Module 16: Medical Specialties Condition Atlas

This version is organized by specialty, not body system. Each specialty lists the conditions it commonly assesses and treats, with pathophysiology, assessment, diagnosis, first-line, second-line, third-line/advanced care, and progression. Similar diseases are not repeated unless the specialty role is different.

Clinical safety: This is a study atlas and navigation layer. Verify exact testing, dosing, contraindications, and current local protocols with the cited sources and product labels.

Family Medicine

Specialty role

First-contact, whole-person, longitudinal care across ages; owns prevention, common acute illness, chronic disease, medication safety, and when to refer.

Family Medicine

Hypertension in primary care

Pathophysiology: Primary hypertension is sustained elevation of systemic arterial pressure from vascular tone, renal sodium handling, sympathetic activity, endothelial dysfunction, genetics, age, obesity, sleep apnea, diet, alcohol, and medication contributors; chronic pressure load injures brain, heart, kidneys, retina, and arteries.

How Family Medicine assesses it: Assess correct cuff size and technique, repeated office BP, home or ambulatory BP readings, ASCVD risk, diabetes/CKD, pregnancy potential, NSAIDs/decongestants/stimulants/OCPs, alcohol/sodium intake, sleep apnea symptoms, secondary hypertension clues, and symptoms of end-organ injury such as chest pain, dyspnea, neurologic deficit, or vision change.

Diagnosis: Confirm with repeated office measurements and preferably home or ambulatory monitoring; evaluate BMP/CMP with creatinine/eGFR and potassium, urine albumin-creatinine ratio or urinalysis, fasting lipids, A1c/glucose, ECG for LVH/ischemia, TSH when suggested, and aldosterone-renin ratio, renal artery imaging, or sleep study for resistant/secondary patterns.

First-line treatment: Lifestyle therapy includes sodium reduction, DASH-style diet, weight loss, exercise, alcohol reduction, sleep apnea treatment, and smoking cessation. First-line drugs include chlorthalidone (Thalitone), hydrochlorothiazide (Microzide), amlodipine (Norvasc), lisinopril (Zestril/Prinivil), or losartan (Cozaar), selected by comorbidity, kidney function, potassium, pregnancy potential, and adverse effects.

Second-line treatment: If above goal, combine complementary first-line classes such as ACE inhibitor/ARB plus calcium-channel blocker or thiazide-like diuretic; check adherence, home readings, diet sodium, NSAID/stimulant use, and adverse effects before intensifying.

Third-line / advanced care: Resistant hypertension needs secondary-cause workup and often spironolactone (Aldactone) if potassium/eGFR allow; urgent ED transfer is needed for hypertensive emergency with acute target-organ injury. Nephrology/cardiology referral is appropriate for resistant, secondary, or complicated disease.

Progression and follow-up: Poor control increases stroke, MI, heart failure, atrial fibrillation, CKD, retinopathy, peripheral arterial disease, vascular dementia, aortic disease, and medication harm from overly aggressive treatment.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Type 2 diabetes longitudinal management

Pathophysiology: Type 2 diabetes combines insulin resistance, progressive beta-cell dysfunction, hepatic glucose overproduction, adipose inflammation, incretin abnormalities, and renal glucose handling, leading to hyperglycemia, microvascular injury, ASCVD, CKD, neuropathy, infection risk, and acute HHS/DKA in severe stress.

How Family Medicine assesses it: Assess symptoms, A1c history, hypoglycemia, diet/activity, weight, steroid/antipsychotic use, ASCVD/HF/CKD, albuminuria, neuropathy/foot risk, retinopathy screening, BP/lipids, injection technique, affordability, health literacy, and pregnancy potential.

Diagnosis: Use A1c, fasting plasma glucose, random glucose with classic symptoms, or 2-hour OGTT; monitor CMP/eGFR, urine albumin-creatinine ratio, fasting lipids, B12 with chronic metformin, foot monofilament/pulse exam, retinal exam, and ketones/anion gap/VBG or serum osmolality when DKA/HHS is possible.

First-line treatment: Use individualized A1c goal, nutrition/activity/weight plan, and metformin (Glucophage) when tolerated. Prefer GLP-1/GIP therapy such as semaglutide (Ozempic/Rybelsus/Wegovy) or tirzepatide (Mounjaro/Zepbound) for weight/A1c needs, and SGLT2 inhibitors empagliflozin (Jardiance) or dapagliflozin (Farxiga) for heart failure or CKD benefit when appropriate.

Second-line treatment: Add or intensify therapy based on phenotype: basal insulin glargine (Lantus/Basaglar/Semglee) for symptomatic or very uncontrolled disease, prandial insulin lispro (Humalog) or aspart (NovoLog) when needed, DPP-4 inhibitor sitagliptin (Januvia), sulfonylurea glipizide (Glucotrol), or pioglitazone (Actos) only when benefits outweigh risks.

Third-line / advanced care: Use CGM such as Dexcom G7 or FreeStyle Libre, diabetes education, endocrinology referral, pump/concentrated insulin for complex insulin needs, and emergency DKA/HHS protocol with IV fluids, regular insulin, potassium, and trigger treatment.

Progression and follow-up: Follow A1c/CGM, renal function, albuminuria, feet, eyes, BP/lipids, vaccine status, hypoglycemia, affordability, and complications including ASCVD, CKD, retinopathy, neuropathy, foot ulcer, infection, HHS/DKA, and treatment-related hypoglycemia.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Hyperlipidemia and ASCVD prevention

Pathophysiology: Atherogenic apoB-containing lipoproteins enter arterial walls, oxidize, trigger inflammation, and form plaques that can rupture or narrow vessels, producing MI, ischemic stroke, PAD, and aortic disease; severe triglyceride elevation can trigger pancreatitis.

How Family Medicine assesses it: Assess known ASCVD, LDL-C level, diabetes, CKD, hypertension, smoking, family history of premature ASCVD, inflammatory disease, premature menopause/preeclampsia, diet/alcohol, secondary causes such as hypothyroidism/nephrotic syndrome, and medication adherence/tolerance.

Diagnosis: Use fasting or nonfasting lipid panel, ASCVD risk estimate for primary prevention, A1c/glucose, TSH and CMP when secondary causes are possible, urine albumin/eGFR when metabolic disease is present, and coronary artery calcium CT when the primary-prevention decision remains uncertain.

First-line treatment: Lifestyle includes Mediterranean/DASH-style eating, reduced saturated/trans fat, exercise, weight management, tobacco cessation, and BP/diabetes control. Drug therapy uses statins when indicated: atorvastatin (Lipitor), rosuvastatin (Crestor), pravastatin (Pravachol), or simvastatin (Zocor); aspirin (Bayer/Ecotrin) is routine for secondary prevention but selective in primary prevention.

Second-line treatment: If LDL-C remains above risk-based goal or statin intolerance occurs, add ezetimibe (Zetia), bempedoic acid (Nexletol/Nexlizet), or PCSK9 therapy alirocumab (Praluent), evolocumab (Repatha), or inclisiran (Leqvio). Use icosapent ethyl (Vascepa) for selected high-triglyceride patients with ASCVD or diabetes risk.

Third-line / advanced care: Refer to lipid/cardiology for familial hypercholesterolemia, recurrent ASCVD despite therapy, very high LDL-C, severe hypertriglyceridemia, or complex statin intolerance; consider fibrate or omega-3 strategy for pancreatitis prevention when triglycerides are very high.

Progression and follow-up: Monitor lipid response, adherence, myalgias, liver symptoms when present, diabetes risk, ASCVD events, pancreatitis risk with severe triglycerides, and medication interactions.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Obesity and metabolic risk

Pathophysiology: Obesity is a chronic adiposity-based disease involving neurohormonal appetite regulation, genetics, sleep, medications, environment, insulin resistance, inflammation, and ectopic fat, increasing diabetes, MASLD/MASH, OSA, hypertension, infertility, osteoarthritis, and ASCVD risk.

How Family Medicine assesses it: Assess BMI, waist circumference, weight trajectory, BP, A1c/glucose, lipids, ALT/AST, sleep apnea symptoms, depression/eating disorder screen, medications that increase weight, pregnancy plans, joint pain, readiness, food access, and prior weight-loss attempts.

Diagnosis: Diagnose by BMI/clinical adiposity and screen complications with A1c, fasting lipids, CMP/liver enzymes, TSH only when symptoms suggest thyroid disease, urine albumin/eGFR with diabetes/HTN, sleep study for OSA symptoms, and fibrosis scoring/elastography when fatty liver risk is present.

First-line treatment: First-line care is intensive lifestyle treatment: nutrition pattern, calorie strategy, physical activity, sleep, behavioral support, and treatment of weight-promoting medications when possible. Anti-obesity medication may include semaglutide (Wegovy), tirzepatide (Zepbound), liraglutide (Saxenda), orlistat (Alli/Xenical), phentermine-topiramate (Qsymia), or naltrexone-bupropion (Contrave) based on contraindications.

Second-line treatment: Treat complications directly with metformin (Glucophage) for diabetes prevention/diabetes when appropriate, GLP-1/GIP or SGLT2 therapy for diabetes/CKD/HF indications, statin/BP therapy, CPAP for OSA, PT for joint limitation, and behavioral health support for binge eating or depression.

Third-line / advanced care: Refer for obesity medicine/endocrinology, dietitian, bariatric/metabolic surgery evaluation such as sleeve gastrectomy or Roux-en-Y gastric bypass, or multidisciplinary care when BMI/comorbidity criteria, medication failure, or severe complications are present.

Progression and follow-up: Follow weight, waist, BP, A1c, lipids, liver risk, OSA, mood, adverse effects, pregnancy risk with medications, muscle preservation, and long-term recurrence prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Depression screening and treatment

Pathophysiology: Major depression involves mood, reward, stress-hormone, sleep, inflammatory, genetic, trauma, substance, and psychosocial pathways that cause persistent low mood or anhedonia with cognitive, somatic, functional, and safety effects.

How Family Medicine assesses it: Use PHQ-9, suicide/self-harm assessment, bipolar screen, substance screen, grief/trauma context, sleep, thyroid/anemia/medication mimics, pregnancy/postpartum status, chronic pain, social stressors, and functional impairment.

Diagnosis: Diagnosis is clinical using DSM criteria supported by PHQ-9 severity; consider TSH, CBC, B12, CMP, pregnancy test, medication review, and urgent safety evaluation for suicidality, psychosis, mania, catatonia, or inability to care for self.

First-line treatment: First-line treatment is shared decision-making with psychotherapy such as CBT/interpersonal therapy, exercise/sleep/substance interventions, and SSRI/SNRI when indicated: sertraline (Zoloft), escitalopram (Lexapro), fluoxetine (Prozac), venlafaxine (Effexor XR), or duloxetine (Cymbalta) when pain/anxiety overlap.

Second-line treatment: If inadequate after an adequate trial, optimize dose, switch medication, or augment with bupropion XL (Wellbutrin XL), mirtazapine (Remeron), buspirone (Buspar), lithium (Lithobid), or aripiprazole (Abilify) depending on symptoms, adverse effects, and bipolar risk.

Third-line / advanced care: Refer urgently for active suicidal intent, psychosis, mania, severe functional collapse, pregnancy complexity, treatment resistance, ECT, TMS, ketamine/esketamine (Spravato), intensive outpatient, or inpatient care.

Progression and follow-up: Follow PHQ-9, sleep, function, suicidality, adherence, adverse effects, sexual side effects, weight, recurrence, substance use, chronic disease adherence, and relapse-prevention duration.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Anxiety disorders in primary care

Pathophysiology: Anxiety disorders reflect threat-circuit sensitization, autonomic arousal, avoidance learning, trauma/substance effects, sleep disruption, and medical mimics, causing excessive worry, panic, somatic symptoms, and avoidance-related disability.

How Family Medicine assesses it: Use GAD-7 or panic symptom review, assess panic attacks/agoraphobia, depression/suicide, bipolar disorder, trauma, caffeine/stimulants/decongestants, substance use, hyperthyroid symptoms, arrhythmia/chest pain, pregnancy, and functional avoidance.

Diagnosis: Diagnosis is clinical using DSM criteria; consider TSH, CBC/CMP, pregnancy test, ECG for palpitations/chest pain, and targeted cardiopulmonary/endocrine testing only when symptoms suggest a mimic.

First-line treatment: First-line care includes CBT/exposure-based therapy, sleep/caffeine reduction, exercise, and SSRI/SNRI such as sertraline (Zoloft), escitalopram (Lexapro), fluoxetine (Prozac), paroxetine (Paxil), venlafaxine XR (Effexor XR), or duloxetine (Cymbalta).

Second-line treatment: For partial response, optimize dose/duration, switch SSRI/SNRI, add buspirone (Buspar) for generalized anxiety, hydroxyzine (Vistaril/Atarax) short-term, propranolol (Inderal) for performance anxiety when safe, or trauma-focused therapy when PTSD features dominate.

Third-line / advanced care: Avoid routine long-term benzodiazepines; limited lorazepam (Ativan) or clonazepam (Klonopin) may be carefully used for short bridging in selected patients. Refer for suicidality, bipolar/psychosis, severe OCD/PTSD, substance use, pregnancy complexity, or treatment resistance.

Progression and follow-up: Follow GAD-7/panic frequency, avoidance, sleep, substance use, medication adverse effects, driving/work impairment, depression/suicide risk, and relapse during taper.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Acute upper respiratory infection

Pathophysiology: Most acute upper respiratory infections are viral inflammation of nasal, pharyngeal, sinus, and airway mucosa; bacterial sinusitis, streptococcal pharyngitis, influenza, COVID-19, pertussis, pneumonia, and asthma/COPD exacerbation are key differentials.

How Family Medicine assesses it: Assess duration, fever pattern, cough, dyspnea, chest pain, wheeze, sore throat, sinus/tooth pain, ear pain, exposure risk, pregnancy, immunocompromise, COPD/asthma, oxygen saturation, lung exam, hydration, and red flags such as hypoxia, meningismus, drooling, or sepsis.

Diagnosis: Usually clinical. Use COVID/flu/RSV testing when results change isolation or antivirals, rapid strep/NAAT when Centor/McIsaac supports testing, chest X-ray for hypoxia/focal lung findings/tachypnea, and avoid routine antibiotics or sinus imaging in uncomplicated viral illness.

First-line treatment: Supportive care includes fluids, honey for cough when age-appropriate, saline, acetaminophen (Tylenol), ibuprofen (Advil/Motrin), guaifenesin (Mucinex), dextromethorphan (Delsym), intranasal fluticasone (Flonase), and ipratropium nasal (Atrovent) for rhinorrhea. Use nirmatrelvir-ritonavir (Paxlovid) or oseltamivir (Tamiflu) only when criteria and timing are met.

Second-line treatment: Treat confirmed strep with penicillin V (Pen VK) or amoxicillin (Amoxil); treat bacterial sinusitis meeting persistent/severe/worsening criteria with amoxicillin-clavulanate (Augmentin) or doxycycline (Vibramycin) when appropriate.

Third-line / advanced care: Escalate to ED/urgent imaging for hypoxia, respiratory distress, sepsis, dehydration, altered mental status, immunocompromised severe illness, peritonsillar abscess, epiglottitis concern, or pneumonia requiring inpatient care.

Progression and follow-up: Most viral URIs resolve in 7-10 days, cough may persist longer; complications include sinusitis, otitis media, pneumonia, asthma/COPD flare, dehydration, inappropriate antibiotic adverse effects, and missed severe infection.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Community-acquired pneumonia outpatient triage

Pathophysiology: Community-acquired pneumonia is infection of alveoli and interstitium, commonly from Streptococcus pneumoniae, respiratory viruses, Haemophilus influenzae, atypicals, aspiration, or gram-negative pathogens in risk groups, causing impaired gas exchange and systemic inflammation.

How Family Medicine assesses it: Assess fever, cough/sputum, pleuritic pain, dyspnea, oxygen saturation, respiratory rate, BP, mental status, age, comorbid heart/lung/liver/kidney disease, immunocompromise, aspiration risk, recent antibiotics, and ability to take oral therapy.

Diagnosis: Use chest X-ray to confirm infiltrate when pneumonia is suspected; check pulse oximetry. CBC/CMP, blood cultures, sputum culture, procalcitonin, or CT chest are reserved for severe, unclear, recurrent, immunocompromised, or nonresponding cases. Use CURB-65/PSI plus clinical judgment for site of care.

First-line treatment: Low-risk outpatient adults without comorbidities may receive amoxicillin (Amoxil), doxycycline (Vibramycin), or azithromycin (Zithromax) only where macrolide resistance is acceptable. Provide antipyretics, hydration, smoking cessation, and follow-up.

Second-line treatment: Outpatients with comorbidities often need amoxicillin-clavulanate (Augmentin) or cefpodoxime/cefuroxime plus doxycycline or azithromycin, or respiratory fluoroquinolone levofloxacin (Levaquin) or moxifloxacin (Avelox) when benefits outweigh risks.

Third-line / advanced care: Send to ED/admit for hypoxia, sepsis, hypotension, confusion, inability to take PO, multilobar disease, empyema, immunocompromise, failed outpatient therapy, or high severity score; inpatient regimens commonly use ceftriaxone (Rocephin) plus azithromycin or levofloxacin by local protocol.

Progression and follow-up: Reassess within 48-72 hours if not improving; complications include respiratory failure, sepsis, pleural effusion/empyema, abscess, arrhythmia, dehydration, C difficile, and missed malignancy if infiltrate fails to clear in high-risk patients.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Urinary tract infection in adult women

Pathophysiology: Uncomplicated cystitis is bacterial infection of the bladder mucosa, usually Escherichia coli ascending from periurethral flora; pyelonephritis involves renal parenchyma and may cause bacteremia or sepsis.

How Family Medicine assesses it: Assess dysuria, frequency, urgency, suprapubic pain, hematuria, fever/flank pain, nausea/vomiting, pregnancy, diabetes/immunocompromise, kidney stone, urologic abnormality, recurrent UTI, vaginal discharge/STI risk, recent antibiotics, and local resistance/allergy history.

Diagnosis: Uncomplicated cystitis can be diagnosed clinically with urinalysis support; obtain urine culture for pregnancy, pyelonephritis, recurrent/complicated infection, recent antibiotics/resistance risk, persistent symptoms, or treatment failure. Use pregnancy test or STI NAAT when history suggests; imaging is for obstruction, stone, sepsis, or nonresponse.

First-line treatment: Uncomplicated cystitis first-line options include nitrofurantoin (Macrobid) for 5 days when renal function is adequate, TMP-SMX (Bactrim DS) for 3 days when resistance/allergy permit, or fosfomycin (Monurol) single dose. Phenazopyridine (Pyridium/AZO) may be used briefly for dysuria.

Second-line treatment: Use cephalexin (Keflex), amoxicillin-clavulanate (Augmentin), or culture-directed therapy when first-line agents are unsuitable. Pyelonephritis needs urine culture and oral fluoroquinolone such as ciprofloxacin (Cipro) or levofloxacin (Levaquin) only when appropriate, often with initial ceftriaxone if resistance risk exists.

Third-line / advanced care: Escalate/admit for pregnancy pyelonephritis, sepsis, obstruction/stone, vomiting/inability to take PO, renal transplant/immunocompromise, resistant organism, or persistent fever; urology evaluation is needed for recurrent complicated infection or anatomic concern.

Progression and follow-up: Complications include pyelonephritis, bacteremia, renal abscess, recurrent UTI, antibiotic resistance, C difficile, yeast vaginitis, and missed STI/vaginitis if symptoms are atypical.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Low back pain initial evaluation

Pathophysiology: Most acute low back pain is mechanical from muscle/ligament strain, disc/facet degeneration, or nonspecific pain sensitization; dangerous causes include fracture, malignancy, infection, cauda equina, inflammatory disease, abdominal/aortic disease, and severe radiculopathy.

How Family Medicine assesses it: Assess onset/trauma, neurologic symptoms, bowel/bladder retention or incontinence, saddle anesthesia, fever, cancer history, injection drug use, steroid/osteoporosis risk, anticoagulation, night pain, weight loss, occupational demands, psychosocial yellow flags, and focused neurologic exam.

Diagnosis: Do not image uncomplicated acute low back pain. Use MRI lumbar spine for cauda equina, infection, malignancy, progressive neurologic deficit, or persistent radiculopathy when intervention is considered; X-ray/CT for trauma/fracture risk; ESR/CRP/CBC for infection/malignancy clues.

First-line treatment: First-line care is reassurance, staying active, heat, time-limited NSAID such as ibuprofen (Advil/Motrin) or naproxen (Aleve/Naprosyn) when safe, acetaminophen (Tylenol) as adjunct, and early PT/exercise for persistent or recurrent pain.

Second-line treatment: Short-term cyclobenzaprine (Flexeril) or methocarbamol (Robaxin) may help selected acute spasm; duloxetine (Cymbalta), gabapentin (Neurontin), or pregabalin (Lyrica) is reserved for chronic/neuropathic patterns after diagnosis is clear. Avoid routine opioids, benzodiazepines, and systemic steroids for nonspecific back pain.

Third-line / advanced care: Urgent ED/spine referral for cauda equina, progressive motor deficit, epidural abscess, fracture instability, cancer cord compression, or severe refractory radiculopathy; consider epidural steroid injection/surgery only for selected imaging-confirmed radiculopathy/stenosis.

Progression and follow-up: Most improves within weeks; monitor pain, function, work status, neurologic changes, medication adverse effects, chronicity risk, opioid exposure, deconditioning, and recurrence prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Osteoarthritis long-term care

Pathophysiology: Osteoarthritis is whole-joint disease involving cartilage loss, subchondral bone remodeling, synovitis, osteophytes, meniscal/ligament change, muscle weakness, pain sensitization, age, obesity, trauma, and genetics.

How Family Medicine assesses it: Assess affected joints, pain pattern, morning stiffness duration, swelling, function, falls, obesity, prior injury, inflammatory signs, joint instability, occupational limits, kidney/GI/CV risk for NSAIDs, and patient goals.

Diagnosis: Usually clinical for hands/knees/hips; weight-bearing X-ray helps when diagnosis is unclear, severity guides referral, or surgery is considered. ESR/CRP, RF/anti-CCP, uric acid, aspiration, or MRI is reserved for inflammatory, crystal, infection, trauma, or atypical disease.

First-line treatment: Core treatment is exercise/PT, weight loss when relevant, assistive devices/bracing, heat/cold, topical diclofenac (Voltaren), acetaminophen (Tylenol) selectively, and oral NSAID such as naproxen (Aleve/Naprosyn) or ibuprofen (Advil/Motrin) only when renal/GI/CV risk is acceptable.

Second-line treatment: Consider duloxetine (Cymbalta) for chronic knee/hip OA pain, intra-articular triamcinolone (Kenalog) for flares, capsaicin for selected hand/knee symptoms, and fall-prevention/strength training. Avoid chronic opioids when possible.

Third-line / advanced care: Orthopedics referral for severe pain/function loss despite conservative therapy, deformity, advanced radiographic disease, or joint replacement evaluation; urgent referral for suspected septic arthritis, fracture, or rapidly destructive joint disease.

Progression and follow-up: Follow pain, function, walking tolerance, sleep, falls, NSAID toxicity, BP/kidney/GI effects, injection frequency, disability, and readiness for surgical discussion.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Migraine initial management

Pathophysiology: Migraine is a recurrent neurovascular brain disorder involving trigeminovascular activation, CGRP signaling, cortical spreading depression, sensory hypersensitivity, genetics, hormones, sleep, stress, and environmental triggers.

How Family Medicine assesses it: Assess headache onset, duration, unilateral/pulsating quality, nausea, photophobia/phonophobia, aura, menstrual pattern, disability, triggers, medication overuse, pregnancy, neurologic deficits, thunderclap onset, cancer/immunosuppression, fever, papilledema, and red flags using SNOOP features.

Diagnosis: Diagnose clinically using migraine criteria; neuroimaging is not needed for stable typical migraine with normal exam. Use MRI/CT urgently for thunderclap, new focal deficit, papilledema, cancer/infection risk, pregnancy/postpartum red flags, trauma, or major pattern change.

First-line treatment: Acute treatment includes early NSAID such as ibuprofen (Advil/Motrin) or naproxen (Aleve/Naprosyn), acetaminophen (Tylenol), antiemetic metoclopramide (Reglan) or prochlorperazine (Compazine), and triptan such as sumatriptan (Imitrex) or rizatriptan (Maxalt) when no vascular contraindication exists.

Second-line treatment: If inadequate, try another triptan or add gepant/ditan such as ubrogepant (Ubrelvy), rimegepant (Nurtec ODT), or lasmiditan (Reyvow). Preventive therapy is considered for frequent/disabling attacks: topiramate (Topamax), propranolol (Inderal), metoprolol (Toprol XL), amitriptyline (Elavil), venlafaxine (Effexor XR), CGRP monoclonal antibodies erenumab (Aimovig), fremanezumab (Ajovy), galcanezumab (Emgality), or atogepant (Qulipta).

Third-line / advanced care: Refer to neurology for refractory migraine, hemiplegic/brainstem aura, medication overuse, chronic migraine needing onabotulinumtoxinA (Botox), pregnancy complexity, or diagnostic uncertainty; ED evaluation for thunderclap or neurologic deficit.

Progression and follow-up: Track headache days, acute medication days, disability, aura changes, medication overuse, triggers, menstrual relation, adverse effects, pregnancy plans, and response after 8-12 weeks of prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

GERD and dyspepsia

Pathophysiology: GERD results from reflux of gastric contents due to lower esophageal sphincter dysfunction, hiatal hernia, impaired clearance, delayed emptying, obesity, pregnancy, and diet/medications; dyspepsia may reflect functional disease, peptic ulcer, H pylori, medication injury, biliary disease, or malignancy.

How Family Medicine assesses it: Assess heartburn/regurgitation, epigastric pain, NSAID/aspirin use, alarm features such as dysphagia, odynophagia, bleeding, anemia, weight loss, persistent vomiting, family GI cancer, age, pregnancy, and cardiac symptoms that can mimic reflux.

Diagnosis: Typical GERD can be treated empirically. Test for H pylori with stool antigen or urea breath test in dyspepsia when appropriate. EGD is indicated for alarm features, dysphagia, GI bleeding, weight loss, persistent vomiting, Barrett risk with chronic reflux, or symptoms refractory to adequate PPI trial.

First-line treatment: Lifestyle care includes weight loss when relevant, head-of-bed elevation, avoiding late meals, tobacco cessation, and trigger review. Use antacids/alginates, famotidine (Pepcid), or PPI such as omeprazole (Prilosec), esomeprazole (Nexium), or pantoprazole (Protonix) for an 8-week trial when indicated.

Second-line treatment: If persistent symptoms, confirm correct PPI timing before breakfast, increase to twice daily temporarily, switch PPI, treat H pylori with guideline regimen such as bismuth quadruple therapy, and review NSAIDs, bisphosphonates, iron, potassium, and GLP-1-related delayed gastric emptying.

Third-line / advanced care: Refer to GI for alarm features, refractory symptoms, suspected Barrett esophagus, strictures, eosinophilic esophagitis, ulcer complications, need for pH impedance/manometry, or anti-reflux procedure evaluation.

Progression and follow-up: Complications include esophagitis, stricture, Barrett esophagus, aspiration, chronic cough/laryngitis, ulcer bleeding, missed cardiac disease, C difficile/fracture/kidney concerns with prolonged PPI use, and recurrent symptoms after stopping therapy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Contraception counseling

Pathophysiology: Contraception counseling matches pregnancy prevention, menstrual control, reproductive goals, medical eligibility, thrombotic risk, drug interactions, STI risk, and patient preference to a safe method.

How Family Medicine assesses it: Assess pregnancy possibility, last menstrual period, postpartum/breastfeeding status, migraine with aura, hypertension, smoking age over 35, VTE/thrombophilia, breast cancer, liver disease, bariatric surgery, antiseizure/rifampin interactions, STI risk, menstrual goals, privacy, and future fertility timing.

Diagnosis: Use urine pregnancy test when pregnancy is uncertain, BP before estrogen-containing methods, STI NAAT when risk is present, Pap/HPV only if due, and CDC medical eligibility criteria to determine method safety; pelvic exam is not required for most hormonal methods but is needed for IUD placement.

First-line treatment: Offer shared decision-making with same-day start when eligible. Highly effective options include levonorgestrel IUD (Mirena/Liletta/Kyleena), copper IUD (Paragard), etonogestrel implant (Nexplanon), depot medroxyprogesterone (Depo-Provera), progestin-only norethindrone (Micronor), drospirenone (Slynd), or combined pills/patch/ring such as ethinyl estradiol/levonorgestrel (Aviane) or etonogestrel/ethinyl estradiol ring (NuvaRing).

Second-line treatment: Emergency contraception options include copper IUD, levonorgestrel (Plan B One-Step), or ulipristal (ella) depending on timing/BMI/contraindications. Manage side effects by switching dose/progestin/route, treating breakthrough bleeding, or choosing nonhormonal/barrier methods.

Third-line / advanced care: Refer for complex medical eligibility, difficult IUD insertion/removal, sterilization counseling, severe adverse effects, suspected pregnancy/ectopic, or contraception in active cancer/thrombosis/transplant settings.

Progression and follow-up: Follow satisfaction, bleeding, BP for estrogen methods, DMPA bone/weight considerations, IUD strings/symptoms, STI prevention, medication interactions, reproductive goals, and warning signs such as severe pelvic pain or VTE symptoms.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Tobacco use disorder

Pathophysiology: Tobacco use disorder is nicotine dependence driven by nicotinic receptor reward pathways, withdrawal avoidance, conditioning, stress, social cues, and product engineering; combustible tobacco causes cancer, COPD, ASCVD, pregnancy harm, and postoperative/wound complications.

How Family Medicine assesses it: Ask every patient about current and past tobacco/nicotine product use, amount, time to first use, quit attempts, triggers, withdrawal, readiness, pregnancy, psychiatric/substance comorbidity, household exposure, lung cancer screening eligibility, and contraindications to medications.

Diagnosis: Clinical diagnosis uses DSM-5 tobacco use disorder features or dependence measures such as time to first cigarette; carbon monoxide testing is optional. Assess pack-years for lung cancer screening, BP/cardiac history for medication choice, and depression/suicide history when using varenicline or bupropion.

First-line treatment: Use brief counseling plus pharmacotherapy unless contraindicated. First-line options include combination nicotine replacement therapy with patch (Nicoderm CQ) plus gum/lozenge (Nicorette/Commit), varenicline (Chantix), or bupropion SR (Zyban/Wellbutrin SR). Provide quit date or reduce-to-quit plan, trigger plan, and quitline/text/app support.

Second-line treatment: If relapse occurs, extend duration, combine varenicline with NRT in selected patients, switch medication, intensify behavioral counseling, address alcohol/cannabis/mental health triggers, and treat withdrawal/weight-gain concerns.

Third-line / advanced care: Refer to tobacco treatment specialist, behavioral health, or pulmonary/cardiology prevention program for repeated relapse, pregnancy complexity, severe psychiatric instability, or high medical risk; screen eligible adults for lung cancer with low-dose CT per USPSTF criteria.

Progression and follow-up: Follow abstinence, slips, withdrawal, mood/suicidality, sleep/vivid dreams, BP, nicotine toxicity, weight, COPD/asthma control, ASCVD risk, cancer screening, and household secondhand exposure.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Alcohol use disorder screening

Pathophysiology: Alcohol use disorder and unhealthy alcohol use reflect reward circuitry, tolerance, withdrawal physiology, genetic risk, trauma/psychiatric comorbidity, and social context; harms include liver disease, pancreatitis, hypertension, cancer, arrhythmias, neuropathy, injury, fetal alcohol exposure, and medication interactions.

How Family Medicine assesses it: Screen with AUDIT-C or single-question screen, quantify drinks/week and binge pattern, assess DSM-5 criteria, withdrawal history/seizures/DTs, liver disease, pancreatitis, falls/injuries, depression/suicide, pregnancy, driving/work safety, and concurrent opioids/benzodiazepines.

Diagnosis: Use AUDIT-C/AUDIT and clinical interview; labs can support harm assessment with CMP/AST/ALT/bilirubin, CBC/MCV, INR, GGT when useful, hepatitis screening when indicated, pregnancy test when relevant, and CIWA-Ar only for withdrawal monitoring, not screening.

First-line treatment: Provide brief intervention, motivational interviewing, harm-reduction or abstinence goal, thiamine when malnutrition/withdrawal risk exists, and medication for moderate/severe AUD when appropriate: naltrexone oral (Revia) or injection (Vivitrol) if no opioid use/severe liver failure, or acamprosate (Campral) when renal function allows.

Second-line treatment: Alternatives include disulfiram (Antabuse) for highly supervised abstinence, gabapentin (Neurontin) or topiramate (Topamax) in selected off-label situations, plus CBT, mutual-help groups, contingency management, or integrated mental health care.

Third-line / advanced care: Medically supervised withdrawal or ED/inpatient care is needed for severe withdrawal history, seizures/DTs, unstable vitals, pregnancy, serious comorbidity, suicidality, polysubstance sedatives, or inability to maintain hydration/safety.

Progression and follow-up: Follow drinking days, heavy drinking days, cravings, liver enzymes, mood/suicide risk, sleep, medication adherence, opioid interaction with naltrexone, relapse triggers, injuries, BP, and family/social safety.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Preventive immunizations

Pathophysiology: Preventive immunization primes adaptive immunity before exposure, reducing severe disease, transmission, cancer risk for HPV/hepatitis B, pregnancy complications, and outbreaks; schedules vary by age, pregnancy, immune status, occupation, travel, and prior vaccines.

How Family Medicine assesses it: Review vaccine records, age, pregnancy, immunocompromise, asplenia, diabetes, CKD/liver/lung/heart disease, smoking, sexual risk, occupational exposure, travel, prior reactions, Guillain-Barre history when relevant, allergies, and live-vaccine contraindications.

Diagnosis: No disease diagnosis is required; reconcile records in the state registry/EHR, identify gaps using the current CDC adult/child schedule, and use targeted serology only when documentation is absent and immunity status matters, such as hepatitis B, varicella, or measles in select patients.

First-line treatment: Use current CDC schedule: annual influenza, updated COVID-19 vaccination, Tdap once then Td/Tdap boosters, RSV vaccine for eligible older or pregnant patients, pneumococcal PCV20 or PCV15/PPSV23 strategy by age/risk, recombinant zoster vaccine Shingrix, HPV vaccine Gardasil 9 through routine/catch-up/shared decision ages, and hepatitis B vaccination for adults by age/risk.

Second-line treatment: Special-risk vaccines include meningococcal ACWY/B, Hib for asplenia/transplant indications, hepatitis A for risk/travel/liver disease, MMR/varicella when nonimmune and not contraindicated, mpox for risk groups, and travel vaccines through travel medicine.

Third-line / advanced care: Defer or specialist-review live vaccines in severe immunocompromise/pregnancy, evaluate anaphylaxis to prior vaccine/component, and coordinate post-exposure prophylaxis or immunoglobulin for rabies, hepatitis B, varicella, measles, or tetanus-prone wounds when indicated.

Progression and follow-up: Follow completion of multi-dose series, adverse events, documentation, future due dates, pregnancy timing, immunocompromise changes, and missed opportunities during chronic disease visits.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Family Medicine

Cancer screening coordination

Pathophysiology: Cancer screening coordination is prevention care that detects precancer or early asymptomatic cancer before symptoms, using age/risk-based tests where benefit outweighs overdiagnosis, false positives, radiation, procedural harm, anxiety, and downstream biopsy risk.

How Family Medicine assesses it: Assess age, sex organs present, family history, genetic syndromes, smoking pack-years, prior abnormal tests/polyps, immunosuppression, DES exposure, HPV status, life expectancy, comorbidities, patient preferences, and whether symptoms require diagnostic rather than screening evaluation.

Diagnosis: Use USPSTF/CDC/specialty-aligned screening: mammography for eligible breast cancer screening, colorectal screening with FIT annually, stool DNA-FIT, CT colonography, sigmoidoscopy, or colonoscopy by risk and prior results; cervical cytology/HPV testing by age/history; annual low-dose CT for eligible smoking history; and individualized PSA discussion for prostate screening.

First-line treatment: Coordinate shared decisions, order the right screening test, ensure bowel prep/navigation when colonoscopy is chosen, track results, and close the loop on abnormal findings. Continue HPV vaccination when eligible and address tobacco cessation, hepatitis B/C, obesity, alcohol, sun protection, and occupational risks.

Second-line treatment: Abnormal screens require disease-specific follow-up: diagnostic mammogram/ultrasound and biopsy for suspicious breast findings, colonoscopy after positive stool test, colposcopy for abnormal cervical screening, Lung-RADS follow-up or pulmonology/thoracic referral after LDCT findings, and urology evaluation after concerning PSA/DRE.

Third-line / advanced care: Refer genetics/high-risk clinic for BRCA/Lynch/polyposis patterns, very strong family history, young cancers, or multiple primaries; stop screening when harms exceed benefit because of limited life expectancy or patient preference after informed discussion.

Progression and follow-up: Track completion, results, pathology, recall intervals, incidental findings, over-screening, under-screening, anxiety, insurance/access barriers, and conversion of positive screening tests into timely diagnostic care.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Specialty role

Adult diagnostic synthesis for complex multimorbidity, inpatient transitions, medication reconciliation, and chronic disease integration.

Internal Medicine

Multimorbidity medication review

Pathophysiology: Multimorbidity medication review prevents therapeutic conflict, prescribing cascades, renal/hepatic dosing errors, duplication, drug-drug interactions, and goal-discordant treatment in adults with several chronic diseases.

How Internal Medicine assesses it: Reconcile every prescription, OTC, supplement, inhaler, injection, topical, and PRN drug with indication, dose, frequency, adherence, cost, adverse effects, allergies, alcohol/substance use, falls, cognition, kidney/liver function, pregnancy potential, and patient goals.

Diagnosis: Use a structured medication list, problem-to-medication mapping, eGFR/creatinine clearance, liver enzymes when relevant, potassium/sodium, A1c/BP/lipids only when they guide therapy, Beers Criteria and STOPP/START concepts for older adults, anticholinergic/sedative burden, QT-risk review, and interaction check for anticoagulants, opioids, benzodiazepines, gabapentinoids, NSAIDs, and RAAS/MRA drugs.

First-line treatment: First-line care is reconciliation plus shared deprescribing: stop duplicate/no-indication drugs, simplify once-daily dosing, align refills, correct renal dosing, replace high-risk agents such as diphenhydramine (Benadryl) or chronic NSAIDs when possible, and prioritize high-value therapies such as statins, BP agents, diabetes agents, and anticoagulation only when benefits fit goals.

Second-line treatment: Taper medications that require tapering, such as benzodiazepines, clonidine (Catapres), beta blockers, gabapentin (Neurontin), opioids, or antidepressants; substitute safer options such as acetaminophen (Tylenol), topical diclofenac (Voltaren), melatonin, or non-drug therapy when appropriate.

Third-line / advanced care: Refer to clinical pharmacy, geriatrics, nephrology, cardiology, psychiatry, or pain/addiction medicine for complex anticoagulation, recurrent falls, delirium, QT prolongation, opioid/benzodiazepine overlap, transplant/chemotherapy regimens, or severe renal/hepatic impairment.

Progression and follow-up: Follow withdrawal symptoms, symptom recurrence, BP/glucose changes, renal function, potassium, INR/DOAC dosing, falls, cognition, adherence, pill burden, cost, hospitalizations, and patient-prioritized outcomes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Hospital discharge follow-up

Pathophysiology: Hospital discharge follow-up reduces post-acute deterioration caused by incomplete diagnostic closure, medication changes, functional decline, infection, volume shifts, procedure complications, and poor handoff communication.

How Internal Medicine assesses it: Review discharge diagnosis, pending tests/cultures/pathology, medication changes, stopped drugs, new oxygen/wound/drain/catheter needs, home services, functional status, red flags, follow-up appointments, patient understanding, and barriers to obtaining medications or equipment.

Diagnosis: Compare discharge summary with prehospital medication list, vitals/weight, focused exam, BMP/CBC/INR/drug levels when indicated by the hospitalization, culture/pathology follow-up, imaging follow-up requirements, and readmission-risk factors such as frailty, HF, CKD, COPD, sepsis, anticoagulation, or poor support.

First-line treatment: First-line care is medication reconciliation, condition-specific action plan, early follow-up timing based on acuity, refill access, warning signs, home BP/glucose/weight plan when relevant, and closed-loop scheduling with specialists, PT/OT, wound care, or home health.

Second-line treatment: Adjust medications based on renal function, BP, volume status, infection response, anticoagulation status, and adverse effects; restart held chronic medications only when safe, such as ACE inhibitors/ARBs/diuretics after AKI or metformin (Glucophage) after contrast/AKI when renal function allows.

Third-line / advanced care: Escalate to ED/readmission for hypoxia, hypotension, sepsis signs, chest pain, neurologic deficit, worsening renal failure/hyperkalemia, uncontrolled pain, bleeding on anticoagulants, inability to take PO meds, unsafe home situation, or worsening wound/procedure complication.

Progression and follow-up: Track readmission, unresolved diagnosis, pending-result closure, adverse drug events, falls, deconditioning, nutrition, caregiver strain, appointment completion, and whether the patient can accurately explain the plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Unintentional weight loss

Pathophysiology: Unintentional weight loss reflects negative energy balance from malignancy, chronic infection, endocrine disease, GI malabsorption, cardiopulmonary disease, renal/liver disease, inflammatory disease, depression, dementia, substance use, food insecurity, or medication adverse effects.

How Internal Medicine assesses it: Quantify percent and time course, appetite, dysphagia, early satiety, bowel changes, fever/night sweats, pain, cough, bleeding, depression, cognition, alcohol/drugs, dental/oral symptoms, food access, medication changes such as GLP-1 agonists/stimulants, and cancer screening status.

Diagnosis: Initial workup usually includes CBC with differential, CMP, TSH, ESR/CRP, urinalysis, HIV/hepatitis/TB testing when risk suggests, A1c, stool occult blood/FIT when appropriate, chest X-ray, age-appropriate cancer screening, and targeted CT/EGD/colonoscopy based on symptoms rather than indiscriminate whole-body imaging.

First-line treatment: Treat identified cause, stop appetite-suppressing/offending medications when possible, address food insecurity, oral/dental disease, nausea/constipation, depression, and provide nutrition support with protein/calorie targets and resistance exercise when safe.

Second-line treatment: Use condition-specific therapy: omeprazole (Prilosec) for ulcer/GERD when indicated, mirtazapine (Remeron) for depression with poor appetite when appropriate, pancreatic enzymes for pancreatic insufficiency, or infection/malignancy therapy after diagnosis. Avoid appetite stimulants as a substitute for evaluation.

Third-line / advanced care: Urgent referral/admission for severe malnutrition, dehydration, GI bleeding, dysphagia/aspiration, suspected cancer with alarm symptoms, systemic infection, adrenal crisis, or inability to maintain intake; involve nutrition, GI, oncology, geriatrics, or social work as indicated.

Progression and follow-up: Follow weight trend, intake, strength/function, labs, symptom evolution, screening completion, medication effects, refeeding risk in severe malnutrition, and whether no diagnosis after observation requires re-evaluation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Fever of unknown origin initial workup

Pathophysiology: Fever of unknown origin is persistent documented fever without diagnosis after initial evaluation; major categories are infection, malignancy, systemic inflammatory/autoimmune disease, drug fever, thromboembolism, endocrine disease, and factitious or periodic fever syndromes.

How Internal Medicine assesses it: Confirm true temperature pattern and duration, travel, animal/tick exposure, TB risk, HIV risk, immunosuppression, prosthetic valves/joints, indwelling lines, dental symptoms, weight loss/night sweats, rash, arthritis, headache/vision symptoms, medications, and focal exam findings including lymph nodes, murmurs, abdomen, skin, and temporal arteries.

Diagnosis: Initial testing includes CBC with differential, CMP/LFTs, ESR/CRP, urinalysis/culture, two or more blood culture sets before antibiotics if bacteremia possible, HIV Ag/Ab, hepatitis testing, TB IGRA when risk, chest X-ray, age-appropriate cancer screening, and targeted CT chest/abdomen/pelvis, echocardiography, PET/CT, biopsy, or rheumatologic tests only when clues support them.

First-line treatment: Avoid empiric antibiotics or steroids in stable immunocompetent adults until cultures/diagnosis are pursued; stop possible culprit drugs when safe, treat dehydration/pain with acetaminophen (Tylenol), and arrange close follow-up with a fever diary and result tracking.

Second-line treatment: Use targeted treatment only after a likely diagnosis emerges, such as ceftriaxone (Rocephin)/vancomycin (Vancocin) for suspected endocarditis per cultures, prednisone (Deltasone) only for confirmed inflammatory disease, or malignancy-specific referral after biopsy.

Third-line / advanced care: Admit/escalate for sepsis, neutropenia, transplant/immunocompromise, endocarditis suspicion with instability, meningitis, temporal arteritis with vision symptoms, hypoxia, severe cytopenias, or inability to complete outpatient evaluation.

Progression and follow-up: Follow fever curve, weight, inflammatory markers, cultures, imaging/biopsy results, new localizing symptoms, medication changes, and harms from premature broad antibiotics or steroids.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Anemia diagnostic approach

Pathophysiology: Anemia is reduced red-cell mass or hemoglobin from blood loss, iron deficiency, B12/folate deficiency, inflammation/CKD, hemolysis, marrow disease, hemoglobinopathy, endocrine disease, or medication/toxin effect.

How Internal Medicine assesses it: Assess fatigue, dyspnea, chest pain, syncope, bleeding, melena, heavy menses, diet, bariatric surgery, alcohol, kidney disease, inflammatory disease, cancer symptoms, anticoagulants/NSAIDs, neurologic symptoms, family history, and hemodynamic stability.

Diagnosis: Start with CBC indices, RDW, reticulocyte count, peripheral smear, ferritin/iron/TIBC/transferrin saturation, B12, folate, creatinine/eGFR, bilirubin/LDH/haptoglobin/DAT for hemolysis, TSH when indicated, stool testing/endoscopy for iron-deficiency or GI symptoms, and bone marrow evaluation for unexplained cytopenias or abnormal smear.

First-line treatment: Treat by cause: ferrous sulfate (Feosol) or alternate-day oral iron for iron deficiency, IV iron sucrose (Venofer) or ferric carboxymaltose (Injectafer) when oral iron fails/rapid repletion needed, cyanocobalamin (Vitamin B12/Nascobal) for B12 deficiency, folic acid (Folvite), and stop bleeding/offending drugs.

Second-line treatment: Use erythropoiesis-stimulating agents such as epoetin alfa (Epogen/Procrit) only for selected CKD/chemo contexts with iron repletion; transfuse packed RBCs for symptomatic severe anemia or unstable bleeding using restrictive thresholds unless active ischemia/bleeding changes the target.

Third-line / advanced care: Urgent ED/hematology/GI referral for hemodynamic instability, acute GI bleeding, hemolytic crisis, severe pancytopenia, blasts, suspected leukemia/aplastic anemia, or neurologic B12 complications.

Progression and follow-up: Follow hemoglobin response, reticulocytes, ferritin/TSAT, source control, occult malignancy evaluation, transfusion reactions, iron constipation, B12 neurologic recovery, and recurrence after treatment.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Syncope in adults

Pathophysiology: Syncope is transient loss of consciousness from global cerebral hypoperfusion due to reflex vasovagal mechanisms, orthostatic hypotension, arrhythmia, structural cardiac disease, pulmonary embolism, bleeding, or medication effect.

How Internal Medicine assesses it: Assess position, prodrome, exertional/supine onset, palpitations, chest pain, dyspnea, neurologic symptoms, seizure features, injury, family sudden death, heart disease, dehydration/bleeding, orthostatic vitals, and medications such as antihypertensives, diuretics, QT-prolongers, sedatives, and alcohol.

Diagnosis: Obtain ECG and orthostatic BP/HR for nearly all adults; use glucose if hypoglycemia possible. CBC/CMP/troponin/D-dimer, echocardiogram, ambulatory monitor, stress test, or CT pulmonary angiography are targeted to history/exam/ECG. Avoid routine head CT, EEG, carotid ultrasound, or broad labs when no neurologic or cardiac clues exist.

First-line treatment: Low-risk vasovagal/orthostatic syncope uses education, hydration, salt if safe, counterpressure maneuvers, medication reduction, compression stockings, and trigger avoidance.

Second-line treatment: Treat cause-specific disease: adjust diuretics/vasodilators, manage anemia/bleeding, use fludrocortisone (Florinef) or midodrine (ProAmatine) for selected refractory orthostatic hypotension, and initiate arrhythmia/structural heart evaluation when suspected.

Third-line / advanced care: ED/admit/cardiology for exertional or supine syncope, abnormal ECG, severe anemia/bleeding, hypotension, heart failure, chest pain/ACS, PE, family sudden death, significant injury, or suspected malignant arrhythmia requiring pacemaker/ICD/ablation.

Progression and follow-up: Track recurrence, injuries, driving/work safety, BP logs, medication changes, arrhythmia detection, hydration/nutrition, and whether the diagnosis remains uncertain after recurrent episodes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Chronic kidney disease with diabetes

Pathophysiology: Diabetic CKD arises from glomerular hyperfiltration, albuminuria, podocyte injury, vascular disease, inflammation, and interstitial fibrosis, accelerating ASCVD, heart failure, anemia, mineral-bone disease, acidosis, and medication toxicity.

How Internal Medicine assesses it: Assess diabetes duration/control, BP, albuminuria, eGFR trend, hematuria/active sediment, retinopathy, neuropathy, HF/ASCVD, NSAID/contrast exposure, recurrent AKI, family kidney disease, urinary obstruction, and hypoglycemia risk as kidney function falls.

Diagnosis: Stage by eGFR and urine albumin-creatinine ratio, repeated for chronicity; monitor BMP/CMP, potassium, bicarbonate, calcium/phosphorus/PTH/vitamin D when advanced, CBC for anemia, lipids, A1c/CGM with awareness of CKD limitations, renal ultrasound or serologic workup when atypical features occur.

First-line treatment: Use BP control, sodium reduction, diabetes optimization, ACE inhibitor/ARB such as lisinopril (Zestril) or losartan (Cozaar) for albuminuria if tolerated, SGLT2 inhibitor empagliflozin (Jardiance) or dapagliflozin (Farxiga) when eGFR criteria allow, statin therapy, and avoid NSAIDs/nephrotoxins.

Second-line treatment: Add finerenone (Kerendia) for selected type 2 diabetes with albuminuric CKD despite ACE/ARB and safe potassium; GLP-1 RA such as semaglutide (Ozempic) or dulaglutide (Trulicity) helps glycemia/weight/CV risk; adjust metformin, insulin, gabapentin, DOACs, and antibiotics for eGFR.

Third-line / advanced care: Nephrology referral for rapid decline, eGFR below 30, severe albuminuria, resistant hypertension, hyperkalemia/acidosis, active urine sediment, uncertain cause, dialysis education, transplant planning, or recurrent AKI.

Progression and follow-up: Follow eGFR slope, albuminuria, potassium, acidosis, anemia, mineral-bone disease, hypoglycemia, HF/ASCVD events, medication dosing, vaccine status, and dialysis/transplant readiness.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Polypharmacy adverse drug events

Pathophysiology: Polypharmacy adverse drug events occur when cumulative pharmacologic burden, interactions, age-related pharmacokinetics, renal/hepatic impairment, duplicate therapy, and prescribing cascades cause symptoms misread as new disease.

How Internal Medicine assesses it: Assess falls, confusion, dizziness, orthostasis, constipation, urinary retention, bleeding, hypoglycemia, sedation, QT symptoms, kidney injury, new symptoms after medication changes, OTC antihistamines/sleep aids, NSAIDs, supplements, alcohol, and adherence complexity.

Diagnosis: Perform medication timeline analysis, renal/hepatic dosing check, orthostatic vitals, glucose/A1c if hypoglycemia possible, BMP for sodium/potassium/creatinine, CBC for bleeding/cytopenias, INR/anti-Xa context when anticoagulated, ECG for QT/bradycardia, and Beers Criteria review in adults 65+.

First-line treatment: Stop or reduce the likely culprit when safe, correct dehydration/electrolytes, simplify dosing, remove duplicate drugs, avoid high-risk combinations such as opioid plus benzodiazepine or gabapentinoid, and educate patient/caregiver on a single accurate medication list.

Second-line treatment: Substitute safer therapy: topical diclofenac (Voltaren) instead of chronic oral NSAID when appropriate, acetaminophen (Tylenol) within safe limits, non-drug insomnia/anxiety care instead of diphenhydramine (Benadryl) or benzodiazepines, and renal-adjusted alternatives.

Third-line / advanced care: Urgent care for major bleeding, severe hypoglycemia, serotonin syndrome, neuroleptic malignant syndrome, severe hyponatremia/hyperkalemia, torsades/QT crisis, overdose, or delirium with unsafe home situation; involve pharmacy/toxicology/geriatrics when complex.

Progression and follow-up: Follow symptom resolution after deprescribing, withdrawal, recurrent pain/anxiety/insomnia, labs, falls, cognition, adherence, caregiver burden, and new prescribing cascades.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Edema differential diagnosis

Pathophysiology: Edema reflects increased hydrostatic pressure, reduced oncotic pressure, lymphatic obstruction, venous disease, capillary leak, medication effect, or sodium/water retention from heart, kidney, liver, endocrine, vascular, or inflammatory disease.

How Internal Medicine assesses it: Assess unilateral vs bilateral, acute vs chronic, pitting, pain/redness, dyspnea/orthopnea, weight gain, JVP, ascites, varicosities, pregnancy, immobility, cancer/VTE risk, kidney/liver disease, proteinuria, thyroid symptoms, and drugs such as amlodipine, NSAIDs, steroids, pioglitazone, and gabapentin.

Diagnosis: Use targeted tests: BMP/eGFR, urinalysis and urine protein/albumin, CMP/albumin/LFTs, BNP/NT-proBNP, TSH when indicated, ECG/chest X-ray/echocardiogram for HF, venous duplex ultrasound for suspected DVT/venous insufficiency, and abdominal imaging for ascites/liver/IVC obstruction when suggested.

First-line treatment: Treat cause: leg elevation/compression for venous disease after arterial disease is excluded, sodium restriction and loop diuretic furosemide (Lasix) for HF/renal volume overload, stop offending drugs when possible, and manage hypothyroidism, nephrotic syndrome, or cirrhosis specifically.

Second-line treatment: Escalate diuretics with torsemide (Demadex), bumetanide (Bumex), or metolazone (Zaroxolyn) only with close electrolyte/renal monitoring; anticoagulate confirmed DVT with apixaban (Eliquis), rivaroxaban (Xarelto), enoxaparin (Lovenox), or warfarin (Coumadin) by context.

Third-line / advanced care: Urgent evaluation for acute unilateral swelling with DVT/compartment/infection concern, pulmonary edema, anasarca with renal/liver failure, cellulitis/sepsis, or suspected SVC/IVC obstruction/malignancy.

Progression and follow-up: Follow weight, edema grade, renal function, potassium/sodium, skin breakdown, ulcers, dyspnea, medication adverse effects, DVT/PE risk, and recurrence after diuretic or compression changes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Dyspnea differential diagnosis

Pathophysiology: Dyspnea arises from cardiopulmonary, hematologic, metabolic, neuromuscular, obesity/deconditioning, anxiety, medication, or systemic disease that increases ventilatory drive, impairs gas exchange, reduces cardiac output, or causes respiratory muscle load.

How Internal Medicine assesses it: Assess onset, exertional/rest symptoms, chest pain, wheeze, cough/fever, orthopnea/PND, edema, hemoptysis, VTE risk, anemia/bleeding, smoking, occupational exposure, pregnancy, panic symptoms, oxygen saturation, lung/cardiac exam, and medication triggers.

Diagnosis: Initial tests often include pulse oximetry, ECG, chest X-ray, CBC, BMP/CMP, BNP/NT-proBNP, troponin when ischemia possible, D-dimer/CT pulmonary angiography when PE risk supports it, spirometry for obstructive disease, echocardiogram for HF/valves/pulmonary hypertension, and ABG/VBG for severe disease.

First-line treatment: Treat the identified cause: albuterol (Ventolin/ProAir) for bronchospasm, furosemide (Lasix) for HF congestion, antibiotics for confirmed pneumonia, iron/B12 therapy for anemia, anticoagulation for PE, and oxygen only when hypoxemia criteria are met.

Second-line treatment: If diagnosis remains unclear, pursue pulmonary function testing, high-resolution CT, stress testing, cardiopulmonary exercise testing, sleep study, or specialist referral guided by abnormal findings rather than repeating nonspecific testing.

Third-line / advanced care: ED/admit for hypoxia, respiratory distress, ACS, PE, pulmonary edema, sepsis, pneumothorax, severe asthma/COPD exacerbation, stridor, neuromuscular weakness, or rapidly progressive symptoms.

Progression and follow-up: Follow exertional capacity, oxygen saturation, weight, lung function, anemia markers, BNP/echo response, medication adverse effects, recurrence, and functional deconditioning.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Fatigue diagnostic approach

Pathophysiology: Fatigue is reduced energy or endurance from sleep disorders, depression/anxiety, anemia, endocrine disease, cardiopulmonary disease, infection/inflammation, CKD/liver disease, medication/substance effects, malignancy, autoimmune disease, or deconditioning.

How Internal Medicine assesses it: Assess duration, sleep quality/OSA, mood, exertional intolerance, weight loss/fever/night sweats, pain, dyspnea, bleeding, menstrual history, thyroid symptoms, medications/sedatives, alcohol/cannabis, work stress, pregnancy, and functional impairment.

Diagnosis: Use focused testing rather than exhaustive panels: CBC, CMP, TSH, A1c/glucose, ferritin/iron or B12 when risk suggests, ESR/CRP when inflammatory symptoms exist, pregnancy test when relevant, sleep apnea screening, PHQ-9/GAD-7, and targeted cardiac/pulmonary/infectious/cancer tests based on clues.

First-line treatment: Treat identifiable causes, optimize sleep, exercise gradually, nutrition, hydration, depression/anxiety therapy, medication reduction, CPAP for OSA, iron/B12 replacement, and chronic disease control.

Second-line treatment: If persistent unexplained fatigue, reassess history/exam, verify sleep/mood/substance factors, review new medications, consider post-viral/long COVID or ME/CFS criteria, and avoid unproven stimulant therapy unless a defined indication exists.

Third-line / advanced care: Urgent evaluation for fatigue with chest pain, severe dyspnea, syncope, neurologic deficit, GI bleeding, severe anemia, adrenal crisis, sepsis, suicidal ideation, or cancer alarm features.

Progression and follow-up: Follow function, sleep metrics, mood scores, weight, lab abnormalities, medication changes, exercise tolerance, and emergence of localizing signs over time.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Electrolyte abnormalities in adults

Pathophysiology: Electrolyte abnormalities reflect kidney function, intake/losses, medications, endocrine disease, acid-base disorders, volume status, and cell shifts; sodium, potassium, calcium, magnesium, and bicarbonate disorders can cause neurologic, cardiac, and muscular emergencies.

How Internal Medicine assesses it: Assess symptoms such as weakness, confusion, seizure, palpitations, paralysis, vomiting/diarrhea, diuretic/laxative use, ACE/ARB/MRA/SGLT2/NSAIDs, kidney disease, adrenal disease, heart failure/cirrhosis, fluid intake, alcohol use, and ECG instability.

Diagnosis: Repeat unexpected critical values, check BMP/CMP, magnesium, phosphorus, serum osmolality, urine sodium/osmolality for hyponatremia, acid-base status with VBG/ABG, glucose correction for sodium, CK for rhabdomyolysis, medication review, and ECG for potassium/calcium abnormalities.

First-line treatment: Treat severity-specific: oral/IV potassium chloride for hypokalemia, calcium gluconate plus insulin/dextrose, albuterol, sodium bicarbonate when indicated, and potassium binders sodium zirconium cyclosilicate (Lokelma) or patiromer (Veltassa) for hyperkalemia; fluid restriction or isotonic saline for hyponatremia based on volume status.

Second-line treatment: Correct magnesium deficiency with magnesium sulfate/oxide, treat hypercalcemia with IV fluids and bisphosphonate zoledronic acid (Zometa) when appropriate, use desmopressin/D5W to prevent overcorrection of severe hyponatremia when needed, and stop culprit medications.

Third-line / advanced care: ICU/nephrology for severe symptomatic hyponatremia needing hypertonic saline, ECG changes from potassium/calcium, severe renal failure, rhabdomyolysis, adrenal crisis, tumor lysis, or need for dialysis.

Progression and follow-up: Follow correction rate, ECG, neurologic status, renal function, recurrence, medication contributors, overcorrection risk such as osmotic demyelination, and outpatient monitoring after drug changes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Frailty with chronic disease

Pathophysiology: Frailty is reduced physiologic reserve from sarcopenia, inflammation, malnutrition, multimorbidity, inactivity, cognitive/mood disease, and social vulnerability, increasing vulnerability to hospitalization, falls, delirium, disability, and medication harm.

How Internal Medicine assesses it: Assess gait speed, grip strength, unintentional weight loss, exhaustion, activity level, ADLs/IADLs, falls, cognition, mood, nutrition, polypharmacy, pain, vision/hearing, social support, goals of care, and chronic disease burden.

Diagnosis: Use Clinical Frailty Scale or phenotype/deficit approach, Timed Up and Go, Mini-Cog/MoCA when cognition concern, PHQ-9, nutrition screen, orthostatic vitals, medication review, and targeted labs such as CBC/CMP/TSH/B12/vitamin D only when clinically indicated.

First-line treatment: First-line care is resistance/balance exercise or PT, protein/calorie optimization, vitamin D only if deficient/at risk, deprescribing high-risk medications, vision/hearing correction, fall prevention, vaccines, and goal-concordant chronic disease targets rather than disease-maximal targets.

Second-line treatment: Treat contributors such as anemia, hypothyroidism, depression, pain, OSA, heart failure, COPD, or diabetes overtreatment; involve OT, nutrition, social work, caregiver support, and community exercise/fall programs.

Third-line / advanced care: Geriatrics/palliative referral for severe frailty, recurrent hospitalizations, advanced dementia, caregiver collapse, unsafe home, complex deprescribing, or need for advance care planning and home-based services.

Progression and follow-up: Follow function, falls, weight, strength, cognition, medication burden, hospitalizations, caregiver stress, home safety, and whether treatment goals remain realistic.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Internal Medicine

Anticoagulation safety review

Pathophysiology: Anticoagulation safety review balances thromboembolism prevention against bleeding risk, renal/hepatic dosing, drug interactions, adherence, procedure timing, falls, and patient goals.

How Internal Medicine assesses it: Confirm indication (AF, VTE, mechanical valve, LV thrombus), intended duration, CHA2DS2-VASc/HAS-BLED or VTE recurrence/bleeding context, renal function, liver disease, age/weight, prior bleeding, falls, alcohol, NSAIDs/antiplatelets, pregnancy, cost/adherence, and upcoming procedures.

Diagnosis: Check CBC, creatinine/eGFR or CrCl, LFTs when indicated, INR for warfarin, medication interaction review including amiodarone/azole/macrolide/antiepileptic/rifampin, and assess DOAC dose criteria for apixaban (Eliquis), rivaroxaban (Xarelto), dabigatran (Pradaxa), or edoxaban (Savaysa).

First-line treatment: Use the safest indicated agent/dose: DOACs for most nonvalvular AF/VTE when appropriate, warfarin (Coumadin/Jantoven) for mechanical valves, moderate-to-severe rheumatic mitral stenosis, or selected renal/cost situations; educate on adherence, bleeding signs, NSAID avoidance, and procedure communication.

Second-line treatment: Adjust dose for renal function/age/weight/interaction, stop unnecessary aspirin/clopidogrel when not indicated, manage INR instability with diet/drug review, and plan peri-procedural interruption/bridging only when thrombotic risk truly requires it.

Third-line / advanced care: Urgent care for major bleeding, head trauma, severe anemia, spinal/retroperitoneal bleed, or thrombosis on therapy. Reversal options include vitamin K and PCC for warfarin, idarucizumab (Praxbind) for dabigatran, and andexanet alfa (Andexxa) or PCC strategies for factor Xa inhibitors by protocol.

Progression and follow-up: Follow bleeding, bruising, hemoglobin, renal function, adherence, missed doses, interactions, falls, procedure needs, recurrent VTE/stroke, and whether anticoagulation remains goal-concordant.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Specialty role

Infant, child, and adolescent care with growth, development, immunization, family context, weight-based dosing, and age-specific red flags.

Pediatrics

Fever in infants and children

Pathophysiology: Pediatric fever is usually viral, but age, appearance, immune status, and source determine risk for UTI, bacteremia, meningitis, pneumonia, Kawasaki disease/MIS-C, sepsis, or focal bacterial infection; infants under 60 days require age-stratified serious bacterial infection evaluation.

How Pediatrics assesses it: Assess exact age, rectal temperature when infant, appearance/toxicity, hydration, respiratory effort, perfusion, immunization status, birth history/prematurity, immune compromise, focal symptoms, exposure/travel, urine symptoms, rash/petechiae, neck stiffness, and caregiver reliability.

Diagnosis: For well-appearing term infants 8-60 days with fever 38 C or higher, follow AAP age bands using urinalysis/urine culture, blood culture, inflammatory markers such as ANC/CRP/procalcitonin where available, and lumbar puncture depending on age/risk results. Older children need targeted testing: UA/culture for UTI risk, rapid viral/strep tests when useful, chest X-ray only for hypoxia/focal lung findings, and CBC/blood culture for toxic or high-risk children.

First-line treatment: Treat distress with weight-based acetaminophen (Tylenol) or ibuprofen (Advil/Motrin) if age-appropriate; avoid aspirin. Stable older children with viral features need fluids, observation, and return precautions rather than antibiotics.

Second-line treatment: Use antibiotics only by suspected source and age: ceftriaxone (Rocephin), cefotaxime, ampicillin, vancomycin (Vancocin), or oral agents such as amoxicillin (Amoxil) or cephalexin (Keflex) based on syndrome, cultures, age, and local guidance.

Third-line / advanced care: Immediate ED/admission for toxic appearance, age under 28 days with fever, hypoxia, poor perfusion, meningismus, petechiae/purpura, dehydration, immunocompromise, incomplete evaluation, unreliable follow-up, or abnormal high-risk infant labs.

Progression and follow-up: Follow culture results, fever curve, hydration, new localizing signs, antibiotic adverse effects, missed UTI/meningitis/sepsis, and caregiver understanding of red flags.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Acute otitis media

Pathophysiology: Acute otitis media is middle-ear infection/inflammation after eustachian tube dysfunction from viral URI, allergy, or anatomy, with bacterial pathogens such as Streptococcus pneumoniae, nontypeable H influenzae, and Moraxella catarrhalis.

How Pediatrics assesses it: Assess ear pain/tugging, fever, sleep disruption, otorrhea, URI symptoms, age, severity, bilateral disease, daycare, prior AOM, recent antibiotics, immunization status, hearing/speech concerns, and mastoid tenderness.

Diagnosis: Diagnose with pneumatic otoscopy/otoscopy showing bulging tympanic membrane, middle-ear effusion, decreased mobility, or new otorrhea not from otitis externa; do not diagnose based only on redness. Tympanometry can support uncertain effusion.

First-line treatment: Analgesia is first for all: weight-based acetaminophen (Tylenol) or ibuprofen (Advil/Motrin). Observation with close follow-up is reasonable for selected older children with mild unilateral disease.

Second-line treatment: When antibiotics are indicated, use high-dose amoxicillin (Amoxil) unless recent amoxicillin, purulent conjunctivitis, or recurrent/nonresponse suggests beta-lactamase coverage; then use amoxicillin-clavulanate (Augmentin). Alternatives include cefdinir (Omnicef), cefuroxime, cefpodoxime, or ceftriaxone (Rocephin) by allergy/severity.

Third-line / advanced care: ENT referral for recurrent AOM, persistent effusion with hearing/language concern, tympanostomy tube evaluation, mastoiditis, facial nerve palsy, intracranial complication, or treatment failure despite appropriate therapy.

Progression and follow-up: Follow pain/fever improvement in 48-72 hours, hearing, speech/language, recurrent episodes, diarrhea/rash from antibiotics, and complications such as mastoiditis or chronic effusion.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Bronchiolitis

Pathophysiology: Bronchiolitis is viral lower-airway infection in infants, usually RSV, causing small-airway edema, mucus plugging, wheeze/crackles, air trapping, feeding difficulty, and apnea risk in young or premature infants.

How Pediatrics assesses it: Assess age, prematurity, chronic lung/heart disease, immune compromise, apnea, feeding/urine output, work of breathing, retractions, nasal flaring, grunting, cyanosis, oxygen saturation, hydration, and caregiver capacity.

Diagnosis: Clinical diagnosis is usually enough. Pulse oximetry guides severity; routine chest X-ray, viral testing, CBC, antibiotics, and blood cultures are not needed in typical mild bronchiolitis. Test for viral pathogens only when it changes isolation/cohorting or high-risk therapy decisions.

First-line treatment: Supportive care: nasal suction, hydration/feeding support, antipyretics, and oxygen when hypoxemic by local threshold. Do not routinely use albuterol, epinephrine, corticosteroids, antibiotics, or chest physiotherapy in typical bronchiolitis.

Second-line treatment: Escalate supportive care with NG/IV fluids, high-flow nasal cannula, or respiratory support when feeding, oxygenation, or work of breathing worsens; treat bacterial coinfection only when evidence exists.

Third-line / advanced care: ED/admit for apnea, persistent hypoxemia, severe work of breathing, dehydration, age under 12 weeks with risk, prematurity, significant cardiopulmonary disease, or unreliable follow-up.

Progression and follow-up: Most peaks days 3-5 and improves over 1-2 weeks; cough/wheeze can persist. Monitor dehydration, apnea, respiratory failure, secondary infection, and recurrent wheeze/asthma risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Croup

Pathophysiology: Croup is viral laryngotracheitis, commonly parainfluenza, causing subglottic edema with barky cough, hoarseness, inspiratory stridor, and variable respiratory distress.

How Pediatrics assesses it: Assess stridor at rest, retractions, agitation/lethargy, cyanosis, drooling, tripod posture, fever/toxic appearance, foreign body risk, epiglottitis/bacterial tracheitis signs, hydration, and prior airway disease.

Diagnosis: Clinical diagnosis; imaging is rarely needed and should not delay treatment. Consider neck/chest imaging or ENT/anesthesia support only when atypical, foreign body, epiglottitis, abscess, or bacterial tracheitis is suspected.

First-line treatment: Give dexamethasone (Decadron) orally/IM/IV for all severity levels using local weight-based dosing; provide calm environment, fluids, and antipyretics.

Second-line treatment: Moderate/severe croup or stridor at rest needs nebulized epinephrine with observation for recurrence. Budesonide nebulized may be used when oral/IM steroid cannot be given.

Third-line / advanced care: ED/admit/airway team for persistent stridor after epinephrine, hypoxia, fatigue, altered mental status, toxic appearance, suspected epiglottitis/bacterial tracheitis, or impending respiratory failure.

Progression and follow-up: Symptoms usually improve within 48 hours; monitor rebound stridor, dehydration, respiratory failure, and missed bacterial/foreign body causes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Pediatric asthma

Pathophysiology: Pediatric asthma is chronic airway inflammation, bronchial hyperresponsiveness, variable airflow obstruction, mucus production, and remodeling risk triggered by viral infections, allergens, smoke, exercise, pollution, and comorbid rhinitis/obesity/GERD.

How Pediatrics assesses it: Assess wheeze/cough, nighttime symptoms, exercise limitation, exacerbations, ED/steroid history, triggers, smoke exposure, allergies/rhinitis, inhaler/spacer technique, adherence, growth, school impact, and red flags for alternative diagnoses.

Diagnosis: Use spirometry with bronchodilator response when age/cooperation allows, symptom pattern and treatment response in younger children, peak flow for monitoring selected patients, allergy evaluation when relevant, and chest X-ray only for atypical presentation or complication.

First-line treatment: Reliever therapy includes albuterol (Ventolin/ProAir) by MDI with spacer or nebulizer. Controller therapy uses inhaled corticosteroid such as fluticasone (Flovent), budesonide (Pulmicort), or beclomethasone (Qvar), with written asthma action plan, trigger control, vaccines, and spacer teaching.

Second-line treatment: Step-up therapy may include ICS-formoterol strategy where age/formulation allows, medium-dose ICS, LABA combination such as budesonide-formoterol (Symbicort) or fluticasone-salmeterol (Advair), montelukast (Singulair) with neuropsychiatric warning, or allergy/rhinitis treatment.

Third-line / advanced care: ED/admit for severe exacerbation, hypoxia, silent chest, exhaustion, poor response to repeated bronchodilator, prior ICU/intubation, or social risk. Specialty referral for frequent oral steroids, diagnostic uncertainty, poor control despite step-up, or biologic consideration.

Progression and follow-up: Follow symptom control, rescue use, exacerbations, spirometry, growth, steroid adverse effects, inhaler technique, adherence, school plan, and trigger reduction.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Pediatric dehydration

Pathophysiology: Pediatric dehydration results from fluid losses through gastroenteritis, fever, vomiting, diarrhea, poor intake, DKA, burns, or renal/endocrine disease; infants decompensate quickly because of higher water needs and limited reserves.

How Pediatrics assesses it: Assess weight change, urine output, tears, mucous membranes, capillary refill, heart rate, mental status, fontanelle, skin turgor, vomiting/diarrhea frequency, blood in stool, fever, travel, diabetes symptoms, and ability to tolerate oral fluids.

Diagnosis: Clinical severity guides care. Check glucose for lethargy or diabetes symptoms; BMP/electrolytes, BUN/creatinine, bicarbonate, ketones, and urinalysis are indicated for moderate/severe dehydration, persistent vomiting, altered mental status, DKA concern, or IV fluid need.

First-line treatment: Mild/moderate dehydration uses oral rehydration solution such as Pedialyte in small frequent volumes; continue breastfeeding/formula/age-appropriate diet. Ondansetron (Zofran) can help vomiting in selected children old enough by local protocol.

Second-line treatment: If oral rehydration fails or dehydration is moderate/severe, use IV isotonic fluids such as normal saline or lactated Ringer bolus, then maintenance/deficit replacement adjusted to sodium/glucose status.

Third-line / advanced care: ED/admit for shock, lethargy, severe dehydration, bilious vomiting, surgical abdomen, bloody diarrhea with toxicity, DKA, electrolyte derangement, young infant risk, or inability of caregivers to maintain hydration.

Progression and follow-up: Follow urine output, weight, mental status, electrolytes when abnormal, ongoing losses, recurrence, and warning signs for sepsis, obstruction, HUS, or DKA.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Pediatric abdominal pain

Pathophysiology: Pediatric abdominal pain may be functional, infectious, constipation-related, urinary, inflammatory, metabolic, gynecologic, testicular, or surgical; appendicitis, obstruction, intussusception, torsion, DKA, HSP/IgA vasculitis, and sepsis must be separated from benign causes.

How Pediatrics assesses it: Assess age, pain location/migration, fever, vomiting/bilious emesis, diarrhea/blood, constipation, urinary symptoms, testicular/pelvic symptoms, menses/pregnancy risk in adolescents, weight loss, trauma, hydration, peritoneal signs, gait/jump test, and genital exam when indicated.

Diagnosis: Use targeted testing: urinalysis/culture, pregnancy test for postmenarchal adolescents, glucose/ketones for DKA concern, CBC/CRP selectively, abdominal ultrasound for appendicitis/intussusception/gallbladder/pelvic disease, scrotal ultrasound for torsion concern without delaying surgery, and CT only when ultrasound/evaluation is nondiagnostic and risk remains.

First-line treatment: Constipation uses polyethylene glycol (MiraLAX) cleanout/maintenance and fiber/fluids; viral gastroenteritis uses oral rehydration; functional pain uses reassurance, school/function plan, constipation treatment, and psychosocial screening.

Second-line treatment: Condition-specific care may include antibiotics for UTI/appendicitis after evaluation, acid suppression such as famotidine (Pepcid) or omeprazole (Prilosec) when dyspepsia pattern is clear, and antiemetic ondansetron (Zofran) for gastroenteritis when appropriate.

Third-line / advanced care: Urgent ED/surgery for peritonitis, bilious emesis, testicular torsion, ovarian torsion, appendicitis concern, intussusception, obstruction, GI bleeding, severe dehydration, DKA, sepsis, or toxic appearance.

Progression and follow-up: Follow pain trajectory, hydration, stooling, weight/growth, school absence, recurrent ED visits, missed surgical disease, and escalation if symptoms localize or persist.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

ADHD in children

Pathophysiology: ADHD is a neurodevelopmental disorder involving inattention, hyperactivity, impulsivity, executive dysfunction, genetics, sleep, learning disorders, trauma, anxiety/depression, and environmental context, with impairment across settings.

How Pediatrics assesses it: Assess symptoms before age 12, impairment in at least two settings, school reports, Vanderbilt or Conners scales from caregivers/teachers, sleep, hearing/vision, learning disorder, anxiety/depression, trauma, substance use in adolescents, tics, cardiac history, BP/HR, appetite, and growth.

Diagnosis: Diagnosis is clinical using DSM criteria supported by standardized rating scales and collateral school information; no routine labs/imaging. Screen for comorbid learning disorder, autism, mood/anxiety, ODD/conduct disorder, sleep apnea, and absence seizures when suggested.

First-line treatment: Preschool children start with evidence-based parent training/behavioral intervention. School-age children use behavioral classroom supports plus stimulant medication when indicated: methylphenidate (Ritalin/Concerta/Focalin) or amphetamine salts/lisdexamfetamine (Adderall XR/Vyvanse), titrated to benefit and adverse effects.

Second-line treatment: If stimulants fail or are contraindicated, use atomoxetine (Strattera), guanfacine ER (Intuniv), or clonidine ER (Kapvay); adjust formulation/timing for rebound, insomnia, appetite suppression, or school coverage.

Third-line / advanced care: Refer developmental-behavioral pediatrics/psychiatry for diagnostic uncertainty, severe comorbidity, preschool complexity, cardiac risk, substance misuse/diversion, treatment resistance, suicidality, or severe aggression.

Progression and follow-up: Follow Vanderbilt/teacher feedback, grades, behavior, sleep, appetite, weight/height, BP/HR, tics, mood, diversion, and medication holidays/coverage needs.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Autism developmental screening

Pathophysiology: Autism spectrum disorder is a neurodevelopmental condition involving social communication differences, restricted/repetitive behaviors, sensory processing differences, language/motor variation, genetics, and frequent comorbid sleep, GI, ADHD, anxiety, or epilepsy.

How Pediatrics assesses it: Assess social reciprocity, eye contact/joint attention, language regression, gestures, repetitive behaviors, sensory sensitivities, play, motor delay, sleep, feeding, hearing, family history, lead risk, seizures, and caregiver concerns.

Diagnosis: Use standardized screening such as M-CHAT-R/F at recommended toddler visits, hearing evaluation, developmental assessment, speech/language evaluation, and formal diagnostic tools such as ADOS-2 by trained clinicians when available; genetic testing with chromosomal microarray/Fragile X is considered after diagnosis.

First-line treatment: Do not wait for final diagnosis to start early intervention: speech therapy, occupational therapy, parent-mediated behavioral/developmental interventions, school evaluation/IEP, sleep routine, and caregiver support.

Second-line treatment: Treat comorbidities specifically: melatonin for selected insomnia, constipation therapy, ADHD treatment, anxiety therapy, or seizure evaluation. Risperidone (Risperdal) or aripiprazole (Abilify) may be used only for severe irritability/aggression under specialist guidance.

Third-line / advanced care: Refer developmental-behavioral pediatrics, child psychology/psychiatry, neurology for seizures/regression, genetics, audiology, and early intervention/school services; urgent evaluation for regression, self-injury, or unsafe behavior.

Progression and follow-up: Follow language/social progress, adaptive function, sleep, feeding, school supports, caregiver stress, safety/elopement, seizures, medication metabolic effects, and transition planning.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Failure to thrive

Pathophysiology: Failure to thrive or pediatric growth faltering occurs when caloric intake, absorption, metabolic demand, or psychosocial caregiving cannot support expected growth; causes include feeding problems, food insecurity, neglect, GERD, oral-motor dysfunction, chronic infection, cardiac/pulmonary disease, endocrine disease, malabsorption, and genetic syndromes.

How Pediatrics assesses it: Plot serial weight/length/head circumference, review birth/prematurity, feeding volume/mixing technique, breastfeeding transfer, vomiting/diarrhea, stool, dysphagia, chronic cough, cardiac symptoms, infections, developmental delay, family heights, food access, caregiver mental health, and neglect/safety.

Diagnosis: Most diagnosis comes from growth data and feeding observation. Targeted tests may include CBC, CMP, urinalysis/culture, TSH, celiac serology, stool studies, sweat chloride, lead, HIV/TB, or cardiac evaluation only when history/exam suggests; avoid broad shotgun testing in a well child with clear intake issue.

First-line treatment: First-line care is nutrition plan with adequate calories/protein, formula mixing correction, lactation support, feeding schedule, high-calorie foods/formula when age-appropriate, vitamin D/iron when indicated, and close weight checks.

Second-line treatment: Treat specific causes such as GERD, constipation, cow milk protein allergy, celiac disease, pancreatic insufficiency, or chronic infection after diagnosis; involve dietitian, speech/feeding therapy, social work, and home visiting when needed.

Third-line / advanced care: Admit or urgently refer for severe malnutrition, dehydration, electrolyte abnormality/refeeding risk, unsafe home/neglect concern, failed outpatient weight gain, significant cardiopulmonary/GI disease, or need for tube feeding.

Progression and follow-up: Follow weight velocity, linear/head growth, developmental progress, caregiver adherence, food security, refeeding risk, micronutrient deficiencies, and recurrence after catch-up growth.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Pediatric rash evaluation

Pathophysiology: Pediatric rashes arise from viral exanthems, bacterial infection, eczema/allergy, drug reactions, infestations, inflammatory disease, vasculitis, trauma, or life-threatening meningococcemia, SJS/TEN, Kawasaki disease, MIS-C, or abuse.

How Pediatrics assesses it: Assess fever/toxicity, rash morphology and distribution, blanching vs petechial/purpuric, mucosal involvement, pain, pruritus, medication/vaccine exposures, travel/ticks, sick contacts, immunization status, immune compromise, joint/abdominal pain, and signs of dehydration or shock.

Diagnosis: Many rashes are clinical. Use rapid strep/culture for scarlet fever/impetigo when needed, KOH for tinea, bacterial culture for purulent lesions, viral testing for varicella/HSV in high-risk cases, CBC/coags/blood culture for petechiae/toxic appearance, and biopsy/dermatology for unclear severe disease.

First-line treatment: Treat common patterns: emollients and low/medium-potency topical steroids such as hydrocortisone or triamcinolone (Kenalog) for eczema, cetirizine (Zyrtec) for urticaria, mupirocin (Bactroban) for localized impetigo, clotrimazole (Lotrimin) for tinea, and permethrin (Elimite) for scabies.

Second-line treatment: Systemic therapy may include cephalexin (Keflex) for cellulitis/impetigo, acyclovir (Zovirax) for significant HSV/varicella risk, or prednisone (Deltasone) only for selected inflammatory/allergic disease after infection is excluded.

Third-line / advanced care: ED/admit for petechiae/purpura with fever, toxic appearance, mucosal sloughing/SJS, Kawasaki/MIS-C concern, cellulitis with sepsis, necrotizing infection, anaphylaxis, dehydration, neonatal vesicles, or abuse concern.

Progression and follow-up: Follow fever, spread, pain, mucosal symptoms, secondary infection, scarring, school/daycare exclusion rules, household treatment for infestations, and drug-allergy documentation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Childhood immunizations

Pathophysiology: Childhood immunizations build adaptive immunity before exposure, reducing severe infection, transmission, outbreaks, congenital/perinatal disease, cancer risk from HPV/hepatitis B, and complications in high-risk children.

How Pediatrics assesses it: Review vaccine record, age, prior reactions, allergies, pregnancy in adolescents, immune compromise, asplenia, chronic heart/lung/kidney/liver disease, diabetes, cochlear implant/CSF leak, travel, outbreak exposure, and caregiver concerns.

Diagnosis: No disease diagnosis is required; reconcile state registry/EHR and use the current CDC/AAP child and adolescent schedule plus catch-up schedule. Check serology only for selected uncertain immunity situations, not as routine replacement for vaccination.

First-line treatment: Offer due vaccines using the current schedule and catch-up rules, explain benefits/risks clearly, coadminister allowed vaccines, document lot/site/VIS, and plan next doses before the family leaves. Use acetaminophen/ibuprofen only for post-vaccine discomfort when age-appropriate, not prophylactically unless advised.

Second-line treatment: Special-risk decisions include pneumococcal, meningococcal, influenza/COVID/RSV, hepatitis A/B, travel vaccines, or immunocompromised schedules based on current CDC/AAP guidance and local/state requirements.

Third-line / advanced care: Allergy/immunology or infectious disease input is needed for suspected vaccine anaphylaxis, complex immunodeficiency, transplant/chemotherapy timing, uncertain contraindications to live vaccines, or post-exposure prophylaxis for measles/varicella/rabies/tetanus/hepatitis B.

Progression and follow-up: Follow series completion, adverse events, school requirements, outbreak needs, high-risk status changes, documentation gaps, and caregiver questions because U.S. vaccine recommendations can change.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Adolescent depression

Pathophysiology: Adolescent depression involves mood/reward circuitry, sleep/circadian disruption, genetics, trauma, social stress, substance use, bullying, chronic illness, and family context, increasing suicide risk and school/social impairment.

How Pediatrics assesses it: Use PHQ-9A or validated screen, assess suicidal ideation/plan/means, self-harm, abuse/bullying, substance use, sleep, eating disorder, bipolar/psychosis symptoms, pregnancy, gender/sexual identity stressors, family support, school function, and confidentiality limits.

Diagnosis: Diagnose clinically with DSM criteria and functional impairment; screen for bipolar disorder before antidepressants. Consider TSH/CBC/B12/CMP/pregnancy/substance testing only when symptoms or history suggest medical/substance contributors.

First-line treatment: Mild depression may start with active support, safety plan, sleep/exercise, problem-solving, and psychotherapy. Moderate/severe or persistent depression uses CBT or interpersonal therapy plus SSRI such as fluoxetine (Prozac) or escitalopram (Lexapro) with family education and close monitoring.

Second-line treatment: If inadequate response, optimize dose/adherence/therapy, switch SSRI, address substance use/trauma/sleep, and involve child psychiatry. Monitor for activation, suicidality, GI effects, sleep changes, and serotonin syndrome.

Third-line / advanced care: Emergency evaluation/inpatient care for active suicidal intent, psychosis, mania, severe self-neglect, abuse/unsafe home, intoxication, or inability of caregivers to maintain safety.

Progression and follow-up: Follow PHQ-9A, school attendance, sleep, self-harm, substance use, family safety plan, medication adverse effects, relapse prevention, and transition planning.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Sports clearance and concussion

Pathophysiology: Sports clearance identifies cardiovascular, neurologic, musculoskeletal, heat, respiratory, and sickle-cell risks before participation; concussion is traumatic brain dysfunction from biomechanical force causing metabolic vulnerability without requiring abnormal imaging.

How Pediatrics assesses it: Preparticipation assessment reviews exertional chest pain/syncope, palpitations, family sudden death, prior concussion, seizures, asthma, heat illness, eating disorder, menstrual history, sickle trait, musculoskeletal injury, supplements, and protective equipment. Concussion assessment reviews mechanism, symptoms, amnesia, vomiting, worsening headache, neurologic deficits, and return-to-play risk.

Diagnosis: Use PPE history/exam; ECG/echo only for concerning cardiac history/exam. Concussion is clinical using symptom scale, neuro exam, balance/vestibular/ocular testing; CT head only for red flags such as worsening mental status, focal deficit, skull fracture concern, repeated vomiting, seizure, or high-risk trauma.

First-line treatment: Clear participation when risk is controlled. Concussion care includes 24-48 hours relative rest, limited screen/school load as needed, sleep, hydration, acetaminophen (Tylenol) initially for headache, and gradual return-to-learn before return-to-play.

Second-line treatment: Persistent symptoms need vestibular/ocular therapy, headache/sleep/mood treatment, school accommodations, and supervised graded aerobic activity. Avoid same-day return to play after suspected concussion.

Third-line / advanced care: Refer sports medicine/neurology/cardiology for exertional syncope/chest pain, abnormal cardiac exam, prolonged concussion symptoms, multiple concussions, focal neurologic deficits, seizure, or worsening symptoms.

Progression and follow-up: Follow symptom resolution, school performance, exertional tolerance, recurrent concussion, mental health, sleep, headache medication overuse, and safe staged return-to-play.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Pediatric obesity

Pathophysiology: Pediatric obesity is chronic adiposity influenced by genetics, family environment, sleep, medications, trauma, food access, activity, endocrine rarity, and neurohormonal regulation, increasing insulin resistance, MASLD, dyslipidemia, hypertension, OSA, orthopedic disease, PCOS, and stigma.

How Pediatrics assesses it: Assess BMI percentile/severe obesity class, growth trajectory, BP, diet/sugary drinks, activity/screen time, sleep/OSA, medications, depression/eating disorder, bullying, family history, food insecurity, readiness, and signs of endocrine disease such as poor linear growth.

Diagnosis: Use BMI percentile and comorbidity screening: BP, fasting lipids, A1c or fasting glucose, ALT/AST for MASLD, sleep study for OSA symptoms, menstrual/androgen evaluation for PCOS when indicated. Endocrine labs are not routine unless linear growth is poor or symptoms suggest.

First-line treatment: First-line treatment is family-based intensive health behavior and lifestyle treatment with nutrition, physical activity, sleep, reduced sugar-sweetened beverages, reduced sedentary time, and non-stigmatizing goals.

Second-line treatment: Adolescents meeting criteria may be considered for anti-obesity medication with specialist support, such as semaglutide (Wegovy), liraglutide (Saxenda), orlistat (Alli/Xenical), or phentermine-topiramate (Qsymia) depending on age/contraindications and current labeling.

Third-line / advanced care: Refer to multidisciplinary pediatric weight-management program, endocrinology, dietitian, behavioral health, sleep medicine, or bariatric surgery program for severe obesity with comorbidities or failed intensive therapy.

Progression and follow-up: Follow BMI trajectory, BP, A1c/lipids/ALT, sleep, mood/eating disorder, medication adverse effects, family goals, stigma, and long-term cardiometabolic risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pediatrics

Pediatric UTI

Pathophysiology: Pediatric UTI is bacterial infection of the bladder or kidney, often E coli, with risk from female sex, uncircumcised male infants, constipation/bladder-bowel dysfunction, vesicoureteral reflux, urinary obstruction, and sexual activity in adolescents.

How Pediatrics assesses it: Assess age, fever without source, dysuria/frequency, abdominal/flank pain, vomiting, prior UTI, constipation, voiding dysfunction, hydration, toxicity, sexual activity/STI risk in adolescents, and congenital urinary history.

Diagnosis: Obtain urinalysis and urine culture before antibiotics when possible. Use catheterized or suprapubic specimen for non-toilet-trained children; avoid bag culture for diagnosis. Renal/bladder ultrasound is considered after febrile UTI in young children or recurrent/atypical cases; VCUG is reserved for abnormal ultrasound or recurrent febrile UTI.

First-line treatment: Treat cystitis with culture-directed oral antibiotics such as cephalexin (Keflex), amoxicillin-clavulanate (Augmentin), cefixime (Suprax), cefdinir (Omnicef), or TMP-SMX (Bactrim) when resistance allows; encourage fluids and manage constipation.

Second-line treatment: Pyelonephritis/febrile UTI may need ceftriaxone (Rocephin) initially or oral third-generation cephalosporin depending on severity, local resistance, vomiting, and age; adjust once culture susceptibilities return.

Third-line / advanced care: Admit/urgent evaluation for toxic appearance, sepsis, age under 2-3 months, dehydration/vomiting, obstruction/stone, immunocompromise, renal abnormality, failed outpatient therapy, or inability to ensure follow-up.

Progression and follow-up: Follow culture result, fever resolution within 48-72 hours, recurrence, constipation/bladder habits, renal ultrasound findings, scarring risk, and antibiotic adverse effects.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Specialty role

Older-adult care with function, cognition, falls, frailty, deprescribing, goals of care, and medication harm reduction.

Geriatrics

Falls and gait instability

Pathophysiology: Falls in older adults usually result from interacting risks: impaired strength/balance, neuropathy, vision loss, vestibular disease, orthostatic hypotension, cognitive impairment, unsafe footwear/home hazards, sedating or BP-lowering medications, alcohol, and acute illness.

How Geriatrics assesses it: Assess fall circumstances, prodrome/syncope, injury, fear of falling, gait speed, Timed Up and Go, orthostatic vitals, feet/footwear, vision/hearing, neuropathy, Parkinsonism, cognition, home hazards, alcohol, osteoporosis risk, and drugs such as benzodiazepines, Z-drugs, anticholinergics, opioids, gabapentinoids, antihypertensives, and hypoglycemics.

Diagnosis: Use focused evaluation: orthostatic BP/HR, ECG when syncope/palpitations/cardiac disease, glucose/A1c if hypoglycemia possible, CBC/CMP/B12/TSH/vitamin D selectively, medication review using Beers Criteria, gait/balance testing, vision assessment, and imaging only for injury, focal neurologic signs, or suspected fracture/subdural bleed.

First-line treatment: First-line prevention is structured exercise/physical therapy emphasizing strength, balance, gait, and mobility; correct vision/footwear/home hazards, treat orthostasis/dehydration, reduce alcohol, optimize assistive devices, and deprescribe fall-risk-increasing medications when possible.

Second-line treatment: Treat contributors: adjust BP regimen, reduce insulin/sulfonylurea hypoglycemia risk, manage neuropathy pain cautiously, treat B12 deficiency, vestibular rehab for BPPV, osteoporosis therapy when fracture risk is high, and OT home safety evaluation.

Third-line / advanced care: Urgent evaluation for head injury on anticoagulants, hip fracture, syncope with cardiac risk, new neurologic deficit, recurrent unexplained falls, suspected abuse/neglect, or inability to ambulate safely at home.

Progression and follow-up: Follow fall frequency, injuries, gait speed, TUG, fear of falling, medication changes, orthostatic symptoms, home modifications, PT adherence, fracture prevention, and caregiver burden.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Delirium

Pathophysiology: Delirium is acute fluctuating brain dysfunction from impaired attention/arousal triggered by infection, hypoxia, dehydration, pain, urinary retention/constipation, sleep disruption, metabolic disturbance, withdrawal, stroke, surgery, or high-risk medications in a vulnerable brain.

How Geriatrics assesses it: Assess acute onset/fluctuation, inattention, altered level of consciousness, hallucinations, sleep-wake reversal, baseline dementia, infection symptoms, pain, oxygenation, urinary retention, constipation, medications, alcohol/benzodiazepine withdrawal, sensory deprivation, and caregiver collateral.

Diagnosis: Use CAM or 4AT plus targeted cause search: vitals, pulse oximetry, glucose, CBC, CMP/electrolytes, urinalysis/culture only if urinary symptoms/systemic signs, ECG, bladder scan, medication/toxin review, and CT head only for trauma, focal deficit, anticoagulated head injury, or unexplained severe change.

First-line treatment: First-line treatment is non-drug: reorientation, glasses/hearing aids, sleep normalization, mobilization, hydration/nutrition, pain control, bowel/bladder relief, family presence, avoid restraints/catheters, and stop deliriogenic drugs such as diphenhydramine (Benadryl), benzodiazepines, anticholinergics, and sedative hypnotics.

Second-line treatment: Treat the cause: fluids for dehydration, oxygen for hypoxia, antibiotics for confirmed infection, bowel regimen, urinary retention relief, and withdrawal protocol when present. Use low-dose antipsychotic such as haloperidol (Haldol) or quetiapine (Seroquel) only for severe distress or danger after QT/Parkinson/Lewy body risks are considered.

Third-line / advanced care: Hospitalize/escalate for sepsis, hypoxia, stroke, severe metabolic derangement, unsafe agitation, inability to take fluids/meds, suspected abuse/neglect, or lack of safe supervision.

Progression and follow-up: Follow attention/arousal, sleep, mobility, hydration, medication changes, caregiver observations, recurrence risk, functional decline, falls, and transition to dementia evaluation only after delirium resolves.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Dementia assessment

Pathophysiology: Dementia is acquired cognitive decline that impairs independence; common etiologies include Alzheimer disease, vascular cognitive impairment, Lewy body dementia, frontotemporal dementia, Parkinson disease dementia, normal pressure hydrocephalus, depression, medications, sleep apnea, B12/thyroid disease, and structural lesions.

How Geriatrics assesses it: Assess onset/course, memory/executive/language/visuospatial symptoms, ADLs/IADLs, driving/finances/medication safety, hallucinations, parkinsonism, REM sleep behavior, behavior changes, depression, alcohol, sleep apnea, falls, caregiver stress, and medication anticholinergic/sedative burden.

Diagnosis: Use MoCA, SLUMS, Mini-Cog, or MMSE plus informant history; check CBC, CMP, TSH, B12, depression screen, medication review, and brain MRI or CT for new diagnosis/atypical features. Consider neuropsychological testing, sleep study, or neurology referral when diagnosis is uncertain or early-onset/rapid/atypical.

First-line treatment: First-line care is safety and function: exercise, cognitive/social activity, hearing/vision correction, sleep, vascular risk control, medication simplification, advance care planning, caregiver education, driving/firearm/financial safety, and community resources.

Second-line treatment: Alzheimer-type dementia may use cholinesterase inhibitors donepezil (Aricept), rivastigmine (Exelon), or galantamine (Razadyne), and memantine (Namenda) for moderate/severe disease; monitor bradycardia, syncope, GI effects, weight loss, and interactions.

Third-line / advanced care: Refer neurology/geriatrics for young onset, rapid progression, prominent hallucinations/parkinsonism, frontotemporal features, NPH signs, seizures, or disease-modifying anti-amyloid therapy consideration requiring biomarker confirmation and MRI safety screening.

Progression and follow-up: Follow cognition, ADLs/IADLs, falls, weight, swallowing, driving, medication adherence, caregiver strain, behavioral symptoms, goals of care, and need for home services or higher level of care.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Frailty syndrome

Pathophysiology: Frailty is reduced physiologic reserve from sarcopenia, chronic inflammation, multimorbidity, malnutrition, inactivity, cognitive/mood disease, and social vulnerability, increasing vulnerability to falls, delirium, hospitalization, disability, and treatment harm.

How Geriatrics assesses it: Assess gait speed, grip strength, exhaustion, weight loss, activity level, ADLs/IADLs, falls, cognition, mood, nutrition, pain, polypharmacy, sensory impairment, social support, caregiver capacity, and patient goals.

Diagnosis: Use Clinical Frailty Scale or frailty phenotype/deficit index, Timed Up and Go, ADL/IADL scales, Mini-Cog/MoCA when indicated, PHQ-9, nutrition screen such as MNA, orthostatic vitals, medication review, and targeted labs like CBC/CMP/TSH/B12/vitamin D when clinically suggested.

First-line treatment: First-line care is resistance/balance exercise, protein-calorie optimization, vitamin D only when deficient/high risk, fall prevention, sensory correction, deprescribing, vaccines, pain control, and individualized chronic disease targets that prioritize function over disease-maximal metrics.

Second-line treatment: Treat drivers such as anemia, heart failure, COPD, depression, hypothyroidism, OSA, malnutrition, pain, and diabetes overtreatment; involve PT/OT, dietitian, social work, and caregiver support.

Third-line / advanced care: Geriatrics/palliative/home-based care referral for severe frailty, recurrent admissions, unsafe home, caregiver collapse, complex deprescribing, or major treatment decisions where burdens may outweigh benefits.

Progression and follow-up: Follow weight, strength, walking speed, ADLs, falls, hospitalizations, cognition, caregiver strain, medication burden, and whether care remains aligned with goals.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Polypharmacy deprescribing

Pathophysiology: Deprescribing reduces medication-related harm from age-related pharmacokinetic changes, renal/hepatic impairment, anticholinergic/sedative burden, interactions, prescribing cascades, and treatments no longer aligned with prognosis or goals.

How Geriatrics assesses it: List every drug/supplement/OTC with indication, benefit timeframe, adverse effects, adherence, cost, renal dosing, falls, cognition, constipation, urinary retention, bleeding, hypoglycemia, orthostasis, and patient priorities.

Diagnosis: Use Beers Criteria, STOPP/START concepts, anticholinergic burden, opioid/benzodiazepine/gabapentinoid overlap review, renal function dosing, duplicate therapy check, and symptom-medication timeline to identify candidates for stopping or tapering.

First-line treatment: Stop drugs without indication or clear benefit; taper high-risk drugs when needed, including benzodiazepines, Z-drugs, opioids, gabapentin/pregabalin, clonidine, beta blockers, antidepressants, antipsychotics, and PPIs when rebound is likely. Use one change at a time when risk of confusion is high.

Second-line treatment: Replace with safer options: sleep CBT/routine instead of sedative hypnotics, topical diclofenac (Voltaren) or acetaminophen (Tylenol) instead of chronic oral NSAIDs when appropriate, bowel regimen reduction after opioid taper, and simplified once-daily regimens/blister packs.

Third-line / advanced care: Pharmacist/geriatrics/psychiatry/pain referral for complex psychotropics, recurrent withdrawal, high-dose opioids, severe anxiety/insomnia, anticoagulant-antiplatelet complexity, or family disagreement about goals.

Progression and follow-up: Follow withdrawal, symptom recurrence, falls, cognition, BP/glucose, pain/sleep/mood, pill burden, adherence, caregiver understanding, and whether deprescribing improved function or quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Urinary incontinence

Pathophysiology: Older-adult urinary incontinence may be urgency/overactive bladder, stress incontinence, overflow retention, functional incontinence, infection, atrophic urogenital change, constipation, neurologic disease, mobility impairment, or medication effect.

How Geriatrics assesses it: Assess urgency/frequency/nocturia, stress leakage, retention symptoms, dysuria/hematuria, fluid/caffeine, constipation, mobility, cognition, pelvic prolapse, prostate symptoms, diabetes, diuretics, sedatives, anticholinergics, alpha blockers, and patient goals.

Diagnosis: Use urinalysis for infection/hematuria, postvoid residual when retention/overflow suspected, bladder diary, cough stress test/pelvic exam when appropriate, medication review, glucose/A1c when polyuria, and avoid routine urine culture for asymptomatic bacteriuria.

First-line treatment: First-line treatment is bladder training, timed voiding, pelvic floor muscle therapy, constipation treatment, caffeine/fluid timing, mobility/toileting support, absorbent product fit, and medication adjustment.

Second-line treatment: For urgency incontinence, consider mirabegron (Myrbetriq) with BP monitoring or antimuscarinics such as trospium (Sanctura) with caution; avoid oxybutynin (Ditropan) when possible due to anticholinergic cognitive/fall risk. Vaginal estrogen such as estradiol (Estrace) may help genitourinary syndrome of menopause.

Third-line / advanced care: Refer urology/urogynecology for retention, recurrent UTI with symptoms, hematuria, prolapse, failed conservative therapy, catheter complications, or procedures such as pessary, sling, botulinum toxin, neuromodulation, or prostate intervention.

Progression and follow-up: Follow leakage episodes, falls/nocturia, skin breakdown, UTIs, cognition, BP, constipation, dry mouth, retention, caregiver burden, and quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Pressure injury prevention

Pathophysiology: Pressure injury develops when sustained pressure, shear, friction, moisture, immobility, malnutrition, poor perfusion, neuropathy, incontinence, or device pressure causes ischemic tissue damage over bony prominences or under medical devices.

How Geriatrics assesses it: Assess mobility, sensation, skin over sacrum/heels/hips, incontinence/moisture, nutrition/protein intake, weight loss, perfusion/diabetes/PAD, pain, support surface, wheelchair seating, caregiver ability, and device contact points.

Diagnosis: Use head-to-toe skin inspection and stage injury by depth/tissue type; measure wound size, tunneling, exudate, odor, surrounding cellulitis, pain, and consider labs/nutrition markers only as part of broader assessment. Image or probe for osteomyelitis when deep nonhealing ulcer or exposed bone suggests it.

First-line treatment: Prevention: repositioning schedule, pressure-redistribution mattress/cushion, heel offloading, moisture/incontinence care, nutrition/protein support, mobilization, device padding, and caregiver education.

Second-line treatment: Treat early injuries with offloading, appropriate dressings, moisture balance, debridement when necrotic tissue, pain control, and management of incontinence/perfusion/nutrition. Antibiotics are for cellulitis, osteomyelitis, or systemic infection, not colonization.

Third-line / advanced care: Wound care/surgery/infectious disease referral for stage 3/4, deep tissue injury, eschar, spreading cellulitis, sepsis, osteomyelitis, uncontrolled pain, or need for debridement/flap planning.

Progression and follow-up: Follow wound size/stage, exudate, pain, infection, nutrition, offloading adherence, equipment fit, caregiver capacity, and recurrence after healing.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Osteoporosis fracture prevention

Pathophysiology: Osteoporosis is reduced bone strength from aging, menopause, glucocorticoids, hypogonadism, low calcium/vitamin D, low weight, smoking/alcohol, CKD/endocrine disease, and immobility, leading to fragility fractures and loss of independence.

How Geriatrics assesses it: Assess prior fragility fracture, falls, height loss, parental hip fracture, steroids, smoking/alcohol, calcium/vitamin D intake, kidney disease, dental plans, GERD/esophageal disease, mobility, and fracture risk using FRAX when appropriate.

Diagnosis: Use DXA hip/spine, vertebral fracture assessment or spine imaging for height loss/back pain, calcium, creatinine/eGFR, vitamin D when risk, TSH/PTH/testosterone/celiac/myeloma tests when secondary causes are suggested.

First-line treatment: First-line prevention includes weight-bearing/resistance/balance exercise, fall prevention, adequate calcium intake, vitamin D repletion if deficient, smoking/alcohol reduction, and bisphosphonate therapy such as alendronate (Fosamax), risedronate (Actonel), or zoledronic acid (Reclast) when fracture risk warrants.

Second-line treatment: Use denosumab (Prolia) when bisphosphonate unsuitable with careful discontinuation planning; anabolic therapy teriparatide (Forteo), abaloparatide (Tymlos), or romosozumab (Evenity) for very high fracture risk depending on contraindications.

Third-line / advanced care: Endocrinology/osteoporosis referral for multiple fractures, very low BMD, CKD complexity, atypical femur fracture, osteonecrosis jaw concern, glucocorticoid osteoporosis, or failure on therapy.

Progression and follow-up: Follow falls, new fractures, height, DXA interval, calcium/vitamin D, renal function, dental issues, thigh/groin pain, adherence, drug holiday timing, and function after fracture.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Malnutrition in older adults

Pathophysiology: Older-adult malnutrition results from inadequate intake, inflammation, dysphagia, dental disease, depression, dementia, social isolation, poverty, medication effects, GI disease, cancer, chronic infection, or increased metabolic demand.

How Geriatrics assesses it: Assess weight loss, appetite, food access, dentition, dysphagia, nausea/constipation, depression, cognition, alcohol, medication effects such as GLP-1 agonists/digoxin, functional ability to shop/cook/eat, caregiver support, and pressure injury risk.

Diagnosis: Use weight/BMI trend, Mini Nutritional Assessment or similar screen, dietary recall, swallowing evaluation when coughing/choking, oral/dental exam, CBC/CMP, B12, TSH, vitamin D/iron selectively, and targeted malignancy/GI/infection evaluation for alarm features.

First-line treatment: First-line care is food-first nutrition: preferred high-protein/high-calorie foods, oral nutrition supplements, meal assistance, dental repair, texture modification, constipation/nausea treatment, social meal programs, and resistance exercise when safe.

Second-line treatment: Treat underlying causes, review/stop appetite-suppressing drugs, consider mirtazapine (Remeron) when depression/insomnia with poor appetite is present, and involve dietitian, speech therapy, social work, and caregiver training.

Third-line / advanced care: Urgent care for severe dehydration, refeeding risk, aspiration, unsafe neglect, pressure injury with poor intake, inability to swallow, or need for enteral feeding discussion aligned with goals of care.

Progression and follow-up: Follow weight, intake, strength, pressure injuries, swallowing safety, labs when abnormal, mood/cognition, food security, caregiver burden, and goals around artificial nutrition.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Sleep disturbance in older adults

Pathophysiology: Sleep disturbance in older adults may reflect circadian shift, insomnia disorder, sleep apnea, restless legs, nocturia, pain, depression/anxiety, dementia, medications, alcohol/caffeine, or poor sleep environment.

How Geriatrics assesses it: Assess sleep schedule, naps, caffeine/alcohol, nocturia, pain, dyspnea, restless legs, snoring/apneas, dream enactment, depression/anxiety, dementia behaviors, medications including diuretics/steroids/SSRIs/stimulants, and falls/night wandering.

Diagnosis: Use sleep diary, Insomnia Severity Index when useful, STOP-Bang/OSA screen, ferritin for restless legs risk, medication review, depression screen, and polysomnography for suspected OSA, REM behavior disorder, periodic limb movement disorder, or atypical events.

First-line treatment: First-line treatment is CBT-I, regular wake time, light exposure, exercise, reduced naps/caffeine/alcohol, pain/nocturia management, and safe sleep environment. Melatonin may help circadian rhythm or dementia-related sleep timing in selected patients.

Second-line treatment: Avoid routine benzodiazepines, Z-drugs, diphenhydramine (Benadryl), and doxepin above low-dose because of falls/delirium. Treat OSA with CPAP/APAP, restless legs with iron repletion if low ferritin and cautious gabapentin (Neurontin) or dopamine agonist when appropriate.

Third-line / advanced care: Refer sleep medicine/geriatrics/psychiatry for refractory insomnia, suspected OSA with cardiopulmonary disease, REM behavior disorder, severe nocturnal behaviors, or medication dependence.

Progression and follow-up: Follow sleep quality, daytime function, falls, cognition, nocturia, CPAP adherence, medication adverse effects, and caregiver sleep burden.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Behavioral symptoms of dementia

Pathophysiology: Behavioral and psychological symptoms of dementia arise from neurodegeneration plus unmet needs, pain, infection, constipation, sleep disruption, overstimulation, caregiver communication mismatch, depression/anxiety, psychosis, or medication effects.

How Geriatrics assesses it: Describe the behavior, timing, trigger, danger, caregiver response, pain, hunger/thirst, toileting, constipation, sleep, infection symptoms, delirium signs, sensory deficits, environment, medication changes, and caregiver strain.

Diagnosis: Rule out delirium and treatable causes with vitals, pain assessment, medication review, constipation/urinary retention check, targeted urinalysis/culture only if urinary/systemic symptoms, CBC/CMP when illness suspected, and depression/psychosis assessment.

First-line treatment: First-line treatment is non-drug: validate, redirect, simplify environment, routines, music/activity, sleep hygiene, glasses/hearing aids, pain treatment with acetaminophen (Tylenol) when appropriate, caregiver training, and respite support.

Second-line treatment: If severe distress or danger persists after causes addressed, cautious medication may include sertraline (Zoloft) for anxiety/depression, trazodone for sleep/agitation in selected cases, or antipsychotic such as risperidone (Risperdal), quetiapine (Seroquel), or olanzapine (Zyprexa) only after discussing stroke/mortality risks.

Third-line / advanced care: Urgent evaluation for violence, suicidality, unsafe wandering, caregiver collapse, suspected abuse/neglect, delirium, psychosis with danger, or need for inpatient geriatric psychiatry/placement.

Progression and follow-up: Follow behavior frequency/severity, sedation, falls, parkinsonism, QT/metabolic effects, caregiver burden, triggers, and attempt dose reduction of antipsychotics when stable.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Advance care planning

Pathophysiology: Advance care planning aligns future medical decisions with values, prognosis, functional trajectory, acceptable tradeoffs, and surrogate decision-making before crisis or loss of capacity.

How Geriatrics assesses it: Assess decision-making capacity, illness understanding, prognosis awareness, values, fears, acceptable quality of life, desired surrogate, cultural/spiritual context, prior experiences, caregiver availability, code status understanding, and specific treatments such as hospitalization, ICU, ventilation, feeding tube, dialysis, and CPR.

Diagnosis: This is not a disease diagnosis; document capacity, health care proxy/surrogate, advance directive/POLST or state form when appropriate, goals-of-care conversation, and whether decisions are informed and voluntary.

First-line treatment: First-line approach is structured conversation using plain language, naming the surrogate, completing advance directive/POLST when desired, sharing documents with family/clinicians, and revisiting after major health changes.

Second-line treatment: For serious illness, use prognosis-specific recommendations, palliative care referral, symptom planning, hospice education when eligible, and conflict mediation if family/surrogate disagreement occurs.

Third-line / advanced care: Ethics, palliative care, legal, or social work involvement is needed for contested capacity, no surrogate, suspected coercion/abuse, complex guardianship, or treatment conflict.

Progression and follow-up: Follow document availability, surrogate understanding, consistency across settings, changes in goals, caregiver readiness, and whether emergency plans match stated values.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Older adult pain management

Pathophysiology: Pain in older adults is often mixed nociceptive, neuropathic, inflammatory, ischemic, cancer-related, or centralized pain, with higher risk of delirium, falls, constipation, renal injury, and drug interactions from analgesics.

How Geriatrics assesses it: Assess pain source, function, sleep, mood, cognition, falls, renal/liver disease, anticoagulants, constipation, substance use, prior opioid exposure, neuropathic features, red flags, and patient-centered functional goals.

Diagnosis: Use focused exam, X-ray for trauma/OA/fracture concern, ESR/CRP for inflammatory/infection concern, neuropathy labs such as B12/A1c/TSH when indicated, and avoid imaging that will not change management.

First-line treatment: First-line care is physical therapy/exercise, heat/cold, assistive devices, topical diclofenac (Voltaren), lidocaine patch (Lidoderm), acetaminophen (Tylenol) within safe total dose, and condition-specific treatment.

Second-line treatment: Use oral NSAIDs such as naproxen (Aleve) or ibuprofen (Advil) only cautiously and briefly with renal/GI/CV review; duloxetine (Cymbalta) may help OA/neuropathic pain; gabapentin (Neurontin) or pregabalin (Lyrica) require renal dosing and fall/sedation monitoring.

Third-line / advanced care: Avoid routine opioids; if necessary for severe acute/cancer/palliative pain, use low-dose short course such as oxycodone (Roxicodone) with bowel regimen naloxone access, risk review, and close follow-up. Refer pain/PM&R/orthopedics/palliative for procedures or complex cases.

Progression and follow-up: Follow function, falls, cognition, constipation, renal function, sedation, mood, opioid misuse risk, pain interference, and whether treatment improves goals rather than only pain score.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Geriatrics

Medication anticholinergic burden

Pathophysiology: Anticholinergic burden blocks central and peripheral muscarinic signaling, worsening cognition, delirium, constipation, urinary retention, dry mouth, blurred vision, tachycardia, heat intolerance, falls, and dementia risk in vulnerable older adults.

How Geriatrics assesses it: Review OTC sleep/cold/allergy drugs, bladder antimuscarinics, tricyclics, antipsychotics, muscle relaxants, antiemetics, Parkinson drugs, and GI antispasmodics; assess memory, delirium, falls, constipation, urinary retention, glaucoma, dry mouth/dental caries, and heat exposure.

Diagnosis: Use medication inventory plus anticholinergic burden scale when helpful, Beers Criteria review, cognitive screen, bowel/bladder assessment, postvoid residual if retention suspected, and symptom timeline after medication changes.

First-line treatment: Deprescribe or replace high-risk agents such as diphenhydramine (Benadryl), hydroxyzine (Vistaril), amitriptyline (Elavil), cyclobenzaprine (Flexeril), oxybutynin (Ditropan), promethazine (Phenergan), and dicyclomine (Bentyl) when possible.

Second-line treatment: Substitute safer options: cetirizine (Zyrtec) or intranasal fluticasone (Flonase) for allergies, mirabegron (Myrbetriq) or behavioral bladder therapy for urgency, SSRI such as sertraline (Zoloft) for depression/anxiety, topical/local pain therapy, and bowel regimen for constipation.

Third-line / advanced care: Urgent evaluation for delirium, acute urinary retention, ileus, heat illness, glaucoma symptoms, severe falls, or unsafe medication misuse; involve pharmacy/geriatrics for complex psychotropic or bladder-drug deprescribing.

Progression and follow-up: Follow cognition, attention, bowel/bladder function, falls, dry mouth/dental health, symptom recurrence after deprescribing, and total anticholinergic score over time.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Specialty role

Heart and vascular specialty care focused on complex cardiac diagnosis, secondary prevention, rhythm, pump function, ischemia, and procedures.

Cardiology

Resistant hypertension and secondary causes

Pathophysiology: Resistant hypertension is BP above goal despite three complementary drugs including a diuretic, or controlled BP requiring four or more agents; causes include inaccurate measurement, nonadherence, high sodium, NSAIDs/stimulants, OSA, primary aldosteronism, renal parenchymal disease, renal artery stenosis, pheochromocytoma, Cushing syndrome, thyroid disease, and coarctation.

How Cardiology assesses it: Confirm true resistance with correct cuff/technique, home or ambulatory BP, adherence, refill history, alcohol/salt/NSAID/decongestant/stimulant use, sleep apnea symptoms, hypokalemia, kidney bruit, episodic headache/palpitations/sweats, and end-organ symptoms.

Diagnosis: Use BMP/CMP with creatinine/eGFR and potassium, urinalysis/urine albumin-creatinine ratio, aldosterone-renin ratio, TSH, sleep study when OSA suspected, renal artery duplex/CTA/MRA for renovascular clues, plasma free metanephrines for pheochromocytoma features, and echocardiogram/ECG for LVH or heart disease.

First-line treatment: Optimize lifestyle and the core regimen: ACE inhibitor/ARB such as lisinopril (Zestril) or losartan (Cozaar), calcium-channel blocker amlodipine (Norvasc), and thiazide-like diuretic chlorthalidone (Thalitone) or indapamide, with loop diuretic furosemide (Lasix) or torsemide (Demadex) when eGFR is low/volume overloaded.

Second-line treatment: Add mineralocorticoid receptor antagonist spironolactone (Aldactone) or eplerenone (Inspra) after checking potassium/eGFR; treat OSA with CPAP, stop offending drugs, and use hydralazine (Apresoline), clonidine (Catapres), carvedilol (Coreg), or alpha blocker only for selected indications.

Third-line / advanced care: Refer to hypertension specialist/nephrology/cardiology for persistent resistance, suspected endocrine/renal artery disease, severe CKD, recurrent hypertensive urgency/emergency, or need for advanced testing/procedures.

Progression and follow-up: Complications include stroke, MI, heart failure, CKD progression, retinopathy, aortic disease, LVH, medication adverse effects, hyperkalemia from add-on therapy, and missed secondary causes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Heart failure with reduced ejection fraction

Pathophysiology: HFrEF is systolic ventricular dysfunction, usually LVEF 40% or lower, from ischemic heart disease, hypertension, cardiomyopathy, toxins, valvular disease, myocarditis, arrhythmia, or genetic disease, causing neurohormonal activation, congestion, low output, remodeling, and sudden death risk.

How Cardiology assesses it: Assess dyspnea, orthopnea/PND, edema, weight trend, BP/HR, volume status, JVP, lung crackles, adherence, sodium intake, alcohol/cocaine/chemo exposure, ischemic symptoms, arrhythmia, renal function, potassium, and NYHA functional class.

Diagnosis: Use transthoracic echocardiogram for EF/valves, BNP/NT-proBNP, ECG, chest X-ray, CMP/eGFR/potassium/magnesium, CBC, TSH, iron studies, A1c/lipids, ischemic evaluation with stress imaging/coronary CTA/angiography when appropriate, and cardiac MRI for infiltrative/myocarditis/scar questions.

First-line treatment: Foundational therapy includes ARNI sacubitril-valsartan (Entresto) or ACE/ARB if not tolerated, evidence beta blocker carvedilol (Coreg), metoprolol succinate (Toprol XL), or bisoprolol, MRA spironolactone (Aldactone) or eplerenone (Inspra), SGLT2 inhibitor dapagliflozin (Farxiga) or empagliflozin (Jardiance), and loop diuretic furosemide (Lasix) or torsemide for congestion.

Second-line treatment: Add hydralazine-isosorbide dinitrate (BiDil) for selected patients, ivabradine (Corlanor) for sinus rhythm with elevated HR despite beta blocker, vericiguat (Verquvo) after recent decompensation, IV iron for iron deficiency, anticoagulation only for AF/VTE/other indication, and cardiac rehab.

Third-line / advanced care: Advanced care includes ICD for persistent low EF after optimized therapy, CRT for qualifying wide QRS/LBBB, revascularization/valve intervention when indicated, LVAD/transplant evaluation, palliative care, and admission for shock, hypoxia, severe congestion, renal failure, or arrhythmia.

Progression and follow-up: Follow weight, symptoms, BP, renal function, potassium, EF reassessment, device eligibility, hospitalizations, arrhythmias, sudden death risk, renal injury, hyperkalemia, hypotension, and goals of care.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Heart failure with preserved ejection fraction

Pathophysiology: HFpEF is heart failure symptoms/signs with preserved LVEF from diastolic dysfunction, ventricular-vascular stiffening, obesity, hypertension, atrial fibrillation, CKD, diabetes, pulmonary hypertension, sleep apnea, valvular disease, or infiltrative disease.

How Cardiology assesses it: Assess exertional dyspnea, edema, orthopnea, obesity, BP, AF, sleep apnea, CKD, diabetes, lung disease, anemia, ischemia, volume status, frailty, and medication causes of fluid retention such as NSAIDs or thiazolidinediones.

Diagnosis: Use echocardiogram for EF, diastolic indices, LVH, LA size, valves, pulmonary pressures; BNP/NT-proBNP may be lower in obesity; check CMP/eGFR, CBC, TSH, iron, A1c/lipids, ECG, chest X-ray, sleep study, stress testing, and consider cardiac MRI or amyloid testing when red flags exist.

First-line treatment: Treat congestion with diuretics such as furosemide (Lasix) or torsemide (Demadex), control BP, treat AF and ischemia, address obesity/OSA, and use SGLT2 inhibitor empagliflozin (Jardiance) or dapagliflozin (Farxiga) when appropriate.

Second-line treatment: Use spironolactone (Aldactone), ARB losartan (Cozaar)/candesartan (Atacand), or sacubitril-valsartan (Entresto) selectively by phenotype, BP, renal function, and potassium; manage AF with rate/rhythm strategy and anticoagulation when CHA2DS2-VASc indicates.

Third-line / advanced care: Refer for amyloidosis evaluation, pulmonary hypertension workup, valve intervention, complex diuretic resistance, recurrent admissions, cardiac rehab, weight-management program, or palliative support for advanced symptoms.

Progression and follow-up: Follow congestion, renal function, potassium, BP, exercise tolerance, AF burden, hospitalizations, pulmonary hypertension, falls/hypotension, and comorbidity control.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Atrial fibrillation rhythm and stroke prevention

Pathophysiology: Atrial fibrillation is chaotic atrial electrical activation causing loss of atrial contraction, irregular ventricular response, atrial remodeling, tachycardia-mediated cardiomyopathy, and left atrial appendage thrombus risk leading to embolic stroke.

How Cardiology assesses it: Assess symptoms, onset/duration, hemodynamic stability, triggers such as infection/alcohol/thyroid disease, heart failure, valvular disease, sleep apnea, stroke/TIA, bleeding risk, medications, renal function, and patient preference for rate versus rhythm control.

Diagnosis: Confirm with 12-lead ECG or ambulatory monitor; evaluate CMP/eGFR, magnesium, TSH, CBC, echocardiogram, sleep apnea risk, troponin only if ischemic symptoms, and CHA2DS2-VASc plus bleeding risk to guide anticoagulation.

First-line treatment: Unstable AF needs immediate synchronized cardioversion. Stable rate control uses metoprolol (Lopressor/Toprol XL), diltiazem (Cardizem), verapamil (Calan), or digoxin (Lanoxin) in selected heart failure/low BP patients. Stroke prevention usually uses apixaban (Eliquis), rivaroxaban (Xarelto), dabigatran (Pradaxa), edoxaban (Savaysa), or warfarin (Coumadin/Jantoven) for valvular AF/mechanical valves.

Second-line treatment: Rhythm control may use electrical cardioversion, flecainide (Tambocor) or propafenone (Rythmol) only without structural/ischemic heart disease, sotalol (Betapace), dofetilide (Tikosyn), dronedarone (Multaq), or amiodarone (Cordarone/Pacerone) with toxicity monitoring.

Third-line / advanced care: Refer electrophysiology for catheter ablation, recurrent symptomatic AF, tachycardia cardiomyopathy, antiarrhythmic failure, or left atrial appendage occlusion when anticoagulation is not tolerated; TEE-guided cardioversion or anticoagulation timing is required when AF duration is uncertain/over 48 hours.

Progression and follow-up: Follow AF burden, rate control, symptoms, EF, renal function for DOAC dosing, bleeding, stroke/TIA, thyroid/liver/lung toxicity with amiodarone, sleep apnea treatment, and recurrence after cardioversion/ablation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Supraventricular tachycardia

Pathophysiology: SVT is usually AV nodal reentrant tachycardia, AV reentrant tachycardia via accessory pathway, or atrial tachycardia producing abrupt regular narrow-complex tachycardia; pre-excitation/WPW can be dangerous with atrial fibrillation.

How Cardiology assesses it: Assess onset/termination, palpitations, chest pain, syncope, dyspnea, triggers, stimulant use, pregnancy, structural heart disease, family sudden death, hemodynamic stability, and ECG evidence of pre-excitation.

Diagnosis: Capture 12-lead ECG during symptoms when possible; use ambulatory monitor/event recorder, electrolytes/magnesium, TSH if recurrent, echocardiogram for structural disease, and EP study for recurrent or uncertain mechanism.

First-line treatment: Unstable SVT needs synchronized cardioversion. Stable regular narrow-complex SVT uses vagal maneuvers followed by adenosine (Adenocard) if no contraindication, with continuous ECG monitoring.

Second-line treatment: Prevention may use metoprolol (Toprol XL), atenolol (Tenormin), diltiazem (Cardizem), or verapamil (Calan) when no pre-excited AF risk; avoid AV nodal blockers in irregular wide-complex tachycardia or suspected pre-excited AF.

Third-line / advanced care: Electrophysiology referral for catheter ablation is preferred for recurrent symptomatic SVT, medication intolerance, WPW, syncope, high-risk occupation, or patient preference.

Progression and follow-up: Complications include syncope/injury, tachycardia-mediated cardiomyopathy with frequent episodes, anxiety, medication bradycardia/hypotension, and rare sudden death in high-risk accessory pathway.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Stable angina

Pathophysiology: Stable angina is predictable myocardial ischemia from fixed coronary atherosclerotic narrowing or microvascular/spasm physiology, where oxygen demand exceeds supply during exertion or stress without acute plaque rupture.

How Cardiology assesses it: Assess exertional chest pressure, radiation, dyspnea, relief with rest/nitroglycerin, diabetes/CKD risk, prior CAD, BP/lipids/smoking, anemia, valvular disease, medication adherence, and unstable features such as rest pain, accelerating pattern, or prolonged symptoms.

Diagnosis: Use ECG, high-sensitivity troponin if symptoms suggest ACS, lipid/A1c/CMP/CBC, and noninvasive testing by pretest probability: exercise ECG when interpretable, stress echo/nuclear/PET, coronary CT angiography, or invasive angiography for high-risk symptoms/tests.

First-line treatment: Antianginal and prevention therapy includes sublingual nitroglycerin (Nitrostat), beta blocker metoprolol (Toprol XL) or carvedilol (Coreg), amlodipine (Norvasc) or diltiazem (Cardizem) when appropriate, high-intensity statin atorvastatin (Lipitor) or rosuvastatin (Crestor), aspirin (Bayer/Ecotrin) for established CAD, BP/diabetes control, smoking cessation, and cardiac rehab/exercise plan.

Second-line treatment: If symptoms persist, add long-acting nitrate isosorbide mononitrate (Imdur), ranolazine (Ranexa), or calcium-channel blocker; optimize LDL with ezetimibe (Zetia) or PCSK9 therapy when needed.

Third-line / advanced care: Urgent ED for unstable features. Revascularization with PCI/CABG is considered for left main/high-risk anatomy, refractory angina despite guideline therapy, or prognostic anatomy; cardiology referral guides testing and procedure selection.

Progression and follow-up: Progression can become ACS/MI, heart failure, arrhythmia, activity limitation, medication hypotension, nitrate tolerance, and missed noncardiac or microvascular/spasm disease.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Acute coronary syndrome

Pathophysiology: ACS results from acute plaque rupture/erosion with coronary thrombosis causing unstable angina, NSTEMI, or STEMI; myocardial necrosis risk depends on vessel occlusion, collateral flow, time to reperfusion, and oxygen demand.

How Cardiology assesses it: Assess chest pressure/radiation, dyspnea, diaphoresis, nausea, syncope, atypical symptoms in women/older adults/diabetes, hemodynamic instability, heart failure, bleeding risk, anticoagulant use, cocaine/stimulants, and time of symptom onset.

Diagnosis: Obtain ECG within 10 minutes and repeat if nondiagnostic, serial high-sensitivity troponins, CMP/eGFR, CBC, coagulation tests when anticoagulated/procedure planned, chest X-ray when alternate diagnosis/heart failure possible, bedside echo for shock/mechanical complication, and risk scores such as HEART/TIMI/GRACE.

First-line treatment: Give aspirin (Bayer/Ecotrin) unless contraindicated, nitroglycerin for pain/HTN if no RV infarct/PDE5 inhibitor/hypotension, high-intensity statin atorvastatin (Lipitor) or rosuvastatin (Crestor), oxygen only for hypoxemia, and anticoagulation such as heparin/enoxaparin per protocol. STEMI requires emergent PCI or fibrinolysis if PCI unavailable within time window.

Second-line treatment: Dual antiplatelet therapy uses ticagrelor (Brilinta), prasugrel (Effient), or clopidogrel (Plavix) by ACS/PCI/fibrinolysis context; beta blocker and ACE inhibitor/ARB are added when stable and indicated.

Third-line / advanced care: Cath lab/PCI, CABG for anatomy, ICU care for shock/arrhythmia/mechanical complications, intra-aortic balloon/Impella in selected shock, and cardiac rehab/discharge secondary prevention are advanced steps.

Progression and follow-up: Complications include death, recurrent MI, ventricular arrhythmias, cardiogenic shock, papillary muscle rupture, VSD, free-wall rupture, pericarditis, heart failure, bleeding, contrast kidney injury, and stent thrombosis.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Post-myocardial infarction secondary prevention

Pathophysiology: After MI, residual atherosclerosis, infarct scar, LV remodeling, platelet activation, inflammation, and risk factors drive recurrent MI, heart failure, arrhythmia, and sudden death risk.

How Cardiology assesses it: Assess MI type, PCI/CABG/stent details, EF, symptoms, BP/HR, LDL/A1c, kidney function, bleeding risk, smoking, rehab access, depression, medication adherence/cost, sexual activity/PDE5 use, and return-to-work/exercise readiness.

Diagnosis: Use discharge cath/echo data, repeat echocardiogram after guideline therapy when EF reduced, lipid panel 4-12 weeks after statin changes, A1c, CMP/eGFR/potassium, ECG for symptoms, and ambulatory monitor for palpitations/syncope.

First-line treatment: Core therapy includes aspirin (Bayer/Ecotrin), P2Y12 inhibitor clopidogrel (Plavix)/ticagrelor (Brilinta)/prasugrel (Effient) for indicated DAPT duration, high-intensity statin atorvastatin (Lipitor) or rosuvastatin (Crestor), beta blocker metoprolol succinate (Toprol XL) or carvedilol (Coreg) when indicated, ACE inhibitor/ARB/ARNI for LV dysfunction/HTN/diabetes/CKD, smoking cessation, and cardiac rehab.

Second-line treatment: Add ezetimibe (Zetia) or PCSK9 inhibitor evolocumab (Repatha)/alirocumab (Praluent) if LDL remains above goal; add eplerenone (Inspra) or spironolactone (Aldactone) after MI with reduced EF/diabetes/HF when renal function and potassium allow.

Third-line / advanced care: ICD evaluation if EF remains low after waiting period and optimized therapy; evaluate recurrent angina with stress imaging/coronary angiography; manage complex antithrombotic needs with cardiology when AF/VTE coexists.

Progression and follow-up: Follow recurrent ischemia, HF symptoms, EF recovery, arrhythmias, bleeding, LDL response, BP, diabetes, depression, rehab completion, medication adverse effects, and adherence.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Valvular aortic stenosis

Pathophysiology: Aortic stenosis is progressive calcific, bicuspid, or rheumatic narrowing of the aortic valve causing LV pressure overload, hypertrophy, diastolic dysfunction, ischemia, syncope, heart failure, and sudden death when severe and symptomatic.

How Cardiology assesses it: Assess exertional dyspnea, angina, syncope/presyncope, heart failure, murmur radiation to carotids, pulse pressure, frailty, bicuspid/aortic disease, dental/infection history, BP, and symptom limitation.

Diagnosis: Use transthoracic echocardiogram for valve area, mean gradient, peak velocity, EF, LVH, and other valves; low-flow/low-gradient disease may need dobutamine stress echo or CT calcium scoring. CT angiography is used for TAVR planning; coronary angiography is used before valve intervention when indicated.

First-line treatment: No medication reverses severe AS. Manage BP carefully, avoid excessive vasodilation/diuresis, treat AF/HF cautiously, address lipids/ASCVD risk, and schedule surveillance echo based on severity.

Second-line treatment: Symptomatic severe AS or severe AS with LV dysfunction needs valve replacement evaluation. Choice of TAVR versus surgical AVR depends on age, anatomy, surgical risk, life expectancy, valve durability, bicuspid anatomy, and patient preference.

Third-line / advanced care: Urgent admission for syncope, angina, pulmonary edema, shock, or decompensated severe AS; balloon valvuloplasty may bridge unstable patients to definitive AVR/TAVR.

Progression and follow-up: Complications include heart failure, syncope/falls, angina, arrhythmias, sudden death, pulmonary hypertension, LV dysfunction, bleeding from acquired von Willebrand disease, and procedural stroke/pacemaker/vascular risks.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Mitral regurgitation

Pathophysiology: Mitral regurgitation is backward systolic flow from LV to LA due to primary leaflet/chordal disease such as prolapse/flail/endocarditis/rheumatic disease or secondary LV remodeling/ischemia; chronic MR causes LA/LV dilation, AF, pulmonary hypertension, and HF.

How Cardiology assesses it: Assess dyspnea, fatigue, palpitations/AF, orthopnea, edema, murmur, endocarditis risk, ischemic history, connective tissue disease, BP, and exercise tolerance; distinguish acute severe MR with pulmonary edema/shock.

Diagnosis: Use transthoracic echocardiogram for mechanism, severity, LV size/EF, LA size, pulmonary pressure; TEE for anatomy/procedure planning or endocarditis; stress echo for exertional symptoms; cardiac MRI when echo quantification is uncertain; coronary evaluation before surgery when indicated.

First-line treatment: Treat contributing hypertension/HF with guideline therapy, diuretics such as furosemide (Lasix) for congestion, anticoagulate AF when indicated, and monitor asymptomatic moderate/severe MR with echo intervals.

Second-line treatment: Primary severe MR with symptoms or LV dysfunction/dilation needs mitral valve repair preferred when durable; secondary MR may improve with HFrEF therapy, CRT/revascularization when indicated, and selected transcatheter edge-to-edge repair such as MitraClip.

Third-line / advanced care: Urgent surgical/cardiology care for acute severe MR from papillary muscle rupture, endocarditis, or chordal rupture with pulmonary edema/shock; advanced valve team decides repair, replacement, or transcatheter option.

Progression and follow-up: Progression causes AF, pulmonary hypertension, LV dysfunction, HF admissions, endocarditis complications, thromboembolism, and worse surgical outcomes if referral is delayed.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Pericarditis

Pathophysiology: Acute pericarditis is inflammation of the pericardial sac from viral/idiopathic, post-MI, autoimmune, uremic, malignancy, bacterial/TB, trauma, or drug causes; inflammation can produce pleuritic pain, effusion, tamponade, or constriction.

How Cardiology assesses it: Assess sharp pleuritic positional chest pain relieved by leaning forward, pericardial rub, fever, dyspnea, recent infection, MI/procedure, autoimmune/renal/cancer/TB risk, anticoagulation, and high-risk features such as fever, large effusion, tamponade, trauma, immunosuppression, or elevated troponin.

Diagnosis: Use ECG for diffuse ST elevation/PR depression, troponin, CBC/CMP/renal function, ESR/CRP, chest X-ray, and echocardiogram for effusion/tamponade. CT/MRI helps recurrent, constrictive, malignant, or unclear cases.

First-line treatment: Low-risk idiopathic/viral pericarditis uses NSAID such as ibuprofen (Advil/Motrin) or aspirin plus colchicine (Colcrys/Mitigare), gastroprotection when needed, exercise restriction, and CRP-guided taper.

Second-line treatment: Treat specific causes; corticosteroids such as prednisone (Deltasone) are reserved for autoimmune disease, NSAID contraindication, pregnancy-specific situations, or refractory disease because they increase recurrence risk.

Third-line / advanced care: Admit for high-risk features, tamponade, bacterial/TB/malignant concern, myopericarditis, renal failure, or anticoagulated trauma. Pericardiocentesis/window is needed for tamponade or diagnostic malignant/purulent effusion; recurrent disease may need anakinra (Kineret) or rilonacept (Arcalyst).

Progression and follow-up: Complications include recurrence, tamponade, constrictive pericarditis, myocarditis, arrhythmias, renal/GI NSAID toxicity, colchicine intolerance, and missed MI/PE/aortic dissection.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Cardiomyopathy

Pathophysiology: Cardiomyopathy includes dilated, hypertrophic, restrictive, arrhythmogenic, stress/Takotsubo, infiltrative, genetic, toxic, tachycardia-mediated, peripartum, and myocarditis-related myocardial disease causing systolic/diastolic dysfunction, arrhythmia, embolic risk, and sudden death.

How Cardiology assesses it: Assess HF symptoms, syncope, palpitations, family sudden death/cardiomyopathy, alcohol/cocaine/chemo exposure, viral illness, pregnancy/postpartum, neuromuscular disease, hypertension, ischemic symptoms, and exam for murmurs/congestion.

Diagnosis: Use ECG, echocardiogram, BNP, CMP/eGFR, TSH, iron studies/ferritin, HIV/hepatitis when indicated, coronary evaluation for ischemia, cardiac MRI for scar/infiltration/myocarditis, ambulatory monitor, genetic testing/counseling for inherited patterns, and endomyocardial biopsy only for selected fulminant or unclear cases.

First-line treatment: Treat phenotype: HFrEF guideline therapy for dilated disease, avoid dehydration/vasodilator excess in obstructive HCM, beta blocker metoprolol (Toprol XL) or nadolol (Corgard) for symptomatic HCM, stop toxins, manage AF, and restrict high-risk exercise when indicated.

Second-line treatment: Use disease-specific therapy such as mavacamten (Camzyos) for selected obstructive HCM, tafamidis (Vyndamax/Vyndaqel) for transthyretin amyloid cardiomyopathy, immunosuppression only for specific inflammatory cardiomyopathies, and anticoagulation for AF/LV thrombus.

Third-line / advanced care: Advanced care includes ICD, CRT, septal reduction therapy, LVAD/transplant evaluation, genetic family screening, myocarditis admission, and specialty cardiomyopathy clinic.

Progression and follow-up: Progression can cause HF, ventricular arrhythmias, sudden death, stroke, LV thrombus, transplant need, medication intolerance, family risk, and pregnancy complications.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Syncope with cardiac risk

Pathophysiology: Cardiac syncope results from transient cerebral hypoperfusion due to arrhythmia, structural obstruction, ischemia, pulmonary embolism, or cardiomyopathy, carrying higher sudden death risk than reflex/orthostatic syncope.

How Cardiology assesses it: Assess exertional or supine syncope, palpitations, chest pain, dyspnea, family sudden death, structural heart disease, abnormal ECG, injury, orthostatic vitals, medications causing hypotension/QT prolongation, dehydration/bleeding, and neurologic seizure mimics.

Diagnosis: Use ECG for all syncope, orthostatic vitals, glucose when indicated, CBC/CMP/troponin only when suggested by history, echocardiogram for murmur/structural disease, ambulatory monitor/event recorder/implantable loop recorder for suspected arrhythmia, and stress testing for exertional symptoms. Avoid routine head CT/carotid imaging without neurologic findings.

First-line treatment: Treat reversible causes: hydration/salt for orthostasis when safe, stop hypotensive/QT drugs, manage anemia/bleeding, and counsel driving/activity restriction until risk clarified.

Second-line treatment: Arrhythmia-specific therapy may include beta blocker, pacemaker for bradyarrhythmia, ICD for malignant ventricular arrhythmia risk, catheter ablation for SVT/VT, or valve intervention for severe AS.

Third-line / advanced care: Admit/urgent cardiology for abnormal ECG, exertional/supine syncope, structural heart disease, severe anemia/bleeding, PE/ACS concern, persistent hypotension, family sudden death, or injury with high-risk features.

Progression and follow-up: Complications include sudden death, recurrent injury/falls, driving accidents, untreated arrhythmia, missed aortic stenosis/HCM/PE/ACS, and overtesting when low-risk reflex syncope is not recognized.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Cardiology

Peripheral arterial disease

Pathophysiology: PAD is atherosclerotic obstruction of lower-extremity arteries causing reduced perfusion, claudication, impaired wound healing, chronic limb-threatening ischemia, and high systemic ASCVD risk.

How Cardiology assesses it: Assess exertional calf/thigh/buttock pain relieved by rest, rest pain, wounds, pulses, bruits, skin temperature/hair loss, diabetes/neuropathy, smoking, kidney disease, prior revascularization, walking limitation, and infection/ischemia severity.

Diagnosis: Use ankle-brachial index at rest, exercise ABI if symptoms with normal resting ABI, toe-brachial index when arteries noncompressible, duplex ultrasound/CTA/MRA for anatomy before revascularization, and wound imaging/culture only when ulcer/infection present.

First-line treatment: Treat ASCVD risk aggressively: smoking cessation, supervised exercise therapy, high-intensity statin atorvastatin (Lipitor) or rosuvastatin (Crestor), antiplatelet aspirin (Bayer/Ecotrin) or clopidogrel (Plavix) for symptomatic PAD, BP/diabetes control, foot care, and vaccines.

Second-line treatment: Cilostazol (Pletal) can improve claudication if no heart failure; rivaroxaban 2.5 mg twice daily (Xarelto) plus aspirin may be used in selected low-bleeding-risk symptomatic PAD/revascularization patients.

Third-line / advanced care: Vascular referral for lifestyle-limiting claudication despite exercise/medical therapy, chronic limb-threatening ischemia, rest pain, gangrene, nonhealing ulcer, acute limb ischemia, or need for endovascular/surgical revascularization.

Progression and follow-up: Complications include MI/stroke, acute limb ischemia, ulcer, infection, amputation, reduced mobility, depression, contrast kidney injury after procedures, and bleeding from antithrombotic therapy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Specialty role

Hormone and metabolic disorders requiring biochemical confirmation, chronic titration, risk reduction, and complication surveillance.

Endocrinology

Type 1 diabetes

Pathophysiology: Type 1 diabetes is autoimmune beta-cell destruction causing absolute insulin deficiency, hyperglycemia, lipolysis, ketogenesis, and risk of diabetic ketoacidosis; long-term risk comes from microvascular and macrovascular complications.

How Endocrinology assesses it: Assess age/onset, weight loss, polyuria/polydipsia, DKA history, hypoglycemia awareness, insulin regimen, carb counting, injection/pump technique, CGM use, exercise, sick-day skills, psychosocial burden, celiac/thyroid autoimmune history, pregnancy plans, and access to insulin/supplies.

Diagnosis: Confirm diabetes with A1c/plasma glucose criteria; distinguish type 1 with clinical phenotype plus autoantibodies such as GAD65, IA-2, ZnT8, insulin autoantibody when useful, and C-peptide in uncertain adults. Screen ketones/anion gap/VBG for DKA; monitor urine albumin-creatinine ratio, eGFR, lipids, retinal and foot exams.

First-line treatment: Requires basal-bolus insulin or pump therapy: insulin glargine (Lantus/Basaglar/Semglee), degludec (Tresiba), or detemir (Levemir) plus rapid insulin lispro (Humalog/Admelog), aspart (NovoLog/Fiasp), or glulisine (Apidra). Use CGM such as Dexcom G7 or FreeStyle Libre, glucagon rescue such as Baqsimi/Gvoke, and education on sick-day rules and ketone testing.

Second-line treatment: Optimize with insulin pump or automated insulin delivery, carb ratio/correction factor adjustment, exercise strategies, nutrition therapy, and treatment of dawn phenomenon or recurrent hypoglycemia. Pramlintide (Symlin) may be considered in selected adults with expert support.

Third-line / advanced care: Urgent care for DKA, severe hypoglycemia, pregnancy, recurrent admissions, inability to afford insulin, eating disorder/insulin omission, or brittle control; endocrinology/diabetes education is central.

Progression and follow-up: Follow CGM time-in-range, A1c, severe hypoglycemia, DKA, lipohypertrophy, kidney/eye/nerve disease, cardiovascular risk, thyroid/celiac screening, distress/burnout, and supply access.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Complex type 2 diabetes pharmacotherapy

Pathophysiology: Complex type 2 diabetes involves insulin resistance, beta-cell failure, obesity/adipose inflammation, hepatic glucose output, incretin dysfunction, renal glucose handling, and comorbid ASCVD, heart failure, CKD, fatty liver, hypoglycemia risk, and medication access barriers.

How Endocrinology assesses it: Assess A1c/CGM pattern, fasting vs postprandial hyperglycemia, hypoglycemia, weight, ASCVD/HF/CKD, albuminuria/eGFR, MASLD risk, steroid use, frailty, pregnancy potential, cost, adherence, GI disease, pancreatitis history, and injection readiness.

Diagnosis: Use A1c, CGM/BGM logs, CMP/eGFR, urine albumin-creatinine ratio, fasting lipids, B12 on metformin, retinal/foot exams, and ketones/anion gap when insulin deficiency or DKA is possible. Consider C-peptide/autoantibodies if phenotype suggests LADA/type 1.

First-line treatment: Base therapy on comorbidity: metformin (Glucophage) if tolerated, GLP-1/GIP therapy semaglutide (Ozempic/Rybelsus/Wegovy), dulaglutide (Trulicity), or tirzepatide (Mounjaro/Zepbound) for weight/A1c/CV risk, and SGLT2 inhibitor empagliflozin (Jardiance) or dapagliflozin (Farxiga) for HF/CKD benefit when eGFR allows.

Second-line treatment: Add basal insulin glargine (Lantus/Basaglar/Semglee) or degludec (Tresiba) for symptomatic/severe hyperglycemia, then prandial insulin lispro/aspart if needed. Alternatives include sitagliptin (Januvia), glipizide (Glucotrol), or pioglitazone (Actos) only when risks fit.

Third-line / advanced care: Use CGM, diabetes education, concentrated insulin U-500 for severe resistance, pump/automated delivery for selected insulin-requiring adults, obesity pharmacotherapy/surgery referral, and urgent DKA/HHS care when metabolic decompensation occurs.

Progression and follow-up: Follow A1c/time-in-range, weight, hypoglycemia, renal function, albuminuria, retinopathy, neuropathy, foot risk, heart failure, ASCVD, medication side effects, affordability, and treatment burden.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Diabetic ketoacidosis transition care

Pathophysiology: DKA is insulin deficiency with counterregulatory hormone excess causing hyperglycemia, ketogenesis, anion-gap metabolic acidosis, dehydration, potassium shifts, and cerebral/arrhythmia risk during correction.

How Endocrinology assesses it: Assess precipitant such as infection, missed insulin, pump failure, new diabetes, MI/stroke, pregnancy, steroid/SGLT2 inhibitor use, vomiting, mental status, volume status, and ability to safely resume subcutaneous insulin.

Diagnosis: Use glucose, beta-hydroxybutyrate or serum/urine ketones, anion gap, bicarbonate, venous/arterial pH, potassium, sodium corrected for glucose, creatinine, osmolality when HHS overlap, infection/ischemia testing by symptoms, and confirm gap closure before transition.

First-line treatment: Acute DKA uses IV isotonic fluids, IV regular insulin, potassium replacement guided by level, dextrose when glucose falls, and treatment of trigger. Transition requires basal insulin overlap before stopping infusion plus prandial/correction insulin plan.

Second-line treatment: For discharge/transition, verify insulin access, pump function if applicable, sick-day rules, ketone strips, glucagon, CGM/BGM supplies, education on when to call/seek care, and follow-up within days to adjust doses.

Third-line / advanced care: ICU/endocrinology for severe acidosis, altered mental status, shock, pregnancy, recurrent DKA, euglycemic DKA from SGLT2 inhibitors, inability to afford insulin, or psychosocial/eating disorder drivers.

Progression and follow-up: Follow recurrent DKA, hypoglycemia after transition, potassium/phosphate, renal recovery, precipitant resolution, insulin adherence/access, pump sites, and diabetes distress.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Hypoglycemia unawareness

Pathophysiology: Hypoglycemia unawareness occurs when recurrent hypoglycemia blunts autonomic warning symptoms and counterregulatory responses, increasing risk of neuroglycopenia, seizure, coma, accidents, and fear-driven hyperglycemia.

How Endocrinology assesses it: Assess frequency/timing of lows, severe episodes, nocturnal hypoglycemia, insulin/sulfonylurea use, renal impairment, alcohol, missed meals, exercise, weight loss, gastroparesis, cognitive impairment, driving/work risk, and whether symptoms occur before neuroglycopenia.

Diagnosis: Use CGM/BGM download to identify time below range, nocturnal patterns, insulin stacking, basal excess, meal mismatch, and hypoglycemia risk medications. Review A1c cautiously because low A1c may mask dangerous variability.

First-line treatment: First-line treatment is strict hypoglycemia avoidance for several weeks, raising glucose targets temporarily, reducing basal/prandial insulin or sulfonylurea, structured meal/exercise planning, CGM alerts, and carrying fast carbohydrate.

Second-line treatment: Use glucagon rescue such as Baqsimi nasal glucagon, Gvoke HypoPen, or Zegalogue; switch from sulfonylurea to lower-risk agents, consider automated insulin delivery/pump suspend, and adjust insulin-to-carb/correction factors.

Third-line / advanced care: Endocrinology/diabetes education for severe or recurrent episodes, impaired cognition, pregnancy, high-risk occupations/driving, adrenal insufficiency concern, insulinoma concern without diabetes drugs, or inability to self-manage.

Progression and follow-up: Follow severe episodes, time below range, awareness recovery, driving safety, caregiver training, CGM use, medication access, and fear of hypoglycemia.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Hypothyroidism

Pathophysiology: Hypothyroidism is inadequate thyroid hormone action from autoimmune thyroiditis, thyroidectomy/radioiodine, iodine/drug effects such as amiodarone/lithium, pituitary disease, or congenital causes, slowing metabolism and affecting lipids, heart, cognition, skin, gut, and reproductive function.

How Endocrinology assesses it: Assess fatigue, cold intolerance, constipation, weight change, dry skin, hair loss, bradycardia, menstrual/fertility issues, pregnancy, goiter, neck surgery/radioiodine, autoimmune history, medications, and myxedema red flags such as hypothermia/altered mental status.

Diagnosis: Primary diagnosis uses elevated TSH with low free T4 for overt disease; TPO antibodies support autoimmune thyroiditis. Central hypothyroidism has low/normal TSH with low free T4 and needs pituitary evaluation. Check pregnancy status when relevant.

First-line treatment: Treat overt hypothyroidism with levothyroxine (Synthroid/Levoxyl/Tirosint) individualized by age, weight, cardiac disease, and pregnancy. Take on empty stomach separated from calcium, iron, bile-acid sequestrants, and PPIs when possible.

Second-line treatment: Adjust dose every 6-8 weeks by TSH for primary disease or free T4 for central disease; increase promptly in pregnancy per obstetric/endocrine guidance. Avoid routine liothyronine (Cytomel) unless specialist-selected.

Third-line / advanced care: Emergency care for myxedema coma with IV levothyroxine, stress-dose hydrocortisone, warming, ventilatory/hemodynamic support, and trigger treatment. Endocrinology for central disease, pregnancy complexity, refractory TSH, malabsorption, or thyroid cancer suppression.

Progression and follow-up: Follow TSH/free T4 targets, symptoms, lipids, weight, AF/osteoporosis from overtreatment, pregnancy outcomes, adherence/absorption interactions, and goiter/nodule changes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Hyperthyroidism and Graves disease

Pathophysiology: Hyperthyroidism is excess thyroid hormone from Graves autoimmune TSH-receptor stimulation, toxic nodular disease, thyroiditis, iodine/amiodarone exposure, or exogenous hormone, causing adrenergic symptoms, weight loss, AF, bone loss, ophthalmopathy, and thyroid storm risk.

How Endocrinology assesses it: Assess weight loss, tremor, heat intolerance, palpitations, diarrhea, anxiety, menstrual change, goiter, eye pain/proptosis/diplopia, neck pain, pregnancy, iodine/amiodarone, cardiac disease, and thyroid storm signs such as fever, delirium, vomiting, heart failure.

Diagnosis: Use TSH, free T4, total/free T3; TRAb/TSI for Graves; radioactive iodine uptake/scan when not pregnant and etiology unclear; thyroid ultrasound when nodules/goiter; CBC and LFTs before antithyroid drugs; ECG for tachyarrhythmia.

First-line treatment: Control symptoms with beta blocker such as propranolol (Inderal) or atenolol (Tenormin) when safe. Graves disease treatment options include methimazole (Tapazole), radioactive iodine, or thyroidectomy; PTU is preferred in first trimester pregnancy or thyroid storm.

Second-line treatment: Monitor thyroid labs, CBC/LFT symptoms, agranulocytosis warning with fever/sore throat, hepatic toxicity, and Graves orbitopathy. Definitive therapy is favored for relapse, toxic nodules, large goiter, medication intolerance, or patient preference.

Third-line / advanced care: Thyroid storm needs ICU, high-dose PTU or methimazole, iodine after thionamide, beta blockade, glucocorticoids, cooling/support, and trigger treatment. Ophthalmology for moderate/severe eye disease; high-volume thyroid surgeon for surgery.

Progression and follow-up: Follow TSH/T4/T3, relapse/hypothyroidism after therapy, AF, bone loss, weight, orbitopathy, pregnancy/fetal risk, and medication adverse effects.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Thyroid nodule evaluation

Pathophysiology: Thyroid nodules are common structural lesions from benign hyperplasia/cysts, thyroiditis, adenoma, or malignancy; cancer risk depends on ultrasound pattern, size, radiation/family history, lymph nodes, growth, and compressive symptoms.

How Endocrinology assesses it: Assess radiation exposure, family thyroid cancer/MEN2, rapid growth, hoarseness, dysphagia/dyspnea, neck nodes, thyroid dysfunction symptoms, pregnancy, prior thyroid disease, and exam for fixation/lymphadenopathy.

Diagnosis: Check TSH first. If low, radionuclide scan determines hot vs cold nodule. Ultrasound characterizes size and features using ACR TI-RADS or ATA pattern; FNA is based on size/risk category. Suspicious nodes need ultrasound-guided FNA with thyroglobulin washout when appropriate.

First-line treatment: Benign or low-risk nodules are monitored with ultrasound interval based on risk; treat thyroid dysfunction separately. Hot autonomous nodules are rarely malignant and may need radioactive iodine, surgery, or antithyroid bridging if hyperthyroid.

Second-line treatment: Indeterminate cytology may use molecular testing, repeat FNA, diagnostic lobectomy, or surveillance depending on risk, size, and patient preference.

Third-line / advanced care: Surgery/endocrine referral for malignant/suspicious cytology, compressive symptoms, high-risk history, large/growing nodules, suspicious nodes, or patient preference; medullary/anaplastic concern needs urgent specialty care.

Progression and follow-up: Follow ultrasound growth, compressive symptoms, cytology results, thyroid function, post-FNA complications, and over-biopsy/over-treatment risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Adrenal insufficiency

Pathophysiology: Adrenal insufficiency is inadequate cortisol with or without aldosterone deficiency from autoimmune adrenalitis, adrenal hemorrhage/infiltration, pituitary ACTH deficiency, chronic glucocorticoid suppression, or congenital/metabolic causes, risking adrenal crisis.

How Endocrinology assesses it: Assess fatigue, weight loss, orthostasis, hyperpigmentation, salt craving, GI symptoms, hyponatremia/hyperkalemia, hypoglycemia, autoimmune disease, steroid/opioid use, pituitary disease, infection, pregnancy, and crisis signs such as shock/vomiting/altered mental status.

Diagnosis: Use 8 AM cortisol with ACTH, cosyntropin stimulation test, BMP sodium/potassium/glucose, renin/aldosterone for primary disease, 21-hydroxylase antibodies when autoimmune suspected, and pituitary/adrenal imaging based on ACTH pattern.

First-line treatment: Stable primary disease uses hydrocortisone (Cortef) or prednisone replacement plus fludrocortisone (Florinef) for mineralocorticoid deficiency; educate on sick-day dose increases, medical alert identification, and emergency hydrocortisone injection.

Second-line treatment: Secondary adrenal insufficiency uses glucocorticoid replacement without fludrocortisone and evaluation/treatment of pituitary causes; taper chronic steroids carefully and test HPA recovery.

Third-line / advanced care: Adrenal crisis requires immediate hydrocortisone IV/IM, isotonic saline with dextrose as needed, electrolyte correction, and trigger treatment; do not delay steroids for labs in unstable patients.

Progression and follow-up: Follow symptoms, BP/orthostasis, sodium/potassium, renin for primary disease, weight/Cushingoid overtreatment, bone health, infection/crisis frequency, and steroid emergency preparedness.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Cushing syndrome

Pathophysiology: Cushing syndrome is chronic glucocorticoid excess from exogenous steroids, ACTH-secreting pituitary adenoma, ectopic ACTH, or adrenal cortisol production, causing central adiposity, proximal weakness, diabetes, hypertension, osteoporosis, infection risk, thrombosis, mood disease, and skin fragility.

How Endocrinology assesses it: Assess steroid exposure including injections/creams/inhaled, weight gain, dorsocervical fat, wide purple striae, bruising, proximal weakness, menstrual/sexual dysfunction, diabetes/HTN, fractures, infections, depression, and hypokalemia/rapid virilization suggesting ectopic/adrenal disease.

Diagnosis: Screen with two abnormal first-line tests: late-night salivary cortisol, 1-mg overnight dexamethasone suppression, or 24-hour urinary free cortisol. Then measure ACTH to classify ACTH-dependent vs independent; use pituitary MRI, adrenal CT, inferior petrosal sinus sampling, or ectopic tumor imaging as indicated.

First-line treatment: Stop/taper exogenous glucocorticoids safely when possible and treat comorbid HTN/diabetes/osteoporosis/infection risk. Endogenous disease usually requires surgical source control by experienced pituitary/adrenal surgeon.

Second-line treatment: Medical therapy while awaiting surgery or for persistent disease may include ketoconazole, metyrapone (Metopirone), osilodrostat (Isturisa), mifepristone (Korlym) for hyperglycemia, or pituitary-directed therapy in selected cases.

Third-line / advanced care: Urgent endocrine care for severe hypercortisolism with infection, psychosis, hypokalemia, VTE, uncontrolled diabetes/HTN, or adrenal crisis after treatment; consider radiation or bilateral adrenalectomy for refractory disease.

Progression and follow-up: Follow cortisol remission/recurrence, adrenal insufficiency, BP/glucose, bone density, VTE, infections, mood/cognition, muscle recovery, and long-term pituitary/adrenal surveillance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Primary hyperaldosteronism

Pathophysiology: Primary hyperaldosteronism is autonomous aldosterone secretion from bilateral adrenal hyperplasia or aldosterone-producing adenoma, causing sodium retention, hypertension, potassium wasting, metabolic alkalosis, LVH, AF, CKD, and excess cardiovascular risk.

How Endocrinology assesses it: Screen in resistant HTN, hypokalemia, adrenal incidentaloma with HTN, early-onset HTN/stroke family history, sleep apnea with HTN, or severe hypertension. Assess potassium supplements, diuretics, ACE/ARB/MRA use, and BP medication effects on testing.

Diagnosis: Use aldosterone-renin ratio with corrected potassium and appropriate medication context; confirm with saline infusion, oral sodium loading, captopril, or fludrocortisone suppression when needed. Adrenal CT evaluates anatomy; adrenal venous sampling distinguishes unilateral from bilateral disease in surgical candidates.

First-line treatment: Unilateral disease can be treated with laparoscopic adrenalectomy after AVS confirmation when appropriate. Bilateral disease or nonsurgical patients use mineralocorticoid receptor antagonists spironolactone (Aldactone) or eplerenone (Inspra), plus sodium restriction and BP therapy.

Second-line treatment: Titrate MRA to BP, potassium, renin response when used, and tolerability; amiloride (Midamor) is an alternative when MRA not tolerated.

Third-line / advanced care: Refer endocrinology/hypertension specialist for diagnostic confirmation, AVS, young patients, adrenal mass, severe hypokalemia, CKD, or difficult BP control.

Progression and follow-up: Follow BP, potassium, renal function, renin/aldosterone context, AF/LVH risk, gynecomastia/menstrual side effects, and persistent hypertension after surgery.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Osteoporosis endocrine evaluation

Pathophysiology: Osteoporosis reflects low bone strength from estrogen/testosterone deficiency, aging, glucocorticoids, hyperthyroidism, hyperparathyroidism, malabsorption, CKD, diabetes, medications, low weight, smoking/alcohol, and immobility, leading to fragility fracture.

How Endocrinology assesses it: Assess prior fragility fracture, height loss, falls, steroid use, menopause/hypogonadism, kidney stones/hypercalcemia, thyroid/parathyroid disease, malabsorption/bariatric surgery, CKD, myeloma symptoms, dental plans, and medication risks.

Diagnosis: Use DXA hip/spine, vertebral imaging for height loss/back pain, FRAX when applicable, calcium/albumin, creatinine/eGFR, phosphorus, alkaline phosphatase, 25-OH vitamin D, PTH, TSH, CBC, celiac/myeloma/testosterone testing when indicated, and 24-hour urine calcium in selected cases.

First-line treatment: Ensure calcium intake, vitamin D repletion, resistance/balance exercise, fall prevention, smoking/alcohol reduction, and first-line antiresorptive therapy such as alendronate (Fosamax), risedronate (Actonel), or zoledronic acid (Reclast) when fracture risk warrants.

Second-line treatment: Use denosumab (Prolia) when appropriate with no abrupt stopping; anabolic agents teriparatide (Forteo), abaloparatide (Tymlos), or romosozumab (Evenity) for very high risk, followed by antiresorptive consolidation.

Third-line / advanced care: Endocrinology referral for young age, multiple fractures, very low BMD, CKD-mineral bone disease, hyperparathyroidism, osteomalacia, atypical femur fracture, osteonecrosis jaw concern, or treatment failure.

Progression and follow-up: Follow fracture incidence, falls, DXA interval, calcium/vitamin D, renal function, dental issues, thigh/groin pain, adherence, drug holiday timing, and secondary cause correction.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Polycystic ovary syndrome metabolic care

Pathophysiology: PCOS involves ovarian hyperandrogenism, ovulatory dysfunction, insulin resistance, genetics, adiposity, and neuroendocrine changes, increasing infertility, endometrial hyperplasia, type 2 diabetes, dyslipidemia, MASLD, OSA, and mood risk.

How Endocrinology assesses it: Assess menstrual pattern, hirsutism/acne/alopecia, infertility goals, weight, BP, acanthosis, sleep apnea, mood/eating disorder, pregnancy plans, medications, and symptoms suggesting mimics such as rapid virilization, Cushing syndrome, thyroid/prolactin disease, or adrenal tumor.

Diagnosis: Use Rotterdam-style criteria after excluding mimics: pregnancy test, TSH, prolactin, total/free testosterone, DHEAS when adrenal concern, 17-hydroxyprogesterone for nonclassic CAH risk, A1c or 2-hour OGTT, lipids, ALT/AST, and pelvic ultrasound only when needed.

First-line treatment: Lifestyle/weight management when relevant, combined hormonal contraceptive such as ethinyl estradiol/drospirenone (Yaz) or other COC for cycle control/hyperandrogenism if eligible, and metformin (Glucophage) for metabolic risk/prediabetes or cycle support.

Second-line treatment: Add spironolactone (Aldactone) for hirsutism/acne with reliable contraception and potassium monitoring; use topical eflornithine (Vaniqa) or dermatologic therapy. Letrozole (Femara) is commonly first-line ovulation induction when pregnancy desired.

Third-line / advanced care: Refer endocrinology/reproductive endocrinology for infertility, severe hyperandrogenism/virilization, diagnostic uncertainty, diabetes, suspected tumor/Cushing/CAH, or complex metabolic disease.

Progression and follow-up: Follow cycles/endometrial protection, A1c/OGTT, lipids, BP, weight, liver risk, hirsutism response, mood, pregnancy goals, and spironolactone teratogenic/potassium risks.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Pituitary adenoma

Pathophysiology: Pituitary adenomas cause symptoms by hormone excess, pituitary hormone deficiency, stalk effect hyperprolactinemia, optic chiasm compression, cavernous sinus invasion, apoplexy, or incidental mass effect.

How Endocrinology assesses it: Assess headache, visual field loss, diplopia, galactorrhea, menstrual/sexual dysfunction, infertility, acromegaly features, Cushing features, thyroid/adrenal symptoms, polyuria/polydipsia, pregnancy, and apoplexy signs such as sudden severe headache/vision loss/ophthalmoplegia.

Diagnosis: Use pituitary MRI with contrast, visual field testing for macroadenoma/optic proximity, prolactin, IGF-1, morning cortisol/ACTH or stimulation testing, TSH/free T4, LH/FSH/estradiol/testosterone, and evaluation for diabetes insipidus when polyuria. Confirm Cushing/acromegaly with dynamic testing.

First-line treatment: Prolactinomas usually use dopamine agonist cabergoline (Dostinex) or bromocriptine (Parlodel). Nonfunctioning microadenomas may be observed with MRI/labs. Replace deficient hormones carefully, giving glucocorticoid before thyroid hormone if adrenal insufficiency possible.

Second-line treatment: Functioning adenomas may need transsphenoidal surgery, somatostatin analogs octreotide (Sandostatin) or lanreotide (Somatuline), pegvisomant (Somavert), ketoconazole/metyrapone/osilodrostat for Cushing, or radiation for residual/recurrent disease.

Third-line / advanced care: Pituitary apoplexy or acute visual compromise needs urgent steroids, neurosurgery/endocrinology/ophthalmology evaluation, and possible decompression.

Progression and follow-up: Follow MRI size, visual fields, hormone excess/remission, hypopituitarism, fertility/pregnancy issues, medication adverse effects, and recurrence after surgery/radiation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Endocrinology

Obesity pharmacotherapy

Pathophysiology: Obesity pharmacotherapy treats chronic adiposity disease driven by appetite/satiety neurobiology, insulin resistance, genetics, environment, sleep, medications, and comorbid metabolic disease; medications require long-term benefit-risk monitoring rather than short cosmetic use.

How Endocrinology assesses it: Assess BMI/waist, obesity complications, BP/HR, diabetes, ASCVD, CKD, liver disease, sleep apnea, pregnancy potential, eating disorder, pancreatitis/gallbladder history, medullary thyroid cancer/MEN2 history, psychiatric history, current weight-promoting drugs, and prior treatment response.

Diagnosis: Confirm BMI eligibility and screen complications with A1c/glucose, lipids, CMP/ALT/AST, TSH only when clinically suggested, pregnancy test when relevant, OSA screen, and medication contraindication review.

First-line treatment: Use intensive lifestyle foundation plus FDA-approved medication when indicated: semaglutide (Wegovy), tirzepatide (Zepbound), liraglutide (Saxenda), phentermine-topiramate (Qsymia), naltrexone-bupropion (Contrave), or orlistat (Alli/Xenical), individualized by comorbidities and contraindications.

Second-line treatment: Adjust or switch therapy if inadequate response after an appropriate trial, manage nausea/constipation with GLP-1/GIP agents, monitor BP/HR with sympathomimetic therapy, mood/seizure risk with naltrexone-bupropion, and fat-soluble vitamins/GI effects with orlistat.

Third-line / advanced care: Refer obesity medicine/endocrinology/bariatric surgery for severe obesity, diabetes/OSA/MASH complications, medication contraindications, inadequate response, or eating disorder/pregnancy complexity.

Progression and follow-up: Follow percent weight loss, waist, A1c/BP/lipids, renal/liver function, GI adverse effects, gallbladder/pancreatitis symptoms, pregnancy avoidance where required, muscle preservation, and weight regain if therapy stops.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Specialty role

Lung and breathing specialty care for airway disease, interstitial/parenchymal disease, sleep breathing, nodules, hypoxemia, and procedures.

Pulmonology

Severe asthma phenotype assessment

Pathophysiology: Severe asthma is asthma that remains uncontrolled despite high-dose inhaled corticosteroid plus additional controller or requires that therapy to stay controlled; phenotypes include allergic, eosinophilic/type 2-high, aspirin-exacerbated, occupational, obesity-related, neutrophilic, and mimic-driven disease.

How Pulmonology assesses it: Confirm asthma diagnosis, inhaler technique, adherence, trigger exposure, smoking/vaping, occupational sensitizers, rhinitis/sinusitis/polyps, GERD/OSA/obesity, aspirin/NSAID reactions, exacerbation/steroid history, ICU/intubation history, and steroid adverse effects.

Diagnosis: Use spirometry with bronchodilator response, peak-flow variability, FeNO, blood eosinophils, total/specific IgE or allergy testing, chest imaging if atypical, CBC/CMP before biologics, and evaluate mimics such as vocal cord dysfunction, bronchiectasis, ABPA, heart failure, COPD, and eosinophilic granulomatosis with polyangiitis.

First-line treatment: Optimize fundamentals: high-dose ICS/LABA such as budesonide-formoterol (Symbicort/Breyna) or fluticasone-salmeterol (Advair/Wixela), SMART/MART strategy when appropriate, albuterol (Ventolin/ProAir) rescue, spacer technique, trigger control, vaccines, smoking cessation, and comorbidity treatment.

Second-line treatment: Add tiotropium (Spiriva Respimat), leukotriene receptor antagonist montelukast (Singulair) with neuropsychiatric warning, allergen immunotherapy in selected allergic disease, or phenotype-matched biologic such as omalizumab (Xolair), mepolizumab (Nucala), benralizumab (Fasenra), dupilumab (Dupixent), tezepelumab (Tezspire), or reslizumab (Cinqair).

Third-line / advanced care: Refer severe asthma/allergy-pulmonary specialist for biologic selection, frequent oral steroid bursts, steroid dependence, diagnostic uncertainty, occupational asthma, ABPA/EGPA concern, or life-threatening exacerbations.

Progression and follow-up: Follow exacerbations, oral steroid exposure, ACT/ACQ score, spirometry, FeNO/eosinophils when useful, biologic response, inhaler adherence, steroid toxicity, and remission/step-down opportunities.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

COPD with frequent exacerbations

Pathophysiology: COPD is chronic airflow obstruction from airway inflammation, emphysema, small-airway disease, mucus hypersecretion, and impaired gas exchange, usually from tobacco or biomass exposure; frequent exacerbations accelerate lung-function decline, hospitalization, and mortality.

How Pulmonology assesses it: Assess dyspnea, cough/sputum, exacerbation frequency, smoking/vaping/biomass, inhaler technique/adherence, oxygen saturation, eosinophil count, pneumonia history, alpha-1 antitrypsin risk, weight/cachexia, anxiety/depression, sleep apnea, and heart failure overlap.

Diagnosis: Confirm with post-bronchodilator spirometry showing obstruction, stage symptoms/exacerbations, check pulse oximetry, chest X-ray/CT when indicated, CBC/eosinophils, alpha-1 antitrypsin level for early/family/basilar disease, 6-minute walk, and ABG for chronic hypercapnia or severe hypoxemia.

First-line treatment: Core treatment is smoking cessation, vaccines, pulmonary rehab, rescue albuterol (Ventolin/ProAir) or ipratropium-albuterol (DuoNeb), and long-acting bronchodilator therapy such as tiotropium (Spiriva), umeclidinium-vilanterol (Anoro Ellipta), or tiotropium-olodaterol (Stiolto).

Second-line treatment: Frequent exacerbations may need triple therapy ICS/LABA/LAMA such as fluticasone-umeclidinium-vilanterol (Trelegy) or budesonide-glycopyrrolate-formoterol (Breztri), roflumilast (Daliresp) for chronic bronchitis with severe obstruction, or azithromycin prophylaxis in selected nonsmokers after QT/hearing risk review.

Third-line / advanced care: Exacerbations use short-acting bronchodilators, prednisone (Deltasone) short course when indicated, antibiotics such as doxycycline (Vibramycin), azithromycin (Zithromax), or amoxicillin-clavulanate (Augmentin) for purulent/severe cases, oxygen/NIV for respiratory failure, and admission for hypoxemia, hypercapnia, pneumonia, or poor support.

Progression and follow-up: Follow exacerbations, CAT/mMRC, spirometry, oxygen need, hypercapnia, inhaler technique, pneumonia, osteoporosis, weight loss, pulmonary hypertension, lung cancer screening eligibility, and advance care planning.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Interstitial lung disease

Pathophysiology: Interstitial lung disease is a group of inflammatory/fibrotic parenchymal lung disorders including idiopathic pulmonary fibrosis, connective-tissue disease ILD, hypersensitivity pneumonitis, sarcoidosis, drug-induced ILD, pneumoconiosis, and organizing pneumonia, causing restrictive physiology and impaired diffusion.

How Pulmonology assesses it: Assess dyspnea/cough trajectory, crackles/clubbing, autoimmune symptoms, exposures to birds/mold/silica/asbestos, smoking/vaping, occupational history, medications such as amiodarone/nitrofurantoin/methotrexate, family history, GERD, oxygen desaturation, and acute worsening.

Diagnosis: Use high-resolution CT chest with ILD protocol, full PFTs with DLCO, 6-minute walk/oxygen titration, autoimmune serologies guided by symptoms, hypersensitivity exposure workup, echocardiogram for pulmonary hypertension, and multidisciplinary review; bronchoscopy/BAL or surgical/cryobiopsy only when diagnosis remains uncertain and risk acceptable.

First-line treatment: Remove offending exposure/drug, vaccinate, pulmonary rehab, oxygen for exertional/resting hypoxemia, treat GERD/OSA when present, and use disease-specific therapy after ILD subtype is identified.

Second-line treatment: IPF/progressive pulmonary fibrosis may use antifibrotics nintedanib (Ofev) or pirfenidone (Esbriet); inflammatory/CTD ILD may use prednisone (Deltasone), mycophenolate (CellCept), azathioprine (Imuran), rituximab (Rituxan), or cyclophosphamide by diagnosis.

Third-line / advanced care: Refer ILD center for uncertain diagnosis, progressive fibrosis, transplant evaluation, acute exacerbation, pulmonary hypertension, or need for biopsy/advanced immunosuppression; admit for acute hypoxemic worsening.

Progression and follow-up: Follow FVC, DLCO, 6-minute walk, oxygen needs, HRCT progression, liver tests with antifibrotics, diarrhea/photosensitivity, infection risk from immunosuppression, pulmonary hypertension, and transplant timing.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Pulmonary nodule evaluation

Pathophysiology: Pulmonary nodules may represent benign granuloma, scar, infection, hamartoma, inflammatory lesion, metastasis, or primary lung cancer; malignancy risk depends on size, growth, solid/subsolid type, spiculation, upper-lobe location, smoking, age, cancer history, and immune status.

How Pulmonology assesses it: Assess prior imaging, nodule size/type, smoking pack-years, lung cancer screening status, occupational/radon exposure, cancer history, immunosuppression, infection/TB/fungal risk, symptoms, family history, and surgical candidacy.

Diagnosis: Compare prior CTs, use thin-slice chest CT, apply Fleischner for incidental nodules or Lung-RADS for screening nodules, and estimate pretest malignancy risk. PET/CT, CT-guided biopsy, bronchoscopy/robotic navigation, or surgical excision is considered for larger/growing/high-risk nodules.

First-line treatment: Low-risk small nodules often need no follow-up or interval CT only; intermediate nodules need scheduled CT surveillance based on size/type/risk. Counsel smoking cessation and ensure closed-loop tracking of follow-up dates.

Second-line treatment: Nodules over 8 mm, growth, suspicious morphology, or high-risk clinical context may need PET/CT, tissue diagnosis, or thoracic surgery/pulmonary nodule clinic review.

Third-line / advanced care: Urgent referral for suspected cancer, hemoptysis, obstructing lesion, mediastinal nodes, immunocompromised infection concern, or missed follow-up. Multidisciplinary tumor board is appropriate when malignancy probability is significant.

Progression and follow-up: Follow nodule growth/doubling time, change from ground-glass to solid, biopsy complications, radiation exposure, patient anxiety, smoking cessation, and transition to lung cancer staging if malignant.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Chronic cough

Pathophysiology: Chronic cough over 8 weeks commonly arises from upper airway cough syndrome, asthma/cough-variant asthma, nonasthmatic eosinophilic bronchitis, GERD/laryngopharyngeal reflux, ACE inhibitor use, smoking/COPD, bronchiectasis, ILD, infection, or malignancy.

How Pulmonology assesses it: Assess duration, sputum/hemoptysis, dyspnea/wheeze, rhinitis/postnasal drip, reflux, ACE inhibitor, smoking/vaping, occupational exposure, asthma history, infection/TB risk, weight loss, fever, and red flags.

Diagnosis: Initial evaluation includes chest X-ray, spirometry with bronchodilator, medication review, and targeted tests: FeNO/eosinophils, methacholine challenge, sinus evaluation, reflux evaluation, CT chest for abnormal X-ray/red flags, and sputum studies when infection/bronchiectasis suspected.

First-line treatment: Treat likely causes sequentially: stop ACE inhibitor, intranasal fluticasone (Flonase) plus antihistamine for upper airway cough syndrome, inhaled corticosteroid such as budesonide (Pulmicort) or fluticasone for asthma/eosinophilic bronchitis, smoking cessation, and GERD lifestyle/PPI trial when reflux features exist.

Second-line treatment: If refractory, confirm adherence/technique and consider CT chest, ENT laryngoscopy, pulmonology referral, speech therapy for cough hypersensitivity, gabapentin (Neurontin) in selected refractory cough, or disease-specific therapy.

Third-line / advanced care: Urgent evaluation for hemoptysis, hypoxia, weight loss, abnormal imaging, recurrent pneumonia, immunocompromise, aspiration, suspected malignancy, or TB.

Progression and follow-up: Follow cough frequency/severity, sleep/work impact, spirometry, imaging resolution, medication adverse effects, and emergence of red flags.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Hemoptysis

Pathophysiology: Hemoptysis is bleeding from lower respiratory tract due to bronchitis, pneumonia, bronchiectasis, TB/fungal infection, cancer, pulmonary embolism, vasculitis, diffuse alveolar hemorrhage, anticoagulation, or vascular malformation; massive bleeding threatens airway before blood loss.

How Pulmonology assesses it: Quantify volume/rate, confirm pulmonary vs GI/nasal source, assess airway, oxygenation, hemodynamics, anticoagulants/antiplatelets, TB/cancer risk, infection symptoms, bronchiectasis, PE risk, renal/vasculitis symptoms, and recurrent episodes.

Diagnosis: Use chest X-ray initially, CBC/coags/type and screen for significant bleeding, CMP/renal function, CT angiography chest or contrast CT to localize source, sputum AFB/culture when TB/infection risk, bronchoscopy for airway control/localization or persistent high-risk bleeding.

First-line treatment: Small-volume stable hemoptysis is treated by cause, such as antibiotics for pneumonia/bronchitis when bacterial features exist, holding/reversing anticoagulation when safe, and close follow-up with imaging.

Second-line treatment: Persistent or moderate bleeding needs pulmonology evaluation, CT-guided localization, bronchoscopy, and treatment of bronchiectasis/infection/PE/vasculitis; tranexamic acid may be used in selected settings by specialist/local protocol.

Third-line / advanced care: Massive or unstable hemoptysis requires ED/ICU, airway protection bleeding-side down, large-bore access, reversal of coagulopathy, bronchoscopy, bronchial artery embolization, and thoracic surgery backup.

Progression and follow-up: Follow recurrence, anemia, oxygenation, imaging resolution, malignancy/TB exclusion, anticoagulation restart timing, and complications of embolization/bronchoscopy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Pleural effusion

Pathophysiology: Pleural effusion is fluid accumulation from transudative hydrostatic/oncotic imbalance such as heart failure/cirrhosis/nephrosis or exudative inflammation/malignancy/infection/PE/pancreatitis/autoimmune disease.

How Pulmonology assesses it: Assess dyspnea, pleuritic pain, fever, weight loss, cancer history, heart/liver/kidney disease, PE risk, TB exposure, trauma, medications, oxygenation, and whether effusion is unilateral, large, loculated, or recurrent.

Diagnosis: Use chest X-ray and ultrasound; thoracentesis for new unilateral, large, febrile, atypical, or non-heart-failure effusions. Send pleural protein/LDH for Light criteria, cell count/differential, Gram stain/culture, pH/glucose for parapneumonic effusion, cytology, triglycerides, ADA/TB studies when indicated.

First-line treatment: Treat underlying cause: diuretics such as furosemide (Lasix) for heart failure effusion when typical, antibiotics for parapneumonic infection, anticoagulation for PE, and therapeutic thoracentesis for symptomatic large effusion.

Second-line treatment: Complicated parapneumonic effusion/empyema may need chest tube drainage, intrapleural tPA/DNase, or VATS; malignant effusion may need repeated thoracentesis, indwelling pleural catheter, or pleurodesis.

Third-line / advanced care: Urgent admission for hypoxemia, empyema/sepsis, massive effusion, tension physiology, hemothorax, or rapidly recurrent malignant effusion.

Progression and follow-up: Follow symptom relief, recurrence, pleural fluid results, pneumothorax after thoracentesis, infection control, malignancy diagnosis, and need for definitive pleural procedure.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Sleep apnea

Pathophysiology: Obstructive sleep apnea is recurrent upper-airway collapse during sleep causing intermittent hypoxemia, arousals, sympathetic activation, sleep fragmentation, pulmonary/systemic hypertension risk, AF, insulin resistance, and daytime sleepiness.

How Pulmonology assesses it: Assess snoring, witnessed apneas, gasping, daytime sleepiness, morning headaches, resistant hypertension, AF, heart failure, stroke, obesity/neck circumference, sedatives/opioids/alcohol, driving risk, nasal obstruction, and occupational safety.

Diagnosis: Use STOP-Bang or similar screen, home sleep apnea test for uncomplicated high-probability OSA, in-lab polysomnography for cardiopulmonary disease, hypoventilation, neuromuscular disease, opioids, central apnea concern, or negative home test with high suspicion.

First-line treatment: First-line therapy is CPAP/APAP with mask fitting, humidification, adherence coaching, weight management, side-sleeping, avoiding alcohol/sedatives near bedtime, and treating nasal obstruction.

Second-line treatment: Alternatives include mandibular advancement oral appliance for mild/moderate OSA or CPAP-intolerant patients, positional therapy, bilevel PAP for hypoventilation/pressure intolerance, and GLP-1/GIP weight therapy or bariatric referral when obesity drives disease.

Third-line / advanced care: Refer sleep medicine/ENT for PAP failure, central sleep apnea, obesity hypoventilation, severe hypoxemia, commercial driver clearance, surgical options such as hypoglossal nerve stimulation, or complex cardiopulmonary disease.

Progression and follow-up: Follow PAP adherence, residual AHI, leak, sleepiness, BP, AF burden, driving safety, weight, nocturnal oxygenation, and mask/skin complications.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Pulmonary hypertension

Pathophysiology: Pulmonary hypertension is elevated pulmonary pressures from pulmonary arterial vascular remodeling, left heart disease, chronic lung disease/hypoxia, chronic thromboembolic disease, or multifactorial causes, leading to RV strain, failure, syncope, and death.

How Pulmonology assesses it: Assess exertional dyspnea, syncope, chest pain, edema, connective tissue disease, congenital heart disease, portal HTN, HIV, methamphetamine/anorexigen exposure, PE/VTE history, OSA/COPD/ILD, left heart disease, oxygen saturation, and signs of RV failure.

Diagnosis: Screen with echocardiogram, BNP/NT-proBNP, ECG, chest imaging, PFTs/DLCO, sleep testing, V/Q scan for CTEPH, CT angiography when needed, autoimmune/HIV/liver testing by risk, and confirm/classify with right-heart catheterization before PAH-specific therapy.

First-line treatment: Treat underlying cause: diuretics for right-heart congestion, oxygen for hypoxemia, CPAP for OSA, anticoagulation for CTEPH/VTE when indicated, and optimize left heart/lung disease. Avoid empiric PAH vasodilators without classification.

Second-line treatment: Confirmed PAH may use endothelin receptor antagonists ambrisentan (Letairis) or bosentan (Tracleer), PDE-5 inhibitors sildenafil (Revatio) or tadalafil (Adcirca), soluble guanylate cyclase stimulator riociguat (Adempas), prostacyclin therapies epoprostenol (Flolan/Veletri), treprostinil (Remodulin/Tyvaso), or selexipag (Uptravi) by risk.

Third-line / advanced care: Refer pulmonary hypertension center for right-heart cath, PAH therapy, CTEPH operability/pulmonary endarterectomy or balloon angioplasty, transplant evaluation, pregnancy counseling, or high-risk features.

Progression and follow-up: Follow WHO functional class, 6-minute walk, BNP, echo/RV function, oxygen, syncope, edema, liver/kidney function, medication toxicity, and hospitalization risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Bronchiectasis

Pathophysiology: Bronchiectasis is irreversible bronchial dilation from chronic infection/inflammation and impaired mucus clearance due to prior infection, immune deficiency, cystic fibrosis/CFTR disease, primary ciliary dyskinesia, aspiration, ABPA, autoimmune disease, or obstruction.

How Pulmonology assesses it: Assess chronic productive cough, sputum volume, hemoptysis, recurrent pneumonia, sinus disease, aspiration/GERD, asthma/ABPA, immune deficiency, NTM/TB risk, smoking, exacerbation frequency, and prior cultures including Pseudomonas.

Diagnosis: Confirm with high-resolution CT chest; obtain sputum culture including AFB/NTM, spirometry, CBC, immunoglobulins, ABPA testing (IgE/Aspergillus), alpha-1 antitrypsin when indicated, swallow/aspiration evaluation, and CF/PCD testing for suggestive history.

First-line treatment: Daily airway clearance with oscillatory PEP/chest physiotherapy, exercise, hydration, vaccines, smoking cessation, and bronchodilator if obstructive symptoms. Treat exacerbations with culture-guided antibiotics such as amoxicillin-clavulanate (Augmentin), doxycycline (Vibramycin), levofloxacin (Levaquin), or ciprofloxacin (Cipro) when Pseudomonas risk.

Second-line treatment: Frequent exacerbators may need long-term macrolide azithromycin after NTM exclusion/QT-hearing review, inhaled antibiotics for chronic Pseudomonas, hypertonic saline, or treatment of ABPA/immune deficiency/aspiration.

Third-line / advanced care: Hospitalize for hypoxemia, sepsis, massive hemoptysis, resistant organisms, failed oral therapy, or severe exacerbation needing IV antibiotics. Bronchial artery embolization for significant hemoptysis.

Progression and follow-up: Follow exacerbations, sputum microbiology, lung function, CT progression, hemoptysis, NTM risk, hearing/QT with macrolides, antibiotic resistance, and quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Respiratory failure follow-up

Pathophysiology: Post-respiratory failure recovery involves residual lung injury, respiratory muscle weakness, deconditioning, dysphagia/aspiration, oxygen or ventilatory dependence, cognitive/psychological ICU sequelae, and recurrence risk from unresolved cardiopulmonary disease.

How Pulmonology assesses it: Review cause of respiratory failure, intubation/NIV course, tracheostomy, oxygen requirement, exertional dyspnea, cough, swallowing, sleep symptoms, weakness, cognition/mood, medications, imaging, cultures, and readmission triggers.

Diagnosis: Use pulse oximetry at rest/exertion, oxygen titration/6-minute walk, PFTs when stable, chest X-ray/CT follow-up when infiltrates/ARDS/ILD suspected, ABG/VBG for hypercapnia, sleep study for OSA/hypoventilation, swallow evaluation when aspiration risk, and medication review.

First-line treatment: Create recovery plan: oxygen weaning if criteria met, pulmonary rehab/PT, inhaler optimization, nutrition, vaccines, smoking cessation, secretion clearance, and follow-up imaging/testing based on original disease.

Second-line treatment: Use CPAP/BiPAP/NIV for OSA, obesity hypoventilation, neuromuscular weakness, or chronic hypercapnic COPD when indicated; treat anxiety/PTSD, dysphagia, and deconditioning actively.

Third-line / advanced care: Urgent care for worsening hypoxemia, hypercapnia, recurrent pneumonia, hemoptysis, chest pain/PE concern, trach complications, inability to clear secretions, or failed home oxygen/NIV support.

Progression and follow-up: Follow oxygen/NIV adherence, exertional capacity, PFT recovery, imaging resolution, readmissions, cognition/mood, swallowing, nutrition, and goals of care after severe illness.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Occupational lung disease

Pathophysiology: Occupational lung disease results from inhaled dusts, fumes, vapors, sensitizers, or fibers causing asthma, COPD, pneumoconiosis, hypersensitivity pneumonitis, metal fume fever, bronchiolitis, malignancy, or pleural disease.

How Pulmonology assesses it: Take detailed job/exposure history, tasks, materials, PPE, symptom timing at work vs away, coworkers affected, silica/asbestos/coal/beryllium/isocyanate/grain/mold exposure, smoking, latency, and workers compensation documentation needs.

Diagnosis: Use spirometry with bronchodilator, serial peak flows at and away from work for occupational asthma, DLCO, chest X-ray/HRCT for pneumoconiosis/ILD/pleural plaques, specific IgE or sensitizer testing when available, beryllium lymphocyte proliferation test for beryllium, and exposure records/SDS review.

First-line treatment: Primary treatment is exposure removal or reduction, workplace controls/PPE, smoking cessation, vaccines, and disease-specific therapy such as inhaled corticosteroid/LABA for occupational asthma or bronchodilators for COPD.

Second-line treatment: Progressive fibrotic disease may need ILD evaluation, oxygen, pulmonary rehab, antifibrotic or immunosuppressive therapy depending on subtype, and occupational medicine support for accommodations/claims.

Third-line / advanced care: Refer occupational medicine/pulmonology for diagnostic documentation, severe or progressive disease, suspected silicosis/asbestosis/berylliosis, malignancy, cluster/outbreak, or workplace reporting needs.

Progression and follow-up: Follow lung function, exposure cessation, imaging progression, work capacity, compensation documentation, cancer screening when indicated, and mental/financial impact.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Sarcoidosis pulmonary disease

Pathophysiology: Sarcoidosis is multisystem granulomatous inflammation of unclear cause, commonly involving lungs and lymph nodes, with possible skin, eye, cardiac, neurologic, hepatic, renal, and calcium metabolism involvement.

How Pulmonology assesses it: Assess cough, dyspnea, chest pain, fatigue, erythema nodosum, uveitis/vision symptoms, palpitations/syncope, neurologic symptoms, kidney stones, hypercalcemia symptoms, occupational/infectious mimics, and medication/exposure history.

Diagnosis: Use chest X-ray/CT pattern, PFTs/DLCO, calcium, creatinine, liver tests, ECG, eye exam, and biopsy showing noncaseating granulomas when diagnosis uncertain or treatment needed, while excluding TB/fungal infection, lymphoma, berylliosis, and other granulomatous disease.

First-line treatment: Asymptomatic stage I or mild disease may be observed with monitoring. Treat symptomatic/progressive pulmonary or organ-threatening disease with prednisone (Deltasone) using the lowest effective dose and taper plan.

Second-line treatment: Steroid-sparing therapy includes methotrexate (Trexall), azathioprine (Imuran), mycophenolate (CellCept), hydroxychloroquine (Plaquenil) for skin/calcium symptoms, or anti-TNF infliximab (Remicade) for refractory disease.

Third-line / advanced care: Urgent specialty care for cardiac sarcoid, neurosarcoid, severe ocular disease, pulmonary hypertension, advanced fibrosis, hypercalcemia renal injury, or respiratory failure; consider transplant referral for end-stage disease.

Progression and follow-up: Follow symptoms, PFTs, imaging, calcium/renal/liver labs, ECG/cardiac symptoms, eye disease, steroid toxicity, relapse, and fibrosis/pulmonary hypertension.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pulmonology

Long COVID dyspnea

Pathophysiology: Long COVID dyspnea may reflect post-viral airway hyperreactivity, dysautonomia, deconditioning, dysfunctional breathing, residual parenchymal disease, pulmonary vascular disease, cardiac injury, anemia, sleep disorder, or mood/anxiety overlap.

How Pulmonology assesses it: Assess initial COVID severity, hospitalization/PE/ARDS history, exertional desaturation, chest pain, palpitations, cough/wheeze, fatigue/post-exertional malaise, orthostatic symptoms, sleep, mood, anemia risk, and functional baseline.

Diagnosis: Use pulse oximetry including exertion, chest X-ray, PFTs with DLCO, CBC/CMP/TSH when indicated, ECG/echo for cardiac symptoms, CT chest for abnormal imaging or persistent hypoxemia, CT pulmonary angiography/VQ when PE risk, and cardiopulmonary exercise testing for unclear exertional limitation.

First-line treatment: Treat identified drivers: pulmonary rehab or paced rehabilitation when post-exertional malaise absent, breathing retraining, albuterol (Ventolin/ProAir) or inhaled corticosteroid when airway disease documented, sleep optimization, and gradual return-to-activity plan.

Second-line treatment: Manage dysautonomia with fluids/salt/compression and specialist input, treat OSA/anemia/asthma/ILD/PE specifically, and address anxiety/depression without dismissing physiologic symptoms.

Third-line / advanced care: Refer pulmonology/cardiology/long-COVID clinic for hypoxemia, abnormal CT/PFT/DLCO, suspected pulmonary vascular disease, post-ICU syndrome, severe functional impairment, or diagnostic uncertainty.

Progression and follow-up: Follow exertional oxygen saturation, 6-minute walk, PFTs, symptom scores, post-exertional crashes, work/school function, mood/sleep, and new cardiopulmonary red flags.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Specialty role

Digestive and liver specialty care focused on endoscopy, inflammatory disease, motility, hepatobiliary disease, and cancer prevention.

Gastroenterology and Hepatology

GERD refractory symptoms

Pathophysiology: Refractory GERD symptoms may reflect persistent acid reflux, weakly acidic/nonacid reflux, reflux hypersensitivity, functional heartburn, eosinophilic esophagitis, gastroparesis, rumination, pill injury, cardiac disease, or poor PPI timing/adherence.

How Gastroenterology and Hepatology assesses it: Assess heartburn/regurgitation, dysphagia, odynophagia, weight loss, bleeding/anemia, vomiting, chest pain cardiac evaluation, PPI timing before meals, NSAIDs/bisphosphonates/potassium/iron, obesity, pregnancy, tobacco, alcohol, late meals, and prior endoscopy.

Diagnosis: Alarm symptoms need EGD. If no alarm symptoms, confirm optimized 8-week PPI trial. Persistent symptoms may need EGD off PPI when possible, biopsies for eosinophilic esophagitis, ambulatory pH or pH-impedance monitoring on/off PPI depending on prior objective GERD, and manometry before antireflux procedures.

First-line treatment: Optimize PPI use: omeprazole (Prilosec), esomeprazole (Nexium), pantoprazole (Protonix), or rabeprazole before breakfast; lifestyle includes weight loss when relevant, head-of-bed elevation, avoiding late meals, tobacco cessation, and trigger review.

Second-line treatment: Escalate to twice-daily PPI temporarily, switch PPI, add bedtime famotidine (Pepcid) for nocturnal symptoms, alginate antacid, or baclofen only for selected regurgitation with side-effect caution. Treat EoE, gastroparesis, or functional heartburn specifically if found.

Third-line / advanced care: GI referral for alarm features, refractory symptoms, Barrett risk, strictures, suspected EoE, need for pH/manometry, or antireflux surgery/endoscopic therapy evaluation such as fundoplication or magnetic sphincter augmentation.

Progression and follow-up: Follow symptom response, dysphagia/bleeding, PPI adverse risks, need for long-term lowest effective dose, Barrett/stricture complications, and whether symptoms are truly reflux-driven.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Barrett esophagus surveillance

Pathophysiology: Barrett esophagus is intestinal metaplasia of distal esophageal mucosa from chronic reflux injury, increasing risk for dysplasia and esophageal adenocarcinoma; risk rises with segment length, male sex, age, obesity, smoking, and family history.

How Gastroenterology and Hepatology assesses it: Assess GERD duration, dysphagia, weight loss, bleeding, prior endoscopy/pathology, segment length, dysplasia history, PPI adherence, obesity/tobacco, family esophageal cancer, and procedure fitness.

Diagnosis: Confirm with EGD showing columnar mucosa plus biopsies demonstrating intestinal metaplasia; use Seattle protocol biopsies and targeted biopsies of visible lesions. Expert pathology review is recommended for dysplasia.

First-line treatment: Use daily PPI such as omeprazole (Prilosec) or pantoprazole (Protonix), reflux risk reduction, tobacco cessation, weight management, and surveillance EGD intervals based on nondysplastic vs indefinite/low-grade/high-grade dysplasia and segment length.

Second-line treatment: Confirmed low-grade dysplasia generally prompts endoscopic eradication therapy or close surveillance; high-grade dysplasia/intramucosal carcinoma requires endoscopic mucosal resection of visible lesions and radiofrequency ablation/eradication therapy in expert centers.

Third-line / advanced care: Refer advanced endoscopy/esophageal center for dysplasia, nodularity, long-segment disease with uncertainty, recurrent strictures, or post-ablation surveillance; surgery/oncology for invasive cancer.

Progression and follow-up: Follow dysplasia progression/regression, eradication of intestinal metaplasia, strictures after ablation, reflux control, adherence to surveillance, and cancer symptoms.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Peptic ulcer disease

Pathophysiology: Peptic ulcer disease is mucosal injury from H. pylori, NSAIDs/aspirin, acid-pepsin imbalance, physiologic stress, smoking, malignancy, or rare hypersecretory states, causing epigastric pain, bleeding, perforation, gastric outlet obstruction, or anemia.

How Gastroenterology and Hepatology assesses it: Assess epigastric pain relation to meals, melena/hematemesis, anemia symptoms, NSAID/aspirin/anticoagulant/steroid/SSRI use, H. pylori history, weight loss, vomiting, dysphagia, older age, cancer risk, and hemodynamic stability.

Diagnosis: Use H. pylori stool antigen or urea breath test when uncomplicated; EGD for alarm features, bleeding, severe/recurrent symptoms, older/high-risk patients, or suspected gastric ulcer needing biopsy. Check CBC/iron, BUN/creatinine, and type/screen if bleeding.

First-line treatment: Stop NSAIDs when possible, treat with PPI such as pantoprazole (Protonix) or omeprazole (Prilosec), eradicate H. pylori if present, avoid smoking, and use gastroprotection if antiplatelet/NSAID must continue.

Second-line treatment: For persistent/recurrent ulcers, confirm H. pylori eradication, review NSAID/salicylate exposure, assess adherence, consider Zollinger-Ellison with fasting gastrin/gastric pH when severe/refractory/multiple, and repeat EGD for gastric ulcer healing/excluding cancer.

Third-line / advanced care: Urgent endoscopy for bleeding; surgery/interventional radiology for perforation, uncontrolled bleeding, or obstruction; admit for hemodynamic instability, severe anemia, peritonitis, or high-risk bleeding stigmata.

Progression and follow-up: Follow pain, bleeding recurrence, hemoglobin/iron, H. pylori test-of-cure, ulcer healing when indicated, PPI duration, and medication risk modification.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

H pylori infection

Pathophysiology: Helicobacter pylori colonizes gastric mucosa, causing chronic gastritis, peptic ulcer disease, iron deficiency, B12 deficiency, MALT lymphoma, and gastric cancer risk through inflammation, urease activity, and virulence factors.

How Gastroenterology and Hepatology assesses it: Assess ulcer/dyspepsia symptoms, prior eradication regimens, macrolide/fluoroquinolone exposure, penicillin allergy, pregnancy, GI bleeding, family gastric cancer, MALT lymphoma, unexplained iron deficiency, and need for test-of-cure.

Diagnosis: Use urea breath test, stool antigen, or biopsy-based testing. Avoid false negatives by holding PPIs about 2 weeks and bismuth/antibiotics about 4 weeks when feasible. Endoscopy is used for alarm features, bleeding, older/high-risk dyspepsia, or gastric ulcer.

First-line treatment: When susceptibility is unknown, preferred empiric treatment is optimized bismuth quadruple therapy for 14 days: PPI twice daily plus bismuth subsalicylate/subcitrate, tetracycline, and metronidazole (Flagyl). Avoid clarithromycin or levofloxacin regimens unless susceptibility is known.

Second-line treatment: Salvage depends on prior regimen: use bismuth quadruple if not used, rifabutin triple therapy with rifabutin/amoxicillin/PPI, or susceptibility-guided therapy. Vonoprazan-amoxicillin dual or vonoprazan-based regimens may be options depending on availability/allergy.

Third-line / advanced care: GI referral for multiple failures, penicillin allergy complexity, MALT lymphoma, gastric premalignant lesions, bleeding ulcers, or need for susceptibility testing/endoscopy.

Progression and follow-up: Confirm eradication in all treated patients with stool antigen or urea breath test at least 4 weeks after therapy and off PPI when possible; follow ulcer healing, anemia, recurrence, antibiotic adverse effects, and reinfection risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Irritable bowel syndrome

Pathophysiology: IBS is a disorder of gut-brain interaction involving visceral hypersensitivity, altered motility, microbiome changes, postinfectious immune activation, bile acid effects, diet triggers, stress, and central pain processing without structural disease.

How Gastroenterology and Hepatology assesses it: Assess abdominal pain related to defecation and stool change, diarrhea/constipation pattern, bloating, alarm features, nocturnal symptoms, weight loss, GI bleeding, anemia, family IBD/colon cancer/celiac, medications, diet, stress, and pelvic floor symptoms.

Diagnosis: Use Rome criteria with limited testing: CBC, CRP or fecal calprotectin when diarrhea/IBD concern, celiac serology for IBS-D/mixed, stool tests for infection when risk, colonoscopy for age-appropriate screening or alarm features. Avoid broad imaging/endoscopy without red flags.

First-line treatment: Education, reassurance, exercise, sleep/stress care, soluble fiber psyllium for IBS-C/mixed, low-FODMAP trial with reintroduction, peppermint oil, and loperamide (Imodium) only for diarrhea control when safe.

Second-line treatment: IBS-C options include polyethylene glycol (MiraLAX), linaclotide (Linzess), plecanatide (Trulance), lubiprostone (Amitiza), or tenapanor (Ibsrela). IBS-D options include rifaximin (Xifaxan), eluxadoline (Viberzi) when no contraindications, bile-acid sequestrant trial, or low-dose tricyclic such as nortriptyline (Pamelor).

Third-line / advanced care: GI referral for alarm features, refractory symptoms, suspected IBD/celiac/microscopic colitis, severe weight loss, complex pelvic floor dysfunction, or diagnostic uncertainty.

Progression and follow-up: Follow stool pattern, pain interference, diet restriction/nutrition, medication adverse effects, mood/anxiety, opioid avoidance, and red-flag evolution.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Inflammatory bowel disease

Pathophysiology: IBD includes Crohn disease and ulcerative colitis, immune-mediated intestinal inflammation with genetic, microbial, barrier, and environmental drivers; Crohn can be transmural/skip lesions anywhere GI tract, while UC is continuous colonic mucosal disease.

How Gastroenterology and Hepatology assesses it: Assess diarrhea, blood, urgency, nocturnal stools, abdominal pain, weight loss, fever, perianal disease, extraintestinal symptoms, growth/fertility, smoking, NSAIDs, infection risks, vaccines, TB/hepatitis status, and prior biologic/immunomodulator exposure.

Diagnosis: Use CBC, CMP, CRP/ESR, fecal calprotectin, stool C. difficile/culture when flare, colonoscopy with ileoscopy and biopsies, CT/MR enterography for Crohn small bowel/complications, and pelvic MRI for fistulizing perianal disease.

First-line treatment: Mild UC may use mesalamine (Lialda/Asacol/Canasa). Induction of moderate/severe flares may require corticosteroids such as prednisone or budesonide formulations, but steroids are not maintenance. Optimize vaccines and nutrition.

Second-line treatment: Maintenance/advanced therapy includes anti-TNF infliximab (Remicade), adalimumab (Humira), vedolizumab (Entyvio), ustekinumab (Stelara), risankizumab (Skyrizi), ozanimod (Zeposia), upadacitinib (Rinvoq), thiopurines, or methotrexate by phenotype and risk.

Third-line / advanced care: Urgent care for toxic megacolon, severe bleeding, perforation, abscess, obstruction, severe steroid-refractory colitis, sepsis, or perianal abscess; surgery for refractory UC, dysplasia/cancer, strictures, fistulas, or complications.

Progression and follow-up: Follow symptoms, fecal calprotectin/CRP, drug levels/antibodies when relevant, colonoscopy mucosal healing, infection/malignancy risk, bone health, vaccines, pregnancy planning, and colorectal cancer surveillance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Celiac disease

Pathophysiology: Celiac disease is immune-mediated small-intestinal injury triggered by gluten in genetically susceptible individuals, causing villous atrophy, malabsorption, iron deficiency, diarrhea, bloating, osteoporosis, infertility, neuropathy, dermatitis herpetiformis, and lymphoma risk.

How Gastroenterology and Hepatology assesses it: Assess diarrhea/constipation, bloating, weight loss, anemia, fatigue, rash, mouth ulcers, neuropathy, infertility, osteoporosis, type 1 diabetes/autoimmune thyroid disease, family history, IgA deficiency, and whether the patient is already gluten-free.

Diagnosis: Test while eating gluten: tissue transglutaminase IgA plus total IgA; use deamidated gliadin IgG or tTG IgG for IgA deficiency. Confirm adults commonly with EGD/duodenal biopsies. Check CBC, iron/ferritin, folate/B12, vitamin D, calcium, liver enzymes, and bone density when indicated.

First-line treatment: Strict lifelong gluten-free diet with dietitian education, label/cross-contamination counseling, correction of iron/vitamin deficiencies, and vaccines/health maintenance as needed.

Second-line treatment: If symptoms or serologies persist, check gluten exposure first, then evaluate lactose intolerance, IBS, microscopic colitis, pancreatic insufficiency, SIBO, or refractory celiac disease.

Third-line / advanced care: GI referral for diagnostic uncertainty, severe malnutrition, refractory disease, ulcerative jejunoileitis/lymphoma concern, pregnancy/fertility issues, or complicated nutrient deficiencies.

Progression and follow-up: Follow symptom response, tTG normalization, weight/nutrition, iron/vitamin levels, bone health, adherence barriers, and malignancy warning signs.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Chronic constipation

Pathophysiology: Chronic constipation results from slow transit, defecatory disorder/pelvic floor dyssynergia, IBS-C, low fiber/fluid, immobility, neurologic disease, endocrine/metabolic disease, obstruction, or medications such as opioids, anticholinergics, calcium, iron, and calcium-channel blockers.

How Gastroenterology and Hepatology assesses it: Assess stool frequency/form, straining, incomplete evacuation, manual maneuvers, alarm symptoms, opioid/anticholinergic use, diet/fluid, mobility, neurologic symptoms, hypothyroid/hypercalcemia symptoms, pelvic surgery, and colon cancer screening status.

Diagnosis: Use clinical diagnosis and digital rectal exam. Colonoscopy for alarm features or screening indications. Check TSH, calcium, glucose, or CBC only when suggested. Refractory cases need anorectal manometry, balloon expulsion, defecography, or transit study.

First-line treatment: First-line treatment is fiber/psyllium with fluids, exercise, toileting routine after meals, medication review, and osmotic laxative polyethylene glycol (MiraLAX). Senna or bisacodyl can be used short-term/rescue.

Second-line treatment: Prescription options include lubiprostone (Amitiza), linaclotide (Linzess), plecanatide (Trulance), prucalopride (Motegrity), or methylnaltrexone (Relistor)/naloxegol (Movantik) for opioid-induced constipation.

Third-line / advanced care: Pelvic floor biofeedback for dyssynergia; urgent evaluation for obstruction, severe pain/distention, vomiting, GI bleeding, weight loss, fecal impaction with complications, or suspected volvulus.

Progression and follow-up: Follow stool pattern, bloating, electrolyte issues from laxatives, dependence concerns, impaction, quality of life, and alarm symptom development.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Chronic diarrhea

Pathophysiology: Chronic diarrhea arises from osmotic, secretory, inflammatory, malabsorptive, bile-acid, medication-related, endocrine, infectious, pancreatic, or functional causes.

How Gastroenterology and Hepatology assesses it: Assess duration, stool volume/nocturnal symptoms, blood/fat/oil, weight loss, fever, travel, antibiotics, immunosuppression, diet sweeteners/lactose, metformin/PPIs/NSAIDs/magnesium, prior surgery/cholecystectomy, IBD/celiac family history, and HIV risk.

Diagnosis: Initial tests may include CBC, CMP, CRP, celiac serology, TSH when indicated, fecal calprotectin/lactoferrin, stool C. difficile if antibiotic/healthcare risk, Giardia/ova/parasite by exposure, fecal fat/elastase when malabsorption suspected, colonoscopy with biopsies for microscopic colitis/IBD/alarm features.

First-line treatment: Treat dehydration/electrolytes, stop culprit medications, use oral rehydration, dietary lactose/FODMAP trial when likely, and loperamide (Imodium) only when no inflammatory/infectious red flags.

Second-line treatment: Cause-specific therapy includes cholestyramine (Questran) for bile-acid diarrhea, rifaximin (Xifaxan) for selected IBS-D/SIBO, pancreatic enzymes pancrelipase (Creon) for pancreatic insufficiency, budesonide (Entocort) for microscopic colitis, or IBD/infection treatment.

Third-line / advanced care: Urgent evaluation for severe dehydration, bloody diarrhea, high fever, sepsis, severe electrolyte derangement, immunocompromise, significant weight loss, or suspected severe colitis/toxic megacolon.

Progression and follow-up: Follow stool frequency, weight, hydration, electrolytes, nutritional deficiencies, medication response, colonoscopy/pathology results, and recurrence.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Diverticulitis recurrent disease

Pathophysiology: Diverticulitis is inflammation/microperforation of colonic diverticula, ranging from uncomplicated localized inflammation to abscess, perforation, fistula, obstruction, or sepsis; recurrence risk is influenced by prior severity, age, immune status, obesity, smoking, and NSAID use.

How Gastroenterology and Hepatology assesses it: Assess LLQ pain, fever, bowel changes, peritoneal signs, prior episodes/CT findings, immunosuppression, PO tolerance, pregnancy, urinary/vaginal symptoms, colonoscopy history, and complications such as abscess/fistula.

Diagnosis: CT abdomen/pelvis with contrast confirms diagnosis and complications when first episode, severe, atypical, immunocompromised, or recurrent uncertainty. CBC/CMP/CRP, urinalysis, pregnancy test when relevant. Colonoscopy after recovery if not recently done or cancer concern.

First-line treatment: Uncomplicated mild disease in immunocompetent patients may be managed outpatient with clear diet advancement, analgesia avoiding NSAIDs when possible, and selective antibiotics rather than automatic antibiotics.

Second-line treatment: When antibiotics are indicated use amoxicillin-clavulanate (Augmentin) or ciprofloxacin (Cipro) plus metronidazole (Flagyl) when appropriate; abscess may need percutaneous drainage plus antibiotics.

Third-line / advanced care: Admit/surgery for perforation, peritonitis, sepsis, obstruction, fistula, large abscess, failed outpatient care, immunocompromise, or inability to tolerate PO. Elective colectomy decisions are individualized, not based only on episode count.

Progression and follow-up: Follow recurrence, colonoscopy completion, abscess/fistula/stricture, diet/fiber pattern, smoking/NSAID risk, antibiotic adverse effects, and surgical decision-making.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Acute pancreatitis

Pathophysiology: Acute pancreatitis is pancreatic inflammation from premature enzyme activation, commonly gallstones or alcohol, also hypertriglyceridemia, medications, ERCP, hypercalcemia, trauma, malignancy, or idiopathic causes; severe disease causes necrosis, organ failure, and infection.

How Gastroenterology and Hepatology assesses it: Assess epigastric pain radiating to back, vomiting, alcohol, gallstones, triglyceride risk, meds, prior episodes, fever, hypotension, hypoxia, renal injury, mental status, and severity predictors.

Diagnosis: Diagnosis requires two of three: typical pain, lipase/amylase at least 3 times upper limit, or imaging. Check CBC/CMP/LFTs/bilirubin, calcium, triglycerides, BUN/creatinine, RUQ ultrasound for gallstones, CT abdomen if diagnosis unclear or worsening after 48-72 hours, MRCP/EUS for suspected CBD stone/idiopathic disease.

First-line treatment: Early aggressive but monitored IV lactated Ringer fluids, analgesia such as hydromorphone or morphine when needed, antiemetic ondansetron (Zofran), early oral/enteral feeding as tolerated, and treat cause. Avoid prophylactic antibiotics in sterile pancreatitis.

Second-line treatment: Gallstone pancreatitis needs cholecystectomy during index admission for mild disease; ERCP for cholangitis or persistent biliary obstruction. Hypertriglyceridemia needs insulin infusion/plasmapheresis selectively and fibrate/omega-3 prevention later.

Third-line / advanced care: ICU/admit for organ failure, necrosis, sepsis, cholangitis, severe electrolyte/renal issues, hypoxia, or infected necrosis needing antibiotics/drainage/necrosectomy in step-up approach.

Progression and follow-up: Follow pain, oral tolerance, BUN/creatinine, oxygenation, necrosis/pseudocyst, diabetes/exocrine insufficiency, alcohol cessation, triglycerides, and gallstone definitive management.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Chronic liver disease

Pathophysiology: Chronic liver disease results from MASLD/MASH, alcohol-associated liver disease, viral hepatitis, autoimmune hepatitis, cholestatic disease, hemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency, drug injury, or vascular disease progressing to fibrosis/cirrhosis.

How Gastroenterology and Hepatology assesses it: Assess alcohol, metabolic risk, viral risks, medications/supplements, family history, pruritus, jaundice, ascites/edema, encephalopathy, GI bleeding, sarcopenia, vaccines, and hepatotoxic exposures.

Diagnosis: Use hepatic panel, INR, albumin, platelets, CBC, viral hepatitis serologies, iron studies/ferritin/transferrin saturation, autoimmune markers, ceruloplasmin in young/selected patients, A1AT phenotype, ultrasound, elastography/FibroScan, fibrosis scores such as FIB-4, and biopsy when noninvasive tests are inconclusive.

First-line treatment: Treat cause: weight loss/metabolic control for MASLD, alcohol abstinence with medications such as naltrexone (Revia/Vivitrol) or acamprosate (Campral) when appropriate, antiviral therapy for HBV/HCV, stop hepatotoxins, vaccinate HAV/HBV if nonimmune, and avoid unnecessary NSAIDs.

Second-line treatment: Advanced fibrosis/cirrhosis requires HCC surveillance ultrasound with or without AFP every 6 months, variceal screening, nutrition/protein support, sarcopenia prevention, and management of ascites/encephalopathy/bleeding risk.

Third-line / advanced care: Hepatology referral for cirrhosis, unclear etiology, autoimmune/cholestatic disease, high fibrosis scores, decompensation, transplant evaluation, or suspected HCC.

Progression and follow-up: Follow MELD/Child-Pugh elements, platelets, INR/albumin/bilirubin, fibrosis progression, HCC surveillance, varices, ascites, encephalopathy, renal function, and alcohol/metabolic control.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Cirrhosis complications

Pathophysiology: Cirrhosis is advanced hepatic fibrosis with portal hypertension and liver synthetic dysfunction; complications include ascites, SBP, varices, hepatic encephalopathy, hepatorenal syndrome, HCC, sarcopenia, coagulopathy, and infections.

How Gastroenterology and Hepatology assesses it: Assess ascites/edema, GI bleeding, confusion/sleep reversal, jaundice, fever/abdominal pain, renal function, alcohol use, medications, nutrition, falls, vaccinations, transplant candidacy, and goals of care.

Diagnosis: Use CBC/CMP/INR, bilirubin/albumin/creatinine/sodium for MELD, ultrasound for ascites/HCC, diagnostic paracentesis for new/worsening ascites or hospitalization, ascitic PMN count/culture/albumin/protein, EGD for varices, and evaluate precipitating infection/bleeding/constipation for encephalopathy.

First-line treatment: Ascites: sodium restriction, spironolactone (Aldactone) plus furosemide (Lasix) when tolerated, therapeutic paracentesis with albumin for large-volume removal. Encephalopathy: lactulose (Constulose) titrated to bowel movements; add rifaximin (Xifaxan) for recurrence.

Second-line treatment: Variceal prophylaxis uses nonselective beta blocker carvedilol (Coreg), propranolol (Inderal), or nadolol (Corgard), or endoscopic band ligation. SBP uses ceftriaxone/cefotaxime acutely plus albumin in selected patients and prophylaxis such as ciprofloxacin or TMP-SMX when indicated.

Third-line / advanced care: Urgent admission for GI bleeding, SBP/sepsis, AKI/HRS, severe encephalopathy, hyponatremia, tense ascites with respiratory compromise, or suspected HCC. TIPS, transplant evaluation, and palliative care should be considered when decompensated.

Progression and follow-up: Follow MELD, renal sodium, ascites control, encephalopathy episodes, variceal surveillance, HCC screening, nutrition/sarcopenia, medication renal safety, transplant timing, and goals.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Viral hepatitis

Pathophysiology: Viral hepatitis includes HAV, HBV, HCV, HDV, and HEV causing acute hepatocellular injury, chronic infection for HBV/HCV/HDV, cirrhosis, liver failure, and hepatocellular carcinoma.

How Gastroenterology and Hepatology assesses it: Assess exposure risk, injection/intranasal drug use, transfusion before screening era, birth country, sexual/perinatal risk, tattoos/incarceration, jaundice, fatigue, RUQ pain, alcohol, pregnancy, HIV, immunosuppression, and cirrhosis signs.

Diagnosis: Use HAV IgM for acute HAV; HBV panel with HBsAg, anti-HBs, anti-HBc IgM/total, HBeAg/HBV DNA when infected; HCV antibody with reflex RNA; genotype rarely needed for pangenotypic therapy but cirrhosis staging is essential. Check CMP/INR/CBC, HIV, pregnancy, fibrosis staging, and HCC surveillance if cirrhosis/HBV risk.

First-line treatment: HAV is supportive and prevented by vaccination. HCV is treated with direct-acting antivirals such as glecaprevir-pibrentasvir (Mavyret) or sofosbuvir-velpatasvir (Epclusa) depending on cirrhosis, interactions, and prior therapy. HBV treatment decisions use HBV DNA, ALT, fibrosis, age, and risk; options include tenofovir alafenamide (Vemlidy), tenofovir DF (Viread), or entecavir (Baraclude).

Second-line treatment: Manage coinfections, vaccinate HAV/HBV when nonimmune, counsel transmission prevention, avoid alcohol/hepatotoxins, and monitor HBV reactivation risk before immunosuppression or HCV treatment.

Third-line / advanced care: Hepatology referral for decompensated cirrhosis, HBV pregnancy, HDV, acute liver failure, complex renal disease, prior DAA failure, transplant, or HCC concern.

Progression and follow-up: Follow viral load response/SVR, ALT, fibrosis/cirrhosis, HCC surveillance, renal/bone effects of antivirals, HBV flare/reactivation, and household/sexual contact testing/vaccination.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

Colon cancer screening abnormal result

Pathophysiology: An abnormal colorectal cancer screening test indicates increased probability of adenoma, serrated lesion, cancer, bleeding lesion, or false-positive result; benefit depends on timely diagnostic colonoscopy and complete polyp removal/pathology.

How Gastroenterology and Hepatology assesses it: Assess which test was abnormal (FIT, stool DNA-FIT, CT colonography, sigmoidoscopy, colonoscopy), bleeding/anemia/weight loss, family history, prior polyps, anticoagulants, bowel prep barriers, comorbidity/life expectancy, and access/transportation.

Diagnosis: Positive FIT or stool DNA-FIT requires diagnostic colonoscopy, not repeat stool testing. CT colonography abnormality needs colonoscopy depending on lesion size. Colonoscopy findings require pathology-based surveillance interval using number, size, histology, dysplasia, serrated features, and prep quality.

First-line treatment: Close the loop: schedule colonoscopy, manage anticoagulant/diabetes meds safely, ensure bowel prep instructions, address transportation/cost, and document results/pathology.

Second-line treatment: Large/complex polyps may need advanced endoscopic mucosal resection or surgical referral; iron deficiency anemia or mass requires staging CT, CEA, and oncology/surgery pathway if cancer confirmed.

Third-line / advanced care: Urgent evaluation for obstructive symptoms, overt bleeding with instability, severe anemia, suspected cancer, or failed/incomplete colonoscopy needing alternative completion.

Progression and follow-up: Follow colonoscopy completion, pathology, surveillance interval, family risk update, complications, and patient adherence to the next due date.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Gastroenterology and Hepatology

GI bleeding

Pathophysiology: GI bleeding can be upper, lower, or small-bowel from peptic ulcer, varices, erosive disease, Mallory-Weiss tear, malignancy, angiodysplasia, diverticular bleeding, IBD, ischemic colitis, hemorrhoids, or medication-related mucosal injury/anticoagulation.

How Gastroenterology and Hepatology assesses it: Assess hematemesis, coffee-ground emesis, melena, hematochezia, syncope, abdominal pain, liver disease, NSAIDs/aspirin/anticoagulants/antiplatelets, prior bleed, vitals/orthostasis, comorbid CAD/CKD, and shock.

Diagnosis: Use CBC trend, CMP/BUN/creatinine, INR/coags when anticoagulated/liver disease, type and screen/crossmatch, lactate if shock, risk scores, EGD for suspected upper bleeding, colonoscopy after prep for lower bleeding, CTA abdomen/pelvis for brisk ongoing bleeding, and capsule/enteroscopy for obscure bleeding.

First-line treatment: Stabilize airway/breathing/circulation, two large-bore IVs, restrictive transfusion strategy unless massive bleed/ischemia changes target, hold/reverse anticoagulation when appropriate, IV pantoprazole (Protonix) for suspected ulcer bleeding, and ceftriaxone plus octreotide (Sandostatin) for suspected variceal bleed.

Second-line treatment: Endoscopic therapy may include clips, cautery, injection, band ligation for varices, hemostatic powder, or treatment of angiodysplasia. H. pylori eradication and NSAID cessation prevent recurrent ulcer bleeding.

Third-line / advanced care: ICU/interventional radiology/surgery for shock, ongoing bleeding despite endoscopy, variceal hemorrhage needing TIPS, massive transfusion, or perforation/ischemia concern.

Progression and follow-up: Follow rebleeding, hemoglobin/iron, hemodynamics, endoscopy findings, anticoagulation restart timing, PPI duration, variceal secondary prophylaxis, and malignancy/pathology results.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Specialty role

Kidney, electrolyte, acid-base, hypertension, dialysis, transplant, and renal dosing specialty care.

Nephrology

Chronic kidney disease staging

Pathophysiology: CKD is persistent kidney structure or function abnormality for at least 3 months, staged by eGFR G1-G5 and albuminuria A1-A3; risk is driven by cause, GFR, albuminuria, diabetes, hypertension, ASCVD/HF, age, and complications.

How Nephrology assesses it: Assess cause, eGFR trajectory, albuminuria, BP, diabetes, ASCVD/HF, hematuria, nephrotoxins, NSAIDs/contrast, urinary obstruction, family history, pregnancy potential, diet/salt, medication dosing, and symptoms of uremia or volume overload.

Diagnosis: Confirm chronicity with repeat creatinine/eGFR and urine albumin-creatinine ratio; use urinalysis microscopy, urine protein-creatinine ratio when needed, renal ultrasound for obstruction/size/asymmetry, cystatin C when creatinine is unreliable, and targeted serologies for active sediment/systemic disease.

First-line treatment: Treat cause and risk: BP control, sodium reduction, ACE inhibitor/ARB such as lisinopril (Zestril) or losartan (Cozaar) for albuminuria when tolerated, SGLT2 inhibitor empagliflozin (Jardiance) or dapagliflozin (Farxiga) when criteria fit, statin for ASCVD risk, diabetes optimization, and avoid NSAIDs/nephrotoxins.

Second-line treatment: Manage complications with bicarbonate for metabolic acidosis, iron/ESA for selected anemia, phosphate/PTH/vitamin D strategy in advanced CKD, diuretics for volume, potassium binders for hyperkalemia, vaccines, and renal dose adjustment.

Third-line / advanced care: Nephrology referral for eGFR below 30, rapid decline, severe albuminuria, active urine sediment, resistant HTN, recurrent AKI, electrolyte/acidosis complications, uncertain cause, or dialysis/transplant planning.

Progression and follow-up: Follow eGFR slope, albuminuria, BP, potassium, bicarbonate, anemia, CKD-MBD labs, volume, medication dosing, cardiovascular events, and kidney failure risk prediction.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Rapidly progressive kidney dysfunction

Pathophysiology: Rapid kidney function decline suggests AKI/AKD, rapidly progressive glomerulonephritis, obstruction, renal vascular disease, thrombotic microangiopathy, interstitial nephritis, myeloma kidney, malignant hypertension, or medication/toxin injury.

How Nephrology assesses it: Assess timing, urine output, volume status, BP, hematuria/proteinuria, edema, rash/arthralgia/pulmonary symptoms, infection, new drugs such as NSAIDs/PPIs/antibiotics, contrast, obstruction symptoms, paraprotein symptoms, and systemic red flags.

Diagnosis: Repeat BMP/creatinine, urinalysis with microscopy for casts/dysmorphic RBCs, urine protein/albumin ratio, renal ultrasound for obstruction, CBC/platelets/smear, complements, ANA/dsDNA, ANCA, anti-GBM, hepatitis/HIV, SPEP/UPEP/free light chains, CK, and kidney biopsy when intrinsic disease is suspected and safe.

First-line treatment: Stop nephrotoxins, optimize hemodynamics/volume, relieve obstruction, control severe BP, treat infection, adjust all renally cleared drugs, and urgently involve nephrology when active sediment or rapid decline is present.

Second-line treatment: Disease-specific therapy may include high-dose glucocorticoids, rituximab (Rituxan), cyclophosphamide (Cytoxan), plasma exchange for selected anti-GBM/severe pulmonary hemorrhage cases, or clone-directed therapy for myeloma, but only after urgent nephrology-directed evaluation.

Third-line / advanced care: Emergent dialysis for refractory hyperkalemia, acidosis, pulmonary edema, uremic complications, or toxic ingestion; urgent biopsy/admission for suspected RPGN, TMA, anti-GBM, lupus nephritis, vasculitis, or severe AKI.

Progression and follow-up: Follow creatinine/eGFR daily when acute, urine output, electrolytes, acid-base, biopsy/serology results, drug levels, dialysis need, and transition to CKD follow-up after AKI.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Albuminuria and proteinuria

Pathophysiology: Albuminuria/proteinuria reflects glomerular barrier injury, tubular dysfunction, overflow proteins, orthostatic/transient proteinuria, diabetes, hypertension, obesity, infection, autoimmune disease, or monoclonal gammopathy; higher albuminuria predicts CKD progression and cardiovascular risk.

How Nephrology assesses it: Assess diabetes, BP, edema, hematuria, foamy urine, pregnancy, fever/exercise, UTI symptoms, obesity, autoimmune symptoms, NSAIDs, family kidney disease, and nephrotic symptoms.

Diagnosis: Quantify with urine albumin-creatinine ratio and/or protein-creatinine ratio, repeat to confirm persistence, urinalysis microscopy, serum creatinine/eGFR, albumin/lipids when nephrotic range, and targeted serologies/SPEP/free light chains if hematuria, systemic features, or heavy proteinuria. Consider kidney biopsy for unexplained nephrotic-range or active sediment.

First-line treatment: Treat underlying cause, optimize BP, use ACE inhibitor/ARB such as lisinopril or losartan for albuminuria when tolerated, add SGLT2 inhibitor when indicated, reduce sodium, control diabetes, and stop NSAIDs.

Second-line treatment: Finerenone (Kerendia) may help selected type 2 diabetes with persistent albuminuria; GLP-1 RA may help diabetic/metabolic risk. Nephrotic syndrome may need diuretics, statin, anticoagulation assessment, and immunosuppression by biopsy diagnosis.

Third-line / advanced care: Nephrology referral for ACR A3, nephrotic-range proteinuria, hematuria/casts, rapid eGFR decline, low complements, systemic disease, pregnancy, or suspected monoclonal gammopathy.

Progression and follow-up: Follow albuminuria/proteinuria response, eGFR, potassium, BP, edema, serum albumin, lipids, thrombosis risk, and medication tolerance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Acute kidney injury

Pathophysiology: AKI is abrupt kidney function decline from prerenal hypoperfusion, intrinsic tubular/glomerular/interstitial/vascular injury, or postrenal obstruction; it increases mortality and later CKD risk even after apparent recovery.

How Nephrology assesses it: Assess baseline creatinine, timing, urine output, volume losses, sepsis, hypotension, heart/liver failure, nephrotoxins, contrast, NSAIDs, ACE/ARB/diuretics, urinary obstruction, rhabdomyolysis, hematuria/proteinuria, rash/eosinophilia, and uremic symptoms.

Diagnosis: Use serial creatinine/eGFR, urine output, urinalysis microscopy, urine sodium/FENa or FEUrea only in selected contexts, BMP/electrolytes, CK, renal ultrasound for obstruction risk, medication review, and serologies/biopsy when glomerular or interstitial disease suspected.

First-line treatment: Treat cause: restore perfusion with balanced fluids when hypovolemic, stop nephrotoxins, adjust drug doses, relieve obstruction with catheter/stent/nephrostomy, manage sepsis/hemodynamics, avoid unnecessary contrast, and monitor potassium/acid-base/volume closely.

Second-line treatment: Use diuretics such as furosemide (Lasix) only for volume overload, not to force renal recovery. Treat hyperkalemia, acidosis, and complications specifically; avoid low-value dopamine/fenoldopam strategies.

Third-line / advanced care: Urgent nephrology/dialysis for refractory hyperkalemia, severe acidosis, pulmonary edema/volume overload, uremic pericarditis/encephalopathy/bleeding, certain toxins, or severe/prolonged AKI with unclear cause.

Progression and follow-up: Follow creatinine, urine output, potassium, bicarbonate, volume, medication restart timing, AKI-to-CKD transition, and repeat kidney function/albuminuria after discharge.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Hyperkalemia

Pathophysiology: Hyperkalemia results from reduced renal excretion, RAAS blockade/MRA, potassium supplements, acidosis, insulin deficiency, tissue breakdown, hemolysis, adrenal insufficiency, or pseudohyperkalemia; severe elevations destabilize cardiac conduction.

How Nephrology assesses it: Assess symptoms, ECG risk, CKD/AKI, diabetes/DKA, medications including ACE/ARB/MRA/TMP-SMX/NSAIDs/heparin, supplements/salt substitutes, missed dialysis, weakness/paralysis, and whether sample hemolysis or thrombocytosis suggests pseudohyperkalemia.

Diagnosis: Repeat potassium if unexpected and stable; obtain ECG, BMP/creatinine/bicarbonate/glucose, magnesium, CK when rhabdo possible, VBG/ABG for acidosis, and review medications/diet. Do not delay treatment for ECG changes or severe potassium.

First-line treatment: If ECG changes or severe hyperkalemia: IV calcium gluconate for membrane stabilization, insulin plus dextrose, albuterol nebulization, treat acidosis when appropriate, stop potassium-raising drugs, and use loop diuretic/fluids if volume status allows.

Second-line treatment: Remove potassium with sodium zirconium cyclosilicate (Lokelma), patiromer (Veltassa), sodium polystyrene sulfonate rarely/with caution, diuresis, or dialysis. Chronic management uses diet review and medication adjustment while preserving ACE/ARB/SGLT2/MRA benefits when safe.

Third-line / advanced care: Emergency dialysis for refractory hyperkalemia, severe CKD/AKI, missed dialysis, ongoing tissue breakdown, or life-threatening ECG instability.

Progression and follow-up: Follow repeat potassium after therapy, glucose after insulin, ECG, renal function, bowel tolerance with binders, recurrence after medication restart, and RAAS inhibitor risk-benefit.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Hyponatremia

Pathophysiology: Hyponatremia is low serum sodium from excess water relative to solute due to hypovolemia, SIADH, heart failure/cirrhosis, kidney failure, thiazides, adrenal insufficiency, hypothyroidism, low-solute intake, polydipsia, or hyperglycemia; rapid shifts risk cerebral edema or osmotic demyelination.

How Nephrology assesses it: Assess acuity, neurologic symptoms, seizures, falls, nausea, volume status, medications such as thiazides/SSRIs/carbamazepine, pain/nausea, pulmonary/CNS disease, heart/liver/kidney disease, adrenal symptoms, alcohol/low solute intake, and glucose.

Diagnosis: Check serum osmolality, urine osmolality, urine sodium, glucose-corrected sodium, BMP, TSH and morning cortisol when indicated, and assess chronicity. Severe symptomatic cases require immediate treatment while labs are pending.

First-line treatment: Severe symptomatic hyponatremia uses 3% hypertonic saline bolus protocol with close sodium checks. Hypovolemic hyponatremia uses isotonic saline; SIADH uses fluid restriction and cause/drug treatment; hypervolemic uses sodium/fluid restriction plus loop diuretics.

Second-line treatment: Consider oral urea, salt tablets plus loop diuretic, or vasopressin antagonists such as tolvaptan (Samsca) only in selected monitored cases. Use desmopressin (DDAVP) and D5W to prevent or reverse overcorrection when risk is high.

Third-line / advanced care: ICU/nephrology for seizures, severe sodium derangement, rapid correction risk, liver disease, alcoholism/malnutrition, adrenal crisis, or unclear mixed physiology.

Progression and follow-up: Follow sodium correction rate, neurologic status, urine output, potassium, recurrence, medication causes, and osmotic demyelination risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Metabolic acidosis

Pathophysiology: Metabolic acidosis reflects acid accumulation or bicarbonate loss from CKD, lactic acidosis, ketoacidosis, diarrhea, renal tubular acidosis, toxins, or advanced shock; chronic acidosis accelerates bone/muscle loss and CKD progression.

How Nephrology assesses it: Assess respiratory compensation, shock/sepsis, kidney disease, diarrhea, diabetes/DKA, alcohol/starvation, toxin exposure, medications such as metformin/topiramate/SGLT2 inhibitors, hyperkalemia/hypokalemia, and volume status.

Diagnosis: Use BMP with anion gap, VBG/ABG, lactate, ketones/beta-hydroxybutyrate, glucose, creatinine/eGFR, urinalysis, urine anion gap/osmolal gap when RTA suspected, salicylate/toxic alcohol testing when indicated, and albumin-corrected anion gap.

First-line treatment: Treat cause: fluids/perfusion for lactic acidosis, insulin/fluids/potassium for DKA, stop offending drugs, bicarbonate replacement for CKD or bicarbonate-loss states when indicated, and manage diarrhea/renal tubular acidosis specifically.

Second-line treatment: Oral sodium bicarbonate or sodium citrate can be used in CKD/RTA with monitoring for sodium load/volume/BP; potassium citrate may help selected stone/RTA patients with hypokalemia.

Third-line / advanced care: ICU/nephrology/dialysis for severe acidemia, AKI/CKD with refractory acidosis, toxic alcohols, severe lactic acidosis with shock, or DKA/HHS requiring protocolized care.

Progression and follow-up: Follow bicarbonate, anion gap, potassium, volume/BP, renal function, bone/muscle health, stones in RTA, and recurrence triggers.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Nephrotic syndrome

Pathophysiology: Nephrotic syndrome is heavy proteinuria causing hypoalbuminemia, edema, hyperlipidemia, and thrombosis risk from glomerular diseases such as minimal change disease, FSGS, membranous nephropathy, diabetic kidney disease, lupus, amyloidosis, and infections/drugs.

How Nephrology assesses it: Assess edema/anasarca, foamy urine, weight gain, thrombotic symptoms, infections, diabetes, autoimmune symptoms, malignancy risk, hepatitis/HIV, NSAIDs, family history, and BP.

Diagnosis: Quantify proteinuria with UPCR/24-hour when needed, serum albumin/lipids, creatinine/eGFR, urinalysis microscopy, complements, ANA/dsDNA, PLA2R antibodies, hepatitis B/C/HIV, SPEP/free light chains, diabetes evaluation, and kidney biopsy in most adults without obvious diabetic cause.

First-line treatment: Supportive care: sodium restriction, loop diuretic furosemide (Lasix) or torsemide, ACE/ARB for proteinuria when tolerated, SGLT2 inhibitor when indicated, statin, vaccines, and infection/thrombosis risk assessment.

Second-line treatment: Disease-specific therapy may include prednisone (Deltasone) for minimal change, rituximab (Rituxan) or calcineurin inhibitors tacrolimus/cyclosporine, cyclophosphamide, mycophenolate, or targeted therapy depending on biopsy diagnosis.

Third-line / advanced care: Urgent nephrology for AKI, severe anasarca, nephrotic-range proteinuria, suspected renal vein thrombosis/PE, severe hypoalbuminemia, infection, or need for biopsy/immunosuppression.

Progression and follow-up: Follow proteinuria, albumin, edema/weight, renal function, lipids, thrombosis/infection, immunosuppression toxicity, and relapse/remission.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Glomerulonephritis

Pathophysiology: Glomerulonephritis is immune, complement, infection-related, anti-GBM, ANCA vasculitic, lupus, IgA, membranous, or proliferative glomerular inflammation causing hematuria, proteinuria, casts, hypertension, edema, and kidney decline.

How Nephrology assesses it: Assess hematuria, cola urine, edema, BP, recent infection, rash/purpura, arthritis, sinus/pulmonary symptoms, hemoptysis, neuropathy, autoimmune symptoms, hepatitis/HIV risk, medications, and family history.

Diagnosis: Use urinalysis microscopy for dysmorphic RBCs/RBC casts, UPCR/UACR, creatinine/eGFR, complements C3/C4, ANA/dsDNA, ANCA, anti-GBM, hepatitis B/C/HIV, ASO/anti-DNase B when postinfectious suspected, SPEP/free light chains, and kidney biopsy for diagnosis/prognosis when significant or progressive.

First-line treatment: Control BP/proteinuria with ACE/ARB when safe, manage edema with diuretics, avoid nephrotoxins, treat infection triggers, and urgently classify with nephrology when active sediment or declining GFR.

Second-line treatment: Immunosuppression depends on biopsy and severity: glucocorticoids, rituximab (Rituxan), cyclophosphamide (Cytoxan), mycophenolate (CellCept), calcineurin inhibitors, complement-directed therapy, or plasma exchange in selected anti-GBM/severe pulmonary hemorrhage contexts.

Third-line / advanced care: Hospitalize for RPGN, pulmonary-renal syndrome, severe hypertension, AKI, nephritic-nephrotic syndrome, anti-GBM, ANCA vasculitis, lupus nephritis flare, or dialysis indications.

Progression and follow-up: Follow creatinine/eGFR, proteinuria, hematuria/casts, BP, complements/serologies by disease, infection prophylaxis, immunosuppression toxicity, relapse, and CKD progression.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Kidney stone metabolic prevention

Pathophysiology: Kidney stones form from urinary supersaturation of calcium oxalate/phosphate, uric acid, struvite, or cystine due to low urine volume, hypercalciuria, hypocitraturia, hyperoxaluria, hyperuricosuria, infection, diet, bowel disease, medications, or genetic disorders.

How Nephrology assesses it: Assess stone history, imaging, stone analysis, family history, diet sodium/animal protein/oxalate, fluid intake, bowel disease/bariatric surgery, gout, UTIs, medications such as topiramate/loop diuretics, and solitary kidney/CKD.

Diagnosis: Analyze stone when available; basic evaluation includes BMP/creatinine/calcium, uric acid when indicated, urinalysis/pH/culture, and imaging. Recurrent/high-risk stones need 24-hour urine for volume, calcium, oxalate, citrate, uric acid, sodium, pH, and supersaturation.

First-line treatment: Increase fluids to produce high urine volume, reduce sodium, moderate animal protein, maintain normal dietary calcium with meals, reduce high-oxalate foods when hyperoxaluria, and treat UTIs.

Second-line treatment: Medication prevention by phenotype: thiazide such as chlorthalidone (Thalitone) for hypercalciuria, potassium citrate (Urocit-K) for hypocitraturia/uric acid/cystine support, allopurinol (Zyloprim) for hyperuricosuria or uric acid stones, and urine alkalinization for uric acid stones.

Third-line / advanced care: Urology/nephrology referral for recurrent stones, cystinuria, struvite/staghorn stone, solitary kidney, CKD, obstruction, infection, pregnancy, or failed prevention.

Progression and follow-up: Follow stone recurrence, 24-hour urine response, serum potassium/bicarbonate with citrate, sodium/calcium targets, medication adverse effects, and imaging burden.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Dialysis planning

Pathophysiology: Dialysis planning prepares for kidney replacement therapy before uremic crisis, matching modality and access to prognosis, anatomy, comorbid disease, home support, transplant eligibility, and patient goals.

How Nephrology assesses it: Assess eGFR trend, kidney failure risk, uremic symptoms, volume/electrolyte control, cognition, frailty, vascular anatomy, abdominal surgeries/hernia, home environment, caregiver support, work/travel, transplant interest, and conservative kidney management goals.

Diagnosis: Use eGFR trajectory, albuminuria, complications, kidney failure risk equation, labs for anemia/mineral/acidosis/potassium, modality education, transplant evaluation, vein mapping for hemodialysis access, and peritoneal dialysis candidacy assessment.

First-line treatment: Start education in advanced CKD, preserve arm veins by avoiding PICCs/subclavian lines, manage CKD complications, discuss hemodialysis vs peritoneal dialysis vs transplant vs conservative care, and refer for AV fistula/graft planning when appropriate.

Second-line treatment: Place PD catheter or AV access in time for intended start; use tunneled dialysis catheter only when urgent/no mature access. Optimize vaccines, nutrition, anemia, volume, and medication dosing.

Third-line / advanced care: Urgent dialysis for refractory hyperkalemia, acidosis, pulmonary edema, uremic pericarditis/encephalopathy/bleeding, severe symptoms, or certain toxins; hospitalize when unstable.

Progression and follow-up: Follow access maturation, modality readiness, transplant waitlist status, symptoms, labs, volume, caregiver support, and whether dialysis remains aligned with goals.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Renal transplant follow-up

Pathophysiology: Kidney transplant follow-up balances graft function, rejection risk, infection risk, malignancy risk, cardiovascular/metabolic complications, recurrent kidney disease, and toxicity from calcineurin inhibitors and other immunosuppression.

How Nephrology assesses it: Assess creatinine trend, urine protein, BP, edema, fever, dysuria, graft tenderness, adherence, drug levels, diarrhea/vomiting affecting absorption, new medications/interactions, skin lesions, cancer screening, vaccines, diabetes/lipids, and opportunistic infection symptoms.

Diagnosis: Monitor creatinine/eGFR, urinalysis/UACR or UPCR, tacrolimus/cyclosporine levels, CBC/CMP, BK virus PCR per protocol, donor-specific antibodies when concern, ultrasound for obstruction/vascular issue, and kidney allograft biopsy for unexplained dysfunction/proteinuria or rejection concern.

First-line treatment: Maintenance regimens commonly include tacrolimus (Prograf/Envarsus/Astagraf), mycophenolate mofetil (CellCept/Myfortic), and prednisone; manage BP, diabetes, lipids, bone health, and infection prophylaxis per transplant protocol.

Second-line treatment: Adjust immunosuppression for drug levels, renal toxicity, leukopenia, infection, BK viremia, pregnancy plans, or rejection. Avoid interacting drugs such as azoles/macrolides/diltiazem without transplant input; avoid live vaccines.

Third-line / advanced care: Urgent transplant center contact for rising creatinine, suspected rejection, severe infection, BK nephropathy, obstructive uropathy, medication interruption, pregnancy, malignancy, or inability to obtain immunosuppression.

Progression and follow-up: Follow graft function, proteinuria, drug toxicity, infection, malignancy/skin cancer, cardiovascular risk, adherence, vaccination, recurrent disease, and long-term graft survival.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Medication renal dosing

Pathophysiology: Renal dosing prevents accumulation, toxicity, or underdosing when kidney clearance changes due to CKD, AKI, dialysis, age-related low muscle mass, or tubular secretion competition.

How Nephrology assesses it: Assess current creatinine trend, AKI vs stable CKD, actual/ideal body weight, age/frailty, dialysis modality/timing, indication severity, therapeutic window, nephrotoxins, and drugs needing renal adjustment such as antibiotics, DOACs, diabetes drugs, gabapentinoids, opioids, antivirals, and contrast.

Diagnosis: Estimate kidney function using eGFR and Cockcroft-Gault creatinine clearance when drug labeling requires; consider cystatin C or measured clearance when creatinine is unreliable. Check drug levels for vancomycin, aminoglycosides, lithium, digoxin, and selected antiseizure drugs.

First-line treatment: Adjust dose/interval or choose safer alternatives. Examples: reduce gabapentin (Neurontin), pregabalin (Lyrica), levetiracetam (Keppra), many antibiotics, metformin by eGFR thresholds, and DOACs such as apixaban/rivaroxaban per label; avoid NSAIDs and inappropriate nitrofurantoin when renal function is too low.

Second-line treatment: During AKI, hold or reassess ACE/ARB/diuretics/SGLT2/metformin when clinically appropriate, then restart when stable if benefits outweigh risks. Coordinate dialysis-day dosing for dialyzable drugs.

Third-line / advanced care: Pharmacy/nephrology consult for severe AKI/CKD, dialysis, transplant, chemotherapy, narrow-therapeutic-index drugs, obesity/cachexia, pregnancy, or discordant eGFR/CrCl.

Progression and follow-up: Follow efficacy, toxicity, renal recovery/decline, drug levels, electrolytes, sedation/bleeding/hypoglycemia, and dose changes after discharge or dialysis transitions.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Nephrology

Resistant hypertension renal causes

Pathophysiology: Renal causes of resistant hypertension include CKD sodium retention, renal artery stenosis, primary aldosteronism, obstructive sleep apnea with kidney disease, glomerulonephritis, polycystic kidney disease, medication/nephrotoxin effects, and volume overload.

How Nephrology assesses it: Confirm true resistant hypertension with proper technique and home/ambulatory readings; assess sodium intake, adherence, NSAIDs/decongestants/stimulants, CKD/albuminuria, hypokalemia, abdominal bruit, asymmetric kidneys, flash pulmonary edema, sleep apnea, hematuria, and family kidney disease.

Diagnosis: Use BMP/creatinine/eGFR/potassium, urinalysis/UACR, aldosterone-renin ratio, renal ultrasound, renal artery duplex/CTA/MRA when renovascular features, sleep study when indicated, and urine microscopy/serologies if nephritic features.

First-line treatment: Optimize volume and sodium: sodium restriction, chlorthalidone (Thalitone) if kidney function allows, loop diuretic torsemide (Demadex) or furosemide (Lasix) for advanced CKD/volume overload, ACE/ARB for albuminuria when tolerated, and amlodipine (Norvasc) or other complementary agents.

Second-line treatment: Add spironolactone (Aldactone) or eplerenone (Inspra) for resistant HTN if potassium/eGFR allow; potassium binders may help maintain RAAS/MRA therapy. Treat OSA, stop NSAIDs, and manage CKD/metabolic disease.

Third-line / advanced care: Nephrology/hypertension referral for suspected renovascular disease, primary aldosteronism, severe CKD, recurrent hyperkalemia, glomerular disease, hypertensive emergency, or uncontrolled BP despite multidrug therapy.

Progression and follow-up: Follow BP logs, volume/weight, eGFR, potassium, albuminuria, medication adverse effects, secondary-cause results, cardiovascular events, and kidney progression.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Specialty role

Complex infection diagnosis, antimicrobial stewardship, resistance, immunocompromised hosts, HIV, travel, and public health conditions.

Infectious Disease

Sepsis antimicrobial strategy

Pathophysiology: Sepsis is life-threatening organ dysfunction from dysregulated host response to infection; antimicrobial strategy must cover the most likely source and resistant pathogens while preserving source control and later de-escalation.

How Infectious Disease assesses it: Assess shock, lactate, organ dysfunction, suspected source, prior cultures, recent antibiotics/hospitalization, indwelling lines, prosthetic material, neutropenia/transplant/asplenia, renal/hepatic function, allergy history, local antibiogram, and need for drainage or device removal.

Diagnosis: Obtain blood cultures from two sites before antibiotics if this does not delay therapy, lactate, CBC/CMP/coags, urinalysis/culture, respiratory testing, chest X-ray, CT abdomen/pelvis or ultrasound for source, and cultures from abscess, sputum, CSF, or catheter when indicated.

First-line treatment: Give prompt empiric therapy for likely source: piperacillin-tazobactam (Zosyn), cefepime (Maxipime), or meropenem (Merrem) plus vancomycin (Vancocin) when MRSA risk exists; add metronidazole (Flagyl) for anaerobic intra-abdominal coverage if the beta-lactam chosen lacks it.

Second-line treatment: Narrow or stop agents once cultures and clinical course clarify the syndrome; use ceftriaxone (Rocephin), cefazolin (Ancef), ampicillin-sulbactam (Unasyn), ertapenem (Invanz), daptomycin (Cubicin), linezolid (Zyvox), or micafungin (Mycamine) only when the organism/source supports it.

Third-line / advanced care: Infectious disease, ICU, surgery/interventional radiology for septic shock, persistent bacteremia, fungal infection, multidrug resistance, necrotizing infection, uncontrolled abscess, infected hardware, or OPAT planning.

Progression and follow-up: Follow fever curve, MAP/vasopressors, lactate clearance, WBC, creatinine/LFTs, culture susceptibilities, source control, C. difficile risk, drug toxicity, and resistance pressure.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Meningitis

Pathophysiology: Bacterial meningitis causes leptomeningeal inflammation, cerebral edema, vasculitis, raised intracranial pressure, and neuronal injury; viral, fungal, TB, autoimmune, and drug-induced mimics require different therapy.

How Infectious Disease assesses it: Assess fever, headache, neck stiffness, photophobia, altered mental status, seizure, petechiae/purpura, immunocompromise, pregnancy, age over 50, neurosurgery/shunt, otitis/sinusitis, travel, HIV risk, and antibiotic pretreatment.

Diagnosis: Do not delay therapy. Obtain blood cultures, CBC/CMP/coags, lactate if septic, and lumbar puncture with opening pressure, cell count/differential, glucose paired with serum glucose, protein, Gram stain/culture, meningitis/encephalitis PCR when available, and cryptococcal antigen in HIV/immunocompromise. CT head before LP if focal deficit, papilledema, seizure, severe immunocompromise, or depressed consciousness.

First-line treatment: Empiric adult treatment: ceftriaxone (Rocephin) or cefotaxime plus vancomycin (Vancocin); add ampicillin for Listeria risk such as age over 50, pregnancy, alcoholism, or immune compromise. Give dexamethasone before or with first antibiotic when pneumococcal meningitis is possible.

Second-line treatment: Tailor to cultures/PCR: penicillin G or ceftriaxone for susceptible pneumococcus/meningococcus, ampicillin for Listeria, acyclovir (Zovirax) for HSV encephalitis concern, fluconazole/amphotericin-based regimens for fungal disease, and public health prophylaxis for meningococcal contacts.

Third-line / advanced care: ICU/neurology/ID for coma, seizures, hydrocephalus, hearing loss risk, resistant pathogen, immunocompromise, shunt infection, or need for repeat LP/intrathecal therapy.

Progression and follow-up: Complications include septic shock, seizures, stroke, cerebral edema, hearing loss, cognitive impairment, hydrocephalus, cranial neuropathy, adrenal hemorrhage in meningococcemia, and death.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Endocarditis

Pathophysiology: Infective endocarditis is microbial infection of endocardium or valves with vegetations that destroy valves, seed emboli, and maintain bacteremia; risk rises with prosthetic valves, prior endocarditis, injection drug use, devices, and hemodialysis.

How Infectious Disease assesses it: Assess fever, murmur, heart failure symptoms, embolic stroke, back pain, splenomegaly, petechiae, Janeway/Osler lesions, dental procedures, indwelling lines, prosthetic valve/device, injection drug use, and prior blood cultures.

Diagnosis: Obtain at least three blood culture sets before antibiotics when stable, CBC/CMP/urinalysis, ESR/CRP, ECG, transthoracic echo, and transesophageal echo for prosthetic valve, device, S. aureus bacteremia, poor TTE windows, or high suspicion. Image brain/spine/abdomen when embolic or metastatic infection symptoms occur.

First-line treatment: Empiric therapy for unstable native-valve disease often uses vancomycin (Vancocin) plus cefepime (Maxipime) or ceftriaxone (Rocephin) depending on acquisition risk while awaiting cultures; remove infected catheters when possible.

Second-line treatment: Definitive therapy is organism-specific: nafcillin/oxacillin or cefazolin (Ancef) for MSSA, vancomycin or daptomycin (Cubicin) for MRSA, penicillin G or ceftriaxone for susceptible streptococci, ampicillin plus ceftriaxone or gentamicin-selected regimens for Enterococcus.

Third-line / advanced care: Cardiothoracic surgery/device extraction for heart failure, abscess, persistent bacteremia, large/recurrent embolic vegetations, fungal/resistant organisms, prosthetic valve dehiscence, or uncontrolled infection; OPAT only after stability and adherence plan.

Progression and follow-up: Follow blood culture clearance, renal/drug levels, embolic events, valve function, conduction block, heart failure, mycotic aneurysm, relapse after therapy, and substance-use harm-reduction needs.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Osteomyelitis

Pathophysiology: Osteomyelitis is bone infection from hematogenous seeding, contiguous spread from ulcer/trauma/surgery, or hardware infection; necrotic bone and biofilm limit antibiotic penetration.

How Infectious Disease assesses it: Assess pain, ulcer depth, exposed bone, trauma/surgery/hardware, diabetes/PAD, fever, bacteremia, injection drug use, vertebral pain, neurologic deficits, and vascular supply.

Diagnosis: Use CBC, ESR/CRP, blood cultures when febrile or vertebral disease suspected, plain radiographs, MRI with contrast when feasible, and bone biopsy/culture before antibiotics when stable and diagnosis uncertain. CT or nuclear imaging helps when MRI is unavailable or hardware limits views.

First-line treatment: Treat after cultures when stable. Empiric severe disease may use vancomycin (Vancocin) plus cefepime (Maxipime), ceftriaxone (Rocephin), or piperacillin-tazobactam (Zosyn) depending on source, then narrow to agents such as cefazolin (Ancef), nafcillin, daptomycin (Cubicin), levofloxacin (Levaquin), or linezolid (Zyvox) by susceptibility.

Second-line treatment: Surgical debridement, drainage, hardware removal or staged exchange when needed, vascular optimization, offloading, and oral step-down such as doxycycline (Vibramycin), TMP-SMX (Bactrim/Septra), amoxicillin-clavulanate (Augmentin), or fluoroquinolone-rifampin combinations only when organism and hardware context fit.

Third-line / advanced care: Urgent spine/neurosurgery/orthopedics for vertebral osteomyelitis with neurologic deficit, epidural abscess, instability, sepsis, recurrent hardware infection, ischemic limb, or failure of medical therapy.

Progression and follow-up: Follow pain/function, wound healing, ESR/CRP trend, culture response, renal/hepatic toxicity, C. difficile, recurrence, pathologic fracture, epidural abscess, amputation risk, and biofilm relapse.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Diabetic foot infection

Pathophysiology: Diabetic foot infection develops when neuropathy, ischemia, pressure injury, and impaired immunity allow skin, soft tissue, and bone invasion; severity depends on depth, systemic illness, perfusion, and osteomyelitis.

How Infectious Disease assesses it: Assess ulcer size/depth, purulence, erythema, warmth, pain, necrosis, odor, systemic signs, probe-to-bone, neuropathy, pulses/ABI/toe pressures, prior cultures/antibiotics, MRSA/Pseudomonas risk, glycemic control, renal function, and offloading ability.

Diagnosis: Diagnose soft-tissue infection clinically by local/systemic inflammation. Use IWGDF/IDSA severity, ESR/CRP when exam equivocal, deep tissue culture after cleansing/debridement, plain X-ray, probe-to-bone, and MRI if osteomyelitis remains uncertain.

First-line treatment: Mild infection without MRSA risk may use cephalexin (Keflex), dicloxacillin, amoxicillin-clavulanate (Augmentin), or clindamycin (Cleocin). Provide debridement, offloading, glycemic optimization, wound care, and vascular assessment.

Second-line treatment: Moderate/severe infection may need ampicillin-sulbactam (Unasyn), ceftriaxone plus metronidazole (Flagyl), ertapenem (Invanz), piperacillin-tazobactam (Zosyn), or vancomycin (Vancocin) added for MRSA risk; tailor to deep cultures.

Third-line / advanced care: Hospitalize for severe infection, necrotizing infection, gangrene, ischemia, abscess, systemic toxicity, inability to offload, or moderate infection with major comorbidity; surgery/podiatry/vascular/ID for drainage, revascularization, bone resection, or OPAT.

Progression and follow-up: Follow wound size, erythema, drainage, perfusion, glucose, renal function, culture response, antibiotic toxicity, osteomyelitis recurrence, Charcot changes, amputation risk, and footwear prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Complicated UTI

Pathophysiology: Complicated UTI occurs with urinary tract abnormality, obstruction, catheter, stone, male sex, pregnancy, transplant, renal impairment, resistant organism, or systemic illness, increasing risk of bacteremia and relapse.

How Infectious Disease assesses it: Assess fever/flank pain, sepsis, urinary retention, catheter, stones, prostate symptoms, pregnancy, transplant/CKD, recent antibiotics, prior ESBL/Pseudomonas, procedures, allergies, renal dosing, and local resistance.

Diagnosis: Obtain urinalysis and urine culture before antibiotics, blood cultures if febrile/septic, BMP/creatinine, pregnancy test when relevant, postvoid residual if retention, and renal ultrasound or CT when obstruction, stone, abscess, emphysematous infection, or failure to improve is suspected.

First-line treatment: Stable lower complicated UTI can use culture-guided oral therapy such as nitrofurantoin (Macrobid) only for cystitis with adequate renal function, TMP-SMX (Bactrim/Septra), amoxicillin-clavulanate (Augmentin), cephalexin (Keflex), or fosfomycin (Monurol) in selected cystitis scenarios.

Second-line treatment: Systemic illness or resistance risk may need ceftriaxone (Rocephin), cefepime (Maxipime), piperacillin-tazobactam (Zosyn), ertapenem (Invanz), or meropenem (Merrem), then oral step-down such as ciprofloxacin (Cipro), levofloxacin (Levaquin), or TMP-SMX when susceptible and safe.

Third-line / advanced care: Urology/ID for obstruction, infected stone, abscess, recurrent ESBL/carbapenem-resistant organisms, transplant infection, prostatitis, catheter biofilm, or OPAT; drain obstruction urgently.

Progression and follow-up: Follow symptom resolution, culture susceptibilities, renal function, recurrence, C. difficile, tendon/QT risks with fluoroquinolones, bacteremia, pyelonephritis, renal abscess, and sepsis.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Pyelonephritis with resistance risk

Pathophysiology: Pyelonephritis is bacterial infection of renal pelvis/parenchyma; resistance risk from prior antibiotics, healthcare exposure, ESBL history, urinary devices, travel, or recurrent UTI can make standard oral therapy fail.

How Infectious Disease assesses it: Assess fever, flank pain, nausea/vomiting, sepsis, pregnancy, diabetes, stones/obstruction, catheter, recent cultures, prior ESBL/Pseudomonas, oral tolerance, allergies, renal function, and admission criteria.

Diagnosis: Use urinalysis, urine culture with susceptibilities, blood cultures when septic/admitted, CBC/CMP, pregnancy test when relevant, and CT abdomen/pelvis or renal ultrasound for stone/obstruction, persistent fever beyond 48-72 hours, severe illness, or atypical presentation.

First-line treatment: Outpatient low-risk patients may receive ceftriaxone (Rocephin) initial dose then ciprofloxacin (Cipro), levofloxacin (Levaquin), or TMP-SMX (Bactrim/Septra) if susceptibility is likely/known; avoid nitrofurantoin for pyelonephritis.

Second-line treatment: Resistance or admission risk: cefepime (Maxipime), piperacillin-tazobactam (Zosyn), ertapenem (Invanz), meropenem (Merrem), or aminoglycoside-selected therapy such as gentamicin with renal monitoring, then de-escalate.

Third-line / advanced care: Urgent urology for obstructed infected system, emphysematous pyelonephritis, renal/perinephric abscess, infected stone, pregnancy complications, septic shock, or failure to improve.

Progression and follow-up: Follow fever curve, flank pain, cultures, renal function, oral tolerance, obstruction imaging, bacteremia, relapse, abscess, sepsis, pregnancy outcomes, and antimicrobial adverse effects.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

C difficile infection

Pathophysiology: C. difficile infection follows microbiome disruption, toxin-mediated colitis, and inflammatory injury; recurrence is driven by persistent spores, impaired antibody response, age, acid suppression, antibiotics, and immunocompromise.

How Infectious Disease assesses it: Assess diarrhea frequency, abdominal pain, fever, ileus, leukocytosis, creatinine rise, hypotension, megacolon, recent antibiotics/hospitalization, prior CDI, IBD, immunosuppression, and ability to stop inciting antibiotics.

Diagnosis: Test only unformed stool in symptomatic patients using NAAT/toxin algorithm per local lab; avoid test-of-cure. Check CBC/CMP and CT abdomen/pelvis for severe pain, ileus, toxic megacolon, or diagnostic uncertainty.

First-line treatment: Initial non-fulminant CDI: fidaxomicin (Dificid) preferred when available or oral vancomycin (Vancocin). Stop unnecessary antibiotics and acid suppressants, hydrate, and use contact precautions.

Second-line treatment: First recurrence: fidaxomicin standard/extended-pulsed or vancomycin taper/pulse; consider bezlotoxumab (Zinplava) for high-risk recurrence. Further recurrences may use fecal microbiota products under guideline pathways.

Third-line / advanced care: Fulminant CDI needs high-dose oral/NG vancomycin plus IV metronidazole (Flagyl), rectal vancomycin if ileus, surgical consultation for colectomy/diverting loop ileostomy, ICU support, and ID/GI input.

Progression and follow-up: Follow stool frequency, WBC/creatinine, hydration, abdominal distention, recurrence within 8 weeks, medication access, transmission control, toxic megacolon, perforation, shock, and death risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

HIV initial evaluation

Pathophysiology: HIV infects CD4 lymphocytes and establishes chronic immune activation; untreated disease progresses to CD4 decline, opportunistic infections, malignancy, neurologic disease, and transmission.

How Infectious Disease assesses it: Assess prior HIV tests, acute retroviral symptoms, opportunistic infection symptoms, STI/hepatitis/TB risk, pregnancy potential, medications/interactions, renal/hepatic disease, mental health/substance use, insurance/access, partner safety, and readiness for rapid ART.

Diagnosis: Confirm with HIV Ag/Ab and HIV-1/2 differentiation assay, HIV RNA viral load, CD4 count, genotype resistance including integrase if indicated, HLA-B*5701 if abacavir considered, CMP/CBC/lipids/A1c, hepatitis A/B/C serologies, TB IGRA, STI NAAT/RPR, pregnancy test, urinalysis, and vaccines review.

First-line treatment: Start antiretroviral therapy rapidly unless a specific opportunistic infection timing issue exists. Common first-line options include bictegravir/tenofovir alafenamide/emtricitabine (Biktarvy) or dolutegravir (Tivicay) plus tenofovir/emtricitabine (Truvada or Descovy).

Second-line treatment: Tailor ART for resistance, kidney/bone disease, hepatitis B coinfection, pregnancy, drug interactions, and adherence barriers; provide TMP-SMX (Bactrim/Septra) for Pneumocystis prophylaxis when CD4 criteria are met and treat coinfections.

Third-line / advanced care: ID/HIV specialist for resistance, pregnancy, opportunistic infection, virologic failure, severe renal/hepatic disease, long-acting cabotegravir/rilpivirine (Cabenuva) eligibility, or complex psychosocial barriers.

Progression and follow-up: Follow viral load suppression, CD4 recovery, renal/hepatic/lipid effects, STI prevention, vaccines, adherence, resistance, opportunistic infections, malignancy screening, and U=U counseling.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

HIV PrEP and PEP

Pathophysiology: PrEP prevents HIV acquisition before exposure, while PEP blocks early viral replication after a substantial exposure; both require rapid risk assessment, baseline testing, and adherence support.

How Infectious Disease assesses it: Assess exposure type, timing within 72 hours for PEP, source HIV status/viral suppression, sexual/injection risks, kidney function, hepatitis B status, pregnancy, drug interactions, symptoms of acute HIV, STI risk, and ability to return for follow-up.

Diagnosis: Use HIV Ag/Ab plus HIV RNA if acute infection possible, creatinine/eGFR, hepatitis B/C serology, pregnancy test when relevant, STI NAAT/RPR, and source testing when available; do not delay PEP while awaiting results if indicated.

First-line treatment: PEP: start as soon as possible and within 72 hours for 28 days, commonly dolutegravir (Tivicay) plus tenofovir/emtricitabine (Truvada) or bictegravir/TAF/FTC (Biktarvy) per current protocols and availability. PrEP options include tenofovir/emtricitabine (Truvada), tenofovir alafenamide/emtricitabine (Descovy) for eligible groups, or long-acting cabotegravir (Apretude).

Second-line treatment: Manage nausea with ondansetron (Zofran) if needed, treat STIs, provide emergency contraception when indicated, transition PEP to PrEP for ongoing risk, and use doxycycline PEP only where guideline-appropriate for selected STI prevention.

Third-line / advanced care: Specialist/public health input for renal disease, hepatitis B, pregnancy/breastfeeding complexity, sexual assault care coordination, occupational exposure, delayed presentation, acute HIV suspicion, or positive HIV testing.

Progression and follow-up: Follow HIV testing at recommended intervals, renal function, hepatitis B flare risk after stopping tenofovir, STI screening, adherence/injection schedule, side effects, ongoing prevention, and source results.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Tuberculosis latent and active

Pathophysiology: Tuberculosis arises when Mycobacterium tuberculosis survives in macrophages; latent infection is contained without symptoms, while active pulmonary or extrapulmonary TB can cavitate, disseminate, and transmit by airborne droplets.

How Infectious Disease assesses it: Assess cough, fever, night sweats, weight loss, hemoptysis, exposure, prior TB treatment, birth/travel/residence risk, congregate settings, immunosuppression/TNF inhibitors, HIV, pregnancy, liver disease, and drug interactions.

Diagnosis: Latent TB uses IGRA or TST plus symptom screen and chest X-ray to exclude active disease. Active TB requires airborne isolation, chest imaging, sputum AFB smear/culture and NAAT, drug susceptibility testing, HIV testing, and extrapulmonary sampling when relevant.

First-line treatment: Latent TB preferred regimens include once-weekly isoniazid plus rifapentine (3HP), daily rifampin (Rifadin) for 4 months, or daily isoniazid/rifampin for 3 months when appropriate. Active drug-susceptible TB commonly uses isoniazid, rifampin, pyrazinamide, and ethambutol initially with pyridoxine (vitamin B6).

Second-line treatment: Selected adults/adolescents with drug-susceptible pulmonary TB may use CDC/ATS/IDSA-endorsed shorter rifapentine/moxifloxacin-containing regimens when eligible; adjust for resistance, cavitation/culture status, CNS/bone disease, pregnancy, and interactions.

Third-line / advanced care: Public health TB program/ID for active TB, drug resistance, HIV coinfection, pregnancy, liver toxicity, adherence concerns, directly observed therapy, contact investigation, or isolation clearance.

Progression and follow-up: Follow symptoms, sputum culture conversion, LFTs, vision with ethambutol, neuropathy, adherence, interactions with ART/warfarin/OCPs, relapse, resistance, transmission, and post-TB lung disease.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Opportunistic infection in immunocompromise

Pathophysiology: Immunocompromise from HIV, transplant, chemotherapy, neutropenia, biologics, steroids, or congenital disease changes pathogen spectrum and blunts inflammatory signs, allowing rapid invasive fungal, viral, bacterial, and parasitic disease.

How Infectious Disease assesses it: Identify immune defect, ANC/CD4, transplant type/date, immunosuppressants, prophylaxis adherence, fever pattern, respiratory/CNS/GI/skin symptoms, travel, pets, foods, molds, lines, and prior resistant organisms.

Diagnosis: Use syndrome-directed testing: CBC/CMP, blood cultures, CT chest/sinuses/abdomen as indicated, respiratory viral PCR, fungal markers such as galactomannan or beta-D-glucan when appropriate, CMV/BK/EBV PCR by host, cryptococcal antigen, toxoplasma testing, BAL/biopsy, and medication levels.

First-line treatment: Treat urgently by host and syndrome: cefepime (Maxipime) or piperacillin-tazobactam (Zosyn) for neutropenic fever, TMP-SMX (Bactrim/Septra) for Pneumocystis, ganciclovir/valganciclovir (Cytovene/Valcyte) for CMV, and mold-active therapy such as voriconazole (Vfend) or liposomal amphotericin B (AmBisome) when invasive fungal disease suspected.

Second-line treatment: Adjust immunosuppression when possible, add corticosteroids for moderate/severe Pneumocystis with hypoxemia, choose prophylaxis based on CD4/transplant regimen, and tailor therapy to microbiology and drug interactions.

Third-line / advanced care: ID/transplant/oncology urgent involvement for shock, hypoxemia, CNS infection, persistent fever, mold disease, resistant virus, graft rejection balance, or need for bronchoscopy/biopsy.

Progression and follow-up: Follow oxygenation, viral loads/fungal markers, drug levels, renal/hepatic marrow toxicity, immune reconstitution, prophylaxis gaps, relapse, graft rejection, and mortality risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Travel fever

Pathophysiology: Travel fever may reflect malaria, dengue, chikungunya, Zika, typhoid/paratyphoid, rickettsial disease, viral hemorrhagic fever, acute HIV, hepatitis, traveler diarrhea complications, or routine respiratory/urinary infection acquired abroad.

How Infectious Disease assesses it: Assess itinerary, dates, rural/urban exposure, mosquito/tick/animal/freshwater/sexual exposures, vaccines/prophylaxis, sick contacts, outbreaks, incubation period, pregnancy, immune status, rash, hemorrhage, jaundice, diarrhea, neurologic symptoms, and severe malaria signs.

Diagnosis: Malaria testing is urgent for fever after travel to endemic areas: thick/thin smear or rapid antigen repeated if initially negative. Add CBC/CMP/LFTs, blood cultures for typhoid, dengue/chikungunya/Zika testing by timing, stool testing if diarrhea, hepatitis/HIV testing, chest X-ray/urinalysis when indicated, and public health notification for high-consequence pathogens.

First-line treatment: If malaria is possible and severe features exist, treat immediately with IV artesunate through CDC pathway; uncomplicated malaria therapy depends on species/resistance and may include atovaquone-proguanil (Malarone), artemether-lumefantrine (Coartem), or chloroquine where sensitive.

Second-line treatment: Typhoid may need ceftriaxone (Rocephin), azithromycin (Zithromax), or carbapenem for resistant disease; rickettsial illness uses doxycycline (Vibramycin); dengue care is supportive with acetaminophen and avoidance of NSAIDs until bleeding risk clarified.

Third-line / advanced care: ID/public health/CDC consultation for severe malaria, hemorrhagic fever concern, encephalitis, pregnancy, immunocompromise, outbreak exposure, resistant typhoid, or undiagnosed fever after initial workup.

Progression and follow-up: Follow platelets/hematocrit, LFTs, parasitemia clearance, hydration, shock/bleeding warning signs, relapse species needing primaquine/tafenoquine after G6PD testing, transmission precautions, and travel-contact implications.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Tick-borne disease

Pathophysiology: Tick-borne diseases include Lyme disease, anaplasmosis, ehrlichiosis, Rocky Mountain spotted fever, babesiosis, tularemia, and regional viruses; early treatment matters because labs may be negative initially.

How Infectious Disease assesses it: Assess geography, season, tick attachment duration, erythema migrans, fever, headache, myalgias, rash on palms/soles, cytopenias, transaminitis, hemolysis, neurologic/cardiac symptoms, pregnancy, asplenia, and immune compromise.

Diagnosis: Erythema migrans is clinical. Use two-tier Lyme serology when indicated after early window, CBC/CMP, peripheral smear for babesiosis, PCR/serology for anaplasma/ehrlichia/RMSF as available, ECG for Lyme carditis symptoms, and CSF studies for neuroborreliosis when clinically needed.

First-line treatment: Doxycycline (Vibramycin) treats Lyme disease in eligible patients and is first-line for RMSF/anaplasmosis/ehrlichiosis; do not delay RMSF treatment for labs. Amoxicillin (Amoxil) or cefuroxime (Ceftin) are alternatives for certain Lyme presentations.

Second-line treatment: Babesiosis with symptoms uses atovaquone (Mepron) plus azithromycin (Zithromax), or clindamycin plus quinine for severe disease; severe neuro/cardiac Lyme may need IV ceftriaxone (Rocephin).

Third-line / advanced care: Hospitalize for RMSF severe illness, meningitis/encephalitis, high-grade AV block, severe babesiosis with hemolysis/organ failure, pregnancy complexity, or immunocompromised persistent infection.

Progression and follow-up: Follow fever resolution, cytopenias/LFTs, hemolysis/parasitemia, heart block, neurologic deficits, Jarisch-Herxheimer reaction, post-treatment Lyme symptoms, and prevention counseling.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Recurrent cellulitis

Pathophysiology: Recurrent cellulitis is repeated dermal/subcutaneous infection, usually streptococcal or staphylococcal, promoted by edema, venous disease, lymphedema, tinea pedis, obesity, skin breakdown, wounds, and prior lymphatic injury.

How Infectious Disease assesses it: Assess frequency, location, portals of entry, toe-web maceration/tinea, edema/lymphedema, venous insufficiency, diabetes, wounds/ulcers, MRSA history, trauma, animal bites, injection drug use, and mimics such as stasis dermatitis or gout.

Diagnosis: Usually clinical. Culture purulence/abscess, obtain ultrasound if abscess/DVT uncertainty, CBC/CRP only for severe disease, and evaluate vascular/edema drivers; blood cultures only for systemic toxicity, immunocompromise, unusual exposures, or severe infection.

First-line treatment: Acute nonpurulent cellulitis: cephalexin (Keflex), cefadroxil (Duricef), amoxicillin (Amoxil), or IV cefazolin (Ancef)/ceftriaxone (Rocephin) by severity; purulent/MRSA risk may need doxycycline (Vibramycin), TMP-SMX (Bactrim/Septra), clindamycin (Cleocin), or vancomycin (Vancocin).

Second-line treatment: Prevent recurrence with compression/edema control, weight management, skin moisturization, treatment of tinea pedis with terbinafine (Lamisil) or clotrimazole (Lotrimin), wound care, and selected prophylactic penicillin V (Veetids) or benzathine penicillin G for frequent nonpurulent recurrences.

Third-line / advanced care: ID/dermatology/vascular/lymphedema referral for frequent recurrence, unusual organisms, immunocompromise, necrotizing concern, chronic ulcers, failure of prophylaxis, or diagnostic uncertainty.

Progression and follow-up: Follow recurrence rate, edema control, skin integrity, antibiotic adverse effects, C. difficile, resistance, abscess formation, bacteremia, necrotizing infection, and functional impairment.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Infectious Disease

Antibiotic allergy evaluation

Pathophysiology: Many antibiotic allergy labels reflect intolerance, viral exanthem, remote childhood rash, or non-IgE reactions rather than persistent true allergy; inaccurate labels drive broader antibiotics, resistance, toxicity, and worse outcomes.

How Infectious Disease assesses it: Document culprit drug, reaction timing, symptoms, treatment, mucosal/skin pain/blistering, organ injury, hypotension/wheeze, years since reaction, tolerated beta-lactams since, infection urgency, pregnancy, and severe cutaneous adverse reaction history.

Diagnosis: Risk-stratify. Low-risk penicillin histories may undergo direct oral amoxicillin challenge; moderate-risk immediate reactions may need penicillin skin testing followed by challenge. Avoid challenge in SJS/TEN, DRESS, AGEP, serum sickness-like severe reactions, interstitial nephritis, hepatitis, or hemolytic anemia.

First-line treatment: For low-risk labels, supervised delabeling can permit amoxicillin (Amoxil), ampicillin, cefazolin (Ancef), cephalexin (Keflex), or other beta-lactams when indicated; update the EHR allergy field with reaction details and tolerated drugs.

Second-line treatment: When true allergy or high-risk history exists, select alternatives based on syndrome and susceptibilities, such as doxycycline (Vibramycin), azithromycin (Zithromax), clindamycin (Cleocin), vancomycin (Vancocin), aztreonam (Azactam), or fluoroquinolones only when benefits outweigh risks.

Third-line / advanced care: Allergy/ID referral for perioperative cefazolin need, recurrent infections, pregnancy, cystic fibrosis/complex resistance, need for desensitization, or unclear severe reaction. Desensitization is temporary and requires monitored setting.

Progression and follow-up: Follow delabeling documentation, future tolerance, avoidance of severe culprit reactions, antimicrobial stewardship benefits, adverse drug events, and patient understanding of true allergy versus side effect.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Specialty role

Blood disorders, clotting, bleeding, anemia, cytopenias, hemoglobinopathies, and anticoagulation complexity.

Hematology

Iron deficiency anemia

Pathophysiology: Iron deficiency anemia reflects depleted iron stores causing impaired hemoglobin synthesis; in adults it is blood loss until proven otherwise, especially menstrual bleeding, GI bleeding, malabsorption, pregnancy, bariatric surgery, or dietary deficiency.

How Hematology assesses it: Assess fatigue, dyspnea, pica, restless legs, menorrhagia, pregnancy, GI symptoms, NSAID/aspirin/anticoagulant use, bariatric surgery, diet, celiac risk, family history, and hemodynamic symptoms from active bleeding.

Diagnosis: Use CBC with indices, reticulocyte count, ferritin, serum iron/TIBC/transferrin saturation, CRP when inflammation may mask ferritin, B12/folate if mixed picture, stool/GI evaluation by age/risk, celiac serology when suggested, and endoscopy/colonoscopy for unexplained adult IDA or alarm features.

First-line treatment: Treat cause and replete iron: oral ferrous sulfate (Feosol), ferrous gluconate, or ferrous fumarate every other day or daily as tolerated with vitamin C/food strategy individualized; separate from calcium, PPIs, levothyroxine, and tetracyclines when possible.

Second-line treatment: Use IV iron such as iron sucrose (Venofer), ferric carboxymaltose (Injectafer), ferumoxytol (Feraheme), or ferric derisomaltose (Monoferric) for intolerance, malabsorption, CKD/IBD, late pregnancy need, severe deficiency, or ongoing losses.

Third-line / advanced care: Transfuse packed RBCs for unstable bleeding, severe symptomatic anemia, cardiac ischemia, or very low hemoglobin by clinical context; hematology/GI/GYN referral for refractory anemia, suspected marrow disease, or unclear bleeding source.

Progression and follow-up: Follow hemoglobin response in 2-4 weeks, ferritin/transferrin saturation after repletion, adherence, constipation/nausea, source control, recurrence, missed malignancy, and heart strain from severe anemia.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

B12 and folate deficiency

Pathophysiology: Vitamin B12 deficiency impairs DNA synthesis and myelin maintenance from pernicious anemia, gastric/ileal disease, metformin/PPI exposure, vegan diet, nitrous oxide, or bariatric surgery; folate deficiency reflects poor intake, alcohol use, pregnancy, hemolysis, or antifolate drugs.

How Hematology assesses it: Assess neuropathy, gait imbalance, cognitive/mood change, glossitis, diarrhea, alcohol use, diet, pregnancy, gastric/ileal surgery, autoimmune disease, metformin, PPIs, methotrexate, trimethoprim, phenytoin, and neurologic red flags.

Diagnosis: Use CBC with MCV, reticulocyte count, smear for macro-ovalocytes/hypersegmented neutrophils, B12, folate, methylmalonic acid, homocysteine, intrinsic factor/parietal cell antibodies when pernicious anemia suspected, TSH/LFTs, and marrow evaluation only if cytopenias fail to correct or MDS suspected.

First-line treatment: B12 deficiency: cyanocobalamin (Vitamin B12/Nascobal) oral high-dose or IM injections depending on severity, malabsorption, and neurologic disease. Folate deficiency: folic acid (Folvite) after B12 deficiency is excluded or treated.

Second-line treatment: Treat cause: stop/reduce offending drugs when possible, manage celiac/IBD, nutrition counseling, alcohol treatment, prenatal folate, and lifelong B12 for pernicious anemia or irreversible malabsorption.

Third-line / advanced care: Urgent neurology/hematology for progressive neurologic deficits, severe pancytopenia, hemolysis-like ineffective erythropoiesis, suspected marrow disorder, or failure to respond despite confirmed adherence.

Progression and follow-up: Follow reticulocyte response, CBC normalization, potassium early in severe repletion, neurologic recovery, recurrence risk, gastric cancer surveillance considerations in pernicious anemia, and irreversible neuropathy if delayed.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Hemolytic anemia

Pathophysiology: Hemolytic anemia is premature RBC destruction from immune antibodies, membrane/enzyme defects, hemoglobinopathy, microangiopathy, infection, drugs, mechanical valves, or complement-mediated disease.

How Hematology assesses it: Assess jaundice, dark urine, back/abdominal pain, fever, new drugs, transfusion history, pregnancy, autoimmune disease, infections, valve/LVAD, thrombosis, neurologic/renal symptoms suggesting TMA, family history, and splenomegaly.

Diagnosis: Use CBC, reticulocyte count, smear, LDH, indirect bilirubin, haptoglobin, direct antiglobulin test, urinalysis for hemoglobin, CMP, G6PD testing when appropriate after acute phase, cold agglutinin testing, ADAMTS13 if TTP concern, and PNH flow cytometry when thrombosis/cytopenias suggest it.

First-line treatment: Stabilize and remove triggers; warm autoimmune hemolysis often starts prednisone (Deltasone) plus folate and transfusion if needed using least-incompatible blood under blood-bank guidance.

Second-line treatment: Rituximab (Rituxan), IVIG (Privigen/Gamunex), splenectomy-selected cases, complement inhibitors eculizumab (Soliris) or ravulizumab (Ultomiris) for PNH/complement disease, and infection-directed therapy by cause.

Third-line / advanced care: Emergency plasma exchange for suspected TTP, ICU for severe anemia/shock, hematology/transfusion medicine for complex antibodies, acute transfusion reaction, hemolytic disease of pregnancy/newborn, or refractory disease.

Progression and follow-up: Follow hemoglobin, retic count, LDH/bilirubin/haptoglobin, thrombosis, renal injury, gallstones, steroid toxicity, infection risk after complement blockade/splenectomy, and relapse.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Sickle cell disease pain crisis

Pathophysiology: Sickle cell vaso-occlusive crisis occurs when HbS polymerization causes RBC sickling, hemolysis, endothelial activation, microvascular occlusion, ischemia, and inflammatory pain; triggers include infection, dehydration, hypoxia, cold, stress, and menstruation.

How Hematology assesses it: Assess pain location/severity versus baseline plan, fever, chest pain, dyspnea, neurologic deficit, priapism, pregnancy, splenic symptoms, hydration, opioid tolerance, prior acute chest/stroke, transfusion history/alloantibodies, and infection signs.

Diagnosis: Use CBC/reticulocyte count, CMP/bilirubin, type/screen if transfusion possible, pulse oximetry, pregnancy test when relevant, chest X-ray for chest symptoms/hypoxia/fever, cultures if febrile, and do not delay analgesia for labs.

First-line treatment: Rapid individualized analgesia: IV morphine or hydromorphone (Dilaudid) or patient-specific opioid plan, NSAID such as ketorolac (Toradol) if renal/bleeding risk allows, acetaminophen (Tylenol), oral/IV hydration avoiding overload, oxygen only for hypoxemia, incentive spirometry, and treat trigger.

Second-line treatment: Disease-modifying prevention includes hydroxyurea (Hydrea/Droxia), L-glutamine (Endari), crizanlizumab (Adakveo) where appropriate, voxelotor (Oxbryta) only if available/appropriate under current regulatory status, vaccination, penicillin prophylaxis in children, and transfusion programs for selected stroke/ACS risk.

Third-line / advanced care: Urgent transfusion/exchange transfusion, hematology, ICU, or stroke team for acute chest syndrome, stroke/TIA, severe anemia/aplastic crisis, splenic sequestration, priapism, sepsis, multiorgan failure, or pain uncontrolled by protocol.

Progression and follow-up: Follow pain relief, sedation/respiratory status, hypoxia, fever, hemoglobin/retic, opioid adverse effects, acute chest evolution, renal function, alloimmunization, chronic organ damage, and individualized care plan access.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Thrombocytopenia

Pathophysiology: Thrombocytopenia results from decreased production, immune destruction, consumption, sequestration, dilution, drugs, infection, liver disease, marrow failure, TMA, DIC, HIT, or inherited platelet disorders.

How Hematology assesses it: Assess bleeding pattern, platelet trend, recent heparin, quinine/TMP-SMX/linezolid/valproate, alcohol, viral symptoms, pregnancy, liver disease, autoimmune disease, thrombosis, neurologic/renal symptoms, splenomegaly, and pseudothrombocytopenia risk.

Diagnosis: Repeat CBC in citrate tube if clumping suspected, review peripheral smear, PT/INR/aPTT/fibrinogen/D-dimer when DIC possible, CMP/LFTs, HIV/HCV, pregnancy test, B12/folate, hemolysis labs, HIT 4Ts/PF4 testing when relevant, and bone marrow biopsy for unexplained cytopenias or older adult marrow concern.

First-line treatment: Treat cause and bleeding risk. ITP with significant bleeding or very low platelets often uses corticosteroids such as dexamethasone or prednisone and/or IVIG (Privigen/Gamunex); avoid platelet-impairing drugs and anticoagulation unless benefit clearly outweighs risk.

Second-line treatment: Second-line ITP options include rituximab (Rituxan), thrombopoietin receptor agonists eltrombopag (Promacta), romiplostim (Nplate), or avatrombopag (Doptelet), and selected splenectomy after shared decision-making.

Third-line / advanced care: Emergency platelet transfusion for life-threatening bleeding or procedures, plasma exchange for TTP suspicion, stop heparin and start non-heparin anticoagulant for HIT, obstetric/hematology care for pregnancy HELLP/TTP/ITP complexity.

Progression and follow-up: Follow platelet count, bleeding, thrombosis, smear changes, medication triggers, infection testing, steroid toxicity, TPO-RA thrombosis/liver effects, relapse, and missed marrow malignancy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Neutropenia

Pathophysiology: Neutropenia is reduced neutrophil defense from chemotherapy, marrow failure, autoimmune disease, drugs, viral infection, nutritional deficiency, congenital syndromes, hypersplenism, or benign ethnic/Duffy-null associated neutrophil count.

How Hematology assesses it: Assess ANC severity/duration, fever, oral ulcers, infections, chemo timing, medications such as antithyroid drugs/clozapine/TMP-SMX, autoimmune symptoms, HIV/hepatitis risk, B12/folate/copper risk, splenomegaly, and ethnicity/baseline counts.

Diagnosis: Use CBC differential trend, smear, CMP, B12/folate/copper, HIV/hepatitis/EBV/CMV testing when indicated, autoimmune markers by clues, medication review, and bone marrow biopsy with flow/cytogenetics if severe, persistent, unexplained, or with other cytopenias.

First-line treatment: Afebrile mild chronic neutropenia may need observation and infection precautions; stop offending drugs when safe and correct B12/folate/copper deficiency.

Second-line treatment: Febrile neutropenia requires urgent antipseudomonal therapy such as cefepime (Maxipime), piperacillin-tazobactam (Zosyn), or meropenem (Merrem); add vancomycin (Vancocin) only for line infection, pneumonia, skin infection, instability, or MRSA risk.

Third-line / advanced care: Hematology for severe chronic neutropenia, suspected marrow failure, congenital syndromes, G-CSF filgrastim (Neupogen/Zarxio) selection, recurrent infections, or need for antimicrobial prophylaxis.

Progression and follow-up: Follow ANC trend, fever plan, infection frequency, marrow evolution, medication toxicity, G-CSF bone pain/splenomegaly, fungal infection risk, and need for vaccination/prophylaxis.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Pancytopenia

Pathophysiology: Pancytopenia reflects failure or suppression of multiple marrow lineages, peripheral destruction/sequestration, nutritional deficiency, aplastic anemia, myelodysplastic syndrome, leukemia/lymphoma infiltration, infection, autoimmune disease, hypersplenism, or drugs/toxins.

How Hematology assesses it: Assess fatigue, infection, bleeding, weight loss/night sweats, bone pain, alcohol, chemotherapy/radiation, benzene/toxin exposure, medications, autoimmune symptoms, viral risks, diet/bariatric surgery, splenomegaly, lymphadenopathy, and hemodynamic stability.

Diagnosis: Use CBC with differential, reticulocyte count, smear, CMP/LFTs, LDH/uric acid, B12/folate/copper, iron studies, viral testing HIV/hepatitis/EBV/CMV/parvovirus as indicated, hemolysis labs, coagulation tests, flow cytometry when blasts/lymphocytosis, and bone marrow biopsy with cytogenetics/molecular testing for unexplained or severe cases.

First-line treatment: Stabilize with RBC transfusion for symptomatic severe anemia, platelet transfusion for serious bleeding/very low platelets/procedures, infection precautions, stop marrow-toxic drugs, and correct nutritional deficiencies.

Second-line treatment: Treat identified cause: immunosuppression for aplastic anemia, hypomethylating agents for selected MDS, leukemia/lymphoma therapy, antivirals/antibiotics when infectious, or steroids/immune therapy only when immune cause is supported.

Third-line / advanced care: Urgent hematology/admission for blasts, severe neutropenia with fever, platelets with bleeding, hemoglobin instability, DIC/TMA, suspected acute leukemia/aplastic anemia, or need for marrow biopsy/transplant evaluation.

Progression and follow-up: Follow cell lines, reticulocyte recovery, infections, bleeding, transfusion needs/iron overload, clonal evolution to AML/MDS, treatment toxicity, and transplant candidacy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Venous thromboembolism duration decision

Pathophysiology: VTE duration depends on whether thrombosis was provoked by transient risk, persistent risk, cancer, antiphospholipid syndrome, recurrence, clot location, bleeding risk, and patient preference.

How Hematology assesses it: Assess DVT/PE site, provoking factors surgery/trauma/immobility/estrogen/pregnancy, active cancer, prior VTE, family history, antiphospholipid features, renal/liver function, bleeding history, falls, drug interactions, weight, pregnancy potential, and adherence/cost.

Diagnosis: Confirm index event with compression ultrasound, CT pulmonary angiography or V/Q scan, baseline CBC/CMP/PT/INR/aPTT, cancer screening by history/age-appropriate screening, and thrombophilia testing only when it will change management, not during acute anticoagulation for most patients.

First-line treatment: Most proximal DVT/PE receives at least 3 months anticoagulation with apixaban (Eliquis), rivaroxaban (Xarelto), dabigatran (Pradaxa), edoxaban (Savaysa), warfarin (Coumadin/Jantoven), or enoxaparin (Lovenox) selected by renal function, cancer, pregnancy, APS, interactions, and cost.

Second-line treatment: Stop after 3 months for major transient provoked VTE when risk resolved and bleeding risk favors stopping; consider extended low-dose apixaban or rivaroxaban for unprovoked or persistent-risk VTE when bleeding risk acceptable.

Third-line / advanced care: Hematology for recurrent VTE, unusual sites, suspected APS needing warfarin, cancer-associated thrombosis complexity, pregnancy, severe thrombophilia, bleeding conflict, or IVC filter only when anticoagulation is impossible.

Progression and follow-up: Follow recurrence risk, bleeding, renal/liver function, adherence, drug interactions, post-thrombotic syndrome, chronic thromboembolic pulmonary hypertension, and peri-procedure interruption plans.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Anticoagulation complications

Pathophysiology: Anticoagulation complications include bleeding, thrombosis despite therapy, supratherapeutic anticoagulant effect, drug interactions, renal accumulation, HIT, pregnancy exposure, and procedure-related interruption errors.

How Hematology assesses it: Assess bleeding site/severity, last dose, indication, thrombotic risk, renal/liver function, CBC trend, INR or anti-Xa where relevant, antiplatelets/NSAIDs, CYP/P-gp interactions, falls/trauma, adherence, overdose, and upcoming procedures.

Diagnosis: Use CBC, type/screen, CMP/creatinine, PT/INR/aPTT, fibrinogen when major bleeding, drug-specific anti-Xa/dilute thrombin time when available, CT head for head trauma/neuro symptoms, CT angiography/endoscopy by bleeding site, and HIT testing when platelet fall/thrombosis follows heparin.

First-line treatment: Hold anticoagulant for clinically significant bleeding, apply local control, transfuse/support, and reverse warfarin with vitamin K plus 4-factor PCC (Kcentra) for major bleeding; reverse dabigatran with idarucizumab (Praxbind) when severe.

Second-line treatment: Factor Xa inhibitor major bleeding may use andexanet alfa (Andexxa) where appropriate or 4-factor PCC per protocol; protamine reverses heparin and partially LMWH. Restart timing depends on bleed control and thrombosis risk.

Third-line / advanced care: Emergency medicine/hematology/procedural specialists for intracranial, retroperitoneal, GI unstable, airway, compartment, spinal, or life-threatening bleeding; switch agents or investigate malignancy/APS/adherence for breakthrough thrombosis.

Progression and follow-up: Follow rebleeding, thrombosis during interruption, hemoglobin, renal function, reversal complications, INR/drug levels, medication reconciliation, fall prevention, and documented restart plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Warfarin INR instability

Pathophysiology: Warfarin INR instability reflects variable vitamin K intake, adherence, genetics, illness, liver/thyroid disease, alcohol, interacting drugs, antibiotics, amiodarone, antifungals, anticonvulsants, heart failure, and inconsistent monitoring.

How Hematology assesses it: Assess indication/target INR, missed/extra doses, diet changes, alcohol, diarrhea/vomiting, new medications/supplements, antibiotics, acetaminophen use, liver/thyroid symptoms, bleeding/thrombosis, health literacy, and access to INR testing.

Diagnosis: Check INR trend, CBC if bleeding/anemia, CMP/LFTs, TSH if suggested, medication interaction review, and confirm whether warfarin remains preferred over DOAC, especially for mechanical valve, moderate-severe mitral stenosis, or high-risk APS.

First-line treatment: For minor out-of-range INR, adjust weekly dose using anticoagulation clinic protocol, reinforce consistent vitamin K intake, adherence tools, and repeat INR at an appropriate interval.

Second-line treatment: Supratherapeutic INR without bleeding may require holding warfarin and sometimes oral vitamin K depending on INR/risk; subtherapeutic INR may require dose increase or bridging only for selected very high thrombosis-risk indications.

Third-line / advanced care: Major bleeding requires vitamin K plus 4-factor PCC (Kcentra) and emergency evaluation. Refer anticoagulation clinic/hematology for recurrent instability, APS/mechanical valve complexity, peri-procedure bridging, or inability to monitor.

Progression and follow-up: Follow time in therapeutic range, bleeding, thrombosis, interacting drugs, diet stability, falls, renal/liver changes, and whether conversion to apixaban/rivaroxaban/dabigatran is safe for the indication.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Bleeding disorder evaluation

Pathophysiology: Bleeding disorders arise from platelet number/function defects, von Willebrand disease, coagulation factor deficiency, liver disease, anticoagulants, connective tissue disease, or acquired inhibitors.

How Hematology assesses it: Assess mucocutaneous bleeding, epistaxis, menorrhagia, surgical/dental bleeding, postpartum bleeding, joint/muscle bleeding, bruising, family history, medications/NSAIDs/SSRIs, anticoagulants, liver/renal disease, and bleeding assessment tool score.

Diagnosis: Initial tests include CBC/platelets, smear, PT/INR, aPTT, fibrinogen, CMP/LFTs, von Willebrand antigen/activity and factor VIII when mucocutaneous pattern, platelet function testing when indicated, mixing study for prolonged aPTT/PT, and specific factor assays/inhibitor testing guided by results.

First-line treatment: Avoid aspirin/NSAIDs when platelet/vWD pattern suspected, use local pressure/topical hemostatics, iron repletion for chronic blood loss, and coordinate procedure planning before surgery/dental work.

Second-line treatment: Condition-specific therapy may include desmopressin (DDAVP/Stimate where available), tranexamic acid (Lysteda/Cyklokapron), aminocaproic acid (Amicar), von Willebrand factor concentrate (Humate-P/Wilate/Vonvendi), or factor VIII/IX replacement.

Third-line / advanced care: Emergency hematology for major bleeding, intracranial bleed, acquired hemophilia, severe factor deficiency, pregnancy/delivery planning, urgent surgery, or suspected DIC/TMA.

Progression and follow-up: Follow bleeding frequency, ferritin/anemia, procedure outcomes, thrombosis risk with concentrates/antifibrinolytics, inhibitor development, and family testing.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Hypercoagulable workup

Pathophysiology: Hypercoagulability may be inherited, acquired, cancer-associated, inflammatory, estrogen/pregnancy-related, antiphospholipid-mediated, myeloproliferative, paroxysmal nocturnal hemoglobinuria, or simply unprovoked without detectable thrombophilia.

How Hematology assesses it: Assess VTE age/site, provoking factors, recurrence, family history, pregnancy morbidity, arterial thrombosis, autoimmune disease, cancer symptoms, CBC abnormalities, hemolysis, estrogen/testosterone use, nephrotic syndrome, and whether results would alter duration or drug choice.

Diagnosis: Avoid broad acute-phase testing that will not change care. Consider antiphospholipid antibodies for unprovoked/recurrent/arterial/pregnancy morbidity; factor V Leiden/prothrombin mutation/protein C/S/antithrombin only in selected patients; JAK2 for splanchnic thrombosis or high counts; PNH flow for unusual thrombosis with cytopenias/hemolysis.

First-line treatment: Treat the acute clot with standard anticoagulation first; counsel family history and modifiable risks such as estrogen avoidance, smoking cessation, weight, mobility, and perioperative prophylaxis.

Second-line treatment: Use results to guide therapy: warfarin (Coumadin/Jantoven) preferred over DOACs for high-risk APS; indefinite anticoagulation considered for recurrent/unprovoked high-risk VTE if bleeding risk acceptable.

Third-line / advanced care: Hematology for unusual-site thrombosis, recurrent VTE on therapy, pregnancy planning, suspected APS/MPN/PNH, strong family history, or complex stop/continue decisions.

Progression and follow-up: Follow recurrent thrombosis, bleeding, pregnancy outcomes, family counseling, false-positive tests from acute thrombosis/anticoagulants, and overtesting harms.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Myeloproliferative neoplasm suspicion

Pathophysiology: Myeloproliferative neoplasms are clonal stem-cell disorders such as polycythemia vera, essential thrombocythemia, and myelofibrosis driven often by JAK2, CALR, or MPL mutations, causing thrombosis, bleeding, splenomegaly, constitutional symptoms, marrow fibrosis, and AML transformation risk.

How Hematology assesses it: Assess persistent erythrocytosis, thrombocytosis, leukocytosis, pruritus after bathing, erythromelalgia, headaches/visual symptoms, thrombosis especially splanchnic/cerebral, bleeding, constitutional symptoms, splenomegaly, iron deficiency, hypoxia/smoking/testosterone, and family history.

Diagnosis: Repeat CBC with smear, EPO level for erythrocytosis, iron studies, oxygen saturation/carboxyhemoglobin when relevant, JAK2 V617F/exon 12, CALR/MPL testing if JAK2-negative thrombocytosis/myelofibrosis suspected, BCR-ABL to exclude CML, LDH/uric acid, and bone marrow biopsy with cytogenetics/molecular risk stratification.

First-line treatment: Low-risk PV often uses phlebotomy to hematocrit target plus low-dose aspirin (Bayer/Ecotrin) if no contraindication; ET risk-adapted aspirin may be used for microvascular symptoms. Correct cardiovascular risks and avoid iron replacement in PV unless specialist-directed.

Second-line treatment: Cytoreduction with hydroxyurea (Hydrea), peginterferon alfa-2a/ropeginterferon (Besremi), or anagrelide (Agrylin) for selected ET/PV risk; myelofibrosis symptom/spleen therapy may include ruxolitinib (Jakafi), fedratinib (Inrebic), momelotinib (Ojjaara), or pacritinib (Vonjo) by cytopenias/risk.

Third-line / advanced care: Hematology/MPN specialist for all suspected cases, pregnancy, unusual thrombosis, severe thrombocytosis with acquired vWD, progressive splenomegaly, constitutional symptoms, transplant evaluation, or AML transformation concern.

Progression and follow-up: Follow CBC targets, thrombosis/bleeding, splenomegaly, symptoms, iron deficiency, marrow fibrosis, mutation/risk score, drug cytopenias/infections, skin cancer with hydroxyurea, and leukemic transformation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Hematology

Lymphadenopathy evaluation

Pathophysiology: Lymphadenopathy may be reactive infection/inflammation, autoimmune disease, medication-related, metastatic cancer, lymphoma, leukemia, or granulomatous disease; risk depends on node size, location, persistence, systemic symptoms, and exam context.

How Hematology assesses it: Assess duration, tenderness, growth, generalized versus localized nodes, supraclavicular/epitrochlear location, fever/night sweats/weight loss, infections, dental/skin/STI exposure, travel/TB, cat exposure, autoimmune symptoms, medications, malignancy history, and hepatosplenomegaly.

Diagnosis: Use targeted CBC with differential, CMP/LDH, ESR/CRP, HIV, EBV/CMV, TB testing, syphilis or toxoplasma/cat-scratch testing when suggested, ultrasound for superficial nodes, CT neck/chest/abdomen/pelvis for deep/high-risk nodes, and excisional biopsy preferred when lymphoma suspected.

First-line treatment: Observe short-term only for clearly benign localized nodes with infectious trigger and no red flags; treat identified infection such as dental/skin source with appropriate therapy and reassess node resolution.

Second-line treatment: If persistent beyond several weeks, enlarging, hard/fixed, supraclavicular, generalized, or with B symptoms, expedite imaging and tissue diagnosis rather than repeated empiric antibiotics or steroids.

Third-line / advanced care: Hematology/oncology or ENT/surgery for excisional biopsy, flow cytometry, core biopsy when excision impractical, PET-CT after diagnosis, or urgent evaluation for airway compromise, SVC syndrome, cytopenias, or suspected aggressive lymphoma.

Progression and follow-up: Follow node size, systemic symptoms, CBC/LDH, biopsy results, infection resolution, steroid exposure before biopsy, missed lymphoma/metastatic cancer, and patient follow-through.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Specialty role

Cancer diagnosis and systemic treatment coordination, staging, surveillance, toxicity management, and survivorship.

Oncology

Breast cancer treatment coordination

Pathophysiology: Breast cancer is biologically defined by histology, grade, ER/PR hormone-receptor status, HER2 status, Ki-67/proliferation, nodal involvement, and metastatic pattern; ductal carcinoma in situ, invasive ductal, invasive lobular, triple-negative, HER2-positive, and hormone-receptor-positive disease behave and respond differently.

How Oncology assesses it: Assess palpable mass, nipple discharge/skin change, axillary nodes, prior mammograms, family/genetic risk, menopausal status, fertility goals, cardiac history, bone health, and symptoms of metastasis such as bone pain, dyspnea, liver pain, or neurologic deficits.

Diagnosis: Diagnostic mammogram plus targeted breast/axillary ultrasound; breast MRI for selected extent/high-risk cases; core needle biopsy with ER, PR, HER2 IHC/FISH when equivocal, grade, and histology; stage with AJCC TNM plus prognostic markers. CT chest/abdomen/pelvis, bone scan, or PET/CT is reserved for node-positive, locally advanced, aggressive biology, or metastatic symptoms rather than every early cancer.

First-line treatment: Local disease is treated with surgery (lumpectomy plus radiation or mastectomy) and axillary staging. Sentinel lymph node biopsy remains common for invasive cancer, while omission may be considered only for carefully selected small clinically node-negative tumors with negative axillary ultrasound and planned breast-conserving surgery/radiation. ER/PR-positive disease uses tamoxifen (Soltamox) or aromatase inhibitors anastrozole (Arimidex), letrozole (Femara), exemestane (Aromasin). HER2-positive disease adds trastuzumab (Herceptin/Kanjinti) often with pertuzumab (Perjeta) and chemotherapy such as paclitaxel (Taxol) or docetaxel (Taxotere). Triple-negative disease often uses anthracycline/taxane chemotherapy and selected pembrolizumab (Keytruda) in higher-risk settings.

Second-line treatment: Use genomic recurrence assays such as Oncotype DX in selected ER-positive/HER2-negative early disease; neoadjuvant therapy for large/node-positive/HER2-positive/triple-negative tumors; capecitabine (Xeloda), T-DM1 ado-trastuzumab emtansine (Kadcyla), olaparib (Lynparza) for germline BRCA-selected high-risk disease, or CDK4/6 inhibitors such as abemaciclib (Verzenio) in selected high-risk hormone-receptor-positive disease.

Third-line / advanced care: Metastatic care is subtype-driven: endocrine therapy plus CDK4/6 inhibitor palbociclib (Ibrance)/ribociclib (Kisqali)/abemaciclib, HER2-directed therapy including trastuzumab deruxtecan (Enhertu), sacituzumab govitecan (Trodelvy) for selected triple-negative disease, bone agents zoledronic acid (Zometa) or denosumab (Xgeva), palliative radiation, clinical trials, and early palliative care.

Progression and follow-up: Follow for local recurrence, contralateral disease, lymphedema, cardiomyopathy from anthracyclines/HER2 therapy, neuropathy, ovarian/fertility effects, bone loss from endocrine therapy, and metastases to bone, liver, lung, or brain.

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Oncology

Lung cancer workup

Pathophysiology: Lung cancer separates first into non-small cell lung cancer (adenocarcinoma, squamous, large cell) versus small cell lung cancer. Smoking, radon, asbestos, and molecular drivers such as EGFR, ALK, ROS1, BRAF, MET, RET, NTRK, KRAS, and PD-L1 expression shape prognosis and treatment.

How Oncology assesses it: Assess cough, hemoptysis, dyspnea, chest pain, weight loss, smoking/exposure history, performance status, paraneoplastic symptoms, superior vena cava syndrome, brain/bone symptoms, and pulmonary reserve.

Diagnosis: Chest CT with contrast, PET/CT for staging, brain MRI for stage II/III or neurologic symptoms and most small-cell/advanced cases, tissue biopsy by bronchoscopy/EBUS, CT-guided biopsy, or thoracentesis, mediastinal nodal staging, histology, PD-L1, and broad molecular testing for nonsquamous or advanced NSCLC.

First-line treatment: Early-stage NSCLC: surgical resection with lymph node sampling if operable, stereotactic body radiation therapy if medically inoperable, and adjuvant/neoadjuvant systemic therapy by stage/biomarker. Advanced NSCLC: biomarker-directed therapy such as osimertinib (Tagrisso) for EGFR, alectinib (Alecensa) for ALK, pembrolizumab (Keytruda) for PD-L1-high disease, or platinum doublet chemotherapy such as carboplatin plus pemetrexed (Alimta) for nonsquamous disease when no targetable driver. Small-cell lung cancer: platinum etoposide plus immunotherapy such as atezolizumab (Tecentriq) or durvalumab (Imfinzi) for extensive-stage disease.

Second-line treatment: Stage III unresectable NSCLC often uses concurrent chemoradiation followed by durvalumab (Imfinzi) consolidation. Progression after targeted therapy needs resistance testing and next-line targeted agent, chemoimmunotherapy, docetaxel (Taxotere) plus ramucirumab (Cyramza), or clinical trial.

Third-line / advanced care: Urgent oncology/radiation for SVC syndrome, hemoptysis, airway obstruction, spinal cord compression, or brain metastases. Use palliative radiation, bronchoscopic stenting/debulking, pleural catheter, bone agents, hospice/palliative care when appropriate.

Progression and follow-up: Progression causes malignant pleural effusion, brain/bone/adrenal/liver metastases, cachexia, hypercalcemia, SIADH or Cushing syndrome in small-cell disease, respiratory failure, and treatment pneumonitis or immune toxicity.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Colon cancer treatment coordination

Pathophysiology: Colon cancer usually arises through adenoma-carcinoma or serrated pathways with molecular features such as mismatch-repair deficiency/MSI-H, KRAS/NRAS/BRAF status, sidedness, and metastatic pattern guiding therapy.

How Oncology assesses it: Assess rectal bleeding, iron-deficiency anemia, bowel habit change, obstruction/perforation symptoms, family history/Lynch syndrome features, prior polyps, CEA baseline, performance status, neuropathy risk, and symptoms of liver/lung/peritoneal spread.

Diagnosis: Colonoscopy with biopsy is diagnostic; CT chest/abdomen/pelvis for staging; CEA baseline; CBC/CMP/iron studies; MMR/MSI testing for all colon cancers; KRAS/NRAS/BRAF and HER2/NTRK testing for metastatic disease. MRI pelvis applies to rectal cancer rather than colon cancer.

First-line treatment: Localized colon cancer: surgical colectomy with lymph node harvest. Stage III and selected high-risk stage II disease receive adjuvant fluoropyrimidine/oxaliplatin therapy such as FOLFOX (5-FU/leucovorin/oxaliplatin) or CAPOX (capecitabine/Xeloda plus oxaliplatin/Eloxatin).

Second-line treatment: Metastatic disease uses systemic combinations such as FOLFOX, FOLFIRI (5-FU/leucovorin/irinotecan/Camptosar), CAPOX, plus bevacizumab (Avastin) or EGFR antibody cetuximab (Erbitux)/panitumumab (Vectibix) for RAS wild-type left-sided tumors. MSI-H/dMMR metastatic disease can use pembrolizumab (Keytruda) or nivolumab (Opdivo).

Third-line / advanced care: Consider liver/lung metastasectomy or ablation for oligometastatic disease, HIPEC only in selected peritoneal disease centers, regorafenib (Stivarga), trifluridine-tipiracil (Lonsurf), fruquintinib (Fruzaqla), targeted BRAF therapy encorafenib (Braftovi) plus cetuximab for BRAF V600E, clinical trials, and palliative obstruction/stent/ostomy care.

Progression and follow-up: Progression causes bowel obstruction, perforation, bleeding/anemia, liver failure, peritoneal carcinomatosis, cachexia, neuropathy from oxaliplatin, diarrhea from irinotecan, and recurrence requiring CEA/imaging/colonoscopy surveillance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Prostate cancer risk stratification

Pathophysiology: Prostate cancer ranges from indolent localized adenocarcinoma to aggressive metastatic castration-resistant disease. Risk is stratified by PSA, Grade Group/Gleason score, clinical T stage, MRI findings, genomic risk in selected cases, nodal disease, and metastases, especially bone.

How Oncology assesses it: Assess PSA trend, urinary obstructive symptoms, bone pain, neurologic symptoms, family history/BRCA/Lynch risk, life expectancy, comorbidities, sexual/urinary priorities, and prior biopsy/MRI findings.

Diagnosis: PSA, digital rectal exam, multiparametric prostate MRI, transrectal or transperineal biopsy with Grade Group/Gleason score, and risk stratification. Staging imaging is risk-based: PSMA PET/CT, bone scan, CT/MRI pelvis/abdomen for high-risk or suspected metastatic disease, not routinely for very-low/low-risk localized disease.

First-line treatment: Very-low/low-risk disease often uses active surveillance with PSA, MRI, and repeat biopsy. Localized intermediate/high-risk disease uses radical prostatectomy with pelvic lymph node evaluation when indicated, or external-beam radiation/brachytherapy plus androgen deprivation therapy such as leuprolide (Lupron/Eligard) or degarelix (Firmagon) depending on risk.

Second-line treatment: Biochemical recurrence is managed by salvage radiation, ADT, or PSMA-guided evaluation. Metastatic hormone-sensitive disease uses ADT plus intensification such as abiraterone (Zytiga) with prednisone, enzalutamide (Xtandi), apalutamide (Erleada), darolutamide (Nubeqa), or docetaxel (Taxotere) in selected patients.

Third-line / advanced care: Castration-resistant disease may use enzalutamide, abiraterone, docetaxel/cabazitaxel (Jevtana), radium-223 (Xofigo) for symptomatic bone-predominant disease, lutetium Lu-177 vipivotide tetraxetan (Pluvicto) for PSMA-positive disease, PARP inhibitors olaparib (Lynparza)/rucaparib (Rubraca) for HRR mutations, bone protection denosumab (Xgeva) or zoledronic acid (Zometa), palliative radiation, and clinical trials.

Progression and follow-up: Monitor PSA kinetics, testosterone castration level, urinary obstruction, bone metastases/fracture/spinal cord compression, ADT metabolic/bone/sexual effects, hot flashes, fatigue, anemia, and treatment-resistant progression.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Lymphoma suspicion and staging

Pathophysiology: Lymphoma is not one disease: Hodgkin lymphoma, diffuse large B-cell lymphoma, follicular lymphoma, mantle cell lymphoma, marginal zone lymphoma, Burkitt lymphoma, T-cell lymphomas, and CLL/SLL differ in growth rate, staging, curability, and treatment sensitivity.

How Oncology assesses it: Assess painless lymphadenopathy, B symptoms (fever/night sweats/weight loss), pruritus, alcohol-related node pain, extranodal symptoms, autoimmune/immunosuppression history, HIV/hepatitis risk, performance status, and bulky mediastinal/airway/SVC symptoms.

Diagnosis: Excisional lymph node biopsy is preferred when feasible; pathology with flow cytometry, immunohistochemistry, cytogenetics/FISH, and molecular studies. Stage with PET/CT for FDG-avid lymphomas, CT when appropriate, CBC/CMP/LDH/uric acid, hepatitis B/C/HIV testing, bone marrow biopsy in selected cases, and Ann Arbor/Lugano staging.

First-line treatment: Treatment is subtype-specific. Hodgkin lymphoma often uses ABVD (doxorubicin/bleomycin/vinblastine/dacarbazine) or brentuximab vedotin (Adcetris)-containing regimens by stage/risk. DLBCL commonly uses R-CHOP or polatuzumab-based chemoimmunotherapy. Indolent follicular lymphoma may use observation, rituximab (Rituxan), bendamustine-rituximab, or radiation for localized disease.

Second-line treatment: Relapsed disease depends on histology: salvage chemo plus autologous stem-cell transplant for eligible aggressive lymphoma, CAR-T therapies such as axicabtagene ciloleucel (Yescarta) or tisagenlecleucel (Kymriah), bispecific antibodies, BTK inhibitors for mantle cell/CLL biology, or lenalidomide (Revlimid) regimens.

Third-line / advanced care: Urgent treatment for tumor lysis risk, spinal cord compression, airway/SVC compromise, HLH concern, CNS lymphoma, or severe cytopenias. Use infection prophylaxis, growth factors, transfusion support, and clinical trials when appropriate.

Progression and follow-up: Progression may cause marrow failure, bulky organ compression, transformation of indolent lymphoma, infections from immune dysfunction/therapy, infertility, cardiopulmonary toxicity, neuropathy, and secondary malignancies.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Leukemia acute presentation

Pathophysiology: Leukemia is divided into acute myeloid leukemia, acute lymphoblastic leukemia, chronic lymphocytic leukemia, chronic myeloid leukemia, and other entities; lineage, blast percentage, cytogenetics, mutations, and patient fitness determine urgency and treatment.

How Oncology assesses it: Assess fatigue, infections, fever, bleeding/bruising, bone pain, leukostasis symptoms (dyspnea, neurologic deficits, vision changes), splenomegaly, medication/exposure history, prior chemo/radiation, and tumor lysis/DIC risk.

Diagnosis: CBC with differential, peripheral smear, CMP, LDH, uric acid, phosphorus, coagulation panel/fibrinogen, flow cytometry, bone marrow biopsy/aspirate, cytogenetics/FISH, molecular testing such as FLT3/NPM1/IDH/BCR-ABL/PML-RARA as appropriate, HLA typing for transplant candidates, and infection baseline testing.

First-line treatment: Suspected acute leukemia is urgent hematology care. APL is a medical emergency treated immediately with all-trans retinoic acid (ATRA, Vesanoid) plus arsenic trioxide (Trisenox) or anthracycline-based therapy by risk. Fit AML may use cytarabine/daunorubicin induction; older/unfit AML often uses azacitidine (Vidaza) or decitabine plus venetoclax (Venclexta). CML uses tyrosine kinase inhibitors such as imatinib (Gleevec), dasatinib (Sprycel), nilotinib (Tasigna), or bosutinib (Bosulif).

Second-line treatment: ALL uses multiagent induction/consolidation/maintenance with CNS prophylaxis; Philadelphia-positive ALL adds TKI. Add targeted AML agents such as midostaurin (Rydapt) for FLT3, ivosidenib (Tibsovo) for IDH1, enasidenib (Idhifa) for IDH2 when indicated. CLL treatment may use acalabrutinib (Calquence), zanubrutinib (Brukinsa), venetoclax-obinutuzumab, or observation for asymptomatic early disease.

Third-line / advanced care: Allogeneic stem-cell transplant, CAR-T therapy for selected ALL, leukapheresis/cytoreduction for leukostasis, ICU support, broad antimicrobials, transfusions, tumor lysis prophylaxis with allopurinol (Zyloprim) or rasburicase (Elitek), and clinical trials.

Progression and follow-up: Complications include leukostasis, DIC especially APL, tumor lysis syndrome, severe infection, bleeding, relapse, graft-versus-host disease after transplant, infertility, cardiotoxicity, and long-term secondary cancers.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Neutropenic fever

Pathophysiology: Neutropenic fever is an oncologic emergency because chemotherapy- or marrow-related neutrophil depletion prevents localizing signs while bacteremia, fungal infection, or sepsis can progress rapidly.

How Oncology assesses it: Assess ANC, fever pattern, time since chemo/transplant, mucositis, central line, skin/perianal pain, cough/dyspnea, abdominal pain/diarrhea, urinary symptoms, prior resistant organisms, antifungal/antibacterial prophylaxis, and hemodynamic stability.

Diagnosis: Do not delay antibiotics. Obtain CBC with differential, CMP/lactate when ill, two sets of blood cultures including central line and peripheral when possible, urinalysis/culture if symptoms, chest X-ray or CT chest for respiratory symptoms, stool C. difficile if diarrhea, and site cultures/imaging for focal symptoms.

First-line treatment: Give empiric antipseudomonal beta-lactam promptly: cefepime (Maxipime), piperacillin-tazobactam (Zosyn), meropenem (Merrem), or imipenem-cilastatin (Primaxin). Add vancomycin (Vancocin) only for catheter infection, skin/soft tissue infection, pneumonia, hemodynamic instability, known MRSA, or severe mucositis with resistant gram-positive risk.

Second-line treatment: Low-risk selected patients may use oral ciprofloxacin (Cipro) plus amoxicillin-clavulanate (Augmentin) under protocol. Persistent fever after several days or high-risk features may require antifungal coverage such as micafungin (Mycamine), voriconazole (Vfend), or liposomal amphotericin B (AmBisome) guided by risk/imaging.

Third-line / advanced care: ICU for sepsis/shock, remove infected catheter when indicated, G-CSF filgrastim (Neupogen/Zarxio) in selected high-risk cases, infectious disease consultation, and tailor therapy to cultures and clinical course.

Progression and follow-up: Complications include septic shock, invasive mold infection, typhlitis/neutropenic enterocolitis, pneumonia, catheter sepsis, organ failure, chemotherapy delay, and death.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Chemotherapy nausea and vomiting

Pathophysiology: Chemotherapy-induced nausea/vomiting is mediated by serotonin 5-HT3, substance P/NK1, dopamine, vestibular, anticipatory, and delayed inflammatory pathways; risk depends on the emetogenic regimen and patient factors.

How Oncology assesses it: Assess chemo regimen emetogenicity, prior CINV, pregnancy, bowel obstruction/brain metastasis/hypercalcemia/opioids, hydration, weight loss, QT risk, constipation, steroid contraindications, and anticipatory anxiety.

Diagnosis: Clinical diagnosis after excluding emergencies: bowel obstruction, increased intracranial pressure, infection, metabolic derangement, adrenal insufficiency, or medication toxicity. Check BMP/Mg, calcium, LFTs, and imaging if symptoms are atypical/severe.

First-line treatment: Highly emetogenic regimens typically use 5-HT3 antagonist ondansetron (Zofran) or palonosetron (Aloxi), dexamethasone (Decadron), NK1 antagonist aprepitant (Emend)/fosaprepitant, and often olanzapine (Zyprexa). Moderate-risk regimens use 5-HT3 antagonist plus dexamethasone with NK1/olanzapine when indicated.

Second-line treatment: Breakthrough therapy can use prochlorperazine (Compazine), metoclopramide (Reglan), olanzapine, lorazepam (Ativan) for anticipatory component, or cannabinoid dronabinol (Marinol) in selected refractory cases.

Third-line / advanced care: IV fluids/electrolyte replacement, hospital evaluation for dehydration or obstruction, nutrition support, palliative care, and chemo regimen antiemetic escalation next cycle.

Progression and follow-up: Poor control causes dehydration, AKI, electrolyte abnormalities, malnutrition, anticipatory nausea, treatment refusal, aspiration risk, and hospitalization.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Immune checkpoint inhibitor toxicity

Pathophysiology: Checkpoint inhibitors such as pembrolizumab, nivolumab, ipilimumab, atezolizumab, durvalumab, and cemiplimab activate antitumor immunity but can cause immune-related adverse events in any organ.

How Oncology assesses it: Ask specifically about diarrhea/colitis, cough/dyspnea/pneumonitis, rash, hepatitis symptoms, endocrinopathy fatigue/headache/hypotension, arthritis, nephritis, myocarditis chest pain, neurologic weakness, and timing since immunotherapy.

Diagnosis: Grade severity; labs include CBC/CMP/LFTs/creatinine, TSH/free T4, cortisol/ACTH when adrenal concern, troponin/ECG for myocarditis concern, stool studies before colitis immunosuppression, chest CT for pneumonitis, and organ-specific imaging/biopsy when unclear.

First-line treatment: Grade 1 often monitor/continue with close follow-up except dangerous organs. Grade 2 generally hold immunotherapy and start prednisone (Deltasone) or equivalent for many toxicities. Endocrine toxicity often requires hormone replacement such as levothyroxine (Synthroid) or hydrocortisone (Cortef) rather than permanent immunosuppression alone.

Second-line treatment: Grade 3-4 toxicity needs high-dose corticosteroids such as methylprednisolone (Solu-Medrol), specialist consultation, and slow taper. Steroid-refractory colitis may require infliximab (Remicade) or vedolizumab (Entyvio); hepatitis may use mycophenolate (CellCept) and avoid infliximab.

Third-line / advanced care: ICU/cardiology/neurology for myocarditis, myasthenia-like syndrome, Guillain-Barre-like syndrome, severe pneumonitis, adrenal crisis, or neurologic toxicity. Rechallenge decisions are oncology-specialist, risk-based, and toxicity-specific.

Progression and follow-up: Delayed recognition can cause bowel perforation, respiratory failure, liver failure, adrenal crisis, myocarditis death, chronic endocrine replacement needs, and permanent discontinuation of effective cancer therapy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Cancer pain

Pathophysiology: Cancer pain may be nociceptive from tumor invasion, visceral obstruction, bone metastases, or procedures; neuropathic from nerve compression or chemotherapy; and total pain from psychosocial/spiritual distress.

How Oncology assesses it: Assess pain mechanism, site, severity, breakthrough pattern, opioid exposure/tolerance, bowel function, sedation, renal/hepatic function, substance-use risk, goals, and emergencies such as fracture, cord compression, infection, or bowel obstruction.

Diagnosis: Clinical pain phenotype plus targeted imaging: X-ray/CT/MRI for bone/spine/structural pain, labs for hypercalcemia/infection, neurologic exam for cord/nerve compression, and medication review for neuropathy.

First-line treatment: Mild pain: acetaminophen (Tylenol), NSAID such as ibuprofen (Advil/Motrin) or naproxen (Aleve) if safe. Moderate/severe cancer pain: opioids such as morphine, oxycodone (OxyContin/Roxicodone), hydromorphone (Dilaudid), or fentanyl patch (Duragesic) with bowel regimen senna (Senokot) plus polyethylene glycol (MiraLAX). Neuropathic pain: duloxetine (Cymbalta), gabapentin (Neurontin), or pregabalin (Lyrica).

Second-line treatment: Bone metastasis pain may need radiation, dexamethasone (Decadron), bisphosphonate zoledronic acid (Zometa), or denosumab (Xgeva). Refractory pain may use methadone (Dolophine), ketamine protocols, nerve blocks, or intrathecal pump specialist care.

Third-line / advanced care: Urgent oncology/radiation/surgery for spinal cord compression, pathologic fracture, bowel obstruction, or uncontrolled pain crisis; palliative care for complex opioid rotation, goals, and psychosocial support.

Progression and follow-up: Poorly controlled pain causes immobility, delirium, depression, caregiver distress, constipation, falls, opioid toxicity, hospitalization, and suffering near end of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Malignant spinal cord compression

Pathophysiology: Epidural tumor extension or vertebral metastasis compresses the spinal cord/cauda equina, causing edema, ischemia, demyelination, and potentially irreversible neurologic injury.

How Oncology assesses it: Assess new severe back pain, nocturnal pain, radicular pain, weakness, sensory level, gait change, bowel/bladder dysfunction, known cancer type, steroid contraindications, and anticoagulant use.

Diagnosis: Emergency MRI of the entire spine with contrast is preferred; CT myelogram if MRI impossible. Perform neurologic exam, postvoid residual, CBC/CMP/coags, and identify tissue diagnosis if cancer unknown without delaying decompression/radiation decisions.

First-line treatment: Give dexamethasone (Decadron) promptly when suspected unless contraindicated, immobilize if unstable spine concern, urgent radiation oncology/neurosurgery consultation, analgesia, and DVT/pressure injury prevention.

Second-line treatment: Definitive therapy is tumor- and stability-dependent: external-beam radiation for radiosensitive disease or nonsurgical candidates; surgical decompression/stabilization followed by radiation for selected patients with instability, radioresistant tumor, solitary compression, or good functional prognosis.

Third-line / advanced care: Systemic therapy for chemo-sensitive tumors, vertebroplasty/kyphoplasty in selected painful compression fractures, rehab, bladder/bowel program, palliative care, and hospice when neurologic recovery is unlikely or goals prioritize comfort.

Progression and follow-up: Delay can cause permanent paralysis, urinary retention/incontinence, fecal incontinence, pressure injuries, VTE, severe pain, and loss of independence.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Tumor lysis syndrome

Pathophysiology: Rapid tumor cell breakdown releases potassium, phosphate, and nucleic acids, causing hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, AKI, arrhythmias, seizures, and death; risk is high in bulky, chemo-sensitive hematologic cancers.

How Oncology assesses it: Assess cancer type/burden, baseline uric acid, LDH, creatinine/eGFR, electrolytes, urine output, planned cytotoxic therapy, dehydration, and prior kidney disease.

Diagnosis: Use serial BMP, phosphorus, calcium, uric acid, LDH, creatinine, ECG for hyperkalemia, strict intake/output, and Cairo-Bishop style lab/clinical TLS criteria when needed.

First-line treatment: Prevention/treatment includes aggressive IV hydration when appropriate, frequent labs, avoid nephrotoxins, allopurinol (Zyloprim) for lower/intermediate risk prevention, and rasburicase (Elitek) for high-risk or established hyperuricemia/TLS when not G6PD deficient.

Second-line treatment: Treat hyperkalemia urgently with calcium gluconate, insulin/dextrose, albuterol, potassium binders, and dialysis if refractory; manage hyperphosphatemia with binders and avoid routine calcium unless symptomatic hypocalcemia.

Third-line / advanced care: ICU/nephrology for severe electrolyte abnormalities, arrhythmia, seizures, AKI, oliguria, or dialysis indications. Delay chemotherapy only when clinically necessary and oncology-directed.

Progression and follow-up: Complications include fatal arrhythmia, seizure, acute kidney injury, volume overload, dialysis need, and interruption of curative cancer therapy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Palliative oncology transition

Pathophysiology: Palliative transition occurs when disease trajectory, treatment burden, functional decline, or patient goals shift from tumor-directed escalation toward symptom-focused care, quality of life, and support for patient/family.

How Oncology assesses it: Assess prognosis understanding, performance status, symptom burden, treatment options/benefit probability, decision-making capacity, caregiver support, spiritual distress, code status, advance directive, and hospice eligibility.

Diagnosis: This is a goals-of-care and clinical trajectory diagnosis: document cancer status, treatment response, ECOG/Karnofsky function, weight loss/cachexia, hospitalizations, uncontrolled symptoms, and patient values.

First-line treatment: Primary palliative care includes serious-illness conversation, symptom control, opioid/nonopioid pain plan, bowel regimen, antiemetics such as ondansetron (Zofran) or prochlorperazine (Compazine), dyspnea support, depression/anxiety treatment, and caregiver planning.

Second-line treatment: Specialty palliative care for complex pain, refractory nausea/dyspnea/delirium, family conflict, prognostic uncertainty, or high distress. Hospice referral when life expectancy and goals align with comfort-focused care.

Third-line / advanced care: Inpatient palliative unit, home hospice, continuous care for crisis symptoms, palliative sedation only for refractory suffering under strict ethical protocols, and bereavement support.

Progression and follow-up: Good transition reduces unwanted ICU care, uncontrolled symptoms, caregiver distress, and goal-discordant treatment while improving quality of life and often care satisfaction.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oncology

Cancer survivorship care

Pathophysiology: Survivorship care addresses late effects of cancer and treatment: cardiomyopathy, neuropathy, endocrine dysfunction, infertility, sexual health, cognitive changes, fatigue, lymphedema, bone loss, second malignancies, and psychosocial recovery.

How Oncology assesses it: Assess original cancer/stage/treatments, recurrence symptoms, surveillance schedule, medications, neuropathy, fatigue, sleep, mood/PTSD, fertility/sexual function, bone health, cardiovascular risk, vaccines, work/financial toxicity, and health behaviors.

Diagnosis: Use survivorship care plan, treatment summary, cancer-specific surveillance such as mammography/colonoscopy/PSA/imaging only when indicated, CBC/CMP/TSH/endocrine labs as treatment-specific, echocardiogram after anthracycline/HER2 therapy when indicated, DEXA for bone risk, and validated distress/fatigue tools.

First-line treatment: Coordinate primary care and oncology surveillance; manage risk factors with statins/antihypertensives/diabetes care, vaccines, exercise/rehab, nutrition, smoking cessation varenicline (Chantix) or nicotine replacement, and symptom-specific meds such as duloxetine (Cymbalta) for neuropathy or venlafaxine (Effexor XR) for hot flashes.

Second-line treatment: Refer to cardio-oncology, fertility/sexual medicine, lymphedema therapy, psycho-oncology, PT/OT, pain clinic, endocrinology, or genetics based on treatment exposure and symptoms.

Third-line / advanced care: Evaluate urgently for recurrence red flags, second malignancy, severe depression/suicidality, cardiopulmonary symptoms, progressive neurologic deficits, or late radiation/chemo complications.

Progression and follow-up: Unaddressed survivorship problems can cause preventable cardiovascular disease, fractures, chronic pain, disability, infertility distress, depression/anxiety, missed recurrence, and poor adherence to surveillance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Specialty role

Brain, nerve, neuromuscular, seizure, movement, headache, cognition, and stroke specialty care.

Neurology

Ischemic stroke acute and secondary prevention

Pathophysiology: Acute ischemic stroke is focal brain, retinal, or spinal cord ischemia from large-artery atherosclerosis, cardioembolism, small-vessel occlusion, dissection, hypercoagulability, or other mechanisms; salvageable penumbra and large-vessel occlusion determine acute options.

How Neurology assesses it: Assess exact last-known-well, baseline function, NIHSS, glucose, BP, anticoagulant/DOAC timing, seizure/migraine/hypoglycemia mimics, airway/swallowing, disabling deficit, trauma/surgery/bleeding contraindications, and thrombectomy transfer eligibility.

Diagnosis: Immediate noncontrast CT head excludes hemorrhage; CTA head/neck identifies large-vessel occlusion and carotid disease; CT perfusion or MRI DWI/FLAIR helps selected extended-window cases. Obtain CBC/CMP/PT/INR/aPTT, troponin, ECG/telemetry, lipids, A1c, echocardiography, and mechanism-directed vascular/cardiac workup.

First-line treatment: Eligible disabling ischemic stroke may receive IV thrombolysis with tenecteplase (TNKase) or alteplase (Activase) per institutional/AHA criteria. Give aspirin (Bayer/Ecotrin) after hemorrhage exclusion when thrombolysis timing allows, high-intensity atorvastatin (Lipitor) or rosuvastatin (Crestor), DVT prevention, swallow screen, and BP/glucose/temperature control.

Second-line treatment: Mechanical thrombectomy for eligible anterior-circulation large-vessel occlusion and selected extended-window patients; short-course dual antiplatelet aspirin plus clopidogrel (Plavix) for selected minor noncardioembolic stroke; anticoagulation such as apixaban (Eliquis) for atrial fibrillation after timing based on infarct size/bleeding risk.

Third-line / advanced care: Neuro ICU/stroke center for thrombectomy, malignant edema, basilar occlusion, hemorrhagic transformation, fluctuating deficits, decompressive hemicraniectomy, carotid endarterectomy/stenting, rehab, and secondary prevention clinic.

Progression and follow-up: Follow neurologic exam/NIHSS, dysphagia/aspiration, cerebral edema, hemorrhagic transformation, recurrent stroke, AF detection, BP/lipid/A1c goals, depression/cognition, spasticity, and functional recovery.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Transient ischemic attack

Pathophysiology: TIA is transient focal retinal or cerebral ischemia without infarction on imaging, most often from embolic, large-artery, small-vessel, or hemodynamic mechanisms; early recurrent stroke risk is front-loaded.

How Neurology assesses it: Assess symptom localization, duration, ABCD2 features, crescendo events, amaurosis fugax, carotid bruit, AF symptoms, anticoagulant use, vascular risk factors, mimics such as seizure/migraine/syncope, and ability to complete urgent evaluation.

Diagnosis: MRI brain with DWI is preferred when available; CT head if MRI unavailable/urgent. CTA/MRA/carotid ultrasound evaluates cervicocephalic vessels; ECG/telemetry or ambulatory rhythm monitoring, echocardiography when embolic source suspected, CBC/CMP/coags, lipids, and A1c are typical.

First-line treatment: Start antiplatelet therapy after hemorrhage is excluded: aspirin (Bayer/Ecotrin) or clopidogrel (Plavix). High-risk TIA or minor noncardioembolic stroke often uses short-course aspirin plus clopidogrel, then single antiplatelet; start high-intensity statin and aggressive BP/diabetes/tobacco management.

Second-line treatment: Anticoagulate atrial fibrillation or other cardioembolic source with apixaban (Eliquis), rivaroxaban (Xarelto), dabigatran (Pradaxa), edoxaban (Savaysa), or warfarin (Coumadin) when indicated. Symptomatic high-grade carotid stenosis needs urgent vascular evaluation.

Third-line / advanced care: Admit or rapid-access stroke clinic for high-risk/crescendo TIA, symptomatic carotid stenosis, new AF needing anticoagulation plan, persistent/recurrent symptoms, posterior circulation symptoms, or inability to complete workup within 24-48 hours.

Progression and follow-up: Follow recurrent neurologic symptoms, vascular imaging results, AF monitoring, antithrombotic adherence/bleeding, carotid intervention timing, BP/lipids/A1c, and lifestyle changes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Seizure first episode

Pathophysiology: A first seizure may be provoked by metabolic, toxic, infectious, structural, vascular, traumatic, or withdrawal triggers, or unprovoked from an enduring epileptogenic brain tendency; recurrence risk is higher with epileptiform EEG, structural lesion, prior brain insult, or nocturnal seizure.

How Neurology assesses it: Assess witness description, focal onset, duration, postictal state, tongue bite/incontinence, injury, pregnancy, fever/meningismus, substance/withdrawal, sleep deprivation, medications lowering threshold, prior neurologic insult, family history, driving/work safety, and functional seizure clues.

Diagnosis: Check glucose, sodium/CMP, CBC, pregnancy test when relevant, toxicology when suggested, antiseizure levels if already prescribed, ECG for syncope mimic, brain MRI epilepsy protocol for unprovoked seizure, EEG ideally early, CT head urgently for trauma, focal deficit, cancer, anticoagulation, immunocompromise, or persistent altered mental status.

First-line treatment: Treat reversible causes and provide safety counseling: no driving per state law, avoid swimming alone/heights/open flames, sleep hygiene, alcohol/substance counseling. Immediate antiseizure medication is individualized after recurrence-risk discussion rather than automatic for every first unprovoked seizure.

Second-line treatment: If high recurrence risk or patient preference supports treatment, options include levetiracetam (Keppra), lamotrigine (Lamictal), oxcarbazepine (Trileptal), or lacosamide (Vimpat) chosen by seizure type, comorbid mood, pregnancy potential, interactions, renal/hepatic status, and adverse effects.

Third-line / advanced care: Emergency care for status epilepticus, persistent altered mental status, meningitis/encephalitis, mass/bleed/stroke, pregnancy/eclampsia, severe metabolic abnormality, cluster seizures, or serious injury; neurology follow-up for EEG/MRI interpretation and recurrence plan.

Progression and follow-up: Follow recurrence, EEG/MRI results, medication adverse effects, mood/suicidality, driving restrictions, occupational risk, pregnancy counseling, and distinction from syncope or functional seizures.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Epilepsy medication management

Pathophysiology: Epilepsy medication management aims for seizure freedom without unacceptable adverse effects by matching drug to seizure type, epilepsy syndrome, comorbidity, reproductive plans, interactions, adherence, and serum level needs.

How Neurology assesses it: Assess seizure diary, classification, triggers, adherence, sleep/alcohol, adverse effects, cognition/mood, bone health, contraception/pregnancy potential, renal/hepatic function, rescue medication access, SUDEP risk, and whether events are epileptic versus functional.

Diagnosis: Review EEG/MRI and syndrome diagnosis; monitor CBC/CMP/sodium or drug levels when medication-specific. Check levels for phenytoin, carbamazepine, valproate, phenobarbital, adherence questions, pregnancy, toxicity, or breakthrough seizures. Reassess diagnosis with video EEG when events persist despite therapy.

First-line treatment: Common first-line choices include levetiracetam (Keppra), lamotrigine (Lamictal), lacosamide (Vimpat), oxcarbazepine (Trileptal), carbamazepine (Tegretol), valproate/divalproex (Depakote) when appropriate, or topiramate (Topamax), chosen by seizure type and patient factors; avoid valproate when pregnancy is possible unless no safer effective option.

Second-line treatment: If uncontrolled, optimize dose/adherence, switch or add rational polytherapy, address sleep/substance triggers, prescribe rescue midazolam nasal spray (Nayzilam) or diazepam nasal spray (Valtoco) for clusters, and consider ketogenic diet in selected refractory cases.

Third-line / advanced care: Refer epilepsy center for drug-resistant epilepsy after failure of two appropriate medications, presurgical evaluation, vagus nerve stimulation, responsive neurostimulation, deep brain stimulation, video EEG clarification, or complex pregnancy planning.

Progression and follow-up: Follow seizure frequency, injuries, SUDEP counseling, mood/cognition, rash/SJS risk with lamotrigine/carbamazepine, sodium with oxcarbazepine, liver/platelets/weight with valproate, bone health, and medication withdrawal only after careful risk review.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Migraine preventive care

Pathophysiology: Migraine is a genetic sensory network disorder involving trigeminovascular activation, CGRP signaling, cortical spreading depression, brainstem/hypothalamic modulation, and central sensitization; prevention reduces attack frequency, disability, and medication overuse.

How Neurology assesses it: Assess headache days/month, migraine days, aura, disability, acute-medication days, menstrual pattern, sleep/OSA, caffeine, pregnancy plans, depression/anxiety, BP/asthma/kidney stones/obesity, red flags, and patient preference for oral versus injectable therapy.

Diagnosis: Clinical ICHD pattern; brain MRI or CT/CTA is used for thunderclap onset, abnormal neurologic exam, papilledema, cancer/immunosuppression, pregnancy/postpartum concern, new headache after age 50, exertional/positional headache, or major pattern change.

First-line treatment: Prevention is indicated for frequent/disabling attacks or medication overuse risk. Options include propranolol (Inderal), metoprolol (Toprol XL), topiramate (Topamax), divalproex (Depakote) when pregnancy not possible, amitriptyline (Elavil), venlafaxine (Effexor XR), candesartan (Atacand), and CGRP-targeting therapies as first-line options such as erenumab (Aimovig), fremanezumab (Ajovy), galcanezumab (Emgality), eptinezumab (Vyepti), atogepant (Qulipta), or rimegepant (Nurtec ODT).

Second-line treatment: Acute therapy uses NSAIDs, acetaminophen, triptans such as sumatriptan (Imitrex) or rizatriptan (Maxalt), gepants ubrogepant (Ubrelvy)/rimegepant, or lasmiditan (Reyvow) based on vascular risk and sedation; limit overuse and add antiemetic metoclopramide (Reglan) or prochlorperazine (Compazine) when needed.

Third-line / advanced care: Neurology/headache referral for chronic migraine needing onabotulinumtoxinA (Botox), refractory attacks, hemiplegic/brainstem aura, pregnancy complexity, secondary-headache concern, status migrainosus, or medication-overuse detoxification.

Progression and follow-up: Follow monthly migraine days, acute-medication days, MIDAS/HIT-6 disability, BP/weight/mood, constipation or hypertension with erenumab, cognitive/paresthesia effects with topiramate, pregnancy safety, and medication overuse.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Parkinson disease

Pathophysiology: Parkinson disease is progressive alpha-synuclein neurodegeneration affecting nigrostriatal dopamine pathways and extranigral autonomic, sleep, mood, and cognitive circuits; motor signs include bradykinesia plus rest tremor, rigidity, or postural instability.

How Neurology assesses it: Assess asymmetric tremor, bradykinesia, rigidity, gait/freezing/falls, anosmia, constipation, REM sleep behavior disorder, depression/anxiety, cognition, hallucinations, orthostasis, urinary symptoms, dysphagia, medication-induced parkinsonism, and atypical red flags such as early falls, gaze palsy, severe autonomic failure, or poor levodopa response.

Diagnosis: Clinical diagnosis by neurologic exam; dopamine transporter scan (DaTscan) helps distinguish degenerative parkinsonism from essential tremor/drug-induced cases when uncertain. Brain MRI is used for atypical signs, vascular parkinsonism, normal-pressure hydrocephalus, or structural mimics.

First-line treatment: Function-limiting motor symptoms generally use carbidopa-levodopa (Sinemet/Rytary). Dopamine agonists pramipexole (Mirapex), ropinirole (Requip), or rotigotine (Neupro), MAO-B inhibitors rasagiline (Azilect)/selegiline, and amantadine (Gocovri) are selected by age, cognition, impulse-control risk, and symptom pattern.

Second-line treatment: Motor fluctuations may need levodopa schedule adjustment, entacapone (Comtan), opicapone (Ongentys), safinamide (Xadago), istradefylline (Nourianz), or apomorphine rescue. Treat nonmotor symptoms: constipation regimen, melatonin/clonazepam for REM sleep behavior disorder, orthostatic measures, PT/exercise, speech/swallow therapy.

Third-line / advanced care: Movement-disorders referral for atypical disease, hallucinations/psychosis, cognitive decline, disabling dyskinesia/fluctuations, deep brain stimulation, levodopa intestinal gel, focused ultrasound, recurrent falls, or complex medication adverse effects.

Progression and follow-up: Follow motor function, wearing off, dyskinesia, falls, swallowing/aspiration, orthostasis, hallucinations, impulse-control disorders, cognition, caregiver strain, driving safety, and advance care planning.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Multiple sclerosis relapse

Pathophysiology: MS relapse is new or worsening inflammatory demyelinating CNS dysfunction lasting at least 24 hours without fever/infection, separated from prior relapse by about 30 days; pseudo-relapse occurs with infection, heat, sleep loss, or metabolic stress.

How Neurology assesses it: Assess symptom onset/duration, optic neuritis, myelitis, brainstem/cerebellar signs, bladder infection symptoms, fever, pregnancy/postpartum, current disease-modifying therapy, infection exposure, disability impact, and alternate diagnoses such as stroke, migraine, compressive myelopathy, or PML.

Diagnosis: Use neurologic exam, urinalysis/culture and infection screen when suggested, CBC/CMP before steroids, MRI brain/spine with gadolinium for unclear/severe/new localization or treatment decisions, and compare with prior imaging; CSF is not routine for known MS relapse unless diagnosis uncertain.

First-line treatment: Mild sensory relapse may be observed. Function-limiting relapse uses high-dose corticosteroids such as IV methylprednisolone (Solu-Medrol) 1 g daily for 3-5 days or high-dose oral prednisone/methylprednisolone equivalent, with gastric/glucose/mood precautions.

Second-line treatment: If steroid-refractory severe relapse, use plasma exchange for optic neuritis, myelitis, brainstem, or severe motor relapse. Review DMT adherence/neutralizing issues and optimize therapy after relapse recovery.

Third-line / advanced care: Urgent neurology/admission for severe weakness, bilateral vision loss, brainstem symptoms, respiratory compromise, spinal cord syndrome, pregnancy complexity, PML concern, or inability to safely receive steroids/PLEX outpatient.

Progression and follow-up: Follow EDSS/function, vision, gait, bladder, MRI activity, infections, steroid adverse effects, relapse recovery, DMT escalation, vaccine timing, and transition to progressive disease.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Peripheral neuropathy

Pathophysiology: Peripheral neuropathy reflects length-dependent axonal loss, demyelination, small-fiber dysfunction, immune attack, metabolic injury, toxins, hereditary disease, infection, or entrapment; diabetes, alcohol, chemotherapy, B12 deficiency, CKD, and monoclonal gammopathy are common causes.

How Neurology assesses it: Assess distribution, sensory versus motor/autonomic features, pain, falls, weakness, rapid progression, asymmetry, back/radicular symptoms, diabetes, alcohol, chemo, medications, toxins, family history, weight loss, rash, and autonomic symptoms.

Diagnosis: Use A1c/glucose, B12 with methylmalonic acid, TSH, CMP/eGFR/LFTs, CBC, SPEP/free light chains, ESR/CRP/ANA/HIV/hepatitis/Lyme only by context, EMG/NCS for large-fiber, motor, asymmetric, or progressive neuropathy; skin biopsy or autonomic testing for small-fiber cases.

First-line treatment: Treat cause: glucose optimization, stop neurotoxins, B12 replacement, alcohol treatment, renal/thyroid management, PT/balance, foot care. Neuropathic pain options include duloxetine (Cymbalta), gabapentin (Neurontin), pregabalin (Lyrica), nortriptyline (Pamelor), topical lidocaine, or capsaicin.

Second-line treatment: Immune neuropathies such as CIDP may need IVIG (Privigen/Gamunex), corticosteroids, or plasma exchange after confirmation; entrapment neuropathies need splinting, ergonomic change, injection, or surgery by site.

Third-line / advanced care: Urgent neurology for rapidly progressive weakness, respiratory/bulbar symptoms, Guillain-Barre concern, asymmetric vasculitic neuropathy, foot drop, severe autonomic instability, or suspected paraneoplastic/infiltrative disease.

Progression and follow-up: Follow pain, sensation, strength, gait/falls, ulcers, autonomic dysfunction, medication sedation, renal dosing, cause-specific labs, and progression from treatable immune or toxic etiologies.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Bell palsy

Pathophysiology: Bell palsy is acute peripheral facial nerve palsy, likely inflammatory/viral edema within the facial canal; mimics include stroke, Ramsay Hunt zoster, Lyme disease, otitis/mastoiditis, tumor, and parotid disease.

How Neurology assesses it: Assess onset within 72 hours, complete forehead involvement, taste/lacrimation, ear pain/vesicles, hyperacusis, eye closure, tick exposure, rash, neurologic deficits, recurrent/bilateral palsy, pregnancy, diabetes, and immunocompromise.

Diagnosis: Clinical diagnosis when isolated unilateral lower motor neuron facial weakness; image MRI/CT or test Lyme/HIV/VZV when atypical, bilateral, recurrent, gradual, forehead sparing, other cranial nerves, vesicles, cancer, or no improvement.

First-line treatment: Start prednisone (Deltasone) within 72 hours unless contraindicated; protect eye with artificial tears, lubricating ointment, taping/patch at night, and urgent eye care if corneal exposure.

Second-line treatment: Add valacyclovir (Valtrex) or acyclovir (Zovirax) for severe palsy or suspected viral contribution; Ramsay Hunt needs antiviral plus steroid and ENT/ophthalmology attention.

Third-line / advanced care: Neurology/ENT/ophthalmology for complete paralysis, corneal injury, atypical features, no recovery by 3 months, progressive weakness, recurrent palsy, or synkinesis needing facial rehab/botulinum toxin.

Progression and follow-up: Follow facial recovery, eye injury, neuropathic pain, synkinesis, contracture, psychosocial distress, and missed central/structural causes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Vertigo central versus peripheral

Pathophysiology: Vertigo arises from peripheral vestibular disorders such as BPPV, vestibular neuritis, Meniere disease, or labyrinthitis, or central causes such as cerebellar/brainstem stroke, demyelination, tumor, or migraine.

How Neurology assesses it: Assess timing/triggers, continuous versus episodic, neurologic symptoms, headache/neck pain, hearing loss/tinnitus, vascular risk, gait inability, anticoagulation, recent infection, trauma, nystagmus pattern, and HINTS exam only when clinician trained and patient has acute vestibular syndrome.

Diagnosis: BPPV is diagnosed by Dix-Hallpike or supine roll test. Central concern needs MRI brain with diffusion and vascular imaging CTA/MRA when stroke/dissection possible; audiology for hearing symptoms; avoid relying on normal early MRI alone if posterior circulation stroke suspicion remains high.

First-line treatment: Posterior canal BPPV: Epley maneuver; vestibular neuritis: short antiemetic/vestibular suppressant such as meclizine (Antivert) or prochlorperazine (Compazine) only briefly plus vestibular rehab; migraine vertigo uses migraine strategy.

Second-line treatment: Meniere disease may use salt reduction, diuretics such as hydrochlorothiazide-triamterene (Dyazide), betahistine where used, and ENT therapy; persistent vestibular hypofunction benefits from vestibular PT.

Third-line / advanced care: Emergency stroke pathway for focal deficits, direction-changing/vertical nystagmus, severe truncal ataxia, new severe headache/neck pain, inability to walk, high vascular risk, or central HINTS; ENT/neurology for refractory or atypical vertigo.

Progression and follow-up: Follow falls, gait, hearing, recurrent attacks, medication sedation, vestibular compensation, stroke recurrence risk, and missed posterior circulation infarct.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Dementia differential diagnosis

Pathophysiology: Dementia syndromes reflect neurodegenerative, vascular, Lewy body, frontotemporal, Parkinson-related, normal-pressure hydrocephalus, medication, mood, sleep, metabolic, infectious, or structural causes of cognitive and functional decline.

How Neurology assesses it: Assess time course, memory/language/executive/behavioral pattern, hallucinations/fluctuations, parkinsonism, gait/urinary symptoms, depression, sleep apnea, alcohol, anticholinergic/sedative burden, ADLs/IADLs, driving/finances/med safety, caregiver concerns, and safety risks.

Diagnosis: Use MoCA/MMSE/SLUMS plus informant history, PHQ-9, medication review, CBC/CMP/TSH/B12, HIV/RPR when risk, sleep evaluation when suggested, brain MRI or CT for structural/vascular/NPH pattern, and neuropsychology or PET/CSF/amyloid biomarkers when diagnosis affects management.

First-line treatment: Address reversible contributors, deprescribe anticholinergics/benzodiazepines when possible, treat depression/sleep apnea, exercise/social/cognitive routines, caregiver education, advance planning, and safety interventions.

Second-line treatment: Alzheimer disease symptomatic therapy may include donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne), and memantine (Namenda) by stage/tolerance; vascular cognitive impairment focuses BP/lipid/diabetes/smoking control; Lewy body dementia avoids dopamine-blocking antipsychotics when possible.

Third-line / advanced care: Neurology/memory clinic for young-onset, rapidly progressive dementia, prominent behavioral/language syndrome, hallucinations/parkinsonism, NPH evaluation, seizure concern, anti-amyloid therapy eligibility/ARIA monitoring, or unsafe home situation.

Progression and follow-up: Follow cognition/function, caregiver strain, wandering/falls, nutrition, medication adherence, driving, finances, delirium risk, behavioral symptoms, dysphagia, goals of care, and institutional support needs.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Myasthenia gravis

Pathophysiology: Myasthenia gravis is autoimmune neuromuscular junction failure, usually from acetylcholine receptor antibodies or MuSK/LRP4 antibodies, causing fatigable skeletal muscle weakness and risking respiratory or bulbar crisis.

How Neurology assesses it: Assess fluctuating ptosis/diplopia, dysarthria, dysphagia, chewing fatigue, neck/limb weakness, dyspnea, infection/surgery triggers, pregnancy, medications that worsen MG (aminoglycosides, fluoroquinolones, magnesium, beta blockers), and crisis warning signs.

Diagnosis: Test AChR binding/blocking/modulating antibodies, MuSK antibodies if AChR-negative, repetitive nerve stimulation or single-fiber EMG, bedside ice-pack test for ptosis, pulmonary function with FVC/NIF when bulbar/respiratory symptoms, and chest CT/MRI for thymoma.

First-line treatment: Symptomatic therapy with pyridostigmine (Mestinon) plus trigger avoidance. Immunotherapy often uses prednisone (Deltasone) with steroid-sparing azathioprine (Imuran), mycophenolate (CellCept), cyclosporine, or tacrolimus selected by severity and comorbidity.

Second-line treatment: Rapid worsening, severe bulbar symptoms, or preoperative optimization may use IVIG (Privigen/Gamunex) or plasma exchange. Refractory AChR-positive disease may use eculizumab (Soliris), ravulizumab (Ultomiris), efgartigimod (Vyvgart), rozanolixizumab (Rystiggo), or rituximab (Rituxan), especially MuSK disease.

Third-line / advanced care: ICU for myasthenic crisis with respiratory failure, aspiration, rapidly falling FVC/NIF, or severe bulbar weakness; thymectomy for thymoma and selected generalized AChR-positive MG; neuromuscular specialist for pregnancy, refractory disease, or biologic therapy.

Progression and follow-up: Follow MG-ADL/QMG, ocular/bulbar/respiratory strength, FVC when severe, infections, steroid toxicity, immunosuppression labs, meningococcal vaccination for complement inhibitors, thymoma surveillance, and medication avoidance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Restless legs syndrome

Pathophysiology: Restless legs syndrome is a sensorimotor disorder causing urge to move legs, worse at rest/evening, relieved by movement; mechanisms involve brain iron handling and dopaminergic pathways, with secondary causes including iron deficiency, pregnancy, CKD, neuropathy, and medications.

How Neurology assesses it: Assess classic four criteria, sleep disruption, periodic limb movements, ferritin/iron intake, pregnancy, kidney disease, neuropathy, caffeine/alcohol, family history, antidepressants, antipsychotics, dopamine-blocking antiemetics, sedating antihistamines, and prior dopamine agonist augmentation.

Diagnosis: Clinical diagnosis; check ferritin and transferrin saturation, CBC when iron deficiency possible, renal function, and neuropathy labs when indicated. PSG is reserved for unclear cases, suspected PLMD/OSA, or refractory symptoms. Differentiate leg cramps, akathisia, neuropathy, venous disease, and positional discomfort.

First-line treatment: Correct contributors: stop exacerbating drugs when possible, reduce caffeine/alcohol, manage sleep deprivation, and replete iron. Oral ferrous sulfate or IV iron is considered when ferritin/TSAT are low by sleep-medicine thresholds and symptoms justify treatment.

Second-line treatment: First-line pharmacologic options increasingly favor alpha-2-delta ligands: gabapentin enacarbil (Horizant), gabapentin (Neurontin), or pregabalin (Lyrica), especially with pain/insomnia. Dopamine agonists pramipexole (Mirapex), ropinirole (Requip), or rotigotine (Neupro) can work but require augmentation/impulse-control counseling.

Third-line / advanced care: Sleep specialist for augmentation, refractory RLS, severe insomnia, opioid consideration for severe refractory disease, pregnancy/CKD complexity, or diagnostic uncertainty. Avoid escalating dopamine agonist indefinitely when symptoms start earlier/spread/worsen.

Progression and follow-up: Follow symptom timing, sleep quality, ferritin/TSAT, augmentation, impulse-control behaviors, sedation/dizziness/edema, pregnancy changes, and medication interactions.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Neurology

Traumatic brain injury follow-up

Pathophysiology: Traumatic brain injury follow-up addresses evolving neurologic, cognitive, vestibular, mood, sleep, headache, seizure, and functional effects after concussion, mild TBI, or moderate/severe injury; secondary injury can arise from bleeding, edema, hypoxia, seizures, or medication/substance effects.

How Neurology assesses it: Assess mechanism, loss of consciousness/amnesia, anticoagulants, initial imaging, worsening headache, vomiting, seizure, focal deficit, dizziness, vision, sleep, cognition, mood/PTSD, return-to-work/school/driving, alcohol/substance use, and red flags for delayed bleed or cervical injury.

Diagnosis: Use neurologic exam, symptom scales, cognitive screen, vestibular/ocular motor assessment, medication review, and CT head for acute red flags or decision-rule criteria. MRI brain, neuropsychological testing, EEG, sleep study, or vestibular testing is reserved for persistent, focal, seizure-like, or complex symptoms.

First-line treatment: Early management includes relative rest for 24-48 hours, then graded return to activity, headache care with acetaminophen (Tylenol) or NSAID when bleeding risk is excluded, sleep regularization, screen-time pacing, hydration, and education to avoid repeat head injury.

Second-line treatment: Persistent symptoms use targeted therapy: vestibular PT, vision therapy, cognitive rehab, graded aerobic exercise, CBT/trauma therapy, migraine prevention such as amitriptyline (Elavil), topiramate (Topamax), or propranolol (Inderal) when phenotype fits, and treatment of depression/anxiety/sleep disorders.

Third-line / advanced care: Urgent ED/neurosurgery for worsening headache, repeated vomiting, seizure, focal deficit, declining consciousness, anticoagulation with concerning symptoms, suspected CSF leak, or new severe neck pain; neurology/PM&R/concussion clinic for symptoms beyond expected recovery or moderate/severe TBI.

Progression and follow-up: Follow symptom burden, school/work accommodations, driving risk, falls, post-traumatic epilepsy, medication overuse headache, depression/suicidality, sleep disorder, vestibular dysfunction, and cumulative concussion risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Specialty role

Mental health specialty care for diagnosis, psychotherapy/medication strategy, safety, severe illness, and substance comorbidity.

Psychiatry

Major depressive disorder treatment resistance

Pathophysiology: Treatment-resistant major depressive disorder is persistent clinically significant depression after adequate dose, duration, adherence, and measurement-based trials, often complicated by anxiety, trauma, substance use, bipolar spectrum, sleep disorder, pain, medical illness, or psychosocial stress.

How Psychiatry assesses it: Assess PHQ-9 trajectory, suicide risk, psychosis/catatonia, bipolar history before antidepressant escalation, prior medication doses/durations/adherence, psychotherapy exposure, substance use, sleep apnea/insomnia, trauma, pain, thyroid/anemia/B12 mimics, pregnancy, and functional impairment.

Diagnosis: Confirm unipolar MDD with DSM interview and PHQ-9; review medication history for adequate trials, check TSH/CBC/CMP/B12 or other labs only when clinically suggested, screen with MDQ/C-SSRS/AUDIT-C/DAST, and consider pharmacogenomic testing only as adjunctive, not diagnostic.

First-line treatment: Optimize current antidepressant and psychotherapy first: CBT, interpersonal therapy, behavioral activation, exercise/sleep intervention, and SSRI/SNRI such as sertraline (Zoloft), escitalopram (Lexapro), fluoxetine (Prozac), venlafaxine XR (Effexor XR), or duloxetine (Cymbalta).

Second-line treatment: Switch or augment based on phenotype: bupropion XL (Wellbutrin XL) for fatigue/sexual adverse effects, mirtazapine (Remeron) for insomnia/weight loss, lithium (Lithobid) for augmentation/suicide reduction, thyroid liothyronine (Cytomel), or atypical antipsychotic augmentation aripiprazole (Abilify), brexpiprazole (Rexulti), or quetiapine XR (Seroquel XR).

Third-line / advanced care: Psychiatry/interventional referral for ECT, transcranial magnetic stimulation, ketamine infusion, esketamine nasal spray (Spravato REMS), partial hospital/intensive outpatient care, or inpatient care for active suicidal intent, psychosis, mania, catatonia, or grave disability.

Progression and follow-up: Follow PHQ-9, function, sleep, substance use, suicidality, sexual/weight/metabolic adverse effects, lithium level/renal/thyroid monitoring, antipsychotic metabolic/EPS effects, relapse prevention, and missed bipolar disorder.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Generalized anxiety disorder

Pathophysiology: Generalized anxiety disorder is chronic excessive worry with threat-circuit sensitization, intolerance of uncertainty, autonomic arousal, muscle tension, sleep disruption, avoidance, and frequent overlap with depression, trauma, substance use, and medical mimics.

How Psychiatry assesses it: Use GAD-7, assess worry domains, panic/agoraphobia, OCD/PTSD symptoms, depression/suicide, bipolar disorder, caffeine/stimulants/decongestants, cannabis/alcohol, hyperthyroid symptoms, arrhythmia/chest pain, pregnancy, and functional avoidance.

Diagnosis: DSM-based diagnosis with impairment and duration; consider TSH, CBC/CMP, pregnancy test, ECG, or targeted endocrine/cardiopulmonary testing only when symptoms suggest a medical mimic.

First-line treatment: First-line treatment is CBT with worry exposure/problem-solving plus SSRI/SNRI such as escitalopram (Lexapro), sertraline (Zoloft), paroxetine (Paxil), fluoxetine (Prozac), venlafaxine XR (Effexor XR), or duloxetine (Cymbalta), titrated slowly to reduce activation.

Second-line treatment: For partial response, optimize dose/duration, switch SSRI/SNRI, add buspirone (Buspar), hydroxyzine (Vistaril/Atarax) short-term, pregabalin/gabapentin in selected off-label cases, or propranolol (Inderal) for performance-only symptoms when safe.

Third-line / advanced care: Refer psychiatry/therapy specialty for treatment resistance, severe avoidance/agoraphobia, suicidality, bipolar/psychosis, substance-use disorder, pregnancy complexity, benzodiazepine dependence, or need for intensive exposure work.

Progression and follow-up: Follow GAD-7, sleep, avoidance, panic frequency, work/school function, substance use, antidepressant activation/sexual effects, benzodiazepine avoidance, relapse during taper, and comorbid depression.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Panic disorder

Pathophysiology: Panic disorder involves recurrent unexpected panic attacks with conditioned fear of bodily sensations and avoidance; differential includes arrhythmia, hyperthyroidism, asthma/COPD, vestibular disease, stimulant/cannabis use, and withdrawal.

How Psychiatry assesses it: Assess attack onset/peak, palpitations, dyspnea, chest pain, dizziness, derealization, fear of dying/losing control, avoidance/agoraphobia, ED visits, caffeine/stimulants, substance use, trauma, depression/suicide, and cardiac/endocrine red flags.

Diagnosis: DSM-based diagnosis after excluding dangerous mimics when indicated. Use ECG for chest pain/palpitations/syncope risk, TSH/CBC/CMP as clinically suggested, pregnancy test when relevant, and panic-specific scales such as PDSS if available.

First-line treatment: CBT with interoceptive exposure and SSRI/SNRI such as sertraline (Zoloft), escitalopram (Lexapro), fluoxetine (Prozac), paroxetine (Paxil), or venlafaxine XR (Effexor XR); start low and titrate slowly.

Second-line treatment: Short-term bridge may use limited clonazepam (Klonopin) or lorazepam (Ativan) only for carefully selected patients while SSRI/CBT starts; alternatives include hydroxyzine (Vistaril) or propranolol for prominent autonomic symptoms when appropriate.

Third-line / advanced care: Psychiatry referral for refractory panic, severe agoraphobia, benzodiazepine dependence, suicidality, bipolar/psychosis, substance use, or diagnostic uncertainty with cardiopulmonary mimics.

Progression and follow-up: Follow panic frequency, avoidance radius, rescue-medication use, driving/work impairment, ER utilization, depression/suicide risk, substance use, and medication adverse effects.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Bipolar disorder

Pathophysiology: Bipolar disorder is recurrent mood dysregulation with manic/hypomanic and depressive episodes linked to circadian disruption, reward circuitry, genetics, stress, substances, and antidepressant sensitivity.

How Psychiatry assesses it: Assess lifetime mania/hypomania, decreased need for sleep, impulsivity, psychosis, mixed features, rapid cycling, postpartum episodes, family history, antidepressant-induced activation, substance use, suicide risk, violence risk, medical mimics, and current polarity/severity.

Diagnosis: DSM-based interview supported by MDQ, collateral history, PHQ-9/C-SSRS, urine drug testing when indicated, TSH/CBC/CMP, pregnancy test, and baseline renal/thyroid/calcium for lithium or metabolic labs for antipsychotics; rule out stimulant, steroid, thyroid, neurologic, or substance-induced mood disorder.

First-line treatment: Acute mania often uses lithium (Lithobid), valproate/divalproex (Depakote), or antipsychotic such as quetiapine (Seroquel), risperidone (Risperdal), olanzapine (Zyprexa), aripiprazole (Abilify), or cariprazine (Vraylar). Stop antidepressant monotherapy when mania/mixed state is suspected.

Second-line treatment: Bipolar depression options include quetiapine, lurasidone (Latuda) with lithium/valproate or alone per indication, lamotrigine (Lamictal) for maintenance/depressive prevention, cariprazine, or olanzapine-fluoxetine (Symbyax), plus psychoeducation and sleep/circadian stabilization.

Third-line / advanced care: Hospitalize for mania with dangerous behavior, psychosis, inability to sleep/eat, suicidal intent, severe mixed state, catatonia, or postpartum psychosis. ECT for severe mania/depression/catatonia or pregnancy complexity; psychiatry for maintenance planning.

Progression and follow-up: Follow mood chart, sleep, suicide risk, substance use, lithium levels/renal/thyroid, valproate LFT/CBC/teratogenicity, lamotrigine rash/SJS, antipsychotic metabolic/EPS/prolactin effects, adherence, and relapse warning signs.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Schizophrenia

Pathophysiology: Schizophrenia is a chronic psychotic disorder involving dopamine/glutamate signaling, neurodevelopmental vulnerability, cognitive impairment, negative symptoms, and functional decline, with relapse strongly tied to medication interruption and substance use.

How Psychiatry assesses it: Assess hallucinations, delusions, disorganization, negative symptoms, cognition, duration/prodrome, mood episodes, catatonia, suicide/violence risk, command hallucinations, substance use especially cannabis/stimulants, trauma, medical mimics, housing/support, and medication history.

Diagnosis: DSM-based diagnosis with collateral history; initial workup often includes CBC/CMP/TSH/B12, urine toxicology, pregnancy test, HIV/syphilis or autoimmune/neurologic testing when indicated, and brain imaging/EEG when atypical, focal, late-onset, delirious, or seizure-like.

First-line treatment: Start antipsychotic using shared decision-making: risperidone (Risperdal), aripiprazole (Abilify), olanzapine (Zyprexa), quetiapine (Seroquel), lurasidone (Latuda), ziprasidone (Geodon), paliperidone (Invega), or haloperidol (Haldol) based on metabolic/EPS/QT/prolactin risks; combine with family psychoeducation, CBT for psychosis, supported employment, and substance-use treatment.

Second-line treatment: Use long-acting injectable antipsychotics such as paliperidone palmitate (Invega Sustenna/Trinza/Hafyera), aripiprazole LAI (Abilify Maintena/Aristada), risperidone LAI, or haloperidol decanoate for adherence/relapse prevention.

Third-line / advanced care: Clozapine (Clozaril/Versacloz) for treatment-resistant schizophrenia or recurrent suicidality, with ANC monitoring and myocarditis/seizure/metabolic surveillance. Hospitalize for danger to self/others, grave disability, catatonia, severe command hallucinations, or inability to care for basic needs.

Progression and follow-up: Follow psychosis severity, negative/cognitive symptoms, function, suicide risk, substance use, adherence, A1c/lipids/weight/BP, EPS/tardive dyskinesia, prolactin/QT, clozapine ANC, housing, and relapse plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

PTSD

Pathophysiology: PTSD follows trauma exposure with persistent threat conditioning, intrusive memories, avoidance, negative mood/cognition, hyperarousal, sleep disruption, moral injury, and frequent comorbid depression, substance use, chronic pain, and TBI.

How Psychiatry assesses it: Assess trauma type/timing, PCL-5 symptoms, dissociation, nightmares, avoidance, hypervigilance, depression/suicide, substance use, intimate partner violence/safety, TBI, chronic pain, sleep apnea, and readiness for trauma-focused therapy.

Diagnosis: DSM-based diagnosis with PCL-5 or CAPS-5 when available; evaluate comorbid MDD, panic, OCD, bipolar, psychosis, substance use, TBI, and medical contributors. Labs are not routine unless medications or mimics require them.

First-line treatment: First-line care is trauma-focused psychotherapy such as prolonged exposure, cognitive processing therapy, or EMDR. Medications with best support include sertraline (Zoloft), paroxetine (Paxil), or venlafaxine XR (Effexor XR), chosen by comorbidity and tolerability.

Second-line treatment: Nightmares may respond to prazosin (Minipress) in selected patients; treat insomnia with CBT-I and avoid routine benzodiazepines because they can worsen outcomes and dependence risk. Address substance use and safety concurrently rather than delaying PTSD treatment indefinitely.

Third-line / advanced care: Specialty trauma program, intensive outpatient/residential care, or inpatient care for active suicidal intent, severe dissociation, unsafe home/IPV, psychosis/mania, severe substance withdrawal, or inability to function. Consider adjunctive treatments only after evidence-based therapy/medication review.

Progression and follow-up: Follow PCL-5, sleep/nightmares, avoidance, substance use, suicidality, relationships, work function, medication sexual/GI/BP effects, retraumatization risk, and relapse triggers.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Obsessive compulsive disorder

Pathophysiology: OCD is intrusive obsessions and compulsions maintained by cortico-striato-thalamo-cortical circuitry, threat overestimation, intolerance of uncertainty, and ritual reinforcement; insight varies.

How Psychiatry assesses it: Assess obsession themes, compulsions/avoidance, time spent, insight, functional impairment, tic disorder, hoarding/body dysmorphic/eating disorder overlap, depression/suicide, psychosis differential, family accommodation, and substance use.

Diagnosis: Clinical DSM-based diagnosis supported by Y-BOCS; screen for depression, bipolar disorder before antidepressants, tic disorder, and medical/substance mimics only when suggested.

First-line treatment: First-line treatment is exposure and response prevention CBT plus SSRI at often higher OCD doses and longer trials: fluoxetine (Prozac), sertraline (Zoloft), fluvoxamine (Luvox), paroxetine (Paxil), or escitalopram (Lexapro).

Second-line treatment: If inadequate response, optimize SSRI for 10-12 weeks, switch SSRI or use clomipramine (Anafranil) with ECG/anticholinergic/seizure risk review, and augment selected resistant cases with antipsychotic such as risperidone (Risperdal) or aripiprazole (Abilify), especially with tics.

Third-line / advanced care: Specialty OCD program for severe disability, poor insight, suicidality, comorbid psychosis/bipolar, pediatric/family accommodation complexity, intensive ERP, or neuromodulation consideration.

Progression and follow-up: Follow Y-BOCS/time spent, avoidance, family accommodation, depression/suicide, SSRI sexual/GI effects, clomipramine toxicity, antipsychotic metabolic/EPS effects, and relapse prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Insomnia with psychiatric comorbidity

Pathophysiology: Insomnia with psychiatric comorbidity is hyperarousal and conditioned wakefulness interacting with depression, anxiety, PTSD, bipolar disorder, substance use, pain, circadian disruption, medications, and sleep apnea.

How Psychiatry assesses it: Assess sleep schedule, time in bed, naps, caffeine/alcohol/cannabis, screens, shift work, nightmares, restless legs, OSA symptoms, mania/hypomania, depression/suicide, pain, medications, and hypnotic dependence.

Diagnosis: Use sleep diary, Insomnia Severity Index, PHQ-9/GAD-7/PTSD screen, medication/substance review, and polysomnography only when OSA, periodic limb movements, parasomnia, narcolepsy, or treatment-resistant diagnostic uncertainty is suspected.

First-line treatment: CBT-I is first-line: stimulus control, sleep restriction, cognitive restructuring, relaxation, regular wake time, and circadian light timing. Treat the underlying psychiatric disorder and avoid destabilizing bipolar disorder with sleep loss.

Second-line treatment: Short-term medication options include doxepin low-dose (Silenor), trazodone, mirtazapine (Remeron) when depression/weight loss fits, hydroxyzine (Vistaril), zolpidem (Ambien), eszopiclone (Lunesta), zaleplon (Sonata), ramelteon (Rozerem), or suvorexant/lemborexant (Belsomra/Dayvigo) chosen by age, falls, substance risk, and next-day sedation.

Third-line / advanced care: Sleep medicine/psychiatry for refractory insomnia, suspected OSA/parasomnia, bipolar mania risk, PTSD nightmares, sedative-hypnotic dependence, older adults with falls/cognitive risk, or complex polypharmacy.

Progression and follow-up: Follow sleep efficiency, daytime function, mood/suicide, falls, cognition, parasomnias, tolerance/dependence, respiratory risk with sedatives, and relapse after medication taper.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

ADHD in adults

Pathophysiology: Adult ADHD is persistent neurodevelopmental impairment in attention, inhibition, working memory, time management, and emotional regulation beginning in childhood and often complicated by anxiety, depression, sleep disorder, substance use, and learning problems.

How Psychiatry assesses it: Assess childhood onset, cross-setting impairment, ASRS symptoms, collateral/school history when possible, sleep, anxiety/depression/bipolar, substance use, trauma, cardiac history, BP/HR, diversion risk, and functional goals.

Diagnosis: DSM-based diagnosis requiring childhood onset and impairment; rule out sleep apnea, substance use, mania, anxiety/depression, thyroid disease when suggested. Baseline BP/HR and cardiac history guide stimulant safety; ECG only when cardiac risk suggests.

First-line treatment: First-line pharmacotherapy often uses stimulants: methylphenidate ER (Concerta/Ritalin LA), mixed amphetamine salts (Adderall XR), lisdexamfetamine (Vyvanse), or dextroamphetamine, with behavioral skills coaching, CBT for ADHD, calendars, reminders, and sleep regularity.

Second-line treatment: Nonstimulants include atomoxetine (Strattera), guanfacine ER (Intuniv), clonidine ER (Kapvay), or bupropion XL (Wellbutrin XL), especially when anxiety, tics, substance-risk, or stimulant intolerance is present.

Third-line / advanced care: Psychiatry/neuropsychology for diagnostic uncertainty, active substance use, bipolar/psychosis, severe anxiety, cardiovascular complexity, pregnancy, diversion concern, or failure of multiple medication classes.

Progression and follow-up: Follow ASRS/function, BP/HR, appetite/weight, insomnia, anxiety/irritability, misuse/diversion, substance use, driving/work performance, and periodic need for medication.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Alcohol withdrawal

Pathophysiology: Alcohol withdrawal is CNS hyperexcitability after reduced alcohol intake from GABA downregulation and glutamate upregulation, ranging from tremor/anxiety to seizures and delirium tremens.

How Psychiatry assesses it: Assess time since last drink, daily amount, prior withdrawal seizures/DTs, CIWA-Ar symptoms, vitals, hallucinosis, comorbid liver disease, pregnancy, older age, polysubstance benzodiazepine/barbiturate use, suicidality, dehydration, and social support.

Diagnosis: Clinical diagnosis; use CIWA-Ar or RASS-based protocols, glucose, CMP/Mg/phosphate, CBC, LFTs/INR when liver disease, ethanol level, urine drug testing when indicated, pregnancy test, ECG if cardiac risk, and evaluate infection/trauma/pancreatitis when symptoms suggest.

First-line treatment: Give thiamine before glucose when malnourished/risk, fluids/electrolytes, folate/multivitamin, and benzodiazepine protocol such as lorazepam (Ativan), diazepam (Valium), or chlordiazepoxide (Librium) based on liver function and setting.

Second-line treatment: Adjuncts include phenobarbital protocols in monitored settings, gabapentin (Neurontin) or carbamazepine (Tegretol) for selected mild outpatient withdrawal, clonidine/beta blockers only for autonomic symptoms after adequate GABAergic therapy, and transition to AUD treatment naltrexone (Vivitrol/Revia) or acamprosate (Campral).

Third-line / advanced care: Inpatient/ICU for history of seizures/DTs, severe withdrawal, unstable vitals, delirium, pregnancy, serious medical/psychiatric illness, polysubstance sedatives, inability to take PO, or unsafe home; treat seizures/DTs emergently.

Progression and follow-up: Follow CIWA/RASS, sedation/respiratory status, electrolytes, Wernicke encephalopathy, seizures, delirium tremens, aspiration, suicidality, relapse prevention, and linkage to ongoing AUD care.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Opioid use disorder

Pathophysiology: Opioid use disorder is chronic relapsing reward, tolerance, withdrawal, craving, and compulsive-use physiology with high overdose risk, especially with fentanyl exposure, benzodiazepines, alcohol, reduced tolerance, and injection complications.

How Psychiatry assesses it: Assess DSM criteria, last opioid/fentanyl use, withdrawal severity with COWS, overdose history, route, infections, pain, pregnancy, psychiatric comorbidity, benzodiazepines/alcohol, housing, legal stress, readiness, and harm-reduction needs.

Diagnosis: Clinical DSM diagnosis; urine drug testing supports care but does not replace history. Check pregnancy test, HIV/HCV/HBV/STI testing, LFTs when using naltrexone, PDMP review, and evaluate endocarditis/abscess/withdrawal complications when suggested.

First-line treatment: Offer medication treatment: buprenorphine-naloxone (Suboxone/Zubsolv) or buprenorphine (Subutex in pregnancy/selected cases), initiated when moderate withdrawal is present or by low-dose/microinduction for fentanyl risk; provide naloxone (Narcan/Kloxxado), fentanyl test strips where legal, and counseling/support.

Second-line treatment: Methadone through an opioid treatment program is preferred for high tolerance, unsuccessful buprenorphine, or need for structured dosing. Extended-release naltrexone (Vivitrol) requires full detoxification and is suitable only for selected motivated patients.

Third-line / advanced care: Urgent care for overdose, severe withdrawal/dehydration, pregnancy, suicidality, endocarditis/serious infection, polysubstance sedative use, or inability to stabilize outpatient. Coordinate addiction medicine, psychiatry, infectious disease, and pain care.

Progression and follow-up: Follow retention, cravings, urine toxicology trends, overdose events, injection harms, constipation, QT risk with methadone, precipitated withdrawal, pregnancy outcomes, HIV/HCV care, and recovery supports.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Suicide risk assessment

Pathophysiology: Suicide risk is dynamic and arises from psychiatric illness, acute stress, substance use, trauma, pain, insomnia, impulsivity, hopelessness, access to lethal means, prior attempts, and protective factors.

How Psychiatry assesses it: Ask directly about suicidal thoughts, intent, plan, preparation, access to firearms/medications, prior attempts, recent losses, intoxication/withdrawal, psychosis/command hallucinations, agitation, insomnia, pain, protective factors, supports, and ability to collaborate on safety.

Diagnosis: Use structured tools such as C-SSRS or ASQ plus clinical formulation; stratify acute and chronic risk rather than relying on a score alone. Assess capacity, intoxication, medical lethality of attempts, collateral information when needed, and co-occurring MDD, bipolar, psychosis, PTSD, substance use, or personality disorder.

First-line treatment: For non-imminent risk, create collaborative Safety Planning Intervention, lethal-means counseling including firearm/medication safety, crisis contacts such as 988 in the U.S., rapid follow-up, caring contacts, and treat underlying disorders.

Second-line treatment: Higher acute risk needs same-day mental health evaluation, increased contact, family/support involvement with consent or safety necessity, medication quantity limits, substance-use intervention, and possible intensive outpatient/partial hospitalization.

Third-line / advanced care: Emergency/inpatient care is needed for active intent with plan/access, inability to maintain safety, severe intoxication/withdrawal, psychosis/mania, recent high-lethality attempt, lack of supports, or grave disability.

Progression and follow-up: Follow suicidal ideation intensity, access to means, adherence to safety plan, substance use, sleep, agitation, treatment engagement, post-discharge period, and recurrence after medication or psychosocial changes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Eating disorder

Pathophysiology: Eating disorders include anorexia nervosa, bulimia nervosa, binge-eating disorder, ARFID, and OSFED; they involve altered eating/weight-control behavior, body image or sensory/fear drivers, malnutrition, reward/anxiety circuitry, and serious medical complications.

How Psychiatry assesses it: Assess weight trajectory, BMI percent expected, restriction, bingeing, purging, laxatives/diuretics, compulsive exercise, body image, menstrual/endocrine effects, syncope, chest pain, GI symptoms, dental erosion, family history, trauma, diabetes/insulin omission, suicidality, and substance use.

Diagnosis: Use DSM interview plus vitals including orthostatics, weight history, ECG, CMP/Mg/phosphate, CBC, TSH when indicated, pregnancy test, urinalysis/ketones, bone health when chronic restriction, and screen for depression/OCD/anxiety. Do not rely on normal BMI to exclude severe disorder.

First-line treatment: Treatment is multidisciplinary with nutritional rehabilitation, psychotherapy, medical monitoring, and family-based treatment for adolescents with anorexia. CBT-E is useful for bulimia/binge eating; fluoxetine (Prozac) is FDA-approved for bulimia; lisdexamfetamine (Vyvanse) is approved for binge-eating disorder in selected adults.

Second-line treatment: Manage complications: phosphate/thiamine and monitored refeeding when high risk, constipation care, dental care, stop purging agents, treat comorbid anxiety/depression after nutrition plan, and avoid bupropion in bulimia/anorexia due to seizure risk.

Third-line / advanced care: Higher level of care or hospitalization for bradycardia, hypotension, syncope, electrolyte abnormalities, arrhythmia/QTc prolongation, acute food refusal, rapid weight loss, severe purging, suicidality, pregnancy complications, or failure of outpatient care.

Progression and follow-up: Follow weight/vitals/orthostatics, electrolytes/phosphate, ECG, menstrual/bone health, purging frequency, binge frequency, exercise compulsion, suicidality, refeeding syndrome, relapse, and family support.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Psychiatry

Medication-induced mood symptoms

Pathophysiology: Medication-induced mood symptoms occur when steroids, stimulants, antidepressants, isotretinoin, interferon, dopaminergic drugs, hormonal agents, antiepileptics, sedatives, withdrawal states, or substances trigger depression, anxiety, mania, psychosis, irritability, or suicidality.

How Psychiatry assesses it: Create a timeline of symptom onset versus medication starts/stops/dose changes, OTC/supplements, substances, sleep loss, prior bipolar/psychosis, steroid dose, stimulant use, dopaminergic therapy, withdrawal, medical illness, and safety risk.

Diagnosis: DSM substance/medication-induced disorder is clinical; use PHQ-9/GAD-7/MDQ/C-SSRS, medication reconciliation, PDMP when relevant, urine drug testing when indicated, TSH/CMP/CBC/B12 or neurologic/endocrine tests based on symptoms, and collateral history.

First-line treatment: If safe, reduce/stop or substitute the offending agent with the prescriber, treat insomnia/substance use, and provide close follow-up. Avoid adding antidepressant monotherapy when medication-induced mania is possible.

Second-line treatment: Short-term symptom treatment may include hydroxyzine (Vistaril) for anxiety, trazodone for insomnia, or antipsychotic/mood stabilizer such as quetiapine (Seroquel), olanzapine (Zyprexa), or lithium (Lithobid) for severe mania/psychosis while the trigger is addressed.

Third-line / advanced care: Emergency/psychiatry for suicidality, mania/psychosis, aggression, delirium, severe withdrawal, inability to stop medically necessary culprit, or complex neurologic/endocrine medication interactions.

Progression and follow-up: Follow symptom resolution after dose change, recurrence with rechallenge, sleep, safety, metabolic/EPS effects if antipsychotic used, underlying psychiatric disorder unmasked, and documentation of culprit reaction.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Specialty role

Female reproductive, pregnancy, postpartum, gynecologic, pelvic, hormonal, and preventive care.

Obstetrics and Gynecology

Prenatal care risk stratification

Pathophysiology: Prenatal care risk stratification separates routine pregnancy from maternal, fetal, placental, genetic, infectious, hypertensive, metabolic, thrombotic, and psychosocial risks that change visit frequency, testing, medication safety, and delivery planning.

How Obstetrics and Gynecology assesses it: Assess gestational age by last menstrual period/early ultrasound, obstetric history, prior cesarean/preterm birth/preeclampsia/GDM, chronic hypertension/diabetes/renal/cardiac disease, medications/teratogens, substance use, IPV, depression, BMI, blood type/Rh, vaccine status, genetic history, and fetal movement later in pregnancy.

Diagnosis: Use dating ultrasound when needed, BP and urine protein risk review, CBC, blood type/Rh/antibody screen, rubella/varicella immunity, HIV, hepatitis B/C, syphilis, GC/CT when indicated, urine culture, Pap/HPV if due, carrier screening, aneuploidy screening or cell-free DNA, anatomy ultrasound at about 18-22 weeks, glucose screening at 24-28 weeks, GBS culture at 36-37 weeks, and growth ultrasound/NST/BPP for high-risk pregnancies.

First-line treatment: Routine care includes prenatal vitamin with folic acid, low-dose aspirin 81 mg (Bayer/Ecotrin) starting after 12 weeks for preeclampsia-risk patients, influenza/COVID/Tdap vaccination when indicated, nausea therapy such as doxylamine-pyridoxine (Diclegis/Bonjesta) or ondansetron (Zofran) when appropriate, nutrition/weight counseling, and avoidance of teratogens.

Second-line treatment: High-risk findings trigger maternal-fetal medicine referral, serial growth ultrasound, antenatal testing, Rh immune globulin (RhoGAM) for Rh-negative patients, iron therapy ferrous sulfate (Feosol) for iron-deficiency anemia, and condition-specific treatment for hypertension, diabetes, thyroid disease, infection, or thrombosis.

Third-line / advanced care: Escalate urgently for severe hypertension, preeclampsia symptoms, heavy bleeding, PPROM/preterm labor, decreased fetal movement, ectopic concern early, suspected fetal anomaly, placenta previa/accreta concern, or maternal instability; advanced care may include admission, magnesium sulfate, betamethasone (Celestone) for fetal lung maturity, induction, or cesarean delivery.

Progression and follow-up: Poorly identified risk can lead to fetal growth restriction, preterm birth, stillbirth, congenital infection/anomaly missed follow-up, severe preeclampsia/eclampsia, hemorrhage, thromboembolism, maternal ICU care, or avoidable medication exposure.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Gestational diabetes

Pathophysiology: Gestational diabetes results from placental hormone-driven insulin resistance exceeding maternal beta-cell reserve, causing fetal hyperinsulinemia, macrosomia, neonatal hypoglycemia, and higher maternal lifetime type 2 diabetes risk.

How Obstetrics and Gynecology assesses it: Assess prior GDM/macrosomia, BMI, family history, PCOS, ethnicity-related risk, steroid use, diet/activity, home glucose logs after diagnosis, fetal growth, polyhydramnios, hypertension/preeclampsia risk, and hypoglycemia if medication is used.

Diagnosis: Screen most patients at 24-28 weeks with a 50-g 1-hour glucose challenge followed by a diagnostic 100-g 3-hour oral glucose tolerance test if abnormal, or use a one-step 75-g OGTT where that protocol is used. Check A1c/fasting glucose early only for high-risk pregestational diabetes concern, and use ultrasound for fetal growth surveillance when medication or poor control is present.

First-line treatment: First-line treatment is medical nutrition therapy, carbohydrate distribution, exercise as safe, and self-monitoring fasting and postprandial glucose. Treat nausea/food insecurity/barriers so the plan is realistic; metformin (Glucophage) or glyburide (Diabeta/Glynase) are alternatives in selected patients but insulin is the usual preferred medication when lifestyle is insufficient.

Second-line treatment: Use insulin when glucose targets remain above goal: NPH insulin (Humulin N/Novolin N), insulin detemir (Levemir) where available, insulin lispro (Humalog/Admelog), or insulin aspart (NovoLog/Fiasp) matched to fasting or post-meal elevations. Add antenatal testing and growth ultrasound when medication-treated or poorly controlled.

Third-line / advanced care: Maternal-fetal medicine/endocrinology co-management for severe hyperglycemia, suspected pregestational diabetes, fetal overgrowth, polyhydramnios, recurrent hypoglycemia, or complex insulin titration; delivery timing is individualized by control, fetal size, comorbid hypertension, and obstetric factors.

Progression and follow-up: Complications include shoulder dystocia, cesarean delivery, neonatal hypoglycemia, jaundice, respiratory distress, preeclampsia, stillbirth risk with poor control, and later maternal type 2 diabetes; follow with postpartum 75-g OGTT and long-term diabetes screening.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Hypertensive disorders of pregnancy

Pathophysiology: Hypertensive disorders of pregnancy include chronic hypertension, gestational hypertension, preeclampsia, preeclampsia with severe features, HELLP syndrome, and eclampsia; abnormal placentation, endothelial dysfunction, vasospasm, and organ injury drive maternal-fetal risk.

How Obstetrics and Gynecology assesses it: Assess gestational age, repeated properly measured BP, headache, visual symptoms, RUQ/epigastric pain, dyspnea/pulmonary edema, neurologic symptoms, edema, fetal movement, prior preeclampsia, chronic HTN/renal disease/diabetes, medication exposures, and severe-range BP or seizure symptoms.

Diagnosis: Use BP criteria plus urine protein-creatinine ratio or 24-hour protein when needed; CBC/platelets, CMP with AST/ALT/creatinine, urine protein, LDH/haptoglobin if HELLP/hemolysis concern, fetal ultrasound for growth, amniotic fluid assessment, NST/BPP, and evaluation for pulmonary edema or neurologic complication when symptomatic.

First-line treatment: Non-severe chronic or gestational hypertension commonly uses labetalol (Trandate), nifedipine ER (Procardia XL/Adalat CC), or methyldopa (Aldomet) when medication is indicated; low-dose aspirin 81 mg (Bayer/Ecotrin) is used preventively in risk-eligible pregnancies. Avoid ACE inhibitors/ARBs such as lisinopril (Zestril) or losartan (Cozaar) during pregnancy.

Second-line treatment: Severe-range BP needs urgent treatment with IV labetalol, IV hydralazine (Apresoline), or oral immediate-release nifedipine; preeclampsia with severe features uses magnesium sulfate for seizure prophylaxis and corticosteroids such as betamethasone (Celestone) when fetal lung maturity benefit is relevant.

Third-line / advanced care: Delivery is definitive therapy for preeclampsia/eclampsia/HELLP when maternal or fetal risk requires it; admit for severe features, eclampsia, HELLP, pulmonary edema, renal/liver injury, neurologic symptoms, or nonreassuring fetal status, with maternal-fetal medicine/anesthesia/neonatal planning.

Progression and follow-up: Progression can cause eclampsia, stroke, pulmonary edema, placental abruption, DIC, liver hematoma/rupture, renal failure, fetal growth restriction, stillbirth, preterm delivery, and increased long-term maternal cardiovascular risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Postpartum depression

Pathophysiology: Postpartum depression is major depression occurring during pregnancy or within the first postpartum year, shaped by sleep deprivation, hormonal transition, prior mood/anxiety disorder, trauma, pain, lactation stress, thyroid disease, anemia, social stress, and genetic vulnerability.

How Obstetrics and Gynecology assesses it: Screen with EPDS or PHQ-9, ask directly about self-harm, infant-harm intrusive thoughts, bonding, sleep when baby sleeps, anxiety/panic/OCD symptoms, trauma birth experience, bipolar history before antidepressants, psychosis symptoms, substance use, IPV, supports, breastfeeding, thyroid/anemia symptoms, and medication preferences.

Diagnosis: Clinical DSM diagnosis supported by EPDS/PHQ-9 and functional assessment; screen for bipolar disorder and postpartum psychosis. Consider CBC, TSH, B12, CMP, or substance testing only when suggested. Any psychosis, command hallucinations, delusions about the infant, or active suicidal/infanticidal intent is an emergency.

First-line treatment: Mild to moderate illness uses psychotherapy such as CBT or interpersonal therapy, sleep protection, partner/family support, lactation-safe planning, and SSRI such as sertraline (Zoloft) or escitalopram (Lexapro) when medication is indicated; continue previously effective medication when benefits outweigh risks.

Second-line treatment: Moderate-severe or rapid-response needs may use medication plus therapy, psychiatric consultation, and FDA-approved postpartum depression agents brexanolone IV (Zulresso REMS) or zuranolone (Zurzuvae) for eligible patients, with sedation/driving/breastfeeding counseling.

Third-line / advanced care: Urgent perinatal psychiatry, ED, or inpatient care for suicidal intent, infant-harm intent, psychosis, mania, catatonia, inability to care for self/infant, severe substance use, or unsafe home; involve supports and crisis plan immediately.

Progression and follow-up: Follow EPDS/PHQ-9 response, sleep, bonding, feeding, medication adverse effects, suicidality, infant safety, relapse risk in future pregnancies, bipolar conversion, and access to therapy/support.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Ectopic pregnancy

Pathophysiology: Ectopic pregnancy implants outside the uterine cavity, most often in the fallopian tube, risking tubal rupture and life-threatening hemorrhage.

How Obstetrics and Gynecology assesses it: Assess pregnancy test positivity, unilateral pelvic pain, vaginal bleeding, syncope/shoulder pain, hemodynamic stability, prior ectopic/tubal surgery/PID, fertility treatment, and Rh status.

Diagnosis: Use quantitative serum hCG trend, transvaginal ultrasound for intrauterine pregnancy/adnexal mass/free fluid, CBC/type and screen/Rh, CMP before methotrexate, and diagnostic laparoscopy if unstable or unclear.

First-line treatment: Stable selected patients may receive methotrexate (Trexall) with strict hCG follow-up; give Rh immune globulin (RhoGAM) if Rh-negative and indicated.

Second-line treatment: Repeat methotrexate protocols or close expectant management only for carefully selected declining hCG cases with reliable follow-up.

Third-line / advanced care: Immediate OB/GYN surgery with laparoscopy/laparotomy and salpingostomy/salpingectomy for rupture, instability, contraindication to methotrexate, high-risk imaging, or failed medical therapy.

Progression and follow-up: Rupture can cause massive hemoperitoneum, shock, transfusion, infertility risk, and death.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Abnormal uterine bleeding

Pathophysiology: Abnormal uterine bleeding can result from pregnancy, ovulatory dysfunction, fibroids, polyps, adenomyosis, coagulopathy, endometrial hyperplasia/cancer, thyroid disease, medications, or iatrogenic hormones.

How Obstetrics and Gynecology assesses it: Assess hemodynamic stability, pregnancy possibility, bleeding volume/clots, anemia symptoms, anticoagulants, cycle pattern, pelvic pain, obesity/PCOS risk, age, and cancer risk factors.

Diagnosis: Use urine/serum hCG, CBC/ferritin, TSH when indicated, coagulation testing if history suggests, pelvic/transvaginal ultrasound for structural disease, Pap/HPV if due, and endometrial biopsy for age/risk/persistent bleeding.

First-line treatment: Stable acute bleeding can use NSAIDs such as ibuprofen (Advil/Motrin), tranexamic acid (Lysteda), combined oral contraceptives such as ethinyl estradiol/levonorgestrel (Aviane), or progestins such as medroxyprogesterone (Provera) depending on contraindications.

Second-line treatment: Long-term control may use levonorgestrel IUD (Mirena/Liletta), cyclic/continuous progestin, combined hormonal contraception, iron replacement ferrous sulfate (Feosol), or treatment of thyroid/PCOS contributors.

Third-line / advanced care: Urgent care for instability; OB/GYN for hysteroscopy/polypectomy, myomectomy, endometrial ablation, uterine artery embolization, hysterectomy, or malignancy evaluation.

Progression and follow-up: Untreated bleeding can cause iron-deficiency anemia, syncope, transfusion need, missed pregnancy complication, endometrial hyperplasia/cancer delay, and poor quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Dysmenorrhea

Pathophysiology: Dysmenorrhea is painful menses from prostaglandin-mediated uterine contractions in primary disease or from secondary causes such as endometriosis, adenomyosis, fibroids, pelvic inflammatory disease, cervical stenosis, or obstructive anomalies.

How Obstetrics and Gynecology assesses it: Assess onset after menarche, cyclic pattern, severity, school/work impairment, dyspareunia, dyschezia, infertility, heavy bleeding, fever/discharge, pelvic mass symptoms, family history of endometriosis, sexual activity/pregnancy risk, and response to NSAIDs/hormonal therapy.

Diagnosis: Primary dysmenorrhea is clinical when typical and pelvic exam is not otherwise indicated. Use pregnancy test when relevant, pelvic exam/STI testing for sexually active patients with infection symptoms, transvaginal or pelvic ultrasound for secondary features, and MRI/laparoscopy when endometriosis or structural disease remains likely.

First-line treatment: NSAIDs started 1-2 days before menses when predictable: ibuprofen (Advil/Motrin), naproxen (Aleve/Naprosyn), or mefenamic acid (Ponstel), plus heat/exercise. Hormonal suppression options include combined oral contraceptives such as ethinyl estradiol/levonorgestrel (Aviane), patch/ring, norethindrone, depot medroxyprogesterone (Depo-Provera), etonogestrel implant (Nexplanon), or levonorgestrel IUD (Mirena/Liletta).

Second-line treatment: If persistent after 3-6 months, evaluate secondary causes and treat suspected endometriosis with continuous hormonal suppression, norethindrone acetate (Aygestin), elagolix (Orilissa) in selected adults, or pelvic floor PT when myofascial pain overlaps.

Third-line / advanced care: OB/GYN referral for refractory pain, suspected endometriosis/adenomyosis/fibroid, obstructive anomaly, pelvic mass, infertility, severe dyspareunia, or need for diagnostic/therapeutic laparoscopy.

Progression and follow-up: Follow pain days, function, NSAID GI/renal risk, bleeding pattern, contraception goals, anemia, endometriosis progression, opioid avoidance, and quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Endometriosis

Pathophysiology: Endometrial-like tissue outside the uterus drives estrogen-responsive inflammation, fibrosis, adhesions, neuroangiogenesis, and pelvic pain that may worsen with menses.

How Obstetrics and Gynecology assesses it: Assess cyclic pelvic pain, dysmenorrhea, dyspareunia, dyschezia, infertility, urinary/bowel symptoms, prior surgeries, response to hormones/NSAIDs, and red flags for acute abdomen.

Diagnosis: Clinical diagnosis is common; use pregnancy test, pelvic exam, transvaginal ultrasound for endometrioma/structural disease, MRI for deep infiltrating disease when needed, and laparoscopy with pathology when diagnosis or treatment requires confirmation.

First-line treatment: NSAIDs such as naproxen (Aleve/Naprosyn) plus hormonal suppression with combined oral contraceptive, norethindrone acetate (Aygestin), depot medroxyprogesterone (Depo-Provera), or levonorgestrel IUD (Mirena/Liletta).

Second-line treatment: GnRH antagonist elagolix (Orilissa) or relugolix/estradiol/norethindrone (Myfembree), GnRH agonist leuprolide (Lupron Depot) with add-back therapy, and pelvic floor PT for pain overlap.

Third-line / advanced care: OB/GYN surgery for excision/ablation, endometrioma management, fertility referral, multidisciplinary pain care, or bowel/bladder specialist involvement.

Progression and follow-up: Progression can cause chronic pelvic pain, adhesions, infertility, ovarian endometriomas, bowel/bladder involvement, central sensitization, and repeated surgery.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Pelvic inflammatory disease

Pathophysiology: Ascending infection from cervix to uterus, fallopian tubes, ovaries, or peritoneum causes endometritis, salpingitis, tubo-ovarian abscess, and inflammatory scarring.

How Obstetrics and Gynecology assesses it: Assess pelvic/lower abdominal pain, cervical motion/adnexal/uterine tenderness, fever, discharge, STI exposure, pregnancy, IUD timing, vomiting, severe illness, and ability to follow outpatient therapy.

Diagnosis: Clinical diagnosis is treated empirically; test pregnancy, NAAT for gonorrhea/chlamydia/trichomonas, wet prep, HIV/syphilis as indicated, CBC/CRP if severe, and transvaginal ultrasound or CT when abscess/appendicitis/torsion is possible.

First-line treatment: Outpatient: ceftriaxone (Rocephin) plus doxycycline (Vibramycin) plus metronidazole (Flagyl), with partner evaluation/treatment and abstinence until therapy complete.

Second-line treatment: Inpatient/severe disease: cefoxitin (Mefoxin) or cefotetan (Cefotan) plus doxycycline, or clindamycin (Cleocin) plus gentamicin (Garamycin), tailored to response.

Third-line / advanced care: Hospitalize for pregnancy, tubo-ovarian abscess, severe illness, inability to tolerate oral meds, failed outpatient therapy, or surgical emergency concern; drain abscess when needed.

Progression and follow-up: Complications include infertility, ectopic pregnancy, chronic pelvic pain, tubo-ovarian abscess rupture, peritonitis, and recurrent PID.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Vaginitis differential diagnosis

Pathophysiology: Vaginitis is usually caused by disruption of vaginal flora or infection: bacterial vaginosis with anaerobe overgrowth, vulvovaginal candidiasis with Candida inflammation, trichomoniasis with protozoal infection, or atrophic/genitourinary syndrome after estrogen decline.

How Obstetrics and Gynecology assesses it: Assess discharge color/odor, itching/burning, dysuria, dyspareunia, pregnancy, diabetes/immunosuppression, recent antibiotics, STI exposure, pelvic pain, fever, cervical motion tenderness, and recurrent episodes.

Diagnosis: Use vaginal pH, saline wet mount, KOH whiff test, microscopy for clue cells/yeast/trichomonads, NAAT for trichomonas/gonorrhea/chlamydia when indicated, pregnancy test when relevant, and pelvic exam if PID/cervicitis is possible.

First-line treatment: Bacterial vaginosis: metronidazole (Flagyl) oral or gel, or clindamycin (Cleocin) cream. Candidiasis: fluconazole (Diflucan) oral when appropriate or topical azole such as clotrimazole (Lotrimin) or miconazole (Monistat). Trichomoniasis: metronidazole (Flagyl) or tinidazole (Tindamax) with partner treatment.

Second-line treatment: Recurrent BV may need suppressive metronidazole gel; recurrent candidiasis may need longer induction plus weekly fluconazole; non-albicans Candida may need boric acid under clinician guidance.

Third-line / advanced care: Refer for recurrent/refractory symptoms, pregnancy complexity, pelvic pain/fever, suspected PID, immunocompromise, or concern for vulvar dermatosis/neoplasia.

Progression and follow-up: Missed STI/PID can progress to chronic pelvic pain, infertility, ectopic pregnancy risk, pregnancy complications, persistent symptoms, and reinfection if partners are not treated.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Menopause symptoms

Pathophysiology: Menopause reflects ovarian follicle depletion and estrogen decline, causing vasomotor symptoms, sleep disturbance, mood changes, urogenital atrophy, bone loss, and cardiometabolic shifts.

How Obstetrics and Gynecology assesses it: Assess hot flashes/night sweats, sleep, mood, vaginal/urinary symptoms, bleeding after menopause, VTE/stroke/breast cancer history, uterus status, osteoporosis risk, and patient goals.

Diagnosis: Usually clinical after 12 months amenorrhea at typical age; use pregnancy test when uncertain, TSH/prolactin/FSH selectively for atypical age, evaluate postmenopausal bleeding with transvaginal ultrasound and/or endometrial biopsy.

First-line treatment: Lifestyle and trigger management; for eligible bothersome vasomotor symptoms use estradiol (Estrace/Vivelle-Dot/Climara) plus progesterone (Prometrium) if uterus present, or estrogen alone after hysterectomy.

Second-line treatment: Nonhormonal options include paroxetine (Brisdelle/Paxil), venlafaxine (Effexor XR), gabapentin (Neurontin), clonidine (Catapres), or fezolinetant (Veozah); vaginal estrogen (Vagifem/Estrace cream/Estring) for genitourinary syndrome.

Third-line / advanced care: Gynecology referral for complex contraindications, postmenopausal bleeding, refractory symptoms, osteoporosis treatment such as alendronate (Fosamax), or cancer-risk counseling.

Progression and follow-up: Untreated severe symptoms can impair sleep/function; estrogen deficiency contributes to vaginal atrophy, dyspareunia, recurrent urinary symptoms, bone loss, and fracture risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Contraception with medical comorbidity

Pathophysiology: Contraception prevents ovulation, fertilization, or implantation depending on method; medical comorbidities change estrogen, progestin, device, and drug-interaction safety.

How Obstetrics and Gynecology assesses it: Assess pregnancy status, BP, migraine with aura, VTE/stroke/CAD risk, smoking age over 35, breast cancer, liver disease, postpartum/breastfeeding timing, enzyme-inducing medications, and reproductive goals.

Diagnosis: Use quick-start criteria, urine pregnancy test if uncertain, BP before estrogen-containing methods, STI screening when indicated for IUD placement, and medical eligibility risk review.

First-line treatment: Long-acting options: levonorgestrel IUD (Mirena/Liletta/Kyleena), copper IUD (Paragard), etonogestrel implant (Nexplanon). Short-acting: combined pill ethinyl estradiol/levonorgestrel (Aviane), patch (Xulane), ring (NuvaRing), norethindrone POP (Micronor), or drospirenone POP (Slynd).

Second-line treatment: Depot medroxyprogesterone (Depo-Provera), barrier methods, emergency contraception levonorgestrel (Plan B), ulipristal (Ella), or copper IUD; choose progestin-only/nonhormonal when estrogen is contraindicated.

Third-line / advanced care: Refer for difficult IUD insertion/removal, sterilization counseling, complex thrombotic/cancer/liver disease, or contraception after teratogenic medication exposure.

Progression and follow-up: Poor method fit can lead to unintended pregnancy, medication-teratogen exposure, worsening comorbidity risk, irregular bleeding, or discontinuation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Cervical cancer screening abnormality

Pathophysiology: Persistent high-risk HPV infection causes cervical dysplasia that can progress through CIN stages to invasive cervical cancer over years.

How Obstetrics and Gynecology assesses it: Assess age, prior Pap/HPV results, immunosuppression/HIV, DES exposure, pregnancy, smoking, HPV vaccination, abnormal bleeding, and follow-up reliability.

Diagnosis: Use age-appropriate Pap cytology and/or high-risk HPV testing; abnormal results are triaged with risk-based colposcopy, cervical biopsy, endocervical sampling, and excisional procedure such as LEEP when indicated.

First-line treatment: Low-risk abnormalities may receive surveillance repeat HPV/Pap; treat cervicitis/STIs when present and update HPV vaccination with Gardasil 9 when eligible.

Second-line treatment: High-grade lesions often need colposcopy-directed biopsy and excisional treatment such as LEEP or cold-knife cone, with pathology margin review.

Third-line / advanced care: Gynecologic oncology for invasive cancer, adenocarcinoma in situ complexity, pregnancy-associated high-grade disease, or recurrent high-grade dysplasia.

Progression and follow-up: Missed follow-up can allow CIN2/3 to progress to invasive cervical cancer, bleeding, pain, infertility from treatment, and metastatic disease.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Ovarian cyst evaluation

Pathophysiology: Ovarian cysts include functional follicular/corpus luteum cysts, hemorrhagic cysts, endometriomas, dermoids, tubo-ovarian abscess, ectopic-related adnexal masses, and benign or malignant neoplasms; risk depends on age, menopausal status, morphology, size, symptoms, and torsion/rupture.

How Obstetrics and Gynecology assesses it: Assess pregnancy status, acute unilateral pain, nausea/vomiting, syncope, fever, discharge, hemodynamic stability, LMP, menopausal status, cancer family history/BRCA risk, endometriosis symptoms, prior cysts, and torsion risk from mass size or fertility treatment.

Diagnosis: First test is urine/serum hCG. Use transvaginal ultrasound with Doppler and morphology description (simple, hemorrhagic, septations, solid components, papillary projections, ascites), CBC if bleeding/infection, GC/CT if PID possible, CA-125 or risk algorithms mainly for suspicious masses/postmenopause, and CT/MRI only for staging/unclear non-gynecologic or complex findings.

First-line treatment: Simple functional cysts in reproductive-age patients often need observation, NSAIDs such as ibuprofen (Advil/Motrin) or naproxen (Aleve), and repeat ultrasound based on size/features. Combined hormonal contraception may prevent new functional cysts but does not rapidly resolve an existing cyst.

Second-line treatment: Endometrioma, dermoid, persistent large cyst, recurrent symptoms, or indeterminate ultrasound needs OB/GYN follow-up, serial imaging, MRI characterization, or cystectomy planning depending on fertility goals and malignancy risk.

Third-line / advanced care: Emergency surgery/ED for ovarian torsion concern, ruptured cyst with hemodynamic instability, ectopic pregnancy, tubo-ovarian abscess/sepsis, or imaging suspicious for malignancy; gynecologic oncology for high-risk mass features.

Progression and follow-up: Follow cyst size/morphology, pain recurrence, torsion risk, hemoperitoneum, fertility impact, endometriosis association, tumor marker context, and missed malignancy in postmenopausal or complex masses.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Infertility initial workup

Pathophysiology: Infertility reflects ovulatory dysfunction, diminished ovarian reserve, tubal/peritoneal disease, endometriosis, uterine/cervical factors, male factor, sexual dysfunction, age-related oocyte decline, endocrine disease, or unexplained factors.

How Obstetrics and Gynecology assesses it: Assess duration trying to conceive, age, menstrual regularity, ovulation symptoms, prior pregnancies/losses, STI/PID/ectopic history, endometriosis pain, surgeries, chemo/radiation, medications, BMI, thyroid/galactorrhea symptoms, intercourse timing, semen exposure, male partner history, and genetic/family risks.

Diagnosis: Start evaluation after 12 months if under 35, after 6 months if 35 or older, or immediately for known risk factors. Test ovulation with mid-luteal progesterone or cycle history, ovarian reserve with AMH/antral follicle count/day-3 FSH-estradiol when useful, TSH/prolactin if indicated, semen analysis, uterine/tubal evaluation with hysterosalpingography or saline infusion sonography, and pelvic ultrasound.

First-line treatment: Optimize timing of intercourse, prenatal vitamin with folic acid, smoking/alcohol/substance reduction, weight/metabolic health, and treat thyroid/prolactin or infection issues. Ovulatory PCOS may respond to letrozole (Femara) for ovulation induction under clinician guidance.

Second-line treatment: Condition-specific care includes clomiphene (Clomid) when appropriate, metformin (Glucophage) for selected PCOS metabolic issues, endometriosis/fibroid/polyp treatment, tubal surgery in selected cases, intrauterine insemination, or IVF depending on findings and age.

Third-line / advanced care: Reproductive endocrinology referral for age 35 or older, severe male factor, diminished ovarian reserve, tubal occlusion, recurrent pregnancy loss, endometriosis, genetic concerns, failed ovulation induction, or need for IVF/PGT/fertility preservation.

Progression and follow-up: Follow ovulation, pregnancy outcomes, multiple gestation risk, ovarian hyperstimulation risk, ectopic risk, emotional distress, time-sensitive age factors, and transition to higher-level fertility care.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Obstetrics and Gynecology

Urinary symptoms in pregnancy

Pathophysiology: Urinary symptoms in pregnancy may reflect asymptomatic bacteriuria, cystitis, pyelonephritis, stones, vaginitis/STIs, physiologic frequency, or preterm labor mimic; untreated bacteriuria increases pyelonephritis and adverse pregnancy risk.

How Obstetrics and Gynecology assesses it: Assess dysuria, frequency, urgency, hematuria, flank pain, fever, contractions, vaginal discharge/bleeding, gestational age, prior UTI/pyelo, resistant organisms, allergies, renal disease, diabetes, and ability to tolerate oral intake.

Diagnosis: Obtain urinalysis and urine culture before antibiotics when possible; screen for asymptomatic bacteriuria early in pregnancy. Use CBC/CMP if febrile or flank pain, renal ultrasound for stone/obstruction concern, and STI/vaginitis testing when discharge/pelvic symptoms exist. Test-of-cure culture is commonly used after treatment in pregnancy.

First-line treatment: Treat cystitis/asymptomatic bacteriuria with pregnancy-appropriate antibiotics guided by culture: nitrofurantoin (Macrobid) when appropriate outside contraindicated contexts, cephalexin (Keflex), amoxicillin-clavulanate (Augmentin), or fosfomycin (Monurol). Avoid empiric fluoroquinolones; avoid TMP-SMX in first trimester/near term unless benefits outweigh risks.

Second-line treatment: Recurrent UTI may need suppressive cephalexin or nitrofurantoin after culture-guided treatment; address hydration, postcoital pattern, diabetes control, and resistant-organism history.

Third-line / advanced care: Pyelonephritis generally requires hospital evaluation with IV antibiotics such as ceftriaxone (Rocephin), fluids, antiemetics, fetal/uterine assessment, and monitoring for sepsis, ARDS, anemia, or preterm labor; urology for obstruction/infected stone.

Progression and follow-up: Follow symptom resolution, culture clearance, recurrence, pyelonephritis, sepsis, preterm contractions, fetal well-being when indicated, antibiotic allergy/resistance, and renal complications.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Specialty role

Skin, hair, nail, mucosal, inflammatory, infectious, allergic, neoplastic, and procedural dermatologic care.

Dermatology

Atopic dermatitis

Pathophysiology: Atopic dermatitis combines epidermal barrier dysfunction, filaggrin-related susceptibility, type 2 inflammation, itch-scratch cycle, and Staphylococcus aureus colonization.

How Dermatology assesses it: Assess age-specific distribution, itch severity, sleep loss, triggers/irritants, allergic rhinitis/asthma, infection signs, steroid use, and impact on school/work.

Diagnosis: Clinical diagnosis; culture if impetiginized or recurrent infection, patch testing if allergic contact dermatitis suspected, and biopsy only if atypical or lymphoma/psoriasis mimic concern.

First-line treatment: Daily emollients, fragrance avoidance, short lukewarm bathing, topical corticosteroids by site/potency such as hydrocortisone or triamcinolone (Kenalog), and oral antihistamine only for sleep-limited itch when appropriate.

Second-line treatment: Topical calcineurin inhibitors tacrolimus (Protopic) or pimecrolimus (Elidel), crisaborole (Eucrisa), ruxolitinib cream (Opzelura), wet wraps, bleach baths for recurrent infection, and antibiotics only for clear bacterial infection.

Third-line / advanced care: Dermatology for phototherapy, dupilumab (Dupixent), tralokinumab (Adbry), upadacitinib (Rinvoq), abrocitinib (Cibinqo), or evaluation for allergic contact dermatitis.

Progression and follow-up: Poor control causes sleep disruption, lichenification, infection, eczema herpeticum, psychosocial distress, and steroid adverse effects.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Allergic contact dermatitis

Pathophysiology: Irritant contact dermatitis results from direct barrier injury; allergic contact dermatitis is delayed type IV T-cell hypersensitivity to allergens such as nickel, fragrance, poison ivy, rubber, or preservatives.

How Dermatology assesses it: Map rash distribution to exposures, occupation/hobbies, cosmetics, gloves, metals, plants, topical meds, and timing after exposure; assess vesicles, weeping, facial/genital involvement, and infection.

Diagnosis: Clinical pattern plus exposure history; patch testing for recurrent/chronic allergic cases; KOH/culture/biopsy only when infection, tinea, psoriasis, or autoimmune mimic is possible.

First-line treatment: Avoid/remove trigger, wash exposed skin, emollients, topical corticosteroid such as triamcinolone (Kenalog) for trunk/extremities or hydrocortisone for face/folds, and cool compresses.

Second-line treatment: Extensive poison ivy/allergic dermatitis may need oral prednisone (Deltasone) taper; secondary infection may need cephalexin (Keflex) or doxycycline (Vibramycin) based on MRSA risk.

Third-line / advanced care: Dermatology/allergy for patch testing, occupational evaluation, refractory hand dermatitis, systemic immunosuppression, or severe facial/genital disease.

Progression and follow-up: Persistent exposure causes chronic fissuring, lichenification, infection, work impairment, and repeated steroid exposure.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Psoriasis

Pathophysiology: Immune-mediated IL-23/Th17 inflammation accelerates keratinocyte turnover, causing plaques and systemic comorbidity including psoriatic arthritis and cardiometabolic risk.

How Dermatology assesses it: Assess body surface area, nails/scalp/genitals, joint pain/dactylitis, infection risk, liver disease, pregnancy, depression, metabolic syndrome, and prior steroid/biologic exposure.

Diagnosis: Clinical diagnosis; biopsy if uncertain, screen for psoriatic arthritis, CBC/CMP/hepatitis/TB testing before systemic immunosuppression, and evaluate cardiovascular risk.

First-line treatment: Topical corticosteroids such as triamcinolone (Kenalog) or clobetasol (Temovate), vitamin D analog calcipotriene (Dovonex), moisturizers, and phototherapy for broader disease.

Second-line treatment: Methotrexate (Trexall), apremilast (Otezla), cyclosporine (Neoral), acitretin (Soriatane), or biologics such as adalimumab (Humira), ustekinumab (Stelara), secukinumab (Cosentyx), ixekizumab (Taltz), or guselkumab (Tremfya).

Third-line / advanced care: Dermatology/rheumatology co-management for severe skin/joint disease, biologic switching, infection monitoring, and pregnancy-safe planning.

Progression and follow-up: Progression can include psoriatic arthritis, nail destruction, erythroderma/pustular flares, metabolic syndrome, and quality-of-life impairment.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Acne vulgaris

Pathophysiology: Follicular hyperkeratinization, Cutibacterium acnes, androgen-driven sebum, and inflammation cause comedones, papules, pustules, nodules, and scarring.

How Dermatology assesses it: Assess lesion type, severity, scarring, pregnancy potential, menstrual/androgen symptoms, medication triggers, skin care, psychosocial impact, and prior therapy adherence.

Diagnosis: Clinical diagnosis; consider pregnancy test before teratogenic drugs, androgen labs for severe hyperandrogenism, and culture if unusual gram-negative folliculitis or treatment failure.

First-line treatment: Topical benzoyl peroxide, adapalene (Differin), tretinoin (Retin-A), clindamycin (Cleocin T) only with benzoyl peroxide, and gentle noncomedogenic skin care.

Second-line treatment: Oral doxycycline (Doryx/Vibramycin), minocycline (Minocin), combined oral contraceptives such as ethinyl estradiol/drospirenone (Yaz/Yasmin), or spironolactone (Aldactone) for appropriate patients.

Third-line / advanced care: Dermatology for isotretinoin (Accutane/Claravis/Absorica) with iPLEDGE requirements, intralesional triamcinolone (Kenalog), scar procedures, or severe acne fulminans care.

Progression and follow-up: Untreated inflammatory acne can cause permanent scarring, dyspigmentation, pain, and depression/anxiety.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Rosacea

Pathophysiology: Rosacea is a chronic centrofacial inflammatory and neurovascular disorder with flushing, persistent erythema, papules/pustules, telangiectasias, phymatous change, and ocular involvement; triggers include heat, alcohol, spicy foods, sun, stress, and topical steroids.

How Dermatology assesses it: Assess erythematotelangiectatic versus papulopustular versus phymatous features, ocular dryness/grittiness/blepharitis, flushing triggers, photosensitivity, steroid use, acneiform drug eruptions, demodex/seborrheic overlap, skin of color diagnostic clues, and psychosocial impact.

Diagnosis: Clinical diagnosis based on phenotype and distribution; check ocular symptoms, medication triggers, and mimics such as acne vulgaris, lupus malar rash, seborrheic dermatitis, perioral dermatitis, carcinoid flushing, or dermatomyositis. Biopsy or ANA is reserved for atypical photosensitive or systemic presentations.

First-line treatment: Trigger reduction, gentle skin care, daily broad-spectrum sunscreen, and phenotype-directed topical therapy: metronidazole (MetroGel/MetroCream), azelaic acid (Finacea), ivermectin cream (Soolantra), brimonidine (Mirvaso), or oxymetazoline (Rhofade).

Second-line treatment: Papulopustular or ocular disease may need doxycycline low-dose modified release (Oracea) or doxycycline/minocycline, plus eyelid hygiene and artificial tears. Persistent telangiectasia/erythema may respond to pulsed dye laser or intense pulsed light.

Third-line / advanced care: Dermatology/ophthalmology for ocular keratitis/vision symptoms, phymatous rhinophyma needing laser/surgery, severe refractory disease, diagnostic uncertainty, or steroid-induced rosacea/perioral dermatitis.

Progression and follow-up: Follow flushing triggers, inflammatory lesion count, ocular symptoms, medication irritation, photosensitivity, antibiotic stewardship, phymatous change, and quality-of-life burden.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Hidradenitis suppurativa

Pathophysiology: Hidradenitis suppurativa is chronic follicular occlusion and immune dysregulation in intertriginous skin, producing painful nodules, abscesses, draining tunnels, scarring, and flares; smoking, obesity, friction, family history, and hormonal factors increase risk.

How Dermatology assesses it: Assess axilla/groin/inframammary/perineal distribution, recurrent painful nodules, sinus tracts, scarring, Hurley stage, drainage/odor, fever/cellulitis, menstrual flares, pregnancy, smoking, weight, depression, pain, IBD/spondyloarthritis/PCOS overlap, and prior antibiotic/biologic/surgery response.

Diagnosis: Clinical diagnosis from typical lesions, location, and recurrence. Culture only if secondary infection is suspected; ultrasound can map tunnels; biopsy if squamous cell carcinoma or Crohn disease mimic is suspected; screen comorbid depression, metabolic syndrome, IBD, and inflammatory arthritis by symptoms.

First-line treatment: General care includes smoking cessation, weight/friction reduction, loose clothing, antiseptic wash such as chlorhexidine, pain control, and topical clindamycin (Cleocin T) for mild disease; intralesional triamcinolone (Kenalog) can calm isolated inflamed nodules.

Second-line treatment: Moderate disease may use doxycycline (Vibramycin), minocycline, or clindamycin plus rifampin protocols, hormonal therapy such as spironolactone (Aldactone) or combined oral contraceptives in selected patients, and biologic therapy adalimumab (Humira) or secukinumab (Cosentyx) for moderate-severe disease.

Third-line / advanced care: Dermatology/surgery for deroofing, local excision, wide excision, laser hair reduction, severe tunnels/scarring, refractory pain, recurrent abscesses, pregnancy complexity, or suspected SCC in chronic perineal/gluteal disease.

Progression and follow-up: Follow flare frequency, pain, drainage, tunnels/scars, function, depression, opioid exposure, antibiotic adverse effects, biologic infection risk, and squamous cell carcinoma risk in long-standing severe disease.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Urticaria

Pathophysiology: Urticaria is mast-cell mediator release causing transient pruritic wheals, angioedema, or both; acute disease is often infection, food, medication, venom, or idiopathic, while chronic spontaneous urticaria is usually autoimmune/idiopathic rather than allergic.

How Dermatology assesses it: Assess duration under or over 6 weeks, individual lesion duration under 24 hours, angioedema, anaphylaxis symptoms, NSAIDs/opioids/ACE inhibitors, inducible triggers such as cold/pressure/heat/exercise, infections, autoimmune thyroid disease symptoms, pregnancy, and quality-of-life/sleep impact.

Diagnosis: Clinical diagnosis. No broad allergy panel is needed for chronic spontaneous urticaria without a clear trigger. Use CBC/ESR/CRP/TSH only when history suggests systemic disease; biopsy lesions lasting over 24 hours, painful/bruising, purpuric, or leaving hyperpigmentation to evaluate urticarial vasculitis.

First-line treatment: Second-generation H1 antihistamines are first-line: cetirizine (Zyrtec), levocetirizine (Xyzal), fexofenadine (Allegra), loratadine (Claritin), or desloratadine (Clarinex); avoid triggers and treat anaphylaxis with epinephrine autoinjector (EpiPen/Auvi-Q) when systemic symptoms occur.

Second-line treatment: If chronic symptoms persist, increase second-generation antihistamine dose up to guideline-supported higher dosing under clinician guidance; add short steroid burst only for severe flares, and consider H2 blocker or leukotriene receptor antagonist montelukast (Singulair) selectively.

Third-line / advanced care: Allergy/dermatology for omalizumab (Xolair), cyclosporine (Neoral) in refractory cases, recurrent angioedema without hives needing C4/C1 inhibitor evaluation, cold urticaria with systemic reactions, or suspected urticarial vasculitis.

Progression and follow-up: Follow wheal/angioedema frequency, sleep, sedation, anaphylaxis risk, NSAID/ACE inhibitor triggers, steroid overuse, omalizumab response, autoimmune clues, and impact on school/work.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Tinea infections

Pathophysiology: Dermatophyte fungi invade keratinized skin, hair, or nails; moisture, occlusion, diabetes, immunosuppression, and communal exposure increase risk.

How Dermatology assesses it: Assess annular scale, feet/groin/scalp/nails, household contacts, pets, steroid use that may mask tinea, diabetes/immunosuppression, and bacterial superinfection.

Diagnosis: KOH prep of scale/hair/nail confirms hyphae; fungal culture or PAS nail clipping for uncertain onychomycosis; avoid diagnosing by appearance alone when steroid-modified or atypical.

First-line treatment: Localized tinea corporis/cruris/pedis: topical terbinafine (Lamisil), clotrimazole (Lotrimin), or ketoconazole (Nizoral); keep area dry and avoid topical steroid monotherapy.

Second-line treatment: Extensive, scalp, nail, or refractory disease may need oral terbinafine (Lamisil) or itraconazole (Sporanox) after liver/drug-interaction review; tinea capitis may use griseofulvin (Gris-PEG) or terbinafine.

Third-line / advanced care: Dermatology for treatment failure, immunocompromised host, diagnostic uncertainty, Majocchi granuloma, or severe onychomycosis.

Progression and follow-up: Untreated infection can spread, recur, cause cellulitis from skin breaks, transmit to contacts, and become steroid-modified tinea incognito.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Scabies

Pathophysiology: Sarcoptes scabiei mites burrow in the stratum corneum, triggering delayed hypersensitivity with intense pruritus, especially at night.

How Dermatology assesses it: Assess nocturnal itch, burrows, web spaces/wrists/genitals/beltline, household or institutional contacts, immunosuppression, crusted lesions, and secondary impetigo.

Diagnosis: Clinical diagnosis supported by dermoscopy, mineral oil skin scraping, tape test, or microscopy of mite/eggs/scybala when uncertain.

First-line treatment: Permethrin 5% cream (Elimite) from neck down overnight, repeat in 7 days; treat close contacts simultaneously and wash/bag bedding/clothing.

Second-line treatment: Oral ivermectin (Stromectol) for outbreaks, adherence barriers, or crusted scabies protocols when appropriate; treat secondary infection with mupirocin (Bactroban) or oral antibiotics if cellulitis/impetigo.

Third-line / advanced care: Dermatology/infectious disease for crusted scabies, institutional outbreaks, infant/pregnancy complexity, or persistent symptoms after correct therapy.

Progression and follow-up: Complications include excoriations, impetigo, cellulitis, post-scabetic itch, outbreaks, and severe crusted scabies in immunocompromised patients.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Impetigo

Pathophysiology: Staphylococcus aureus or Streptococcus pyogenes infect superficial epidermis, producing honey-colored crusts or bullae, often after skin barrier disruption.

How Dermatology assesses it: Assess lesion number/location, bullae, fever, cellulitis, outbreaks, MRSA risk, eczema/scabies/tinea trigger, and school/daycare exposure.

Diagnosis: Usually clinical; culture purulent or recurrent lesions, outbreak cases, MRSA concern, or treatment failure.

First-line treatment: Limited disease: topical mupirocin (Bactroban) or retapamulin (Altabax). Gently remove crusts and improve hygiene.

Second-line treatment: Numerous lesions/outbreaks: cephalexin (Keflex) or dicloxacillin; use clindamycin (Cleocin), doxycycline (Vibramycin), or TMP-SMX (Bactrim/Septra) when MRSA risk and age/pregnancy allow.

Third-line / advanced care: Evaluate for cellulitis, abscess, post-strep complications, recurrent colonization, or immunodeficiency when severe/recurrent.

Progression and follow-up: Complications include cellulitis, abscess, transmission, post-streptococcal glomerulonephritis, and recurrence if underlying dermatitis/scabies persists.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Herpes zoster

Pathophysiology: Varicella-zoster virus reactivates from dorsal root or cranial nerve ganglia, causing a unilateral dermatomal vesicular eruption with neuropathic pain.

How Dermatology assesses it: Assess rash onset within 72 hours, dermatome, eye/ear involvement, immunocompromise, pregnancy, severe pain, fever, dissemination, and vaccination history.

Diagnosis: Usually clinical; use VZV PCR from lesion swab when atypical, disseminated, immunocompromised, or diagnosis uncertain. Urgent eye exam if V1/ocular symptoms; consider HIV/immunosuppression evaluation when severe or recurrent.

First-line treatment: Start antiviral therapy when indicated: valacyclovir (Valtrex), famciclovir (Famvir), or acyclovir (Zovirax); analgesia with acetaminophen (Tylenol), NSAIDs, topical lidocaine (Lidoderm), and gabapentin (Neurontin) or pregabalin (Lyrica) for neuropathic pain.

Second-line treatment: Ophthalmic zoster needs urgent ophthalmology and systemic antivirals; severe pain may require short opioid course plus neuropathic agent; vaccinate later with recombinant zoster vaccine (Shingrix) when eligible.

Third-line / advanced care: IV acyclovir for disseminated, CNS/visceral, or severely immunocompromised disease; pain/palliative or neurology referral for refractory postherpetic neuralgia.

Progression and follow-up: Complications include postherpetic neuralgia, keratitis/uveitis/vision loss, Ramsay Hunt syndrome, bacterial superinfection, meningitis/encephalitis, and disseminated infection.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Melanoma screening

Pathophysiology: Melanoma is malignant melanocyte transformation driven by UV injury, nevus biology, genetic susceptibility, and mutations such as BRAF, NRAS, or KIT; prognosis depends heavily on Breslow depth, ulceration, mitotic activity, nodal disease, and metastasis.

How Dermatology assesses it: Assess ABCDE change, ugly duckling lesion, new or changing pigmented lesion, bleeding/itching, personal/family melanoma, atypical nevi, tanning bed/UV exposure, immunosuppression, skin type, total body skin exam, lymph nodes, and symptoms of metastasis when lesion is invasive/high-risk.

Diagnosis: Use dermoscopy and biopsy suspicious lesions with narrow-margin excisional biopsy when feasible, saucerization/deep shave or punch only when anatomically appropriate and deep enough for microstaging. Pathology must report Breslow depth, ulceration, mitotic rate, margins, and subtype; sentinel lymph node biopsy and imaging are stage/risk-based.

First-line treatment: Melanoma in situ and invasive primary melanoma are treated with wide local excision using margin based on stage. Counsel sun protection, self-skin exams, total body photography/dermoscopic monitoring for high nevus burden, and family risk awareness.

Second-line treatment: Sentinel lymph node biopsy is considered for appropriate Breslow depth/high-risk features. Stage III/IV or high-risk resected disease may need oncology-directed immunotherapy such as pembrolizumab (Keytruda), nivolumab (Opdivo), or targeted BRAF/MEK therapy dabrafenib (Tafinlar) plus trametinib (Mekinist) when BRAF V600-positive.

Third-line / advanced care: Dermatology/oncology/surgical oncology for positive margins, sentinel node decisions, high-risk pathology, nodal disease, metastatic symptoms, lentigo maligna on constrained sites where staged excision/Mohs may be chosen, or immunotherapy toxicity.

Progression and follow-up: Follow recurrence, new primary melanoma, nodal/distant metastasis, lymphedema after nodal surgery, immune-related adverse events, brain/liver/lung/bone spread, and adherence to skin surveillance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Basal cell carcinoma

Pathophysiology: Basal cell carcinoma is a slow-growing keratinocyte cancer driven mainly by UV and hedgehog pathway activation; it rarely metastasizes but can deeply invade and destroy local tissue, especially on central face, ears, scalp, hands, feet, and genital sites.

How Dermatology assesses it: Assess pearly papule, rolled border, telangiectasia, ulceration, nonhealing sore, scar-like morpheaform plaque, lesion size, high-risk location, recurrence, immunosuppression, radiation history, genetic syndromes, anticoagulation, and patient preference/cosmesis.

Diagnosis: Confirm with shave, punch, or excisional biopsy adequate to define subtype: nodular, superficial, infiltrative, micronodular, morpheaform, basosquamous, or perineural features. Risk stratify by size, location, borders, histology, recurrence, and immune status; imaging only for suspected deep invasion/perineural spread.

First-line treatment: Low-risk BCC is usually treated with standard surgical excision, electrodesiccation and curettage in appropriate nonterminal hair-bearing low-risk sites, or topical imiquimod (Aldara) or fluorouracil (Efudex) for selected superficial BCC when surgery is not preferred.

Second-line treatment: High-risk, recurrent, aggressive histology, or cosmetically sensitive tumors often need Mohs micrographic surgery. Radiation is an option when surgery is not feasible; photodynamic therapy has lower cure rates and is selected cautiously.

Third-line / advanced care: Advanced unresectable or metastatic BCC may need hedgehog inhibitors vismodegib (Erivedge) or sonidegib (Odomzo), or PD-1 inhibitor cemiplimab (Libtayo) after hedgehog inhibitor failure/intolerance; refer dermatologic surgery/oncology for complex disease.

Progression and follow-up: Follow for recurrence, new keratinocyte cancers, perineural/deep invasion, surgical wound issues, cosmetic/functional impact, hedgehog-inhibitor muscle cramps/dysgeusia/alopecia, and annual full-skin exams.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Squamous cell carcinoma

Pathophysiology: Cutaneous squamous cell carcinoma arises from UV-driven keratinocyte atypia and actinic damage, with higher metastatic risk than BCC; risk increases with immunosuppression, chronic wounds, radiation, high-risk sites, depth, poor differentiation, and perineural invasion.

How Dermatology assesses it: Assess tender hyperkeratotic papule/nodule, nonhealing ulcer, rapid growth, actinic keratoses, field cancerization, transplant/immunosuppression, chronic scars/ulcers, HPV-related genital/periungual lesions, high-risk ear/lip location, neurologic symptoms, and regional lymph nodes.

Diagnosis: Biopsy with shave, punch, or excision deep enough to assess invasion, differentiation, depth, perineural/lymphovascular invasion, and margins. Palpate lymph nodes; ultrasound/CT/MRI/PET is reserved for high-risk tumors, palpable nodes, deep invasion, or perineural symptoms.

First-line treatment: Low-risk SCC is treated with standard excision or electrodesiccation and curettage in selected low-risk locations; actinic keratoses/field disease may use cryotherapy, fluorouracil (Efudex), imiquimod (Aldara), tirbanibulin (Klisyri), or photodynamic therapy.

Second-line treatment: High-risk SCC generally needs Mohs micrographic surgery or excision with margin control; radiation may be adjuvant or definitive when surgery is not feasible, especially perineural or nodal-risk disease.

Third-line / advanced care: Dermatologic surgery/oncology for high-risk, recurrent, nodal, perineural, transplant-associated, or unresectable disease. Advanced disease may use PD-1 therapy cemiplimab (Libtayo) or pembrolizumab (Keytruda), nodal surgery/radiation, and immunosuppression adjustment with transplant team.

Progression and follow-up: Follow local recurrence, nodal metastasis, perineural spread, additional SCCs/actinic keratoses, transplant medication risk, wound healing, radiation effects, and functional/cosmetic outcomes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Drug eruption

Pathophysiology: Drug eruptions range from benign morbilliform T-cell reactions to severe cutaneous adverse reactions such as SJS/TEN with keratinocyte apoptosis and mucosal necrosis.

How Dermatology assesses it: List all new drugs in prior 1-8 weeks, timing, fever, facial edema, mucosal pain, skin pain, blistering, target lesions, lymph nodes, eosinophilia symptoms, liver/kidney symptoms, and percent body surface area.

Diagnosis: Stop suspect drug; use CBC with differential, CMP/LFTs/creatinine, urinalysis, skin biopsy when severe/uncertain, and SCORTEN or burn-unit criteria for SJS/TEN. Rule out viral exanthem and infection when needed.

First-line treatment: Mild morbilliform eruption: discontinue culprit if possible, topical corticosteroid such as triamcinolone (Kenalog), oral antihistamine cetirizine (Zyrtec), and close follow-up.

Second-line treatment: DRESS or severe eruption needs systemic corticosteroids under specialist guidance, organ monitoring, and strict avoidance documentation.

Third-line / advanced care: SJS/TEN concern requires emergency hospitalization/burn or ICU-level care, ophthalmology, wound/fluid/electrolyte management, pain control, and specialist-directed immunomodulation.

Progression and follow-up: Severe reactions can progress to ocular scarring, sepsis, multiorgan injury, chronic mucosal disease, and death.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Dermatology

Stevens Johnson syndrome concern

Pathophysiology: Drug eruptions range from benign morbilliform T-cell reactions to severe cutaneous adverse reactions such as SJS/TEN with keratinocyte apoptosis and mucosal necrosis.

How Dermatology assesses it: List all new drugs in prior 1-8 weeks, timing, fever, facial edema, mucosal pain, skin pain, blistering, target lesions, lymph nodes, eosinophilia symptoms, liver/kidney symptoms, and percent body surface area.

Diagnosis: Stop suspect drug; use CBC with differential, CMP/LFTs/creatinine, urinalysis, skin biopsy when severe/uncertain, and SCORTEN or burn-unit criteria for SJS/TEN. Rule out viral exanthem and infection when needed.

First-line treatment: Mild morbilliform eruption: discontinue culprit if possible, topical corticosteroid such as triamcinolone (Kenalog), oral antihistamine cetirizine (Zyrtec), and close follow-up.

Second-line treatment: DRESS or severe eruption needs systemic corticosteroids under specialist guidance, organ monitoring, and strict avoidance documentation.

Third-line / advanced care: SJS/TEN concern requires emergency hospitalization/burn or ICU-level care, ophthalmology, wound/fluid/electrolyte management, pain control, and specialist-directed immunomodulation.

Progression and follow-up: Severe reactions can progress to ocular scarring, sepsis, multiorgan injury, chronic mucosal disease, and death.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Specialty role

Autoimmune, inflammatory joint, connective tissue, vasculitis, crystal, and systemic inflammatory disease specialty care.

Rheumatology

Rheumatoid arthritis

Pathophysiology: Rheumatoid arthritis is systemic autoimmune synovitis driven by loss of tolerance, RF/anti-CCP autoantibodies, cytokine inflammation, pannus formation, erosions, deformity, and extra-articular lung, eye, vascular, and cardiovascular risk.

How Rheumatology assesses it: Assess symmetric small-joint pain/swelling, morning stiffness duration, MCP/PIP/wrist/MTP involvement, nodules, sicca, lung symptoms, smoking, infection risk, pregnancy plans, baseline function, erosive disease risk, and comorbid ASCVD/osteoporosis.

Diagnosis: Use joint exam with tender/swollen counts, ESR/CRP, RF, anti-CCP, CBC/CMP, hepatitis B/C and TB screening before biologics/JAK inhibitors, hand/foot X-rays or ultrasound/MRI for synovitis/erosions, and exclude mimics such as gout, CPPD, viral arthritis, psoriatic arthritis, and lupus.

First-line treatment: Start disease-modifying therapy early, usually methotrexate (Trexall/Rasuvo) with folic acid if no contraindication; NSAIDs such as naproxen (Aleve/Naprosyn) or short prednisone (Deltasone) bridge may reduce symptoms but should not replace DMARDs.

Second-line treatment: If not at target, add or switch conventional DMARDs hydroxychloroquine (Plaquenil), sulfasalazine (Azulfidine), leflunomide (Arava), or biologic/targeted therapy such as adalimumab (Humira), etanercept (Enbrel), abatacept (Orencia), tocilizumab (Actemra), rituximab (Rituxan), or upadacitinib (Rinvoq).

Third-line / advanced care: Rheumatology urgently for rapidly progressive erosive disease, vasculitis, ILD, scleritis, severe infection on immunosuppression, pregnancy medication planning, or refractory disease needing biologic/JAK strategy.

Progression and follow-up: Follow CDAI/DAS28 or tender/swollen joints, function, erosions, CBC/CMP with DMARDs, infection/vaccine status, lung symptoms, steroid exposure, osteoporosis, cardiovascular risk, and treat-to-target remission/low disease activity.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Systemic lupus erythematosus

Pathophysiology: Systemic lupus erythematosus is immune-complex and autoantibody-mediated multisystem disease affecting skin, joints, kidneys, blood, serosa, CNS, and pregnancy; complement activation and interferon pathways drive flares.

How Rheumatology assesses it: Assess photosensitive rash, oral/nasal ulcers, inflammatory arthritis, serositis, Raynaud, alopecia, fevers, cytopenia symptoms, renal edema/foamy urine, neurologic symptoms, thrombosis/pregnancy loss, medications, infection risk, pregnancy plans, and organ-threatening features.

Diagnosis: Use ANA as entry screen, anti-dsDNA, anti-Smith, complements C3/C4, CBC, CMP/creatinine, urinalysis with microscopy, urine protein-creatinine ratio, antiphospholipid antibodies, ESR/CRP pattern, pregnancy test when relevant, and kidney biopsy for suspected lupus nephritis with significant proteinuria/active sediment.

First-line treatment: Hydroxychloroquine (Plaquenil) is foundational unless contraindicated, with eye screening. Use sun protection, vaccines, cardiovascular risk control, topical steroids/calcineurin inhibitors for skin, NSAIDs cautiously, and short glucocorticoid courses only when needed.

Second-line treatment: Organ-specific steroid-sparing therapy may include methotrexate (Trexall), azathioprine (Imuran), mycophenolate mofetil (CellCept/Myfortic), belimumab (Benlysta), anifrolumab (Saphnelo), or voclosporin (Lupkynis) in lupus nephritis regimens with nephrology/rheumatology guidance.

Third-line / advanced care: Urgent admission/specialty care for nephritis, CNS lupus, alveolar hemorrhage, myocarditis, severe cytopenias, catastrophic antiphospholipid syndrome, pregnancy flare, or severe infection; high-dose steroids, cyclophosphamide (Cytoxan), rituximab, plasma exchange, or anticoagulation may be needed by syndrome.

Progression and follow-up: Follow disease activity, complements/dsDNA, CBC/CMP, urine protein/sediment, BP, hydroxychloroquine retinal toxicity, steroid burden, infection, thrombosis, pregnancy outcomes, CKD, and damage accrual.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Gout urate-lowering strategy

Pathophysiology: Monosodium urate crystal deposition triggers neutrophilic synovitis and recurrent inflammatory arthritis; chronic hyperuricemia can form tophi and kidney stones.

How Rheumatology assesses it: Assess joint pattern, tophi, kidney disease, diuretics, alcohol/fructose, urate level timing, fever/septic arthritis risk, and medication contraindications.

Diagnosis: Joint aspiration with crystal analysis is most specific; use serum uric acid, CBC/CRP/ESR, renal function, X-ray or ultrasound/dual-energy CT for chronic or uncertain disease, and culture if infection is possible.

First-line treatment: Acute flare: NSAID such as naproxen (Aleve/Naprosyn) or indomethacin (Indocin), colchicine (Colcrys/Mitigare), or prednisone (Deltasone). Long-term urate lowering: allopurinol (Zyloprim/Aloprim) with flare prophylaxis when indicated.

Second-line treatment: Febuxostat (Uloric) when allopurinol is unsuitable, probenecid (Probalan) for selected underexcretion with adequate kidney function, and intra-articular steroid injection for monoarticular flares.

Third-line / advanced care: Rheumatology for refractory/tophaceous gout, pegloticase (Krystexxa), complex CKD/transplant drug interactions, or diagnostic uncertainty.

Progression and follow-up: Recurrent flares can progress to erosive arthritis, tophi, disability, uric acid nephrolithiasis, and medication toxicity.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Pseudogout

Pathophysiology: Monosodium urate crystal deposition triggers neutrophilic synovitis and recurrent inflammatory arthritis; chronic hyperuricemia can form tophi and kidney stones.

How Rheumatology assesses it: Assess joint pattern, tophi, kidney disease, diuretics, alcohol/fructose, urate level timing, fever/septic arthritis risk, and medication contraindications.

Diagnosis: Joint aspiration with crystal analysis is most specific; use serum uric acid, CBC/CRP/ESR, renal function, X-ray or ultrasound/dual-energy CT for chronic or uncertain disease, and culture if infection is possible.

First-line treatment: Acute flare: NSAID such as naproxen (Aleve/Naprosyn) or indomethacin (Indocin), colchicine (Colcrys/Mitigare), or prednisone (Deltasone). Long-term urate lowering: allopurinol (Zyloprim/Aloprim) with flare prophylaxis when indicated.

Second-line treatment: Febuxostat (Uloric) when allopurinol is unsuitable, probenecid (Probalan) for selected underexcretion with adequate kidney function, and intra-articular steroid injection for monoarticular flares.

Third-line / advanced care: Rheumatology for refractory/tophaceous gout, pegloticase (Krystexxa), complex CKD/transplant drug interactions, or diagnostic uncertainty.

Progression and follow-up: Recurrent flares can progress to erosive arthritis, tophi, disability, uric acid nephrolithiasis, and medication toxicity.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Polymyalgia rheumatica

Pathophysiology: Polymyalgia rheumatica is inflammatory pain and stiffness of shoulder and hip girdles in adults over 50, likely related to innate immune activation and overlapping large-vessel vasculitis biology with giant cell arteritis.

How Rheumatology assesses it: Assess bilateral shoulder/hip aching, morning stiffness, difficulty rising or lifting arms, constitutional symptoms, age over 50, true weakness versus pain inhibition, peripheral synovitis, GCA symptoms such as headache/jaw claudication/vision change, and mimics including RA, statin myopathy, hypothyroid, malignancy, infection.

Diagnosis: Use ESR/CRP, CBC/CMP, CK to exclude myositis/statin myopathy, TSH when indicated, RF/anti-CCP if RA mimic, and ultrasound shoulders/hips for bursitis/tenosynovitis when uncertain. Rapid glucocorticoid response supports but does not prove diagnosis.

First-line treatment: Prednisone (Deltasone) low-to-moderate dose with gradual taper is standard; add calcium/vitamin D, osteoporosis risk assessment, bisphosphonate such as alendronate (Fosamax) when indicated, exercise/physical therapy, and monitor glucose/BP.

Second-line treatment: Relapsing or steroid-toxic disease may use methotrexate (Trexall) or IL-6 inhibition such as tocilizumab (Actemra) or sarilumab (Kevzara) in selected cases with rheumatology guidance.

Third-line / advanced care: Immediate high-dose steroid/urgent evaluation if any GCA symptoms occur; rheumatology referral for atypical features, poor steroid response, relapse, very high inflammatory markers, or steroid complications.

Progression and follow-up: Follow pain/stiffness, ESR/CRP, prednisone adverse effects, osteoporosis, diabetes/hypertension, occult GCA, relapse during taper, and functional recovery.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Giant cell arteritis

Pathophysiology: Giant cell arteritis is granulomatous large- and medium-vessel vasculitis in adults over 50, affecting extracranial carotid branches and aorta; ischemia can cause irreversible vision loss, stroke, jaw claudication, and aortic aneurysm.

How Rheumatology assesses it: Assess new headache/scalp tenderness, jaw or tongue claudication, transient or permanent vision symptoms, diplopia, constitutional symptoms, PMR symptoms, limb claudication, bruits, pulse/BP asymmetry, neurologic symptoms, and infection/malignancy mimics.

Diagnosis: Check ESR/CRP, CBC/platelets, CMP; do not delay treatment for testing when suspected. Confirm with temporal artery ultrasound/biopsy and/or large-vessel imaging CTA/MRA/PET-CT depending on phenotype and local expertise; ophthalmology exam for visual symptoms.

First-line treatment: Start high-dose glucocorticoids immediately when GCA suspected: prednisone (Deltasone) for no visual symptoms or IV methylprednisolone (Solu-Medrol) for threatened/established vision loss per protocol; add gastric/bone/PJP risk planning as appropriate.

Second-line treatment: Tocilizumab (Actemra) can reduce relapse and steroid exposure in selected patients; methotrexate may be considered when IL-6 therapy unsuitable. Use aspirin only for selected vascular indications after bleeding risk review.

Third-line / advanced care: Emergency ophthalmology/rheumatology/ED for visual symptoms, stroke/TIA, aortic dissection symptoms, limb ischemia, or diagnostic uncertainty with high risk; monitor for large-vessel involvement and aneurysm.

Progression and follow-up: Follow vision, headache/jaw symptoms, ESR/CRP with clinical context, steroid toxicity, infection, aortic aneurysm/dissection surveillance, relapse, and IL-6 inhibitor masking of CRP.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Ankylosing spondylitis

Pathophysiology: Ankylosing spondylitis or radiographic axial spondyloarthritis is inflammatory sacroiliac/spinal disease driven by IL-17/IL-23/TNF pathways, enthesitis, new bone formation, uveitis, IBD, psoriasis, and HLA-B27 association.

How Rheumatology assesses it: Assess inflammatory back pain before age 45, morning stiffness improving with exercise, alternating buttock pain, nocturnal pain, enthesitis, dactylitis, uveitis, psoriasis, IBD symptoms, family history, smoking, function, posture, and infection risk before biologics.

Diagnosis: Use pelvic X-ray for sacroiliitis, MRI SI joints/spine for nonradiographic disease or early inflammation, CRP/ESR, HLA-B27 when diagnosis uncertain, and screen TB/hepatitis before biologic therapy. Avoid overdiagnosis from nonspecific back pain without SpA features.

First-line treatment: Daily exercise/posture PT and NSAID trial such as naproxen (Aleve/Naprosyn), celecoxib (Celebrex), or indomethacin (Indocin) if safe; smoking cessation and osteoporosis/fall prevention.

Second-line treatment: Active disease despite NSAIDs uses biologics: TNF inhibitors adalimumab (Humira), etanercept (Enbrel), infliximab (Remicade), certolizumab (Cimzia), golimumab (Simponi), IL-17 inhibitors secukinumab (Cosentyx) or ixekizumab (Taltz), or JAK inhibitor upadacitinib (Rinvoq) in selected patients.

Third-line / advanced care: Rheumatology for biologic selection, recurrent uveitis needing ophthalmology, IBD coordination, severe hip disease, spinal fracture/neurologic symptoms, pregnancy planning, or refractory disease.

Progression and follow-up: Follow BASDAI/ASDAS or function, spinal mobility, uveitis, IBD/psoriasis, infections, TB/hepatitis screening, radiographic progression, osteoporosis/fracture, and cardiovascular risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Psoriatic arthritis

Pathophysiology: Psoriatic arthritis is heterogeneous inflammatory arthritis linked to psoriasis, nail disease, enthesitis, dactylitis, axial disease, and IL-23/IL-17/TNF pathways; untreated disease can erode joints and impair function.

How Rheumatology assesses it: Assess psoriasis/nail pitting/onycholysis, peripheral joint pattern, dactylitis, enthesitis heel pain, inflammatory back pain, uveitis, IBD, metabolic syndrome, depression, infection risk, pregnancy plans, and prior biologic exposure.

Diagnosis: Clinical diagnosis supported by inflammatory exam, ESR/CRP, X-ray/ultrasound/MRI for erosions/enthesitis/sacroiliitis, RF/anti-CCP to distinguish RA overlap, and skin/nail exam. Screen TB/hepatitis before biologics/JAK inhibitors.

First-line treatment: NSAIDs such as naproxen for mild symptoms, local steroid injections, topical psoriasis therapy, and conventional DMARD methotrexate (Trexall) for peripheral arthritis/skin when appropriate.

Second-line treatment: Moderate-severe or domain-specific disease uses biologics/targeted therapy: TNF inhibitors adalimumab (Humira), etanercept (Enbrel), IL-17 inhibitors secukinumab (Cosentyx)/ixekizumab (Taltz), IL-23 inhibitors guselkumab (Tremfya)/risankizumab (Skyrizi), ustekinumab (Stelara), apremilast (Otezla), or JAK inhibitors such as upadacitinib (Rinvoq) by phenotype.

Third-line / advanced care: Rheumatology/dermatology co-management for erosive disease, axial disease, severe skin/nail disease, IBD/uveitis, biologic failure, pregnancy, or high infection risk.

Progression and follow-up: Follow joint counts, dactylitis/enthesitis, skin/nails, function, radiographic damage, metabolic risk, depression, infection, medication labs, and treat-to-target response.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Scleroderma

Pathophysiology: Systemic sclerosis is autoimmune vasculopathy and fibrosis causing Raynaud, skin thickening, digital ischemia, GI dysmotility, interstitial lung disease, pulmonary arterial hypertension, renal crisis, and cardiac involvement.

How Rheumatology assesses it: Assess Raynaud onset, puffy fingers/sclerodactyly, digital ulcers, telangiectasias, calcinosis, reflux/dysphagia, dyspnea/cough, BP, renal symptoms, chest pain/palpitations, skin score, tendon friction rubs, and RNA polymerase III risk.

Diagnosis: Use ANA with centromere, topoisomerase I/Scl-70, RNA polymerase III antibodies, nailfold capillaroscopy, baseline PFTs with DLCO, high-resolution CT chest when ILD suspected/high risk, echocardiogram/NT-proBNP for PAH screening, CMP/creatinine/urinalysis, BP monitoring, and GI testing by symptoms.

First-line treatment: Raynaud care includes cold avoidance, smoking cessation, calcium-channel blocker nifedipine ER (Procardia XL) or amlodipine (Norvasc), PPI such as omeprazole (Prilosec) for reflux, vaccines, and regular lung/PAH/renal surveillance.

Second-line treatment: ILD may use mycophenolate mofetil (CellCept), cyclophosphamide (Cytoxan), rituximab (Rituxan), tocilizumab (Actemra), or antifibrotic nintedanib (Ofev) in selected progressive fibrosing disease. Digital ulcers may need PDE-5 inhibitor sildenafil (Revatio) or prostacyclin therapy.

Third-line / advanced care: Scleroderma renal crisis needs immediate ACE inhibitor such as captopril even in renal dysfunction and urgent nephrology; pulmonary hypertension center for PAH; rheumatology for all systemic disease, ILD progression, severe GI dysmotility, or digital ischemia.

Progression and follow-up: Follow modified Rodnan skin score, BP/creatinine, PFT/DLCO, HRCT, echo/NT-proBNP, digital ulcers, reflux/aspiration, malnutrition, arrhythmia, renal crisis, and medication toxicity.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Sjogren syndrome

Pathophysiology: Sjogren syndrome is autoimmune exocrinopathy with lymphocytic salivary/lacrimal gland injury causing sicca symptoms, systemic fatigue/arthralgia/neuropathy/ILD/renal tubular acidosis, and increased lymphoma risk.

How Rheumatology assesses it: Assess dry eyes/mouth, dental caries, parotid swelling, dysphagia, vaginal dryness, fatigue, arthralgia, Raynaud, neuropathy, purpura, cough/dyspnea, kidney stones/acidosis symptoms, medications with anticholinergic effects, hepatitis C/HIV risk, and lymphoma red flags.

Diagnosis: Use ANA, SSA/Ro, SSB/La, RF, ESR/CRP, CBC/CMP, urinalysis, complements, SPEP when systemic/lymphoma concern; objective dryness tests include Schirmer, ocular staining, unstimulated salivary flow, and minor salivary gland biopsy when serology is negative but suspicion remains.

First-line treatment: Symptom care: preservative-free artificial tears, ocular lubricants, topical cyclosporine (Restasis) or lifitegrast (Xiidra) with ophthalmology, saliva substitutes, sugar-free lozenges, fluoride dental care, hydration, and avoid anticholinergic drugs when possible.

Second-line treatment: Secretagogues pilocarpine (Salagen) or cevimeline (Evoxac) for xerostomia when safe; hydroxychloroquine (Plaquenil) may help inflammatory arthralgia/fatigue in selected patients; systemic organ disease needs targeted immunosuppression.

Third-line / advanced care: Rheumatology/ophthalmology/dentistry for systemic disease, corneal damage, recurrent parotid swelling, vasculitis, neuropathy, ILD, renal disease, cryoglobulinemia, low complements, monoclonal gammopathy, or lymphoma concern.

Progression and follow-up: Follow ocular surface, dental decay, salivary gland swelling, CBC/complements/SPEP if high risk, neuropathy/ILD/renal features, fatigue/function, medication dryness burden, and lymphoma warning signs.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Vasculitis initial evaluation

Pathophysiology: Vasculitis is vessel-wall inflammation causing ischemia, hemorrhage, aneurysm, thrombosis, or organ damage; classification depends on vessel size, ANCA/immune-complex biology, infection/drug triggers, and organ pattern.

How Rheumatology assesses it: Assess constitutional symptoms, palpable purpura, ulcers, mononeuritis multiplex, sinus/otitis, hemoptysis/dyspnea, renal hematuria/proteinuria, abdominal pain, testicular pain, ocular inflammation, headache/jaw claudication, limb claudication, drug/infection exposure, hepatitis/HIV risk, and cancer clues.

Diagnosis: Use CBC/CMP/creatinine, urinalysis microscopy and protein-creatinine ratio, ESR/CRP, ANCA PR3/MPO, complements, ANA, cryoglobulins, hepatitis B/C/HIV, blood cultures when infection possible, chest imaging, CTA/MRA/PET for large vessels, EMG/nerve studies, and tissue biopsy of involved organ/skin/kidney/artery when feasible.

First-line treatment: Do not give chronic immunosuppression before excluding infection/malignancy when stable, but organ- or life-threatening disease needs urgent glucocorticoids after key cultures/biopsy planning. Supportive care includes BP/renal protection, vaccines, PJP prophylaxis when high-dose immunosuppression is used.

Second-line treatment: Induction depends on subtype/severity: rituximab (Rituxan) or cyclophosphamide (Cytoxan) for severe ANCA vasculitis, glucocorticoids plus tocilizumab (Actemra) for selected GCA, antiviral therapy for HBV/HCV-associated disease, or colchicine/dapsone for limited cutaneous disease by diagnosis.

Third-line / advanced care: Urgent rheumatology/nephrology/pulmonology/neurology for pulmonary-renal syndrome, rapidly progressive GN, alveolar hemorrhage, CNS disease, mesenteric ischemia, vision symptoms, mononeuritis multiplex, digital ischemia, or suspected infection mimicking vasculitis.

Progression and follow-up: Follow organ-specific activity, creatinine/urine, pulmonary symptoms, neuropathy, skin lesions, ESR/CRP with caution, ANCA trends only as adjunct, infection, cytopenias, infertility/bladder risk with cyclophosphamide, relapse, and damage accrual.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Fibromyalgia

Pathophysiology: Fibromyalgia is chronic nociplastic pain with central sensitization, altered pain processing, sleep disturbance, fatigue, cognitive symptoms, autonomic sensitivity, and frequent overlap with migraine, IBS, mood disorders, hypermobility, and trauma history.

How Rheumatology assesses it: Assess widespread pain index/symptom severity, sleep quality, fatigue, cognitive fog, exercise tolerance, mood/PTSD, medication/substance use, hypermobility, headaches/IBS, red flags for inflammatory, neurologic, endocrine, or malignant disease, and patient goals.

Diagnosis: Clinical diagnosis using ACR-style widespread pain/symptom criteria; limited labs such as CBC, CMP, TSH, ESR/CRP, CK, B12/vitamin D only when history/exam suggests mimics. Avoid repeated broad autoimmune testing when exam lacks inflammatory features.

First-line treatment: Education that pain is real and nervous-system mediated, graded low-impact exercise, sleep regularity, CBT/ACT or trauma-informed therapy when helpful, pacing, and treatment of comorbid mood/sleep disorders.

Second-line treatment: Medications may include duloxetine (Cymbalta), milnacipran (Savella), pregabalin (Lyrica), low-dose amitriptyline (Elavil), or cyclobenzaprine (Flexeril) at night in selected patients; avoid chronic opioids and routine steroids.

Third-line / advanced care: Refer rheumatology only for diagnostic uncertainty/inflammatory signs; pain rehab, sleep medicine, psychiatry/psychology, PT, or PM&R for severe disability, opioid taper complexity, refractory insomnia, or functional restoration.

Progression and follow-up: Follow function, sleep, activity tolerance, flares, mood/suicidality, medication sedation/weight gain/BP, opioid exposure, work accommodations, and avoidance of low-value testing/procedures.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Myositis

Pathophysiology: Idiopathic inflammatory myopathies include dermatomyositis, polymyositis, immune-mediated necrotizing myopathy, antisynthetase syndrome, and inclusion body myositis, causing muscle inflammation/necrosis plus skin, lung, cardiac, swallowing, and malignancy associations by subtype.

How Rheumatology assesses it: Assess proximal weakness more than pain, dysphagia, dyspnea/cough, mechanic hands, Raynaud, arthritis, Gottron papules, heliotrope rash, statin exposure, cancer symptoms, falls, respiratory weakness, and rapid progression.

Diagnosis: Use CK, aldolase, AST/ALT/LDH, ESR/CRP, myositis antibody panel such as Jo-1/Mi-2/MDA5/TIF1-gamma/SRP/HMGCR, ANA, EMG, MRI muscle, muscle biopsy when needed, PFT/HRCT for ILD risk, ECG/troponin/echo for cardiac concern, and age-appropriate malignancy screening especially dermatomyositis/TIF1-gamma.

First-line treatment: High-dose glucocorticoids such as prednisone (Deltasone) are typical initial therapy for significant inflammatory myositis, paired early with steroid-sparing methotrexate (Trexall), azathioprine (Imuran), or mycophenolate (CellCept) depending on lung/liver/pregnancy factors; PT preserves function.

Second-line treatment: IVIG (Privigen/Gamunex), rituximab (Rituxan), tacrolimus, cyclophosphamide, or JAK inhibitors in selected refractory or antibody-defined disease; inclusion body myositis emphasizes rehab, fall prevention, dysphagia care, and assistive devices because immunotherapy response is limited.

Third-line / advanced care: Urgent care for respiratory weakness, rapidly progressive ILD especially MDA5 disease, severe dysphagia/aspiration, myocarditis/arrhythmia, rhabdomyolysis-level CK/AKI, or malignancy concern; co-manage pulmonology/neurology/oncology.

Progression and follow-up: Follow strength/function, CK/aldolase, swallowing, PFT/HRCT, cardiac signs, steroid/DMARD toxicity, falls, cancer surveillance, calcinosis, and ILD progression.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Rheumatology

Raynaud phenomenon

Pathophysiology: Raynaud phenomenon is episodic digital vasospasm causing triphasic or biphasic color change, numbness, and pain; primary Raynaud is benign, while secondary Raynaud from systemic sclerosis, lupus, myositis, vasculitis, antiphospholipid syndrome, drugs, vibration, or occlusive disease can ulcerate or cause ischemia.

How Rheumatology assesses it: Assess age at onset, symmetry, thumb involvement, ulcers/pitting, severe pain, tissue loss, systemic sclerosis signs, inflammatory arthritis, rash, dyspnea, dysphagia/reflux, migraine/vasospastic meds, stimulants, beta blockers, smoking, occupational vibration, and cold exposure.

Diagnosis: Clinical pattern plus nailfold capillaroscopy when available; test ANA with reflex ENA/scleroderma antibodies, ESR/CRP, CBC/CMP/urinalysis, TSH when suggested, antiphospholipid testing if thrombosis/pregnancy loss, and vascular studies if asymmetric pulses, ulcers, or macrovascular disease suspected.

First-line treatment: Cold protection, layered gloves, hand warmers, smoking cessation, avoid vasoconstrictors/stimulants when possible, stress management, and calcium-channel blocker nifedipine ER (Procardia XL) or amlodipine (Norvasc) for frequent or painful attacks.

Second-line treatment: Refractory or digital ulcer disease may use PDE-5 inhibitor sildenafil (Revatio/Viagra) or tadalafil (Cialis), topical nitroglycerin, losartan, fluoxetine, or prostacyclin infusion such as epoprostenol/iloprost where available under specialist care.

Third-line / advanced care: Urgent vascular/rheumatology evaluation for digital ulcer, critical ischemia, gangrene, severe asymmetric attacks, suspected systemic sclerosis, or new adult-onset Raynaud with abnormal nailfold/autoantibodies.

Progression and follow-up: Follow attack frequency, ulcers/pitting, BP/headache/edema from vasodilators, smoking status, autoantibody evolution, systemic sclerosis organ screening, and tissue loss.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Specialty role

Allergic disease, asthma overlap, immune deficiency, anaphylaxis, food/drug allergy, and immunotherapy.

Allergy and Immunology

Anaphylaxis aftercare

Pathophysiology: Anaphylaxis is acute systemic mast-cell/basophil mediator release that can cause airway edema, bronchospasm, vasodilation, shock, GI symptoms, urticaria/angioedema, and biphasic recurrence after apparent recovery.

How Allergy and Immunology assesses it: Assess trigger timing, foods, drugs, venom, latex, exercise/cofactors, asthma, mast-cell disease, hypotension/airway symptoms, epinephrine timing/number of doses, ED observation course, beta blocker/ACE inhibitor use, pregnancy, and access to autoinjectors.

Diagnosis: Clinical diagnosis is based on multisystem acute reaction; obtain acute serum tryptase ideally 1-4 hours after onset and baseline tryptase later when severe, hypotensive, idiopathic, or venom-related. Use targeted skin testing/specific IgE or supervised challenge later, not broad panels.

First-line treatment: Discharge planning includes two epinephrine autoinjectors such as EpiPen, Auvi-Q, or generic epinephrine, written action plan, trigger avoidance, technique teaching, medical alert identification, and asthma control. Antihistamines such as cetirizine (Zyrtec) treat hives but do not replace epinephrine.

Second-line treatment: Allergist evaluation for trigger confirmation, food/drug/venom testing, cofactor counseling, and immunotherapy/desensitization when appropriate; review need for glucagon if on beta blocker and emergency plan for future reactions.

Third-line / advanced care: Urgent re-evaluation for recurrent symptoms, airway compromise, hypotension, multiple epinephrine doses, severe asthma, pregnancy, or unclear idiopathic episodes; evaluate mastocytosis or hereditary alpha-tryptasemia if baseline tryptase is persistently high.

Progression and follow-up: Follow epinephrine carriage/use, recurrence, trigger labeling, school/work plans, asthma control, anxiety/avoidance burden, biphasic reactions, and allergy documentation accuracy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Food allergy evaluation

Pathophysiology: Food allergy evaluation separates IgE-mediated immediate allergy, pollen-food allergy syndrome, food-dependent exercise-induced anaphylaxis, non-IgE disease, intolerance, and sensitization without clinical allergy.

How Allergy and Immunology assesses it: Assess exact food, amount, preparation, timing, reproducibility, hives/angioedema/wheeze/vomiting/hypotension, cofactors such as exercise/NSAIDs/alcohol, tolerated forms, atopic disease, infant eczema, nutritional impact, and prior epinephrine use.

Diagnosis: Testing must follow history: skin prick test or serum specific IgE/component testing such as peanut Ara h 2 can support IgE allergy but does not diagnose allergy alone. Oral food challenge is the diagnostic standard when risk is acceptable. Avoid broad food IgG panels.

First-line treatment: For confirmed IgE food allergy: strict targeted avoidance, epinephrine autoinjectors, label reading, cross-contact counseling, school/work plan, nutrition support, and treatment of accidental reactions with epinephrine for systemic symptoms.

Second-line treatment: Selected patients may consider oral immunotherapy such as peanut allergen powder (Palforzia) or supervised food ladder/baked milk/egg approaches when appropriate; manage eczema/asthma because uncontrolled asthma increases reaction risk.

Third-line / advanced care: Allergy referral for anaphylaxis, multiple-food restriction, uncertain diagnosis, infant high-risk peanut introduction, occupational food exposure, eosinophilic GI symptoms, or oral challenge/immunotherapy decisions.

Progression and follow-up: Follow reaction frequency, epinephrine use, nutrition/growth, anxiety, asthma control, tolerance development, test trends only when clinically useful, and accidental exposure planning.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Drug allergy delabeling

Pathophysiology: Drug allergy delabeling identifies patients whose antibiotic or medication allergy label reflects side effect, viral exanthem, remote benign rash, or resolved sensitivity rather than persistent immune allergy; inaccurate labels worsen antimicrobial choice and outcomes.

How Allergy and Immunology assesses it: Document drug, indication, age/time since reaction, timing after dose, symptoms, treatment, hospitalization, mucosal lesions, blistering/skin pain, organ injury, hypotension/bronchospasm, tolerated related drugs, and current need for beta-lactam or other culprit class.

Diagnosis: Risk-stratify: low-risk penicillin histories may undergo direct oral amoxicillin challenge; moderate-risk immediate reactions may use penicillin skin testing then challenge. Avoid challenge/desensitization shortcuts for SJS/TEN, DRESS, AGEP, serum sickness-like severe reactions, hepatitis, nephritis, hemolytic anemia, or severe mucosal disease.

First-line treatment: Low-risk delabeling uses supervised oral challenge with observation, then exact EHR allergy update listing tolerated amoxicillin/penicillin or cephalosporins such as cefazolin (Ancef) or cephalexin (Keflex). Educate patient that side effect is not allergy.

Second-line treatment: If true allergy persists but a drug is needed, choose alternatives by infection/susceptibility or perform desensitization in monitored setting for time-limited need, such as penicillin in pregnancy syphilis or selected chemotherapy/biologic reactions.

Third-line / advanced care: Allergy specialist for high-risk history, perioperative cefazolin need, multiple drug labels, complex antibiotic resistance, pregnancy, cystic fibrosis, mast-cell disease, or need for desensitization/challenge to non-beta-lactam drugs.

Progression and follow-up: Follow delabeling durability, future beta-lactam tolerance, antibiotic stewardship, EHR accuracy, severe-reaction avoidance, and patient confidence using formerly labeled drugs.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Allergic rhinitis immunotherapy

Pathophysiology: Allergic rhinitis is IgE-mediated nasal and ocular inflammation from aeroallergens such as pollen, dust mite, animals, molds, or cockroach; immunotherapy induces immune tolerance and can reduce symptoms/medication needs over time.

How Allergy and Immunology assesses it: Assess seasonal/perennial pattern, triggers, nasal obstruction, conjunctivitis, asthma control, sinusitis/otitis, sleep/work impairment, medication response, beta blocker use, pregnancy, adherence ability, and whether symptoms match candidate allergens.

Diagnosis: Confirm clinically relevant sensitization with skin prick testing or serum specific IgE matched to exposure history. Spirometry/asthma assessment is needed before immunotherapy in asthma patients; uncontrolled asthma is a major risk factor for systemic reactions.

First-line treatment: Optimize avoidance and pharmacotherapy first: intranasal corticosteroid fluticasone (Flonase), budesonide (Rhinocort), or mometasone (Nasonex), intranasal antihistamine azelastine (Astelin/Astepro), oral antihistamine cetirizine (Zyrtec) or fexofenadine (Allegra), saline irrigation, and eye drops such as olopatadine (Pataday).

Second-line treatment: Subcutaneous immunotherapy or FDA-approved sublingual tablets such as grass pollen (Oralair/Grastek), ragweed (Ragwitek), or dust mite (Odactra) are options when symptoms remain significant and sensitization is relevant; prescribe epinephrine for SLIT per protocol.

Third-line / advanced care: Allergy supervision is required for SCIT build-up/maintenance, systemic reaction management, venom/asthma overlap, pregnancy continuation decisions, beta blocker/ACE inhibitor complexity, or severe uncontrolled asthma.

Progression and follow-up: Follow symptom-medication scores, asthma control, systemic/local reactions, adherence over 3-5 years, anaphylaxis preparedness, and whether allergen selection matches exposure.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Chronic urticaria

Pathophysiology: Urticaria is mast-cell mediator release causing transient pruritic wheals, angioedema, or both; acute disease is often infection, food, medication, venom, or idiopathic, while chronic spontaneous urticaria is usually autoimmune/idiopathic rather than allergic.

How Allergy and Immunology assesses it: Assess duration under or over 6 weeks, individual lesion duration under 24 hours, angioedema, anaphylaxis symptoms, NSAIDs/opioids/ACE inhibitors, inducible triggers such as cold/pressure/heat/exercise, infections, autoimmune thyroid disease symptoms, pregnancy, and quality-of-life/sleep impact.

Diagnosis: Clinical diagnosis. No broad allergy panel is needed for chronic spontaneous urticaria without a clear trigger. Use CBC/ESR/CRP/TSH only when history suggests systemic disease; biopsy lesions lasting over 24 hours, painful/bruising, purpuric, or leaving hyperpigmentation to evaluate urticarial vasculitis.

First-line treatment: Second-generation H1 antihistamines are first-line: cetirizine (Zyrtec), levocetirizine (Xyzal), fexofenadine (Allegra), loratadine (Claritin), or desloratadine (Clarinex); avoid triggers and treat anaphylaxis with epinephrine autoinjector (EpiPen/Auvi-Q) when systemic symptoms occur.

Second-line treatment: If chronic symptoms persist, increase second-generation antihistamine dose up to guideline-supported higher dosing under clinician guidance; add short steroid burst only for severe flares, and consider H2 blocker or leukotriene receptor antagonist montelukast (Singulair) selectively.

Third-line / advanced care: Allergy/dermatology for omalizumab (Xolair), cyclosporine (Neoral) in refractory cases, recurrent angioedema without hives needing C4/C1 inhibitor evaluation, cold urticaria with systemic reactions, or suspected urticarial vasculitis.

Progression and follow-up: Follow wheal/angioedema frequency, sleep, sedation, anaphylaxis risk, NSAID/ACE inhibitor triggers, steroid overuse, omalizumab response, autoimmune clues, and impact on school/work.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Angioedema

Pathophysiology: Angioedema is deep dermal/submucosal swelling. Histamine-mediated angioedema often has urticaria/anaphylaxis; bradykinin-mediated angioedema from ACE inhibitors or C1-inhibitor deficiency lacks hives and can threaten airway or cause abdominal attacks.

How Allergy and Immunology assesses it: Assess airway/tongue/larynx, abdominal pain, urticaria/itching, hypotension/wheeze, ACE inhibitor/ARB/neprilysin/DPP-4 inhibitor use, estrogen exposure, family history, recurrent episodes, trauma/dental triggers, age at onset, and response to epinephrine/antihistamines.

Diagnosis: Airway first. If recurrent angioedema without hives, check C4, C1 inhibitor antigen and function, and C1q for acquired forms; tryptase when anaphylaxis suspected; medication review for ACE inhibitor angioedema; imaging only for severe abdominal attacks or alternative diagnosis.

First-line treatment: Histamine-mediated episodes: epinephrine for anaphylaxis, H1 antihistamine such as cetirizine/diphenhydramine, corticosteroid adjunct, and trigger avoidance. Stop ACE inhibitor permanently when suspected, even if symptoms resolve.

Second-line treatment: Hereditary angioedema acute attacks use C1 esterase inhibitor (Berinert/Ruconest), icatibant (Firazyr), or ecallantide (Kalbitor); prophylaxis may use lanadelumab (Takhzyro), berotralstat (Orladeyo), or C1 inhibitor (Haegarda/Cinryze) by specialist plan.

Third-line / advanced care: ED/ICU/ENT airway management for tongue/laryngeal involvement, voice change, stridor, progressive swelling, or failed outpatient rescue. Allergy/immunology for all suspected bradykinin-mediated, recurrent idiopathic, acquired C1 inhibitor deficiency, or HAE family screening.

Progression and follow-up: Follow airway episodes, abdominal attacks, medication triggers, C4/C1-INH results, rescue treatment access, prophylaxis response, family testing, estrogen sensitivity, and quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Primary immunodeficiency suspicion

Pathophysiology: Primary immunodeficiency or inborn errors of immunity include antibody, combined cellular, phagocyte, complement, immune dysregulation, and autoinflammatory disorders causing recurrent, severe, unusual, persistent infections, autoimmunity, lymphoproliferation, allergy, or malignancy.

How Allergy and Immunology assesses it: Assess infection type/site/frequency, need for IV antibiotics, opportunistic organisms, poor vaccine response, chronic diarrhea, failure to thrive, bronchiectasis, abscesses, delayed cord separation, autoimmunity, eczema, warts, family history, consanguinity, and secondary causes such as HIV, protein loss, medications, malignancy.

Diagnosis: Initial testing includes CBC with differential, quantitative IgG/IgA/IgM/IgE, vaccine antibody titers to tetanus/pneumococcus, lymphocyte subsets, HIV testing, complement CH50/AH50 when Neisseria or complement signs, neutrophil oxidative burst for CGD suspicion, and genetic testing guided by phenotype.

First-line treatment: Treat active infections aggressively, update non-live vaccines when safe, avoid live vaccines in suspected severe T-cell defects, optimize airway clearance for bronchiectasis, and document organism/culture history.

Second-line treatment: Antibody deficiency may need immunoglobulin replacement IVIG/SCIG such as Gamunex-C, Privigen, Hizentra, or Cuvitru; selected patients use prophylactic antibiotics such as azithromycin or TMP-SMX (Bactrim/Septra) by phenotype.

Third-line / advanced care: Immunology referral for abnormal screening, severe/opportunistic infection, bronchiectasis, family history, immune dysregulation, need for genetic diagnosis, immunoglobulin therapy, or hematopoietic stem-cell transplant/gene therapy consideration.

Progression and follow-up: Follow infection frequency, lung imaging/PFTs, immunoglobulin troughs, vaccine response, autoimmune cytopenias, lymphadenopathy/splenomegaly, malignancy, infusion reactions, and family counseling.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Eosinophilic esophagitis

Pathophysiology: Eosinophilic esophagitis is chronic type 2 antigen-driven esophageal inflammation causing eosinophilic infiltration, remodeling, rings, strictures, dysmotility, dysphagia, and food impaction.

How Allergy and Immunology assesses it: Assess solid-food dysphagia, food impaction, slow eating, food avoidance, heartburn refractory to PPI, atopic dermatitis/asthma/rhinitis/food allergy, growth in children, prior impactions/dilations, and alarm features.

Diagnosis: Upper endoscopy with esophageal biopsies from multiple levels is required; typical findings include rings, furrows, exudates, edema, strictures, but endoscopy can look normal. Diagnosis requires esophageal eosinophilia after excluding other causes; allergy testing does not reliably identify all food triggers.

First-line treatment: First-line options include high-dose proton pump inhibitor such as omeprazole (Prilosec) or pantoprazole (Protonix), swallowed topical steroid budesonide oral suspension/slurry or fluticasone swallowed from inhaler, or empiric elimination diet with dietitian support.

Second-line treatment: Dupilumab (Dupixent) is an option for selected refractory or multi-atopic EoE; endoscopic dilation treats fixed strictures/narrow-caliber esophagus but does not treat inflammation.

Third-line / advanced care: GI/allergy co-management for food impaction, severe stricture, failure of PPI/steroid/diet, pediatric growth issues, complex food allergy, or biologic therapy. Emergency endoscopy for acute impaction with inability to handle secretions.

Progression and follow-up: Follow dysphagia, impactions, endoscopic/histologic response, nutritional adequacy, candidiasis from steroids, stricture recurrence, dilation risk, and adherence to diet/medications.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Severe asthma biologic eligibility

Pathophysiology: Severe asthma biologic eligibility requires confirmed asthma uncontrolled despite optimized high-dose ICS/LABA and correction of modifiable factors, then matching biologic to allergic, eosinophilic, type 2-high, oral-steroid-dependent, or exacerbation-prone phenotype.

How Allergy and Immunology assesses it: Confirm diagnosis, adherence, inhaler technique, high-dose ICS/LABA use, exacerbations/steroid bursts, OCS dependence, ICU/intubation history, allergic rhinitis/nasal polyps, GERD/OSA/obesity, smoking/vaping, occupational exposure, aspirin-exacerbated disease, and contraindications.

Diagnosis: Use spirometry with bronchodilator response or variability, FeNO, blood eosinophils, total IgE, allergen sensitization by skin/specific IgE, CBC/CMP, chest imaging if atypical, and rule out vocal cord dysfunction, COPD, bronchiectasis, ABPA, EGPA, heart failure, and poor adherence before biologics.

First-line treatment: Optimize controller therapy first: high-dose ICS/LABA such as budesonide-formoterol (Symbicort/Breyna) or fluticasone-salmeterol (Advair/Wixela), SMART/MART when appropriate, albuterol (Ventolin) rescue, spacer, trigger control, vaccines, and comorbidity treatment.

Second-line treatment: Biologic selection: omalizumab (Xolair) for allergic asthma with IgE/weight dosing range; mepolizumab (Nucala), benralizumab (Fasenra), or reslizumab (Cinqair) for eosinophilic asthma; dupilumab (Dupixent) for eosinophilic/type 2 or OCS-dependent asthma and nasal polyps; tezepelumab (Tezspire) for severe asthma with recent exacerbations across phenotypes.

Third-line / advanced care: Allergy/pulmonology severe asthma clinic for biologic start/switch, persistent OCS need, frequent exacerbations, diagnostic uncertainty, ABPA/EGPA, pregnancy, or life-threatening attacks. ED/ICU for acute severe exacerbation with hypoxemia, exhaustion, or poor bronchodilator response.

Progression and follow-up: Follow ACT/ACQ, exacerbations, oral steroid exposure, FEV1, FeNO/eosinophils when useful, biologic response by 4-6 months, anaphylaxis/helminth risk, cost/adherence, and step-down opportunities.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Latex allergy

Pathophysiology: Latex allergy may be IgE-mediated immediate allergy to natural rubber latex proteins, irritant contact dermatitis, or allergic contact dermatitis to rubber additives; cross-reactive foods include banana, avocado, kiwi, chestnut, and others.

How Allergy and Immunology assesses it: Assess reactions to gloves/balloons/condoms/dental or surgical exposure, timing, urticaria/angioedema/wheeze/anaphylaxis, hand dermatitis, healthcare/spina bifida/occupational exposure, food cross-reactions, and upcoming procedures.

Diagnosis: Clinical history plus latex-specific IgE or skin testing where available and safe; patch testing evaluates delayed rubber additive dermatitis. Distinguish irritant dermatitis from IgE latex allergy because management and perioperative risk differ.

First-line treatment: Avoid natural rubber latex, use nitrile/vinyl alternatives, carry epinephrine if systemic IgE reactions occurred, and document latex allergy prominently before procedures/dental care. Treat dermatitis with barrier repair and topical corticosteroid such as triamcinolone (Kenalog) when needed.

Second-line treatment: Occupational health planning for healthcare/food-service exposures, workplace substitution, and education about hidden latex sources and cross-reactive foods when clinically relevant.

Third-line / advanced care: Allergy referral for diagnostic uncertainty, systemic reactions, perioperative planning, occupational disability, or anaphylaxis; emergency care for respiratory/cardiovascular symptoms after exposure.

Progression and follow-up: Follow accidental exposures, workplace controls, dermatitis, epinephrine access, surgical/dental precautions, and over-restriction from unconfirmed labels.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Venom allergy

Pathophysiology: Venom allergy is IgE-mediated reaction to Hymenoptera venom such as honeybee, yellow jacket, hornet, wasp, or fire ant, ranging from large local reactions to anaphylaxis; mast-cell disease increases severity risk.

How Allergy and Immunology assesses it: Assess insect identification, sting number, timing, cutaneous-only versus respiratory/cardiovascular/GI symptoms, hypotension/syncope, baseline tryptase risk, outdoor occupation/hobbies, beta blocker/ACE inhibitor use, and epinephrine treatment.

Diagnosis: For systemic reactions, test venom-specific IgE or skin testing after an appropriate interval, and obtain baseline serum tryptase when severe, hypotensive, or recurrent. Large local reactions usually do not require venom immunotherapy unless exceptional exposure/quality-of-life context.

First-line treatment: Provide epinephrine autoinjectors, sting avoidance education, medical alert identification, and treat acute reactions with epinephrine. Large local reactions use cold compresses, antihistamines, NSAIDs, and sometimes short prednisone (Deltasone) course.

Second-line treatment: Venom immunotherapy is highly effective for systemic venom allergy and is selected based on culprit venom testing and exposure risk; fire ant immunotherapy applies in endemic areas.

Third-line / advanced care: Allergy referral for all systemic sting reactions, venom immunotherapy, elevated baseline tryptase/mastocytosis evaluation, occupational high exposure, or recurrent reactions despite therapy.

Progression and follow-up: Follow field stings, epinephrine use, VIT systemic reactions, maintenance duration, quality of life, mast-cell disease evaluation, and continued emergency preparedness.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Allergy and Immunology

Mast cell activation concern

Pathophysiology: Mast-cell activation concern includes episodic mediator release causing flushing, urticaria, angioedema, hypotension, wheeze, GI cramping/diarrhea, and anaphylaxis-like symptoms; differential includes mastocytosis, hereditary alpha-tryptasemia, idiopathic anaphylaxis, carcinoid, pheochromocytoma, panic, and medication reactions.

How Allergy and Immunology assesses it: Assess reproducible episodes, objective signs, triggers, anaphylaxis criteria, flushing pattern, syncope/hypotension, GI symptoms, venom/drug/food reactions, urticaria pigmentosa, osteoporosis/fractures, family history, baseline tryptase, and response to antihistamines/epinephrine.

Diagnosis: Document event tryptase within 1-4 hours and compare with baseline using accepted rise formula; baseline tryptase, CBC/CMP, KIT D816V testing or hematology referral when systemic mastocytosis suspected, urine mediators only by specialist protocol, and targeted testing for mimics.

First-line treatment: Treat confirmed mediator symptoms with trigger avoidance, non-sedating H1 antihistamine such as cetirizine (Zyrtec), H2 blocker famotidine (Pepcid), leukotriene receptor antagonist montelukast (Singulair) when appropriate, cromolyn sodium (Gastrocrom) for GI symptoms, and epinephrine for anaphylaxis.

Second-line treatment: Omalizumab (Xolair) may help recurrent idiopathic anaphylaxis/mast-cell activation symptoms in selected cases; treat comorbid allergic disease and avoid unnecessary restrictive diets or unvalidated testing.

Third-line / advanced care: Allergy/immunology and hematology for recurrent anaphylaxis, elevated baseline tryptase, suspected systemic mastocytosis, severe venom reactions, osteoporosis with mast-cell signs, or unclear episodes with syncope/flushing.

Progression and follow-up: Follow objective event documentation, tryptase pattern, epinephrine use, medication response, bone health, clonal mast-cell markers, trigger burden, and anxiety from unexplained attacks.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Specialty role

Undifferentiated acute care, stabilization, time-sensitive diagnosis, resuscitation, disposition, and emergency procedures.

Emergency Medicine

Chest pain emergency rule-out

Pathophysiology: Emergency chest pain rule-out separates time-sensitive causes: STEMI/NSTEMI/unstable angina, aortic dissection, pulmonary embolism, tension pneumothorax, esophageal rupture, tamponade, myocarditis/pericarditis, pneumonia, and noncardiac pain. ACS results from plaque rupture, thrombosis, vasospasm, or supply-demand mismatch.

How Emergency Medicine assesses it: Triage immediately for airway/breathing/circulation, shock, hypoxia, active chest pain, radiation, diaphoresis, dyspnea, syncope, neurologic deficit, pulse/BP asymmetry, tearing back pain, pregnancy/postpartum status, cocaine/stimulants, anticoagulants, CAD/VTE/aortic risk, and HEART/EDACS elements.

Diagnosis: Obtain ECG within 10 minutes and repeat if symptoms persist, serial high-sensitivity troponins using validated 0/1-, 0/2-, or 0/3-hour pathway, chest X-ray when pulmonary/aortic causes possible, CBC/CMP, pregnancy test when relevant, D-dimer/CTPA only when PE probability supports it, CT angiography for dissection concern, and bedside echo for shock/tamponade/right-heart strain.

First-line treatment: If ACS is possible give chewable aspirin 162-325 mg (Bayer/Ecotrin) unless contraindicated, nitroglycerin (Nitrostat) for ischemic pain if BP/RV infarct/PDE-5 inhibitor status allow, oxygen only for hypoxemia, morphine/fentanyl selectively for refractory pain, and activate cath lab for STEMI or STEMI-equivalent ECG patterns.

Second-line treatment: NSTEMI/unstable angina care uses anticoagulation such as unfractionated heparin or enoxaparin (Lovenox), high-intensity atorvastatin (Lipitor) or rosuvastatin (Crestor), P2Y12 therapy clopidogrel (Plavix) or ticagrelor (Brilinta) when invasive strategy/bleeding risk is defined, and beta blocker such as metoprolol (Lopressor) only when no shock/HF/bradycardia.

Third-line / advanced care: Admit/observe for abnormal ECG/troponin, intermediate-high HEART/EDACS risk, recurrent pain, unstable vitals, suspected dissection/PE/pneumothorax/esophageal rupture, or inability to complete serial testing. Low-risk patients with negative serial troponins may discharge with clear return precautions and outpatient testing when indicated.

Progression and follow-up: Missed ACS can progress to MI, malignant arrhythmia, cardiogenic shock, heart failure, death, or recurrent ED visits; overtesting can cause radiation, contrast nephropathy, false positives, and unnecessary anticoagulation/catheterization.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Stroke alert

Pathophysiology: Stroke alert targets acute ischemic stroke from thromboembolism or large-vessel occlusion, intracerebral hemorrhage, subarachnoid hemorrhage, seizure mimic, migraine, hypoglycemia, intoxication, Bell palsy, and functional deficits; neuronal salvage is time dependent.

How Emergency Medicine assesses it: Record last-known-well, baseline function, anticoagulants/DOAC timing, BP/glucose, seizure at onset, trauma, headache, deficits by NIHSS, airway/swallow risk, pregnancy, recent surgery/bleeding, and goals of care while keeping door-to-imaging fast.

Diagnosis: Check point-of-care glucose immediately, noncontrast CT head to exclude hemorrhage, CT angiography head/neck for suspected LVO, CT perfusion or MRI diffusion/perfusion for selected extended-window cases, ECG/telemetry, CBC/CMP/coags/troponin when they do not delay treatment, and bedside swallow screen before oral intake.

First-line treatment: Eligible disabling ischemic stroke within treatment window receives IV thrombolytic therapy such as alteplase (Activase) or tenecteplase by local protocol after contraindication review and BP control. Use labetalol (Trandate) or nicardipine (Cardene) when BP must be lowered for thrombolysis.

Second-line treatment: Large-vessel occlusion may need mechanical thrombectomy up to 24 hours in selected imaging profiles. Hemorrhage care includes anticoagulant reversal such as idarucizumab (Praxbind) for dabigatran, andexanet alfa (Andexxa) or 4-factor PCC (Kcentra) for factor Xa inhibitors when appropriate, plus neurosurgery/neurocritical care.

Third-line / advanced care: Admit to stroke unit/ICU; transfer to thrombectomy center when indicated. Avoid routine aspirin until hemorrhage excluded and after thrombolysis waiting period. Manage fever, glucose extremes, aspiration, cerebral edema, seizures, and dysphagia.

Progression and follow-up: Follow neurologic worsening, hemorrhagic transformation, recurrent stroke, cerebral edema, aspiration pneumonia, DVT, dysphagia, delirium, functional recovery, rehab needs, and secondary prevention with antiplatelet/statin/anticoagulation when indicated.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Sepsis recognition

Pathophysiology: Sepsis is life-threatening organ dysfunction from dysregulated host response to infection; septic shock adds vasodilation, capillary leak, myocardial depression, mitochondrial dysfunction, and persistent hypoperfusion needing vasopressors.

How Emergency Medicine assesses it: Screen high-risk or acutely ill patients for fever/hypothermia, tachycardia, tachypnea, hypotension, altered mental status, hypoxia, oliguria, mottling, lactate risk, immunocompromise, indwelling devices, recent surgery, resistant organisms, and likely source such as lung, urine, abdomen, skin, CNS, line, or bone.

Diagnosis: Use lactate with repeat if elevated, blood cultures before antibiotics if this will not delay treatment, CBC/CMP/coags, urinalysis/culture, chest X-ray, source-specific CT/ultrasound, respiratory viral PCR when relevant, wound/CSF cultures when indicated, and reassess for noninfectious mimics such as PE, pancreatitis, adrenal crisis, anaphylaxis, or GI bleed.

First-line treatment: Begin resuscitation immediately: oxygen/airway support, balanced crystalloid such as lactated Ringer's for hypotension or lactate 4 mmol/L or higher, broad empiric antibiotics within 1 hour for septic shock/high-likelihood sepsis, and source control planning. Common ED broad regimens include piperacillin-tazobactam (Zosyn) or cefepime (Maxipime) plus vancomycin (Vancocin) when MRSA risk exists.

Second-line treatment: If hypotension persists after fluids, start norepinephrine (Levophed) to target MAP about 65 mm Hg; tailor antibiotics to source/resistance such as meropenem (Merrem) for ESBL risk, ceftriaxone (Rocephin) for selected community sources, metronidazole (Flagyl) for anaerobic abdominal coverage, or micafungin (Mycamine) for high-risk candidemia.

Third-line / advanced care: ICU/critical care for vasopressors, rising lactate, respiratory failure, severe organ dysfunction, need for drainage/surgery, meningitis, neutropenic fever, transplant/immunocompromise, or unclear source with shock. Reassess volume responsiveness dynamically and de-escalate antibiotics when cultures/diagnosis clarify.

Progression and follow-up: Track MAP, lactate clearance, urine output, mental status, oxygenation, creatinine, bilirubin, platelets, source control, antimicrobial toxicity, ARDS, AKI, DIC, delirium, limb ischemia, mortality, and post-sepsis cognitive/functional decline.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Anaphylaxis resuscitation

Pathophysiology: Anaphylaxis resuscitation treats abrupt mast-cell/basophil mediator release causing airway edema, bronchospasm, vasodilation, capillary leak, distributive shock, GI cramping/vomiting, urticaria, and possible biphasic recurrence.

How Emergency Medicine assesses it: Assess airway voice/stridor/tongue swelling, wheeze, oxygen saturation, BP/perfusion, GI symptoms, skin findings, trigger exposure, asthma, pregnancy, beta blocker use, number/timing of epinephrine doses, and whether symptoms meet anaphylaxis criteria even without hives.

Diagnosis: Diagnosis is clinical and treatment must not wait for labs. Obtain tryptase 1-4 hours after onset only after stabilization for severe/idiopathic/venom/mast-cell concern. Consider ECG, glucose, ABG/VBG, chest X-ray, or differential testing only when shock/respiratory mimic remains after resuscitation.

First-line treatment: Give intramuscular epinephrine promptly in the mid-anterolateral thigh, repeat every 5-15 minutes as needed. Place supine with legs elevated unless respiratory distress/vomiting/pregnancy requires positioning, give high-flow oxygen, large-bore IV access, rapid isotonic crystalloid boluses, and nebulized albuterol (Ventolin) for bronchospasm.

Second-line treatment: Adjuncts after epinephrine include H1 antihistamine diphenhydramine (Benadryl) or cetirizine (Zyrtec), H2 blocker famotidine (Pepcid), corticosteroid methylprednisolone (Solu-Medrol) or prednisone (Deltasone), and glucagon for refractory hypotension in beta-blocked patients; these do not replace epinephrine.

Third-line / advanced care: Refractory shock needs epinephrine infusion with continuous monitoring, airway expert/ENT/anesthesia for progressive upper-airway edema, vasopressors, ICU admission, and observation tailored to severity. Discharge only after stability with two epinephrine autoinjectors such as EpiPen/Auvi-Q, action plan, and allergy follow-up.

Progression and follow-up: Follow recurrent airway/shock symptoms, biphasic reaction risk, asthma control, trigger labeling, autoinjector access/technique, beta blocker/ACE inhibitor issues, and anxiety or avoidance after severe reaction.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Acute abdomen

Pathophysiology: Acute abdomen represents surgical, vascular, infectious, inflammatory, urinary, gynecologic, and metabolic emergencies including appendicitis, cholecystitis/cholangitis, pancreatitis, bowel obstruction/perforation/ischemia, diverticulitis, ruptured AAA, ectopic pregnancy, torsion, PID/TOA, renal colic, DKA, and MI.

How Emergency Medicine assesses it: Assess instability, peritonitis, pain onset/migration/location, vomiting/obstipation, GI bleeding, fever, urinary symptoms, pregnancy/LMP, pelvic/testicular symptoms, anticoagulants, vascular disease, prior surgery/hernias, immunosuppression, and analgesic/antibiotic timing.

Diagnosis: Use CBC, CMP/LFTs, lipase, lactate when ischemia/shock possible, urinalysis, pregnancy test in patients with pregnancy potential, ECG/troponin for epigastric/older/cardiac risk, CT abdomen/pelvis with IV contrast for many undifferentiated adults, RUQ ultrasound for biliary disease, pelvic ultrasound for torsion/ectopic, and CTA for mesenteric ischemia/AAA concern.

First-line treatment: Stabilize NPO, IV access, isotonic fluids, antiemetic ondansetron (Zofran), pain control with morphine or hydromorphone (Dilaudid) without delaying exam, early surgery/OB/urology consultation when peritonitis/torsion/ectopic/AAA/ischemia/obstruction is possible, and antibiotics for suspected intra-abdominal infection.

Second-line treatment: Examples: ceftriaxone (Rocephin) plus metronidazole (Flagyl) for appendicitis/diverticulitis, piperacillin-tazobactam (Zosyn) for severe biliary/intra-abdominal sepsis, ceftriaxone plus doxycycline (Vibramycin) plus metronidazole for PID/TOA, and tamsulosin (Flomax)/NSAID strategy for selected ureteral stone after ruling out infection/renal failure.

Third-line / advanced care: Immediate OR/IR/transfer for perforation, peritonitis, bowel ischemia, ruptured AAA, unstable ectopic, ovarian/testicular torsion, necrotizing infection, obstructed infected stone, or septic cholangitis needing ERCP. Admit for uncontrolled pain/vomiting, sepsis, obstruction, pancreatitis severity, or unsafe follow-up.

Progression and follow-up: Follow serial abdominal exams, vitals, lactate, WBC, renal function, urine output, imaging evolution, antibiotic response, missed pregnancy/vascular disease, opioid adverse effects, perforation, abscess, sepsis, and need for source control.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Pulmonary embolism emergency evaluation

Pathophysiology: Pulmonary embolism is thromboembolic obstruction of pulmonary arteries causing V/Q mismatch, hypoxemia, pulmonary vascular resistance, right-ventricular strain, shock, and death; risk rises with VTE history, surgery/immobility, cancer, pregnancy/postpartum, estrogen, thrombophilia, and inflammatory illness.

How Emergency Medicine assesses it: Assess dyspnea, pleuritic chest pain, syncope, hemoptysis, leg swelling, hypoxia, tachycardia, hypotension, VTE risk factors, pregnancy, anticoagulant use, bleeding risk, and pretest probability using gestalt/Wells/Geneva with PERC in truly low-risk adults.

Diagnosis: Low-risk PERC-negative patients need no D-dimer. Low/intermediate risk uses D-dimer, age-adjusted when appropriate; positive D-dimer or high probability generally needs CT pulmonary angiography. Use V/Q scan when contrast/radiation context favors it, leg ultrasound when DVT signs or CTPA unavailable, ECG/troponin/BNP/echo for risk stratification, and pregnancy-specific pathways when relevant.

First-line treatment: If PE is likely and bleeding risk acceptable, start anticoagulation while awaiting imaging when delay is expected: unfractionated heparin for unstable/high-risk or procedure-likely patients, enoxaparin (Lovenox), or DOAC pathway apixaban (Eliquis) or rivaroxaban (Xarelto) for selected stable patients.

Second-line treatment: Confirmed stable low-risk PE may discharge only when oxygenation, vitals, bleeding risk, renal function, social reliability, and follow-up are safe. Intermediate-risk PE needs admission/monitoring, anticoagulation, and evaluation of RV strain/troponin.

Third-line / advanced care: Massive/high-risk PE with hypotension/shock requires resuscitation, norepinephrine if needed, systemic alteplase (Activase) when benefits outweigh bleeding risk, catheter-directed therapy or surgical embolectomy in selected cases, ICU, and PERT consultation where available.

Progression and follow-up: Follow oxygenation, RV strain, troponin/BNP, bleeding, recurrent VTE, chronic thromboembolic pulmonary hypertension, anticoagulant interactions/adherence, cancer/pregnancy evaluation, and duration decisions based on provoked versus unprovoked PE.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

DKA emergency management

Pathophysiology: Diabetic ketoacidosis is insulin deficiency plus counter-regulatory hormone excess causing lipolysis, ketogenesis, anion-gap metabolic acidosis, dehydration, potassium shifts, and hyperosmolar stress; triggers include missed insulin, infection, MI, stroke, pancreatitis, pregnancy, SGLT2 inhibitors, and new type 1 diabetes.

How Emergency Medicine assesses it: Assess airway/mental status, Kussmaul respirations, shock/dehydration, abdominal pain/vomiting, infection/ischemia triggers, insulin pump failure, pregnancy, SGLT2 inhibitor use/euglycemic DKA, weight, urine output, and cerebral edema risk in children/young adults.

Diagnosis: Use bedside glucose, BMP/CMP with anion gap and potassium, venous blood gas pH/bicarbonate, serum beta-hydroxybutyrate, urinalysis/ketones, serum osmolality when HHS overlap, CBC, Mg/phosphate, ECG for potassium effects, pregnancy test, cultures/chest X-ray/troponin/lipase only by trigger clues.

First-line treatment: Start isotonic crystalloid resuscitation, replace potassium before insulin if K is low, begin regular insulin infusion after potassium is safe, monitor glucose hourly and electrolytes/anion gap every 2-4 hours, and add dextrose-containing fluids when glucose falls while acidosis remains.

Second-line treatment: Treat the precipitating cause: antibiotics such as ceftriaxone (Rocephin), piperacillin-tazobactam (Zosyn), or vancomycin (Vancocin) only when infection is likely; manage MI/stroke/pancreatitis/pump failure. Bicarbonate is reserved for extreme acidemia per protocol, not routine DKA.

Third-line / advanced care: ICU/stepdown for severe acidosis, altered mental status, shock, potassium derangement, pregnancy, pediatric DKA, renal failure, or inability to monitor. Transition to subcutaneous basal insulin glargine (Lantus/Basaglar) with overlap before stopping infusion once anion gap closes and patient can eat.

Progression and follow-up: Follow anion gap, beta-hydroxybutyrate, potassium, phosphate, glucose, mental status, fluid balance, cerebral edema, hypoglycemia, hypokalemia, recurrent DKA, sick-day education, insulin access, and trigger prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Hypertensive emergency

Pathophysiology: Hypertensive emergency is severe BP elevation with acute target-organ injury: encephalopathy, ischemic/hemorrhagic stroke, acute coronary syndrome, pulmonary edema, aortic dissection, AKI, eclampsia, retinopathy, or catecholamine/drug crisis. BP number alone without injury is not emergency.

How Emergency Medicine assesses it: Assess neurologic deficits/confusion/seizure, chest/back pain, dyspnea/pulmonary edema, pregnancy/postpartum, cocaine/amphetamine/MAOI use, renal symptoms, visual changes, papilledema, medication adherence/withdrawal, and compare arms/pulses for dissection.

Diagnosis: Confirm BP with correct cuff and repeat measurement; use ECG, troponin, chest X-ray, BMP/creatinine, urinalysis, CBC/platelets, pregnancy test, LFTs/LDH/uric acid for preeclampsia, CT head for neurologic symptoms, CTA chest/abdomen for dissection, and fundoscopic exam when possible.

First-line treatment: Treat the organ syndrome with IV titratable therapy and monitoring; avoid rapid overcorrection except aortic dissection. Common agents include nicardipine (Cardene), clevidipine (Cleviprex), labetalol (Trandate), nitroglycerin for pulmonary edema/ACS, and esmolol (Brevibloc) plus vasodilator for dissection.

Second-line treatment: Special cases: eclampsia/severe preeclampsia needs magnesium sulfate and obstetric delivery planning plus labetalol/hydralazine/nifedipine; catecholamine crisis may need benzodiazepines and phentolamine; intracerebral hemorrhage uses protocol-specific BP targets.

Third-line / advanced care: ICU/admission for all true hypertensive emergencies, dissection, stroke/ICH, ACS, pulmonary edema, AKI, pregnancy-related severe features, or IV infusion needs. Severe asymptomatic hypertension is managed with oral medication adjustment and close follow-up, not aggressive IV lowering.

Progression and follow-up: Follow neurologic status, renal function, urine output, troponin/ECG, pulmonary edema, aortic complications, fetal/maternal status, medication adverse effects, and transition to durable oral regimen with adherence plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Toxic ingestion

Pathophysiology: Toxic ingestion includes intentional, accidental, occupational, pediatric, or substance-use exposure causing toxidromes through cholinergic, anticholinergic, sympathomimetic, opioid, sedative-hypnotic, serotonergic, caustic, cardiotoxic, hepatotoxic, or metabolic mechanisms.

How Emergency Medicine assesses it: Assess airway, breathing, circulation, mental status, glucose, temperature, pupils, skin, bowel sounds, clonus/rigidity, QRS/QT, pill counts, timing, coingestants, extended-release products, suicide risk, pregnancy, access to medications, and call Poison Control early.

Diagnosis: Use ECG immediately and repeat, glucose, acetaminophen level at appropriate timing, salicylate level, ethanol level, BMP/CMP/LFTs, VBG/ABG, lactate, osmol gap when toxic alcohol possible, CK for rhabdo, pregnancy test, urine drug screen only as adjunct, and targeted levels such as lithium, valproate, digoxin, carbamazepine, or iron.

First-line treatment: Stabilize first: oxygen/ventilation, IV access, dextrose for hypoglycemia, naloxone (Narcan) for opioid respiratory depression, benzodiazepines such as lorazepam (Ativan) for seizures/agitation/sympathomimetic toxicity, IV fluids/cooling, and activated charcoal only for appropriate recent protected-airway ingestions.

Second-line treatment: Specific antidotes include N-acetylcysteine (Acetadote) for acetaminophen, sodium bicarbonate for TCA/sodium-channel blockade, atropine plus pralidoxime (2-PAM) for organophosphates, fomepizole (Antizol) for ethylene glycol/methanol, hydroxocobalamin (Cyanokit) for cyanide, digoxin immune Fab (DigiFab), and high-dose insulin euglycemia for calcium-channel/beta-blocker shock.

Third-line / advanced care: ICU/toxicology/nephrology for coma, ventilator need, shock, seizures, wide QRS/QT dysrhythmia, severe acidosis, salicylate/toxic alcohol/lithium needing dialysis, caustic ingestion, body packers, or unsafe psychiatric disposition. Do not rely on third-party labels claiming a product is harmless.

Progression and follow-up: Follow delayed absorption, recurrent opioid toxicity, hepatic failure, renal failure, rhabdomyolysis, aspiration, arrhythmias, serotonin syndrome/NMS, withdrawal, self-harm recurrence, child-safety prevention, and medication access control.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Status epilepticus

Pathophysiology: Convulsive status epilepticus is a seizure lasting 5 minutes or recurrent seizures without recovery; ongoing excitation can cause neuronal injury, lactic acidosis, hyperthermia, rhabdomyolysis, aspiration, hypoxia, and refractory GABA-receptor changes.

How Emergency Medicine assesses it: Protect airway and circulation while identifying seizure onset, prior epilepsy, missed antiseizure meds, trauma, pregnancy/eclampsia, hypoglycemia, infection/meningitis, stroke, alcohol/benzodiazepine withdrawal, toxic ingestion, and continuous seizure versus postictal state.

Diagnosis: Immediate bedside glucose and vitals; labs include BMP sodium/calcium/magnesium, CBC, antiseizure drug levels when relevant, pregnancy test, toxicology/ethanol when indicated, VBG/ABG/lactate/CK, CT head for new focal/trauma/immunocompromise/persistent altered state, lumbar puncture after imaging if CNS infection suspected, and EEG for nonconvulsive/refractory seizures.

First-line treatment: Give dextrose after thiamine when malnourished if hypoglycemic, then benzodiazepine rapidly: lorazepam (Ativan) IV, midazolam (Versed) IM/IN, or diazepam (Valium) IV/rectal, with repeat dosing per protocol while preparing airway support.

Second-line treatment: If seizures continue, load a second-line antiseizure medication such as levetiracetam (Keppra), fosphenytoin/phenytoin (Cerebyx/Dilantin), or valproate (Depacon) based on pregnancy, liver disease, cardiac conduction, and drug interactions; treat causes such as magnesium sulfate for eclampsia or pyridoxine in selected infants/isoniazid toxicity.

Third-line / advanced care: Refractory status needs ICU, intubation, continuous EEG, anesthetic infusion such as propofol (Diprivan), midazolam, or ketamine, plus neurology/critical care. Empiric antibiotics/acyclovir may be needed when meningitis/encephalitis is possible.

Progression and follow-up: Follow seizure cessation time, airway/aspiration, hypoxia, acidosis, hyperthermia, rhabdomyolysis, renal injury, medication hypotension/respiratory depression, EEG recurrence, neurologic outcome, and maintenance antiseizure plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Major trauma initial assessment

Pathophysiology: Major trauma causes death through airway obstruction, hypoxia, hemorrhage, traumatic brain injury, tension pneumothorax, cardiac tamponade, spinal cord injury, pelvic/long-bone bleeding, coagulopathy, hypothermia, and acidosis.

How Emergency Medicine assesses it: Use primary survey: airway with cervical spine protection, breathing, circulation/hemorrhage control, disability/GCS/pupils/glucose, exposure/environment. Assess mechanism, anticoagulants, pregnancy, age/frailty, tourniquets, pelvic stability, chest/abdomen signs, neurologic deficits, and need for massive transfusion.

Diagnosis: Do not let imaging delay resuscitation. Use eFAST, chest/pelvis X-ray when indicated, trauma labs CBC/CMP/coags/type and cross/fibrinogen/TEG or ROTEM where available, lactate/base deficit, CT head/c-spine/chest/abdomen/pelvis after stabilization, CT angiography for vascular injury, and repeat exams because early findings can be absent.

First-line treatment: Control hemorrhage with direct pressure/tourniquet/pelvic binder, give oxygen, secure airway with ketamine/etomidate plus paralytic when needed, decompress tension pneumothorax, start balanced blood-product resuscitation with PRBC/plasma/platelets, give tranexamic acid (TXA) early when major hemorrhage criteria are met, calcium replacement, and warming.

Second-line treatment: Treat specific injuries: chest tube for hemothorax/pneumothorax, cefazolin (Ancef) for open fractures, tetanus update/Tdap, hypertonic saline or mannitol for impending herniation, levetiracetam (Keppra) for selected severe TBI seizure prophylaxis, and analgesia fentanyl or hydromorphone while avoiding hypotension.

Third-line / advanced care: Activate trauma surgery; transfer to trauma center for major mechanism, shock, penetrating torso/head/neck, severe TBI, spinal deficit, pelvic fracture, burns, pediatric/geriatric high-risk trauma, or need for OR/IR/neurosurgery. ICU/OR/IR decisions are made from physiology, not CT alone.

Progression and follow-up: Follow hemorrhage, coagulopathy, hypothermia, acidosis, compartment syndrome, missed injuries, TBI swelling, spinal precautions, infection, rhabdomyolysis, pain control, delirium, PTSD, rehab needs, and safe discharge instructions.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Severe headache red flags

Pathophysiology: Severe headache red flags identify subarachnoid hemorrhage, intracerebral hemorrhage, meningitis/encephalitis, cerebral venous thrombosis, cervical artery dissection, giant cell arteritis, acute angle-closure glaucoma, carbon monoxide poisoning, preeclampsia, brain mass, and idiopathic intracranial hypertension rather than uncomplicated migraine.

How Emergency Medicine assesses it: Assess thunderclap onset/maximal intensity within 1 minute, worst headache, neurologic deficit, syncope, seizure, fever/neck stiffness, papilledema, pregnancy/postpartum, cancer/immunosuppression, anticoagulants, trauma, exertion/sex trigger, age over 50/new pattern, jaw claudication/vision symptoms, eye pain/redness, and CO exposure.

Diagnosis: Noncontrast CT head urgently for thunderclap/neurologic/trauma/anticoagulant concern; if SAH concern persists after negative CT, use lumbar puncture or CT angiography per timing/local pathway. CTA/MRA head-neck for dissection/aneurysm/RCVS, MRV/CTV for venous thrombosis, ESR/CRP/platelets for GCA, pregnancy/BP/urine protein for preeclampsia, and tonometry for angle closure.

First-line treatment: Stabilize ABCs, treat pain/nausea with acetaminophen, metoclopramide (Reglan) or prochlorperazine (Compazine) plus diphenhydramine when migraine likely, IV fluids if dehydrated, and avoid triptans/ergots until vascular causes are excluded in red-flag presentations.

Second-line treatment: Disease-specific emergency treatment: ceftriaxone/vancomycin plus dexamethasone for suspected bacterial meningitis, acyclovir (Zovirax) for encephalitis concern, nimodipine (Nimotop) and neurosurgery for SAH, magnesium sulfate for eclampsia, high-dose prednisone for GCA with vision risk, acetazolamide/timolol/brimonidine for angle closure while calling ophthalmology.

Third-line / advanced care: Admit/transfer for SAH/ICH, meningitis/encephalitis, venous thrombosis, dissection, GCA with visual symptoms, papilledema/mass, pregnancy severe features, immunocompromised infection, persistent neurologic deficit, or uncontrolled pain/vomiting with diagnostic uncertainty.

Progression and follow-up: Follow neurologic exams, repeat imaging/LP results, vision, fever, BP, seizure, hyponatremia, vasospasm after SAH, steroid/antibiotic adverse effects, medication-overuse headache, and return precautions for recurrent thunderclap or deficits.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Syncope risk disposition

Pathophysiology: Syncope is transient global cerebral hypoperfusion from reflex/vasovagal, orthostatic, cardiac arrhythmic, structural heart, PE, hemorrhage, medication, autonomic, or metabolic causes; emergency care identifies short-term risk rather than proving every benign cause.

How Emergency Medicine assesses it: Assess exertional or supine syncope, palpitations, chest pain, dyspnea, family sudden death, heart disease, abnormal vitals, bleeding/melena, pregnancy, neurologic deficit/seizure mimic, trauma from fall, dehydration, new medications, older age/frailty, and recurrence.

Diagnosis: Minimum ED evaluation includes history, orthostatic vitals when feasible, cardiac/pulmonary/neuro exam, 12-lead ECG, glucose, pregnancy test when relevant, hemoglobin/electrolytes/troponin/D-dimer/CT only when suggested by history or exam, and telemetry for suspected arrhythmia. Head CT is not routine without trauma, focal deficit, anticoagulation, or concerning headache.

First-line treatment: Treat the cause: oral/IV fluids for dehydration, stop or reduce offending antihypertensives/diuretics when safe, compression/counterpressure education for reflex syncope, antiemetics if volume loss, transfusion/GI bleed protocol if hemorrhage, and ACLS care for dysrhythmia.

Second-line treatment: Cardiac-risk patients need monitoring, echocardiography, cardiology/electrophysiology, pacemaker/ICD evaluation, or ambulatory rhythm monitor. PE, aortic stenosis, hypertrophic cardiomyopathy, ACS, and pulmonary hypertension need disease-specific admission workup.

Third-line / advanced care: Admit/observe for abnormal ECG, exertional/supine syncope, structural heart disease, CHF, persistent hypotension, severe anemia/bleeding, dyspnea/PE concern, serious injury, older frailty without safe support, or recurrent unexplained episodes. Low-risk vasovagal/orthostatic syncope can discharge with follow-up and precautions.

Progression and follow-up: Follow recurrent episodes, injuries, arrhythmias, medication hypotension, driving/work restrictions, dehydration triggers, anemia/bleeding, device findings, and diagnostic yield of outpatient monitoring.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Emergency Medicine

Acute psychosis safety

Pathophysiology: Acute psychosis in the ED may reflect primary psychotic disorder, mania, severe depression, delirium, intoxication/withdrawal, stimulant/cannabis use, steroid/medication effect, endocrine/metabolic disease, CNS infection, seizure, trauma, or autoimmune/neurologic disease.

How Emergency Medicine assesses it: Prioritize safety: assess agitation/violence, suicidality/homicidality, command hallucinations, grave disability, capacity, delirium signs, vitals, glucose, intoxication/withdrawal, trauma, pregnancy, medication/substance exposure, first episode versus known illness, collateral, and medical red flags such as fever, focal deficit, catatonia, or fluctuating attention.

Diagnosis: Use targeted medical screening rather than blanket panels: glucose, vitals, mental status exam, pregnancy test when relevant, urine toxicology/ethanol when clinically useful, CBC/CMP/TSH/UA/CK/ECG/CT head/LP only by presentation. First-episode, older-onset, delirious, febrile, focal, or immunocompromised patients need broader workup.

First-line treatment: Verbal de-escalation, reduced stimulation, trauma-informed approach, remove hazards, treat pain/hypoxia/hypoglycemia/withdrawal, and use oral medication when possible: olanzapine (Zyprexa), risperidone (Risperdal), quetiapine (Seroquel), or lorazepam (Ativan) depending on likely cause.

Second-line treatment: Severe agitation threatening safety may need IM haloperidol (Haldol) plus lorazepam, droperidol (Inapsine), or IM olanzapine, with ECG/QT, respiratory, and dystonia monitoring. Avoid combining IM olanzapine and benzodiazepines too closely because of respiratory risk.

Third-line / advanced care: Emergency psychiatry/inpatient hold when danger to self/others, grave disability, command hallucinations, mania/psychosis with unsafe behavior, inability to complete medical evaluation, catatonia, delirium, intoxication/withdrawal instability, or unsafe discharge support exists. Medical admission for delirium, infection, metabolic, neurologic, or withdrawal causes.

Progression and follow-up: Follow sedation/airway, QTc/EPS/NMS, restraints duration and injury, capacity changes, suicidality/violence, substance withdrawal, collateral safety planning, medication adherence, housing/support, and linkage to outpatient psychiatry or crisis care.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

Specialty role

ICU organ support, shock, respiratory failure, sepsis, sedation, delirium, procedures, and high-acuity monitoring.

Critical Care Medicine

Septic shock

Pathophysiology: Septic shock is sepsis with vasoplegia, capillary leak, myocardial depression, mitochondrial dysfunction, microthrombosis, and persistent tissue hypoperfusion requiring vasopressors after fluids; common ICU sources include pneumonia, abdomen, urinary tract, line infection, skin/soft tissue, CNS, and bone.

How Critical Care Medicine assesses it: Assess source, MAP, lactate trend, urine output, mental status, skin perfusion, oxygenation, cardiac function, volume responsiveness, immunosuppression, resistant organisms, indwelling lines, source-control needs, steroid exposure, and whether shock is mixed with cardiogenic, hemorrhagic, obstructive, adrenal, or anaphylactic physiology.

Diagnosis: Use lactate and repeat clearance, blood cultures before antibiotics if no delay, CBC/CMP/coags, ABG/VBG, urinalysis/cultures, respiratory testing, chest imaging, CT/ultrasound for source, bedside echocardiography, dynamic fluid responsiveness such as passive leg raise/stroke volume variation, and SOFA organ dysfunction tracking.

First-line treatment: Give balanced crystalloid such as lactated Ringer's, early broad antibiotics tailored to source such as piperacillin-tazobactam (Zosyn), cefepime (Maxipime), meropenem (Merrem), vancomycin (Vancocin), metronidazole (Flagyl), or micafungin (Mycamine) when fungal risk exists, and obtain urgent source control.

Second-line treatment: Use norepinephrine (Levophed) first-line to target MAP about 65 mm Hg; add vasopressin 0.03 units/min instead of endlessly escalating norepinephrine, then epinephrine for refractory shock. Add dobutamine when myocardial dysfunction and persistent hypoperfusion remain despite MAP restoration.

Third-line / advanced care: Hydrocortisone 200 mg/day is considered for ongoing vasopressor requirement. ICU care includes arterial/central access, ventilation/renal support when needed, drainage/surgery/line removal, antimicrobial de-escalation, DVT/stress-ulcer/nutrition planning, and goals-of-care review for refractory multiorgan failure.

Progression and follow-up: Follow MAP, vasopressor dose, lactate, urine output, creatinine, bilirubin, platelets, oxygenation, delirium, source control, culture narrowing, limb/digital ischemia, arrhythmias, steroid hyperglycemia, AKI, ARDS, DIC, mortality, and post-sepsis disability.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

ARDS

Pathophysiology: ARDS is acute inflammatory alveolar-capillary injury causing noncardiogenic pulmonary edema, surfactant dysfunction, atelectasis, shunt physiology, reduced compliance, refractory hypoxemia, and ventilator-induced lung-injury risk after sepsis, pneumonia, aspiration, pancreatitis, trauma, transfusion, or shock.

How Critical Care Medicine assesses it: Assess timing within 1 week of insult, bilateral opacities, PaO2/FiO2 severity with PEEP/CPAP, plateau/driving pressures, recruitability, fluid balance, shock, sedation/paralysis needs, aspiration risk, pneumothorax, and alternative causes such as cardiogenic edema or diffuse alveolar hemorrhage.

Diagnosis: Use Berlin criteria, ABG, chest X-ray or CT showing bilateral opacities, echocardiography/BNP/hemodynamics when cardiac edema is uncertain, respiratory cultures/viral testing, lung ultrasound, plateau pressure measurement, and daily readiness for spontaneous awakening/breathing when improving.

First-line treatment: Use lung-protective ventilation with tidal volume 4-8 mL/kg predicted body weight, plateau pressure under 30 cm H2O when possible, adequate PEEP, conservative fluid strategy after shock resolves, treat the cause, and avoid excessive FiO2 when oxygen targets are met.

Second-line treatment: Moderate-severe ARDS may need prone positioning 12-16 hours/day or longer, neuromuscular blockade such as cisatracurium (Nimbex) for severe ventilator dyssynchrony/early severe ARDS, deeper sedation only when necessary, inhaled pulmonary vasodilator as short rescue, and recruitment/PEEP strategy by experienced team.

Third-line / advanced care: VV-ECMO referral for refractory severe hypoxemia or hypercapnia despite optimized ventilation/proning in appropriate candidates; evaluate barotrauma, right-ventricular failure, ventilator-associated pneumonia, and goals of care if lung failure remains refractory.

Progression and follow-up: Follow PaO2/FiO2, driving pressure, compliance, plateau pressure, ventilator days, sedation/paralysis complications, pressure injuries from proning, VAP, pneumothorax, ICU weakness, cognitive impairment, fibrotic lung disease, and long-term functional recovery.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

Mechanical ventilation liberation

Pathophysiology: Ventilator liberation fails when respiratory muscle load exceeds capacity or when neurologic, cardiac, metabolic, secretion, airway, sedation, delirium, malnutrition, or diaphragmatic weakness prevents sustained spontaneous breathing.

How Critical Care Medicine assesses it: Assess improvement of the original cause, oxygenation/PEEP/FiO2 needs, hemodynamic stability, mental status/airway protection, cough/secretions, sedation depth, pain/anxiety, acid-base status, fluid overload, anemia, nutrition, and prior failed extubation reason.

Diagnosis: Use daily spontaneous awakening trial plus spontaneous breathing trial with pressure support/CPAP or T-piece, rapid shallow breathing index as adjunct, negative inspiratory force/vital capacity selectively, cuff leak when airway edema risk, ABG/VBG when uncertain, and bedside ultrasound/echo for diaphragm or cardiac weaning failure clues.

First-line treatment: Lighten sedation, treat pain, correct electrolytes, mobilize early, optimize bronchodilators/diuresis, suction/airway clearance, and perform protocolized SAT/SBT when criteria are met. Extubate to nasal cannula, high-flow nasal cannula, or noninvasive ventilation based on risk.

Second-line treatment: High-risk extubation such as COPD, hypercapnia, heart failure, obesity hypoventilation, or repeated failure may benefit from planned BiPAP/NIV or high-flow nasal cannula. Dexamethasone may help selected patients with absent cuff leak/high airway edema risk before extubation.

Third-line / advanced care: Tracheostomy discussion for prolonged ventilation, repeated extubation failure, severe neurologic impairment, secretion burden, or expected slow recovery. ENT/anesthesia support for difficult airway extubation; palliative review when liberation is inconsistent with goals or prognosis.

Progression and follow-up: Follow reintubation within 48-72 hours, aspiration, stridor, respiratory muscle weakness, delirium, ICU-acquired weakness, ventilator-associated pneumonia, tracheostomy complications, communication/swallowing, and rehab trajectory.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

Vasopressor titration

Pathophysiology: Vasopressor titration corrects distributive, cardiogenic, obstructive, neurogenic, or mixed shock by manipulating vascular tone, heart rate, contractility, and venous capacitance; wrong drug or excessive dose can worsen arrhythmia, ischemia, afterload, and tissue perfusion.

How Critical Care Medicine assesses it: Assess shock phenotype, MAP target, lactate, urine output, mentation, skin perfusion, central venous/arterial access, rhythm, LV/RV function by echo, preload responsiveness, bleeding, infection source, adrenal risk, limb ischemia, and medication extravasation risk.

Diagnosis: Use arterial-line BP when high-dose or rapidly changing support, serial lactate, urine output, ECG/telemetry, bedside echo, ScvO2 or venous saturation selectively, ABG/VBG, electrolytes, troponin/BNP when cardiac shock possible, and dynamic fluid tests rather than static CVP alone.

First-line treatment: Norepinephrine (Levophed) is usual first-line for septic/distributive shock. Titrate to a syndrome-appropriate MAP, often 65 mm Hg, while giving adequate fluids and source control. Use push-dose pressors only as a monitored bridge during peri-intubation or crashing hypotension.

Second-line treatment: Add vasopressin 0.03 units/min for septic shock needing moderate norepinephrine, epinephrine for refractory distributive shock or anaphylaxis, phenylephrine for selected tachyarrhythmia contexts, dobutamine or milrinone for low-output cardiogenic physiology, and inodilator/vasopressor combinations for RV failure with specialist input.

Third-line / advanced care: High-dose multi-pressor shock needs ICU/critical care, central access confirmation, extravasation treatment with phentolamine when needed, hydrocortisone for refractory septic shock, mechanical circulatory support evaluation for cardiogenic shock, and early goals-of-care conversation when refractory.

Progression and follow-up: Follow vasopressor dose trend, lactate, mottling/capillary refill, urine output, arrhythmias, myocardial ischemia, digital/mesenteric ischemia, line infection/thrombosis, extravasation, rebound hypotension during wean, and organ recovery.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

ICU delirium

Pathophysiology: Delirium is acute fluctuating brain dysfunction from impaired attention/arousal triggered by infection, hypoxia, dehydration, pain, urinary retention/constipation, sleep disruption, metabolic disturbance, withdrawal, stroke, surgery, or high-risk medications in a vulnerable brain.

How Critical Care Medicine assesses it: Assess acute onset/fluctuation, inattention, altered level of consciousness, hallucinations, sleep-wake reversal, baseline dementia, infection symptoms, pain, oxygenation, urinary retention, constipation, medications, alcohol/benzodiazepine withdrawal, sensory deprivation, and caregiver collateral.

Diagnosis: Use CAM or 4AT plus targeted cause search: vitals, pulse oximetry, glucose, CBC, CMP/electrolytes, urinalysis/culture only if urinary symptoms/systemic signs, ECG, bladder scan, medication/toxin review, and CT head only for trauma, focal deficit, anticoagulated head injury, or unexplained severe change.

First-line treatment: First-line treatment is non-drug: reorientation, glasses/hearing aids, sleep normalization, mobilization, hydration/nutrition, pain control, bowel/bladder relief, family presence, avoid restraints/catheters, and stop deliriogenic drugs such as diphenhydramine (Benadryl), benzodiazepines, anticholinergics, and sedative hypnotics.

Second-line treatment: Treat the cause: fluids for dehydration, oxygen for hypoxia, antibiotics for confirmed infection, bowel regimen, urinary retention relief, and withdrawal protocol when present. Use low-dose antipsychotic such as haloperidol (Haldol) or quetiapine (Seroquel) only for severe distress or danger after QT/Parkinson/Lewy body risks are considered.

Third-line / advanced care: Hospitalize/escalate for sepsis, hypoxia, stroke, severe metabolic derangement, unsafe agitation, inability to take fluids/meds, suspected abuse/neglect, or lack of safe supervision.

Progression and follow-up: Follow attention/arousal, sleep, mobility, hydration, medication changes, caregiver observations, recurrence risk, functional decline, falls, and transition to dementia evaluation only after delirium resolves.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

Acute respiratory failure

Pathophysiology: Acute respiratory failure is failure of oxygenation, ventilation, or both from pneumonia, ARDS, asthma/COPD, pulmonary edema, PE, pneumothorax, sepsis, neuromuscular weakness, overdose, airway obstruction, aspiration, or obesity hypoventilation.

How Critical Care Medicine assesses it: Assess work of breathing, mental status, airway protection, SpO2, ABG/VBG CO2 and pH, hemodynamics, wheeze/crackles/stridor, secretion burden, aspiration risk, neuromuscular strength, opioid/sedative exposure, DNR/intubation preferences, and likely reversibility.

Diagnosis: Use ABG/VBG, chest X-ray/ultrasound, ECG, BMP/CBC, BNP/troponin when cardiac, D-dimer/CTPA when PE probability supports it, respiratory PCR/cultures, peak flow for asthma, NIF/vital capacity for neuromuscular weakness, and bedside echo for pulmonary edema/RV strain.

First-line treatment: Provide oxygen delivery matched to severity: nasal cannula, nonrebreather, high-flow nasal cannula, CPAP/BiPAP for COPD/cardiogenic edema/selected hypoxemia, bronchodilators albuterol-ipratropium (DuoNeb), diuresis furosemide (Lasix) for pulmonary edema, antibiotics for pneumonia, and naloxone for opioid ventilatory failure.

Second-line treatment: Intubate for inability to protect airway, refractory hypoxemia/hypercapnia/acidosis, exhaustion, shock, severe agitation preventing support, or unsafe NIV. Use lung-protective ventilation, appropriate PEEP, post-intubation sedation/analgesia, and treat the cause quickly.

Third-line / advanced care: ICU escalation for mechanical ventilation, shock, severe ARDS, neuromuscular failure, difficult airway, need for bronchoscopy, ECMO consideration, or goals-of-care conflict. Avoid prolonged NIV when failure signs are clear because delayed intubation worsens outcomes.

Progression and follow-up: Follow oxygenation, pH/CO2, work of breathing, ventilator pressures, aspiration, VAP, barotrauma, delirium, ICU weakness, tracheostomy need, and post-ICU dyspnea or functional decline.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

Cardiogenic shock

Pathophysiology: Cardiogenic shock is inadequate tissue perfusion from pump failure due to acute MI, decompensated heart failure, myocarditis, valvular catastrophe, arrhythmia, mechanical MI complication, Takotsubo, or RV failure; high filling pressures and low cardiac output cause multiorgan hypoperfusion.

How Critical Care Medicine assesses it: Assess ACS symptoms, ECG, rhythm, BP/MAP, lactate, urine output, cool extremities, JVP, pulmonary edema, murmur, RV infarct/PE signs, mechanical complications, vasoactive needs, congestion versus hypovolemia, and candidacy for cath/mechanical circulatory support.

Diagnosis: Use ECG, serial troponin, lactate, CMP/renal/liver markers, ABG/VBG, bedside echocardiography for LV/RV/valves/tamponade, chest X-ray/lung ultrasound, coronary angiography for suspected MI, pulmonary artery catheter in selected complex shock, and evaluate mimics such as sepsis/PE/dissection.

First-line treatment: Stabilize oxygenation, avoid excessive fluids unless RV preload-responsive, use norepinephrine (Levophed) for hypotension, add dobutamine or milrinone for low-output state when BP allows, treat arrhythmias, and pursue urgent revascularization for MI shock.

Second-line treatment: Manage congestion with cautious IV furosemide (Lasix) once perfusion allows, vasodilators nitroglycerin/nitroprusside only if BP adequate, anticoagulation/antiplatelet per ACS pathway, and targeted therapy for RV infarct, valvular rupture, myocarditis, or tamponade.

Third-line / advanced care: Shock team/cardiology for intra-aortic balloon pump in selected mechanical complications, Impella, VA-ECMO, surgical repair, transplant/LVAD evaluation, or palliative cardiology when irreversible. ICU monitoring is required for escalating vasoactives, lactate, renal failure, or respiratory failure.

Progression and follow-up: Follow lactate, urine output, end-organ labs, pulmonary edema, arrhythmia, limb ischemia from MCS, hemolysis, bleeding, AKI, neurologic status, recovery of EF, need for durable support, and mortality risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

Massive transfusion

Pathophysiology: Massive transfusion treats life-threatening hemorrhagic shock from trauma, GI bleed, obstetric hemorrhage, ruptured aneurysm, surgery, or coagulopathy; death is driven by exsanguination, hypothermia, acidosis, hypocalcemia, dilutional coagulopathy, and traumatic coagulopathy.

How Critical Care Medicine assesses it: Assess source/control of bleeding, shock index, MAP, mental status, active external/internal bleeding, anticoagulants/antiplatelets, pregnancy, temperature, calcium, fibrinogen, base deficit/lactate, INR/PTT, platelets, and need for OR/IR/endoscopy/OB/trauma activation.

Diagnosis: Activate massive transfusion protocol by physiology, not hemoglobin alone. Use type and cross, CBC, PT/INR/PTT, fibrinogen, ionized calcium, ABG/VBG, lactate/base deficit, TEG/ROTEM where available, pregnancy test, and source imaging only if stable enough.

First-line treatment: Give balanced blood products early such as PRBC/plasma/platelets in trauma-style ratios, control hemorrhage with direct pressure/tourniquet/pelvic binder/surgery/IR/endoscopy, warm patient and products, give calcium chloride or calcium gluconate for hypocalcemia, and minimize crystalloid dilution.

Second-line treatment: Use tranexamic acid (TXA) early for trauma hemorrhage within 3 hours or selected postpartum hemorrhage protocols, reverse anticoagulation with 4-factor PCC (Kcentra), vitamin K, idarucizumab (Praxbind), andexanet alfa (Andexxa) or PCC depending on drug/setting, and give cryoprecipitate/fibrinogen concentrate for low fibrinogen.

Third-line / advanced care: ICU/OR/IR/endoscopy/OB/trauma team for definitive hemorrhage control; monitor for transfusion reactions, TRALI/TACO, hyperkalemia, hypocalcemia, hypothermia, DIC, abdominal compartment syndrome, and need to stop MTP once hemostasis achieved.

Progression and follow-up: Follow bleeding control, hemoglobin trend, lactate/base deficit, INR/PTT/fibrinogen/platelets, ionized calcium, temperature, pH, potassium, renal function, thrombosis, organ failure, and delayed complications from both hemorrhage and transfusion.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

Acute renal replacement decision

Pathophysiology: ICU renal replacement therapy supports severe AKI when kidney failure causes life-threatening electrolyte, acid-base, volume, uremic, or toxin problems; timing is driven by complications and trajectory rather than creatinine alone.

How Critical Care Medicine assesses it: Assess urine output, volume overload/pulmonary edema, potassium, pH/bicarbonate, uremic encephalopathy/pericarditis/bleeding, toxin ingestion, hemodynamics/pressor dose, catabolic state, rhabdomyolysis/tumor lysis, drug dosing, vascular access, anticoagulation risk, and goals of care.

Diagnosis: Use BMP/Mg/phosphate, ABG/VBG, urinalysis/sediment, urine output trend, renal ultrasound for obstruction when relevant, CK/uric acid for rhabdo/tumor lysis, toxicology levels for dialyzable poisons, fluid balance, and nephrology assessment for modality.

First-line treatment: Treat reversible causes: optimize perfusion/MAP, stop nephrotoxins, dose-adjust drugs, relieve obstruction, manage sepsis/shock, loop diuretic furosemide (Lasix) only for volume management not renal recovery, potassium temporization with calcium/insulin/dextrose/albuterol, and bicarbonate for selected severe acidosis.

Second-line treatment: Start RRT for refractory hyperkalemia, severe metabolic acidosis, pulmonary edema/volume overload unresponsive to diuretics, uremic complications, severe azotemia with symptoms, or dialyzable toxins such as lithium, ethylene glycol, methanol, or severe salicylate poisoning.

Third-line / advanced care: Choose CRRT for hemodynamic instability/cerebral edema/liver failure, intermittent hemodialysis for stable patients or rapid toxin/electrolyte removal, and SLED where available. ICU/nephrology manage catheter placement, anticoagulation citrate/heparin choice, ultrafiltration goals, and discontinuation when renal recovery occurs.

Progression and follow-up: Follow potassium, acid-base, volume status, solute clearance, filter clotting, hypophosphatemia, hypothermia, hypotension, line infection/thrombosis, drug underdosing, renal recovery, dialysis dependence, and whether RRT remains aligned with prognosis/goals.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

ICU sedation and analgesia

Pathophysiology: ICU sedation and analgesia balance pain, ventilator synchrony, anxiety, procedures, safety, sleep, delirium, respiratory drive, hemodynamics, and long-term cognition; oversedation prolongs ventilation and immobility while undersedation causes suffering and device removal.

How Critical Care Medicine assesses it: Assess pain with numeric scale or CPOT/BPS, RASS target, ventilator synchrony, delirium by CAM-ICU, hemodynamics, renal/liver function, alcohol/benzodiazepine/opioid tolerance, neuromuscular blockade need, withdrawal risk, sleep, and daily SAT/SBT eligibility.

Diagnosis: Use protocolized pain/sedation/delirium scores, medication review, triglycerides with prolonged propofol, CK/lactate/acidosis for propofol infusion syndrome concern, QTc for antipsychotics, bowel function, and respiratory mechanics to distinguish pain/anxiety from hypoxemia or dyssynchrony.

First-line treatment: Use analgesia-first strategy: fentanyl, hydromorphone (Dilaudid), morphine, or enteral oxycodone plus nonopioids such as acetaminophen when safe. Target light sedation, often RASS -2 to 0, with propofol (Diprivan) or dexmedetomidine (Precedex) for many ventilated adults.

Second-line treatment: Use benzodiazepines such as midazolam (Versed) or lorazepam (Ativan) for alcohol/benzodiazepine withdrawal, seizures, deep sedation needs, or propofol intolerance; ketamine can help analgesia/bronchospasm/opioid-sparing. Treat agitation causes before escalating sedatives.

Third-line / advanced care: Deep sedation/paralysis requires clear indication such as severe ARDS proning or refractory intracranial pressure, with eye care, DVT prevention, train-of-four when paralyzed, and daily reassessment. Palliative sedation differs and requires goals-of-care clarity.

Progression and follow-up: Follow ventilator days, delirium, hypotension/bradycardia, hypertriglyceridemia, ileus, withdrawal, tolerance, ICU weakness, pressure injuries, accidental extubation, awareness/distress, PTSD, and medication accumulation in renal/liver failure.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

Severe pancreatitis ICU care

Pathophysiology: Severe acute pancreatitis causes pancreatic enzyme-mediated inflammation, capillary leak, SIRS, third-spacing, necrosis, infected collections, abdominal compartment physiology, hypocalcemia, ARDS, AKI, shock, and multiorgan failure; gallstones and alcohol are common causes.

How Critical Care Medicine assesses it: Assess onset, alcohol/gallstone history, organ failure, SIRS, hypoxia, shock, urine output, pain, vomiting, ileus, fever, jaundice/cholangitis, calcium/triglycerides, medication causes, abdominal compartment signs, and early severity scores such as BISAP/APACHE II as adjuncts.

Diagnosis: Diagnose by two of three: typical pain, lipase/amylase over 3 times upper limit, or imaging. Use CMP/LFTs, CBC/BUN/creatinine, calcium, triglycerides, lactate, RUQ ultrasound for gallstones, CT abdomen with contrast only when diagnosis unclear or complications/nonimprovement after 48-72 hours, and MRCP/ERCP for biliary obstruction/cholangitis.

First-line treatment: Early ICU care is aggressive but reassessed lactated Ringer's resuscitation, opioid analgesia such as hydromorphone (Dilaudid) or fentanyl, antiemetic ondansetron (Zofran), oxygen/organ support, early enteral nutrition when possible, and treatment of the cause such as ERCP for cholangitis/ongoing obstruction.

Second-line treatment: Do not give prophylactic antibiotics for sterile necrosis. Use antibiotics that penetrate necrosis such as piperacillin-tazobactam (Zosyn), carbapenem, or quinolone plus metronidazole only for infected necrosis/cholangitis/other infection. Drain infected collections with step-up endoscopic/percutaneous/surgical approach when mature or unstable.

Third-line / advanced care: ICU/surgery/GI/IR for persistent organ failure, infected necrosis, abdominal compartment syndrome, hemorrhage/pseudoaneurysm, refractory shock, ARDS, AKI/RRT, or need for cholecystectomy timing after gallstone pancreatitis.

Progression and follow-up: Follow BUN/creatinine, hematocrit, calcium, glucose, oxygenation, urine output, pain/nutrition, necrosis/collections, infection, GI bleeding, splenic/portal vein thrombosis, pancreatic insufficiency, pseudocyst/walled-off necrosis, and recurrence prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

Post-cardiac arrest care

Pathophysiology: Post-cardiac arrest syndrome includes hypoxic-ischemic brain injury, myocardial stunning, systemic ischemia-reperfusion inflammation, shock, lung injury, seizures, metabolic derangements, and recurrent arrest risk after return of spontaneous circulation.

How Critical Care Medicine assesses it: Assess airway/oxygenation/ventilation, MAP/shock, rhythm/STEMI or ongoing ischemia, arrest etiology, downtime/no-flow/low-flow, neurologic exam before sedation/paralysis, temperature, glucose, seizures/myoclonus, aspiration, trauma, electrolyte/toxic causes, and family goals.

Diagnosis: Use ECG, troponin trend, bedside echo, ABG/VBG, lactate, CMP/Mg/phosphate, glucose, chest X-ray, CT head when indicated, EEG for coma/seizures, coronary angiography for STEMI/shock/electrical instability/ongoing ischemia, and targeted CT/CTA/toxicology for suspected PE, hemorrhage, overdose, or neurologic cause.

First-line treatment: Optimize oxygenation without hyperoxia, target normocapnia unless special neuro indication, maintain MAP often at least 65 mm Hg with norepinephrine (Levophed) and fluids/inotropes as needed, treat STEMI/ischemia, correct electrolytes, control fever, and use deliberate temperature control for comatose adults after ROSC.

Second-line treatment: Temperature strategy uses a constant target between 33 C and 37.5 C per protocol, avoid rapid rewarming, treat shivering with buspirone, magnesium, meperidine, dexmedetomidine, propofol, or neuromuscular blockade when needed, and manage seizures/status epilepticus with EEG-guided levetiracetam (Keppra), valproate, or other antiseizure therapy.

Third-line / advanced care: ICU bundle includes ventilator care, hemodynamic support, coronary/PE/toxin/source treatment, continuous EEG where available, delayed multimodal neuroprognostication after confounders clear, family meetings, organ donation consideration, and palliative care when prognosis/goals require.

Progression and follow-up: Follow recurrent arrest, shock, EF recovery, oxygen/CO2, fever, seizures, cerebral edema, AKI, aspiration pneumonia, ICU delirium, neurologic awakening, withdrawal of life-sustaining therapy timing, rehabilitation needs, ICD/secondary prevention, and family psychological support.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Critical Care Medicine

Multiorgan failure goals of care

Pathophysiology: Multiorgan failure is progressive dysfunction of two or more organ systems from sepsis, shock, ARDS, trauma, pancreatitis, liver failure, malignancy, or cardiac arrest; prognosis depends on reversibility, baseline function, frailty, organ count, trajectory, and patient values.

How Critical Care Medicine assesses it: Assess each failing organ, reversibility, SOFA/lactate/vasopressor/ventilator/RRT trajectory, baseline cognition/function, frailty, serious comorbidities, surrogate decision-maker, advance directive, code status, acceptable outcomes, spiritual/cultural priorities, and family understanding.

Diagnosis: Use objective trajectory rather than a single score: serial SOFA components, ventilator/pressor/RRT dependence, nutrition, delirium/coma, infection/source control, imaging/labs for reversibility, and multidisciplinary input from ICU, primary teams, palliative care, ethics, and specialists.

First-line treatment: Continue time-limited ICU trial when recovery is plausible and aligned with goals: clear milestones such as lower vasopressor dose, improving oxygenation, renal recovery, neurologic awakening, source control, and daily communication in plain language.

Second-line treatment: Treat distress aggressively regardless of code status: fentanyl or hydromorphone for pain/dyspnea, anxiolysis when appropriate, delirium management, family presence, chaplain/social work, and avoid nonbeneficial labs/procedures that do not support the agreed plan.

Third-line / advanced care: If burdens outweigh benefits or goals change, transition to DNR/DNI, no escalation, comfort-focused care, or withdrawal of life support with palliative care support. Ethics consultation helps when conflict persists or surrogate decisions do not match known patient values.

Progression and follow-up: Follow organ trajectory, suffering, communication quality, family conflict, moral distress, ICU-acquired weakness, long-term disability, hospice eligibility, bereavement needs, and documentation of decisions so all teams honor the same plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Specialty role

Perioperative risk, airway, anesthesia, procedural sedation, regional anesthesia, acute/chronic pain, and safety.

Anesthesiology and Pain Medicine

Preoperative medication assessment

Pathophysiology: Preoperative medication assessment prevents anesthesia-related hypotension, bleeding, aspiration, withdrawal, adrenal crisis, hypoglycemia, serotonin/toxin interactions, and drug-device complications while avoiding unnecessary cancellation or undertreatment of chronic disease.

How Anesthesiology and Pain Medicine assesses it: Review procedure urgency/bleeding risk, anesthesia type, renal/liver function, frailty, OSA, pregnancy, allergies, anticoagulants/antiplatelets, GLP-1/GIP agents, SGLT2 inhibitors, insulin, steroids, ACE/ARB/diuretics, beta blockers, opioids/benzodiazepines, MAOIs/SSRIs, herbal supplements, and implanted devices.

Diagnosis: Use medication reconciliation with exact last dose, indication, thrombotic risk, renal function/eGFR, CBC/platelets/coags when anticoagulated or bleeding risk, A1c/glucose when diabetes, ECG when cardiac risk, pregnancy test when appropriate, and cardiology/device clinic input for pacemaker/ICD or recent stent.

First-line treatment: Continue most beta blockers, calcium-channel blockers, inhalers, antiseizure drugs, Parkinson drugs, and psychiatric medications unless a specific interaction exists. Hold or adjust drugs by risk: SGLT2 inhibitors such as empagliflozin (Jardiance) before major surgery, warfarin (Coumadin/Jantoven), apixaban (Eliquis), rivaroxaban (Xarelto), dabigatran (Pradaxa), clopidogrel (Plavix), and insulin plans by procedure/renal function.

Second-line treatment: Coordinate bridging only for high thrombotic-risk situations using heparin/enoxaparin (Lovenox) when appropriate; manage chronic steroids with perioperative hydrocortisone if adrenal suppression risk, avoid abrupt opioid/benzodiazepine withdrawal, and individualize GLP-1 agents such as semaglutide (Ozempic/Wegovy) or tirzepatide (Mounjaro/Zepbound) when aspiration symptoms or delayed gastric emptying risk exists.

Third-line / advanced care: Anesthesia/cardiology/hematology/endocrinology input for recent PCI/stent, mechanical valve, LVAD, severe pulmonary hypertension, brittle diabetes, adrenal insufficiency, severe OSA/OHS, complex anticoagulation, malignant hyperthermia history, or inability to safely interrupt essential medication.

Progression and follow-up: Follow day-of-surgery glucose/BP, aspiration risk, bleeding/thrombosis, withdrawal, adrenal crisis, postoperative restart timing, renal function, delirium, medication omissions, and discharge instructions that restore chronic therapy safely.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Difficult airway risk

Pathophysiology: Difficult airway risk arises when anatomy, physiology, pathology, positioning, or emergency context makes mask ventilation, supraglottic ventilation, intubation, oxygenation, or emergency front-of-neck access difficult; hypoxemia and failed rescue are the lethal pathways.

How Anesthesiology and Pain Medicine assesses it: Assess prior difficult airway, Mallampati, mouth opening, thyromental distance, neck mobility, dentition, beard/obesity/OSA, pregnancy, cervical spine disease, facial/airway trauma, tumors/infection/angioedema, aspiration risk, hemodynamic reserve, oxygen reserve, and whether awake airway is safer than induction.

Diagnosis: Use focused airway exam plus review prior anesthesia records, imaging for neck mass/trauma when relevant, flexible nasolaryngoscopy for upper-airway pathology, oxygenation/ventilation reserve assessment, and a written primary/rescue plan including equipment and skilled help.

First-line treatment: Prepare oxygenation first: preoxygenation, apneic oxygenation, ramped positioning, suction, two working IVs, video laryngoscope, bougie, supraglottic airway, fiberoptic scope, difficult-airway cart, and explicit call for help. Awake intubation is favored when difficult ventilation/intubation or aspiration/airway obstruction risk is high.

Second-line treatment: If asleep approach is chosen, limit attempts, optimize between attempts, change technique early, maintain oxygenation with mask/SAD, and use drugs suited to physiology such as ketamine, etomidate, propofol, rocuronium, succinylcholine, phenylephrine, or norepinephrine as appropriate.

Third-line / advanced care: Cannot intubate/cannot oxygenate requires emergency front-of-neck access, usually cricothyrotomy, without prolonged repeated laryngoscopy. ENT/anesthesia backup, ECMO consideration for extreme airway obstruction, and postoperative airway plan/ICU monitoring are needed for high-risk extubation.

Progression and follow-up: Follow hypoxemia time, aspiration, airway edema, dental/soft-tissue injury, hemodynamic collapse, awareness, failed extubation, documentation in the record, patient notification, and future difficult-airway alert.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Procedural sedation

Pathophysiology: Procedural sedation intentionally depresses consciousness and pain perception, but can unintentionally progress to deep sedation/general anesthesia with airway obstruction, hypoventilation, aspiration, hypotension, dysrhythmia, or failed procedure conditions.

How Anesthesiology and Pain Medicine assesses it: Assess ASA class, airway/OSA/obesity, fasting status, aspiration risk, pregnancy, age/frailty, cardiopulmonary disease, renal/liver disease, opioid/benzodiazepine tolerance, allergies, prior sedation events, procedure pain/duration, and need for moderate versus deep sedation or anesthesia support.

Diagnosis: Before sedation document focused airway/heart/lung exam, baseline vitals, oxygen saturation, pregnancy/glucose testing when relevant, last oral intake, consent, rescue plan, and medication dosing plan. Monitoring includes continuous pulse oximetry, blood pressure, ECG when risk, level of consciousness, and capnography when feasible especially for moderate/deep sedation.

First-line treatment: Use supplemental oxygen unless contraindicated, dedicated monitor, suction/airway equipment, bag-mask, reversal agents naloxone (Narcan) and flumazenil (Romazicon), and titrated agents such as midazolam (Versed), fentanyl, ketamine (Ketalar), propofol (Diprivan), etomidate, nitrous oxide, or dexmedetomidine (Precedex) by procedure and clinician privileges.

Second-line treatment: Manage complications immediately: airway reposition/jaw thrust/oral airway, bag-mask ventilation, reduce/stop sedative, IV fluids/vasopressors for hypotension, antiemetic ondansetron (Zofran), treat laryngospasm with CPAP/succinylcholine if severe, and reverse opioids/benzodiazepines only when clinically necessary because pain/withdrawal can recur.

Third-line / advanced care: Anesthesia consultation for anticipated difficult airway, severe OSA/OHS, unstable cardiopulmonary disease, high aspiration risk, prolonged painful procedure, prior sedation failure, pregnancy complexity, or need for deep sedation beyond local capability.

Progression and follow-up: Follow return to baseline mental status, oxygenation/ventilation, pain/nausea, delayed respiratory depression, paradoxical reactions, emergence agitation, aspiration, discharge escort criteria, procedure success, and documentation of adverse events.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Postoperative nausea and vomiting

Pathophysiology: Chemotherapy-induced nausea/vomiting is mediated by serotonin 5-HT3, substance P/NK1, dopamine, vestibular, anticipatory, and delayed inflammatory pathways; risk depends on the emetogenic regimen and patient factors.

How Anesthesiology and Pain Medicine assesses it: Assess chemo regimen emetogenicity, prior CINV, pregnancy, bowel obstruction/brain metastasis/hypercalcemia/opioids, hydration, weight loss, QT risk, constipation, steroid contraindications, and anticipatory anxiety.

Diagnosis: Clinical diagnosis after excluding emergencies: bowel obstruction, increased intracranial pressure, infection, metabolic derangement, adrenal insufficiency, or medication toxicity. Check BMP/Mg, calcium, LFTs, and imaging if symptoms are atypical/severe.

First-line treatment: Highly emetogenic regimens typically use 5-HT3 antagonist ondansetron (Zofran) or palonosetron (Aloxi), dexamethasone (Decadron), NK1 antagonist aprepitant (Emend)/fosaprepitant, and often olanzapine (Zyprexa). Moderate-risk regimens use 5-HT3 antagonist plus dexamethasone with NK1/olanzapine when indicated.

Second-line treatment: Breakthrough therapy can use prochlorperazine (Compazine), metoclopramide (Reglan), olanzapine, lorazepam (Ativan) for anticipatory component, or cannabinoid dronabinol (Marinol) in selected refractory cases.

Third-line / advanced care: IV fluids/electrolyte replacement, hospital evaluation for dehydration or obstruction, nutrition support, palliative care, and chemo regimen antiemetic escalation next cycle.

Progression and follow-up: Poor control causes dehydration, AKI, electrolyte abnormalities, malnutrition, anticipatory nausea, treatment refusal, aspiration risk, and hospitalization.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Malignant hyperthermia

Pathophysiology: Malignant hyperthermia is pharmacogenetic skeletal-muscle ryanodine receptor dysregulation, often RYR1 or CACNA1S-related, triggered by volatile anesthetics or succinylcholine, causing uncontrolled calcium release, hypermetabolism, hypercarbia, rigidity, acidosis, hyperkalemia, rhabdomyolysis, hyperthermia, and cardiac arrest.

How Anesthesiology and Pain Medicine assesses it: Suspect MH with rapidly rising end-tidal CO2 despite ventilation, tachycardia, masseter/generalized rigidity, acidosis, hyperkalemia, temperature rise late, dark urine, arrhythmia, family/personal anesthesia reaction, or unexplained perioperative collapse after triggering agents.

Diagnosis: Diagnosis is clinical during crisis; send ABG/VBG, electrolytes, CK, myoglobin/urine myoglobin, lactate, coagulation studies, renal function, and temperature/core monitoring after treatment starts. Later confirmation may involve caffeine-halothane contracture testing or genetic testing through MH specialists.

First-line treatment: Stop volatile anesthetic and succinylcholine, call MH hotline/team, hyperventilate with 100% oxygen, give IV dantrolene (Dantrium/Ryanodex) immediately using institutional/MHAUS dosing protocol, switch to nontriggering anesthesia, actively cool if hyperthermic, and treat hyperkalemia/acidosis.

Second-line treatment: Continue dantrolene redosing/infusion per response, manage arrhythmias avoiding calcium-channel blockers with dantrolene, give insulin/dextrose/calcium/albuterol for hyperkalemia, IV fluids and diuresis for rhabdomyolysis, monitor CK/potassium/temperature, and prepare ICU transfer.

Third-line / advanced care: ICU observation at least 24 hours after crisis because recrudescence occurs. Refer patient and family for MH susceptibility evaluation, medical alert identification, and future trigger-free anesthetic plan using total IV anesthesia/nondepolarizing paralytics.

Progression and follow-up: Follow recurrent hypermetabolism, hyperkalemic arrest, DIC, AKI from rhabdomyolysis, compartment syndrome, pulmonary edema, dantrolene weakness/hepatotoxicity, family screening, and clear documentation of trigger avoidance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Acute postoperative pain

Pathophysiology: Acute postoperative pain arises from tissue injury, inflammatory mediators, nerve injury, muscle spasm, drains/tubes, and central sensitization; undertreated pain impairs breathing, mobility, sleep, and recovery, while overtreatment causes respiratory depression, ileus, delirium, and persistent opioid use.

How Anesthesiology and Pain Medicine assesses it: Assess procedure expected pain, pain score/function, opioid tolerance/OUD, OSA/OHS, age/frailty, renal/liver disease, bleeding risk, regional anesthesia options, neuropathic features, nausea/ileus, sedation/respiratory rate, bowel regimen, and patient goals.

Diagnosis: Pain is clinical but severe or escalating pain requires evaluation for bleeding, compartment syndrome, anastomotic leak, infection, ischemia, urinary retention, hardware problem, or nerve injury. Use sedation scores, pulse oximetry/capnography when high risk, and targeted imaging/labs by complication concern.

First-line treatment: Use multimodal analgesia: scheduled acetaminophen (Tylenol), NSAID such as ibuprofen/ketorolac/celecoxib when renal/bleeding/anastomosis risk allows, local/regional block, ice/elevation/splinting, and short-acting opioids such as oxycodone, hydromorphone (Dilaudid), or morphine only when needed for function.

Second-line treatment: For severe pain use PCA hydromorphone or morphine with monitoring, ketamine infusion for opioid-tolerant or hyperalgesia risk, gabapentin/pregabalin selectively for neuropathic pain with sedation caution, muscle relaxant only when spasm is clear, and bowel regimen with senna/polyethylene glycol.

Third-line / advanced care: Acute pain/anesthesia service for epidural/nerve catheter, uncontrolled pain despite escalating opioids, OSA with opioid needs, opioid tolerance/OUD, regional block complication, or concern for surgical complication. Naloxone (Narcan) and airway support are required for opioid-induced respiratory depression.

Progression and follow-up: Follow pain with coughing/deep breathing/ambulation, sedation, oxygenation, bowel function, nausea, falls, delirium, renal/GI bleeding from NSAIDs, opioid quantity at discharge, taper plan, persistent postsurgical pain, and safe storage/disposal.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Regional anesthesia complications

Pathophysiology: Regional anesthesia complications include local anesthetic systemic toxicity, neuraxial hematoma/abscess, nerve injury, pneumothorax, intravascular injection, high spinal, hypotension, urinary retention, infection, falls/weakness, and block failure; risk depends on site, dose, anticoagulation, anatomy, and monitoring.

How Anesthesiology and Pain Medicine assesses it: Assess block site, local anesthetic type/dose, epinephrine use, ultrasound/nerve stimulator details, anticoagulants/antiplatelets, coagulopathy, infection, neurologic baseline, new tinnitus/metallic taste/seizure, hypotension/bradycardia, dyspnea, motor/sensory deficit, back pain, fever, or bladder dysfunction.

Diagnosis: LAST is clinical; monitor ECG and neurologic symptoms. Suspected neuraxial hematoma/abscess needs urgent MRI and neurosurgery. Persistent focal deficit needs neurologic exam and possible EMG/imaging. Dyspnea after interscalene/supraclavicular block may need chest imaging or ultrasound.

First-line treatment: For LAST: stop local anesthetic, call for help, airway/oxygenation, seizure control with benzodiazepine, and 20% lipid emulsion per ASRA checklist while avoiding additional local anesthetic, large epinephrine doses, beta blockers, calcium-channel blockers, and vasopressin.

Second-line treatment: Treat high spinal with airway/ventilation, fluids, vasopressors such as phenylephrine/ephedrine/norepinephrine, and bradycardia treatment atropine/epinephrine. Manage hypotension, urinary retention, falls risk, and block failure with alternative analgesia.

Third-line / advanced care: Urgent decompression pathway for neuraxial hematoma/abscess symptoms; ICU/ED for cardiovascular LAST, refractory seizure, pneumothorax, respiratory compromise, or persistent neurologic deficit. Document event and adjust future regional plans.

Progression and follow-up: Follow neurologic recovery, catheter site infection, anticoagulant restart timing, rebound pain, falls/pressure injury from numb limb, persistent neuropathy, litigation/documentation needs, and patient counseling for future anesthesia.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Opioid-tolerant perioperative care

Pathophysiology: Opioid-tolerant perioperative care manages receptor tolerance, physical dependence, opioid-induced hyperalgesia, withdrawal risk, OUD treatment continuity, respiratory depression, and higher analgesic needs after surgery.

How Anesthesiology and Pain Medicine assesses it: Assess daily morphine milligram equivalents, last opioid dose, long-acting opioids, buprenorphine/methadone/naltrexone, OUD history, benzodiazepines/alcohol, OSA/OHS/COPD, renal/liver disease, pain diagnosis, prior ketamine/regional response, withdrawal symptoms, PDMP, and discharge prescriber.

Diagnosis: Use accurate medication reconciliation, PDMP, urine toxicology only when clinically useful, baseline pain/function goals, sedation/respiratory risk assessment, ECG/QTc for methadone, pregnancy status when relevant, and coordinate with addiction/pain prescribers before surgery.

First-line treatment: Continue baseline opioid or MOUD in most cases, including methadone and often buprenorphine (Suboxone/Subutex/Sublocade) with split dosing or supplemental full agonist plan. Use multimodal analgesia: acetaminophen, NSAID if safe, regional anesthesia, ketamine, dexmedetomidine, clonidine, gabapentinoid selectively, and nonpharmacologic measures.

Second-line treatment: Expect higher opioid requirements with PCA hydromorphone/morphine/fentanyl titrated to function and monitoring; avoid mixed agonist-antagonists that precipitate withdrawal. For naltrexone (Vivitrol/Revia), elective planning may require timing/alternative analgesia and relapse prevention.

Third-line / advanced care: Pain/addiction/anesthesia consult for high-dose opioids, OUD, methadone/buprenorphine complexity, severe OSA, benzodiazepine co-use, uncontrolled pain, or discharge taper planning. Provide naloxone, bowel regimen, safe storage, and clear single-prescriber handoff.

Progression and follow-up: Follow withdrawal, oversedation/respiratory depression, pain function, hyperalgesia, ileus, delirium, relapse/overdose risk, QTc with methadone, opioid taper, and transition back to preoperative regimen or safer long-term plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Chronic neuropathic pain

Pathophysiology: Chronic neuropathic pain arises from lesion or disease of somatosensory pathways causing ectopic firing, peripheral/central sensitization, allodynia, hyperalgesia, dysesthesia, sleep disturbance, mood impairment, and functional decline.

How Anesthesiology and Pain Medicine assesses it: Assess distribution, burning/electric/allodynia/numbness, diabetes, shingles, radiculopathy, chemotherapy, HIV, alcohol/B12, entrapment, spinal cord injury, CRPS signs, depression/anxiety/sleep, substance risk, falls, renal function, and red flags such as progressive weakness, myelopathy, cancer, infection, or cauda equina.

Diagnosis: Clinical phenotype plus neurologic exam; use A1c, B12, TSH, SPEP, HIV/hepatitis when indicated, EMG/NCS for large-fiber neuropathy/radiculopathy/entrapment, MRI spine for radicular or myelopathic red flags, and skin biopsy/autonomic testing for suspected small-fiber neuropathy.

First-line treatment: First-line drugs include duloxetine (Cymbalta), venlafaxine (Effexor XR), gabapentin (Neurontin), pregabalin (Lyrica), nortriptyline/amitriptyline when safe, topical lidocaine 5% patch, and capsaicin; combine with PT, sleep treatment, mood care, and disease-specific control such as diabetes management.

Second-line treatment: If inadequate, optimize dose/duration, rotate class, combine complementary agents cautiously, consider tramadol or tapentadol only selectively, and use interventional options such as epidural steroid injection for radicular pain or peripheral nerve procedures when anatomy supports it.

Third-line / advanced care: Pain medicine/neurology for progressive neurologic deficit, refractory pain, spinal cord stimulation or dorsal root ganglion stimulation, intrathecal therapy, complex polypharmacy, opioid risk, or unclear diagnosis. Avoid chronic full-agonist opioids as routine first-line neuropathic therapy.

Progression and follow-up: Follow pain interference, sleep, mood/suicide, falls/sedation, edema/weight gain from gabapentinoids, anticholinergic effects from TCAs, serotonin/BP effects from SNRIs, function, work, and central sensitization.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Complex regional pain syndrome

Pathophysiology: Complex regional pain syndrome is disproportionate regional pain after injury/surgery/immobilization with peripheral and central sensitization, autonomic dysregulation, neurogenic inflammation, motor dysfunction, edema, sweating, temperature/color change, trophic changes, and cortical reorganization.

How Anesthesiology and Pain Medicine assesses it: Assess inciting event, pain disproportion, allodynia/hyperalgesia, temperature/color asymmetry, edema/sweating, ROM weakness/tremor/dystonia, skin/hair/nail changes, immobilization, mood/sleep, function, opioid exposure, and mimics such as infection, DVT, compartment syndrome, neuropathy, fracture, or inflammatory arthritis.

Diagnosis: Use Budapest criteria clinically; imaging/labs only to exclude mimics. X-ray may show osteopenia late, triple-phase bone scan/MRI can support selected cases but do not replace clinical criteria. Evaluate for nerve injury if type II CRPS suspected.

First-line treatment: Early aggressive functional restoration is central: PT/OT with graded exposure, desensitization, mirror therapy/graded motor imagery, edema control, sleep/mood treatment, and analgesics such as NSAIDs/acetaminophen, gabapentin/pregabalin, duloxetine, nortriptyline, or topical lidocaine.

Second-line treatment: Selected early inflammatory CRPS may use short prednisone course; bisphosphonates such as alendronate/pamidronate or calcitonin may be considered in some protocols. Sympathetic blocks can facilitate therapy in sympathetically maintained pain.

Third-line / advanced care: Pain medicine/rehab/psychology for refractory disability, ketamine infusion consideration, spinal cord or dorsal root ganglion stimulation, dystonia management, severe depression/suicidality, or diagnostic uncertainty. Avoid immobilization and escalating opioids without functional gains.

Progression and follow-up: Follow limb temperature/color, edema, ROM, strength, gait/hand use, pain interference, fear avoidance, mood, sleep, opioid dependence, spread, contracture, osteopenia, and return-to-work/school function.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Epidural analgesia monitoring

Pathophysiology: Epidural analgesia delivers local anesthetic/opioid near neuraxial nerves for thoracic/abdominal/obstetric/orthopedic pain but can cause sympathectomy hypotension, motor block, respiratory depression, urinary retention, pruritus, infection, catheter migration, high neuraxial block, hematoma, or abscess.

How Anesthesiology and Pain Medicine assesses it: Assess dermatome level, pain relief, motor strength, sensory level, BP/HR, respiratory rate/sedation, oxygenation, pruritus/nausea, urinary retention, anticoagulants, platelet/coagulation status, fever/back pain, catheter site, infusion concentration/rate, and breakthrough pain pattern.

Diagnosis: Use scheduled neuraxial checks with motor/sensory exam, sedation/respiratory scoring when neuraxial opioid used, catheter site inspection, anticoagulation timing per ASRA/institution protocol, CBC/coags when clinically needed, and urgent MRI for new severe back pain, motor weakness, sensory loss, or bowel/bladder dysfunction.

First-line treatment: Adjust infusion of local anesthetic such as bupivacaine (Marcaine) or ropivacaine plus opioid fentanyl/hydromorphone as appropriate; treat hypotension with fluids, phenylephrine/ephedrine, dose reduction, or vasopressor support by setting; use naloxone (Narcan) for significant opioid respiratory depression.

Second-line treatment: Manage pruritus/nausea with nalbuphine, ondansetron, or low-dose naloxone infusion per protocol; unilateral block may need repositioning/bolus/catheter adjustment; inadequate analgesia needs acute pain service review and multimodal adjuncts.

Third-line / advanced care: Stop infusion and urgently evaluate for high spinal, epidural hematoma/abscess, local anesthetic toxicity, catheter infection, or progressive neurologic deficit. Coordinate safe catheter removal around heparin, LMWH, DOACs, warfarin, antiplatelets, and thrombolytics.

Progression and follow-up: Follow pain with breathing/mobilization, hypotension, falls from motor block, respiratory depression, urinary retention, ileus, pruritus, infection, neuraxial hematoma timing, anticoagulant restart, and transition to oral analgesia.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Anesthesiology and Pain Medicine

Perioperative anticoagulation coordination

Pathophysiology: Perioperative anticoagulation coordination balances surgical bleeding and neuraxial hematoma risk against thrombosis from atrial fibrillation, VTE, mechanical valves, recent PCI/stent, stroke, LVAD, thrombophilia, or active cancer.

How Anesthesiology and Pain Medicine assesses it: Assess drug, indication, last dose, renal function, bleeding risk of procedure, neuraxial/regional plan, thrombotic risk, prior stroke/VTE timing, mechanical valve type/location, CHA2DS2-VASc, recent stent/ACS, platelet count, liver disease, and surgeon/anesthesia/cardiology priorities.

Diagnosis: Use medication reconciliation, eGFR, CBC/platelets, PT/INR for warfarin, anti-Xa/dilute thrombin time only in selected urgent DOAC situations, ECG/cardiology notes for stent/valve risk, and ASRA/institution neuraxial timing tables for block/catheter placement and removal.

First-line treatment: For elective cases, hold warfarin (Coumadin/Jantoven), apixaban (Eliquis), rivaroxaban (Xarelto), edoxaban (Savaysa), dabigatran (Pradaxa), clopidogrel (Plavix), prasugrel (Effient), ticagrelor (Brilinta), and aspirin only when bleeding risk outweighs thrombosis risk, with timing based on renal function/procedure risk.

Second-line treatment: Bridge with unfractionated heparin or enoxaparin (Lovenox) only for selected high-thrombotic-risk patients; many atrial fibrillation or remote VTE patients should not be bridged. Continue aspirin for many secondary-prevention/stent situations unless surgical bleeding risk is prohibitive.

Third-line / advanced care: Urgent reversal may require vitamin K and 4-factor PCC (Kcentra) for warfarin, idarucizumab (Praxbind) for dabigatran, andexanet alfa (Andexxa) or PCC for factor Xa inhibitors by protocol, platelet strategy for antiplatelet-associated life-threatening bleeding, and multidisciplinary decision-making.

Progression and follow-up: Follow postoperative bleeding, hematoma/neuraxial symptoms, VTE/stroke/MI/stent thrombosis, catheter removal timing, renal function, restart time, patient instructions, and handoff so anticoagulation is not accidentally omitted or restarted too early.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Specialty role

Operative and perioperative management of abdominal, soft tissue, endocrine, breast, emergency, and procedural surgical disease.

General Surgery

Appendicitis

Pathophysiology: Appendicitis usually begins with luminal obstruction from lymphoid hyperplasia, fecalith, tumor, or parasite, causing bacterial overgrowth, venous congestion, ischemia, suppuration, and possible gangrene/perforation with abscess or diffuse peritonitis.

How General Surgery assesses it: Assess migratory periumbilical-to-RLQ pain, anorexia, nausea/vomiting after pain onset, fever, Rovsing/psoas/obturator signs, peritonitis, pregnancy status, immunosuppression, older age, prior antibiotics, duration over 48 hours, palpable mass, and mimics such as ovarian/testicular torsion, ectopic pregnancy, ureteral stone, Crohn disease, and gastroenteritis.

Diagnosis: Use CBC with differential, CMP, urinalysis, pregnancy test when relevant, CRP selectively, and imaging by patient: ultrasound can be first-line in children/pregnancy, CT abdomen/pelvis with IV contrast is highly definitive in many adults, and MRI is useful in pregnancy or radiation avoidance. Look for appendicolith, perforation, abscess, phlegmon, or alternative disease.

First-line treatment: Keep NPO, give IV fluids, analgesia such as morphine or hydromorphone (Dilaudid), antiemetic ondansetron (Zofran), and antibiotics covering gram-negatives/anaerobes such as ceftriaxone (Rocephin) plus metronidazole (Flagyl), cefoxitin, or piperacillin-tazobactam (Zosyn) for complicated/septic cases.

Second-line treatment: Laparoscopic appendectomy is definitive and favored by many surgical pathways, especially with appendicolith, perforation, abscess, diffuse peritonitis, immunocompromise, or unreliable follow-up. Carefully selected uncomplicated appendicitis may use antibiotics-first after shared decision-making and clear recurrence counseling.

Third-line / advanced care: Percutaneous drainage plus antibiotics may stabilize selected appendiceal abscess/phlegmon; urgent operation is needed for generalized peritonitis, sepsis, failed nonoperative management, obstruction, or concern for malignancy in older adults. Postop complicated cases usually receive short-course antibiotics after source control.

Progression and follow-up: Follow fever/WBC, pain, oral intake, abscess, ileus, wound infection, stump leak, recurrent appendicitis after antibiotics, missed appendiceal neoplasm, C. difficile, and return precautions for worsening pain or fever.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Cholecystitis

Pathophysiology: Acute cholecystitis is gallbladder inflammation usually from cystic duct obstruction by gallstone, causing distention, ischemia, bile inflammation, bacterial infection, empyema, gangrene, perforation, and sepsis; acalculous disease occurs in critical illness or vascular compromise.

How General Surgery assesses it: Assess RUQ/epigastric pain lasting over 4-6 hours, fever, nausea/vomiting, Murphy sign, jaundice suggesting CBD stone/cholangitis, sepsis, diabetes, pregnancy, cirrhosis, anticoagulants, prior biliary colic, organ dysfunction, and operative risk by ASA/frailty.

Diagnosis: Use CBC, CMP with bilirubin/AST/ALT/alk phos, lipase, blood cultures if septic, RUQ ultrasound for stones, wall thickening, pericholecystic fluid, sonographic Murphy sign, and bile duct dilation. HIDA scan helps when ultrasound is equivocal; MRCP/EUS/ERCP evaluate suspected choledocholithiasis/cholangitis.

First-line treatment: NPO, IV fluids, analgesia with ketorolac when safe or opioids, antiemetic ondansetron (Zofran), and antibiotics for moderate/severe/systemic disease such as ceftriaxone plus metronidazole, ampicillin-sulbactam (Unasyn), piperacillin-tazobactam, or cefepime plus metronidazole when resistant/healthcare-associated risk exists.

Second-line treatment: Early laparoscopic cholecystectomy during index admission is standard for suitable patients. If common bile duct stone or cholangitis is present, ERCP with sphincterotomy/stone extraction usually precedes or accompanies cholecystectomy planning.

Third-line / advanced care: Percutaneous cholecystostomy is used for unstable or prohibitive operative-risk patients, with interval cholecystectomy or tube management later. Emergency surgery/ICU for gangrene, perforation, emphysematous cholecystitis, abscess, diffuse peritonitis, or septic shock.

Progression and follow-up: Follow pain/fever, bilirubin/LFTs, WBC, sepsis, bile leak, retained CBD stone, pancreatitis, surgical site infection, recurrent cholecystitis after drainage, diarrhea after cholecystectomy, and need for definitive gallbladder removal.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Choledocholithiasis

Pathophysiology: Choledocholithiasis is a stone in the common bile duct causing intermittent or persistent biliary obstruction; complications include cholangitis, gallstone pancreatitis, biliary cirrhosis, hepatic abscess, and sepsis.

How General Surgery assesses it: Assess RUQ/epigastric pain, jaundice, dark urine/pale stool, fever/rigors, hypotension/confusion, pancreatitis symptoms, prior cholecystectomy, anticoagulation, pregnancy, and predictors such as bilirubin elevation, CBD dilation, visible duct stone, or cholangitis.

Diagnosis: Use CMP/LFTs with bilirubin/alk phos, CBC, lipase, blood cultures if febrile, RUQ ultrasound for duct dilation/stones, MRCP or EUS for intermediate probability, and ERCP for high-probability therapeutic cases rather than purely diagnostic use.

First-line treatment: If stable without cholangitis, keep NPO, IV fluids, analgesia, antiemetics, and plan MRCP/EUS or ERCP based on probability. Antibiotics are used when cholangitis, cholecystitis, or sepsis is present, such as ceftriaxone plus metronidazole or piperacillin-tazobactam.

Second-line treatment: ERCP with sphincterotomy, balloon/basket extraction, lithotripsy, or biliary stent clears duct stones; laparoscopic cholecystectomy follows during the same admission when gallbladder remains, especially after gallstone pancreatitis once clinically improved.

Third-line / advanced care: Urgent ERCP/biliary drainage for acute cholangitis, persistent obstruction, rising bilirubin, sepsis, or severe pancreatitis with cholangitis. Surgery/IR alternatives apply when ERCP fails or anatomy is altered.

Progression and follow-up: Follow bilirubin/LFT normalization, fever, pancreatitis, post-ERCP pancreatitis/bleeding/perforation, retained stones, recurrent cholangitis, stent occlusion, and timing of cholecystectomy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Pancreatitis surgical complication

Pathophysiology: Surgical complications of pancreatitis include infected necrosis, walled-off necrosis, pseudocyst, hemorrhage/pseudoaneurysm, abdominal compartment syndrome, gastric outlet or biliary obstruction, colon fistula, disconnected duct syndrome, and recurrent gallstone pancreatitis.

How General Surgery assesses it: Assess persistent organ failure, fever/leukocytosis after early phase, sepsis, worsening abdominal pain, inability to tolerate enteral nutrition, GI bleeding, jaundice, distention/oliguria, prior CT findings, gallstones, alcohol/triglyceride causes, and timing from onset because collections mature over weeks.

Diagnosis: Use contrast CT or MRI/MRCP to define necrosis and collections, blood cultures if septic, CBC/CMP, CRP trend selectively, CTA for bleeding/pseudoaneurysm, ultrasound/MRCP/EUS for biliary obstruction, and avoid FNA unless diagnosis of infected necrosis remains unclear and would change management.

First-line treatment: Supportive care includes enteral nutrition, analgesia, fluids guided by status, oxygen/organ support, and ERCP only for cholangitis or persistent biliary obstruction. Do not use prophylactic antibiotics for sterile necrosis.

Second-line treatment: Infected necrosis uses antibiotics with pancreatic penetration such as piperacillin-tazobactam, meropenem (Merrem), or quinolone plus metronidazole when appropriate, plus delayed step-up drainage when possible: endoscopic cystgastrostomy/necrosectomy or percutaneous drainage.

Third-line / advanced care: Surgery is reserved for failure of less invasive step-up care, abdominal compartment syndrome, bowel ischemia/perforation, uncontrolled bleeding after IR, or unstable sepsis. Cholecystectomy is needed for gallstone pancreatitis timing based on severity and collections.

Progression and follow-up: Follow organ failure, nutrition, infected necrosis, bleeding, fistula, diabetes/exocrine insufficiency, disconnected duct, recurrent admissions, drain complications, and need for multidisciplinary HPB/GI/IR/surgery care.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Incarcerated hernia

Pathophysiology: Incarcerated hernia is trapped abdominal content through a fascial defect; strangulation compromises venous and arterial flow, causing bowel ischemia, necrosis, perforation, obstruction, sepsis, and death.

How General Surgery assesses it: Assess hernia location, irreducibility duration, pain severity, skin erythema, fever, tachycardia, vomiting/obstipation, abdominal distention, peritonitis, prior repairs/mesh, pregnancy, cirrhosis/ascites, anticoagulation, and whether the hernia was forcibly reduced before evaluation.

Diagnosis: Clinical exam is key. CT abdomen/pelvis with IV contrast evaluates bowel obstruction, transition point, ischemia, perforation, and occult hernia when diagnosis is uncertain. Labs include CBC, CMP, lactate, type/screen, and coagulation tests if surgery likely; lactate can be normal early.

First-line treatment: NPO, IV access/fluids, analgesia, antiemetics, and urgent surgical evaluation. Gentle reduction may be attempted only when no strangulation/peritonitis/skin compromise/systemic toxicity is present, followed by observation and elective repair planning.

Second-line treatment: If obstruction or incarceration persists, operative repair is needed. Antibiotics such as cefazolin (Ancef) for clean repair or broader ceftriaxone plus metronidazole/piperacillin-tazobactam when bowel compromise is suspected; mesh choice depends on contamination and tissue quality.

Third-line / advanced care: Emergency surgery for strangulation, peritonitis, bowel ischemia/perforation, sepsis, skin necrosis, failed reduction, or reduction-en-masse concern. Bowel resection/stoma may be required when nonviable bowel is present.

Progression and follow-up: Follow recurrence, wound/mesh infection, chronic pain, bowel obstruction, missed ischemia after reduction, seroma/hematoma, urinary retention, and risk-factor modification such as smoking, obesity, constipation, ascites, or heavy lifting.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Small bowel obstruction

Pathophysiology: Small bowel obstruction blocks intestinal contents from adhesions, hernia, tumor, Crohn stricture, volvulus, intussusception, gallstone ileus, or radiation; closed-loop obstruction can impair perfusion and cause ischemia, necrosis, perforation, and sepsis.

How General Surgery assesses it: Assess prior abdominal surgery, hernias, cancer/Crohn history, pain colicky versus continuous, vomiting, obstipation/flatus, distention, fever, tachycardia, peritonitis, dehydration, anticoagulants, and signs of strangulation including constant pain, leukocytosis, acidosis, lactate rise, or shock.

Diagnosis: CT abdomen/pelvis with IV contrast identifies transition point, complete versus partial obstruction, closed loop, ischemia, mass, hernia, free air/fluid. Labs include CBC, CMP/Mg, lactate, VBG/ABG when ill. Plain films can support but should not delay CT when serious features exist.

First-line treatment: Initial care: NPO, IV isotonic fluids, electrolyte correction, antiemetic ondansetron, analgesia, VTE prophylaxis, and nasogastric decompression for significant vomiting/distention or complete obstruction. Antibiotics are not routine unless ischemia/perforation/sepsis suspected.

Second-line treatment: Adhesive partial SBO without ischemia may receive nonoperative management with serial exams and water-soluble contrast challenge such as Gastrografin to predict/accelerate resolution. Treat cause-specific obstruction such as incarcerated hernia or malignancy with surgery/oncology planning.

Third-line / advanced care: Immediate operation for peritonitis, closed-loop obstruction, strangulation/ischemia, perforation, incarcerated hernia, volvulus, clinical deterioration, or failure of nonoperative management. Laparoscopy may be used selectively; dense adhesions/distention often require open approach.

Progression and follow-up: Follow pain, distention, NG output, flatus/stool, electrolytes, renal function, aspiration, bowel ischemia, perforation, recurrent adhesive SBO, short bowel after resection, wound infection, and nutrition needs.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Diverticulitis surgical indications

Pathophysiology: Diverticulitis occurs when diverticular microperforation triggers localized colonic inflammation; complicated disease includes abscess, fistula, obstruction/stricture, free perforation with peritonitis, or sepsis.

How General Surgery assesses it: Assess LLQ pain, fever, bowel/urinary symptoms, immunosuppression, prior episodes, peritonitis, sepsis, abscess history, fistula symptoms such as pneumaturia/fecaluria/vaginal stool, obstruction, anticoagulants, and colon cancer screening status.

Diagnosis: CT abdomen/pelvis with IV contrast defines uncomplicated versus abscess/perforation/fistula/obstruction and excludes mimics. Labs include CBC, CMP, CRP selectively, urinalysis, pregnancy test if relevant. Colonoscopy is delayed after recovery when indicated to exclude cancer, not during acute perforation risk.

First-line treatment: Uncomplicated mild disease may be outpatient with clear liquids/advance diet, analgesia, and selective antibiotics based on risk. When antibiotics are used: amoxicillin-clavulanate (Augmentin) or ciprofloxacin (Cipro) plus metronidazole (Flagyl), avoiding fluoroquinolones when safer alternatives fit.

Second-line treatment: Complicated disease needs admission, IV fluids, bowel rest as needed, IV antibiotics such as ceftriaxone plus metronidazole or piperacillin-tazobactam, and percutaneous drainage for larger accessible abscesses, commonly around 3 cm or larger depending on clinical context.

Third-line / advanced care: Emergency surgery for diffuse peritonitis/free perforation, uncontrolled sepsis, failed drainage/antibiotics, obstruction, or clinical deterioration. Elective sigmoid colectomy is individualized for recurrent attacks, fistula, stricture, immunosuppression, or quality-of-life impact rather than episode count alone.

Progression and follow-up: Follow abscess recurrence, fistula/stricture, colonoscopy completion, C. difficile/antibiotic harm, ostomy reversal planning, recurrent diverticulitis, bowel function, and missed colorectal cancer.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Abscess incision and drainage

Pathophysiology: Cutaneous abscess is a localized pus collection from bacterial infection, often Staphylococcus aureus including MRSA, with necrotic debris and pressure that limits antibiotic penetration until drainage occurs.

How General Surgery assesses it: Assess size, fluctuance, surrounding cellulitis, fever/systemic toxicity, immunosuppression, diabetes, injection drug use, perineal/hand/face/breast location, recurrent abscesses, hidradenitis, foreign body, necrotizing infection signs, and need for procedural sedation or ultrasound guidance.

Diagnosis: Clinical exam plus bedside ultrasound when cellulitis versus abscess is uncertain or depth/location matters. Culture pus for recurrent, severe, immunocompromised, systemic, or treatment-failure cases. Check glucose/CBC only when systemic illness, diabetes, or deeper infection concern exists.

First-line treatment: Perform incision and drainage with local anesthesia such as lidocaine, adequate incision, loculation breakdown, irrigation as needed, and dressing. Routine packing is often unnecessary for small simple abscesses and increases pain; tetanus update if wound context requires.

Second-line treatment: Add antibiotics when systemic signs, extensive cellulitis, immunocompromise, extremes of age, difficult location, multiple lesions, MRSA risk, or inadequate drainage: TMP-SMX (Bactrim/Septra), doxycycline (Vibramycin), clindamycin (Cleocin), or cephalexin (Keflex) when streptococcal cellulitis predominates and MRSA risk is low.

Third-line / advanced care: Surgery/ED escalation for necrotizing infection, perirectal/deep space/hand/facial danger triangle abscess, breast abscess needing imaging/drainage planning, hidradenitis tunnels, septic patient, foreign body, or failed outpatient drainage.

Progression and follow-up: Follow pain, drainage, cellulitis spread, fever, culture results, recurrence, scarring, fistula, MRSA decolonization needs, hygiene/contact precautions, and underlying diabetes, hidradenitis, or immune compromise.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Breast mass surgical workup

Pathophysiology: Breast mass may represent cyst, fibroadenoma, abscess, fat necrosis, phyllodes tumor, papilloma, DCIS, invasive carcinoma, lymphoma, or metastasis; malignancy risk depends on age, imaging features, growth, family/genetic risk, and pathology.

How General Surgery assesses it: Assess age, pregnancy/lactation, mass duration/growth, pain, cyclicity, nipple discharge/blood, skin/nipple retraction, erythema, fever, trauma, prior biopsies, hormone use, axillary nodes, family history, BRCA/Lynch patterns, and last breast imaging.

Diagnosis: Use triple assessment: clinical exam, diagnostic mammography/tomosynthesis plus targeted ultrasound by age and pregnancy/lactation context, and image-guided core needle biopsy for BI-RADS 4/5 or discordant findings. MRI is reserved for selected extent/high-risk/occult cases.

First-line treatment: Simple cyst can be reassured or aspirated if symptomatic; abscess uses ultrasound-guided aspiration/drainage plus antibiotics such as dicloxacillin/cephalexin or MRSA-active TMP-SMX/clindamycin when indicated. Benign concordant fibroadenoma may be observed with imaging follow-up.

Second-line treatment: High-risk lesions, phyllodes tumor, discordant pathology, enlarging mass, atypia, papilloma with atypia, radial scar depending on context, or patient preference may need excisional biopsy/lumpectomy. Cancer workup adds receptor testing ER/PR/HER2 and oncology planning.

Third-line / advanced care: Breast surgery/oncology for invasive cancer/DCIS, inflammatory breast cancer concern, suspicious nodes, genetic high-risk, pregnancy-associated cancer, recurrent abscess/fistula, or imaging-pathology discordance.

Progression and follow-up: Follow pathology concordance, imaging interval, wound/hematoma after biopsy, delayed cancer diagnosis, lymphedema risk after nodal surgery, fertility/pregnancy needs, and genetic counseling when family history indicates.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Thyroid nodule surgical referral

Pathophysiology: Thyroid nodules arise from benign hyperplasia, cyst, thyroiditis, follicular neoplasm, papillary/follicular/medullary/anaplastic cancer, or metastasis; surgical concern depends on ultrasound pattern, cytology, molecular risk, compressive symptoms, growth, and thyroid function.

How General Surgery assesses it: Assess radiation exposure, family thyroid cancer/MEN2, rapid growth, hoarseness, dysphagia, dyspnea, compressive symptoms, cervical nodes, hyperthyroid symptoms, pregnancy, anticoagulants, prior ultrasound/FNA, and patient preference.

Diagnosis: Use TSH first. If TSH low, radionuclide scan determines hyperfunctioning nodule. High-resolution thyroid/neck ultrasound reports size, TI-RADS/ATA suspicious features, and lymph nodes. FNA is based on size and ultrasound risk; cytology uses Bethesda categories, with calcitonin/RET testing when medullary risk.

First-line treatment: Benign low-risk nodules use ultrasound surveillance by risk pattern, levothyroxine suppression is generally avoided, and hyperfunctioning nodules use endocrinology treatment. Symptomatic cysts may be aspirated or treated with ethanol ablation in selected centers.

Second-line treatment: Indeterminate cytology may use repeat FNA, molecular testing, diagnostic lobectomy, or surveillance depending on Bethesda category, ultrasound, size, molecular results, and patient factors.

Third-line / advanced care: Surgical referral for malignant/suspicious cytology, compressive symptoms, substernal extension, significant growth with concern, suspicious lymph nodes, medullary/anaplastic concern, or indeterminate nodules where diagnostic lobectomy is chosen. Total thyroidectomy versus lobectomy depends on cancer type/size/risk.

Progression and follow-up: Follow ultrasound growth, lymph nodes, voice changes, calcium/vocal cord risks after surgery, hypothyroidism, radioactive iodine need, thyroglobulin/calcitonin surveillance, and recurrence risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Bowel perforation

Pathophysiology: Bowel perforation releases gas, enteric contents, bacteria, and inflammatory mediators into the peritoneum or retroperitoneum, causing peritonitis, abscess, sepsis, feculent contamination, shock, and multiorgan failure.

How General Surgery assesses it: Assess sudden severe abdominal pain, peritonitis, fever, tachycardia, hypotension, immunosuppression/steroids, diverticulitis/ulcer/ischemia/cancer/IBD, recent endoscopy/surgery, trauma, foreign body, anticoagulation, and goals/operative candidacy.

Diagnosis: CT abdomen/pelvis with IV contrast is key when stable, showing free air, extraluminal contrast, focal defect, abscess, ischemia, or source. Upright chest/abdominal X-ray can show free air but is less sensitive. Labs include CBC, CMP, lactate, blood cultures if septic, coags, and type/screen.

First-line treatment: NPO, two large-bore IVs, aggressive resuscitation, broad antibiotics such as piperacillin-tazobactam, cefepime plus metronidazole, or meropenem for severe/healthcare-associated infection, analgesia, antiemetics, NG tube when obstruction/ileus/vomiting, and urgent surgical consultation.

Second-line treatment: Stable contained perforations, such as selected diverticular microperforation or small sealed iatrogenic perforation, may be managed with antibiotics, bowel rest, serial exams, and percutaneous drainage of abscess if accessible.

Third-line / advanced care: Emergency operation for diffuse peritonitis, free perforation, sepsis/shock, uncontrolled leak, ischemic bowel, cancer perforation, or failed nonoperative management. Procedures range from laparoscopic washout/repair to resection, anastomosis, Hartmann procedure, or ostomy based on contamination and physiology.

Progression and follow-up: Follow source control, lactate, WBC, fever, abscess, anastomotic leak, ostomy needs, wound infection/dehiscence, sepsis, ICU complications, nutrition, and recovery or palliative decisions in frail/high-risk patients.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Postoperative wound infection

Pathophysiology: Postoperative wound infection ranges from superficial incisional cellulitis/abscess to deep incisional infection, organ-space abscess, anastomotic leak, necrotizing infection, or infected mesh/hardware; risk rises with contamination, diabetes, obesity, smoking, immunosuppression, poor perfusion, and hematoma/seroma.

How General Surgery assesses it: Assess postop day, fever, wound pain, erythema, warmth, drainage/pus/odor, fluctuance, wound separation, crepitus, severe pain out of proportion, foreign material/mesh, systemic toxicity, glucose control, antibiotics received, and operation type including bowel/anastomosis.

Diagnosis: Open/inspect suspicious wound; culture purulence in severe/recurrent/healthcare-associated cases. Use CBC/CMP, blood cultures if septic, bedside ultrasound for fluid collection, CT abdomen/pelvis when deep/organ-space infection or leak is possible, and evaluate necrotizing infection immediately.

First-line treatment: Superficial infection requires opening part of incision, drainage, irrigation, local wound care, and antibiotics only when cellulitis/systemic signs/high-risk patient: cephalexin (Keflex), cefazolin (Ancef), or MRSA-active TMP-SMX/doxycycline/vancomycin by severity/risk.

Second-line treatment: Deep or organ-space infection needs source control with drainage, debridement, or reoperation plus broader antibiotics such as piperacillin-tazobactam, cefepime plus metronidazole, or vancomycin added for MRSA risk. Optimize glucose, nutrition, smoking cessation, and wound VAC when appropriate.

Third-line / advanced care: Emergency surgery for necrotizing soft tissue infection, fascial dehiscence/evisceration, anastomotic leak with sepsis, infected mesh with systemic illness, or uncontrolled abscess. ID/wound care/plastics for resistant organisms, chronic wounds, or complex reconstruction.

Progression and follow-up: Follow erythema/drainage, wound depth, culture narrowing, dehiscence, fistula, mesh infection, C. difficile, scarring/hernia risk, readmission, home wound care ability, and prevention for future operations.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Hemorrhoids procedural care

Pathophysiology: Hemorrhoids are symptomatic enlargement/displacement of anal cushions with venous congestion, mucosal prolapse, bleeding, thrombosis, pain, itching, or hygiene difficulty; internal hemorrhoids are graded I-IV and external thrombosis is a separate painful entity.

How General Surgery assesses it: Assess bleeding pattern, prolapse reducibility, pain severity/onset, thrombosis duration, constipation/straining, pregnancy, anticoagulants, anemia symptoms, weight loss, bowel habit change, family colorectal cancer risk, prior colonoscopy, and anorectal exam tolerance.

Diagnosis: Use inspection, digital rectal exam, anoscopy when tolerated, CBC if significant bleeding, and colonoscopy when red flags, age/screening due, persistent bleeding, iron deficiency, no clear anorectal source, or concerning symptoms exist. Do not attribute all rectal bleeding to hemorrhoids without evaluation.

First-line treatment: First-line: fiber such as psyllium, fluids, stool softening with polyethylene glycol (MiraLAX) if constipated, avoid straining/prolonged toilet sitting, sitz baths, topical hydrocortisone or lidocaine short term, and treat diarrhea/constipation drivers.

Second-line treatment: Grade I-II and selected grade III internal hemorrhoids refractory to conservative care: rubber band ligation is usually most effective office therapy; alternatives include infrared coagulation or sclerotherapy, especially when bleeding and anticoagulation context matters.

Third-line / advanced care: Excisional hemorrhoidectomy for large external or combined grade III-IV disease, recurrent/prolapsing symptoms, or failed office therapy; urgent excision may help selected severe external thrombosis within about 72 hours. Stapled hemorrhoidopexy is not routine first-line because of recurrence/complication concerns.

Progression and follow-up: Follow bleeding, anemia, pain, urinary retention after procedures, delayed post-band bleeding, thrombosis, recurrence, constipation control, anal stenosis/incontinence rare risks, and completion of colon cancer screening.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

General Surgery

Bariatric surgery complications

Pathophysiology: Bariatric surgery complications vary by procedure and timing: leak, hemorrhage, marginal ulcer, stricture, internal hernia, small bowel obstruction, gallstones, dumping, hypoglycemia, malnutrition, vitamin deficiency, GERD, weight regain, and alcohol-use vulnerability.

How General Surgery assesses it: Identify procedure (sleeve, Roux-en-Y gastric bypass, duodenal switch, band), postop timing, tachycardia, fever, abdominal/shoulder pain, vomiting/dysphagia, GI bleeding, melena, reflux, obstructive symptoms, pregnancy, NSAID/tobacco use, supplements adherence, and neurologic symptoms of thiamine deficiency.

Diagnosis: Early severe pain/tachycardia needs CT abdomen/pelvis with oral/IV contrast when feasible, upper GI contrast study or diagnostic laparoscopy if high suspicion persists. Labs: CBC, CMP, lactate, lipase, thiamine/B12/iron/vitamin D/calcium/PTH/fat-soluble vitamins by timing. Endoscopy evaluates marginal ulcer/stricture/bleeding.

First-line treatment: Stabilize NPO, IV fluids, antiemetics, analgesia, thiamine before glucose if vomiting/malnourished, broad antibiotics such as piperacillin-tazobactam for suspected leak/sepsis, proton pump inhibitor pantoprazole (Protonix) or omeprazole (Prilosec) for ulcer/reflux, and urgent bariatric surgeon contact.

Second-line treatment: Stricture may need endoscopic balloon dilation; marginal ulcer requires PPI, sucralfate (Carafate), stop NSAIDs/tobacco, test/treat H. pylori; gallstones may need cholecystectomy; deficiencies require targeted replacement; dumping/hypoglycemia uses diet adjustment and endocrine/nutrition support.

Third-line / advanced care: Emergency surgery or transfer to bariatric center for leak, internal hernia, closed-loop obstruction, perforated ulcer, uncontrolled bleeding, sepsis, or ischemia. Do not falsely reassure a post-bypass patient with intermittent severe pain and normal early imaging if internal hernia remains likely.

Progression and follow-up: Follow recurrent pain/vomiting, hydration, protein intake, micronutrients, bone health, anemia, neurologic deficits, ulcer recurrence, obstruction, weight regain, substance-use risk, pregnancy nutrition, and long-term bariatric follow-up.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Specialty role

Bone, joint, ligament, tendon, spine, sports, trauma, arthritis, and procedural musculoskeletal care.

Orthopedics and Sports Medicine

Fracture initial management

Pathophysiology: Fracture disrupts cortical/trabecular bone and periosteum; morbidity depends on displacement, joint involvement, open wound contamination, neurovascular injury, compartment pressure, bleeding, osteoporosis, and growth-plate involvement in children.

How Orthopedics and Sports Medicine assesses it: Assess mechanism, pain/deformity, open wound, skin tenting, distal pulses/capillary refill, motor/sensation, adjacent joints, anticoagulants, age/bone risk, intoxication/falls, high-energy trauma, and red flags for compartment syndrome or nonaccidental trauma when relevant.

Diagnosis: Obtain X-rays with AP/lateral/oblique views including joints above and below when needed. CT defines complex intra-articular, pelvis, spine, calcaneus, and occult fracture patterns; MRI helps occult hip/scaphoid/stress fracture. Check CBC/CMP/coags/type-screen in major trauma or operative cases.

First-line treatment: Immobilize in position of comfort, remove constricting items, give analgesia such as acetaminophen (Tylenol), ibuprofen (Advil/Motrin) or naproxen (Aleve) when safe, opioid such as oxycodone or hydromorphone for severe acute pain, ice/elevation, tetanus update, and IV cefazolin (Ancef) plus broader coverage for open fractures by severity/contamination.

Second-line treatment: Closed reduction with hematoma block, procedural sedation, splint/cast, and repeat neurovascular exam/X-ray when alignment requires. Nonoperative care is appropriate for stable, nondisplaced fractures with reliable follow-up; DVT prophylaxis is individualized for lower-extremity immobilization risk.

Third-line / advanced care: Urgent orthopedics for open fracture, neurovascular compromise, compartment syndrome, dislocation-fracture, unstable pelvic/femur fracture, displaced intra-articular fracture, pediatric physeal injury, fight bite/contamination, or failed reduction. Operative fixation depends on stability, alignment, function, and soft tissue.

Progression and follow-up: Follow pain, swelling, neurovascular status, compartment signs, skin pressure from splint, infection, nonunion/malunion, stiffness, complex regional pain syndrome, DVT, osteoporosis evaluation after fragility fracture, and rehab milestones.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Osteoarthritis procedural referral

Pathophysiology: Osteoarthritis is whole-joint degeneration with cartilage loss, subchondral remodeling, osteophytes, synovitis, meniscal/ligament changes, malalignment, muscle weakness, obesity/trauma/genetic risk, and pain sensitization.

How Orthopedics and Sports Medicine assesses it: Assess joint location, weight-bearing pain, stiffness under 30 minutes, effusion, deformity, instability, walking tolerance, falls, BMI, prior injury, inflammatory symptoms, kidney/GI/CV risk for NSAIDs, injection history, X-ray severity, and patient goals for surgery versus symptom control.

Diagnosis: Use weight-bearing X-rays for knee/hip and targeted hand/shoulder imaging when diagnosis or procedural planning needs confirmation. MRI is not routine for typical OA but helps when occult fracture, osteonecrosis, tumor, infection, or repairable meniscal/ligament pathology is suspected.

First-line treatment: Core therapy is exercise/PT, weight loss when relevant, cane/bracing, topical diclofenac (Voltaren), acetaminophen selectively, oral NSAID such as naproxen/ibuprofen/celecoxib when risk allows, and intra-articular triamcinolone (Kenalog) for flares or function-limiting pain.

Second-line treatment: Duloxetine (Cymbalta) may help chronic knee/hip OA pain; hyaluronic acid, platelet-rich plasma, or other injections depend on joint, evidence, cost, and local practice. Avoid repeated steroid injections too close to arthroplasty because of infection concern.

Third-line / advanced care: Refer orthopedics for severe pain/function loss despite optimized nonoperative care, advanced radiographic OA, deformity/instability, night/rest pain, failed injections, or arthroplasty discussion. Urgent referral for hot swollen joint, fracture, rapidly destructive hip, or suspected tumor/infection.

Progression and follow-up: Follow pain/function, walking distance, falls, NSAID renal/GI/BP toxicity, injection frequency, weight/strength, readiness for joint replacement, postop expectations, and revision/infection risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Rotator cuff tear

Pathophysiology: Rotator cuff tear involves partial or full-thickness disruption of supraspinatus, infraspinatus, subscapularis, or teres minor tendon from degenerative tendinopathy, impingement, acute trauma, or massive tear with fatty atrophy and cuff-tear arthropathy.

How Orthopedics and Sports Medicine assesses it: Assess traumatic versus atraumatic onset, night pain, overhead weakness, pseudoparalysis, drop-arm, external rotation strength, belly-press/lift-off, stiffness suggesting adhesive capsulitis, cervical radiculopathy, occupation/sport, smoking/diabetes, and prior injections/PT.

Diagnosis: Shoulder X-rays assess arthritis, superior migration, fracture, calcific tendinitis, and acromial morphology. Ultrasound or MRI confirms tear size, retraction, muscle atrophy/fatty infiltration, biceps/labrum pathology, and surgical reparability; MRI is prioritized for acute traumatic weakness.

First-line treatment: Initial nonoperative care for many degenerative or small tears includes activity modification, PT emphasizing scapular control/rotator strengthening, acetaminophen/NSAIDs if safe, topical diclofenac, and subacromial corticosteroid injection selectively for pain limiting rehab.

Second-line treatment: Acute traumatic full-thickness tear, high-demand patient, persistent weakness/pain after structured rehab, or large/retracted tear warrants orthopedic discussion for arthroscopic/open repair, biceps procedure, or debridement depending on tissue quality.

Third-line / advanced care: Massive irreparable tears may need superior capsular reconstruction, tendon transfer, balloon spacer in selected cases, or reverse shoulder arthroplasty when pseudoparalysis/cuff arthropathy exists. Urgent referral for fracture-dislocation, infection, or neurologic deficit.

Progression and follow-up: Follow strength, ROM, night pain, tear enlargement, fatty atrophy, stiffness, injection number/timing, return to work/sport, retear after repair, and progression to cuff-tear arthropathy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

ACL injury

Pathophysiology: ACL injury is rupture or sprain of the anterior cruciate ligament from pivoting, deceleration, valgus/internal rotation, or contact trauma, causing anterior/rotational instability and risk of meniscal/cartilage injury and later osteoarthritis.

How Orthopedics and Sports Medicine assesses it: Assess pop, immediate swelling/hemarthrosis, giving way, sport demands, Lachman/pivot shift/anterior drawer, collateral/PCL signs, meniscal locking, neurovascular status, growth plate maturity, prior injury, and goals for return to cutting/pivoting activity.

Diagnosis: Knee X-rays rule out fracture, Segond avulsion, tibial spine injury, or osteochondral injury. MRI confirms ACL tear and associated meniscal, MCL/LCL, PCL, chondral, bone bruise, or ramp lesions. Aspiration may relieve tense hemarthrosis and clarify lipohemarthrosis/fracture concern.

First-line treatment: Acute care is RICE/relative rest, hinged brace or immobilizer briefly when unstable, crutches, NSAIDs/acetaminophen if safe, swelling control, regain extension, and prehab PT for quadriceps activation and ROM.

Second-line treatment: Nonoperative rehab may fit low-demand or partial-stability patients. ACL reconstruction is often favored for young/high-demand pivoting athletes, recurrent instability, combined injuries, repairable meniscus, or failed rehab; graft choice includes autograft patellar tendon, hamstring, quadriceps tendon, or allograft based on age/activity.

Third-line / advanced care: Urgent ortho for locked knee, displaced bucket-handle meniscus, multiligament injury, tibial spine fracture, vascular injury, open injury, or compartment syndrome. Return to sport requires objective strength/hop/neuromuscular testing and usually many months, not just time since surgery.

Progression and follow-up: Follow swelling, extension loss/cyclops risk, quadriceps strength, instability episodes, meniscal injury, graft failure, contralateral ACL risk, return-to-sport readiness, and osteoarthritis prevention training.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Meniscal tear

Pathophysiology: Meniscal tear disrupts fibrocartilage load-sharing, shock absorption, and joint stability; traumatic vertical/bucket-handle tears differ from degenerative horizontal/root tears often associated with osteoarthritis.

How Orthopedics and Sports Medicine assesses it: Assess twisting injury, joint-line pain, effusion timing, locking/catching versus pain-only clicking, inability to fully extend, squat/Thessaly/McMurray, age/OA symptoms, ACL injury signs, prior surgery, and sport/work kneeling or pivoting demands.

Diagnosis: Weight-bearing knee X-rays evaluate OA/fracture. MRI confirms tear pattern, root involvement, displacement, chondral disease, and associated ligament injury when surgery is considered or mechanical locking persists. Arthroscopy is therapeutic rather than a diagnostic first step.

First-line treatment: Degenerative or nonlocking tears often start with PT, activity modification, weight loss when relevant, topical/oral NSAIDs if safe, acetaminophen, and corticosteroid injection for inflammatory OA flare.

Second-line treatment: Traumatic repairable tears in vascular zone, root tears with extrusion, or persistent mechanical symptoms may need arthroscopic repair or partial meniscectomy. Repair is preferred when healing potential is good because meniscal preservation reduces OA risk.

Third-line / advanced care: Urgent orthopedics for locked knee/bucket-handle tear, multiligament injury, fracture, septic arthritis concern, or inability to bear weight after acute trauma. Avoid arthroscopy for degenerative meniscal tear with OA unless true mechanical obstruction or selected failure of conservative care.

Progression and follow-up: Follow effusion, extension, mechanical locking, quadriceps strength, return to sport/work, OA progression, recurrent tear, postoperative stiffness, DVT risk, and pain that reflects OA rather than meniscus alone.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Tendinopathy

Pathophysiology: Tendinopathy is failed tendon homeostasis with collagen disorganization, matrix change, neovascularity, load intolerance, and pain; examples include Achilles, patellar, lateral epicondyle, gluteal, and rotator cuff tendinopathy.

How Orthopedics and Sports Medicine assesses it: Assess tendon site, training/workload change, focal load-related pain, morning stiffness, rupture pop/gap/weakness, fluoroquinolone or steroid exposure, inflammatory arthritis, diabetes, biomechanics, footwear/equipment, and red flags such as infection, tumor, or acute complete rupture.

Diagnosis: Usually clinical; ultrasound or MRI helps when rupture, partial tear, atypical pain, refractory symptoms, or procedural planning is suspected. X-ray can assess calcific tendinitis, enthesophyte, Haglund deformity, or bony avulsion.

First-line treatment: First-line treatment is relative load modification, progressive eccentric/heavy-slow resistance rehab, PT biomechanics, ice/heat by preference, topical diclofenac, short oral NSAID only for reactive inflammatory flares, and correction of training errors.

Second-line treatment: Adjuncts may include counterforce strap/heel lift/orthotics, extracorporeal shockwave therapy for selected chronic cases, nitroglycerin patch in select tendons, or ultrasound-guided procedures. Avoid corticosteroid injection into/near Achilles or patellar tendon because rupture risk can outweigh benefit.

Third-line / advanced care: Orthopedics/sports medicine for complete rupture, high-grade partial tear, persistent disability after 3-6 months rehab, insertional Achilles with deformity, calcific tendinitis needing barbotage, or surgical debridement/repair consideration.

Progression and follow-up: Follow pain with load, tendon capacity, return-to-sport progression, rupture signs, recurrence from rapid loading, NSAID/steroid harms, adherence to rehab, and psychosocial fear-avoidance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Carpal tunnel syndrome

Pathophysiology: Carpal tunnel syndrome is median nerve compression under the transverse carpal ligament causing ischemia/demyelination and then axonal loss; risks include repetitive wrist load, pregnancy, diabetes, hypothyroidism, obesity, rheumatoid arthritis, amyloid, and renal disease.

How Orthopedics and Sports Medicine assesses it: Assess nocturnal numbness/tingling in thumb-index-middle/radial ring fingers, shaking hand relief, thenar weakness/atrophy, Phalen/Tinel/Durkan, neck/radicular symptoms, ulnar distribution, pregnancy, diabetes/thyroid symptoms, work ergonomics, and severity/duration.

Diagnosis: Clinical diagnosis is often enough for typical mild disease. EMG/NCS confirms severity, axonal loss, atypical symptoms, workers compensation context, or preoperative baseline. Ultrasound can show median nerve enlargement. Check A1c/TSH only when clinically suggested.

First-line treatment: Neutral wrist splint at night, activity/ergonomic modification, short NSAID or acetaminophen for pain, manage pregnancy/diabetes/thyroid contributors, and nerve-gliding/hand therapy as adjunct. Avoid prolonged wrist flexion during sleep/work.

Second-line treatment: Corticosteroid injection with triamcinolone (Kenalog) or methylprednisolone can provide temporary relief and diagnostic support; repeat injections are limited. Persistent moderate symptoms, failed splint/injection, or EMG denervation should move toward surgical decompression.

Third-line / advanced care: Urgent hand surgery for thenar atrophy, objective weakness, severe EMG axonal loss, progressive sensory loss, acute CTS after fracture/bleeding/infection, or recurrence after release. Carpal tunnel release is open or endoscopic depending on surgeon/patient factors.

Progression and follow-up: Follow nocturnal symptoms, sensory recovery, grip/pinch strength, thenar wasting, work function, recurrence, pillar pain after surgery, scar sensitivity, and missed cervical radiculopathy/polyneuropathy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Septic arthritis

Pathophysiology: Septic arthritis is microbial infection of a joint causing rapid neutrophilic cartilage destruction, synovial inflammation, effusion, bacteremia risk, and sepsis; common causes include Staphylococcus aureus, streptococci, gram-negatives, and gonococcal disease.

How Orthopedics and Sports Medicine assesses it: Assess acute hot swollen painful joint, fever, inability to bear weight or move joint, prosthetic joint, immunosuppression, diabetes, RA, IVDU, recent injection/surgery, skin infection, STI risk, anticoagulation, and whether crystals are also possible.

Diagnosis: Urgent arthrocentesis before antibiotics when feasible: synovial WBC/differential, Gram stain, culture, crystals, and glucose/protein if useful. Blood cultures, CBC, ESR/CRP, CMP; X-ray for baseline, ultrasound for effusion guidance, MRI for adjacent osteomyelitis/abscess. Crystals do not exclude infection.

First-line treatment: After cultures, start empiric IV antibiotics: vancomycin (Vancocin) for MRSA plus ceftriaxone (Rocephin), cefepime (Maxipime), or piperacillin-tazobactam (Zosyn) based on gram-negative/healthcare risk; gonococcal arthritis uses ceftriaxone and STI partner management.

Second-line treatment: Drainage is required: repeated aspiration, arthroscopic lavage, or open irrigation/debridement depending on joint, organism, pus burden, hip/shoulder location, prosthesis, and response. Immobilize briefly for pain, then early ROM/PT after infection controlled.

Third-line / advanced care: Urgent orthopedics/ID for hip/shoulder infection, prosthetic joint, bacteremia/sepsis, immunocompromise, delayed presentation, adjacent osteomyelitis, or failure to improve within 24-48 hours. Do not inject steroid into a joint until infection is excluded.

Progression and follow-up: Follow pain, fever, CRP/ESR trend, culture clearance, joint ROM, cartilage destruction, osteomyelitis, prosthesis failure, antibiotic toxicity, C. difficile, and long-term postinfectious arthritis.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Osteomyelitis surgical concern

Pathophysiology: Orthopedic osteomyelitis surgical concern includes bone infection from open fracture, contiguous ulcer, hardware biofilm, postoperative infection, diabetic foot, hematogenous seeding, or vertebral spread; necrotic bone and implants prevent cure without source control in selected cases.

How Orthopedics and Sports Medicine assesses it: Assess exposed bone/probe-to-bone ulcer, open fracture contamination, hardware pain/loosening/drainage, fever, bacteremia, diabetes/PAD, immunosuppression, spine pain/neurologic deficit, sinus tract, prior antibiotics, vascular supply, and limb salvage goals.

Diagnosis: Use CBC, ESR/CRP, blood cultures when febrile or vertebral disease suspected, plain X-ray, MRI with contrast when feasible, CT for sequestrum/hardware anatomy, nuclear imaging when MRI limited, vascular studies for limb ischemia, and bone biopsy/culture before antibiotics when stable and diagnosis uncertain.

First-line treatment: If stable, obtain deep cultures before antibiotics; if septic or neurologically threatened, start empiric vancomycin plus cefepime/ceftriaxone/piperacillin-tazobactam by source and narrow to organism. Offload wounds, optimize glucose, nutrition, smoking, and perfusion.

Second-line treatment: Surgical debridement removes necrotic bone, drains abscess, manages dead space, and may require hardware removal, DAIR, staged exchange, flap coverage, or amputation when limb is unsalvageable. Oral step-down is culture-specific and may include doxycycline, TMP-SMX, fluoroquinolone-rifampin combinations, linezolid, or beta-lactams.

Third-line / advanced care: Urgent orthopedics/spine/ID/vascular for epidural abscess, neurologic deficit, unstable spine, sepsis, limb ischemia, gas/necrotizing infection, infected nonunion, prosthetic joint infection, or failure of antibiotics alone.

Progression and follow-up: Follow wound closure, pain/function, ESR/CRP, recurrence, hardware loosening, pathologic fracture, antibiotic renal/hepatic/marrow toxicity, C. difficile, amputation risk, and biofilm relapse.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Low back pain with radiculopathy

Pathophysiology: Lumbar radiculopathy is nerve-root inflammation/compression from disc herniation, foraminal stenosis, spondylolisthesis, facet/ligament hypertrophy, tumor, infection, fracture, or diabetic radiculoplexus neuropathy, causing dermatomal pain, numbness, weakness, and reflex changes.

How Orthopedics and Sports Medicine assesses it: Assess pain distribution, neurologic deficits, straight-leg raise/slump, bowel/bladder retention or saddle anesthesia, fever, cancer, trauma, steroid/IVDU/immunosuppression, weight loss, osteoporosis, progressive weakness, work demands, mood, and prior spine surgery.

Diagnosis: No immediate imaging for uncomplicated acute radiculopathy without red flags. MRI lumbar spine is indicated for cauda equina, infection/tumor/fracture concern, progressive deficit, or persistent disabling symptoms when injection/surgery considered. X-ray assesses instability/trauma; EMG helps unclear chronic radiculopathy versus neuropathy.

First-line treatment: Encourage activity as tolerated, PT/exercise, heat, NSAID such as naproxen/ibuprofen if safe, acetaminophen, short muscle relaxant such as cyclobenzaprine (Flexeril) for spasm, and neuropathic agent gabapentin/pregabalin/duloxetine selectively. Avoid routine early opioids or bed rest.

Second-line treatment: Epidural steroid injection may help short-term radicular pain in selected disc herniation/stenosis after imaging. Oral prednisone burst has mixed benefit and should be individualized. Address sleep, work modification, and psychosocial barriers.

Third-line / advanced care: Emergency spine surgery for cauda equina, rapidly progressive motor deficit, epidural abscess, tumor compression, unstable fracture, or severe refractory neurologic pain. Elective surgery such as microdiscectomy/laminectomy is considered for persistent disabling radiculopathy with concordant imaging.

Progression and follow-up: Follow strength/reflex/sensation, pain/function, opioid exposure, falls, work status, recurrent episodes, injection response, foot drop, bladder symptoms, and postsurgical recurrence.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Hip fracture

Pathophysiology: Hip fracture in older adults is usually fragility fracture of femoral neck, intertrochanteric, or subtrochanteric region, causing pain, immobility, bleeding, delirium risk, VTE, pneumonia, loss of independence, and high 1-year mortality.

How Orthopedics and Sports Medicine assesses it: Assess fall mechanism/syncope, anticoagulants, head injury, pain with log roll/axial load, leg shortening/external rotation, distal neurovascular status, delirium/dementia, baseline mobility, frailty, osteoporosis, pressure injury, and goals of care.

Diagnosis: AP pelvis and cross-table lateral hip X-rays are first-line; MRI detects occult fracture when X-ray negative but suspicion remains, CT if MRI unavailable. Labs include CBC/CMP/coags/type-screen, ECG, troponin selectively, vitamin D, and evaluation of reversible fall causes without delaying surgery unnecessarily.

First-line treatment: Provide fascia iliaca/femoral nerve block when available, acetaminophen plus cautious opioids such as morphine/hydromorphone, avoid traction routinely, correct dehydration/electrolytes, manage anticoagulation, delirium prevention, pressure/VTE prophylaxis, and early ortho/geriatrics co-management.

Second-line treatment: Surgery within 24-48 hours is generally associated with better outcomes when medically feasible. Displaced femoral neck fractures often need hemiarthroplasty or total hip arthroplasty in selected active patients; intertrochanteric/subtrochanteric fractures usually need intramedullary nail or sliding hip screw by pattern.

Third-line / advanced care: ICU/medicine/anesthesia optimization for unstable cardiac, sepsis, or anticoagulation reversal issues; palliative nonoperative care only when surgery does not match prognosis/goals. Postop care emphasizes early mobilization, VTE prophylaxis, osteoporosis therapy, and rehab placement.

Progression and follow-up: Follow delirium, pneumonia, VTE, pressure injury, anemia, surgical infection/dislocation/fixation failure, pain control, walking recovery, falls prevention, osteoporosis treatment such as alendronate/zoledronic acid, and mortality risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Compartment syndrome

Pathophysiology: Acute compartment syndrome occurs when pressure within a closed fascial compartment exceeds capillary perfusion, causing muscle/nerve ischemia and necrosis; triggers include tibia/forearm fractures, crush injury, reperfusion, burns, tight casts, bleeding, and exertional causes.

How Orthopedics and Sports Medicine assesses it: Assess escalating pain out of proportion, pain with passive stretch, tense compartment, paresthesia, weakness, analgesic-resistant pain, high-risk fracture/crush, anticoagulation/bleeding, obtunded or regional-anesthesia patient, and remember pulses can remain present until late.

Diagnosis: Diagnosis is clinical in awake patients. Measure compartment pressures or delta pressure when exam is unreliable or equivocal; do not delay fasciotomy for classic findings. Check CK, renal function, potassium, lactate/ABG when rhabdomyolysis or systemic injury is present.

First-line treatment: Immediately remove casts/dressings, keep limb at heart level, stop circumferential compression, provide analgesia, oxygen/resuscitation, treat hypotension, and call orthopedics emergently. Avoid elevating high above heart because perfusion may worsen.

Second-line treatment: Definitive treatment is urgent fasciotomy of all involved compartments. Associated fracture stabilization, vascular repair, debridement, and staged wound management/skin grafting may be needed. Rhabdomyolysis requires IV fluids and electrolyte management.

Third-line / advanced care: Delay causes permanent nerve palsy, Volkmann contracture, muscle necrosis, infection, amputation, hyperkalemia, AKI, and death. Chronic exertional compartment syndrome is separate and uses exercise pressure testing and elective fasciotomy only after evaluation.

Progression and follow-up: Follow pain relief, motor/sensory recovery, CK/renal function, wound closure, infection, grafting, chronic weakness/contracture, return to activity, and medicolegal-quality documentation of serial exams.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Plantar fasciitis

Pathophysiology: Plantar fasciitis is degenerative fasciopathy at the medial calcaneal tubercle from repetitive tensile load, limited ankle dorsiflexion, obesity, prolonged standing/running, poor footwear, and intrinsic foot weakness; heel spur is often incidental.

How Orthopedics and Sports Medicine assesses it: Assess first-step morning heel pain, medial plantar calcaneal tenderness, running/standing load, footwear, BMI, calf tightness, pes planus/cavus, neurologic symptoms, inflammatory arthritis, stress fracture red flags, infection, and bilateral/systemic symptoms.

Diagnosis: Clinical diagnosis. X-ray if trauma, atypical pain, failure of care, or bony lesion/stress fracture concern. Ultrasound or MRI can show plantar fascia thickening/tear or alternative diagnosis; labs only if inflammatory/systemic disease suspected.

First-line treatment: Treat with plantar fascia-specific stretching, calf stretching, activity/load modification, supportive shoes, heel cup/orthotic, night splint, ice massage, topical/oral NSAID if safe, and PT for foot/ankle strength. Most improve over months.

Second-line treatment: Persistent symptoms may use supervised PT, taping, walking boot short term, extracorporeal shockwave therapy, or carefully placed corticosteroid injection with counseling about fascia rupture/fat-pad atrophy. Platelet-rich plasma evidence and cost vary.

Third-line / advanced care: Foot/ankle referral for symptoms refractory after 6-12 months, suspected rupture, neurologic entrapment, stress fracture, inflammatory arthritis, or surgical plantar fascia release/gastrocnemius recession consideration.

Progression and follow-up: Follow first-step pain, walking/running tolerance, calf flexibility, footwear adherence, steroid injection number, rupture symptoms, chronic heel pain, compensation injuries, and gradual return-to-load plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Orthopedics and Sports Medicine

Shoulder dislocation

Pathophysiology: Shoulder dislocation, most often anterior glenohumeral, occurs after abduction/external rotation trauma or seizure/electrocution; complications include Bankart lesion, Hill-Sachs defect, rotator cuff tear, axillary nerve injury, vascular injury, and recurrent instability.

How Orthopedics and Sports Medicine assesses it: Assess mechanism, direction, first-time versus recurrent, age, seizure/electrical cause, deformity, skin tenting, distal pulses, axillary nerve sensation over deltoid, motor function, associated fracture, rotator cuff weakness in older adults, and locked posterior dislocation clues.

Diagnosis: Obtain pre-reduction X-rays when fracture, first dislocation, trauma, older age, or uncertain direction; do not delay reduction for obvious recurrent atraumatic dislocation without fracture concern per local practice. Post-reduction X-ray confirms alignment/fracture. CT for complex fracture; MRI for cuff/labrum planning.

First-line treatment: Provide analgesia/sedation or intra-articular lidocaine, perform gentle reduction technique such as traction-countertraction, external rotation, scapular manipulation, or Milch, reassess neurovascular status, immobilize in sling, ice, NSAID/acetaminophen if safe, and arrange follow-up.

Second-line treatment: Early PT restores ROM then rotator cuff/scapular strength. Young athletes/high recurrence risk, bony Bankart, engaging Hill-Sachs, recurrent instability, or contact sports need orthopedic/sports referral for stabilization discussion.

Third-line / advanced care: Urgent ortho/vascular for irreducible dislocation, fracture-dislocation, open injury, vascular compromise, persistent neurologic deficit, posterior dislocation, seizure-related bilateral injury, or older adult with acute cuff tear/pseudoparalysis.

Progression and follow-up: Follow recurrent instability, stiffness/frozen shoulder, axillary nerve recovery, rotator cuff tear, return-to-sport/work, surgical stabilization decision, and avoidance of prolonged immobilization in older adults.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Specialty role

Urinary tract, male reproductive, stone, prostate, malignancy, incontinence, procedural, and surgical urologic care.

Urology

Benign prostatic hyperplasia

Pathophysiology: Benign prostatic hyperplasia is androgen-influenced stromal and glandular enlargement in the transition zone of the prostate, increasing bladder outlet resistance, detrusor hypertrophy, incomplete emptying, nocturia, urgency, and retention risk.

How Urology assesses it: Assess IPSS/AUA-SI symptom score, weak stream, hesitancy, intermittency, straining, nocturia, urgency, retention, recurrent UTI, hematuria, stones, renal insufficiency, anticholinergics/decongestants/opioids, neurologic disease, sleep apnea/nocturnal polyuria, prostate cancer risk, and bother/goals.

Diagnosis: Use urinalysis, postvoid residual bladder scan, DRE, PSA when it would alter cancer/prostate-volume decisions, creatinine/eGFR if retention/renal concern, uroflowmetry, renal/bladder ultrasound for high residual or complications, and cystoscopy/urodynamics before procedures or atypical symptoms.

First-line treatment: Mild symptoms: watchful waiting, evening fluid/alcohol/caffeine reduction, timed voiding, constipation care, and medication review. Moderate symptoms: alpha-1 blocker tamsulosin (Flomax), alfuzosin (Uroxatral), silodosin (Rapaflo), doxazosin (Cardura), or tadalafil (Cialis) when erectile dysfunction coexists.

Second-line treatment: Large prostate/progression risk uses finasteride (Proscar) or dutasteride (Avodart), often with alpha blocker; storage symptoms may add mirabegron (Myrbetriq) or cautious antimuscarinic such as solifenacin (Vesicare) only after retention risk is checked.

Third-line / advanced care: Catheterize acute retention. Refractory bother, recurrent retention/UTI, bladder stones, renal dysfunction, gross hematuria from BPH, or high residual may need TURP, HoLEP, Rezum, UroLift, aquablation, simple prostatectomy, or suprapubic catheter planning.

Progression and follow-up: Follow IPSS, PVR, renal function, UTIs, hematuria, retention, falls from nocturia, alpha-blocker orthostasis/ejaculatory effects, 5-alpha-reductase sexual effects/PSA interpretation, and procedure complications.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Acute urinary retention

Pathophysiology: Acute urinary retention is painful inability to void from bladder outlet obstruction, detrusor underactivity, medications, constipation, infection, neurologic disease, postoperative state, urethral stricture, clot retention, or prostate enlargement; overdistention can injure detrusor and kidneys.

How Urology assesses it: Assess time since last void, suprapubic pain/distention, BPH history, urethral trauma/stricture, hematuria/clots, fever, back pain/saddle anesthesia/leg weakness, constipation, anticholinergics/opioids/decongestants, recent anesthesia, and renal failure symptoms.

Diagnosis: Bladder scan confirms high volume; urinalysis/culture when infection/hematuria, BMP/creatinine for prolonged retention or renal concern, CBC if infection/bleeding, renal ultrasound for hydronephrosis, and urgent spine MRI if cauda equina signs exist.

First-line treatment: Immediate bladder decompression with urethral Foley catheter using lidocaine jelly; coude catheter for suspected BPH. Start tamsulosin (Flomax) or alfuzosin when BPH likely and arrange trial without catheter after several days if stable.

Second-line treatment: If urethral catheter fails or urethral injury/stricture is suspected, call urology for cystoscopic placement or suprapubic catheter. Clot retention needs large-bore 3-way catheter, manual irrigation, continuous bladder irrigation, and hematuria workup.

Third-line / advanced care: Admit/urgent urology for sepsis, AKI/hydronephrosis, gross hematuria/clots, neurologic deficit, post-obstructive diuresis, difficult catheterization, urethral trauma, or recurrent retention. Treat precipitating constipation, infection, medication trigger, or neurologic cause.

Progression and follow-up: Follow urine output for post-obstructive diuresis, creatinine, catheter trauma/UTI, recurrent retention, bladder atony, hematuria source, alpha-blocker adverse effects, and definitive BPH/stricture/neurogenic bladder plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Prostatitis

Pathophysiology: Prostatitis includes acute bacterial prostatitis with ascending urinary infection and prostatic edema, chronic bacterial prostatitis with recurrent infection, and chronic pelvic pain syndrome with noninfectious pelvic floor/inflammatory pain.

How Urology assesses it: Assess fever/chills, dysuria, pelvic/perineal pain, obstructive symptoms, retention, tender/boggy prostate, recent instrumentation, STI risk, immunosuppression, sepsis, recurrent UTIs with same organism, ejaculatory pain, and chronic pain phenotype.

Diagnosis: Acute disease: urinalysis and urine culture, blood cultures if febrile/septic, CBC/CMP if ill. Avoid vigorous prostate massage. NAAT for gonorrhea/chlamydia when STI risk. CT or TRUS if abscess suspected or persistent fever. Chronic disease may use pre/post-massage urine cultures selectively.

First-line treatment: Stable acute bacterial prostatitis uses culture-guided antibiotics with prostate penetration: TMP-SMX (Bactrim/Septra), ciprofloxacin (Cipro) or levofloxacin (Levaquin) when benefits outweigh risks/resistance, or ceftriaxone (Rocephin) plus doxycycline (Vibramycin) for STI concern.

Second-line treatment: Severe/septic cases need IV ceftriaxone, cefepime, piperacillin-tazobactam (Zosyn), or carbapenem by risk plus fluids and admission. Add tamsulosin for obstruction; urinary retention may require suprapubic catheter rather than traumatic urethral catheter attempts.

Third-line / advanced care: Urology for abscess drainage, sepsis, retention, failure after 48-72 hours, recurrent bacterial prostatitis, anatomic obstruction, or chronic pelvic pain requiring pelvic floor PT, NSAIDs, alpha blocker, neuropathic pain treatment, and multimodal care.

Progression and follow-up: Follow fever, urine culture, retention, abscess, recurrent UTI, chronic pelvic pain, sexual dysfunction, antibiotic toxicity/C. difficile, fluoroquinolone tendon/QT/CNS risks, and malignancy evaluation if symptoms/PSA remain abnormal after infection resolves.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Kidney stone acute management

Pathophysiology: Acute kidney stone pain occurs when ureteral obstruction raises collecting-system pressure and triggers ureteral spasm; risk depends on stone size/location, infection, renal function, solitary kidney, pregnancy, obstruction duration, and stone composition.

How Urology assesses it: Assess colicky flank-to-groin pain, hematuria, nausea/vomiting, fever/rigors, dysuria, solitary kidney, CKD, pregnancy, immunosuppression, prior stones/procedures, anticoagulation, uncontrolled pain, and ability to hydrate/take oral meds.

Diagnosis: Noncontrast CT stone protocol is most sensitive in nonpregnant adults; renal ultrasound is first-line in pregnancy and often initial in children. Use urinalysis, urine culture if infection signs, BMP/creatinine, CBC when febrile/ill, pregnancy test, and stone analysis when passed/captured.

First-line treatment: Pain control with NSAID ketorolac/ibuprofen when renal/GI/bleeding risk allows, acetaminophen, opioids such as oxycodone/hydromorphone only for refractory pain, antiemetic ondansetron (Zofran), fluids to euvolemia, urine strainer, and tamsulosin (Flomax) for selected distal ureteral stones.

Second-line treatment: Outpatient management fits afebrile stable patients with controlled symptoms, preserved renal function, and likely passage. Antibiotics only for UTI; culture-directed options include ceftriaxone, cephalexin, TMP-SMX, or fluoroquinolone when appropriate.

Third-line / advanced care: Emergency decompression with ureteral stent or percutaneous nephrostomy is required for obstructed infected stone, sepsis, anuria, solitary kidney obstruction, AKI, intractable pain/vomiting, or high-grade obstruction. Definitive ureteroscopy/laser lithotripsy, shockwave lithotripsy, or PCNL depends on size/location.

Progression and follow-up: Follow stone passage, fever, renal function, hydronephrosis, recurrent ED visits, opioid exposure, stricture, infection, and metabolic prevention with fluids, stone analysis, and 24-hour urine for recurrent/high-risk stones.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Recurrent UTI urologic evaluation

Pathophysiology: Recurrent UTI is repeated symptomatic bacterial cystitis from reinfection or relapse; urologic concerns include stones, obstruction, incomplete emptying, fistula, foreign body, atrophic tissue, catheterization, resistant organisms, or upper-tract source.

How Urology assesses it: Confirm true symptomatic episodes, culture organisms, hematuria, pyelonephritis, stones, urinary retention/PVR, incontinence, pelvic organ prolapse, menopause/genitourinary syndrome, sexual triggers, spermicide, diabetes, immunosuppression, prior urologic surgery, and antibiotic exposure.

Diagnosis: Document urine cultures before treatment when possible. Use urinalysis/culture, PVR bladder scan, pelvic exam when relevant, renal/bladder ultrasound or CT for stones/obstruction/relapse, cystoscopy only for hematuria, suspected fistula/foreign body, cancer risk, or complicated features.

First-line treatment: Behavioral prevention: hydration, avoid spermicides, postcoital voiding optional, vaginal estrogen such as estradiol cream/tablet/ring for postmenopausal GSM, treat constipation/emptying issues, and use nonantibiotic options such as methenamine hippurate (Hiprex) in selected patients.

Second-line treatment: Antibiotic strategies include patient-initiated therapy, postcoital prophylaxis, or continuous low-dose nitrofurantoin (Macrobid), TMP-SMX, cephalexin, or fosfomycin by cultures/allergies/renal function, with stewardship and adverse-effect monitoring.

Third-line / advanced care: Urology/ID for relapsing same organism, MDR infection, stones, obstruction, high PVR/neurogenic bladder, fistula, gross hematuria, recurrent pyelonephritis, transplant/immunocompromise, or need for cystoscopy/upper tract imaging.

Progression and follow-up: Follow culture pattern, resistance, C. difficile, nitrofurantoin lung/liver toxicity, TMP-SMX renal/potassium effects, renal scarring rare in adults, quality of life, and avoidance of treating asymptomatic bacteriuria except pregnancy/procedure indications.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Hematuria workup

Pathophysiology: Hematuria may arise from bladder/upper tract cancer, kidney cancer, stones, infection, BPH, glomerular disease, trauma, exercise, anticoagulation-unmasked lesions, radiation cystitis, or gynecologic contamination; gross hematuria carries higher malignancy risk.

How Urology assesses it: Assess gross versus microscopic, smoking/occupational exposure, age, irritative symptoms, flank pain/stone history, infection symptoms, anticoagulants, pelvic radiation/cyclophosphamide, trauma, menses/gynecologic source, proteinuria/casts/edema, family renal cancer/Lynch, and prior negative workup.

Diagnosis: Confirm microhematuria by microscopy (not dipstick alone). Initial evaluation includes BP, creatinine/eGFR, urinalysis microscopy/protein, culture if infection. Risk-stratify: low-risk may repeat UA; intermediate/high-risk generally need cystoscopy plus upper tract imaging such as renal ultrasound or multiphasic CT urography, with MR urography if CT contraindicated.

First-line treatment: Treat obvious benign causes such as UTI and repeat urinalysis after resolution; do not dismiss hematuria solely because the patient takes anticoagulants. Hydrate and manage clots if gross hematuria.

Second-line treatment: Persistent or risk-based hematuria requires cystoscopy to inspect bladder/urethra; CT urogram evaluates kidneys/ureters. Urine cytology is selective for high-risk, equivocal cystoscopy, persistent hematuria with irritative symptoms, or carcinoma-in-situ concern.

Third-line / advanced care: Urgent urology/ED for gross hematuria with clot retention, anemia, AKI/obstruction, trauma, solitary kidney, or suspected malignancy. Nephrology for proteinuria, dysmorphic RBCs, casts, reduced kidney function, or systemic glomerular disease.

Progression and follow-up: Follow completion of cystoscopy/imaging, recurrence, cancer diagnosis, stone/infection treatment, renal disease markers, clot retention, patient anxiety, and shared decision-making after negative evaluation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Overactive bladder

Pathophysiology: Overactive bladder is urgency with frequency/nocturia with or without urge incontinence from detrusor overactivity, sensory urgency, neurologic disease, bladder outlet obstruction, atrophy, medications, caffeine, constipation, or sleep/volume disorders.

How Urology assesses it: Assess urgency episodes, frequency/nocturia, incontinence type, fluids/caffeine/alcohol, constipation, UTIs, hematuria, pelvic organ prolapse, neurologic symptoms, diabetes, sleep apnea, diuretics, mobility/cognition, anticholinergic burden, and PVR risk.

Diagnosis: Use urinalysis, bladder diary, symptom questionnaires, PVR when retention risk, pelvic/prostate exam as appropriate, and culture if UTI symptoms. Cystoscopy/urodynamics/imaging are reserved for hematuria, recurrent infections, pain, retention, neurologic disease, or refractory/unclear cases.

First-line treatment: First-line treatment is bladder training, timed voiding, urgency suppression, pelvic floor PT, fluid/caffeine adjustment, constipation treatment, weight loss if relevant, and manage sleep apnea/nocturnal polyuria contributors.

Second-line treatment: Medications include beta-3 agonist mirabegron (Myrbetriq) or vibegron (Gemtesa), or antimuscarinics oxybutynin (Ditropan), solifenacin (Vesicare), tolterodine (Detrol), trospium, or darifenacin; choose around BP, glaucoma, constipation, cognition, and retention risk.

Third-line / advanced care: Refractory OAB may use intradetrusor onabotulinumtoxinA (Botox) with retention/UTI counseling, percutaneous tibial nerve stimulation, or sacral neuromodulation. Urology for high PVR, hematuria, recurrent UTI, neurologic disease, or failure of medications.

Progression and follow-up: Follow urgency/incontinence diary, BP with beta-3 agonists, dry mouth/constipation/cognition with antimuscarinics, PVR/retention, UTIs after Botox, nocturia causes, falls, and quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Stress urinary incontinence

Pathophysiology: Older-adult urinary incontinence may be urgency/overactive bladder, stress incontinence, overflow retention, functional incontinence, infection, atrophic urogenital change, constipation, neurologic disease, mobility impairment, or medication effect.

How Urology assesses it: Assess urgency/frequency/nocturia, stress leakage, retention symptoms, dysuria/hematuria, fluid/caffeine, constipation, mobility, cognition, pelvic prolapse, prostate symptoms, diabetes, diuretics, sedatives, anticholinergics, alpha blockers, and patient goals.

Diagnosis: Use urinalysis for infection/hematuria, postvoid residual when retention/overflow suspected, bladder diary, cough stress test/pelvic exam when appropriate, medication review, glucose/A1c when polyuria, and avoid routine urine culture for asymptomatic bacteriuria.

First-line treatment: First-line treatment is bladder training, timed voiding, pelvic floor muscle therapy, constipation treatment, caffeine/fluid timing, mobility/toileting support, absorbent product fit, and medication adjustment.

Second-line treatment: For urgency incontinence, consider mirabegron (Myrbetriq) with BP monitoring or antimuscarinics such as trospium (Sanctura) with caution; avoid oxybutynin (Ditropan) when possible due to anticholinergic cognitive/fall risk. Vaginal estrogen such as estradiol (Estrace) may help genitourinary syndrome of menopause.

Third-line / advanced care: Refer urology/urogynecology for retention, recurrent UTI with symptoms, hematuria, prolapse, failed conservative therapy, catheter complications, or procedures such as pessary, sling, botulinum toxin, neuromodulation, or prostate intervention.

Progression and follow-up: Follow leakage episodes, falls/nocturia, skin breakdown, UTIs, cognition, BP, constipation, dry mouth, retention, caregiver burden, and quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Erectile dysfunction

Pathophysiology: Erectile dysfunction reflects impaired neurovascular erection from endothelial disease, diabetes, hypertension, dyslipidemia, hypogonadism, pelvic surgery/radiation, neurologic disease, medications, Peyronie disease, depression/anxiety, relationship factors, or substance use; it can signal occult ASCVD.

How Urology assesses it: Assess onset, rigidity/maintenance, morning erections, libido, ejaculation/orgasm, penile curvature/pain, diabetes/ASCVD risk, BP/lipids, smoking, depression, medications such as SSRIs/beta blockers/opioids, testosterone symptoms, prostate cancer treatment, and contraindications to PDE-5 inhibitors.

Diagnosis: Use focused genital/vascular/neuro exam, A1c/glucose, lipids, morning total testosterone when low libido or suggestive symptoms, TSH/prolactin selectively, and ASCVD risk evaluation. Penile duplex or specialized testing is reserved for trauma, Peyronie, surgery planning, or refractory cases.

First-line treatment: Lifestyle/ASCVD risk reduction, medication review, relationship/psychosexual support, and PDE-5 inhibitors sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra), or avanafil (Stendra) when no nitrates/riociguat and cardiac status permits.

Second-line treatment: If PDE-5 response inadequate, optimize timing/dose, testosterone replacement only for confirmed symptomatic hypogonadism after prostate/hematocrit risk review, vacuum erection device, intraurethral alprostadil (Muse), or intracavernosal alprostadil/Trimix teaching.

Third-line / advanced care: Urology for penile prosthesis, Peyronie disease, post-prostatectomy rehab, priapism risk, complex endocrine/cardiac issues, or failure of less invasive therapy. ED with chest pain/nitrate use requires cardiac care, not PDE-5 use.

Progression and follow-up: Follow erectile function, adverse effects/headache/hypotension, nitrate interactions, testosterone hematocrit/PSA, relationship distress, depression, ASCVD events, priapism, and prosthesis infection/mechanical failure.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Testicular torsion

Pathophysiology: Testicular torsion is twisting of the spermatic cord, usually from bell-clapper deformity, causing venous congestion, arterial ischemia, infarction, and fertility/endocrine harm; salvage is time-critical, best within hours.

How Urology assesses it: Assess sudden unilateral testicular pain, nausea/vomiting, high-riding or transverse testis, absent cremasteric reflex, swelling, abdominal pain in children, intermittent prior episodes, trauma, fever/urinary symptoms, and time from onset.

Diagnosis: Torsion is clinical when suspicion is high and should go directly to surgery without imaging delay. Color Doppler scrotal ultrasound helps equivocal cases but false negatives occur. Urinalysis/NAAT can assess epididymitis/STI only when torsion is less likely.

First-line treatment: Immediate urology consultation and surgical exploration with detorsion and bilateral orchiopexy. Provide analgesia, antiemetic, NPO, and preop preparation. Manual detorsion may be attempted while awaiting surgery but does not replace orchiopexy.

Second-line treatment: If nonviable testis, orchiectomy plus contralateral orchiopexy may be required. Intermittent torsion needs elective orchiopexy even if pain resolves and ultrasound is normal.

Third-line / advanced care: Do not delay for antibiotics or imaging when classic torsion. Transfer urgently if no urology available, with accepting surgeon; document neurovascular-style timing, exam, and counseling.

Progression and follow-up: Follow testicular viability/atrophy, pain resolution, wound infection, fertility, endocrine function, contralateral fixation, psychological impact, and return precautions for recurrent acute scrotum.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Epididymitis

Pathophysiology: Epididymitis is inflammation/infection of epididymis from sexually transmitted pathogens such as Chlamydia trachomatis or Neisseria gonorrhoeae, enteric gram-negatives from urinary reflux/obstruction, instrumentation, or less commonly TB/amiodarone; torsion must be excluded.

How Urology assesses it: Assess gradual posterior testicular pain, swelling, dysuria/urethral discharge, STI exposure, insertive anal sex, age, urinary obstruction/BPH, catheter/instrumentation, fever, scrotal elevation relief, cremasteric reflex, and torsion red flags.

Diagnosis: Urinalysis, urine culture, NAAT for gonorrhea/chlamydia, HIV/syphilis testing when STI risk, and scrotal Doppler ultrasound when torsion cannot be confidently excluded or abscess/mass suspected. Do not let ultrasound delay torsion surgery when classic.

First-line treatment: STI-associated: ceftriaxone (Rocephin) plus doxycycline (Vibramycin). Insertive anal sex or enteric risk may use ceftriaxone plus levofloxacin; enteric-only older men may use levofloxacin when gonorrhea excluded and risks acceptable. Add NSAIDs, scrotal elevation, ice, rest, and abstinence until treated.

Second-line treatment: Treat partners for STI, review culture results, address BPH/obstruction, and reassess within 48-72 hours if not improving. Fluoroquinolone risks require careful selection and counseling.

Third-line / advanced care: Urology/ED for severe pain, abscess, infarction, sepsis, immunocompromise, recurrent episodes, suspected tumor, prepubertal epididymitis, or diagnostic uncertainty with torsion.

Progression and follow-up: Follow pain/swelling resolution, STI reinfection, infertility/chronic scrotal pain, abscess, testicular infarction, missed torsion, and partner notification/testing.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Prostate cancer screening discussion

Pathophysiology: Prostate cancer screening seeks clinically significant adenocarcinoma while limiting overdiagnosis and overtreatment of indolent disease; risk varies by age, family history, ancestry, germline mutations, PSA density, MRI findings, and life expectancy.

How Urology assesses it: Assess age, life expectancy, urinary/prostatitis symptoms, prior PSA/biopsy/MRI, family history of prostate/breast/ovarian/pancreatic cancer, BRCA/Lynch risk, patient values about biopsy/treatment harms, medications such as finasteride, and DRE findings.

Diagnosis: Shared decision PSA testing; repeat elevated PSA before biopsy when appropriate, account for 5-alpha-reductase inhibitors, use DRE, percent free PSA/PHI/4Kscore or other biomarkers selectively, prostate MRI, PSA density, and transperineal/transrectal biopsy with targeted/systematic cores when risk remains significant.

First-line treatment: Screening interval and start age are individualized; avoid routine PSA screening when life expectancy is limited. Treat prostatitis/UTI and repeat PSA after resolution rather than biopsy during acute inflammation.

Second-line treatment: Abnormal PSA/MRI leads to urology counseling on biopsy risks, infection prevention, MRI-targeted biopsy, and active surveillance versus definitive treatment if cancer is found based on Grade Group, PSA, stage, genomic tests, and preferences.

Third-line / advanced care: Refer urology for persistently elevated PSA, abnormal DRE, high-risk family/genetic history, concerning MRI, or prior negative biopsy with rising PSA. Genetics referral for strong hereditary patterns.

Progression and follow-up: Follow PSA trend, biopsy complications, anxiety, overdiagnosis, active surveillance adherence, urinary/sexual/bowel treatment effects, metastasis risk in aggressive disease, and shared decision updates as health status changes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Bladder cancer suspicion

Pathophysiology: Bladder cancer is usually urothelial carcinoma linked to smoking, aromatic amines, chronic irritation, cyclophosphamide, pelvic radiation, and age; it presents with painless gross hematuria or irritative voiding and ranges from non-muscle-invasive to muscle-invasive/metastatic disease.

How Urology assesses it: Assess gross/microscopic hematuria, clots, dysuria/urgency without infection, smoking, occupational exposures, pelvic radiation/cyclophosphamide, recurrent UTIs, stones/catheters, flank pain, weight loss, anemia, and anticoagulant use.

Diagnosis: Cystoscopy with transurethral resection/biopsy is diagnostic. Upper tract imaging, often CT urography, evaluates kidneys/ureters. Urine cytology helps high-grade/CIS suspicion. Stage with pathology including muscle presence; CT chest/abdomen/pelvis when muscle-invasive or metastatic concern.

First-line treatment: Non-muscle-invasive disease is treated with complete TURBT, immediate intravesical gemcitabine or mitomycin in selected low-risk cases, and risk-stratified intravesical BCG for high-risk disease plus surveillance cystoscopy.

Second-line treatment: Muscle-invasive disease usually needs radical cystectomy with pelvic lymph node dissection and urinary diversion plus cisplatin-based neoadjuvant chemotherapy when eligible, or bladder-preserving trimodality therapy in selected patients.

Third-line / advanced care: Urgent urology for gross hematuria/clot retention, suspected tumor, hydronephrosis, or anemia. Oncology for locally advanced/metastatic disease using cisplatin/gemcitabine, immunotherapy pembrolizumab (Keytruda), nivolumab (Opdivo), enfortumab vedotin (Padcev), or targeted therapy by biomarkers.

Progression and follow-up: Follow recurrence/progression with cystoscopy, cytology, upper-tract surveillance, renal function after diversion, urinary infections, sexual function, neuropathy/hearing/renal toxicity from cisplatin, and smoking cessation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Urology

Renal mass

Pathophysiology: Renal mass may be simple cyst, angiomyolipoma, oncocytoma, renal cell carcinoma, urothelial carcinoma, lymphoma, infection, or metastasis; malignancy risk depends on solid enhancement, size, growth, fat, cyst complexity, hereditary syndrome, and symptoms.

How Urology assesses it: Assess incidental versus symptomatic mass, hematuria, flank pain, weight loss, fever, hypertension, varicocele, smoking, obesity, dialysis/acquired cystic disease, family renal cancer, hereditary syndromes, renal function, solitary kidney, and surgical fitness.

Diagnosis: Use multiphasic contrast CT or MRI renal mass protocol to assess enhancement, fat, venous invasion, nodes, and Bosniak cyst class. Renal ultrasound helps cyst characterization; chest imaging for suspicious RCC; biopsy when result would change management such as ablation, surveillance, lymphoma/metastasis/infection, or poor surgical candidate.

First-line treatment: Small renal masses may use active surveillance with serial imaging in older/comorbid patients; partial nephrectomy is preferred when feasible for cT1 masses to preserve renal function. Ablation cryoablation/radiofrequency is an option for selected small peripheral tumors.

Second-line treatment: Radical nephrectomy for large/central/invasive tumors when partial not feasible; manage angiomyolipoma by size/symptoms/bleeding risk with surveillance, embolization, or mTOR therapy in TSC contexts. Urothelial features require different evaluation such as CT urogram/ureteroscopy.

Third-line / advanced care: Urologic oncology for enhancing solid mass, complex Bosniak III/IV cyst, venous thrombus, hereditary/multifocal disease, solitary kidney, CKD, or metastatic concern. Medical oncology for advanced RCC using immunotherapy/VEGF-TKI combinations.

Progression and follow-up: Follow tumor growth, renal function/eGFR, proteinuria, recurrence/metastasis, post-nephrectomy CKD, bleeding from angiomyolipoma, hereditary screening, and surveillance adherence.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Specialty role

Eye and vision specialty care for medical and surgical diseases of cornea, retina, glaucoma, uveitis, trauma, and neuro-ophthalmology.

Ophthalmology

Acute angle closure glaucoma

Pathophysiology: Acute angle-closure glaucoma occurs when the anterior chamber angle abruptly closes, blocking trabecular outflow and rapidly raising intraocular pressure enough to ischemically injure the optic nerve within hours.

How Ophthalmology assesses it: Assess sudden painful red eye, blurred vision, halos, headache, nausea/vomiting, mid-dilated fixed pupil, corneal haze, shallow chamber, hyperopia, prior narrow-angle warning, and triggers such as anticholinergics, sympathomimetics, topiramate, or dilation.

Diagnosis: Check visual acuity, pupils/RAPD, slit lamp, corneal edema, anterior chamber depth, tonometry/IOP, gonioscopy by ophthalmology when feasible, and evaluate the fellow eye. Avoid dilation until angle status is safe.

First-line treatment: Emergency treatment while calling ophthalmology: topical timolol (Timoptic), brimonidine (Alphagan P), dorzolamide (Trusopt), systemic acetazolamide (Diamox) if not contraindicated, antiemetic/analgesia, and avoid precipitating medications.

Second-line treatment: When IOP begins to fall, ophthalmology may add pilocarpine (Isopto Carpine). Severe or refractory pressure may need IV mannitol or oral glycerol if safe. Definitive care is laser peripheral iridotomy, usually both eyes.

Third-line / advanced care: Immediate transfer/admission if ophthalmology unavailable, vision threatened, vomiting/dehydration, very high IOP, medication contraindications, or suspected secondary angle closure. Surgical iridectomy or lens extraction is selected by ophthalmology.

Progression and follow-up: Follow IOP, optic nerve, corneal clarity, recurrent attack, medication adverse effects, fellow-eye prophylaxis, permanent visual field loss, and cataract/lens contribution.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Conjunctivitis versus keratitis

Pathophysiology: Conjunctivitis is superficial conjunctival inflammation, while keratitis is corneal epithelial/stromal infection or inflammation that can ulcerate and scar; contact lenses, trauma, HSV, bacteria, acanthamoeba, and dry eye raise keratitis risk.

How Ophthalmology assesses it: Assess pain severity, photophobia, vision change, contact lens use, discharge, unilateral versus bilateral, foreign body/trauma, vesicles, dendritic history, immunosuppression, chemical exposure, ciliary flush, corneal opacity, and preauricular node.

Diagnosis: Measure visual acuity first, inspect pupils, fluorescein stain for epithelial defect/dendrite/ulcer, slit lamp if available, evert lids for foreign body, and culture/contact lens case for corneal ulcer, severe purulence, gonococcal concern, or refractory disease.

First-line treatment: Simple viral/allergic conjunctivitis uses hygiene, cool compresses, artificial tears, and antihistamine/mast-cell drops such as ketotifen (Zaditor/Alaway) or olopatadine (Pataday). Bacterial conjunctivitis may use polymyxin B-trimethoprim (Polytrim) or erythromycin ointment.

Second-line treatment: Contact lens wearer or suspected bacterial keratitis needs immediate lens cessation and antipseudomonal fluoroquinolone drops such as moxifloxacin (Vigamox) or ofloxacin/ciprofloxacin with same-day ophthalmology. Avoid steroid drops unless ophthalmology directs.

Third-line / advanced care: Emergency ophthalmology for corneal ulcer/infiltrate, decreased vision, severe pain/photophobia, HSV dendrite, gonococcal hyperpurulence, chemical injury, immunocompromise, contact lens keratitis, or failure to improve.

Progression and follow-up: Follow corneal staining, vision, pain, lens hygiene, recurrence, corneal scar, perforation, endophthalmitis rare risk, and accurate documentation of HSV/contact-lens disease.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Diabetic retinopathy

Pathophysiology: Diabetic retinopathy results from chronic hyperglycemia-driven retinal microvascular damage, capillary nonperfusion, leakage, ischemia, VEGF upregulation, neovascularization, vitreous hemorrhage, traction, and diabetic macular edema.

How Ophthalmology assesses it: Assess diabetes type/duration, A1c trajectory, BP/lipids/kidney disease, pregnancy, visual symptoms, prior injections/laser, OCT history, foot/kidney complications, and ability to attend frequent retina visits.

Diagnosis: Dilated retinal exam with severity staging, fundus photography, OCT for macular edema, OCT angiography/fluorescein angiography when ischemia/neovascularization or treatment planning requires, and pregnancy-specific screening for preexisting diabetes.

First-line treatment: Optimize systemic control with primary/endocrine care: glucose, BP, lipids, kidney disease, smoking. Mild/moderate nonproliferative disease often uses surveillance intervals; refer retina for DME, severe NPDR, or proliferative disease.

Second-line treatment: Center-involving DME or proliferative disease commonly uses intravitreal anti-VEGF such as aflibercept (Eylea), ranibizumab (Lucentis), faricimab (Vabysmo), or bevacizumab (Avastin off-label); steroid implants/laser are selected by lens/IOP/response context.

Third-line / advanced care: Panretinal photocoagulation treats proliferative disease and reduces severe vision loss risk; vitrectomy for nonclearing vitreous hemorrhage, tractional retinal detachment threatening macula, or combined traction/rhegmatogenous detachment.

Progression and follow-up: Follow OCT thickness, neovascularization, hemorrhage, traction, injection interval adherence, cataract/IOP steroid risks, pregnancy worsening, renal/cardiovascular risk, and irreversible vision loss.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Macular degeneration

Pathophysiology: Age-related macular degeneration involves drusen, retinal pigment epithelium dysfunction, complement/inflammatory injury, geographic atrophy, or choroidal neovascularization causing central vision loss while peripheral vision is often preserved.

How Ophthalmology assesses it: Assess age, smoking, family history, metamorphopsia, central scotoma, reading/driving difficulty, drusen history, AREDS use, anticoagulants, cardiovascular risk, and monocular symptoms.

Diagnosis: Use visual acuity, Amsler grid, dilated fundus exam, OCT to distinguish dry AMD/geographic atrophy from exudative fluid, fundus autofluorescence for atrophy, and fluorescein/OCT angiography when neovascular diagnosis is uncertain.

First-line treatment: Dry intermediate AMD: smoking cessation, AREDS2 vitamins when indicated, cardiovascular risk optimization, UV protection, home Amsler monitoring, and low-vision support. AREDS is not for people without AMD or only early minimal drusen.

Second-line treatment: Wet AMD requires prompt retina care with intravitreal anti-VEGF such as aflibercept (Eylea), ranibizumab (Lucentis), bevacizumab (Avastin off-label), faricimab (Vabysmo), or ranibizumab port delivery in selected cases.

Third-line / advanced care: Geographic atrophy may use complement inhibitors pegcetacoplan (Syfovre) or avacincaptad pegol (Izervay) in selected patients after retina counseling. Urgent evaluation for new distortion, central dark spot, hemorrhage, or sudden decline.

Progression and follow-up: Follow OCT fluid, injection response, atrophy expansion, fellow-eye conversion, endophthalmitis warning after injection, adherence, low-vision needs, driving safety, and quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Retinal detachment

Pathophysiology: Retinal detachment separates neurosensory retina from retinal pigment epithelium; rhegmatogenous detachment follows retinal tear, tractional detachment occurs in proliferative diabetic or scar disease, and exudative detachment comes from fluid leakage/inflammation/tumor.

How Ophthalmology assesses it: Assess flashes, new floaters, curtain/shadow, field loss, trauma, high myopia, prior cataract surgery, lattice degeneration, family history, diabetic retinopathy, uveitis, and whether macula appears on or off by symptoms/exam.

Diagnosis: Dilated peripheral retinal exam with scleral depression is definitive; ocular ultrasound B-scan if view obscured by vitreous hemorrhage/cataract. OCT helps macular status. Avoid delaying retina referral for nonessential imaging.

First-line treatment: Same-day emergency ophthalmology/retina referral. Keep patient NPO if surgery likely, avoid heavy activity, protect eye after trauma, and educate that painless symptoms can still be vision-threatening.

Second-line treatment: Treatment depends on tear/detachment: laser retinopexy or cryopexy for retinal tear/localized detachment, pneumatic retinopexy for selected superior uncomplicated detachments, scleral buckle, pars plana vitrectomy, or combined repair.

Third-line / advanced care: Immediate retina surgery priority for macula-on rhegmatogenous detachment, giant tear, trauma, proliferative vitreoretinopathy, tractional macular threat, or combined traction/rhegmatogenous disease. Gas bubble requires positioning and no air travel/nitrous oxide.

Progression and follow-up: Follow reattachment, proliferative vitreoretinopathy, recurrent detachment, cataract after vitrectomy, IOP, infection, visual recovery by macular status, and fellow-eye tear risk.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Uveitis

Pathophysiology: Uveitis is intraocular inflammation of iris/ciliary body/choroid/retina from autoimmune, HLA-B27 spondyloarthritis, sarcoid, Behcet, JIA, infection such as HSV/VZV/syphilis/TB/toxoplasma, drug reaction, masquerade lymphoma, or idiopathic disease.

How Ophthalmology assesses it: Assess photophobia, deep aching pain, redness/ciliary flush, blurred vision, floaters, laterality, granulomatous signs, prior episodes, back pain, psoriasis/IBD, oral/genital ulcers, pulmonary symptoms, rash, arthritis, immunosuppression, travel/TB, and STI risk.

Diagnosis: Ophthalmology slit-lamp exam identifies anterior chamber cells/flare, keratic precipitates, synechiae, IOP, vitreous/retinal involvement. Workup is targeted for recurrent, bilateral, posterior, granulomatous, severe, or systemic cases: HLA-B27, syphilis serology, TB testing, chest imaging, ACE/lysozyme, CBC/CMP, and infectious PCR when indicated.

First-line treatment: Anterior noninfectious uveitis often uses topical prednisolone acetate (Pred Forte) plus cycloplegic such as cyclopentolate or homatropine under ophthalmology direction. Check IOP and rule out herpetic/infectious keratitis before steroids.

Second-line treatment: Posterior/intermediate, severe, or recurrent disease may need periocular/intravitreal steroids, systemic prednisone, methotrexate, mycophenolate (CellCept), adalimumab (Humira), or infection-specific therapy such as acyclovir/valacyclovir, toxoplasmosis regimen, or syphilis/TB treatment.

Third-line / advanced care: Urgent ophthalmology for any suspected uveitis with pain/photophobia/vision loss, hypopyon, high IOP, posterior involvement, immunocompromise, trauma, or pediatric disease. Rheumatology/ID co-management when systemic/infectious disease suspected.

Progression and follow-up: Follow visual acuity, cells/flare, IOP/steroid response, cataract, glaucoma, cystoid macular edema, synechiae, recurrence, systemic disease activity, and immunosuppression toxicity.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Optic neuritis

Pathophysiology: Optic neuritis is inflammatory demyelination or immune optic nerve injury from multiple sclerosis, MOG antibody disease, neuromyelitis optica spectrum disorder, infection, sarcoid, lupus, drugs, or idiopathic causes.

How Ophthalmology assesses it: Assess subacute monocular vision loss, pain with eye movement, color desaturation, RAPD, visual field defect, prior neurologic symptoms, bilateral/severe/no-pain atypical features, optic disc swelling, infection/systemic symptoms, pregnancy, and recurrence.

Diagnosis: MRI brain and orbits with gadolinium evaluates optic nerve enhancement and MS lesions. OCT/visual fields document injury. Atypical or severe cases need AQP4-IgG, MOG-IgG, ESR/CRP in older patients, syphilis/Lyme/TB/HIV/sarcoid tests by context, and neurology/ophthalmology input.

First-line treatment: Typical demyelinating optic neuritis may be observed or treated with high-dose IV methylprednisolone (Solu-Medrol) or equivalent to speed recovery; avoid low-dose oral prednisone alone because recurrence risk increased in classic trial data.

Second-line treatment: AQP4/MOG or severe bilateral/recurrent disease often needs IV steroids followed by taper and plasma exchange for poor response; long-term relapse prevention uses neurology-directed immunotherapy.

Third-line / advanced care: Emergency evaluation for bilateral severe vision loss, chiasmal/neurologic deficits, older age with GCA concern, marked disc edema/hemorrhage, infection, or poor steroid response. Coordinate MS disease-modifying therapy if diagnostic criteria met.

Progression and follow-up: Follow acuity, color vision, visual fields, OCT RNFL/GCL, MRI lesions, recurrence, MS conversion risk, steroid adverse effects, and driving/work accommodations.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Corneal abrasion contact lens

Pathophysiology: Contact-lens corneal abrasion disrupts epithelium and increases risk of Pseudomonas microbial keratitis, corneal ulcer, stromal melt, scar, and vision loss, especially with overnight wear, poor hygiene, or contaminated lenses.

How Ophthalmology assesses it: Assess contact lens type/overnight wear, pain/foreign body sensation, photophobia, vision decrease, discharge, trauma/foreign body, water exposure, dendritic lesions, corneal infiltrate/opacity, and tetanus context for penetrating trauma.

Diagnosis: Measure visual acuity, fluorescein stain under cobalt blue/slit lamp, evert lids, inspect for infiltrate/ulcer/rust ring/foreign body, avoid patching contact lens abrasions, and culture only if ulcer/infiltrate or severe/refractory keratitis.

First-line treatment: Stop contact lenses. Use antipseudomonal topical antibiotic such as ofloxacin, ciprofloxacin, or moxifloxacin drops; lubricating drops/ointment; oral NSAID/acetaminophen; cycloplegic selectively for severe photophobia. Avoid topical anesthetic outpatient use unless tightly protocolized.

Second-line treatment: Small uncomplicated abrasions need follow-up within 24-48 hours, sooner if contact-lens related. Do not restart lenses until healed and asymptomatic; discard contaminated lenses/case and review hygiene.

Third-line / advanced care: Same-day ophthalmology for infiltrate/ulcer, decreased vision, large/central abrasion, contact lens wearer with severe pain, penetrating injury, dendrite/HSV concern, hypopyon, immunocompromise, or no improvement within 24 hours.

Progression and follow-up: Follow epithelial healing, infiltrate, ulcer, scar, recurrent erosion, lens hygiene, steroid avoidance unless ophthalmology directs, and return precautions for worsening pain/vision.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Orbital cellulitis

Pathophysiology: Orbital cellulitis is infection posterior to the orbital septum, often from sinusitis, causing orbital fat/muscle inflammation, abscess, optic neuropathy, cavernous sinus thrombosis, meningitis, or intracranial extension.

How Ophthalmology assesses it: Assess fever, toxic appearance, eyelid swelling/erythema, proptosis, pain with eye movement, ophthalmoplegia, diplopia, decreased vision, RAPD, color vision, chemosis, sinus/dental infection, trauma, immunocompromise, diabetes, and age.

Diagnosis: Check visual acuity, pupils/RAPD, EOMs, color vision, proptosis, IOP when safe, CBC/blood cultures if febrile, and urgent CT orbit/sinuses with contrast or MRI if intracranial/cavernous sinus concern. Distinguish preseptal cellulitis, which lacks orbital signs.

First-line treatment: Admit for IV antibiotics covering staph including MRSA, streptococci, anaerobes, and sinus pathogens: vancomycin plus ceftriaxone/cefepime/ampicillin-sulbactam, adding metronidazole when anaerobic/intracranial concern exists; nasal decongestant/sinus care by ENT as appropriate.

Second-line treatment: Drainage is needed for large subperiosteal/orbital abscess, vision compromise, afferent defect, ophthalmoplegia/proptosis progression, intracranial extension, fungal concern, dental source, or failure to improve within 24-48 hours.

Third-line / advanced care: Emergency ophthalmology and ENT; ICU/neurosurgery for cavernous sinus thrombosis, meningitis, intracranial abscess, sepsis, or invasive fungal sinusitis. Diabetic/immunocompromised patients with black eschar need urgent amphotericin-based fungal evaluation.

Progression and follow-up: Follow vision/color/RAPD, EOMs, fever/WBC, abscess size, sinus source control, antibiotic narrowing, optic neuropathy, cavernous sinus thrombosis, intracranial spread, and recurrence.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Eyelid disorders

Pathophysiology: Eyelid disorders include blepharitis/meibomian gland dysfunction, hordeolum, chalazion, ectropion/entropion, ptosis, dermatitis, trichiasis, preseptal cellulitis, and eyelid malignancy such as basal cell, squamous cell, sebaceous carcinoma, or melanoma.

How Ophthalmology assesses it: Assess lid margin crusting, focal tender nodule versus painless chalazion, lash misdirection, tearing/exposure, ptosis variability, contact dermatitis triggers, fever/cellulitis, recurrent same-site lesion, madarosis, ulceration, pearly border, pigment, and vision/corneal symptoms.

Diagnosis: Exam lid margin, lashes, meibomian glands, cornea with fluorescein if irritation/exposure, ocular motility for orbital signs, and biopsy suspicious or recurrent atypical lesions. Culture only for severe/recurrent infection.

First-line treatment: Blepharitis/MGD: warm compresses, lid hygiene, artificial tears, omega-3 selectively, topical antibiotic ointment erythromycin/bacitracin for anterior disease; hordeolum/chalazion starts warm compresses and massage, avoiding squeezing.

Second-line treatment: Persistent chalazion may need intralesional triamcinolone or incision/curettage; doxycycline can help rosacea/MGD; preseptal cellulitis uses oral amoxicillin-clavulanate or MRSA-active regimen when indicated after excluding orbital signs.

Third-line / advanced care: Ophthalmology/oculoplastics for recurrent chalazion in same location, suspicious malignancy features, corneal abrasion from entropion/trichiasis, significant ptosis, orbital signs, abscess, or failure of conservative care.

Progression and follow-up: Follow corneal exposure/abrasion, recurrence, scarring, lash loss, cellulitis spread, medication irritation, biopsy results, and ocular surface disease.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Dry eye disease

Pathophysiology: Dry eye disease is tear film instability from aqueous deficiency, evaporative meibomian gland dysfunction, inflammation, mucin deficiency, neurotrophic disease, medications, Sjogren syndrome, rosacea, screens, contact lenses, or environment.

How Ophthalmology assesses it: Assess burning/grittiness, fluctuating vision, reflex tearing, photophobia, contact lens tolerance, screen use, meds with anticholinergic effects, autoimmune sicca, rosacea/blepharitis, LASIK/cataract surgery, lagophthalmos, and severe pain out of proportion suggesting neuropathic pain.

Diagnosis: Use ocular surface exam, tear breakup time, staining with fluorescein/lissamine, Schirmer test when aqueous deficiency suspected, meibomian gland assessment, and Sjogren labs/referral when dry mouth, parotid swelling, arthritis, neuropathy, or systemic signs exist.

First-line treatment: Artificial tears, preservative-free if frequent, lubricating ointment at night, warm compress/lid hygiene for MGD, screen breaks, humidification, avoid airflow, stop offending drops/meds when possible, and treat blepharitis/rosacea.

Second-line treatment: Anti-inflammatory therapy may include topical cyclosporine (Restasis/Cequa), lifitegrast (Xiidra), short ophthalmologist-directed steroid pulse such as loteprednol, punctal plugs after inflammation controlled, oral doxycycline for rosacea/MGD, or autologous serum tears in severe disease.

Third-line / advanced care: Ophthalmology for moderate-severe symptoms, corneal staining/ulceration, Sjogren concern, neurotrophic keratopathy, exposure keratopathy, graft-versus-host disease, contact lens intolerance, or pain out of proportion.

Progression and follow-up: Follow staining, tear film, vision fluctuation, infection risk with plugs, steroid IOP/cataract risk, autoimmune features, corneal ulcer/scar, and quality-of-life/work impact.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Vision loss emergency

Pathophysiology: Acute vision loss may be retinal artery/vein occlusion, retinal detachment, vitreous hemorrhage, optic neuritis, ischemic optic neuropathy/GCA, acute glaucoma, endophthalmitis, stroke, trauma/globe injury, or functional/migraine mimic.

How Ophthalmology assesses it: Assess monocular versus binocular, onset/time last normal, pain/redness, flashes/floaters/curtain, neurologic deficits, headache/jaw claudication, trauma/surgery/injection, contact lens, vascular risks, anticoagulants, and eye movement pain.

Diagnosis: Measure visual acuity, pupils/RAPD, confrontation fields, IOP, slit lamp/fluorescein, dilated fundus if safe, ocular ultrasound if media opaque and no globe rupture, ESR/CRP/platelets for GCA concern, stroke workup for retinal artery occlusion or binocular field loss, and MRI orbits/brain for optic neuritis/neuro concern.

First-line treatment: Same-day ophthalmology or ED transfer. Treat syndrome: high-dose steroids for suspected GCA after labs without delay, IOP-lowering for angle closure, eye shield/NPO/antiemetic for globe injury, and stroke-center evaluation for central retinal artery occlusion.

Second-line treatment: Retinal detachment/tear needs retina procedure; endophthalmitis needs intravitreal antibiotics; vitreous hemorrhage needs retinal evaluation; optic neuritis may need IV methylprednisolone depending phenotype; retinal vein occlusion later uses anti-VEGF for macular edema.

Third-line / advanced care: Emergency escalation for CRAO, GCA symptoms, retinal detachment, globe injury, endophthalmitis, orbital cellulitis, acute glaucoma, neurologic deficits, or severe pain. Do not patch or press on suspected globe rupture.

Progression and follow-up: Follow visual recovery, fellow-eye risk, stroke/GCA workup completion, retinal complications, treatment timing, driving safety, and low-vision rehab.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Cataract evaluation

Pathophysiology: Cataract is crystalline lens opacity from aging, diabetes, steroids, trauma, radiation, uveitis, congenital disease, or prior surgery, causing glare, halos, reduced contrast, myopic shift, and functional vision decline.

How Ophthalmology assesses it: Assess visual function for driving/reading/falls, glare/night driving, monocular diplopia, diabetes/retinopathy, alpha-1 blocker use such as tamsulosin, anticoagulants, prior LASIK, uveitis, trauma, pseudoexfoliation, corneal disease, macular disease, and patient refractive goals.

Diagnosis: Use visual acuity with refraction, glare testing when relevant, slit-lamp lens grading, dilated retinal exam, IOP, corneal topography/biometry for intraocular lens planning, OCT macula when retinal disease or unexplained reduced vision exists.

First-line treatment: Update refraction, lighting, glare control, treat dry eye/blepharitis, optimize diabetes and ocular surface before measurements, and proceed to surgery when cataract limits activities and benefits outweigh risks.

Second-line treatment: Phacoemulsification with intraocular lens is standard; lens choice monofocal/toric/multifocal/extended-depth depends on astigmatism, macular disease, ocular surface, cost, and expectations. Tamsulosin history alerts surgeon to floppy iris risk.

Third-line / advanced care: Complex cataract referral for zonular weakness, pseudoexfoliation, small pupil, corneal disease, uveitis, prior vitrectomy, dense/brunescent lens, monocular patient, or combined glaucoma/retina procedure.

Progression and follow-up: Follow postop infection/endophthalmitis warning, cystoid macular edema, posterior capsular opacification needing YAG capsulotomy, refractive surprise, falls/driving function, and second-eye timing.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Ophthalmology

Glaucoma chronic care

Pathophysiology: Chronic glaucoma is progressive optic neuropathy, most often open-angle, with retinal ganglion cell loss and visual field damage driven by IOP susceptibility, age, family history, thin cornea, myopia, vascular factors, steroid response, and angle anatomy.

How Ophthalmology assesses it: Assess family history, race/ancestry risk, steroid use, trauma, migraine/Raynaud/sleep apnea, adherence, drop side effects, prior laser/surgery, central corneal thickness, optic nerve appearance, visual field symptoms, and angle status.

Diagnosis: Use IOP, gonioscopy, optic nerve/RNFL OCT, pachymetry, dilated optic disc exam, standard automated visual fields, optic disc photos, and staging by structure/function. Check for secondary causes such as pigment dispersion, pseudoexfoliation, uveitis, or steroid response.

First-line treatment: Lower IOP to individualized target. First-line drops often include prostaglandin analog latanoprost (Xalatan), travoprost, bimatoprost, or beta blocker timolol when no asthma/bradycardia contraindication; alternatives include brimonidine, dorzolamide, or fixed combinations.

Second-line treatment: Selective laser trabeculoplasty is first-line or add-on for open-angle glaucoma; add/switch drops based on target, adherence, cost, ocular surface, and systemic contraindications. Avoid chronic steroid exposure when possible.

Third-line / advanced care: Surgery such as trabeculectomy, tube shunt, MIGS, or cyclophotocoagulation is considered for progression despite maximal tolerated therapy, advanced disease, poor adherence, or need for cataract-combined procedure. Acute angle symptoms require emergency care.

Progression and follow-up: Follow visual fields/OCT trend, optic nerve, IOP variability, adherence, ocular surface toxicity, drop systemic effects, cataract, surgical bleb/tube complications, and vision-related function.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Specialty role

Ear, nose, throat, sinus, voice, swallowing, hearing, sleep airway, head/neck, and procedural ENT care.

Otolaryngology ENT

Chronic sinusitis

Pathophysiology: Chronic rhinosinusitis is persistent nasal and sinus mucosal inflammation lasting at least 12 weeks, driven by impaired mucociliary clearance, ostial obstruction, allergy, asthma/AERD, immune dysfunction, biofilm, fungal or eosinophilic inflammation, and sometimes nasal polyps.

How Otolaryngology ENT assesses it: Assess obstruction, purulent drainage, facial pressure, smell loss, duration, prior antibiotics/steroids, asthma, aspirin/NSAID reactions, allergic rhinitis, immune deficiency, dental symptoms, prior sinus surgery, occupational irritants, and red flags such as unilateral bleeding, cranial neuropathy, orbital symptoms, severe headache, or immunocompromise.

Diagnosis: Diagnosis requires symptoms plus objective inflammation on anterior rhinoscopy, nasal endoscopy, or CT sinus without contrast. Culture purulence endoscopically for refractory disease, evaluate allergy/immune deficiency when recurrent, and use dental imaging or CT when odontogenic sinusitis is suspected.

First-line treatment: First-line therapy is daily high-volume saline irrigation plus intranasal corticosteroid such as fluticasone (Flonase), budesonide respules mixed in irrigation (Pulmicort, off-label), mometasone (Nasonex), or triamcinolone (Nasacort). Treat comorbid allergic rhinitis with azelastine (Astelin/Astepro) or cetirizine (Zyrtec) when relevant.

Second-line treatment: Acute bacterial exacerbations may use amoxicillin-clavulanate (Augmentin) or doxycycline (Vibramycin) guided by severity, allergy, and culture. Short oral prednisone (Deltasone) can help severe polypoid/eosinophilic inflammation when risks are acceptable.

Third-line / advanced care: ENT rhinology referral for endoscopic sinus surgery, image-guided surgery, polypectomy, culture-directed therapy, evaluation for allergic fungal rhinosinusitis, CSF leak, invasive fungal disease, or biologics such as dupilumab (Dupixent), omalizumab (Xolair), or mepolizumab (Nucala) for severe nasal polyps.

Progression and follow-up: Follow SNOT-22 symptoms, smell, endoscopic inflammation, CT burden, asthma control, steroid exposure, antibiotic adverse effects, recurrence after surgery, orbital/intracranial complications, and unilateral tumor mimics.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Recurrent otitis media

Pathophysiology: Recurrent acute otitis media reflects repeated middle-ear infection from eustachian tube dysfunction, viral URIs, adenoid hypertrophy, daycare exposure, tobacco smoke, allergy, craniofacial anatomy, and bacterial pathogens including Streptococcus pneumoniae, nontypeable H influenzae, and Moraxella catarrhalis.

How Otolaryngology ENT assesses it: Assess episode count and documentation, age, laterality, current middle-ear effusion, fever/otalgia/otorrhea, antibiotic exposure, hearing/speech delay, school performance, allergic rhinitis, adenoid symptoms, tympanic membrane perforation, tube history, vaccines, smoke exposure, and mastoid/facial nerve red flags.

Diagnosis: Confirm AOM episodes with bulging tympanic membrane, middle-ear effusion, decreased mobility on pneumatic otoscopy, tympanometry, or otorrhea not from otitis externa. Audiology is needed for persistent effusion, speech delay, or suspected hearing loss; culture is reserved for tympanocentesis or tube otorrhea when refractory.

First-line treatment: Treat pain every episode with weight-based acetaminophen (Tylenol) or ibuprofen (Advil/Motrin). When antibiotics are indicated, use high-dose amoxicillin (Amoxil); use amoxicillin-clavulanate (Augmentin) if recent amoxicillin, purulent conjunctivitis, beta-lactamase concern, or nonresponse.

Second-line treatment: Alternatives include cefdinir (Omnicef), cefuroxime, cefpodoxime, or ceftriaxone (Rocephin) based on allergy and severity. Avoid prophylactic antibiotics. Manage allergic rhinitis, smoke exposure, and vaccine gaps.

Third-line / advanced care: Tympanostomy tubes are considered for recurrent AOM when middle-ear effusion is present at ENT evaluation, or chronic otitis media with effusion plus hearing or developmental risk; adenoidectomy is considered in selected older children. Admit for mastoiditis, facial nerve palsy, intracranial signs, or toxic appearance.

Progression and follow-up: Follow 48-72 hour response, hearing, language, tympanogram/audiogram, tube otorrhea, persistent perforation, cholesteatoma risk, mastoiditis, antibiotic adverse effects, and recurrence frequency.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Otitis externa

Pathophysiology: Otitis externa is inflammation/infection of the external auditory canal, usually from moisture, trauma, hearing aids/earbuds, eczema, psoriasis, or diabetes; pathogens are often Pseudomonas aeruginosa and Staphylococcus aureus, while fungal disease follows humidity or antibiotic drops.

How Otolaryngology ENT assesses it: Assess tragal/pinna tenderness, canal edema/debris, otorrhea, hearing change, fever, diabetes, immunocompromise, radiation, severe nocturnal pain, cranial neuropathies, mastoid tenderness, tympanic membrane integrity, swimmer exposure, cotton swab trauma, and dermatitis.

Diagnosis: Clinical otoscopy shows canal edema/erythema/debris with pain on tragal or pinna manipulation. Culture is used for recurrent, severe, fungal, immunocompromised, or nonresponsive cases. CT/MRI and ESR/CRP are needed when malignant necrotizing otitis externa is suspected.

First-line treatment: Clean canal when safe, keep ear dry, avoid instrumentation, and use topical therapy: ofloxacin otic (Floxin Otic) or ciprofloxacin/dexamethasone (Ciprodex) if tympanic membrane status is uncertain or perforated; neomycin/polymyxin B/hydrocortisone (Cortisporin) only when membrane is intact and allergy risk is acceptable.

Second-line treatment: Place an ear wick if drops cannot penetrate. Treat fungal disease with clotrimazole solution or ENT debridement. Oral antibiotics are not routine but may be needed for cellulitis beyond the canal or high-risk hosts.

Third-line / advanced care: Urgent ENT/ID for malignant otitis externa with diabetes/immunocompromise, granulation tissue, cranial neuropathy, skull base osteomyelitis, or refractory severe pain; therapy often needs antipseudomonal systemic treatment such as ciprofloxacin (Cipro) or IV cefepime/piperacillin-tazobactam guided by cultures.

Progression and follow-up: Follow pain within 48-72 hours, canal patency, hearing, dermatitis recurrence, tympanic membrane safety, fungal overgrowth, cellulitis, and skull-base osteomyelitis complications.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Sudden sensorineural hearing loss

Pathophysiology: Sudden sensorineural hearing loss is rapid cochlear or retrocochlear dysfunction, classically at least 30 dB over 3 contiguous frequencies within 72 hours, from idiopathic inflammatory/vascular mechanisms, viral injury, autoimmune inner-ear disease, Meniere disease, vestibular schwannoma, stroke, trauma, or ototoxicity.

How Otolaryngology ENT assesses it: Assess exact onset, unilateral/bilateral loss, tinnitus, vertigo, neurologic deficits, ear fullness, otalgia/otorrhea, noise/barotrauma, recent infection, autoimmune symptoms, migraine, vascular risk, anticoagulants, pregnancy, cancer, and ototoxic drugs such as aminoglycosides, cisplatin, or loop diuretics.

Diagnosis: Differentiate conductive loss with otoscopy, tuning forks, and tympanometry. Obtain urgent audiometry within 14 days, MRI internal auditory canals/brain or ABR for retrocochlear pathology, and avoid routine head CT or broad labs unless history points to trauma, stroke, infection, or systemic disease.

First-line treatment: Start time-sensitive corticosteroid therapy when idiopathic SSNHL is likely and no contraindication: prednisone (Deltasone) or methylprednisolone (Medrol) orally, or intratympanic dexamethasone/methylprednisolone by ENT. Counsel that benefit is greatest early.

Second-line treatment: Offer intratympanic steroid salvage for incomplete recovery, typically within 2-6 weeks. Treat identified causes such as Meniere disease, autoimmune disease, Lyme/syphilis when proven, or stroke/TIA when neurologic signs exist.

Third-line / advanced care: Urgent ENT/audiology for same-week audiogram and steroid planning; emergency stroke evaluation for focal deficits or acute vestibular syndrome with central signs. Later care includes hearing aids, CROS aid, cochlear implant evaluation, tinnitus therapy, and vestibular rehab.

Progression and follow-up: Follow repeat audiogram, word recognition, tinnitus distress, vertigo, steroid adverse effects, asymmetric MRI findings, recurrent episodes, permanent hearing loss, and communication safety.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Vertigo ENT evaluation

Pathophysiology: ENT vertigo evaluation separates peripheral vestibular disorders such as BPPV, vestibular neuritis, labyrinthitis, Meniere disease, vestibular migraine, perilymph fistula, and superior canal dehiscence from central causes such as cerebellar stroke or demyelination.

How Otolaryngology ENT assesses it: Assess timing/triggers, seconds versus hours versus continuous vertigo, positional provocation, hearing loss/tinnitus/aural fullness, headache/photophobia, neurologic deficits, gait, stroke risk, recent infection, trauma/barotrauma, ototoxicity, and medication sedatives.

Diagnosis: Use Dix-Hallpike for posterior canal BPPV, supine roll test for horizontal canal BPPV, HINTS only in continuous acute vestibular syndrome by trained clinicians, audiogram for hearing symptoms, vestibular testing selectively, and MRI brain/internal auditory canals when central signs, asymmetric hearing loss, or atypical course occurs.

First-line treatment: Posterior canal BPPV is treated with canalith repositioning such as the Epley maneuver, not chronic meclizine. Vestibular neuritis uses vestibular rehab, hydration/antiemetic support, and very short-term meclizine (Antivert) or diazepam (Valium) only for severe acute nausea.

Second-line treatment: Meniere disease care may use low-sodium diet, trigger reduction, hydrochlorothiazide/triamterene (Dyazide/Maxzide), betahistine where used, intratympanic steroid, or migraine prevention such as nortriptyline (Pamelor), topiramate (Topamax), or propranolol (Inderal) when vestibular migraine fits.

Third-line / advanced care: Emergency referral for new neurologic deficit, inability to walk, direction-changing vertical nystagmus, severe headache, stroke risk with acute vestibular syndrome, sudden hearing loss, or suspected perilymph fistula/superior canal dehiscence needing specialty imaging and surgery.

Progression and follow-up: Follow fall risk, recurrence, hearing fluctuation, migraine control, vestibular compensation, medication sedation, anxiety avoidance, and missed central pathology.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Epistaxis

Pathophysiology: Epistaxis usually arises from anterior septal vessels in Kiesselbach plexus after dryness, trauma, rhinitis, infection, septal deviation, anticoagulants, hypertension association, or hereditary hemorrhagic telangiectasia; posterior bleeding is less common but higher risk.

How Otolaryngology ENT assesses it: Assess airway/hemodynamics, active bleeding side/site, duration, estimated blood loss, posterior drainage, trauma, anticoagulants/antiplatelets, liver/kidney disease, bleeding disorder, intranasal drugs/steroids, recurrent unilateral bleeding, telangiectasias, pregnancy, and anemia symptoms.

Diagnosis: Use anterior rhinoscopy after clot removal and topical vasoconstrictor/anesthetic when safe. CBC/coags/type and screen are for heavy, recurrent, anticoagulated, or unstable bleeding. Nasal endoscopy is needed for recurrent, unilateral, posterior, or unexplained bleeding; CT is for trauma, mass, or invasive disease concern.

First-line treatment: First-line active management is firm sustained compression to the lower third of the nose for at least 5-10 minutes, topical oxymetazoline (Afrin), humidification, saline gel, avoiding nose picking/blowing, and correcting reversible medication or dryness contributors.

Second-line treatment: If a bleeding point is visible, use silver nitrate cautery on one side of septum at a time. If not controlled, use resorbable packing for anticoagulated/bleeding-risk patients or anterior nasal packing such as Merocel/Rapid Rhino with removal plan and analgesia.

Third-line / advanced care: ENT or ED care for posterior packing, endoscopic sphenopalatine artery ligation, embolization, transfusion, reversal of anticoagulation when appropriate, suspected tumor, HHT, or airway/hemodynamic instability.

Progression and follow-up: Follow recurrent bleeding, anemia, packing complications, septal perforation after bilateral cautery, toxic shock warning signs, anticoagulation restart plan, and HHT screening when recurrent/telangiectatic.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Tonsillitis recurrent

Pathophysiology: Recurrent tonsillitis is repeated pharyngeal tonsil infection/inflammation from viral pathogens, group A Streptococcus, EBV, chronic tonsillar crypt biofilm, PFAPA, or peritonsillar abscess tendency; treatment decisions balance episode burden against surgical risk.

How Otolaryngology ENT assesses it: Assess documented episode count, fever, cervical adenitis, tonsillar exudate, positive strep tests, antibiotic courses, school/work impact, sleep-disordered breathing, PFAPA pattern, multiple antibiotic allergies, prior peritonsillar abscess, immunocompromise, and mononucleosis clues.

Diagnosis: Use Centor/McIsaac logic with rapid antigen detection test or NAAT and throat culture when needed; avoid antibiotics for viral features. EBV testing, CBC, or HIV testing is targeted. Sleep symptoms may need polysomnography before tonsillectomy in high-risk children.

First-line treatment: Supportive care includes fluids, acetaminophen (Tylenol), ibuprofen (Advil/Motrin), and corticosteroid such as single-dose dexamethasone only selectively for severe odynophagia. Confirmed group A strep is treated with penicillin V (Pen VK) or amoxicillin (Amoxil).

Second-line treatment: For penicillin allergy or recurrence, use cephalexin (Keflex) if non-anaphylactic, clindamycin (Cleocin), azithromycin (Zithromax), or amoxicillin-clavulanate (Augmentin) based on allergy and local resistance; evaluate carrier state when repeated positives conflict with viral symptoms.

Third-line / advanced care: Tonsillectomy is considered when Paradise-style frequency is met, or modifying factors exist such as PFAPA, multiple antibiotic intolerance, or more than one peritonsillar abscess. Urgent ENT/ED for airway compromise, dehydration, sepsis, or deep neck infection.

Progression and follow-up: Follow episode documentation, strep testing results, antibiotic harms, obstructive sleep symptoms, peritonsillar abscess, post-tonsillectomy bleeding risk, and recurrence despite surgery.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Hoarseness red flags

Pathophysiology: Hoarseness/dysphonia reflects abnormal vocal fold vibration from acute laryngitis, phonotrauma, nodules/polyps, reflux irritation, paresis/paralysis, malignancy, neurologic disease, inhaled steroid effect, intubation injury, or thyroid/chest/neck surgery nerve injury.

How Otolaryngology ENT assesses it: Assess duration, voice demands, tobacco/alcohol, neck mass, dysphagia/odynophagia, hemoptysis, otalgia, weight loss, stridor, respiratory distress, recent intubation or neck/chest surgery, thyroid symptoms, reflux, inhaled corticosteroid use, and professional voice needs.

Diagnosis: Perform laryngoscopy if dysphonia persists beyond 4 weeks or sooner with red flags. Do not obtain CT/MRI before visualizing the larynx unless airway emergency or known mass dictates. Consider stroboscopy, voice evaluation, thyroid/neck imaging, or chest imaging after laryngeal findings.

First-line treatment: For uncomplicated acute laryngitis, use voice conservation, hydration, humidification, avoid smoking/irritants, treat rhinitis/postnasal drip, and optimize inhaler technique/rinse after fluticasone (Flovent/Arnuity) or budesonide (Pulmicort). Avoid empiric antibiotics, steroids, or proton pump inhibitors without a specific indication.

Second-line treatment: Treat identified disease: voice therapy for muscle tension/nodules, omeprazole (Prilosec) or pantoprazole (Protonix) only when reflux syndrome is convincing, antifungal nystatin (Mycostatin) or fluconazole (Diflucan) for candidiasis, and injection medialization for vocal fold paresis when appropriate.

Third-line / advanced care: Urgent ENT for airway symptoms, suspected malignancy, vocal fold paralysis after surgery, neck mass, hemoptysis, professional voice crisis, or persistent unexplained hoarseness; biopsy, microlaryngoscopy, laser, or cancer staging may be needed.

Progression and follow-up: Follow voice handicap, laryngoscopic lesion changes, aspiration risk from paralysis, malignancy delay, occupational impact, reflux medication overuse, and recurrence after surgery or therapy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Dysphagia ENT evaluation

Pathophysiology: ENT dysphagia involves oral, pharyngeal, laryngeal, cricopharyngeal, esophageal inlet, neurologic, structural, inflammatory, iatrogenic, or malignant causes that threaten nutrition and airway safety.

How Otolaryngology ENT assesses it: Assess solids versus liquids, choking/coughing, nasal regurgitation, aspiration pneumonia, weight loss, odynophagia, globus, voice change, reflux, stroke/Parkinson/ALS, radiation or surgery, immunosuppression, pill injury, and alarm symptoms such as progressive dysphagia, bleeding, neck mass, or severe pain.

Diagnosis: Use flexible laryngoscopy for pharyngeal/laryngeal anatomy, modified barium swallow/VFSS or FEES for aspiration and swallow mechanics, barium esophagram for Zenker diverticulum/cricopharyngeal bar, EGD for esophageal mucosal/structural disease, and CT/MRI neck/chest for mass or deep infection concern.

First-line treatment: Stabilize airway and nutrition risk; use speech-language pathology swallow therapy, diet texture/liquid modification, aspiration precautions, medication review, dental/oral care, and treat reflux when clinically present with omeprazole (Prilosec) or pantoprazole (Protonix).

Second-line treatment: Diagnosis-specific treatment may include esophageal dilation, cricopharyngeal botulinum toxin (Botox) or myotomy, Zenker diverticulotomy, antifungal therapy for Candida esophagitis such as fluconazole (Diflucan), or neurologic rehab.

Third-line / advanced care: Urgent ENT/GI/ED for food bolus obstruction, airway compromise, aspiration with hypoxia, rapidly progressive dysphagia, cancer concern, deep neck infection, or inability to maintain hydration/nutrition; feeding tube discussion may be needed in severe neurologic disease.

Progression and follow-up: Follow aspiration pneumonia, weight, hydration, diet tolerance, swallow study response, stricture recurrence, cancer diagnosis, and patient goals for feeding safety versus quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Obstructive sleep apnea airway evaluation

Pathophysiology: Obstructive sleep apnea is recurrent upper-airway collapse during sleep causing intermittent hypoxemia, arousals, sympathetic activation, sleep fragmentation, pulmonary/systemic hypertension risk, AF, insulin resistance, and daytime sleepiness.

How Otolaryngology ENT assesses it: Assess snoring, witnessed apneas, gasping, daytime sleepiness, morning headaches, resistant hypertension, AF, heart failure, stroke, obesity/neck circumference, sedatives/opioids/alcohol, driving risk, nasal obstruction, and occupational safety.

Diagnosis: Use STOP-Bang or similar screen, home sleep apnea test for uncomplicated high-probability OSA, in-lab polysomnography for cardiopulmonary disease, hypoventilation, neuromuscular disease, opioids, central apnea concern, or negative home test with high suspicion.

First-line treatment: First-line therapy is CPAP/APAP with mask fitting, humidification, adherence coaching, weight management, side-sleeping, avoiding alcohol/sedatives near bedtime, and treating nasal obstruction.

Second-line treatment: Alternatives include mandibular advancement oral appliance for mild/moderate OSA or CPAP-intolerant patients, positional therapy, bilevel PAP for hypoventilation/pressure intolerance, and GLP-1/GIP weight therapy or bariatric referral when obesity drives disease.

Third-line / advanced care: Refer sleep medicine/ENT for PAP failure, central sleep apnea, obesity hypoventilation, severe hypoxemia, commercial driver clearance, surgical options such as hypoglossal nerve stimulation, or complex cardiopulmonary disease.

Progression and follow-up: Follow PAP adherence, residual AHI, leak, sleepiness, BP, AF burden, driving safety, weight, nocturnal oxygenation, and mask/skin complications.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Thyroid neck mass

Pathophysiology: A thyroid or neck mass may be benign thyroid nodule, thyroid cancer, reactive lymph node, branchial cleft cyst, salivary lesion, lymphoma, metastatic head/neck squamous cell carcinoma, or infectious/inflammatory disease; adult persistent neck mass is malignant until proven otherwise.

How Otolaryngology ENT assesses it: Assess duration, growth, pain, compressive symptoms, dysphagia/dyspnea, hoarseness, radiation exposure, family thyroid cancer/MEN2, tobacco/alcohol, HPV risk, B symptoms, URI/dental infection, thyroid dysfunction symptoms, and fixation or lymphadenopathy.

Diagnosis: For thyroid nodules, obtain TSH and high-resolution thyroid/neck ultrasound with TI-RADS or ATA risk pattern; FNA is based on size and sonographic risk. Low TSH prompts radionuclide scan. Adult unexplained neck mass needs contrast CT or MRI and FNA, not open biopsy first.

First-line treatment: Benign thyroid nodules are observed with ultrasound intervals based on risk. Hyperfunctioning nodules are managed with endocrinology using methimazole (Tapazole), radioactive iodine, or surgery. Infectious lymphadenitis may use amoxicillin-clavulanate (Augmentin) or clindamycin (Cleocin) when bacterial features exist.

Second-line treatment: Indeterminate thyroid FNA may use molecular testing such as Afirma or ThyroSeq where available, repeat FNA, diagnostic lobectomy, or surveillance by risk. Suspicious lateral neck nodes require ultrasound-guided FNA with thyroglobulin washout when thyroid cancer is possible.

Third-line / advanced care: ENT/endocrine surgery for malignant/suspicious nodules, compressive goiter, vocal fold paralysis, rapidly enlarging mass, anaplastic concern, or metastatic neck disease; laryngoscopy before thyroid surgery when voice symptoms or invasive disease exist.

Progression and follow-up: Follow ultrasound growth, cytology/molecular results, compressive symptoms, voice, calcium/vocal cord surgical risks, recurrence markers such as thyroglobulin, and missed aerodigestive cancer.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Salivary gland disease

Pathophysiology: Salivary gland disease includes sialolithiasis, acute bacterial sialadenitis, viral parotitis, Sjogren disease, medication-related xerostomia, autoimmune IgG4 disease, benign tumors such as pleomorphic adenoma, and malignant salivary tumors.

How Otolaryngology ENT assesses it: Assess meal-related swelling/pain, fever, purulence from duct, dehydration, xerostomia/eye dryness, autoimmune symptoms, stones, recurrent parotitis, facial nerve weakness, firm/fixed mass, tobacco, radiation, medications with anticholinergic burden, and immunocompromise.

Diagnosis: Examine ducts and massage for purulence, culture drainage when present, check CBC if systemic illness, ultrasound or noncontrast CT for stones, contrast CT/MRI for abscess/tumor, Sjogren testing with SSA/SSB/ANA/RF and objective dryness tests, and FNA/core biopsy for salivary mass.

First-line treatment: Sialolithiasis/sialadenitis initial care is hydration, warm compresses, gland massage, sialogogues such as lemon drops, NSAIDs, and oral hygiene. Acute bacterial disease uses anti-staphylococcal/oral flora coverage such as amoxicillin-clavulanate (Augmentin) or dicloxacillin; clindamycin (Cleocin) if selected allergy/MRSA context.

Second-line treatment: Recurrent stones or stenosis may need sialendoscopy, duct dilation, basket retrieval, or lithotripsy. Xerostomia uses medication reduction, saliva substitutes, dental fluoride, pilocarpine (Salagen), or cevimeline (Evoxac) when not contraindicated.

Third-line / advanced care: ENT for abscess drainage, IV antibiotics such as ampicillin-sulbactam (Unasyn) plus MRSA coverage when severe, facial nerve weakness, suspected tumor, deep lobe parotid mass, or parotidectomy/submandibular gland excision planning.

Progression and follow-up: Follow recurrence, abscess, dehydration, dental caries, xerostomia complications, facial nerve function, tumor growth, malignant transformation risk in pleomorphic adenoma, and autoimmune systemic disease.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Peritonsillar abscess

Pathophysiology: Peritonsillar abscess is pus between tonsillar capsule and pharyngeal constrictor, usually polymicrobial group A strep, Streptococcus anginosus group, Staphylococcus aureus, and anaerobes after tonsillitis, causing trismus, uvular deviation, dehydration, and possible airway spread.

How Otolaryngology ENT assesses it: Assess severe unilateral sore throat, muffled hot-potato voice, drooling, trismus, fever, neck swelling, uvular deviation, toxic appearance, dehydration, immunocompromise, airway symptoms, prior PTA, and Lemierre/deep neck infection clues.

Diagnosis: Diagnosis is usually clinical. Intraoral ultrasound can confirm abscess and guide drainage; CT neck with IV contrast is used when exam is limited, deep neck spread is suspected, or diagnosis is uncertain. Test for group A strep/EBV when relevant, but do not delay drainage if clear abscess.

First-line treatment: Provide analgesia, hydration, airway assessment, and drainage by needle aspiration or incision and drainage when abscess is present. Antibiotics should cover strep and anaerobes: amoxicillin-clavulanate (Augmentin), clindamycin (Cleocin), or penicillin plus metronidazole (Flagyl).

Second-line treatment: A single dose of dexamethasone (Decadron) or methylprednisolone can reduce pain/trismus in selected patients. Culture drainage for severe, recurrent, immunocompromised, or treatment-failure cases. Observation/admission depends on airway, oral intake, and comorbidity.

Third-line / advanced care: ENT for difficult drainage, recurrent PTA, airway compromise, spread to parapharyngeal/retropharyngeal space, sepsis, or quinsy tonsillectomy/interval tonsillectomy in selected recurrent disease.

Progression and follow-up: Follow oral intake within 24 hours, fever/pain, trismus, recurrence, bleeding, deep neck infection, internal jugular thrombophlebitis, aspiration, and antibiotic adverse effects.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Otolaryngology ENT

Nasal polyps

Pathophysiology: Nasal polyps are benign inflammatory outgrowths of sinonasal mucosa, commonly type 2/eosinophilic inflammation linked with asthma, allergic rhinitis, chronic rhinosinusitis, and aspirin-exacerbated respiratory disease; unilateral polyps require tumor/inverted papilloma evaluation.

How Otolaryngology ENT assesses it: Assess bilateral obstruction, smell loss, rhinorrhea, facial pressure, asthma control, NSAID/aspirin respiratory reactions, recurrent sinus infections, prior surgery, steroid burden, allergy symptoms, cystic fibrosis/primary ciliary dyskinesia clues in children, and unilateral bleeding or pain.

Diagnosis: Use anterior rhinoscopy or nasal endoscopy to confirm polyps, CT sinus for extent and surgical planning, allergy/asthma/AERD assessment, and biopsy/imaging for unilateral, atypical, bleeding, painful, or destructive lesions.

First-line treatment: First-line therapy is saline irrigation plus intranasal corticosteroid spray or delivery system such as fluticasone (Flonase/Xhance), mometasone (Nasonex), budesonide irrigation (Pulmicort, off-label), or triamcinolone (Nasacort). Short oral prednisone (Deltasone) can be used for severe obstruction when risks are acceptable.

Second-line treatment: Treat comorbid allergic rhinitis/asthma; consider aspirin desensitization for AERD in experienced centers. Biologics for severe recurrent polyps include dupilumab (Dupixent), omalizumab (Xolair), or mepolizumab (Nucala) when criteria are met.

Third-line / advanced care: Functional endoscopic sinus surgery with polypectomy is used for persistent obstruction, recurrent infections, smell loss, complications, or failure of medical therapy; urgent evaluation for orbital/intracranial complication or unilateral neoplasm concern.

Progression and follow-up: Follow smell, nasal airflow, SNOT-22, endoscopic polyp score, asthma/AERD control, steroid adverse effects, recurrence after surgery, biologic response, and unilateral lesion pathology.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Specialty role

Imaging selection, interpretation, procedural guidance, radiation safety, interventional diagnosis, and disease staging.

Radiology

Imaging choice for headache

Pathophysiology: Headache imaging triage detects secondary causes such as hemorrhage, aneurysm, mass, infection, venous thrombosis, dissection, hydrocephalus, intracranial hypertension or hypotension, and pituitary apoplexy while avoiding low-yield imaging for stable primary headache.

How Radiology assesses it: Assess thunderclap onset, worst headache, neurologic deficit, papilledema, fever or meningismus, cancer, immunocompromise, pregnancy or postpartum state, anticoagulation, trauma, age over 50, giant-cell arteritis symptoms, exertional or sexual trigger, positional pattern, Valsalva trigger, and change from baseline.

Diagnosis: No imaging is usually needed for stable migraine or tension pattern with normal neurologic exam. Use noncontrast CT head first for acute thunderclap or suspected hemorrhage; CTA head/neck for aneurysm or dissection; MRI brain with/without contrast for progressive, cancer, infection, posterior fossa, pressure, or abnormal-exam concerns; MRV/CTV for venous sinus thrombosis.

First-line treatment: Select the modality that answers the danger question: CT for fast hemorrhage/trauma, MRI for mass/inflammation/posterior fossa, CTA/MRA for arterial disease, and MRV/CTV for venous thrombosis. Communicate hemorrhage, mass effect, hydrocephalus, or vascular occlusion immediately.

Second-line treatment: If CT is negative but subarachnoid hemorrhage remains possible, coordinate lumbar puncture or CTA based on timing and local protocol. Use contrast when infection, neoplasm, inflammatory disease, or vascular lesion characterization requires it.

Third-line / advanced care: Emergency neurology, neurosurgery, stroke, or interventional neuroradiology for intracranial hemorrhage, aneurysm, dissection, venous sinus thrombosis, meningitis/abscess, mass effect, hydrocephalus, pituitary apoplexy, or papilledema.

Progression and follow-up: Follow result communication, repeat imaging need, radiation/contrast exposure, incidental aneurysm or Chiari findings, and whether symptoms evolve beyond the original indication.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

CT pulmonary angiography for PE

Pathophysiology: CT pulmonary angiography evaluates pulmonary arterial thrombus that can obstruct pulmonary blood flow, cause right-heart strain, hypoxemia, pulmonary infarction, shock, and death; imaging should follow pretest probability and contraindication review.

How Radiology assesses it: Assess Wells/Geneva or clinician gestalt, D-dimer eligibility, pregnancy, renal function/eGFR, iodinated contrast reaction history, hemodynamic instability, oxygen need, prior PE, anticoagulation, body habitus, IV access, chest X-ray, and whether V/Q scan would be interpretable.

Diagnosis: Use D-dimer to avoid imaging in low or intermediate-risk patients when appropriate. CTPA with IV iodinated contrast is first-line when PE is likely or D-dimer positive without major contraindication. V/Q scan is preferred for major contrast contraindication or some pregnancy/young patients with normal chest X-ray. Leg venous ultrasound can support diagnosis when chest imaging is delayed or contraindicated.

First-line treatment: Protocol CTA chest PE with timing bolus, adequate IV access, and motion reduction. Report central/lobar/segmental clot, RV/LV ratio, septal bowing, reflux into IVC, infarct, effusion, and alternate diagnoses such as pneumonia or aortic disease.

Second-line treatment: If CTPA is nondiagnostic, repeat only for fixable technical failure; otherwise use V/Q scan, lower-extremity duplex ultrasound, echocardiography for unstable patients, or clinical anticoagulation decision with the treating team.

Third-line / advanced care: Massive or submassive PE with shock, severe RV strain, saddle/central clot, or deterioration requires PE response team, ICU, systemic alteplase (Activase) consideration by clinicians, catheter thrombectomy/thrombolysis, or surgical embolectomy.

Progression and follow-up: Follow anticoagulation decision support, incidental nodules, chronic thromboembolic disease, contrast reaction or extravasation, kidney risk in high-risk patients, and repeat imaging only when symptoms or management change.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Abdominal pain imaging selection

Pathophysiology: Abdominal pain imaging targets emergencies such as appendicitis, diverticulitis, bowel obstruction, perforation, ischemia, cholecystitis, pancreatitis complications, renal stone, ectopic pregnancy, ovarian torsion, abdominal aortic aneurysm, and abscess.

How Radiology assesses it: Assess pain location, pregnancy status, age, fever/sepsis, peritonitis, vomiting/obstruction, GI bleeding, renal colic, RUQ pain, pelvic symptoms, vascular risk, prior surgery, immunocompromise, renal function, contrast allergy, and whether ultrasound can answer the question.

Diagnosis: RUQ pain usually starts with ultrasound. Adult RLQ/LLQ pain often uses CT abdomen/pelvis with IV contrast; pregnancy and many pediatric cases start with ultrasound and MRI when needed. Renal colic uses noncontrast CT or ultrasound in selected patients. Mesenteric ischemia uses CTA abdomen/pelvis. Perforation/obstruction usually uses CT with IV contrast and oral contrast selectively.

First-line treatment: Choose the lowest-risk definitive test: ultrasound for biliary, pelvic, obstetric, and AAA screening; CT with IV contrast for inflammatory/infectious abdominal emergencies; noncontrast CT for stones; MRI/MRCP for biliary, pregnancy, or problem-solving; CTA for vascular catastrophe.

Second-line treatment: If ultrasound is equivocal, escalate to CT or MRI based on pregnancy, age, and clinical risk. Use image-guided aspiration or drainage for a drainable abscess when source control is needed and a safe window exists.

Third-line / advanced care: Immediate surgical/IR escalation for free air, ischemic bowel, ruptured AAA, active bleeding, closed-loop obstruction, perforated appendicitis/diverticulitis, emphysematous infection, ovarian torsion, ectopic pregnancy, or unstable patient.

Progression and follow-up: Follow whether imaging answered the question, incidental findings, abscess size/drain output, repeat imaging triggers, radiation dose in recurrent pain, contrast reaction/extravasation, and missed evolving surgical disease.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Back pain imaging red flags

Pathophysiology: Mechanical overload, cartilage degeneration, tendon/ligament injury, bone stress, disc/facet disease, or trauma causes pain, inflammation, instability, and functional limitation.

How Radiology assesses it: Assess mechanism, neurologic deficits, red flags including fever/cancer/trauma/bowel-bladder symptoms, gait, joint range of motion, swelling, instability, occupational or sport demands, and medication risks.

Diagnosis: Use X-ray for trauma/deformity/advanced OA, MRI for neurologic deficit/ligament/meniscus/stress injury or persistent red flags, CT for complex fracture, ultrasound for tendon/bursa/effusion, and ESR/CRP/CBC if infection or inflammatory disease is possible.

First-line treatment: Activity modification, PT/exercise, weight reduction when relevant, topical diclofenac (Voltaren), acetaminophen (Tylenol), NSAID such as naproxen (Aleve/Naprosyn) or ibuprofen (Advil/Motrin) when safe, braces/orthotics, heat/ice, and return-to-activity plan.

Second-line treatment: Duloxetine (Cymbalta) for chronic OA/back pain, gabapentin (Neurontin) or pregabalin (Lyrica) for neuropathic features, short muscle relaxant cyclobenzaprine (Flexeril) selectively, corticosteroid injection triamcinolone (Kenalog), or image-guided procedure.

Third-line / advanced care: Orthopedic/PM&R/pain referral for surgery, joint replacement, fracture fixation, epidural steroid injection, radiofrequency ablation, concussion specialty care, or multidisciplinary rehab.

Progression and follow-up: Poorly controlled disease can cause chronic pain, falls, opioid exposure, deformity, neurologic compromise, nonunion, disability, and deconditioning.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Lung nodule imaging follow-up

Pathophysiology: Pulmonary nodule follow-up estimates malignancy risk from size, growth, attenuation, morphology, upper-lobe location, smoking/exposure history, age, prior cancer, and immune status; many small nodules are benign granulomas or scars.

How Radiology assesses it: Assess nodule size in mm, solid versus subsolid/ground-glass/part-solid, number, prior stability, smoking pack-years, age, family/prior cancer, infection symptoms, endemic fungi/TB risk, immunosuppression, occupational exposure, and whether found on screening or incidental CT.

Diagnosis: Thin-section chest CT is the baseline test. Fleischner-style follow-up applies to incidental nodules in adults without known cancer or immunosuppression, while Lung-RADS applies to lung cancer screening. PET/CT is more useful for solid nodules generally 8 mm or larger with sufficient risk; biopsy depends on risk, size, location, and patient fitness.

First-line treatment: Low-risk very small solid nodules often need no follow-up; larger or high-risk nodules need interval low-dose CT at guideline intervals. Persistent part-solid nodules require closer surveillance because the solid component increases invasive adenocarcinoma risk.

Second-line treatment: Growth, suspicious morphology, or size/risk threshold may require PET/CT, navigational bronchoscopy, CT-guided biopsy, or thoracic surgery referral. Treat obvious infection only when clinical syndrome supports it, then confirm radiographic resolution.

Third-line / advanced care: Urgent multidisciplinary evaluation for spiculated enlarging nodule, PET-avid lesion, associated lymphadenopathy, hemoptysis, superior vena cava syndrome, or suspected metastatic disease; staging CT/PET/MRI brain may be needed once cancer is suspected.

Progression and follow-up: Follow measurement method, volume/diameter growth, doubling time, radiation-minimizing CT technique, biopsy pneumothorax/bleeding risk, patient anxiety, and avoiding duplicate follow-up systems.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Breast imaging abnormality

Pathophysiology: Breast imaging abnormalities may represent cyst, fibroadenoma, fat necrosis, infection, high-risk lesion, ductal carcinoma in situ, invasive carcinoma, or metastatic nodes; management is driven by BI-RADS category and imaging-pathology concordance.

How Radiology assesses it: Assess age, pregnancy/lactation, palpable lump, nipple discharge, skin/nipple change, focal pain, prior mammograms, breast density, implants, personal/family cancer, genetic risk, prior biopsy, anticoagulants, and whether this is screening recall or diagnostic presentation.

Diagnosis: Diagnostic mammography with tomosynthesis and targeted ultrasound evaluate most adult palpable or recalled findings. Ultrasound is first for many patients under 30 and during pregnancy/lactation. Breast MRI is used for high-risk screening, extent of disease, implant rupture, occult primary, or problem solving. BI-RADS 4/5 requires tissue diagnosis.

First-line treatment: Assign BI-RADS clearly: 0 additional imaging, 1/2 routine, 3 short-interval usually 6-month follow-up, 4 suspicious biopsy, 5 highly suggestive malignancy, 6 known cancer. Communicate suspicious findings and biopsy recommendations directly.

Second-line treatment: Use image-guided core needle biopsy by the modality that best sees the lesion: ultrasound-guided, stereotactic/tomosynthesis-guided, or MRI-guided biopsy. Clip placement and post-biopsy mammogram confirm target sampling; pathology must be concordant with imaging.

Third-line / advanced care: Discordant benign pathology, high-risk lesion, malignancy, inflammatory breast cancer concern, abscess needing drainage, or axillary nodal disease requires breast surgery/oncology coordination and possible MRI or staging by cancer type.

Progression and follow-up: Follow biopsy result, concordance, clip position, BI-RADS 3 stability, post-biopsy hematoma/infection, screening interval, genetic-risk referral, and treatment response imaging when neoadjuvant therapy is used.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Stroke imaging workflow

Pathophysiology: Stroke imaging rapidly distinguishes ischemic stroke, intracranial hemorrhage, large-vessel occlusion, salvageable penumbra, mimics, and complications so reperfusion or hemorrhage management can begin without delay.

How Radiology assesses it: Assess last-known-well, NIHSS, deficits, anticoagulants, BP/glucose, seizure/migraine mimic, renal function if CTA delay would be minimal, pregnancy, contrast allergy, posterior circulation signs, and whether thrombectomy window/perfusion imaging applies.

Diagnosis: Noncontrast CT head is first to exclude hemorrhage and large established infarct. CTA head/neck detects large-vessel occlusion and stenosis/dissection. CT perfusion or MRI diffusion/perfusion helps select late-window thrombectomy or unclear onset. MRI DWI is most sensitive for small/posterior infarct when it will not delay acute therapy.

First-line treatment: Immediate CT/CTA protocol with critical-result communication: hemorrhage, ASPECTS/early ischemic change, LVO site, carotid dissection/stenosis, basilar occlusion, mass mimic, or perfusion mismatch.

Second-line treatment: If CT/CTA is negative but symptoms persist, MRI brain DWI/FLAIR and MRA/MRV can evaluate small infarct, venous thrombosis, posterior circulation, demyelination, tumor, or seizure-related mimic. Carotid ultrasound is adjunctive, not a substitute for acute LVO imaging.

Third-line / advanced care: Activate stroke neurology/interventional neuroradiology for LVO thrombectomy, thrombolysis eligibility, basilar occlusion, hemorrhage, aneurysm/AVM, malignant edema, or dissection. Do not delay reperfusion for nonessential imaging.

Progression and follow-up: Follow hemorrhagic transformation, edema/mass effect, vessel recanalization, carotid intervention planning, incidental aneurysm, contrast/kidney risk, and repeat imaging when neurologic status changes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Trauma CT decision

Pathophysiology: Trauma CT decision-making balances rapid detection of life-threatening hemorrhage, solid-organ injury, vascular injury, brain/spine injury, hollow viscus injury, and fractures against radiation/contrast risk, especially in children and pregnancy.

How Radiology assesses it: Assess mechanism, hemodynamics, GCS, anticoagulants, neurologic deficit, distracting injury, intoxication, chest/abdomen/pelvis tenderness, seatbelt sign, FAST result, pregnancy, age, renal risk, and whether whole-body CT or selective imaging fits stability and mechanism.

Diagnosis: Unstable patients often need FAST/eFAST, portable chest/pelvis X-ray, and operative/interventional pathway rather than delayed CT. Stable high-energy polytrauma may use CT head/c-spine/chest/abdomen/pelvis with IV contrast. CTA is used for suspected vascular injury; CT cystography for bladder rupture; MRI for ligament/cord injury after stabilization.

First-line treatment: Protocol by mechanism: noncontrast head/c-spine, contrast CT chest/abdomen/pelvis, arterial phase/CTA for vascular injury, delayed phase for urinary collecting system injury, and immediate communication of active extravasation, aortic injury, intracranial bleed, unstable spine, or solid-organ injury grade.

Second-line treatment: Use interventional radiology for embolization of pelvic, splenic, hepatic, renal, or arterial bleeding when appropriate. Repeat CT is driven by clinical change, nonoperative management protocols, or suspected delayed complication.

Third-line / advanced care: Emergency trauma surgery/neurosurgery/orthopedics/IR for shock, active bleeding, expanding hematoma, traumatic aortic injury, unstable pelvic fracture, intracranial mass effect, spinal cord compression, or hollow viscus perforation.

Progression and follow-up: Follow radiation dose, contrast exposure, missed hollow viscus/pancreatic/diaphragm injury, delayed bleeding, nonoperative solid-organ monitoring, incidental findings, and pregnancy/fetal dose counseling.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Interventional abscess drainage

Pathophysiology: Image-guided abscess drainage provides source control for infected fluid collections by placing a catheter through a safe window, reducing sepsis burden while avoiding or bridging surgery when anatomy allows.

How Radiology assesses it: Assess collection size, location, loculation, maturity, gas, suspected fistula, sepsis, anticoagulation, platelets/INR, access route, nearby bowel/vessels/pleura, pregnancy, allergies, antibiotics already given, and whether surgery is needed for perforation or necrotic tissue.

Diagnosis: CT with IV contrast or ultrasound defines drainability, safe window, and adjacent organs. Labs include CBC, CMP, INR/PTT, platelets, blood cultures if septic, and culture/Gram stain from aspirate. Small phlegmon or nonliquefied collection may not be drainable.

First-line treatment: Use ultrasound- or CT-guided aspiration/drain placement with sterile technique, local anesthetic lidocaine (Xylocaine), moderate sedation such as fentanyl (Sublimaze) plus midazolam (Versed) when appropriate, specimen culture, and catheter flushing/output plan.

Second-line treatment: If output stops but abscess persists, evaluate catheter position with contrast injection or CT, upsize/exchange catheter, break loculations, add another drain, or coordinate antimicrobial narrowing with infectious disease.

Third-line / advanced care: Surgery or advanced intervention is needed for no safe window, uncontrolled sepsis, necrotizing infection, bowel leak requiring repair, multiloculated failure, bleeding, transpleural complication, or fistula requiring definitive management.

Progression and follow-up: Follow fever/WBC, drain output character/volume, culture results, skin leakage, bleeding, pain, catheter dislodgement, fistula, residual cavity, and removal criteria such as low output plus clinical/imaging resolution.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Liver lesion characterization

Pathophysiology: Liver lesions include cyst, hemangioma, focal nodular hyperplasia, hepatic adenoma, abscess, hepatocellular carcinoma, cholangiocarcinoma, and metastasis; characterization depends on enhancement pattern, liver disease risk, hormones, infection, and known malignancy.

How Radiology assesses it: Assess cirrhosis, hepatitis B/C, alcohol/MASLD, oral contraceptive or anabolic steroid use, pregnancy plans, known cancer, fever, RUQ pain, weight loss, AFP history, prior imaging, lesion size/growth, and renal function or contrast constraints.

Diagnosis: Multiphasic contrast MRI liver with extracellular or hepatobiliary agent, or multiphasic CT liver protocol, evaluates arterial enhancement, washout, capsule, diffusion, fat, scar, and hepatobiliary uptake. Ultrasound can identify simple cysts; CEUS may help. LI-RADS applies in at-risk cirrhosis/HBV patients.

First-line treatment: Classic simple cyst or typical hemangioma needs no treatment. FNH is usually observed. Hepatic adenoma requires subtype/risk assessment, stopping estrogen/anabolic drivers when possible, and surveillance or resection/embolization by size, sex, growth, beta-catenin risk, or bleeding.

Second-line treatment: Indeterminate lesions get MRI problem-solving, short-interval follow-up, CEUS, PET/CT when metastasis is possible, or image-guided biopsy only when imaging cannot answer and biopsy risk is acceptable. Abscess uses antibiotics plus drainage when large or not responding.

Third-line / advanced care: Urgent hepatology/oncology/surgery/IR for LI-RADS 5 HCC, portal vein tumor thrombus, hemorrhagic adenoma, large abscess/sepsis, biliary obstruction, or suspected metastases needing staging and tissue diagnosis.

Progression and follow-up: Follow lesion size/enhancement, AFP in at-risk patients, adenoma hemorrhage/malignant transformation risk, biopsy bleeding, contrast safety, and avoiding unnecessary biopsy of classic hemangioma.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Radiation exposure counseling

Pathophysiology: Medical radiation counseling explains ionizing radiation risk while preserving needed diagnosis; risk depends on modality, body region, dose, age, pregnancy, cumulative exposure, and whether nonionizing alternatives can answer the question.

How Radiology assesses it: Assess pregnancy possibility, pediatric/young age, prior repeated CT or nuclear medicine, clinical urgency, ultrasound/MRI alternatives, body part dose sensitivity, patient anxiety, occupational exposure misunderstanding, and whether the exam changes management.

Diagnosis: Estimate relative dose by exam: ultrasound and MRI use no ionizing radiation; chest X-ray is low dose; CT abdomen/pelvis, multiphase CT, CTA, fluoroscopy, and nuclear medicine are higher. Use appropriateness criteria and dose tracking when available rather than denying necessary urgent imaging.

First-line treatment: Use ALARA principles: justify the exam, optimize protocol, scan only needed region/phases, use pediatric or pregnancy protocols, shield when useful and not interfering, and choose ultrasound or MRI when diagnostically equivalent.

Second-line treatment: For pregnancy, do not withhold necessary CT when maternal diagnosis is urgent; use ultrasound/MRI first when appropriate, document fetal-dose discussion for higher-dose pelvic studies, and involve radiology/medical physics for unusual high-dose or repeated fluoroscopy.

Third-line / advanced care: Escalate to radiologist/medical physicist for complex pregnancy exposure, high cumulative fluoroscopy, radiation injury concern, or refusal of medically necessary imaging. Critical diagnoses should not be missed solely from radiation fear.

Progression and follow-up: Follow shared decision documentation, cumulative-dose awareness without overemphasis, incidental repeat imaging, pediatric protocol use, and reassurance that most diagnostic exams carry low absolute cancer risk compared with missed emergency disease.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Radiology

Contrast kidney risk

Pathophysiology: Contrast kidney risk counseling addresses post-contrast acute kidney injury risk, highest in severe CKD, AKI, dehydration, shock, nephrotoxin exposure, and intra-arterial contrast; modern IV iodinated contrast risk is lower than historically feared in stable patients.

How Radiology assesses it: Assess current creatinine/eGFR, AKI versus stable CKD, dialysis status, diabetes with CKD, volume depletion, sepsis/shock, heart failure, NSAIDs and other nephrotoxins, metformin use, prior contrast reaction, and whether contrast is essential for diagnosis.

Diagnosis: Use recent eGFR for high-risk patients; emergency imaging should not be delayed when contrast changes life-saving management. Gadolinium MRI risk focuses on nephrogenic systemic fibrosis in severe CKD/AKI and agent class; group II gadolinium agents have very low NSF risk.

First-line treatment: For stable patients with adequate eGFR, proceed with indicated IV contrast. For high-risk CKD/AKI, use isotonic IV hydration when appropriate, avoid dehydration/NSAIDs, minimize contrast volume, use low- or iso-osmolar iodinated contrast, and choose noncontrast/ultrasound/MRI alternatives only if diagnostically adequate.

Second-line treatment: Metformin is usually held only for AKI, severe CKD, or intra-arterial/high-risk situations per local policy. Dialysis patients do not need urgent dialysis solely for IV contrast unless volume/osmotic issues require it; coordinate if residual renal function matters.

Third-line / advanced care: Radiologist/nephrology discussion for eGFR under 30, active AKI, transplant kidney, repeated contrast, severe heart failure limiting hydration, or gadolinium in severe renal disease. Emergency CTA/CT with contrast still proceeds when benefit outweighs risk.

Progression and follow-up: Follow creatinine in high-risk patients, hydration tolerance, contrast extravasation/reaction, medication restart, duplicate contrast studies, and documentation that risk-benefit favored the indicated exam.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Specialty role

Tissue diagnosis, cytology, lab interpretation, transfusion medicine, microbiology, molecular diagnostics, and autopsy.

Pathology and Laboratory Medicine

Abnormal CBC smear review

Pathophysiology: CBC smear review links automated cell counts to morphology, detecting marrow failure, leukemia, hemolysis, microangiopathy, infection, nutritional deficiency, platelet clumping, blasts, dysplasia, parasites, and analyzer artifacts that change triage.

How Pathology and Laboratory Medicine assesses it: Assess which cell line is abnormal, acuity, symptoms of anemia/bleeding/infection, fever, weight loss, splenomegaly, pregnancy, chemotherapy, anticoagulants, alcohol, liver/kidney disease, nutritional risk, transfusion history, and whether the analyzer flagged blasts, schistocytes, platelet clumps, or atypical lymphocytes.

Diagnosis: Review peripheral smear with CBC differential, reticulocyte count, indices/RDW, platelet estimate, WBC morphology, RBC forms, and artifact check. Reflex testing may include iron studies/ferritin, B12/folate, LDH/haptoglobin/bilirubin/DAT, coagulation panel, flow cytometry for blasts/lymphocytosis, malaria/Babesia smear when exposure fits, and bone marrow biopsy for unexplained cytopenias or blasts.

First-line treatment: First-line lab action is to verify specimen integrity, exclude clotted/hemolyzed sample or EDTA platelet clumping, call critical results, and issue a morphology-guided interpretation such as microcytosis, macro-ovalocytes/hypersegmented neutrophils, schistocytes, blasts, spherocytes, target cells, or platelet satellitism.

Second-line treatment: Escalate to hematopathologist review, manual differential, flow cytometry, cytogenetics/FISH, or molecular testing such as BCR-ABL1, PML-RARA, JAK2, CALR, MPL, or myeloid NGS when smear/counts suggest leukemia, myeloproliferative neoplasm, marrow failure, or clonal cytopenia.

Third-line / advanced care: Urgent clinician notification for blasts or Auer rods, schistocytes suggesting TTP/HUS/DIC, severe neutropenia, severe thrombocytopenia with bleeding risk, hyperleukocytosis, malaria, or platelet count incompatible with procedures/anticoagulation.

Progression and follow-up: Follow repeat CBC trend, smear evolution, transfusion need, treatment response, specimen artifacts, critical value documentation, and whether marrow/flow/molecular findings close the diagnostic loop.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Biopsy diagnosis workflow

Pathophysiology: Biopsy diagnosis converts tissue architecture, cytology, immunophenotype, molecular alterations, and clinical-radiologic context into a diagnosis, grade, stage element, infection/inflammation pattern, or adequacy statement.

How Pathology and Laboratory Medicine assesses it: Assess target lesion, biopsy type, anatomic site/laterality, imaging impression, prior pathology, neoadjuvant therapy, infection precautions, anticoagulation/procedure risk, requested studies, fixation time, orientation, margins, and whether fresh tissue is needed for flow cytometry, culture, cytogenetics, or molecular testing.

Diagnosis: Workflow includes accessioning, specimen adequacy, gross description, fixation in formalin unless fresh studies are required, embedding/sectioning, H&E microscopy, special stains such as AFB/GMS/PAS/Gram, immunohistochemistry, in situ hybridization, flow cytometry, FISH, PCR/NGS, and correlation with imaging/clinical findings. Discordant results require pathologist-clinician communication.

First-line treatment: First-line pathology action is to preserve diagnostic material, identify site and specimen fragments, document adequacy, issue a diagnosis with grade/type when possible, and state limitations such as scant tissue, crush artifact, necrosis, cautery artifact, or sampling mismatch.

Second-line treatment: Use stepwise ancillary testing: cytokeratin, S100/SOX10, CD45, CD3/CD20, ER/PR/HER2, p40/TTF-1/Napsin A, synaptophysin/chromogranin, Ki-67, mismatch repair proteins, PD-L1, or organism stains only when morphology and clinical question justify them.

Third-line / advanced care: Escalate to subspecialty pathology consult, repeat biopsy, radiology-pathology conference, tumor board, or urgent clinician call for unexpected malignancy, transplant rejection, vasculitis, invasive fungal infection, lymphoma, or inadequate sample when delay would harm care.

Progression and follow-up: Follow addenda, amended reports, block exhaustion, turnaround time, tissue stewardship for molecular tests, concordance with imaging, margin/stage completeness, and whether pathology results trigger the correct specialty pathway.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Pap smear cytology abnormality

Pathophysiology: Pap cytology and HPV testing detect cervical squamous or glandular precancer driven mainly by persistent high-risk HPV, especially HPV 16 and 18; cytology reports abnormal cells while HPV-based risk estimates determine management.

How Pathology and Laboratory Medicine assesses it: Assess age, pregnancy, immunosuppression/HIV, prior HPV/cytology/colposcopy/treatment history, hysterectomy status, symptoms such as bleeding or visible lesion, specimen adequacy/transformation zone, HPV genotyping, and whether this is screening versus surveillance.

Diagnosis: Report cytology using Bethesda categories: NILM, ASC-US, LSIL, ASC-H, HSIL, AGC, AIS, or carcinoma, plus specimen adequacy. Management uses ASCCP risk-based thresholds combining current HPV/cytology with prior history; HPV 16/18, HSIL, ASC-H, AGC, AIS, or unsatisfactory cytology have distinct pathways.

First-line treatment: First-line lab role is accurate adequacy and Bethesda interpretation, reflex high-risk HPV testing/genotyping when ordered, and clear recommendation language tied to ASCCP risk logic such as repeat testing, colposcopy, expedited treatment consideration, or endocervical/endometrial sampling for glandular abnormalities.

Second-line treatment: Histology from colposcopy should use LAST terminology where appropriate: LSIL/CIN1 and HSIL/CIN2-3, with p16 immunostain for selected equivocal lesions. Discordant high-grade cytology with negative biopsy requires review and possible repeat colposcopy/excision.

Third-line / advanced care: Urgent gynecology/oncology communication for invasive carcinoma, AIS, AGC favor neoplasia, HSIL in high-risk context, or symptomatic visible lesion because screening algorithms do not replace diagnostic evaluation of symptoms.

Progression and follow-up: Follow closed-loop result notification, colposcopy completion, post-treatment HPV-based surveillance, persistent HPV, CIN2 observation eligibility, unsatisfactory cytology repeat timing, and avoiding overscreening after appropriate exit criteria.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Blood culture interpretation

Pathophysiology: Blood culture interpretation separates true bacteremia/fungemia from contamination by integrating organism identity, number of positive sets, time to positivity, clinical syndrome, source, intravascular devices, and host risk.

How Pathology and Laboratory Medicine assesses it: Assess fever/sepsis, hypotension, endocarditis risk, prosthetic valves/devices, central line, immunocompromise, neutropenia, skin/soft tissue source, urinary/biliary/lung source, prior antibiotics, number of sets drawn, draw sites, and whether only one bottle or multiple sets are positive.

Diagnosis: True pathogens usually include Staphylococcus aureus, Streptococcus pneumoniae, Enterobacterales, Pseudomonas, anaerobes, Candida, Listeria, Neisseria meningitidis, and beta-hemolytic streptococci. Common contaminants include coagulase-negative staphylococci, Cutibacterium acnes, Corynebacterium, Bacillus not anthracis, and Micrococcus, but these can be true with devices or repeated positives. Gram stain, rapid PCR panels, MALDI-TOF, and susceptibilities refine therapy.

First-line treatment: First-line lab action is immediate critical notification of positive blood culture Gram stain, rapid organism ID/resistance marker reporting such as mecA/C, vanA/B, CTX-M/KPC/NDM/OXA/VIM/IMP, and recommendation to draw repeat cultures when clinically needed.

Second-line treatment: If contamination is likely, report context without dismissing high-risk patients. If Staphylococcus aureus, Candida, gram-negative rod sepsis, or persistent positives occur, prompt source control, repeat cultures, echocardiography consideration, and ID involvement are appropriate.

Third-line / advanced care: Urgent escalation for gram-negative rods in septic shock, yeast in blood, S aureus bacteremia, meningococcemia, polymicrobial bacteremia suggesting intraabdominal source, carbapenemase producer, or suspected transfusion-related bacterial contamination.

Progression and follow-up: Follow time to clearance, susceptibility-directed narrowing, central-line removal decisions, endocarditis workup, contamination rates, blood culture stewardship, and whether final results reconcile with empiric antibiotics.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Transfusion reaction

Pathophysiology: Transfusion reactions include acute or delayed hemolytic reaction, febrile nonhemolytic reaction, allergic/anaphylactic reaction, TRALI, TACO, septic reaction, hypotensive reaction, post-transfusion purpura, and transfusion-associated graft-versus-host disease.

How Pathology and Laboratory Medicine assesses it: Assess reaction timing, fever/chills, back/flank pain, dyspnea, hypoxia, hypotension/hypertension, rash/urticaria, angioedema, dark urine, bleeding, volume status, product type, unit number, patient ID, premedications, IgA deficiency history, and comorbid heart/kidney disease.

Diagnosis: Stop transfusion and send clerical check, visual hemolysis check, repeat ABO/Rh, direct antiglobulin test, antibody screen/crossmatch review, plasma free hemoglobin, bilirubin, LDH, haptoglobin, urinalysis for hemoglobin, CBC/coags, and blood cultures from patient/unit when sepsis is possible. Chest X-ray/BNP can help TACO versus TRALI.

First-line treatment: First-line blood bank action is quarantine implicated product, verify patient/unit identity, perform acute reaction workup, notify transfusion medicine physician, and guide supportive care: normal saline, antipyretic for febrile reaction, diphenhydramine (Benadryl) for urticaria, epinephrine (EpiPen/Adrenalin) for anaphylaxis by clinical team, and diuretics such as furosemide (Lasix) for TACO when appropriate.

Second-line treatment: Future product planning may require leukoreduced, irradiated, washed, IgA-deficient, CMV-seronegative, antigen-negative, or phenotype/genotype-matched RBC units depending on reaction type and patient risk.

Third-line / advanced care: Emergency escalation for suspected acute hemolytic reaction, anaphylaxis, TRALI, TACO with respiratory failure, septic transfusion reaction, DIC, renal failure, or hypotension. Report serious reactions per institutional and regulatory requirements.

Progression and follow-up: Follow vital signs, hemolysis labs, renal function/urine output, oxygen requirement, alloantibody formation, delayed hemolysis days later, documentation in transfusion history, and prevention plan for future transfusions.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Coagulation test interpretation

Pathophysiology: Coagulation testing evaluates primary hemostasis, intrinsic/extrinsic/common pathways, fibrinogen, anticoagulant effect, liver synthetic function, vitamin K status, DIC, inherited factor deficiency, inhibitors, and lupus anticoagulant interference.

How Pathology and Laboratory Medicine assesses it: Assess bleeding versus thrombosis history, anticoagulants including warfarin (Coumadin/Jantoven), heparin, enoxaparin (Lovenox), apixaban (Eliquis), rivaroxaban (Xarelto), dabigatran (Pradaxa), liver disease, pregnancy, sepsis, massive transfusion, family history, procedures, and sample quality such as underfilled citrate tube or heparin contamination.

Diagnosis: Initial labs include PT/INR, aPTT, fibrinogen, thrombin time, anti-Xa when heparin/DOAC context fits, D-dimer, platelet count, peripheral smear, liver panel, and mixing study for prolonged PT/aPTT. Factor assays, von Willebrand panel, lupus anticoagulant testing, and inhibitor assays are targeted. DIC pattern often includes thrombocytopenia, prolonged PT/aPTT, low fibrinogen, high D-dimer, and schistocytes.

First-line treatment: First-line lab action is to verify specimen integrity and anticoagulant exposure, distinguish factor deficiency from inhibitor using mixing study, and communicate critical INR/aPTT/fibrinogen values before procedures or in active bleeding.

Second-line treatment: Interpret anticoagulant-specific tests: INR for warfarin, anti-Xa calibrated assays for heparin or some Xa inhibitors, dilute thrombin/ecarin-based tests for dabigatran where available. Reversal decisions may involve vitamin K, 4-factor PCC (Kcentra), protamine, idarucizumab (Praxbind), or andexanet alfa (Andexxa) by clinicians.

Third-line / advanced care: Urgent hematology/transfusion medicine for major bleeding, suspected DIC, acquired hemophilia, TTP mimic, HIT concern, severe factor deficiency, thrombolytic monitoring, or procedure-critical abnormal coagulation tests.

Progression and follow-up: Follow serial coagulation values, fibrinogen replacement response, anticoagulant clearance with renal/hepatic function, inhibitor persistence, thrombosis/bleeding outcomes, and preanalytic errors that could mislead care.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Molecular tumor testing

Pathophysiology: Molecular tumor testing identifies actionable driver alterations, resistance mutations, hereditary clues, tumor mutational features, and diagnostic/classification markers that guide targeted therapy, immunotherapy, prognosis, and clinical trial eligibility.

How Pathology and Laboratory Medicine assesses it: Assess tumor type, stage, recurrence/metastasis, prior therapy, specimen age/site, tumor cellularity, necrosis, decalcification, available tissue blocks, germline implications, turnaround urgency, and whether testing should be single-gene, hotspot panel, broad NGS, FISH, PCR, IHC surrogate, or liquid biopsy.

Diagnosis: Common examples include EGFR/ALK/ROS1/BRAF/MET/RET/NTRK/KRAS in lung cancer, ERBB2/HER2 and MSI/MMR in GI/breast contexts, BRAF V600E in melanoma/thyroid/colon, IDH1/2 and 1p/19q in glioma, BRCA/HRD in ovarian/prostate/breast, and PD-L1 IHC or MSI-high/TMB where immunotherapy decisions require. Reports should include method, limit of detection, tumor fraction, variants, tier/actionability, and limitations.

First-line treatment: First-line pathology action is tissue stewardship: confirm invasive tumor, mark tumor-rich area, avoid exhausting small biopsies, order guideline-supported biomarkers by cancer type/stage, and release integrated results with therapeutic implications and FDA-approved companion diagnostic context when applicable.

Second-line treatment: If tissue is inadequate, consider repeat biopsy, cytology cell block, plasma circulating tumor DNA, or focused IHC/FISH. Negative liquid biopsy does not exclude actionable alteration when tumor shedding is low; tissue testing may still be needed.

Third-line / advanced care: Molecular tumor board or genetics referral for rare variants, discordant results, suspected germline pathogenic variant, resistance after targeted therapy, trial matching, or complex copy-number/fusion interpretation.

Progression and follow-up: Follow turnaround time, treatment start deadlines, resistance mutations, rebiopsy at progression, germline confirmation, insurance/authorization barriers, and whether biomarker results are visible in oncology notes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Thyroid FNA interpretation

Pathophysiology: Thyroid FNA interpretation classifies aspirated follicular cells, colloid, lymphocytes, cyst contents, and malignant features to estimate cancer risk and guide surveillance, repeat FNA, molecular testing, lobectomy, or thyroidectomy.

How Pathology and Laboratory Medicine assesses it: Assess ultrasound risk pattern/TI-RADS, nodule size, solid/cystic nature, calcifications, extrathyroidal extension, suspicious lymph nodes, TSH, radiation exposure, family thyroid cancer/MEN2, prior FNA, rapid growth, compressive symptoms, and whether the sample was ultrasound-guided with adequacy passes.

Diagnosis: Report with Bethesda System categories: I nondiagnostic, II benign, III AUS/FLUS, IV follicular neoplasm/suspicious for follicular neoplasm, V suspicious for malignancy, VI malignant. Adequacy usually requires sufficient follicular groups unless cyst/inflammation exception applies. Ancillary molecular tests such as Afirma or ThyroSeq may refine indeterminate Bethesda III/IV risk.

First-line treatment: First-line pathology action is adequacy assessment when available, Bethesda category, descriptive cytology, and clear malignancy-risk/management correlation. Benign cytology usually returns to ultrasound surveillance; nondiagnostic often repeats ultrasound-guided FNA.

Second-line treatment: Bethesda III/IV may need repeat FNA, molecular testing, or diagnostic lobectomy based on ultrasound risk and patient factors. Bethesda V/VI usually triggers endocrine surgery evaluation; suspicious nodes may need FNA with thyroglobulin washout.

Third-line / advanced care: Urgent communication for anaplastic thyroid carcinoma, medullary thyroid carcinoma, lymphoma, metastatic tumor, or cytology explaining vocal cord paralysis/rapidly enlarging mass. Calcitonin/CEA, flow cytometry, or core biopsy may be needed by suspected diagnosis.

Progression and follow-up: Follow cytology-ultrasound concordance, repeat FNA adequacy, molecular result, surgical pathology correlation, false-negative risk in large/high-risk nodules, and surveillance intervals.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Urine cytology role

Pathophysiology: Urine cytology detects exfoliated malignant urothelial cells, performing best for high-grade urothelial carcinoma and carcinoma in situ but poorly for low-grade papillary tumors; inflammation, stones, instrumentation, and therapy can mimic atypia.

How Pathology and Laboratory Medicine assesses it: Assess indication such as gross hematuria, high-risk microscopic hematuria, bladder cancer surveillance, irritative voiding symptoms, smoking/occupational exposure, prior BCG/chemotherapy/radiation, stones/infection, recent cystoscopy/instrumentation, and specimen type: voided, catheterized, bladder washing, or upper-tract washing.

Diagnosis: Use Paris System categories: nondiagnostic, negative for high-grade urothelial carcinoma, atypical urothelial cells, suspicious for high-grade urothelial carcinoma, high-grade urothelial carcinoma, low-grade neoplasm, or other malignancy. Correlate with cystoscopy, CT urogram/upper tract imaging, urinalysis/culture, and optionally FISH or other urinary markers in selected scenarios.

First-line treatment: First-line role is adjunctive: support detection of high-grade disease/CIS and upper-tract disease, not replace cystoscopy or imaging. Ensure adequate fresh specimen processing and report limitations when cellularity is low or degenerative.

Second-line treatment: Atypical/suspicious results require urology correlation, repeat cytology, cystoscopy with directed biopsy, random bladder biopsies for CIS concern, upper-tract evaluation, or urinary FISH depending on risk and prior cancer history.

Third-line / advanced care: Urgent urology/oncology communication for positive high-grade cytology with negative cystoscopy, suspected upper-tract urothelial carcinoma, post-BCG recurrence, or cytology suggesting nonurothelial malignancy.

Progression and follow-up: Follow cystoscopy/pathology correlation, recurrence surveillance schedule, false positives after treatment/inflammation, specimen adequacy, and whether upper-tract disease was excluded when cytology remains positive.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Surgical margin assessment

Pathophysiology: Surgical margin assessment determines whether tumor, dysplasia, or infected/inflamed target extends to the inked or oriented tissue edge, influencing re-excision, radiation, systemic therapy, surveillance, and prognosis.

How Pathology and Laboratory Medicine assesses it: Assess specimen orientation, surgeon labels/sutures/clips, tumor type, neoadjuvant therapy, anatomic constraints, prior excision, requested frozen section, distance needed by disease type, and whether margin is en face, perpendicular, shaved, or circumferential/radial.

Diagnosis: Grossly ink margins by color/orientation, serially section, map lesion distance, and examine microscopically. Report positive, negative, close distance in mm when relevant, involved margin name, invasive versus in situ component, lymphovascular/perineural invasion, tumor size, grade, nodes, and CAP protocol elements for cancer resections.

First-line treatment: First-line pathology action is accurate inking/orientation, perpendicular margin measurement when distance matters, frozen section only when it will change intraoperative management, and clear synoptic reporting.

Second-line treatment: If margin status is ambiguous because of fragmentation, cautery artifact, unoriented specimen, or tumor at shave margin, issue limitations and communicate with surgeon. Additional levels, immunostains, or specimen radiography may help in breast/skin/head-neck cases.

Third-line / advanced care: Escalate to immediate surgeon call for unexpected positive critical margin on frozen section, cancer at margin in high-risk site, discordant specimen orientation, missing localization clip/lesion, or margin status that changes same-day operative decisions.

Progression and follow-up: Follow re-excision pathology, local recurrence risk, tumor board recommendations, adjuvant radiation/therapy decisions, report addenda, and quality review for orientation or sampling errors.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Hemolysis lab pattern

Pathophysiology: Hemolysis is premature RBC destruction from immune, microangiopathic, mechanical, membrane/enzyme, hemoglobinopathy, infection, toxin, drug, or transfusion causes, producing anemia, jaundice, reticulocytosis, pigment nephropathy, thrombosis, or shock.

How Pathology and Laboratory Medicine assesses it: Assess acute versus chronic anemia, jaundice/dark urine, transfusion, new drugs, infection, prosthetic valve/LVAD, pregnancy, hypertension/renal failure, neurologic symptoms, sickle history, family history, splenomegaly, thrombosis, and specimen hemolysis artifact.

Diagnosis: Core labs include CBC, reticulocyte count, smear, LDH, indirect bilirubin, haptoglobin, plasma free hemoglobin, urinalysis for hemoglobin, DAT/Coombs, type and screen, PT/aPTT/fibrinogen/D-dimer when DIC/TMA possible, creatinine, and G6PD or hemoglobin electrophoresis when indicated. Schistocytes suggest TMA/DIC/mechanical destruction; spherocytes suggest warm AIHA or hereditary spherocytosis.

First-line treatment: First-line lab action is to distinguish in vivo hemolysis from hemolyzed specimen artifact, call critical anemia/schistocytes, and guide urgent pattern recognition: warm AIHA, cold agglutinin disease, TTP/HUS, DIC, transfusion reaction, sickle crisis, or mechanical hemolysis.

Second-line treatment: Reflex/special testing may include eluate, cold agglutinin titer, ADAMTS13 activity/inhibitor, complement testing, PNH flow cytometry, RBC enzyme/membrane studies, and hemoglobin variant analysis. Treatment examples by clinicians include prednisone (Deltasone) or rituximab (Rituxan) for AIHA, plasma exchange for TTP, and eculizumab (Soliris) for selected complement-mediated disease.

Third-line / advanced care: Urgent hematology/transfusion medicine for schistocytes with thrombocytopenia/organ injury, suspected acute hemolytic transfusion reaction, severe AIHA, DIC, sickle acute chest/stroke, PNH thrombosis, or hemolysis with AKI.

Progression and follow-up: Follow hemoglobin, reticulocytes, LDH/bilirubin/haptoglobin, renal function, DAT status, transfusion compatibility, thrombotic complications, relapse, and therapy toxicity.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Pathology and Laboratory Medicine

Inflammatory marker interpretation

Pathophysiology: Inflammatory markers such as CRP, ESR, ferritin, procalcitonin, fibrinogen, D-dimer, and cytokine-related tests reflect acute-phase response, infection, tissue injury, malignancy, autoimmune disease, thrombosis, pregnancy, renal disease, anemia, and age rather than a single diagnosis.

How Pathology and Laboratory Medicine assesses it: Assess clinical syndrome, fever, focal infection, autoimmune symptoms, cancer risk, surgery/trauma, pregnancy, obesity, kidney disease, anemia, medications such as steroids or biologics, timing of symptom onset, and prior baseline marker levels.

Diagnosis: CRP changes faster and tracks many bacterial/inflammatory processes; ESR rises/falls slowly and is affected by age, anemia, pregnancy, renal disease, and immunoglobulins. Procalcitonin may support bacterial infection/antibiotic de-escalation in selected settings but is not definitive. Ferritin can indicate iron stores or severe inflammation/HLH. D-dimer is sensitive but nonspecific and must be paired with pretest probability.

First-line treatment: First-line lab interpretation is context-based: do not diagnose infection, vasculitis, or autoimmune disease from a marker alone. Use markers to support probability, trend response, and decide whether targeted testing such as cultures, imaging, ANA/ANCA, temporal artery evaluation, or malignancy workup is needed.

Second-line treatment: Escalate interpretation when markers are discordant with the patient: high ESR with normal CRP may suggest monoclonal gammopathy, anemia, renal disease, or chronic inflammation; very high ferritin raises concern for Still disease, HLH, severe infection, liver injury, or malignancy by context.

Third-line / advanced care: Urgent clinician notification or escalation for inflammatory markers paired with sepsis, suspected giant cell arteritis with visual symptoms, necrotizing infection, HLH/macrophage activation syndrome, DIC, pulmonary embolism evaluation with high-risk symptoms, or rapidly worsening organ dysfunction.

Progression and follow-up: Follow trends rather than isolated values, lab method differences, false reassurance from normal markers early in disease or under immunosuppression, overtesting cascades, and whether marker changes match clinical improvement.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Specialty role

Serious illness support with symptom control, communication, goals of care, caregiver support, and hospice transition.

Palliative Care

Cancer pain palliative plan

Pathophysiology: Cancer pain may be nociceptive from tumor invasion, visceral obstruction, bone metastases, or procedures; neuropathic from nerve compression or chemotherapy; and total pain from psychosocial, spiritual, financial, and caregiver distress.

How Palliative Care assesses it: Assess pain mechanism, location, severity, breakthrough pattern, functional goal, opioid exposure/tolerance, bowel function, sedation, renal/hepatic function, substance-use risk, caregiver medication handling, goals of care, and emergencies such as fracture, cord compression, infection, or bowel obstruction.

Diagnosis: Use clinical pain phenotype plus targeted evaluation only when it changes care: X-ray/CT/MRI for bone or spine structural pain, labs for hypercalcemia/infection/renal function, neurologic exam for cord or nerve compression, medication review for neuropathy, and ESAS or numeric pain scale to track response.

First-line treatment: Mild pain may use acetaminophen (Tylenol) or NSAID such as ibuprofen (Advil/Motrin) or naproxen (Aleve) if safe. Moderate/severe cancer pain uses opioids such as morphine, oxycodone (Roxicodone/OxyContin), hydromorphone (Dilaudid), or fentanyl patch (Duragesic) with scheduled bowel regimen senna (Senokot) plus polyethylene glycol (MiraLAX). Neuropathic pain may use duloxetine (Cymbalta), gabapentin (Neurontin), or pregabalin (Lyrica).

Second-line treatment: Bone metastasis pain may need palliative radiation, dexamethasone (Decadron), zoledronic acid (Zometa), or denosumab (Xgeva). Refractory pain may require methadone (Dolophine), ketamine protocols, lidocaine infusion, nerve block, intrathecal pump, or opioid rotation by experienced clinicians.

Third-line / advanced care: Urgent oncology/radiation/surgery for spinal cord compression, pathologic fracture, bowel obstruction, uncontrolled pain crisis, opioid toxicity, or pain with delirium. Palliative care coordinates complex opioid safety, goals, family support, and home/hospice medication plans.

Progression and follow-up: Follow pain score and function, breakthrough doses, sedation/respiratory rate, constipation, nausea, falls, delirium, renal changes, opioid storage, caregiver distress, and whether analgesia aligns with the patient's priorities.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Dyspnea in advanced disease

Pathophysiology: Dyspnea in advanced illness arises from lung disease, heart failure, pleural effusion, ascites, anemia, pulmonary embolism, infection, airway obstruction, anxiety, deconditioning, or central perception of air hunger, and distress can be severe even when oxygen saturation is acceptable.

How Palliative Care assesses it: Assess intensity at rest/exertion, oxygen saturation, respiratory rate/work, reversible causes, prognosis, goals, anxiety/panic, cough/secretions, fluid overload, anemia, pleural effusion/ascites, opioid/benzodiazepine exposure, ability to swallow, and caregiver fear.

Diagnosis: Use focused workup only if it changes management: pulse oximetry, exam, chest X-ray, CBC, BNP, infection testing, ultrasound for pleural effusion/ascites, or CT/CTA when PE or obstruction treatment fits goals. Use ESAS or numeric dyspnea score for symptom tracking.

First-line treatment: Treat reversible burdens consistent with goals: oxygen for hypoxemia, fan to face, upright positioning, pursed-lip breathing, relaxation, bronchodilator albuterol (Ventolin/ProAir) for bronchospasm, furosemide (Lasix) for fluid overload, antibiotics only when infection treatment matches goals, and low-dose opioid such as morphine solution or hydromorphone (Dilaudid) for refractory air hunger.

Second-line treatment: If anxiety amplifies dyspnea after opioids/non-drug measures, use cautious lorazepam (Ativan) or midazolam in closely supervised end-of-life settings. Drain symptomatic pleural effusion/ascites by thoracentesis, tunneled pleural catheter, or paracentesis when expected benefit exceeds burden.

Third-line / advanced care: Urgent escalation for stridor/airway obstruction, severe hypoxemia needing acute intervention, pulmonary embolism treatment aligned with goals, uncontrolled terminal dyspnea requiring continuous opioid/benzodiazepine titration, or caregiver inability to manage symptoms at home.

Progression and follow-up: Follow comfort rather than saturation alone, opioid response/toxicity, panic cycles, secretion burden, caregiver confidence, equipment access, repeated procedures, and whether hospitalization remains desired.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Nausea in serious illness

Pathophysiology: Nausea in serious illness may be caused by medications/opioids, constipation, bowel obstruction, gastroparesis, uremia, hypercalcemia, liver failure, infection, vestibular disease, increased intracranial pressure, chemotherapy, radiation, or anxiety.

How Palliative Care assesses it: Assess timing, triggers, vomiting, bowel movements/flatus, abdominal distension/pain, medications, opioid start/escalation, renal/liver failure, calcium, brain metastasis/headache, vestibular symptoms, chemotherapy/radiation timing, hydration, oral intake goals, and route availability.

Diagnosis: Use focused testing only when it changes care: CMP with calcium/creatinine/LFTs, abdominal exam and X-ray/CT for obstruction if intervention fits goals, medication review, brain imaging for new headache/neurologic signs, and constipation assessment. Track with ESAS/numeric nausea score.

First-line treatment: Treat cause and choose receptor-targeted antiemetic: ondansetron (Zofran) for serotonin/chemo-related nausea, prochlorperazine (Compazine) or haloperidol (Haldol) for chemical/metabolic nausea, metoclopramide (Reglan) for gastric stasis when no obstruction, and bowel regimen for constipation.

Second-line treatment: Use olanzapine (Zyprexa) for refractory or multifactorial nausea, dexamethasone (Decadron) for raised intracranial pressure, bowel obstruction, or cancer-related inflammation, scopolamine (Transderm Scop) or meclizine (Antivert) for vestibular nausea, and octreotide (Sandostatin) for malignant bowel obstruction secretions.

Third-line / advanced care: Escalate for intractable vomiting, suspected complete bowel obstruction/perforation, dehydration inconsistent with goals, severe hypercalcemia, increased intracranial pressure, or inability to use oral route requiring subcutaneous/IV/rectal hospice protocols.

Progression and follow-up: Follow symptom score, sedation, QT prolongation risk with dopamine antagonists/ondansetron, extrapyramidal effects, constipation worsening, oral intake goals, caregiver administration, and whether workup/treatment burden matches priorities.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Constipation from opioids

Pathophysiology: Opioid-induced constipation results from mu-receptor slowing of gut motility, reduced secretion, increased sphincter tone, and impaired defecation reflex; tolerance rarely develops, so prophylaxis is needed when opioids start.

How Palliative Care assesses it: Assess last bowel movement, stool consistency, flatus, abdominal pain/distension, nausea/vomiting, oral intake, hydration, immobility, bowel obstruction risk, rectal impaction, renal function, anticholinergics, calcium, and patient privacy/caregiver ability to administer medications.

Diagnosis: Usually clinical. Rectal exam when impaction is possible and consistent with goals; abdominal imaging if bowel obstruction, perforation, ileus, or fecal impaction would change management. Avoid routine extensive workup in actively dying patients unless symptoms require it.

First-line treatment: Start stimulant laxative with opioid: senna (Senokot) or bisacodyl (Dulcolax), often plus osmotic polyethylene glycol (MiraLAX) or lactulose. Encourage fluids/activity only when realistic. Docusate alone is usually inadequate.

Second-line treatment: For refractory OIC without suspected obstruction, consider peripherally acting mu-opioid antagonists such as methylnaltrexone (Relistor), naloxegol (Movantik), or naldemedine (Symproic). Use suppository/enema for rectal stool burden when safe.

Third-line / advanced care: Urgent evaluation for severe abdominal pain, vomiting, absent flatus, peritoneal signs, suspected bowel obstruction, stercoral colitis/perforation, or refractory impaction. Malignant bowel obstruction needs separate goals-based pathway.

Progression and follow-up: Follow bowel movement frequency, comfort, diarrhea/cramping, dehydration, adherence, opioid dose changes, caregiver burden, impaction recurrence, and whether bowel regimen is continued during opioid rotation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Terminal secretions

Pathophysiology: Terminal secretions are noisy pooled oropharyngeal/upper-airway secretions from reduced consciousness, weak swallow/cough, and altered breathing near death; they often distress family more than the patient.

How Palliative Care assesses it: Assess whether secretions appear uncomfortable, respiratory distress, pulmonary edema, infection, aspiration, medication burden, hydration/IV fluids, ability to reposition, urinary retention, delirium, and family understanding of the dying process.

Diagnosis: Clinical diagnosis; avoid burdensome imaging or suctioning unless airway obstruction, tracheostomy, or a reversible cause fits goals. Distinguish wet pulmonary edema from upper-airway pooling because treatment differs.

First-line treatment: First-line care is family education, lateral positioning, gentle mouth care, reduce or stop nonbeneficial IV/subcutaneous fluids, and avoid deep suctioning that causes gagging or distress. Treat dyspnea separately with opioids if present.

Second-line treatment: Anticholinergics may reduce new secretion production: glycopyrrolate (Robinul), scopolamine patch (Transderm Scop), atropine 1% ophthalmic drops used sublingually, or hyoscyamine (Levsin). They work less well for already pooled secretions and can worsen delirium, urinary retention, or dry mouth.

Third-line / advanced care: Escalate to hospice/palliative team for persistent family distress, apparent respiratory discomfort, tracheostomy secretion management, pulmonary edema needing furosemide (Lasix), or terminal symptom crisis requiring continuous nursing support.

Progression and follow-up: Follow observed comfort, family distress, delirium/retention from anticholinergics, mouth dryness, fluid orders, suction-related discomfort, and whether medication burden remains proportionate.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Delirium at end of life

Pathophysiology: End-of-life delirium is acute fluctuating attention/cognition disturbance caused by infection, organ failure, hypoxia, medications/opioids/benzodiazepines/anticholinergics, urinary retention, constipation, dehydration, metabolic abnormalities, brain disease, or the dying process.

How Palliative Care assesses it: Assess onset/fluctuation, hyperactive versus hypoactive features, distress/safety risk, pain, urinary retention, constipation, hypoxia, infection, medication changes, renal/hepatic failure, alcohol/benzodiazepine withdrawal, goals of care, prognosis, and caregiver distress.

Diagnosis: Use bedside tools such as CAM or 4AT when helpful, medication review, focused exam, bladder scan/rectal constipation check when appropriate, and limited labs/imaging only if reversal is desired and plausible. Distinguish terminal delirium from anxiety, depression, dementia, psychosis, or uncontrolled pain.

First-line treatment: Non-drug care: reorientation, calm room, glasses/hearing aids, sleep-wake cues, family presence, reduce tethers, treat pain/retention/constipation, and stop deliriogenic drugs when possible. If distressing agitation threatens safety, use haloperidol (Haldol) or olanzapine (Zyprexa) cautiously.

Second-line treatment: If Parkinson disease/Lewy body dementia, avoid or minimize haloperidol and consider quetiapine (Seroquel). Benzodiazepines such as lorazepam (Ativan) are mainly for alcohol/benzodiazepine withdrawal, severe anxiety with terminal agitation, or palliative sedation protocols.

Third-line / advanced care: Escalate for refractory agitated delirium, severe caregiver distress, unsafe home situation, suspected reversible emergency that patient wants treated, or need for inpatient hospice/palliative sedation using midazolam, phenobarbital, or other specialist protocols.

Progression and follow-up: Follow comfort, ability to interact, falls, extrapyramidal/QT risk, paradoxical benzodiazepine agitation, family understanding that terminal delirium may not reverse, and medication route as swallowing declines.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Goals of care conversation

Pathophysiology: Goals-of-care conversations align medical treatments with a person's values, prognosis understanding, acceptable tradeoffs, and preferred outcomes during serious illness; the intervention is communication, not withdrawal of care.

How Palliative Care assesses it: Assess decision-making capacity, preferred decision-maker/surrogate, understanding of illness, information preferences, values, hopes, worries, spiritual/cultural needs, prior experiences, code status, treatment burdens, language needs, and urgency of decisions.

Diagnosis: Use structured communication such as ask-tell-ask, serious-illness conversation guide, best-case/worst-case, and teach-back. Clarify decisions: disease-directed treatment, hospitalization/ICU, CPR/intubation, artificial nutrition, dialysis, transfusions, hospice, and comfort-focused care.

First-line treatment: First-line action is to name the decision, share prognosis honestly with uncertainty, recommend a plan aligned with stated values, document the conversation in the chart, and enter actionable orders such as code status only after informed discussion.

Second-line treatment: Hold family meeting with interdisciplinary team when conflict, prognostic uncertainty, or multiple specialists exist. Use ethics, chaplaincy, social work, interpreter, or cultural liaison support when needed.

Third-line / advanced care: Escalate to ethics/palliative care for conflict among surrogate/team, unclear surrogate authority, requests for nonbeneficial treatment, high-stakes ICU decisions, or emotional/spiritual distress blocking decision-making.

Progression and follow-up: Follow whether orders match the conversation, revisit after clinical change, ensure surrogate access to documents, communicate across settings, and avoid treating code status as a substitute for broader goals.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Hospice eligibility discussion

Pathophysiology: Hospice is interdisciplinary comfort-focused care for patients expected to live about 6 months or less if the illness follows its usual course, when goals prioritize comfort over curative or life-prolonging treatment; eligibility is prognosis- and goal-based, not only diagnosis-based.

How Palliative Care assesses it: Assess disease trajectory, functional decline such as PPS/Karnofsky, weight loss, recurrent hospitalizations, infections, oxygen dependence, dysphagia/aspiration, pressure injuries, cognitive decline, metastatic/progressive cancer, end-stage heart/lung/liver/kidney/neurologic disease, caregiver capacity, and desired location of care.

Diagnosis: Use hospice benefit criteria as supportive documentation: prognosis under 6 months if natural course continues, decline despite therapy, symptom burden, comorbidities, and patient preference. DNR is not required, but full-code preference should prompt careful clarification of hospice philosophy and emergency plans.

First-line treatment: First-line conversation explains services: nurse/physician oversight, medications/equipment related to terminal diagnosis, social work, chaplain, aides, 24/7 phone support, respite, bereavement, and focus on comfort at home/facility/inpatient hospice when needed.

Second-line treatment: If patient still wants disease-directed therapy, consider concurrent palliative care, home health, clinic-based symptom care, or disease-specific programs until goals change. Some treatments such as palliative radiation, transfusions, or procedures may or may not be covered depending on hospice plan and goals.

Third-line / advanced care: Urgent hospice/palliative referral for uncontrolled symptoms, repeated hospitalizations, caregiver exhaustion, rapid decline, desire to die at home, or need for inpatient hospice for pain, dyspnea, agitation, or secretions unmanageable elsewhere.

Progression and follow-up: Follow enrollment decision, revocation/discharge questions, medication/equipment delivery, caregiver safety, crisis plan, bereavement risk, and revisit eligibility/goals as illness changes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Opioid conversion safety

Pathophysiology: Opioid conversion safety prevents overdose or withdrawal when switching opioid, route, or schedule; incomplete cross-tolerance, renal/hepatic function, age, frailty, drug interactions, and methadone's nonlinear potency make conversions high risk.

How Palliative Care assesses it: Assess current opioid name, dose, schedule, actual 24-hour use including breakthrough, pain control, sedation, respiratory status, renal/hepatic function, age/frailty, QT risk, benzodiazepines/alcohol, swallowing route, patch absorption factors, and reason for rotation.

Diagnosis: Calculate total daily oral morphine equivalents, choose equianalgesic estimate, reduce new opioid dose for incomplete cross-tolerance often 25-50% except special contexts, then provide breakthrough dose usually 5-15% of total daily opioid. Methadone and fentanyl patch conversions require experienced guidance.

First-line treatment: Use immediate-release morphine, oxycodone (Roxicodone), or hydromorphone (Dilaudid) for titration when possible; convert to long-acting morphine ER (MS Contin), oxycodone ER (OxyContin), fentanyl patch (Duragesic), or methadone (Dolophine) only after stable needs are known. Always prescribe bowel regimen and naloxone (Narcan) when appropriate.

Second-line treatment: Adjust for renal disease: avoid or reduce morphine when metabolite accumulation risk is high; consider fentanyl or carefully dosed hydromorphone/methadone with expertise. Reassess within 24-72 hours after changes and sooner in frail or rapidly changing patients.

Third-line / advanced care: Urgent escalation for opioid toxicity, respiratory depression, myoclonus, severe sedation, uncontrolled pain crisis, methadone QT/prolonged sedation concern, complex high-dose rotation, or unsafe home medication administration.

Progression and follow-up: Follow pain, alertness, respiratory rate, breakthrough use, constipation, nausea, myoclonus, falls, caregiver understanding, refill timing, and safe storage/disposal.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Deprescribing in serious illness

Pathophysiology: Deprescribing reduces medication burden when time-to-benefit exceeds prognosis or goals, adverse effects exceed benefit, swallowing is difficult, monitoring is burdensome, or preventive therapy no longer matches priorities.

How Palliative Care assesses it: Assess prognosis, goals, symptom benefit, time-to-benefit, pill burden, swallowing, renal/hepatic function, falls, delirium, anticholinergic load, hypoglycemia/hypotension risk, duplicate drugs, cost, caregiver administration, and medications that should not be abruptly stopped.

Diagnosis: Review medication list by indication: symptom-relieving, disease-modifying, preventive, monitoring-intensive, and potentially harmful. Common candidates include statins, vitamins, bisphosphonates, tight glycemic agents, some antihypertensives, cholinesterase inhibitors, anticoagulants in selected high-bleeding/low-benefit contexts, and PPIs without indication.

First-line treatment: First-line action is shared decision-making: stop one or more low-benefit drugs, simplify dosing, convert essential symptom drugs to available route, and document rationale. Continue medicines that improve comfort, prevent distressing rebound, or meet patient priorities.

Second-line treatment: Taper when needed: benzodiazepines, baclofen, clonidine, beta blockers, corticosteroids, antidepressants, gabapentinoids, and opioids unless imminently dying or toxicity demands faster change. Monitor for withdrawal or symptom recurrence.

Third-line / advanced care: Escalate to pharmacy/palliative care for polypharmacy, anticoagulation dilemmas, insulin simplification, complex psychiatric drugs, seizure medications, or family concern that stopping medicines means abandonment.

Progression and follow-up: Follow symptom burden, withdrawal, BP/glucose only if meaningful, falls/delirium, caregiver workload, cost, adherence, and whether medication list remains aligned after each clinical transition.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Caregiver distress

Pathophysiology: Caregiver distress arises from emotional grief, physical exhaustion, financial/work strain, medication and equipment responsibilities, sleep loss, fear of symptoms, family conflict, cultural expectations, and anticipatory bereavement during serious illness.

How Palliative Care assesses it: Assess caregiver identity, capacity, health literacy, sleep, depression/anxiety, safety, finances/work, family conflict, medication confidence, lifting/toileting burden, spiritual distress, bereavement risk, respite availability, and risk of neglect or abuse in either direction.

Diagnosis: Use caregiver strain index, distress thermometer, PHQ-2/9 or GAD-7 when appropriate, social work assessment, home safety assessment, and direct teach-back for symptom crisis plans. Distinguish normal grief from major depression, trauma, or unsafe caregiving collapse.

First-line treatment: First-line support includes clear care plan, written medication schedule, teach-back for opioids/rescue meds, 24/7 contact instructions, equipment/home nursing/hospice services, respite planning, social work/chaplain support, and permission to rest.

Second-line treatment: Connect to caregiver support groups, counseling, FMLA/benefits resources, paid caregiver options, adult protective services when safety requires, and bereavement support. Treat caregiver depression/anxiety through their own clinician when persistent or severe.

Third-line / advanced care: Escalate urgently for caregiver unable to administer essential meds, unsafe home, suicidal ideation, violence, patient neglect, uncontrolled symptoms exceeding home capacity, or need for inpatient hospice/respite placement.

Progression and follow-up: Follow caregiver sleep, confidence, crisis calls, medication errors, conflict, bereavement risk, physical injury, and whether the care setting remains sustainable.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Palliative Care

Advance directive completion

Pathophysiology: Advance directives document preferences and designate a decision-maker before loss of capacity, reducing unwanted treatment and conflict when serious illness progresses.

How Palliative Care assesses it: Assess capacity, chosen health care proxy/surrogate, state-specific forms, values, acceptable quality of life, CPR/intubation preferences, artificial nutrition/hydration, dialysis, hospitalization, transfusion, religious/cultural needs, organ donation, and where documents will be stored/shared.

Diagnosis: Clarify the difference among advance directive/living will, durable power of attorney for health care, POLST/MOLST/portable medical order, DNR order, and estate/financial documents. POLST-type forms are medical orders for seriously ill or frail patients; advance directives guide future decisions but may not be actionable EMS orders.

First-line treatment: First-line action is to name a surrogate, discuss values and treatment limits, complete valid forms with signatures/witness/notary as required locally, upload to medical record, and give copies to surrogate/family/facility.

Second-line treatment: For complex situations, involve social work, chaplain, interpreter, legal aid/elder law, ethics, or tribal/cultural liaison. Revisit forms after hospitalization, new diagnosis, functional decline, or change in surrogate.

Third-line / advanced care: Escalate urgently when capacity is fluctuating, no surrogate is available, family conflict exists, guardianship may be needed, patient is requesting treatment limits before a high-risk procedure, or documents conflict with current expressed wishes.

Progression and follow-up: Follow document accessibility, surrogate understanding, consistency with code status/POLST, updates after transitions, and whether clinicians can locate the directive during emergencies.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Specialty role

Population health, screening, vaccines, lifestyle risk, occupational/environmental exposure, and prevention policy.

Preventive Medicine and Public Health

Adult vaccine schedule

Pathophysiology: Adult immunization prevents severe respiratory infection, invasive bacterial disease, shingles, hepatitis, HPV-associated cancers, tetanus/pertussis, measles/mumps/rubella, varicella, meningococcal disease, mpox, and travel-associated infections by matching immune risk to ACIP age, pregnancy, occupation, exposure, and medical-condition indications.

How Preventive Medicine and Public Health assesses it: Assess age, pregnancy status, immune compromise, asplenia, cochlear implant/CSF leak, diabetes, CKD/liver/lung/heart disease, HIV status/CD4 when relevant, transplant or biologic therapy, health-care/lab work, travel, military/dormitory exposure, sexual risk, prior vaccine records, prior infection, allergies, Guillain-Barre history, and live-vaccine contraindications.

Diagnosis: Use CDC/ACIP adult schedule by age and medical condition; verify records in state immunization registry when available. Check pregnancy status before live vaccines, hepatitis B serology when indicated, varicella/MMR immunity when history is uncertain and risk is high, and post-vaccine titers only for selected groups such as hepatitis B in dialysis/health-care exposure.

First-line treatment: Give routine vaccines when due: annual influenza vaccine; updated COVID-19 vaccine per current CDC schedule; Tdap once then Td or Tdap every 10 years and Tdap in each pregnancy; recombinant zoster vaccine RZV (Shingrix) 2 doses for adults 50+ or immunocompromised adults 19+; pneumococcal PCV20/PCV21 alone or PCV15 followed by PPSV23 by age/risk; hepatitis B vaccine such as Heplisav-B, Engerix-B, or Recombivax HB for adults 19-59 and risk-based older adults; HPV vaccine Gardasil 9 through age 26 and shared decision age 27-45.

Second-line treatment: Add risk/travel vaccines: RSV vaccine Arexvy, Abrysvo, or mResvia for older adults by current age/risk guidance and Abrysvo in pregnancy when indicated; MMR, varicella, hepatitis A, MenACWY, MenB, Hib, mpox Jynneos, polio IPV, rabies, typhoid, Japanese encephalitis, yellow fever, cholera, and meningococcal boosters when exposure or medical condition fits.

Third-line / advanced care: Refer immunocompromised, transplant, pregnancy, severe allergy, uncertain vaccine reaction, or complex catch-up cases to infectious disease/allergy/travel medicine; report clinically significant adverse events to VAERS and report suspected vaccine-preventable disease outbreaks to public health.

Progression and follow-up: Track vaccine dates, product names, lot/site, adverse reactions, next due dates, booster needs, immune-compromising therapy timing, pregnancy intervals, school/work requirements, and whether refusal was addressed with nonjudgmental counseling.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Cancer screening preventive plan

Pathophysiology: Cancer screening detects precancer or early asymptomatic malignancy before symptoms, but each cancer uses a different test, interval, starting age, stop rule, and abnormal-result pathway to balance mortality benefit against false positives, overdiagnosis, radiation, anxiety, biopsy, and procedure harms.

How Preventive Medicine and Public Health assesses it: Assess age, sex organs present, pregnancy, life expectancy, symptoms, prior abnormal screens, family history, BRCA/Lynch/polyposis risk, immunosuppression, DES exposure, HPV history, smoking pack-years and quit date, occupational exposures, inflammatory bowel disease, prior radiation, and whether the patient needs screening or diagnostic evaluation.

Diagnosis: Use USPSTF/specialty-aligned screening: breast cancer with biennial mammography for average-risk adults 40-74; colorectal cancer from 45-75 with annual FIT, stool DNA-FIT every 1-3 years, CT colonography every 5 years, flexible sigmoidoscopy, or colonoscopy every 10 years; cervical cancer with Pap/HPV strategy by age and cervix status; lung cancer with annual low-dose CT for eligible adults with heavy smoking history; prostate cancer with individualized PSA discussion; hepatitis B/C evaluation when liver cancer risk applies.

First-line treatment: Order the correct test and close the loop: mammography with diagnostic mammogram/ultrasound and core biopsy for BI-RADS 4/5; colonoscopy after any positive stool test; colposcopy after high-risk cervical results; LDCT Lung-RADS follow-up and smoking cessation for lung screening; PSA repeat/risk calculation, prostate MRI, or urology referral when concerning.

Second-line treatment: Escalate screening intensity for high-risk states: genetic counseling/testing for BRCA1/2, Lynch, FAP, or strong family history; breast MRI plus mammography for very high-risk breast cancer; earlier/more frequent colonoscopy for Lynch/polyps/IBD; anal cancer or skin surveillance only when risk profile supports it.

Third-line / advanced care: Do not use screening tests for symptoms such as breast mass, rectal bleeding, hemoptysis, postmenopausal bleeding, or weight loss; these require diagnostic imaging/endoscopy/biopsy. Stop or individualize screening when limited life expectancy, prior total hysterectomy for benign disease, or age/comorbidity makes harm exceed benefit.

Progression and follow-up: Follow completion, results, pathology, recall intervals, high-risk referrals, missed colonoscopy after positive FIT, radiation exposure from LDCT, smoking status, vaccine prevention such as HPV Gardasil 9 and hepatitis B vaccine, and patient preference.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Cardiovascular risk prevention

Pathophysiology: Primary cardiovascular prevention reduces future ASCVD, heart failure, kidney disease, stroke, and vascular death by controlling blood pressure, lipids, tobacco, diabetes, obesity, sleep apnea, diet, activity, and thrombotic risk before the first event.

How Preventive Medicine and Public Health assesses it: Assess age, BP technique/home BP, lipid history, diabetes, CKD, smoking/vaping, pregnancy history such as preeclampsia, premature menopause, family history of premature ASCVD, inflammatory disease, HIV, South Asian ancestry, diet sodium/saturated fat, activity, alcohol, sleep apnea, statin intolerance, and bleeding risk.

Diagnosis: Measure BP on repeated visits or home/ambulatory monitoring, fasting or nonfasting lipid panel, A1c/glucose, creatinine/eGFR, urine albumin-creatinine ratio when diabetes/HTN/CKD risk, ASCVD 10-year risk for adults 40-75, ECG only when symptoms/risk suggests, and coronary artery calcium CT when statin decision remains uncertain after risk discussion.

First-line treatment: First-line prevention is lifestyle plus BP and lipid treatment when indicated: DASH/Mediterranean-style diet, sodium reduction, 150 minutes/week moderate activity, weight reduction, tobacco cessation, sleep apnea treatment, and statin therapy such as atorvastatin (Lipitor) or rosuvastatin (Crestor) for ASCVD risk thresholds, diabetes age 40-75, LDL-C 190 mg/dL or higher, or risk-enhancing features.

Second-line treatment: If risk remains high or LDL goals are not met, intensify statin dose and consider ezetimibe (Zetia) or PCSK9 inhibitor alirocumab (Praluent)/evolocumab (Repatha) in selected very-high-risk or familial hypercholesterolemia cases. Treat hypertension with chlorthalidone (Thalitone), amlodipine (Norvasc), lisinopril (Zestril/Prinivil), or losartan (Cozaar) based on comorbidity.

Third-line / advanced care: Aspirin (Bayer/Ecotrin) for primary prevention is selective and generally avoided when bleeding risk is high; cardiology/lipid clinic referral for familial hypercholesterolemia, severe hypertriglyceridemia, statin intolerance, premature ASCVD family history, abnormal CAC with symptoms, or complex risk decisions.

Progression and follow-up: Follow BP, LDL/non-HDL, A1c, kidney function, potassium after ACE/ARB/diuretic, statin adverse effects, adherence, smoking status, exercise tolerance, weight/waist, and new symptoms that convert prevention into diagnostic cardiology care.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Diabetes prevention

Pathophysiology: Prediabetes reflects insulin resistance and beta-cell stress that can progress to type 2 diabetes, microvascular disease, fatty liver disease, obstructive sleep apnea, and ASCVD; prevention targets weight, muscle insulin sensitivity, sleep, medication contributors, and cardiometabolic risk.

How Preventive Medicine and Public Health assesses it: Assess BMI/waist, family history, gestational diabetes/PCOS, ethnicity-associated risk, hypertension, dyslipidemia, fatty liver, sleep apnea, steroid/antipsychotic exposure, food access, activity, depression, pregnancy plans, and readiness for intensive lifestyle change.

Diagnosis: Screen adults 35-70 with overweight/obesity and others with risk factors using A1c, fasting plasma glucose, or 2-hour OGTT. Prediabetes includes A1c 5.7-6.4%, fasting glucose 100-125 mg/dL, or 2-hour OGTT 140-199 mg/dL; repeat abnormal results when not clearly diagnostic and check lipids, BP, ALT/AST, and urine albumin/eGFR if diabetes is diagnosed.

First-line treatment: Refer to a CDC-recognized Diabetes Prevention Program: goal 5-7% weight loss, at least 150 minutes/week moderate activity, nutrition coaching, sleep support, and relapse prevention. Treat BP/lipids/tobacco concurrently and review weight-promoting drugs.

Second-line treatment: Consider metformin (Glucophage) for high-risk prediabetes, especially younger adults with BMI 35 or higher, prior gestational diabetes, rising A1c, or severe insulin resistance. If obesity criteria are met, consider anti-obesity therapy such as semaglutide (Wegovy) or tirzepatide (Zepbound) with contraception/pregnancy and adverse-effect counseling.

Third-line / advanced care: Endocrinology/obesity medicine referral for suspected type 1/LADA, severe hyperglycemia, recurrent gestational diabetes risk, complex obesity pharmacotherapy, eating disorder, or failure of standard prevention. Bariatric/metabolic surgery evaluation may be appropriate when BMI/comorbidity criteria are met.

Progression and follow-up: Follow A1c or fasting glucose at least yearly, weight/waist, BP, lipids, liver risk, sleep apnea symptoms, medication tolerance, pregnancy plans, and transition promptly to diabetes management if diagnostic thresholds are reached.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Tobacco cessation population approach

Pathophysiology: Nicotine dependence is a chronic relapsing substance-use condition driven by nicotinic receptor reinforcement, cue-triggered craving, withdrawal, stress, social exposure, and industry product design; prevention reduces cancer, COPD, ASCVD, pregnancy harms, surgical complications, and secondhand-smoke exposure.

How Preventive Medicine and Public Health assesses it: Assess product type, cigarettes/day, time to first use, vaping, smokeless tobacco, cannabis co-use, prior quit attempts, withdrawal, pregnancy, psychiatric/substance-use comorbidity, contraindications, household exposure, readiness, social drivers, and eligibility for lung cancer screening.

Diagnosis: Use the 5 A's or Ask-Advise-Refer, document pack-years, Fagerstrom-style dependence clues, CO level only when useful, PHQ-9/substance screen when indicated, and annual low-dose CT eligibility for adults with qualifying smoking history. Do not wait for perfect readiness to offer treatment.

First-line treatment: Offer behavioral counseling plus pharmacotherapy: varenicline (Chantix) is highly effective; nicotine replacement therapy can use patch plus short-acting gum/lozenge/inhaler/nasal spray; bupropion SR (Zyban/Wellbutrin SR) helps when no seizure/eating-disorder risk. Connect to 1-800-QUIT-NOW, text/app supports, and smoke-free home/work policies.

Second-line treatment: For relapse or high dependence, combine long-acting patch with gum/lozenge, extend varenicline duration, switch agents, address alcohol/stress triggers, treat depression/anxiety, and schedule frequent follow-up. In pregnancy, prioritize counseling and weigh NRT only with shared decision-making.

Third-line / advanced care: Refer tobacco treatment specialist, behavioral health, pulmonology, cardiology, or oncology screening program for refractory dependence, severe psychiatric comorbidity, pregnancy complexity, COPD/ASCVD complications, or abnormal LDCT findings.

Progression and follow-up: Track quit date, slips vs relapse, withdrawal, mood/suicidality, BP/weight, medication adverse effects such as nausea/vivid dreams with varenicline or insomnia/seizure risk with bupropion, secondhand exposure, and screening completion.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Obesity prevention counseling

Pathophysiology: Obesity prevention addresses progressive adiposity and metabolic risk before severe complications develop, recognizing neurohormonal appetite regulation, sleep, stress, medications, environment, food insecurity, genetics, pregnancy/postpartum weight retention, and social context.

How Preventive Medicine and Public Health assesses it: Assess BMI percentile/trajectory in youth or BMI/waist in adults, BP, A1c/glucose, lipids, ALT/AST, sleep, depression/binge eating, medications that increase weight, pregnancy plans, family meals, sugary beverages, activity/sedentary time, food access, stigma, and patient priorities.

Diagnosis: Use BMI with clinical context, waist circumference, and complication screening rather than appearance. Order A1c or fasting glucose, lipid panel, CMP/ALT, BP, sleep apnea screen, PCOS evaluation when suggested, and eating-disorder screening before restrictive plans or medications.

First-line treatment: Provide intensive, respectful lifestyle counseling: nutrition pattern with protein/fiber and reduced ultra-processed/sugary drinks, 150-300 minutes/week activity plus resistance training, sleep regularity, reduced sedentary time, family-based changes for children, and motivational interviewing without shaming.

Second-line treatment: When obesity disease is present, consider evidence-based treatment rather than repeated advice alone: semaglutide (Wegovy), tirzepatide (Zepbound), liraglutide (Saxenda), phentermine-topiramate (Qsymia), naltrexone-bupropion (Contrave), or orlistat (Alli/Xenical) based on age, pregnancy potential, contraindications, and coverage; treat HTN, dyslipidemia, prediabetes, OSA, and MASLD directly.

Third-line / advanced care: Refer dietitian, obesity medicine/endocrinology, bariatric surgery, behavioral health, physical therapy, sleep medicine, or social services when severe obesity, complications, eating disorder, disability, medication contraindications, food insecurity, or pregnancy/lactation complexity is present.

Progression and follow-up: Follow weight trajectory, waist, BP, A1c/lipids/liver risk, sleep, mood, physical function, adverse effects, pregnancy avoidance with certain medications, muscle preservation, and long-term recurrence prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Occupational exposure evaluation

Pathophysiology: Occupational exposure evaluation identifies work-related chemical, biologic, physical, ergonomic, radiation, respiratory, skin, noise, heat, violence, and injury hazards early enough to prevent chronic disease and protect co-workers and household contacts.

How Preventive Medicine and Public Health assesses it: Take a job-task history: employer/industry, exact tasks, duration, materials, Safety Data Sheets, ventilation, PPE, respirator fit testing, co-worker illness, symptoms that improve away from work, pregnancy, take-home exposure, OSHA-recordable injuries, and prior monitoring. Ask about solvents, silica/asbestos, lead, pesticides, isocyanates, bloodborne pathogens, latex, noise, heat, and radiation.

Diagnosis: Match testing to hazard: spirometry and chest imaging for respiratory hazards; audiometry for noise; venous blood lead level, CBC, creatinine, and zinc protoporphyrin for lead; carboxyhemoglobin for CO; cholinesterase for organophosphates; hepatitis/HIV testing after needlestick; patch testing for contact dermatitis; and industrial hygiene exposure measurement when clinical testing cannot define risk.

First-line treatment: Remove or reduce exposure using hierarchy of controls: substitution, engineering controls, ventilation, wet methods, machine guarding, administrative controls, PPE, respirator program, vaccination such as hepatitis B, and post-exposure prophylaxis when indicated. Treat the clinical illness while documenting work restrictions clearly.

Second-line treatment: Coordinate with occupational medicine, employer safety staff, workers' compensation, public health, OSHA/NIOSH resources, and union/employee representatives when appropriate. Repeat surveillance testing at hazard-specific intervals and verify that return-to-work does not recreate exposure.

Third-line / advanced care: Urgent referral/emergency care for chemical burns/inhalation injury, carbon monoxide poisoning, heat stroke, acute neurologic toxicity, severe asthma, anaphylaxis, high radiation exposure, or bloodborne pathogen exposure requiring HIV PEP such as tenofovir/emtricitabine (Truvada) plus dolutegravir (Tivicay).

Progression and follow-up: Follow symptom-work timing, objective exposure levels, biologic monitoring, lost workdays, accommodations, PPE fit/adherence, co-worker clusters, reporting requirements, and whether source control was fixed rather than only treating the worker.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Travel medicine prevention

Pathophysiology: Travel medicine prevents destination-specific infection, altitude illness, heat injury, injury/traffic death, thrombosis, animal bites, malaria, travelers' diarrhea, and medication access problems by translating itinerary risk into vaccines, prophylaxis, self-treatment, and contingency planning.

How Preventive Medicine and Public Health assesses it: Assess itinerary by country/region/urban-rural setting, departure date, duration, season, activities, altitude, pregnancy, immune compromise, age, chronic disease, allergies, prior vaccines, medications, sexual exposure risk, animal contact, health-care work, VFR travel, and access to care/insurance abroad.

Diagnosis: Use CDC Yellow Book and destination pages for vaccine and malaria maps. Review routine vaccine status; consider hepatitis A/B, typhoid, yellow fever certificate, Japanese encephalitis, rabies pre-exposure, meningococcal ACWY, polio booster, cholera, influenza/COVID, and measles immunity. No routine lab testing is needed unless risk or disease status requires it.

First-line treatment: Give destination vaccines early and prescribe malaria prophylaxis when indicated: atovaquone-proguanil (Malarone), doxycycline, mefloquine (Lariam), or tafenoquine (Arakoda) after G6PD testing when needed. Counsel insect precautions with DEET/picaridin, permethrin clothing, bed nets, food/water safety, condoms, seatbelts/helmets, sun/heat precautions, and travel medical kit.

Second-line treatment: Provide self-treatment plans: oral rehydration salts; loperamide (Imodium) only when no dysentery/high fever; azithromycin (Zithromax) for severe travelers' diarrhea or dysentery-risk regions; acetazolamide (Diamox) for selected high-altitude prevention; motion sickness therapy such as scopolamine patch; and enough chronic meds in original containers.

Third-line / advanced care: Refer travel medicine/infectious disease for yellow fever contraindication waiver, immunocompromised or pregnant traveler, complex malaria resistance, long-term expatriate travel, humanitarian/health-care work, rabies risk, post-exposure illness, or travel after transplant/biologic therapy.

Progression and follow-up: Follow vaccine series completion, adverse reactions, malaria adherence, fever during or after travel, diarrhea with blood/fever/dehydration, animal bites needing rabies PEP, thrombosis symptoms after long flights, and documentation of country-specific requirements.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Lead exposure

Pathophysiology: Lead toxicity disrupts heme synthesis, mitochondrial and neuronal function, kidney tubules, vascular tone, reproduction, and fetal/child neurodevelopment; adults are commonly exposed through work, firing ranges, renovation, batteries, e-waste, ceramics, hobbies, contaminated supplements, or take-home dust.

How Preventive Medicine and Public Health assesses it: Assess job/hobby sources, home age/renovation, firearms, stained glass, pottery, imported cosmetics/spices/remedies, water/plumbing, pregnancy, children in household, abdominal pain, constipation, neuropathy, cognitive/mood symptoms, anemia, hypertension, CKD, infertility, and co-worker/family symptoms.

Diagnosis: Order venous blood lead level, CBC with indices, peripheral smear when anemia, ferritin/iron status in children/pregnancy, creatinine/eGFR, LFTs when chelation considered, zinc protoporphyrin for chronic exposure context, and environmental/workplace assessment. Capillary tests must be confirmed venously.

First-line treatment: Remove the source: workplace controls/PPE, wet cleaning/HEPA vacuum, no dry sanding, shower/change clothes before home, nutrition with adequate iron/calcium/vitamin C, treat iron deficiency, notify public health when reportable, and test children/pregnant household contacts when take-home exposure is possible.

Second-line treatment: Use BLL-guided follow-up intervals and medical removal from exposure when thresholds are met by OSHA/state/ACOEM guidance. Manage hypertension, kidney disease, abdominal symptoms, neuropathy, and reproductive counseling while exposure is eliminated.

Third-line / advanced care: Consult toxicology/occupational medicine/public health for high or symptomatic BLL, pregnancy, child exposure, encephalopathy, severe abdominal pain, or chelation decisions. Chelators such as succimer (Chemet), calcium disodium EDTA (Calcium Disodium Versenate), or dimercaprol (BAL in Oil) are specialist-directed and not substitutes for source removal.

Progression and follow-up: Follow repeat venous BLL, symptom resolution, CBC/renal function, workplace controls, household contamination, pregnancy/fetal risk, return-to-work criteria, and whether public health remediation prevents re-exposure.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Sexual health prevention

Pathophysiology: Sexual health prevention reduces HIV, syphilis, gonorrhea, chlamydia, hepatitis, HPV-related cancer, unintended pregnancy, and sexual trauma through risk-specific screening, vaccination, barrier methods, PrEP/PEP, contraception, and confidential counseling.

How Preventive Medicine and Public Health assesses it: Ask a nonjudgmental 5 P history: partners, practices, protection, past STIs, pregnancy intentions, plus IPV/sexual assault safety, HIV status, injection drug use, PrEP interest, contraception, allergies, renal/bone disease, pregnancy, and anatomic sites exposed.

Diagnosis: Use HIV Ag/Ab testing with HIV RNA when acute infection is possible, syphilis serology, NAAT for gonorrhea/chlamydia at exposed sites (urine/vaginal/cervical/rectal/pharyngeal), hepatitis B/C testing, pregnancy test, renal function before oral tenofovir PrEP, and baseline STI testing before doxy-PEP or PrEP. Screen cervical cancer/HPV by age and organ status.

First-line treatment: Prevention includes condoms/internal condoms, HPV vaccine Gardasil 9, hepatitis A/B vaccination when indicated, contraception and emergency contraception levonorgestrel (Plan B One-Step), ulipristal (ella), or copper IUD, and HIV PrEP with tenofovir disoproxil fumarate/emtricitabine (Truvada), tenofovir alafenamide/emtricitabine (Descovy, not for receptive vaginal exposure indication), or injectable cabotegravir (Apretude).

Second-line treatment: For selected patients at increased bacterial STI risk, offer doxycycline 200 mg within 72 hours after sex, maximum 200 mg/day, with counseling on photosensitivity/esophagitis and 3-6 month STI follow-up. HIV PEP after high-risk exposure uses a 28-day regimen such as tenofovir/emtricitabine plus dolutegravir (Tivicay) or raltegravir (Isentress), started as soon as possible within 72 hours.

Third-line / advanced care: Refer infectious disease/sexual health clinic for HIV-positive diagnosis, PrEP renal complexity, recurrent STIs, antimicrobial-resistant gonorrhea concern, sexual assault forensic care, pregnancy with STI/HIV exposure, or complex contraception needs.

Progression and follow-up: Follow adherence, renal function for oral PrEP, HIV/STI tests every 3 months or risk-based intervals, pregnancy status, side effects, vaccine completion, partner treatment/expedited partner therapy where legal, and evolving risk without judgment.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Falls prevention program

Pathophysiology: Falls result from interacting gait/balance impairment, sarcopenia, neuropathy, orthostasis, vision loss, vestibular disease, cognitive impairment, unsafe home environment, alcohol, foot problems, and medications such as sedatives, anticholinergics, antihypertensives, opioids, and hypoglycemics.

How Preventive Medicine and Public Health assesses it: Ask about falls in the past year, injury, fear of falling, syncope, dizziness, gait aids, footwear, vision/hearing, neuropathy, Parkinsonism, cognition, urinary urgency, alcohol, osteoporosis/fracture risk, home hazards, and medication list including OTC sleep aids and benzodiazepines.

Diagnosis: Use CDC STEADI-style screening, Timed Up and Go, gait/balance exam, orthostatic vitals, vision exam, foot/footwear assessment, neurologic and cardiac exam when indicated, vitamin D only when deficiency risk, DEXA by osteoporosis criteria, ECG for syncope/arrhythmia clues, and targeted labs for anemia, glucose, B12, TSH, or electrolytes when history suggests.

First-line treatment: First-line prevention is multifactorial: strength and balance exercise such as PT or Tai Chi, home safety modifications, medication deprescribing, correct vision, treat orthostasis/dehydration, appropriate footwear, assistive device fitting, osteoporosis management, and vitamin D replacement when deficient.

Second-line treatment: Address specific causes: vestibular rehab for BPPV, diabetic neuropathy foot care, cataract referral, antihypertensive adjustment, hypoglycemia avoidance, bladder plan that minimizes anticholinergic burden, and alendronate (Fosamax) or other osteoporosis therapy when fracture risk warrants.

Third-line / advanced care: Refer geriatrics, PT/OT, neurology, cardiology, ophthalmology, podiatry, or falls clinic for recurrent injurious falls, unexplained syncope, progressive neurologic signs, unsafe living situation, or inability to implement home modifications.

Progression and follow-up: Track fall frequency, injuries, TUG/gait measures, orthostatic symptoms, medication burden, home hazard completion, fracture risk, confidence/fear of falling, and caregiver support.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Preventive Medicine and Public Health

Health misinformation counseling

Pathophysiology: Health misinformation spreads when fear, identity, distrust, algorithmic amplification, low health literacy, prior harm, and information overload make inaccurate claims feel more usable than evidence; counseling protects safety while preserving the therapeutic relationship.

How Preventive Medicine and Public Health assesses it: Assess the specific claim, source, urgency, decision at stake, patient values, literacy/language needs, prior medical trauma, mistrust, social pressure, and immediate danger such as refusing lifesaving care, using toxic substances, delaying cancer treatment, or avoiding urgent evaluation.

Diagnosis: Verify the claim against primary sources such as CDC, FDA, NIH, USPSTF, specialty society guidelines, DailyMed labels, and local public health advisories. Distinguish uncertainty, evolving guidance, misinformation, disinformation, and reasonable preference-sensitive decisions.

First-line treatment: Use motivational interviewing: ask permission, affirm concerns, elicit what they have heard, share one or two clear facts, explain absolute risk when possible, and offer a trusted source. Avoid shaming, sarcasm, or information dumping; correct the myth and immediately replace it with the safer action.

Second-line treatment: For vaccine, medication, screening, or chronic disease misinformation, use teach-back, printed/plain-language resources, follow-up visits, family/caregiver involvement with consent, and decision aids. Address practical barriers such as cost, transportation, side effects, or prior poor communication that may be driving the false belief.

Third-line / advanced care: Escalate when misinformation creates imminent harm: poison control/toxicology for unsafe remedies, emergency evaluation for delayed red flags, psychiatry for delusional/paranoid intensity with danger, ethics/legal support for capacity or child endangerment, and public health notification for outbreak-related risks.

Progression and follow-up: Follow the behavior change, unresolved concerns, new sources of misinformation, trust, adherence, adverse outcomes, and whether the patient knows exactly when to seek urgent care.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Specialty role

Function, disability, neurorehabilitation, musculoskeletal recovery, spasticity, prosthetics, pain, and return-to-activity.

Physical Medicine and Rehabilitation

Stroke rehabilitation

Pathophysiology: Stroke rehabilitation addresses hemiparesis, aphasia, dysphagia, neglect, cognitive impairment, spasticity, depression, pain, falls, and loss of ADL/IADL independence after ischemic or hemorrhagic brain injury.

How Physical Medicine and Rehabilitation assesses it: Assess premorbid function, NIHSS deficits, motor strength, tone, sensation, balance, vision/neglect, cognition, mood, swallow, bladder/bowel, shoulder pain/subluxation, skin, DVT risk, caregiver support, home barriers, driving/work goals, and rehab tolerance.

Diagnosis: Use functional measures such as AM-PAC, FIM/CARE items, Berg Balance, 6-minute walk, gait speed, Modified Rankin, MoCA, PHQ-9, swallow evaluation, speech-language assessment, OT ADL assessment, and PT gait/balance testing. Imaging is reviewed to understand deficits but therapy prescription is function-driven.

First-line treatment: Early coordinated PT/OT/SLP, mobilization when medically stable, task-specific repetitive practice, dysphagia precautions, shoulder positioning, fall prevention, bowel/bladder program, depression screening, and secondary prevention coordination with neurology/primary care.

Second-line treatment: Use ankle-foot orthosis, cane/walker, constraint-induced movement therapy when criteria fit, functional electrical stimulation, robotic/body-weight-supported gait training selectively, aphasia therapy, cognitive rehab, and spasticity treatment with stretching/splinting plus baclofen (Lioresal), tizanidine (Zanaflex), or botulinum toxin (Botox) for focal tone.

Third-line / advanced care: Inpatient rehab is appropriate when the patient can participate and needs interdisciplinary therapy/medical management. Escalate for aspiration, DVT/PE, severe depression/suicidality, falls, pressure injury, uncontrolled spasticity, or caregiver inability to support discharge.

Progression and follow-up: Follow ADLs, gait speed, falls, swallow/nutrition, aphasia, cognition, mood, shoulder pain, spasticity, community participation, equipment fit, caregiver burden, and plateau versus continued goal-directed progress.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Spinal cord injury rehabilitation

Pathophysiology: Spinal cord injury rehabilitation manages motor/sensory loss, neurogenic bowel/bladder, spasticity, autonomic dysfunction, pressure injury risk, neuropathic pain, respiratory compromise, sexual/fertility issues, and community reintegration based on neurologic level/completeness.

How Physical Medicine and Rehabilitation assesses it: Assess injury level and ASIA/ISNCSCI classification, respiratory function, orthostasis, autonomic dysreflexia risk, skin, bowel/bladder routine, spasticity, pain, DVT risk, contractures, hand function, transfers, wheelchair needs, mood, sexuality, caregiver/home access, and vocational goals.

Diagnosis: Use ISNCSCI exam, functional independence measures, pulmonary function for cervical/high thoracic injury, renal ultrasound/urodynamics when indicated, bladder scan, bowel diary, skin inspection, spasticity scales, pressure mapping, and equipment/home assessment.

First-line treatment: Interdisciplinary SCI rehab includes transfer/mobility training, pressure relief schedule, wheelchair seating, ROM/splinting, respiratory hygiene, DVT prophylaxis coordination, bowel program with senna/bisacodyl suppository/digital stimulation as appropriate, bladder plan with intermittent catheterization when feasible, and education on autonomic dysreflexia.

Second-line treatment: Neuropathic pain may use gabapentin (Neurontin), pregabalin (Lyrica), duloxetine (Cymbalta), or amitriptyline (Elavil). Spasticity may use baclofen (Lioresal), tizanidine (Zanaflex), dantrolene (Dantrium), botulinum toxin, phenol neurolysis, or intrathecal baclofen pump for severe generalized tone.

Third-line / advanced care: Urgent care for autonomic dysreflexia, new neurologic decline, syrinx concern, pressure injury infection, UTI with sepsis, respiratory failure, severe orthostasis, DVT/PE, or unsafe discharge. Specialty SCI clinic coordinates urology, wound, equipment, sexuality, and lifelong surveillance.

Progression and follow-up: Follow neurologic recovery, skin integrity, UTIs/renal function, bowel continence, spasticity, pain, equipment fit, shoulder overuse, bone density/fracture, mood, employment/school, and caregiver sustainability.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Traumatic brain injury rehabilitation

Pathophysiology: TBI rehabilitation addresses cognitive, behavioral, vestibular, visual, sleep, headache, mood, motor, speech/swallow, and participation impairments after mild, moderate, or severe brain injury.

How Physical Medicine and Rehabilitation assesses it: Assess injury severity, PTA duration, seizures, headache, dizziness, vision, sleep, cognition, irritability, depression/PTSD, substance use, balance, cervical pain, school/work demands, driving risk, family safety, and red flags such as worsening headache, repeated vomiting, focal deficit, or declining consciousness.

Diagnosis: Use symptom scales, MoCA or neuropsychological testing, vestibular/ocular motor screening, balance testing, speech/cognitive-communication evaluation, sleep assessment, PHQ-9/GAD-7/PTSD screen, and imaging review. Mild TBI imaging may be normal; function and symptom trajectory guide rehab.

First-line treatment: Early education, relative rest for 24-48 hours then graded return to activity, sleep regularity, headache hygiene, vestibular therapy, cervical PT, school/work accommodations, and avoidance of alcohol/reinjury. Treat pain with acetaminophen (Tylenol) or NSAIDs when safe after bleeding risk is excluded.

Second-line treatment: Persistent symptoms may need amitriptyline (Elavil) or nortriptyline (Pamelor) for headache/sleep, melatonin, trazodone, SSRIs such as sertraline (Zoloft) for mood, stimulant therapy such as methylphenidate (Ritalin) or amantadine (Gocovri/Symmetrel) in selected moderate-severe TBI under specialist care.

Third-line / advanced care: Escalate for seizures, suicidality, aggression unsafe at home, endocrine dysfunction after severe TBI, hydrocephalus, spasticity, dysphagia, inability to return to work/school despite accommodations, or need for inpatient/day neurorehab.

Progression and follow-up: Follow symptom burden, cognition, sleep, headaches, vestibular recovery, mood/safety, return-to-learn/work/play, driving readiness, caregiver strain, and medication sedation or misuse.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Spasticity management

Pathophysiology: Spasticity is velocity-dependent increased tone from upper motor neuron injury after stroke, SCI, MS, cerebral palsy, TBI, or other CNS disease; it can impair hygiene, sleep, gait, transfers, pain, skin, and function but may sometimes support standing/transfers.

How Physical Medicine and Rehabilitation assesses it: Assess distribution, triggers, Modified Ashworth/Tardieu, spasms/clonus, pain, ROM/contracture, skin breakdown, hygiene, gait, orthotic fit, bladder/bowel infection, constipation, pressure injury, medication contributors, functional goals, and whether tone is helpful or harmful.

Diagnosis: Clinical exam distinguishes dynamic spasticity from fixed contracture, dystonia, rigidity, heterotopic ossification, fracture, DVT, or noxious trigger. Use X-ray/ultrasound/labs only when pain, swelling, fever, or loss of ROM suggests another process.

First-line treatment: First-line care is goal-based stretching, positioning, splinting/serial casting when appropriate, trigger treatment, strengthening of antagonists, gait/transfer training, orthotics, and caregiver education.

Second-line treatment: Generalized tone may use baclofen (Lioresal), tizanidine (Zanaflex), dantrolene (Dantrium), diazepam (Valium) selectively, or gabapentin if painful spasms coexist. Focal tone uses botulinum toxin (Botox/Xeomin/Dysport), phenol/alcohol neurolysis, or motor-point blocks paired with therapy.

Third-line / advanced care: Intrathecal baclofen pump, orthopedic tendon lengthening, neurosurgical rhizotomy in selected cases, or inpatient rehab for severe tone causing skin breakdown, hygiene failure, pain crisis, or caregiver collapse. Escalate urgently for sudden worsening from infection, fracture, DVT, or autonomic dysreflexia.

Progression and follow-up: Follow goal attainment, ROM, pain, skin, gait/hand function, sedation/weakness, liver tests with dantrolene, pump withdrawal/overdose risk, injection timing, and whether treatment improves participation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Amputation prosthetic care

Pathophysiology: Amputation rehabilitation manages residual-limb healing, edema shaping, pain, phantom limb pain, contralateral limb protection, prosthetic component selection, gait/upper-limb training, skin safety, and psychosocial adaptation.

How Physical Medicine and Rehabilitation assesses it: Assess amputation level, cause, wound healing, residual-limb shape, contractures, pain/phantom pain, sensation, vascular/diabetes status, contralateral limb, strength/balance, cognition, vision, home/work goals, K-level or functional potential, prosthetic history, and depression/PTSD.

Diagnosis: Use residual-limb exam, skin and volume assessment, gait analysis, AMPPro/AMPnoPRO or functional tests, pain phenotype, vascular/diabetes foot screening, prosthetic socket fit assessment, and imaging only for osteomyelitis, fracture, heterotopic ossification, or painful bony prominence.

First-line treatment: Pre-prosthetic care includes wound care, edema control with shrinker/rigid dressing, knee/hip extension positioning, ROM/strengthening, desensitization, mirror therapy, fall prevention, and temporary prosthesis when ready. Pain may use acetaminophen, NSAIDs if safe, gabapentin (Neurontin), pregabalin (Lyrica), duloxetine (Cymbalta), or topical lidocaine.

Second-line treatment: Prosthetic prescription matches goals: socket design, suspension, liner, foot/knee/hand component, microprocessor knee when indicated, myoelectric or body-powered upper-limb option, and progressive gait/functional training with PT/OT/prosthetist.

Third-line / advanced care: Escalate to amputee clinic, vascular/wound surgery, pain, behavioral health, or revision surgery for nonhealing wound, socket intolerance, recurrent skin breakdown, neuroma, severe phantom pain, contracture, falls, or suspected infection/ischemia.

Progression and follow-up: Follow skin, residual-limb volume, socket fit, pain, falls, gait efficiency, contralateral limb overuse/ulcer risk, component maintenance, weight change, work/community participation, and mental health.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Chronic low back pain rehabilitation

Pathophysiology: Chronic low back pain often reflects mechanical spine changes, deconditioning, fear avoidance, sleep/mood factors, central sensitization, radiculopathy/stenosis in some patients, and social/work contributors rather than imaging severity alone.

How Physical Medicine and Rehabilitation assesses it: Assess pain pattern, neurologic deficits, red flags, function, work demands, yellow flags, sleep, mood, opioid exposure, prior imaging/procedures, activity tolerance, hip/SI contribution, gait, core/hip strength, and goals.

Diagnosis: Use focused neurologic and musculoskeletal exam, Oswestry Disability Index, PROMIS/Pain Catastrophizing or fear-avoidance tools, and MRI only for red flags, progressive deficits, or intervention planning. Imaging degenerative findings must be correlated with symptoms.

First-line treatment: First-line rehab is education, graded activity, exercise therapy, core/hip strengthening, walking/aerobic conditioning, manual therapy as adjunct, CBT-informed pain coping, sleep optimization, weight/tobacco support, and return-to-function goals. Topical diclofenac (Voltaren), acetaminophen, or NSAIDs such as naproxen may be used when safe.

Second-line treatment: Duloxetine (Cymbalta) may help chronic musculoskeletal pain; gabapentin/pregabalin only for clear neuropathic/radicular features with benefit monitoring. Consider epidural steroid injection for imaging-correlated radiculopathy, medial branch blocks/radiofrequency ablation for facet-mediated pain, or multidisciplinary pain rehab.

Third-line / advanced care: Urgent spine referral for cauda equina, progressive motor deficit, infection, malignancy, fracture, or severe refractory radiculopathy. Avoid chronic opioids when possible; taper unsafe regimens with support.

Progression and follow-up: Follow function, walking/sitting tolerance, work participation, sleep, mood, opioid/sedative exposure, procedure response, flare plan, and whether care is reducing disability rather than only pain score.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Osteoarthritis function plan

Pathophysiology: OA function planning treats joint pain, stiffness, weakness, balance impairment, obesity-related load, fear of movement, and environmental barriers that limit walking, stairs, self-care, sleep, and participation.

How Physical Medicine and Rehabilitation assesses it: Assess joint distribution, pain triggers, morning stiffness, swelling/effusion, deformity, gait, falls, strength, ROM, ADLs, work/home demands, BMI, depression/sleep, renal/GI/CV risk for NSAIDs, prior injections, and readiness for joint replacement discussion.

Diagnosis: Use clinical exam plus weight-bearing X-ray when diagnosis/severity affects treatment or surgery referral. Functional tools include WOMAC/KOOS/HOOS, timed up-and-go, gait speed, chair-stand, and falls screen. Labs/aspiration are reserved for inflammatory, crystal, or infectious features.

First-line treatment: First-line plan: land or aquatic exercise, quadriceps/hip strengthening, weight loss when relevant, cane in opposite hand, braces/orthoses, activity pacing, heat/cold, topical diclofenac (Voltaren), acetaminophen (Tylenol) selectively, and oral NSAID such as naproxen/ibuprofen only when safe.

Second-line treatment: Duloxetine (Cymbalta), intra-articular triamcinolone (Kenalog), supervised PT, occupational joint-protection strategies, footwear/insoles, and fall prevention are options. Avoid routine chronic opioids and low-value repeated imaging.

Third-line / advanced care: Orthopedics referral for severe pain/function loss, advanced radiographic disease, deformity, recurrent falls, or joint replacement readiness; urgent evaluation for hot swollen joint, fracture, or rapidly destructive arthritis.

Progression and follow-up: Follow walking distance, stairs, ADLs, falls, sleep, NSAID toxicity, injection frequency, weight, readiness for surgery, and postoperative rehab needs if arthroplasty occurs.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Post-ICU weakness

Pathophysiology: Post-ICU weakness and post-intensive care syndrome result from critical illness polyneuropathy/myopathy, immobility, inflammation, steroid/neuromuscular blocker exposure, sepsis, malnutrition, delirium, sleep disruption, and psychological trauma.

How Physical Medicine and Rehabilitation assesses it: Assess ICU course, ventilation duration, sepsis, steroids/paralytics, strength, sensation, balance, dysphagia, cognition, delirium memories, PTSD/depression/anxiety, nutrition, pressure injuries, respiratory endurance, ADLs, caregiver support, and return-to-work goals.

Diagnosis: Use manual muscle testing or MRC sum score, 6-minute walk, grip strength, gait speed, ADL assessment, MoCA, PHQ-9/GAD-7/PTSD screens, nutrition assessment, swallow evaluation, and EMG/NCS when diagnosis is unclear or recovery is atypical.

First-line treatment: Early progressive mobilization, PT/OT, resistance and aerobic training, energy conservation, nutrition/protein repletion, sleep restoration, delirium education, pulmonary rehab when respiratory limitation persists, and medication simplification.

Second-line treatment: Treat neuropathic pain with gabapentin, pregabalin, or duloxetine only when functionally helpful; manage orthostasis, pressure injury, dysphagia, and mood symptoms. ICU recovery clinic coordinates rehab, pulmonary, cognitive, and behavioral health needs.

Third-line / advanced care: Escalate for severe dysphagia/aspiration, falls, pressure injury, profound weakness without improvement, respiratory failure, suicidality/PTSD crisis, or inability to discharge safely home.

Progression and follow-up: Follow strength, endurance, ADLs, cognition, mood, sleep, nutrition, caregiver strain, readmissions, return to work/driving, and medication adverse effects.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Neuropathic pain rehabilitation

Pathophysiology: Neuropathic pain arises from peripheral nerve, plexus, root, spinal cord, or brain injury causing burning, electric, shooting pain, allodynia, hyperalgesia, numbness, and functional avoidance.

How Physical Medicine and Rehabilitation assesses it: Assess distribution, sensory loss/allodynia, weakness/reflexes, diabetes, chemotherapy, shingles, radiculopathy, entrapment, SCI/stroke/MS, sleep, mood, falls, substance use, work impact, and red flags such as progressive neurologic deficit, cancer, infection, or cauda equina.

Diagnosis: Use focused neuro exam, painDETECT/DN4 selectively, EMG/NCS for entrapment/radiculopathy/polyneuropathy when it changes care, labs for neuropathy causes such as A1c, B12, TSH, SPEP, and MRI for root/spinal cord or malignancy/infection concern.

First-line treatment: Rehab plan includes education, desensitization, graded activity, sleep and mood care, neural mobilization when appropriate, balance/fall prevention, TENS trial, and treatment of cause. Medications include duloxetine (Cymbalta), gabapentin (Neurontin), pregabalin (Lyrica), nortriptyline (Pamelor), topical lidocaine patch (Lidoderm), or capsaicin.

Second-line treatment: If refractory, consider pain psychology, interdisciplinary pain rehab, peripheral nerve block, epidural steroid injection for radiculopathy, spinal cord stimulation for selected failed back surgery/CRPS/neuropathy, or medication rotation with toxicity monitoring.

Third-line / advanced care: Escalate for progressive weakness, myelopathy, bowel/bladder change, CRPS with rapid functional loss, suicidal ideation, opioid dependence, or suspected tumor/infection/compression.

Progression and follow-up: Follow function, sleep, falls, mood, medication sedation/edema/weight gain, misuse risk, sensory injury/ulcers, and whether pain treatment enables activity rather than avoidance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Work injury return plan

Pathophysiology: Work injury return planning reduces disability by matching tissue healing, functional capacity, psychosocial risk, job demands, employer accommodations, and safe activity progression after musculoskeletal or neurologic injury.

How Physical Medicine and Rehabilitation assesses it: Assess injury mechanism, diagnosis, red flags, objective restrictions, essential job tasks, lifting/push/pull/carry, posture, shift length, commute, employer modified duty, workers compensation context, fear avoidance, sleep/mood, medications affecting safety, and patient goals.

Diagnosis: Use functional exam, job-demand analysis, validated disability tools, physical/occupational therapy evaluation, functional capacity evaluation when needed, and imaging/labs only when red flags or management decisions require them.

First-line treatment: First-line plan gives clear temporary restrictions and abilities, graded activity, PT/OT, ergonomic changes, modified duty, home exercise, nonopioid pain plan such as acetaminophen/NSAID/topical diclofenac if safe, and expected reassessment date.

Second-line treatment: If delayed recovery, address yellow flags, workplace conflict, sleep/mood, conditioning, and medication barriers; consider work hardening, occupational medicine, vocational rehab, behavioral pain coping, or specialist evaluation for procedure/surgery only when indicated.

Third-line / advanced care: Escalate for neurologic deficit, unstable injury, unsafe workplace, complex compensation dispute preventing care, opioid/sedative safety issue, or inability to return despite maximal rehab and accommodation.

Progression and follow-up: Follow objective function, work attendance, restrictions, pain interference, medication safety, employer communication, reinjury risk, and transition from temporary restrictions to maximum medical improvement.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Pelvic floor rehabilitation

Pathophysiology: Pelvic floor dysfunction includes weakness, overactivity, poor coordination, nerve injury, childbirth/surgery effects, chronic pelvic pain, urinary/fecal incontinence, constipation, dyspareunia, and prolapse-related symptoms.

How Physical Medicine and Rehabilitation assesses it: Assess urinary urgency/stress leakage, fecal incontinence, constipation, pelvic pain, dyspareunia, childbirth trauma, pelvic surgery/radiation, neurologic disease, medications, fluid/caffeine, red flags such as hematuria, infection, retention, neurologic deficits, or unexplained bleeding, and patient comfort with internal exam.

Diagnosis: Use bladder/bowel diary, postvoid residual when retention possible, urinalysis/culture if infection symptoms, pelvic exam by trained clinician, pelvic floor strength/relaxation assessment, pain mapping, and referral for urodynamics/anorectal manometry/defecography when refractory or surgical planning.

First-line treatment: First-line rehab includes pelvic floor muscle training for stress incontinence, urge suppression/bladder training, bowel habit retraining, diaphragmatic breathing, down-training/relaxation for overactive pelvic floor, biofeedback, manual therapy when appropriate, and home program.

Second-line treatment: Adjuncts include vaginal estrogen for genitourinary syndrome of menopause when appropriate, pessary referral for prolapse/stress leakage, antimuscarinics or beta-3 agonist mirabegron (Myrbetriq) for overactive bladder by clinician, and bowel regimen with polyethylene glycol or fiber strategy.

Third-line / advanced care: Refer urogynecology/urology/colorectal/pelvic pain specialist for retention, recurrent UTIs, hematuria, fistula, severe prolapse, neurologic bowel/bladder, refractory pain, or surgical/injection options such as botulinum toxin, neuromodulation, sling, or prolapse repair.

Progression and follow-up: Follow leakage episodes, pad use, voiding intervals, bowel frequency, pain with intercourse, adherence, adverse medication effects, prolapse symptoms, and quality of life.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Physical Medicine and Rehabilitation

Wheelchair seating

Pathophysiology: Wheelchair seating is a rehab and equipment intervention that prevents pressure injury, improves posture, supports respiration/swallowing/upper-limb access, reduces pain/spasticity, and preserves independence when mobility or trunk control is impaired.

How Physical Medicine and Rehabilitation assesses it: Assess diagnosis, prognosis, transfers, sitting tolerance, skin history, pressure risk, pelvic obliquity/rotation, scoliosis/kyphosis, hip/knee/ankle ROM, spasticity, sensation, cognition, home/vehicle access, caregiver support, propulsion ability, and goals for school/work/community mobility.

Diagnosis: Use functional mobility assessment, mat evaluation, pressure mapping when available, skin inspection, pain scale, spasticity scale, ROM measures, home/environment review, and documentation required for durable medical equipment coverage; imaging is reserved for deformity, pain, fracture, or orthopedic planning.

First-line treatment: Prescribe individualized manual versus power chair, seat width/depth, cushion such as ROHO or Jay, back support, lateral supports, pelvic belt, headrest, tilt-in-space/recline, elevating leg rests, anti-tippers, and pressure-relief schedule with caregiver training.

Second-line treatment: If posture, pain, pressure, or access remains poor, revise cushion/back geometry, add custom molded seating, adjust propulsion setup, treat spasticity with baclofen, tizanidine, or botulinum toxin when indicated, and coordinate OT/PT/vendor home trial.

Third-line / advanced care: Complex rehab technology clinic, wound care, orthopedic/neurosurgical evaluation for severe deformity, power mobility/assistive technology integration, funding appeals, and repeat seating after growth, weight change, surgery, or functional decline.

Progression and follow-up: Follow pressure areas, pain, posture, falls, shoulder overuse, propulsion efficiency, equipment breakdown, caregiver injury, home access, and participation in school/work/community.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Specialty role

Substance use diagnosis and treatment, withdrawal management, harm reduction, medications for addiction treatment, and recovery support.

Addiction Medicine

Opioid use disorder buprenorphine care

Pathophysiology: Opioid use disorder is chronic reward, tolerance, withdrawal, craving, and compulsive-use physiology with high overdose risk, especially with fentanyl exposure, benzodiazepines, alcohol, reduced tolerance after incarceration/detox, and injection complications.

How Addiction Medicine assesses it: Assess DSM-5 criteria, last opioid/fentanyl use, COWS withdrawal score, overdose history, route, prescribed opioids, pain, pregnancy, benzodiazepines/alcohol, psychiatric risk, housing, legal stress, infections, QT risk if methadone considered, and patient goals for treatment intensity.

Diagnosis: Diagnosis is clinical; urine drug testing and PDMP review support care but should not be punitive. Check pregnancy test, HIV, hepatitis B/C, STI testing, LFTs when naltrexone is considered, and evaluate abscess, endocarditis, osteomyelitis, severe withdrawal, or overdose complications when symptoms suggest.

First-line treatment: Offer medication treatment immediately. Buprenorphine-naloxone (Suboxone, Zubsolv, Bunavail) is typical for office-based care; buprenorphine monoproduct (Subutex) is used in pregnancy or selected naloxone-intolerance contexts. Start when moderate withdrawal is present, or use low-dose/microinduction when fentanyl exposure raises precipitated-withdrawal risk. Provide naloxone (Narcan, Kloxxado), fentanyl test strips where legal, safer-use counseling, and bowel regimen if constipated.

Second-line treatment: Methadone through a certified opioid treatment program is often better for very high tolerance, repeated buprenorphine failure, unstable housing needing daily structure, pregnancy preference, or persistent fentanyl use. Extended-release naltrexone (Vivitrol) requires full opioid detoxification and is best for selected highly motivated patients who can tolerate the opioid-free interval.

Third-line / advanced care: Urgent ED/inpatient/addiction referral for overdose, severe dehydration, pregnancy with unstable use, suicidality, endocarditis/sepsis, serious injection infection, polysubstance sedative use, inability to stabilize outpatient, or precipitated withdrawal not manageable in clinic.

Progression and follow-up: Follow retention, cravings, withdrawal, dose adequacy, urine toxicology trends, overdose events, injection harms, HIV/HCV care, constipation, sedation, diversion concerns, pregnancy outcomes, counseling/recovery supports, and patient-centered functional goals rather than abstinence alone.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Alcohol use disorder medications

Pathophysiology: Alcohol use disorder involves dopamine/reward reinforcement, GABA-glutamate adaptation, craving, impaired control, tolerance, withdrawal, and relapse vulnerability; long-term injury includes liver disease, pancreatitis, cardiomyopathy, neuropathy, cancer risk, depression, trauma, and fetal harm.

How Addiction Medicine assesses it: Assess DSM-5 criteria, drinks/day and heavy-drinking days, withdrawal/seizure/DT history, liver disease, renal function, opioid use, pregnancy, suicidality, depression/anxiety/PTSD, pancreatitis, neuropathy, social supports, treatment goals of abstinence versus reduction, and readiness for medication plus counseling.

Diagnosis: Use validated screening such as AUDIT-C, DSM interview, PEth or carbohydrate-deficient transferrin only when useful, CBC/CMP with AST/ALT/bilirubin, INR/albumin when liver disease suspected, magnesium/thiamine status by risk, pregnancy test, hepatitis screening, and CIWA-Ar only for active withdrawal monitoring.

First-line treatment: First-line medications include naltrexone oral (Revia) or extended-release injection (Vivitrol) to reduce heavy drinking/craving when no current opioid use or acute hepatitis/liver failure, and acamprosate (Campral) to support abstinence especially with liver disease or opioid therapy; acamprosate requires renal dosing/avoidance in severe renal impairment. Pair with motivational interviewing, CBT, mutual-help/recovery supports, and thiamine.

Second-line treatment: Disulfiram (Antabuse) is useful only for abstinence goals with reliable supervision and no significant liver/cardiac/psychosis risk; counsel that alcohol in drinks, mouthwash, sauces, and some medicines can trigger reaction. Off-label options in selected patients include topiramate (Topamax) or gabapentin (Neurontin) when benefits outweigh sedation/misuse risks.

Third-line / advanced care: Refer addiction medicine/hepatology/psychiatry for severe AUD, cirrhosis, repeated relapse, polysubstance use, suicidality, pregnancy, cognitive impairment, or consideration of residential/IOP care. Do not start naltrexone if opioids are needed or opioid dependence is present.

Progression and follow-up: Follow drinking days, heavy-drinking days, cravings, LFTs, renal function, mood/suicide risk, medication adherence, injection-site reactions with Vivitrol, pregnancy status, recovery supports, and transition to withdrawal care if abrupt cessation becomes risky.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Alcohol withdrawal risk

Pathophysiology: Alcohol withdrawal occurs when chronic alcohol-enhanced GABA tone and glutamate upregulation are suddenly unopposed, causing autonomic hyperactivity, tremor, anxiety, hallucinosis, seizures, and delirium tremens; withdrawal management alone does not treat AUD.

How Addiction Medicine assesses it: Assess time since last drink, daily intake, prior withdrawal seizures or delirium tremens, CIWA-Ar or other severity scale, age, pregnancy, liver disease, pancreatitis/GI bleed, infection/trauma, electrolyte disturbance, benzodiazepine/barbiturate use, polysubstance use, vitals, hydration, and reliable supervision.

Diagnosis: Clinical diagnosis supported by alcohol history and exclusion of mimics. Check glucose, CMP, magnesium, phosphorus, CBC, LFTs, pregnancy test, ECG when indicated, ethanol level if unclear, and evaluate head injury, sepsis, hepatic encephalopathy, ketoacidosis, or sedative withdrawal when mental status is atypical.

First-line treatment: Give thiamine before glucose when malnourished or Wernicke risk, plus fluids/electrolyte correction. Benzodiazepines are first-line: diazepam (Valium), chlordiazepoxide (Librium), or lorazepam (Ativan) when liver disease/older age/respiratory risk makes shorter metabolism preferable; use symptom-triggered or fixed taper based on setting and monitoring.

Second-line treatment: Phenobarbital can be used by experienced clinicians or protocols for severe/refractory withdrawal or benzodiazepine-sparing strategies. Adjuncts such as gabapentin (Neurontin), carbamazepine (Tegretol), or clonidine (Catapres) may help selected mild cases/symptoms but do not replace benzodiazepines for seizure/DT prevention when risk is high.

Third-line / advanced care: ED/inpatient/ICU care for prior DT/seizure, severe CIWA, hallucinations/confusion, unstable vitals, pregnancy, severe comorbidity, electrolyte derangement, poor oral intake, polysubstance sedative withdrawal, suicidality, or lack of safe monitoring. Treat Wernicke encephalopathy urgently with high-dose parenteral thiamine.

Progression and follow-up: Monitor CIWA/sedation, vitals, seizures, delirium, respiratory depression, electrolytes, nutrition, falls, oversedation, and begin relapse-prevention medication planning before discharge.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Benzodiazepine taper

Pathophysiology: Benzodiazepine physical dependence develops after sustained GABA-A receptor adaptation; abrupt dose reduction can cause rebound anxiety/insomnia, tremor, perceptual disturbance, autonomic symptoms, seizures, delirium, and prolonged withdrawal. Physical dependence is not the same as benzodiazepine use disorder.

How Addiction Medicine assesses it: Assess indication, dose, half-life, duration, prescriber count, early refills, alcohol/opioid use, seizure history, pregnancy, age/falls/cognition, OSA/COPD, PTSD/panic disorder, prior tapers, patient fears, and whether benefits still outweigh harms.

Diagnosis: Review medication history and PDMP; screen for sedative use disorder, depression/suicide risk, alcohol use, OUD, and cognitive/fall risk. Labs are not routine unless comorbidity suggests; urine toxicology may clarify unexpected substances but should not be used punitively.

First-line treatment: Do not stop abruptly. Use a collaborative gradual taper, often reducing total daily dose by about 5-10% at a time with slower reductions near the end; pause or slow for significant withdrawal. Consider converting short-acting alprazolam (Xanax) to longer-acting diazepam (Valium) or clonazepam (Klonopin) only when clinically appropriate. Add CBT-I for insomnia and CBT/SSRI/SNRI options for anxiety disorders.

Second-line treatment: Manage symptoms with non-benzodiazepine strategies: sleep scheduling, melatonin selectively, hydroxyzine (Vistaril) or propranolol (Inderal) for limited symptoms when safe, gabapentin/pregabalin only cautiously because of sedation/misuse risk, and treat underlying PTSD, panic, or depression directly.

Third-line / advanced care: Inpatient or specialty taper is needed for high-dose use, prior seizure/delirium, polysubstance sedatives, pregnancy complexity, suicidality, unstable medical disease, or inability to taper safely outpatient. Avoid flumazenil outside toxicology/emergency indications because it can precipitate seizures.

Progression and follow-up: Follow withdrawal symptoms, sleep, anxiety, cognition, falls, driving risk, alcohol/opioid co-use, dose reductions, patient control/consent, and recurrence of the original condition.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Stimulant use disorder

Pathophysiology: Stimulant use disorder from methamphetamine, cocaine, or prescription stimulants involves dopamine/norepinephrine reward sensitization, craving, binge-crash cycles, sleep deprivation, psychosis, cardiovascular toxicity, hyperthermia, dental/skin harms, and risky sexual/injection exposure.

How Addiction Medicine assesses it: Assess stimulant type/route, binge pattern, sleep, psychosis/paranoia, chest pain, palpitations, neurologic deficits, hyperthermia, weight loss, dental disease, skin picking, HIV/HCV/STI risk, fentanyl contamination risk, ADHD history, depression/suicide risk, and pregnancy.

Diagnosis: DSM-5 diagnosis with urine toxicology as supportive. ECG/troponin for chest pain, CK/renal function for agitation/hyperthermia/rhabdomyolysis, HIV/HCV/STI testing by risk, pregnancy test, dental/skin exam, and psychiatric evaluation for persistent psychosis or suicidality.

First-line treatment: No FDA-approved medication reliably treats stimulant use disorder. First-line evidence-based care is contingency management, CBT/community reinforcement, motivational interviewing, sleep restoration, nutrition, exercise, safer-use counseling, condoms/PrEP when indicated, naloxone and fentanyl test strips due to contamination risk.

Second-line treatment: Treat complications and comorbidities: benzodiazepines such as lorazepam (Ativan) for acute severe agitation; antipsychotic such as olanzapine (Zyprexa) or haloperidol (Haldol) for dangerous psychosis; manage ADHD with careful nonstimulant or monitored stimulant decisions. Some clinicians consider bupropion (Wellbutrin XL) plus extended-release naltrexone (Vivitrol) for methamphetamine use disorder in selected patients based on emerging evidence.

Third-line / advanced care: ED/inpatient care for chest pain/MI, stroke symptoms, hyperthermia, severe agitation, rhabdomyolysis, psychosis with danger, suicidality, pregnancy complications, or severe malnutrition. Refer addiction program offering contingency management when available.

Progression and follow-up: Follow use days, cravings, sleep, weight, psychosis recurrence, mood/suicide risk, infections, sexual health, dental/skin recovery, overdose risk from adulterants, and engagement in contingency management/recovery supports.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Cannabis use disorder

Pathophysiology: Cannabis use disorder reflects cannabinoid receptor adaptation, reward conditioning, withdrawal irritability/sleep disturbance, impaired control, and functional harm; high-potency THC is associated with anxiety, psychosis risk, cyclic vomiting, impaired driving, and cognitive/academic/work effects.

How Addiction Medicine assesses it: Assess product potency/type, daily use, concentrates/vaping/edibles, age at onset, withdrawal, failed cutdowns, school/work impact, driving, pregnancy, psychosis/bipolar history, anxiety/depression, hyperemesis symptoms, tobacco co-use, and reasons for use such as sleep/pain/PTSD.

Diagnosis: DSM-5 diagnosis; urine THC confirms exposure but not impairment or disorder severity. Screen PHQ-9/GAD-7/psychosis/bipolar risk, pregnancy test when relevant, evaluate recurrent vomiting for cannabinoid hyperemesis, and assess lung symptoms in vaping.

First-line treatment: First-line treatment is motivational enhancement therapy, CBT, contingency management, sleep hygiene, exercise, and family-based therapy for adolescents. Counsel on avoiding driving while intoxicated, high-potency concentrates, pregnancy use, and mixing with alcohol/sedatives.

Second-line treatment: No FDA-approved medication treats cannabis use disorder. Treat comorbid anxiety/depression/PTSD with evidence-based therapy and SSRIs/SNRIs when indicated. For cannabinoid hyperemesis, stop cannabis; acute episodes may need IV fluids, ondansetron (Zofran) often limited, haloperidol/droperidol in ED protocols, and topical capsaicin.

Third-line / advanced care: Refer addiction psychiatry or early psychosis program for psychosis, bipolar destabilization, severe adolescent impairment, pregnancy, repeated hyperemesis admissions, or inability to reduce use despite major harms.

Progression and follow-up: Follow use frequency/potency, withdrawal sleep/irritability, mood/psychosis, school/work function, driving safety, pregnancy outcomes, hyperemesis recurrence, and substitution with alcohol/nicotine.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Nicotine dependence

Pathophysiology: Nicotine dependence is nicotinic acetylcholine receptor reinforcement with withdrawal, cue-triggered craving, tolerance, and relapse; combustible tobacco drives cancer, COPD, ASCVD, pregnancy harms, wound complications, and secondhand-smoke exposure.

How Addiction Medicine assesses it: Assess cigarettes/day, time to first cigarette, vaping/smokeless products, prior quit attempts, triggers, pregnancy, psychiatric/substance comorbidity, seizure/eating-disorder risk for bupropion, kidney disease for varenicline dosing, household exposure, and lung cancer screening eligibility.

Diagnosis: Clinical diagnosis; document pack-years and product type. Use CO testing only if helpful. Screen for depression/suicide risk, pregnancy, COPD symptoms/spirometry when indicated, ASCVD risk, and annual low-dose CT eligibility for qualifying smoking history.

First-line treatment: Offer counseling plus medication at every visit: varenicline (Chantix) monotherapy; combination nicotine replacement with patch plus gum/lozenge/inhaler/nasal spray; or bupropion SR (Zyban/Wellbutrin SR) when no seizure/eating-disorder risk. Set quit date or reduction plan and connect to 1-800-QUIT-NOW.

Second-line treatment: If relapse occurs, normalize repeated attempts, extend medication duration, combine NRT with varenicline in selected patients, address alcohol/stress cues, treat depression/anxiety, and use text/app/quitline supports. For pregnancy, behavioral counseling is first-line; medication is individualized.

Third-line / advanced care: Refer tobacco treatment specialist, pulmonology, cardiology, oncology screening, or behavioral health for severe dependence, pregnancy complexity, refractory relapse, COPD/ASCVD complications, or abnormal LDCT.

Progression and follow-up: Follow abstinence/reduction, slips, withdrawal, mood, sleep, weight, BP, medication adverse effects, vaping transition risk, secondhand exposure, and screening completion.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Overdose prevention naloxone

Pathophysiology: Opioid overdose causes mu-opioid respiratory depression, hypoxia, aspiration, pulmonary edema, brain injury, and death; fentanyl and polysubstance use with benzodiazepines/alcohol increase severity and may require repeated naloxone.

How Addiction Medicine assesses it: Assess opioid exposure, fentanyl risk, prior overdose, tolerance loss after detox/jail/hospital, benzodiazepines/alcohol, using alone, route, household members, children, pain prescriptions, OUD treatment access, and willingness to carry naloxone.

Diagnosis: Overdose is recognized by unresponsiveness, slow/absent breathing, cyanosis, pinpoint pupils sometimes absent with polysubstance use, and response to naloxone. In clinic, identify high-risk patients through medication list, PDMP, toxicology when useful, and history.

First-line treatment: Prescribe or dispense naloxone nasal spray (Narcan 4 mg, Kloxxado 8 mg) or injectable naloxone and teach: call 911, give naloxone, rescue breathing/CPR if trained, repeat every 2-3 minutes if no response, and stay until help arrives. Offer buprenorphine or methadone pathway for OUD.

Second-line treatment: Add harm-reduction tools: fentanyl test strips where legal, avoid mixing opioids with alcohol/benzodiazepines, use smaller test dose, avoid using alone, syringe services, HIV/HCV testing, PrEP, and safer storage/disposal of prescribed opioids.

Third-line / advanced care: Emergency care after overdose is needed for recurrent sedation, long-acting opioids, aspiration, trauma, pregnancy, severe hypoxia, polysubstance ingestion, or suicidality. Link directly from ED/hospital to buprenorphine or methadone rather than detox alone.

Progression and follow-up: Follow naloxone possession/refills, overdose events, bystander training, OUD medication uptake, fentanyl exposure, infection prevention, mental health, and household safety.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Medication-assisted treatment retention

Pathophysiology: Retention in medication treatment for OUD/AUD reduces overdose, relapse, infection, hospitalization, incarceration, and mortality; dropout often reflects undertreated withdrawal/craving, stigma, access barriers, psychiatric illness, unstable housing, punitive toxicology responses, and poor fit of medication setting.

How Addiction Medicine assesses it: Assess medication dose adequacy, cravings, withdrawal timing, side effects, transportation, cost, pharmacy access, childcare, work schedule, housing, trauma, depression/anxiety, ongoing fentanyl/alcohol/stimulant use, pain, pregnancy, and patient preferences for visit frequency.

Diagnosis: Use structured follow-up: COWS/craving scales for buprenorphine, drinking-day tracking for AUD, urine toxicology as a clinical tool, PDMP, LFT/renal labs as medication-specific, and screen for depression/suicide, IPV, HIV/HCV/STIs, and social needs.

First-line treatment: Make treatment easy to stay in: adequate buprenorphine or methadone dosing, same-day restarts, longer prescriptions when stable, telehealth when allowed, naloxone, low-barrier follow-up, peer support, contingency management where available, and nonjudgmental response to recurrence.

Second-line treatment: Adjust the plan rather than discharge: increase buprenorphine dose or switch to methadone for persistent fentanyl craving; switch AUD medication among naltrexone, acamprosate, disulfiram, topiramate, or gabapentin based on goals/comorbidity; add behavioral therapy, case management, and treatment for pain/insomnia/psychiatric illness.

Third-line / advanced care: Higher level care such as IOP/residential/inpatient is needed for unsafe withdrawal, repeated overdose, suicidality, severe medical/psychiatric instability, pregnancy with unstable use, or inability to meet basic needs. Keep medications for addiction treatment active during transitions whenever possible.

Progression and follow-up: Follow appointment attendance, medication possession/adherence, cravings, withdrawal, overdose, alcohol heavy-use days, toxicology trends, side effects, quality of life, employment/housing stability, and patient-defined recovery goals.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Harm reduction counseling

Pathophysiology: Harm reduction reduces death and disease without requiring immediate abstinence, addressing overdose, HIV/HCV, bacterial infection, wounds, pregnancy risk, violence, and stigma in people using opioids, stimulants, alcohol, or other substances.

How Addiction Medicine assesses it: Assess substances/routes, overdose history, fentanyl contamination, injection technique, sharing equipment, wounds, sexual risk, housing, violence, pregnancy potential, mental health, readiness for treatment, and what the patient already does to stay safer.

Diagnosis: Screen for HIV, hepatitis C and B, STIs, pregnancy, TB when risk, skin/soft-tissue infection, endocarditis symptoms, alcohol withdrawal risk, and overdose risk. Use toxicology only when it will improve safety or treatment planning.

First-line treatment: Offer naloxone (Narcan/Kloxxado), fentanyl test strips where legal, syringe services, sterile water/cookers/cottons, safer injection/smoking supplies where permitted, wound care, condoms, PrEP, hepatitis A/B vaccination, HIV/HCV treatment linkage, and medication treatment such as buprenorphine/methadone/naltrexone when desired.

Second-line treatment: Counsel practical safety: do not use alone when possible, start with a small test dose, avoid mixing opioids with benzodiazepines/alcohol, rotate injection sites, avoid licking needles, seek care for fever/chest pain/shortness of breath/spreading redness, and create an overdose response plan with trusted people.

Third-line / advanced care: Urgent care for overdose, severe withdrawal, abscess/cellulitis with systemic signs, suspected endocarditis, necrotizing infection, pregnancy complications, sexual assault, suicidality, or unsafe living situation. Engage public health/social work for housing, food, legal, and violence resources.

Progression and follow-up: Follow overdose events, infections, equipment access, HIV/HCV status and treatment, PrEP adherence, wounds, treatment interest, safety planning, and trust; avoid terminating care for ongoing use.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Pregnancy and substance use

Pathophysiology: Substance use in pregnancy can affect placental function, fetal growth, preterm birth, congenital infection risk, neonatal opioid withdrawal syndrome, fetal alcohol spectrum disorders, hypertensive/abruption risk with stimulants, and maternal overdose or withdrawal complications.

How Addiction Medicine assesses it: Use universal nonjudgmental screening at first prenatal visit and during care: substances, dose/route, last use, withdrawal, overdose, prescribed meds, intimate partner violence, housing, nutrition, psychiatric risk, infectious risk, prenatal care access, and patient goals. Consent and legal/reporting implications should be transparent.

Diagnosis: Use validated verbal screening tools first; toxicology testing requires informed consent and should change care. Check pregnancy dating/ultrasound as indicated, HIV/HBV/HCV/syphilis/GC/CT, urine culture, LFTs, CBC, and fetal growth surveillance when risk warrants. Assess alcohol withdrawal and opioid withdrawal urgently.

First-line treatment: For OUD, methadone through OTP or buprenorphine (Subutex or buprenorphine-naloxone when appropriate) is recommended over withdrawal/detox alone. Provide naloxone, prenatal care, infectious disease treatment, tobacco cessation, nutrition, and coordinated obstetric-addiction care. For alcohol, advise abstinence and treat withdrawal medically if present.

Second-line treatment: Treat co-occurring conditions: nicotine replacement may be considered when counseling alone fails; SSRIs for significant depression/anxiety when benefits outweigh risks; hepatitis C linkage postpartum or per evolving guidance; HIV treatment immediately when positive; and social support for housing/IPV. Avoid punitive care that drives patients away.

Third-line / advanced care: Maternal-fetal medicine/addiction specialist referral for polysubstance use, unstable OUD, alcohol/benzodiazepine withdrawal risk, recurrent overdose, severe psychiatric illness, fetal growth restriction, infection, or lack of safe housing. Neonatal team should prepare for neonatal opioid withdrawal syndrome when opioid exposure continues.

Progression and follow-up: Follow prenatal visit retention, medication dose adequacy as pregnancy progresses, overdose risk, fetal growth, infectious labs, mood/suicide risk, delivery pain plan, breastfeeding eligibility, postpartum relapse/overdose risk, contraception, and infant monitoring.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Addiction Medicine

Co-occurring depression and addiction

Pathophysiology: Depression and substance use reinforce each other through reward-circuit dysregulation, sleep disruption, trauma, inflammation/stress biology, withdrawal states, shame, social loss, and medication effects; suicide and overdose risks rise when both are active.

How Addiction Medicine assesses it: Assess timing of mood symptoms relative to use/withdrawal, PHQ-9, anhedonia, sleep, appetite, trauma/PTSD, bipolar symptoms, psychosis, suicide/overdose intent, access to lethal means, pain, medical causes, medications, social isolation, and recovery supports.

Diagnosis: Use DSM interview, PHQ-9/GAD-7, C-SSRS for suicide risk, bipolar screen before antidepressants, toxicology when helpful, TSH/CBC/CMP/B12 when medically suggested, and evaluate intoxication/withdrawal states that can mimic depression. Do not require prolonged abstinence before treating severe depression.

First-line treatment: Integrated treatment is first-line: medication for OUD/AUD/nicotine as indicated, psychotherapy such as CBT/behavioral activation/trauma-informed therapy, sleep regularization, peer support, safety plan, and antidepressant such as sertraline (Zoloft), escitalopram (Lexapro), fluoxetine (Prozac), venlafaxine (Effexor XR), or bupropion (Wellbutrin XL) chosen by substance pattern and contraindications.

Second-line treatment: Address resistant or complex cases by optimizing addiction medication dose, treating insomnia/pain/PTSD, considering mirtazapine (Remeron) for insomnia/weight loss, avoiding bupropion in seizure/eating-disorder or heavy alcohol-withdrawal risk, and coordinating psychiatry/addiction therapy. Contingency management can help stimulant co-use.

Third-line / advanced care: Emergency/inpatient care for active suicidal intent, psychosis, mania, severe withdrawal, repeated overdose, inability to care for self, or unsafe home environment. Consider ECT/TMS/ketamine pathways only with psychiatry and substance-use safety planning.

Progression and follow-up: Follow PHQ-9, substance use days, cravings, overdose/suicide risk, sleep, medication adherence, side effects, mania activation, therapy engagement, social recovery, and relapse warning signs.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

Specialty role

Sleep-disordered breathing, insomnia, circadian disorders, hypersomnia, parasomnias, and sleep-related movement disorders.

Sleep Medicine

Obstructive sleep apnea

Pathophysiology: Obstructive sleep apnea is recurrent pharyngeal airway collapse during sleep causing intermittent hypoxemia, arousals, sympathetic activation, sleep fragmentation, systemic/pulmonary hypertension risk, atrial fibrillation, insulin resistance, and daytime sleepiness.

How Sleep Medicine assesses it: Assess snoring, witnessed apneas, gasping, nonrestorative sleep, Epworth Sleepiness Scale, morning headaches, resistant hypertension, AF/HF/stroke, BMI/neck circumference, craniofacial anatomy, nasal obstruction, alcohol/sedatives/opioids, pregnancy, commercial driving, and drowsy-driving risk.

Diagnosis: Use STOP-Bang or similar screen; home sleep apnea test for uncomplicated high-probability adult OSA; attended polysomnography for significant cardiopulmonary disease, hypoventilation, neuromuscular disease, chronic opioids, suspected central apnea, parasomnia/seizure concern, or negative HSAT with high suspicion. Severity is based on AHI/REI plus oxygen burden and symptoms.

First-line treatment: First-line treatment is CPAP/APAP with mask fitting, heated humidification, pressure comfort settings, adherence coaching, weight management, positional therapy when positional OSA, avoidance of alcohol/sedatives near bedtime, and treatment of nasal obstruction with saline/fluticasone when relevant.

Second-line treatment: Alternatives include custom mandibular advancement oral appliance for mild-moderate OSA or CPAP intolerance, bilevel PAP for pressure intolerance or hypoventilation, GLP-1/GIP weight therapy or bariatric referral when obesity drives disease, and ENT evaluation for anatomic obstruction.

Third-line / advanced care: Refer sleep/ENT for central sleep apnea, obesity hypoventilation, severe nocturnal hypoxemia, PAP failure, commercial driver clearance, hypoglossal nerve stimulation (Inspire) eligibility, maxillomandibular advancement, or complex cardiopulmonary disease.

Progression and follow-up: Follow PAP adherence hours, residual AHI, leak, mask skin injury, sleepiness, BP, AF burden, nocturnal oxygenation, weight, drowsy driving, and cardiovascular/metabolic comorbidities.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

Insomnia disorder

Pathophysiology: Insomnia disorder is persistent difficulty initiating sleep, maintaining sleep, or early awakening despite adequate opportunity, causing daytime impairment; hyperarousal, conditioned wakefulness, irregular schedules, pain, mood disorders, substances, medications, and comorbid sleep disorders contribute.

How Sleep Medicine assesses it: Assess sleep schedule, sleep opportunity, naps, caffeine/alcohol/cannabis/nicotine, screens/light, shift work, pain/nocturia, anxiety/depression/PTSD, restless legs, snoring/apneas, parasomnias, medications such as steroids/stimulants/SSRIs, and hypnotic dependence.

Diagnosis: Diagnosis is clinical with sleep diary and Insomnia Severity Index when useful. PSG is not routine unless OSA, periodic limb movement disorder, parasomnia, seizure, or treatment-refractory diagnostic uncertainty exists. Evaluate comorbid mood, pain, circadian, and medication contributors.

First-line treatment: First-line therapy is CBT-I: stimulus control, sleep restriction/compression, cognitive restructuring, relaxation, and regular wake time. Sleep hygiene alone is insufficient but supports CBT-I. Treat comorbid pain, nocturia, mood, and OSA/restless legs when present.

Second-line treatment: Short-term medications only when benefits outweigh risks: doxepin low dose (Silenor) for sleep maintenance, zolpidem (Ambien) or eszopiclone (Lunesta) selectively, ramelteon (Rozerem) for sleep onset, suvorexant (Belsomra), lemborexant (Dayvigo), or daridorexant (Quviviq). Avoid routine benzodiazepines, diphenhydramine (Benadryl), and antipsychotics for primary insomnia.

Third-line / advanced care: Sleep medicine/behavioral sleep referral for chronic refractory insomnia, hypnotic taper complexity, suspected OSA/parasomnia/RLS, pregnancy, older adult falls/delirium risk, substance use, severe depression/suicidality, or occupational safety concerns.

Progression and follow-up: Follow ISI/sleep diary, daytime function, falls/cognition, medication tolerance/dependence, mood/suicide risk, drowsy driving, and whether sleep effort/anxiety is decreasing.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

Restless legs syndrome

Pathophysiology: Restless legs syndrome is a sensorimotor disorder causing urge to move legs, worse at rest/evening, relieved by movement; mechanisms involve brain iron handling and dopaminergic pathways, with secondary causes including iron deficiency, pregnancy, CKD, neuropathy, and medications.

How Sleep Medicine assesses it: Assess classic four criteria, sleep disruption, periodic limb movements, ferritin/iron intake, pregnancy, kidney disease, neuropathy, caffeine/alcohol, family history, antidepressants, antipsychotics, dopamine-blocking antiemetics, sedating antihistamines, and prior dopamine agonist augmentation.

Diagnosis: Clinical diagnosis; check ferritin and transferrin saturation, CBC when iron deficiency possible, renal function, and neuropathy labs when indicated. PSG is reserved for unclear cases, suspected PLMD/OSA, or refractory symptoms. Differentiate leg cramps, akathisia, neuropathy, venous disease, and positional discomfort.

First-line treatment: Correct contributors: stop exacerbating drugs when possible, reduce caffeine/alcohol, manage sleep deprivation, and replete iron. Oral ferrous sulfate or IV iron is considered when ferritin/TSAT are low by sleep-medicine thresholds and symptoms justify treatment.

Second-line treatment: First-line pharmacologic options increasingly favor alpha-2-delta ligands: gabapentin enacarbil (Horizant), gabapentin (Neurontin), or pregabalin (Lyrica), especially with pain/insomnia. Dopamine agonists pramipexole (Mirapex), ropinirole (Requip), or rotigotine (Neupro) can work but require augmentation/impulse-control counseling.

Third-line / advanced care: Sleep specialist for augmentation, refractory RLS, severe insomnia, opioid consideration for severe refractory disease, pregnancy/CKD complexity, or diagnostic uncertainty. Avoid escalating dopamine agonist indefinitely when symptoms start earlier/spread/worsen.

Progression and follow-up: Follow symptom timing, sleep quality, ferritin/TSAT, augmentation, impulse-control behaviors, sedation/dizziness/edema, pregnancy changes, and medication interactions.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

Narcolepsy

Pathophysiology: Narcolepsy is a central hypersomnolence disorder; type 1 usually involves hypocretin/orexin deficiency with cataplexy, while type 2 lacks cataplexy and requires exclusion of insufficient sleep, OSA, circadian disorder, medication/substance effect, and depression.

How Sleep Medicine assesses it: Assess irresistible daytime sleep attacks, cataplexy, sleep paralysis, hypnagogic hallucinations, automatic behavior, Epworth score, sleep schedule, naps, shift work, medications/substances, depression, OSA symptoms, weight gain, school/work impairment, and driving risk.

Diagnosis: Use sleep diary/actigraphy to confirm adequate sleep, overnight PSG followed by MSLT showing short mean sleep latency and sleep-onset REM periods, urine drug screen when relevant, and CSF hypocretin only for selected unclear cases. Untreated OSA and insufficient sleep can invalidate MSLT.

First-line treatment: Core treatment includes regular sleep schedule, scheduled naps, safety/driving counseling, school/work accommodations, and wake-promoting therapy such as modafinil (Provigil), armodafinil (Nuvigil), solriamfetol (Sunosi), or pitolisant (Wakix), selected by cardiac, psychiatric, pregnancy, and interaction profile.

Second-line treatment: Persistent sleepiness may use methylphenidate (Ritalin/Concerta) or amphetamine salts (Adderall XR) with monitoring. Cataplexy/REM intrusion may use sodium oxybate (Xyrem), low-sodium oxybate (Xywav), pitolisant, venlafaxine (Effexor XR), fluoxetine (Prozac), or atomoxetine (Strattera).

Third-line / advanced care: Sleep specialist for diagnostic uncertainty, children/adolescents, commercial driving, pregnancy planning, oxybate REMS, medication failure, psychiatric/cardiac complexity, or disability accommodation documentation.

Progression and follow-up: Follow Epworth/function, cataplexy frequency, driving/work safety, BP/HR, mood/anxiety, weight, medication misuse/diversion risk, nocturnal sleep quality, and insurance access.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

Shift work sleep disorder

Pathophysiology: Shift work sleep disorder is circadian misalignment from work hours overlapping habitual sleep time, causing insomnia, excessive sleepiness, shortened sleep, impaired performance, metabolic/cardiovascular risk, mood symptoms, and crash/injury risk.

How Sleep Medicine assesses it: Assess shift schedule, rotation direction/speed, sleep duration on work/free days, commute drowsiness, caffeine/alcohol, light exposure, bedroom environment, family obligations, safety-sensitive duties, mood, OSA/RLS symptoms, and medication use.

Diagnosis: Use sleep diary and actigraphy when needed for at least 1-2 weeks across work/free days. Rule out insufficient sleep, OSA, insomnia disorder, depression, narcolepsy, and medication/substance causes. PSG/MSLT only when another sleep disorder is suspected.

First-line treatment: Schedule strategy: anchor sleep period, protected dark/quiet sleep room, naps before/during shift when allowed, bright light during work, sunglasses/light avoidance after night shift, consistent meal/caffeine timing, and employer fatigue-risk mitigation.

Second-line treatment: Timed melatonin can help daytime sleep for some; wake-promoting agents modafinil (Provigil) or armodafinil (Nuvigil) may reduce sleepiness for diagnosed shift work disorder but do not replace sufficient sleep and require safety/interaction review.

Third-line / advanced care: Sleep/occupational medicine referral for safety-sensitive impairment, crashes/near misses, refractory symptoms, comorbid OSA/mood disorder, pregnancy, or need for schedule accommodation under workplace policy.

Progression and follow-up: Follow sleep diary, sleepiness, errors/near misses, commute safety, BP/metabolic health, mood, caffeine/hypnotic use, and whether schedule modification is feasible.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

Delayed sleep-wake phase disorder

Pathophysiology: Delayed sleep-wake phase disorder is a circadian rhythm disorder with sleep onset and wake time delayed relative to required schedule, causing sleep-onset insomnia, morning sleep inertia, daytime impairment, and often normal sleep quality when allowed to follow preferred timing.

How Sleep Medicine assesses it: Assess habitual sleep timing on free days versus work/school days, difficulty waking, light/screen exposure, evening chronotype, ADHD/autism/mood symptoms, caffeine/stimulants, naps, social obligations, family pattern, and whether the schedule has been stable for at least several months.

Diagnosis: Use sleep diary and actigraphy for 1-2 weeks including free days. DLMO is rarely needed clinically. Rule out insomnia disorder, insufficient sleep, depression, substance/medication effects, and OSA/RLS when symptoms suggest.

First-line treatment: Treatment uses fixed wake time, morning bright light shortly after waking, evening dim light/blue-light reduction, consistent meals/activity, and low-dose strategically timed melatonin several hours before desired sleep onset when appropriate.

Second-line treatment: Chronotherapy is rarely used because of relapse and non-24 risk. School/work accommodations, CBT-I elements, and treatment of ADHD/mood disorders may be needed. Avoid hypnotics as primary treatment unless comorbid insomnia persists.

Third-line / advanced care: Sleep specialist for severe school/work failure, non-24 pattern, bipolar disorder risk with light therapy, visual disease limiting light exposure, refractory symptoms, or pediatric/adolescent complexity.

Progression and follow-up: Follow sleep timing, daytime function, attendance, depression/anxiety, light adherence, melatonin timing/dose side effects, relapse during weekends/vacations, and safety with morning driving.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

Parasomnias

Pathophysiology: Parasomnias are undesirable sleep behaviors/events, including NREM sleepwalking, sleep terrors, confusional arousals, REM sleep behavior disorder, nightmare disorder, sleep paralysis, and nocturnal seizures that can mimic parasomnia.

How Sleep Medicine assesses it: Assess event timing in night, dream recall, responsiveness, stereotypy, injury/violence, leaving bed/home, triggers such as sleep deprivation/alcohol/stress, medications, OSA, RLS, neurologic disease, PTSD, family history, and bed-partner observations/video.

Diagnosis: Many NREM parasomnias are clinical. Video PSG with expanded EEG/EMG is indicated for adult onset, violent/injurious events, suspected REM behavior disorder, stereotyped events/seizure concern, or unclear diagnosis. Screen for OSA because arousals can trigger parasomnias.

First-line treatment: Safety first: secure environment, remove weapons/sharp objects, lock windows/doors, pad furniture, treat sleep deprivation, reduce alcohol/sedatives, manage stress, and treat comorbid OSA/RLS. Scheduled awakenings may help predictable NREM events.

Second-line treatment: Medication is reserved for frequent/injurious events: clonazepam (Klonopin) or melatonin for REM behavior disorder; prazosin for PTSD nightmares in selected patients; treat seizures if diagnosed. Avoid unnecessary sedatives that worsen confusion/falls.

Third-line / advanced care: Sleep neurology referral for violent injury, adult-onset RBD, suspected synucleinopathy, seizure concern, refractory events, or forensic/safety implications.

Progression and follow-up: Follow injury risk, bed-partner safety, event frequency/video, medication sedation/falls, OSA control, neurologic symptoms suggesting Parkinson disease/Lewy body disease in RBD, and occupational/driving safety.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

REM sleep behavior disorder

Pathophysiology: REM sleep behavior disorder is dream enactment from loss of normal REM atonia; idiopathic RBD is strongly associated with future alpha-synuclein neurodegenerative disease such as Parkinson disease, dementia with Lewy bodies, or multiple system atrophy.

How Sleep Medicine assesses it: Assess dream enactment, punching/kicking/falling out of bed, injuries, weapons access, antidepressants, alcohol withdrawal, narcolepsy, PTSD/nightmares, OSA pseudo-RBD, cognitive changes, constipation, hyposmia, orthostasis, tremor, gait changes, and bed-partner safety.

Diagnosis: Confirm with video polysomnography showing REM sleep without atonia and excluding mimics such as OSA, NREM parasomnia, nocturnal seizures, and periodic limb movements. Medication-induced RBD-like symptoms need medication review.

First-line treatment: Make sleep environment safe: remove weapons, pad floor/furniture, separate beds temporarily if needed, protect windows, and treat comorbid OSA. Melatonin is often first medication because of tolerability.

Second-line treatment: Clonazepam (Klonopin) can reduce behaviors but requires caution in older adults, OSA, cognitive impairment, falls, and sedative use. Adjust triggering antidepressants only when psychiatric risk allows.

Third-line / advanced care: Refer sleep neurology for confirmed or suspected RBD, injuries, cognitive/motor/autonomic symptoms, diagnostic uncertainty, or counseling about neurodegenerative risk and surveillance.

Progression and follow-up: Follow event frequency/injury, medication adverse effects, OSA control, cognition, parkinsonism, autonomic symptoms, mood, and bed-partner safety.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

CPAP intolerance

Pathophysiology: CPAP intolerance usually reflects mask leak/pressure discomfort, nasal obstruction/dryness, claustrophobia, aerophagia, skin injury, mouth leak, insomnia, pressure-emergent central apnea, poor education, or mismatch between device settings and physiology.

How Sleep Medicine assesses it: Assess download data: usage hours, residual AHI, leak, pressure, central apnea index, mask type/fit, humidification, nasal symptoms, mouth breathing, aerophagia, insomnia/claustrophobia, cleaning burden, skin breakdown, travel/work schedule, and perceived benefit.

Diagnosis: Review PAP download and symptom pattern; check mask fit while pressurized, nasal exam, medication/sedative use, weight change, and whether original diagnosis/titration was correct. Repeat titration PSG if residual events, central apnea, hypoxemia, or pressure intolerance persists despite troubleshooting.

First-line treatment: Interventions include mask refit (nasal pillows/nasal/full-face), heated humidification, ramp/EPR/flex pressure relief, chin strap or mouth leak strategy, nasal saline/fluticasone, desensitization while awake, education, and early follow-up.

Second-line treatment: Switch to bilevel PAP for pressure intolerance/hypoventilation, fixed CPAP or APAP adjustments by download, treat insomnia with CBT-I, manage aerophagia with pressure changes/positioning, and consider oral appliance for mild-moderate OSA if PAP remains unacceptable.

Third-line / advanced care: Sleep specialist/DME escalation for persistent residual AHI, central sleep apnea, severe hypoxemia, skin ulceration, panic/claustrophobia, commercial driver compliance risk, or consideration of hypoglossal nerve stimulation or surgery.

Progression and follow-up: Follow adherence, residual AHI, leak, sleepiness, BP, side effects, equipment replacement, patient confidence, and objective benefit after each change.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

Sleepiness differential diagnosis

Pathophysiology: Excessive daytime sleepiness results from insufficient sleep, OSA, circadian misalignment, sedating medications/substances, depression, narcolepsy, idiopathic hypersomnia, RLS/PLMD, medical illness, neurologic disease, or poor sleep quality.

How Sleep Medicine assesses it: Assess sleep duration/opportunity, schedule variability, Epworth score, snoring/apneas, cataplexy, sleep paralysis/hallucinations, shift work, medications including antihistamines/benzodiazepines/opioids/antiepileptics, alcohol/cannabis, mood, pain, RLS symptoms, and drowsy-driving/work safety.

Diagnosis: Start with sleep diary/actigraphy, medication review, depression screen, CBC/CMP/TSH/ferritin when clinically indicated, HSAT/PSG for suspected OSA, PSG plus MSLT for narcolepsy/idiopathic hypersomnia after adequate sleep and treated OSA, and urine drug screen when relevant.

First-line treatment: Correct sleep deprivation, schedule instability, sedating medications, alcohol/cannabis, and untreated OSA/RLS first. Provide immediate drowsy-driving counseling and workplace safety restrictions when risk is high.

Second-line treatment: If residual sleepiness persists despite adequate treated sleep disorder, consider modafinil/armodafinil, solriamfetol, or pitolisant by diagnosis and contraindications; stimulant therapy requires diagnosis, monitoring, and misuse/cardiac risk assessment.

Third-line / advanced care: Urgent referral for sleep attacks while driving, cataplexy with injury, suspected narcolepsy, severe OSA with hypoxemia, neurologic deficits, or occupational safety-sensitive impairment.

Progression and follow-up: Follow Epworth/function, crash/near-miss events, PAP adherence if applicable, medication effects, sleep duration, mood, substance use, and objective testing validity.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Sleep Medicine

Pediatric sleep apnea

Pathophysiology: Pediatric obstructive sleep apnea is recurrent upper-airway obstruction during sleep from adenotonsillar hypertrophy, obesity, craniofacial anatomy, neuromuscular disease, Down syndrome, allergic rhinitis, or prematurity, causing sleep fragmentation, behavior/learning problems, growth issues, enuresis, and cardiometabolic strain.

How Sleep Medicine assesses it: Assess snoring, witnessed apneas, labored breathing, restless sleep, mouth breathing, daytime behavior/ADHD-like symptoms, school performance, growth, enuresis, tonsil size, nasal obstruction/allergies, obesity, craniofacial syndrome, neuromuscular disease, and surgical risk.

Diagnosis: In-lab polysomnography is preferred for diagnosis and severity, especially before adenotonsillectomy in high-risk children or when exam and symptoms mismatch. HSAT is generally not used for routine pediatric diagnosis. Evaluate comorbid allergic rhinitis and obesity.

First-line treatment: Adenotonsillectomy is first-line for many children with adenotonsillar hypertrophy and OSA. Weight management, nasal saline/intranasal corticosteroid such as fluticasone (Flonase), and montelukast (Singulair) may help selected mild disease/allergic inflammation with neuropsychiatric warning counseling.

Second-line treatment: CPAP/BiPAP is used for persistent OSA after surgery, non-surgical candidates, obesity, craniofacial or neuromuscular disease. Orthodontic/maxillofacial interventions may help selected anatomy.

Third-line / advanced care: Refer pediatric sleep/ENT for severe OSA, oxygen desaturation, hypoventilation, age under 3, Down syndrome, craniofacial/neuromuscular disease, obesity hypoventilation, or residual symptoms after surgery.

Progression and follow-up: Follow behavior/school, growth, enuresis, repeat PSG when high-risk or persistent symptoms, PAP adherence, weight, blood pressure, surgical complications, and caregiver sleep burden.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Specialty role

Workplace injury, exposure, fitness-for-duty, prevention, toxicology, ergonomics, and return-to-work decisions.

Occupational and Environmental Medicine

Needlestick exposure

Pathophysiology: Needlestick or sharps exposure can transmit bloodborne pathogens, especially hepatitis B, hepatitis C, and HIV, depending on source infection status, injury depth, hollow-bore needle, visible blood, device use in vein/artery, and exposed worker immunity.

How Occupational and Environmental Medicine assesses it: Assess time since exposure, device type, depth, blood volume, mucous membrane/nonintact skin exposure, source patient HIV/HBV/HCV status or availability for testing, exposed worker HBV vaccination/anti-HBs status, pregnancy, renal/hepatic disease, interacting medications, and tetanus/wound needs.

Diagnosis: Immediately test source when allowed: HIV Ag/Ab with rapid option, HBsAg, and HCV Ab/RNA per local protocol. Exposed worker baseline HIV Ag/Ab, HBV serology if immune status unknown, HCV Ab/RNA/ALT, pregnancy test when relevant, and creatinine/LFTs before HIV PEP.

First-line treatment: Wash wound with soap/water, report immediately, document exposure, and start HIV PEP as soon as possible ideally within hours when source is HIV-positive or high risk: tenofovir disoproxil fumarate-emtricitabine (Truvada) plus dolutegravir (Tivicay) or raltegravir (Isentress) for 28 days by protocol.

Second-line treatment: HBV management depends on vaccination/anti-HBs and source HBsAg: hepatitis B vaccine booster/series and hepatitis B immune globulin when indicated. No HCV PEP exists; arrange early HCV RNA follow-up to detect acute infection and link to direct-acting antiviral treatment if infected.

Third-line / advanced care: Urgent occupational health/ID for delayed high-risk exposure, pregnancy, renal disease, source with resistant HIV, severe medication intolerance, unknown source with high-risk setting, or seroconversion symptoms. Follow institutional OSHA bloodborne pathogen reporting.

Progression and follow-up: Follow HIV testing schedule, PEP adherence/toxicity, renal/LFTs, HCV RNA/ALT, HBV serology completion, anxiety/trauma, confidentiality, and prevention training for future sharps safety.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Back injury at work

Pathophysiology: Work-related back injury may involve lumbar strain, disc herniation, radiculopathy, fracture, spondylolysis, or flare of chronic pain; disability risk is strongly affected by job demands, fear avoidance, sleep, mood, and workplace accommodation.

How Occupational and Environmental Medicine assesses it: Assess mechanism, load, posture, fall/trauma, neurologic deficits, bowel/bladder symptoms, saddle anesthesia, fever, cancer history, prior injury, job essential functions, lifting/push/pull/carry requirements, shift length, modified duty availability, and medication safety for operating equipment.

Diagnosis: Use focused neurologic and musculoskeletal exam, straight-leg raise when radicular, functional capacity/job-demand comparison, and imaging only for red flags, trauma/fracture risk, progressive deficit, or intervention planning. Document objective restrictions, not just diagnosis.

First-line treatment: First-line care is stay active, heat/ice, early graded return to work, PT/home exercise, ergonomic changes, temporary restrictions, acetaminophen (Tylenol), topical diclofenac (Voltaren), or NSAID such as naproxen (Aleve/Naprosyn) or ibuprofen (Advil/Motrin) when safe.

Second-line treatment: Short course cyclobenzaprine (Flexeril) or methocarbamol (Robaxin) may help acute spasm but can impair safety-sensitive work. Persistent radicular pain may need MRI-guided epidural steroid injection or spine referral if function fails to improve.

Third-line / advanced care: Urgent ED/spine for cauda equina, progressive motor deficit, fracture, infection, malignancy, or severe neurologic compromise. Occupational medicine coordinates restrictions, modified duty, workers compensation documentation, and maximum medical improvement.

Progression and follow-up: Follow pain interference, objective function, neurologic exam, work status, restrictions, medication sedation, psychosocial barriers, reinjury risk, and transition from temporary restrictions to safe full duty.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Repetitive strain injury

Pathophysiology: Repetitive strain injury includes tendinopathy, tenosynovitis, nerve entrapment, epicondylitis, rotator cuff overload, De Quervain tenosynovitis, trigger finger, and nonspecific upper-extremity pain from repetition, force, awkward posture, vibration, and inadequate recovery.

How Occupational and Environmental Medicine assesses it: Assess task cycle, force, grip/pinch, keyboard/mouse/tool use, vibration, overhead work, pace, breaks, duration, symptoms by workday/weekend, numbness/weakness, neck referral, diabetes/thyroid/pregnancy, ergonomic setup, and job modification options.

Diagnosis: Use focused exam by site: Tinel/Phalen for carpal tunnel, Finkelstein for De Quervain, resisted wrist extension for lateral epicondylitis, shoulder impingement/rotator cuff tests, grip/pinch strength, and functional assessment. EMG/NCS for persistent or severe suspected nerve entrapment; ultrasound/MRI only when diagnosis or procedure planning is unclear.

First-line treatment: First-line care is ergonomic redesign, task rotation, microbreaks, reduce force/vibration, neutral wrist/shoulder posture, splint/brace when appropriate, activity modification, PT/OT, tendon loading program, ice/heat, topical diclofenac, acetaminophen, or NSAIDs when safe.

Second-line treatment: Corticosteroid injection such as triamcinolone (Kenalog) may help selected carpal tunnel, trigger finger, De Quervain, or bursitis but repeated injections require caution. Neuropathic symptoms may need night splinting and nerve gliding.

Third-line / advanced care: Refer hand/orthopedics/PM&R for progressive weakness/atrophy, severe carpal tunnel, tendon rupture, persistent function loss despite ergonomic control, or need for surgery. Occupational medicine documents restrictions and prevention plan.

Progression and follow-up: Follow symptom diary, work task tolerance, grip/strength, paresthesias, ergonomic implementation, steroid injection response, recurrence after return to full duty, and disability prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Heat illness

Pathophysiology: Occupational heat illness occurs when metabolic and environmental heat exceed cooling capacity, causing heat cramps, heat syncope, heat exhaustion, rhabdomyolysis, acute kidney injury, or heat stroke with CNS dysfunction and potential death.

How Occupational and Environmental Medicine assesses it: Assess core temperature when possible, mental status, exertion, acclimatization, WBGT/heat index, humidity, clothing/PPE, hydration access, medications such as anticholinergics/diuretics/stimulants, alcohol, obesity, sickle trait, kidney/heart disease, and co-worker cases.

Diagnosis: Heat exhaustion has heavy sweating, weakness, dizziness, nausea, tachycardia without CNS dysfunction. Heat stroke is heat illness with confusion, seizure, coma, ataxia, or other CNS dysfunction. Labs for moderate/severe cases include CMP, CK, urinalysis, CBC, coagulation tests, lactate, and renal function/electrolytes.

First-line treatment: Move to shade/cool area, stop work, remove excess PPE/clothing, active cooling, oral fluids if alert, and monitor. Heat stroke requires immediate EMS and rapid cooling, preferably cold-water immersion or aggressive evaporative/ice cooling; cool first and transport without delaying cooling.

Second-line treatment: Workplace prevention includes acclimatization over 1-2 weeks, water/rest/shade, workload scheduling, buddy system, heat alerts, supervisor training, and PPE/engineering controls. Return to work after significant heat illness needs medical clearance and graduated re-acclimatization.

Third-line / advanced care: ED transfer for altered mental status, syncope with instability, core temp concerning for heat stroke, rhabdomyolysis, AKI, electrolyte derangement, chest pain, persistent vomiting, or symptoms not improving promptly.

Progression and follow-up: Follow CK/creatinine/electrolytes after severe illness, recurrence risk, acclimatization, hydration plan, job modifications, medication contributors, and employer heat illness prevention compliance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Carbon monoxide exposure

Pathophysiology: Carbon monoxide binds hemoglobin and cytochromes with high affinity, causing tissue hypoxia, myocardial injury, neurologic toxicity, and delayed neuropsychiatric syndrome; occupational sources include engines, forklifts, generators, fires, furnaces, and poorly ventilated combustion.

How Occupational and Environmental Medicine assesses it: Assess exposure source, enclosed-space work, co-worker symptoms, duration, headache/dizziness/nausea, confusion, syncope, chest pain, pregnancy, cardiovascular disease, fire/smoke inhalation, pulse oximetry limitations, and whether others at workplace/home are affected.

Diagnosis: Check carboxyhemoglobin by co-oximetry, ABG/VBG when severe, lactate, ECG/troponin for cardiac symptoms/high risk, pregnancy evaluation, and environmental CO measurement. Normal pulse oximetry does not exclude CO poisoning.

First-line treatment: Remove from exposure and give 100% oxygen by nonrebreather or ventilator until symptoms and COHb improve. Notify workplace/emergency services to prevent re-exposure; workers should not return until source is identified and controlled.

Second-line treatment: Hyperbaric oxygen consultation for severe poisoning, loss of consciousness, neurologic deficits, ischemic ECG/troponin elevation, severe acidosis, very high COHb, or pregnancy because fetal risk can be significant even with lower maternal symptoms.

Third-line / advanced care: ED/ICU for altered mental status, syncope, chest pain, pregnancy, fire inhalation/cyanide concern, severe acidosis, or persistent neurologic symptoms. Occupational health coordinates incident investigation and clearance.

Progression and follow-up: Follow delayed cognitive/mood symptoms over days-weeks, cardiac injury, pregnancy/fetal monitoring, workplace remediation, detector installation, and recurrence prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Lead exposure occupational

Pathophysiology: Occupational lead exposure from construction, firing ranges, battery work, smelting, ceramics, renovation, and take-home dust causes neurocognitive, peripheral nerve, renal, hematologic, reproductive, and cardiovascular toxicity by disrupting enzymes and cellular signaling.

How Occupational and Environmental Medicine assesses it: Assess job tasks, airborne/dust exposure, respirator/PPE, hygiene and changing facilities, take-home exposure to family, hobbies, symptoms abdominal pain/constipation/headache/cognition/neuropathy, hypertension, kidney disease, pregnancy/fertility plans, and prior blood lead levels.

Diagnosis: Use venous blood lead level, CBC, creatinine/eGFR, liver tests when treatment considered, zinc protoporphyrin/erythrocyte protoporphyrin for chronic exposure context, and occupational hygiene review. Evaluate children/pregnant household members when take-home exposure is possible.

First-line treatment: Remove or reduce exposure, improve engineering controls/housekeeping, respirator fit program, handwashing, no eating in contaminated areas, shower/change clothes before leaving, and nutritional support with adequate calcium/iron. Manage symptoms and report per state occupational lead surveillance rules when required.

Second-line treatment: Medical removal and return-to-work thresholds depend on OSHA/NIOSH/state guidance and BLL trend. Chelation such as succimer (Chemet), EDTA, or dimercaprol is reserved for significant toxicity and should involve toxicology/occupational medicine, not used to permit continued exposure.

Third-line / advanced care: Urgent toxicology/ED for encephalopathy, severe abdominal pain, very high BLL, pregnancy with significant exposure, severe neuropathy, renal injury, or symptomatic children exposed by take-home dust.

Progression and follow-up: Follow serial venous BLL, renal function, BP, neurocognitive symptoms, anemia, reproductive counseling, workplace controls, respirator compliance, and family exposure prevention.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Chemical dermatitis

Pathophysiology: Occupational chemical dermatitis may be irritant contact dermatitis from wet work, solvents, acids/alkalis, detergents, friction, or occlusion; allergic contact dermatitis from sensitizers such as epoxy, acrylates, rubber accelerators, nickel, chromates, preservatives, fragrances, or plants; or chemical burn.

How Occupational and Environmental Medicine assesses it: Assess exact tasks/products/SDS, wet work/gloves, hand hygiene, timing with shifts/weekends, distribution, coworkers affected, atopy, PPE materials, barrier creams, burns/pain, vesicles, fissures, infection, and potential airborne/contact spread.

Diagnosis: Clinical morphology and exposure pattern guide diagnosis. Patch testing identifies allergic contact dermatitis; KOH/culture rules out fungal infection when suggested; bacterial culture for impetiginization; urgent pH/irrigation assessment for chemical burns. Review SDS for corrosives/sensitizers.

First-line treatment: Remove/substitute offending agent, improve gloves/PPE matched to chemical, reduce wet work, gentle cleansers, emollients, barrier repair, topical corticosteroid such as triamcinolone 0.1% for body or hydrocortisone/desonide for face/folds, and treat secondary infection when present.

Second-line treatment: Severe hand dermatitis may need stronger topical steroid, calcineurin inhibitor tacrolimus (Protopic), phototherapy, systemic therapy by dermatology, or temporary work restriction. Allergic cases need written allergen avoidance and workplace product review.

Third-line / advanced care: Urgent care for chemical burn, eye/genital involvement, extensive blistering, systemic toxicity, cellulitis, occupational cluster, or inability to avoid exposure. Report/coordinate workplace hazard control as appropriate.

Progression and follow-up: Follow skin clearance, fissures/infection, adherence to PPE, allergen avoidance, steroid adverse effects, recurrence on rechallenge, and permanent work modification if sensitization persists.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Fitness for duty evaluation

Pathophysiology: Fitness-for-duty evaluation determines whether a worker can safely perform essential job functions without unreasonable risk to self, coworkers, or the public, while respecting disability law, privacy, and job-specific requirements.

How Occupational and Environmental Medicine assesses it: Assess referral question, essential job functions, safety-sensitive tasks, physical/cognitive/behavioral demands, medications/substances, sleep/fatigue, functional limitations, objective medical data, accommodation options, regulatory standards such as DOT/FAA/OSHA when relevant, and consent/role boundaries.

Diagnosis: Use job description, functional testing, vision/hearing, cognitive or psychiatric evaluation when indicated, medication review, toxicology only when authorized/appropriate, and specialist records. Avoid broad unrelated medical probing; answer ability, restrictions, risk, and accommodation needs.

First-line treatment: Provide clear determination: fit, fit with restrictions/accommodations, temporarily unfit pending treatment/recovery, or unable to determine. State functional limits such as lifting, climbing, driving, respirator use, shift length, or hazardous machinery, not private diagnoses unless authorized/required.

Second-line treatment: Coordinate reasonable accommodations, treatment milestones, re-evaluation date, and communication among worker, employer, HR, treating clinician, and occupational health while maintaining confidentiality.

Third-line / advanced care: Escalate to specialist, independent medical exam, neuropsychology, sleep medicine, psychiatry, or legal/HR review for safety-sensitive impairment, conflicting reports, substance concerns, threats/violence risk, or regulatory certification disputes.

Progression and follow-up: Follow restriction duration, objective improvement, treatment adherence only as relevant to safety, accommodation effectiveness, recurrence risk, and documentation that opinion is job-specific and evidence-based.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Return to work after injury

Pathophysiology: Return-to-work planning after injury prevents prolonged disability by matching tissue healing, functional capacity, symptom control, medication safety, psychosocial risk, and workplace accommodations to essential job demands.

How Occupational and Environmental Medicine assesses it: Assess diagnosis, healing stage, objective functional limits, pain interference, sleep/mood, fear avoidance, medications that impair driving/machinery, job demands, modified duty availability, transportation, supervisor communication, and worker goals.

Diagnosis: Use functional exam, PT/OT reports, job-demand analysis, FCE when needed, and validated function tools. Imaging alone should not determine readiness; restrictions should be based on specific activities and safety risk.

First-line treatment: Write specific temporary restrictions: lifting/carrying, push/pull, overhead work, bending/twisting, sitting/standing/walking tolerance, climbing, driving, shift length, PPE, and medication limitations. Use graded duties and scheduled reassessment.

Second-line treatment: If progress stalls, address barriers with work conditioning, ergonomic evaluation, pain psychology, sleep/mood treatment, supervisor communication, and specialist referral only when objective deficit or procedure target exists.

Third-line / advanced care: Escalate for reinjury, neurologic decline, unsafe job demands, inability to accommodate, complex workers compensation conflict, or need to determine maximum medical improvement/permanent impairment.

Progression and follow-up: Follow function, attendance, restrictions, pain, medication safety, employer accommodation, reinjury, patient confidence, and progression to full duty or permanent restriction.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Occupational hearing loss

Pathophysiology: Occupational hearing loss is usually bilateral high-frequency sensorineural loss from chronic noise exposure, impulse noise, ototoxic solvents/metals, or combined exposures; tinnitus and communication impairment are common.

How Occupational and Environmental Medicine assesses it: Assess noise levels, duration, impulse exposures, hearing protection use/fit, firearm/tool use, military/recreational noise, tinnitus, asymmetry, vertigo, ototoxic medications/chemicals, prior audiograms, and impact on communication/safety.

Diagnosis: Use baseline and annual audiometry with OSHA standard threshold shift logic, otoscopy for conductive causes, audiogram pattern at 3-6 kHz, speech discrimination, tympanometry when indicated, and ENT referral for asymmetric loss, sudden loss, unilateral tinnitus, vertigo, or conductive findings.

First-line treatment: Prevent progression with hearing conservation program: noise measurement, engineering controls, quieter equipment, administrative controls, properly fitted earplugs/earmuffs with training, and worker education. Treat communication needs with hearing aids/assistive devices when indicated.

Second-line treatment: Review standard threshold shift, repeat confirmatory audiogram, refit hearing protection, evaluate ototoxic co-exposures such as solvents or lead, and update work restrictions for safety-critical communication if needed.

Third-line / advanced care: ENT/audiology for sudden sensorineural hearing loss, marked asymmetry, vestibular symptoms, medically treatable ear disease, cochlear implant candidacy, or disputed impairment rating.

Progression and follow-up: Follow serial audiograms, tinnitus distress, hearing protector fit, workplace noise controls, compensation documentation, communication safety, and progression despite controls.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Occupational and Environmental Medicine

Workplace violence trauma

Pathophysiology: Workplace violence trauma can cause acute injuries, concussion, PTSD, depression, anxiety, sleep disturbance, moral injury, chronic pain, and impaired sense of safety, especially in healthcare, public service, retail, education, and isolated work.

How Occupational and Environmental Medicine assesses it: Assess immediate physical injury, strangulation/head injury, sexual assault, threats, weapon exposure, ongoing danger, suicidal/homicidal ideation, dissociation, sleep/nightmares, substance use, prior trauma, social support, reporting needs, and whether returning to the same site is safe.

Diagnosis: Use trauma-informed exam, injury documentation/photos per policy, concussion screen, strangulation evaluation when relevant, PHQ-9/GAD-7/PCL-5 or acute stress screen over time, and occupational incident report. Consider forensic/SANE pathway for sexual assault with consent.

First-line treatment: Ensure safety first: remove from danger, emergency care for injuries, supportive psychological first aid, clear reporting/security plan, temporary work restriction or alternate site, sleep hygiene, and early follow-up. Avoid forcing detailed recounting beyond what care/reporting requires.

Second-line treatment: Persistent symptoms benefit from trauma-focused CBT, EMDR, exposure-based therapy, SSRIs such as sertraline (Zoloft) or paroxetine (Paxil) for PTSD/depression, prazosin for nightmares in selected patients, and graded return-to-work plan.

Third-line / advanced care: Urgent mental health/ED for suicidality, homicidality, psychosis, severe dissociation, unsafe workplace, domestic violence spillover, sexual assault acute care, strangulation symptoms, or inability to function safely.

Progression and follow-up: Follow PTSD/depression symptoms, sleep, substance use, pain/concussion recovery, workplace safety interventions, retaliation fears, accommodation needs, and readiness for return to site or role.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Specialty role

Inherited disease evaluation, family history, testing strategy, counseling, cancer genetics, pharmacogenomics, and newborn screening.

Medical Genetics and Genomics

Hereditary breast ovarian cancer risk

Pathophysiology: Hereditary breast/ovarian/pancreatic/prostate cancer risk is driven by germline pathogenic variants in DNA repair and tumor-suppressor genes such as BRCA1, BRCA2, PALB2, TP53, PTEN, CDH1, STK11, ATM, CHEK2, RAD51C, RAD51D, and BRIP1, with gene-specific penetrance and cancer spectrum.

How Medical Genetics and Genomics assesses it: Assess personal cancer type/age, triple-negative breast cancer, bilateral/multiple primaries, ovarian/fallopian/peritoneal cancer, male breast cancer, pancreatic or metastatic/high-risk prostate cancer, Ashkenazi Jewish ancestry, three-generation pedigree, prior tumor testing, affected relative availability, reproductive goals, and insurance/privacy concerns.

Diagnosis: Test the most informative affected relative first when possible. Use a hereditary cancer multigene panel with deletion/duplication analysis rather than BRCA-only testing when phenotype overlaps. Interpret only pathogenic/likely pathogenic variants as actionable; VUS should not drive prophylactic surgery. Tumor BRCA/HRD results may need germline confirmation.

First-line treatment: For BRCA1/2 or comparable high-risk variants, coordinate high-risk breast screening with annual MRI and mammography by age/gene risk, genetics counseling, cascade testing, and shared decisions about risk-reducing bilateral mastectomy. Risk-reducing salpingo-oophorectomy timing is gene-specific and often earlier for BRCA1 than BRCA2.

Second-line treatment: Use gene-specific management: PALB2 breast MRI/consider mastectomy; TP53 avoid unnecessary radiation and use whole-body/breast MRI surveillance; CDH1 consider prophylactic gastrectomy for hereditary diffuse gastric cancer; pancreatic screening with EUS/MRCP only for selected high-risk genes/family history in expert centers.

Third-line / advanced care: Refer cancer genetics/gynecologic oncology/breast surgery/high-risk clinic for pathogenic variants, very strong family history with negative testing, reproductive planning, prophylactic surgery, or complex VUS discordance. Relatives need targeted familial-variant testing rather than broad unsupervised panels.

Progression and follow-up: Follow surveillance completion, prophylactic surgery decisions, menopause/bone/cardiovascular effects after oophorectomy, psychosocial distress, insurance barriers, variant reclassification, and cascade testing uptake in relatives.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Lynch syndrome risk

Pathophysiology: Lynch syndrome is an autosomal dominant mismatch-repair cancer syndrome caused by pathogenic variants in MLH1, MSH2, MSH6, PMS2, or EPCAM deletion, increasing colorectal, endometrial, ovarian, gastric, small bowel, urinary tract, biliary, brain, sebaceous skin, pancreatic, and prostate cancer risks.

How Medical Genetics and Genomics assesses it: Assess colorectal/endometrial cancer age, multiple Lynch-spectrum tumors, family history across three generations, sebaceous tumors, tumor MMR IHC/MSI results, MLH1 promoter methylation/BRAF testing for sporadic MLH1 loss, prior polyps, hysterectomy/oophorectomy status, ancestry, and reproductive goals.

Diagnosis: Use universal tumor screening for colorectal/endometrial cancers with MMR IHC or MSI; abnormal tumor screen guides germline testing. Germline multigene panel should include MLH1, MSH2, MSH6, PMS2, EPCAM and other colorectal cancer genes when phenotype overlaps. VUS is not diagnostic; somatic tumor testing can clarify double-somatic MMR loss.

First-line treatment: Confirmed Lynch syndrome generally needs colonoscopy every 1-2 years starting by gene/family-history age, often age 20-25 for MLH1/MSH2 and later for some MSH6/PMS2 contexts. Remove polyps promptly, address aspirin chemoprevention through shared decision, and educate about abnormal uterine bleeding.

Second-line treatment: After childbearing, discuss risk-reducing hysterectomy and bilateral salpingo-oophorectomy, especially for MLH1/MSH2/MSH6. Consider upper endoscopy for gastric risk/family history/Asian ancestry, urinalysis for urothelial cancer in selected families, dermatologic exam for Muir-Torre features, and pancreatic screening only in high-risk family contexts.

Third-line / advanced care: Refer genetics/GI high-risk clinic/gynecologic oncology for confirmed pathogenic variants, abnormal tumor screens, early CRC/endometrial cancer, or cascade testing. Urgent diagnostic workup is needed for rectal bleeding, iron deficiency, weight loss, or postmenopausal bleeding rather than routine surveillance scheduling.

Progression and follow-up: Follow colonoscopy quality/interval, pathology, gynecologic risk-reduction decisions, aspirin tolerance, cascade testing, variant reclassification, and cancer-specific survivorship if a tumor develops.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Familial hypercholesterolemia

Pathophysiology: Familial hypercholesterolemia causes lifelong high LDL-C from impaired LDL receptor pathway function, most often LDLR, APOB, PCSK9, or LDLRAP1 variants, leading to premature coronary disease, aortic valve/supravalvular disease in severe biallelic forms, tendon xanthomas, and corneal arcus.

How Medical Genetics and Genomics assesses it: Assess untreated LDL-C, age, premature ASCVD, tendon xanthomas, corneal arcus before age 45, family history of high cholesterol/early MI, secondary causes such as hypothyroidism/nephrotic syndrome/cholestasis, pregnancy potential, childhood lipid history, and relatives needing cascade screening.

Diagnosis: Use LDL-C pattern plus Dutch Lipid Clinic/Simon Broome-style criteria; genetic testing panel includes LDLR sequencing/deletion-duplication, APOB, PCSK9, LDLRAP1, and sometimes other lipid genes. Negative genetic testing does not exclude clinical FH. Screen first-degree relatives with lipid panel and targeted variant testing if familial variant is known.

First-line treatment: Treat aggressively: high-intensity statin such as atorvastatin (Lipitor) or rosuvastatin (Crestor), heart-healthy diet, exercise, no smoking, BP/diabetes control, and early pediatric lipid specialist involvement; statins may start in childhood for heterozygous FH.

Second-line treatment: If LDL-C remains high, add ezetimibe (Zetia), PCSK9 inhibitors alirocumab (Praluent) or evolocumab (Repatha), inclisiran (Leqvio), bempedoic acid (Nexletol), bile-acid sequestrants such as colesevelam (Welchol), or LDL apheresis. Homozygous FH may require evinacumab (Evkeeza), lomitapide (Juxtapid), apheresis, and specialist care.

Third-line / advanced care: Refer lipid/genetics/cardiology for LDL-C 190 mg/dL with family history, suspected homozygous FH, childhood FH, statin intolerance, premature ASCVD, pregnancy planning, or need for PCSK9/apheresis. Avoid teratogenic/insufficiently studied lipid drugs during pregnancy unless specialist-directed.

Progression and follow-up: Follow LDL-C response, adherence, muscle/liver adverse effects, ASCVD symptoms, aortic valve disease in severe FH, family cascade testing, pregnancy interruptions, and access barriers to advanced lipid therapy.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Hypertrophic cardiomyopathy genetic risk

Pathophysiology: Hypertrophic cardiomyopathy is often autosomal dominant sarcomere disease involving genes such as MYH7, MYBPC3, TNNT2, TNNI3, TPM1, ACTC1, MYL2, and MYL3, but phenocopies include Fabry disease, Danon disease, amyloidosis, mitochondrial disease, and RASopathies.

How Medical Genetics and Genomics assesses it: Assess LV wall thickness, obstruction symptoms, syncope, palpitations, family sudden death, exercise history, murmur, hypertension/athlete heart differential, extracardiac clues such as neuropathy/renal disease, pedigree, prior echo/ECG, and relatives at risk.

Diagnosis: Cardiology diagnosis uses echocardiography, ECG, ambulatory rhythm monitoring, cardiac MRI with late gadolinium enhancement, exercise testing when appropriate, and genetic testing with an HCM/cardiomyopathy panel after counseling. A pathogenic familial variant enables cascade testing; a negative panel does not exclude HCM.

First-line treatment: Manage with HCM cardiology: beta-blocker such as metoprolol (Toprol XL) or nadolol (Corgard), nondihydropyridine calcium-channel blocker verapamil (Calan) or diltiazem (Cardizem) when appropriate, avoid dehydration/excess vasodilators in obstruction, and shared exercise recommendations.

Second-line treatment: Obstructive symptomatic HCM may require disopyramide (Norpace), myosin inhibitor mavacamten (Camzyos) in eligible monitored patients, septal myectomy or alcohol septal ablation at experienced centers. Relatives with familial variant need periodic ECG/echo by age/risk.

Third-line / advanced care: ICD evaluation for sudden death risk markers such as prior arrest, sustained VT, unexplained syncope, massive LVH, apical aneurysm, low EF, extensive LGE, or family sudden death. Refer HCM center for complex obstruction, pregnancy, athletes, phenocopy suspicion, or uncertain variant interpretation.

Progression and follow-up: Follow symptoms, LVOT gradient, arrhythmias/AF anticoagulation, SCD risk, medication adverse effects, family screening, variant reclassification, and transition of pediatric relatives into adult surveillance.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Developmental delay genetic evaluation

Pathophysiology: Global developmental delay, intellectual disability, autism with syndromic features, seizures, congenital anomalies, or dysmorphism can reflect chromosomal copy-number changes, single-gene disorders, metabolic disease, teratogens, perinatal injury, or multifactorial neurodevelopmental conditions.

How Medical Genetics and Genomics assesses it: Assess prenatal/perinatal history, newborn screen, growth/head circumference, regression, seizures, tone, feeding, vision/hearing, congenital anomalies, dysmorphology, skin findings, family history/consanguinity, exposures, and developmental domains affected.

Diagnosis: First-tier testing often includes chromosomal microarray and Fragile X testing when indicated; exome or genome sequencing is increasingly recommended early for congenital anomalies/developmental delay/intellectual disability. Add targeted tests for Rett/MECP2, PTEN macrocephaly autism, metabolic labs, brain MRI, EEG, hearing/vision, or mitochondrial studies when phenotype suggests.

First-line treatment: Start early intervention, speech/OT/PT, audiology/vision correction, seizure treatment, nutrition/feeding support, sleep/behavioral care, and family support while testing proceeds; do not wait for a genetic diagnosis to provide services.

Second-line treatment: If testing is negative, consider trio exome/genome, reanalysis in 1-2 years, methylation/episignature testing, repeat expansion testing, or specialist phenotyping. Treat actionable diagnoses specifically, such as biotin (vitamin B7) for biotinidase deficiency or dietary therapy for metabolic disorders.

Third-line / advanced care: Urgent genetics/metabolic/neurology referral for developmental regression, episodic decompensation, seizures, organomegaly, metabolic acidosis/hyperammonemia, hypotonia with respiratory failure, or suspected treatable inborn error.

Progression and follow-up: Follow developmental gains, seizures, feeding/growth, school supports, recurrence risk, parental testing, variant reclassification, reanalysis, and transition planning.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Newborn screen abnormality

Pathophysiology: Newborn screening detects presymptomatic metabolic, endocrine, hemoglobin, immune, cardiac, and genetic conditions where rapid treatment prevents death or disability; abnormal screens are not diagnoses and some are time-critical.

How Medical Genetics and Genomics assesses it: Assess exact analyte/condition, infant age, gestational age, birth weight, feeding, vomiting, lethargy, seizures, jaundice, hypoglycemia, illness, transfusion/TPN, family history, and whether the state lab marked the result time-critical.

Diagnosis: Use ACMG ACT sheet/algorithm for the specific marker. Confirmatory testing may include plasma amino acids, acylcarnitine profile, urine organic acids, ammonia, glucose, ketones, lactate, TSH/free T4, 17-OHP, hemoglobin electrophoresis, sweat chloride/CFTR testing, SCID flow cytometry, or enzyme/molecular testing depending on screen.

First-line treatment: For time-critical metabolic screens, contact metabolic genetics immediately; stop fasting, provide frequent feeds or IV dextrose, avoid catabolism, and send confirmatory labs before special formula when feasible. For endocrine screens, start levothyroxine (Synthroid) for congenital hypothyroidism or hydrocortisone/fludrocortisone for CAH when confirmed/suspected severe.

Second-line treatment: Condition-specific therapy may include phenylalanine-restricted diet/sapropterin (Kuvan) for PKU, carnitine (Carnitor) for fatty-acid oxidation disorders when indicated, vitamin B12 or betaine (Cystadane) for selected methylation disorders, penicillin prophylaxis for sickle cell disease, or CF center care with pancreatic enzymes.

Third-line / advanced care: Emergency evaluation for poor feeding, vomiting, lethargy, seizures, hypoglycemia, hyperammonemia, dehydration, shock, or ambiguous genitalia/salt-wasting concern. Never reassure solely because the baby looks well if the ACT sheet flags time-critical disease.

Progression and follow-up: Follow confirmatory result, false-positive explanation, treatment start time, growth/development, emergency sick-day plan, parental carrier testing, recurrence risk, and state newborn-screen closure documentation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Pharmacogenomic prescribing alert

Pathophysiology: Pharmacogenomic alerts predict altered drug activation, clearance, or immune hypersensitivity from inherited variants, reducing preventable nonresponse or toxicity when the gene-drug pair is actionable and the phenotype is integrated with clinical context.

How Medical Genetics and Genomics assesses it: Assess the exact drug, indication, urgency, genotype/phenotype source, ancestry limitations, liver/kidney function, interacting drugs, prior response, allergies, transplant/cancer context, and whether the result is germline, somatic, or direct-to-consumer and clinically confirmed.

Diagnosis: Use CPIC/FDA label/DailyMed guidance for actionable pairs: CYP2C19-clopidogrel (Plavix), CYP2C19/CYP2D6-SSRIs/TCAs, CYP2D6-codeine/tramadol, CYP2C9/VKORC1/CYP4F2-warfarin (Coumadin/Jantoven), TPMT/NUDT15-thiopurines azathioprine/mercaptopurine, HLA-B*57:01-abacavir (Ziagen), HLA-B*15:02-carbamazepine (Tegretol) in at-risk ancestry, DPYD-fluoropyrimidines, and UGT1A1-irinotecan.

First-line treatment: Act only on high-confidence actionable results: avoid abacavir with HLA-B*57:01; use alternative P2Y12 inhibitor such as prasugrel (Effient) or ticagrelor (Brilinta) for CYP2C19 poor/intermediate metabolizer after PCI when appropriate; reduce/avoid thiopurines with TPMT/NUDT15 poor metabolism; use genotype-guided warfarin only as part of clinical dosing.

Second-line treatment: If result is DTC or unclear, confirm in a CLIA-certified lab before major changes. Document phenotype in the EHR, add decision support, and consider non-genetic causes of toxicity/nonresponse such as adherence, interactions, renal/liver disease, age, and disease severity.

Third-line / advanced care: Pharmacogenomics/pharmacy/genetics consult for multiple alerts, chemotherapy genes, transplant/immunosuppression, rare alleles, conflicting phenotypes, urgent antiplatelet decisions, or when changing therapy could create high clinical risk.

Progression and follow-up: Follow medication outcome, adverse effects, therapeutic drug monitoring when available, updated allele interpretation, EHR portability, family relevance only when appropriate, and avoid overpromising results for non-actionable genes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Carrier screening counseling

Pathophysiology: Carrier screening identifies unaffected people with one pathogenic variant for autosomal recessive or X-linked disease, clarifying reproductive risk for cystic fibrosis, spinal muscular atrophy, hemoglobinopathies, Fragile X, Tay-Sachs, and expanded-panel conditions.

How Medical Genetics and Genomics assesses it: Assess pregnancy status, gestational age, ancestry without stereotyping, family history, consanguinity, partner availability, prior carrier results, IVF plans, donor gametes, values around prenatal diagnosis, and desire for targeted versus expanded screening.

Diagnosis: Offer CFTR and SMN1 carrier screening broadly in preconception/prenatal care; CBC with indices and hemoglobin electrophoresis or molecular testing for hemoglobinopathy risk; Fragile X premutation testing for relevant family/ovarian insufficiency history; and expanded carrier panel if chosen. If one partner is a carrier, test the reproductive partner for the same condition.

First-line treatment: Pretest counseling covers residual risk after negative screening, variable severity, incidental findings, and that carrier status usually does not mean disease. Positive couple results need genetics counseling about 25% autosomal recessive risk or X-linked recurrence, prenatal diagnostic testing, IVF with PGT-M, donor gametes, adoption, or preparation.

Second-line treatment: Do not use newborn screening as a substitute for parental carrier screening. For SMA, explain silent 2+0 carriers and residual risk; for CFTR, explain variants such as 5T/TG only in context; for hemoglobinopathy, distinguish sickle trait, beta-thalassemia trait, and alpha-thalassemia deletion risk.

Third-line / advanced care: Refer reproductive genetics/MFM for both partners carriers, consanguinity, family history with unavailable variant, abnormal fetal ultrasound, positive NIPT requiring diagnostic confirmation, or late pregnancy timing pressure.

Progression and follow-up: Follow partner testing completion, residual-risk documentation, diagnostic testing decisions, fetal/newborn plan, cascade family information, and patient preferences without coercion.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Connective tissue disorder suspicion

Pathophysiology: Heritable connective tissue disorders affect collagen, fibrillin, TGF-beta signaling, or extracellular matrix integrity, including Marfan syndrome, Loeys-Dietz syndrome, vascular/classical/hypermobile Ehlers-Danlos, osteogenesis imperfecta, and related aortopathy syndromes.

How Medical Genetics and Genomics assesses it: Assess aortic aneurysm/dissection, lens dislocation, tall habitus, pectus/scoliosis, hypermobility, skin hyperextensibility/atrophic scars, easy bruising, arterial/organ rupture, pneumothorax, craniofacial/bifid uvula, family sudden death, pregnancy plans, and Beighton score with limitations.

Diagnosis: Use phenotype-directed exam plus echocardiogram/aortic imaging, ophthalmology slit-lamp for ectopia lentis, skeletal imaging when needed, and gene panel including FBN1, TGFBR1/2, SMAD2/3, TGFB2/3, COL3A1, COL5A1/2, COL1A1/2 as phenotype suggests. Hypermobile EDS remains clinical because no single diagnostic gene is established.

First-line treatment: For Marfan/aortopathy, use beta-blocker such as atenolol (Tenormin) or angiotensin receptor blocker losartan (Cozaar) when indicated, activity counseling, BP control, serial echo/CTA/MRA, and family cascade testing if pathogenic variant identified. Treat pain/instability with PT focused on joint protection.

Second-line treatment: Gene-specific management matters: vascular EDS needs arterial surveillance and avoidance of high-risk invasive procedures when possible; Loeys-Dietz may dissect at smaller diameters; Marfan has defined aortic-root surgery thresholds; osteogenesis imperfecta needs fracture/bone care.

Third-line / advanced care: Urgent ED/genetics/cardiothoracic/vascular referral for chest/back/abdominal pain suggesting dissection/rupture, rapidly enlarging aneurysm, pregnancy with aortopathy, arterial rupture, organ rupture, or pneumothorax.

Progression and follow-up: Follow aortic dimensions/growth rate, ocular findings, joint injury, pain/function, pregnancy planning, surgical thresholds, variant reclassification, and relatives needing imaging/genetic testing.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Mitochondrial disease suspicion

Pathophysiology: Mitochondrial disorders impair oxidative phosphorylation from mtDNA or nuclear gene variants, causing multisystem energy failure in brain, muscle, heart, liver, endocrine organs, hearing/vision, GI motility, and kidneys with maternal, autosomal recessive/dominant, or de novo inheritance.

How Medical Genetics and Genomics assesses it: Assess exercise intolerance, episodic decompensation, developmental regression, seizures, stroke-like episodes, migraine, ptosis/ophthalmoplegia, hearing loss, cardiomyopathy/conduction disease, diabetes, liver failure, lactic acidosis, maternal family history, medication triggers, and infection/fasting sensitivity.

Diagnosis: Testing may include lactate/pyruvate interpreted cautiously, CK, CMP, glucose, ammonia, acylcarnitines, urine organic acids, ECG/echo, brain MRI/MRS, ophthalmology/audiology, and combined mtDNA sequencing/deletion plus nuclear mitochondrial gene panel or exome/genome. Muscle biopsy/respiratory-chain enzymology is reserved for selected unresolved cases.

First-line treatment: Avoid catabolism with sick-day plan, prompt IV dextrose during illness when appropriate, hydration, fever control, and avoidance of mitochondrial-toxic drugs when possible, such as valproate in POLG-related disease. Treat seizures, cardiomyopathy, diabetes, hearing/vision, and nutrition issues directly.

Second-line treatment: Supplements such as coenzyme Q10, riboflavin, L-carnitine, creatine, or arginine/citrulline for MELAS-like stroke episodes may be used by specialists with realistic expectations. Genetic counseling must address heteroplasmy, tissue differences, maternal inheritance, nuclear inheritance, and reproductive options.

Third-line / advanced care: Urgent metabolic/genetics/neurology care for regression, status epilepticus, stroke-like episode, liver failure, severe lactic acidosis, rhabdomyolysis, cardiomyopathy/arrhythmia, or recurrent unexplained ICU-level illness.

Progression and follow-up: Follow organ surveillance, growth/nutrition, developmental function, hearing/vision, cardiac rhythm/echo, endocrine disease, medication avoidance list, emergency letter, and variant reinterpretation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Chromosomal microarray result

Pathophysiology: Chromosomal microarray detects pathogenic copy-number variants causing developmental delay, congenital anomalies, autism with syndromic features, miscarriage/stillbirth findings, and dysmorphism, but also finds benign CNVs, susceptibility loci, regions of homozygosity, and variants of uncertain significance.

How Medical Genetics and Genomics assesses it: Assess indication, phenotype, family history/consanguinity, prenatal ultrasound findings, developmental profile, prior karyotype/FISH/exome, and whether the result is deletion, duplication, ROH, mosaicism, or VUS.

Diagnosis: Interpret CNV by size, gene content, known syndrome region, inheritance, ClinGen/ClinVar evidence, phenotype match, penetrance, and parental testing. Microarray does not detect balanced translocations, most single-nucleotide variants, repeat expansions, low-level mosaicism, or methylation disorders.

First-line treatment: For pathogenic CNV, provide syndrome-specific management: organ screening, developmental therapies, neurology/cardiology/renal/ophthalmology/audiology as indicated, and genetics counseling. Parental microarray/karyotype clarifies de novo versus inherited CNV and recurrence risk.

Second-line treatment: For VUS, avoid irreversible management based only on the result; perform parental studies, phenotype reassessment, and periodic reanalysis. ROH may suggest consanguinity/uniparental disomy and can guide recessive-disease testing.

Third-line / advanced care: Refer genetics for pathogenic/likely pathogenic CNV, VUS with phenotype match, prenatal CNV, suspected balanced rearrangement needing karyotype, or complex results with unexpected parentage/consanguinity implications.

Progression and follow-up: Follow clinical surveillance tied to the syndrome, developmental progress, recurrence-risk counseling, parental results, reclassification, and transition to exome/genome if microarray is nondiagnostic.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Medical Genetics and Genomics

Genetic test counseling

Pathophysiology: Genetic test counseling turns a possible inherited diagnosis into an informed decision by clarifying clinical utility, test limits, inheritance, incidental findings, privacy, family implications, and the difference between diagnostic, predictive, carrier, pharmacogenomic, somatic, and direct-to-consumer testing.

How Medical Genetics and Genomics assesses it: Assess the clinical question, affected status, best person to test, family history, prior results, urgency, insurance/GINA limits, life/disability/long-term-care insurance concerns, reproductive plans, patient values, ancestry, and whether the result will change care.

Diagnosis: Choose the narrowest test that answers the question: targeted familial variant, single gene, deletion/duplication, repeat expansion, methylation, chromosomal microarray, karyotype, multigene panel, exome/genome, mtDNA testing, or tumor-germline paired testing. Confirm DTC or research findings in a clinical CLIA lab before care changes.

First-line treatment: Pretest counseling covers possible pathogenic/likely pathogenic, negative, VUS, incidental/secondary findings, nonpaternity/consanguinity, residual risk, and who can access results. Obtain consent and plan how results will be shared with relatives.

Second-line treatment: Posttest counseling links result to action: surveillance, medication choice, surgery, reproductive options, cascade testing, or no change if VUS/negative without explanation. Document the exact variant transcript/nomenclature and lab classification.

Third-line / advanced care: Refer genetics for complex phenotypes, minors being tested for adult-onset conditions, predictive testing for Huntington-like disorders, unexpected results, VUS driving anxiety, consanguinity, prenatal decisions, or variants with major family implications.

Progression and follow-up: Follow variant reclassification, family cascade testing, changes in guidelines, insurance/access issues, psychosocial impact, and whether the result actually changed the medical plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oral Medicine and Dentistry Interface

Specialty role

Oral, dental, jaw, mucosal, salivary, infection, cancer-screening, and medication-related oral conditions.

Oral Medicine and Dentistry Interface

Dental abscess medical triage

Pathophysiology: Odontogenic abscess usually begins with pulpal necrosis, apical periodontitis, periodontal infection, or pericoronitis; spread can remain localized or track into canine, submandibular, masticator, parapharyngeal, orbital, or mediastinal spaces with airway or sepsis risk.

How Oral Medicine and Dentistry Interface assesses it: Assess tooth pain, swelling location, fever/malaise, trismus, dysphagia, drooling, voice change, floor-of-mouth elevation, eye symptoms, immunocompromise, diabetes, pregnancy, anticoagulation, recent dental work, and ability to obtain urgent dental source control.

Diagnosis: Dental exam includes percussion, mobility, periodontal probing, pulp vitality, intraoral/extraoral swelling, and lymph nodes. Dental periapical or panoramic X-ray identifies periapical disease; CT maxillofacial/neck with contrast is used for deep-space infection, orbital spread, osteomyelitis, trismus, or unclear source. Culture is reserved for severe/refractory infection.

First-line treatment: Definitive treatment is dental source control: pulpotomy/pulpectomy/root canal, incision and drainage, extraction, or periodontal therapy. For localized pulpal/periapical disease without systemic involvement, ADA guidance prioritizes dental treatment and analgesia such as ibuprofen (Advil/Motrin) plus acetaminophen (Tylenol) rather than routine antibiotics.

Second-line treatment: Antibiotics are used when systemic involvement, spreading cellulitis, immunocompromise, or delayed source control exists: amoxicillin (Amoxil), penicillin VK, or amoxicillin-clavulanate (Augmentin); alternatives may include azithromycin (Zithromax) or cephalexin (Keflex) depending allergy history. Avoid reflex clindamycin when safer options exist because of C. difficile risk.

Third-line / advanced care: Emergency transfer/oral surgery/ENT for Ludwig angina signs, airway compromise, drooling, dysphagia, rapidly progressive swelling, orbital symptoms, sepsis, dehydration, deep neck infection, necrotizing infection, or failed outpatient therapy. IV ampicillin-sulbactam (Unasyn) or piperacillin-tazobactam (Zosyn) plus surgical drainage may be needed.

Progression and follow-up: Follow pain, fever, swelling, trismus, ability to swallow, completion of source control, antibiotic adverse effects, recurrence, and dental restoration/prevention plan.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oral Medicine and Dentistry Interface

Oral candidiasis

Pathophysiology: Oral candidiasis is Candida overgrowth or invasion promoted by inhaled steroids, dentures, xerostomia, diabetes, HIV/immunosuppression, antibiotics, chemotherapy, malnutrition, and mucosal barrier injury; forms include pseudomembranous thrush, erythematous candidiasis, angular cheilitis, and denture stomatitis.

How Oral Medicine and Dentistry Interface assesses it: Assess removable white plaques, burning, dysgeusia, dysphagia/odynophagia, denture use/hygiene, inhaled corticosteroid technique, diabetes symptoms/A1c, HIV risk, immunosuppressants, antibiotics, xerostomia drugs, chemotherapy/radiation, and recurrence.

Diagnosis: Usually clinical: scrapable plaques leaving erythema support pseudomembranous candidiasis. KOH smear, fungal culture, or biopsy is used for atypical, refractory, or non-scrapable lesions. Dysphagia/odynophagia suggests esophageal candidiasis and needs systemic therapy/evaluation.

First-line treatment: Treat local disease with nystatin oral suspension (Mycostatin) swish/swallow or clotrimazole troches (Mycelex) when feasible; improve denture cleaning/removal overnight, rinse mouth after inhaled steroids, manage dry mouth, and address diabetes or immunosuppression.

Second-line treatment: Use fluconazole (Diflucan) for moderate, recurrent, denture-refractory, or high-risk disease; check interactions such as warfarin, QT drugs, statins, and hepatic risk. Angular cheilitis may need topical antifungal plus barrier and bacterial coverage if crusting.

Third-line / advanced care: Refer oral medicine/ID/GI for refractory disease, suspected azole resistance, esophageal symptoms, unexplained immunosuppression, persistent non-scrapable plaques suggesting leukoplakia, or concern for malignancy.

Progression and follow-up: Follow symptom resolution, lesion clearance, recurrence triggers, denture fit/hygiene, glycemic control, inhaler technique, drug interactions, and need for HIV or immune evaluation.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oral Medicine and Dentistry Interface

Aphthous ulcers

Pathophysiology: Recurrent aphthous stomatitis causes painful non-keratinized mucosal ulcers from immune dysregulation, trauma, stress, nutritional deficiency, celiac/IBD, Behcet disease, cyclic neutropenia, HIV, or medication triggers; it is not caused by herpes simplex.

How Oral Medicine and Dentistry Interface assesses it: Assess ulcer size/number/duration, location, recurrence, fever, genital ulcers, eye inflammation, GI symptoms, weight loss, arthralgia, neutropenia/infections, new drugs, trauma/orthodontics, tobacco cessation, and immune status.

Diagnosis: Clinical diagnosis for typical minor aphthae: shallow round painful ulcers with erythematous halo on labial/buccal mucosa, soft palate, or tongue. Work up severe/recurrent/major ulcers with CBC/differential, ferritin/iron, B12, folate, celiac serology, HIV testing when risk, ESR/CRP and IBD/Behcet evaluation when symptoms fit. Biopsy ulcers persisting beyond 2-3 weeks or atypical indurated lesions.

First-line treatment: Symptomatic care: avoid trauma/SLS toothpaste/spicy acidic foods, topical anesthetic lidocaine viscous, protective paste, and topical corticosteroid such as triamcinolone dental paste (Kenalog in Orabase) or dexamethasone rinse for multiple lesions.

Second-line treatment: For frequent or severe disease, correct iron/B12/folate deficiency, treat underlying celiac/IBD/Behcet, and consider colchicine, dapsone, or short systemic prednisone under specialist guidance. Antivirals do not help aphthae unless HSV is proven.

Third-line / advanced care: Refer oral medicine/rheumatology/GI/hematology for major aphthae, scarring, genital ulcers/uveitis, systemic symptoms, neutropenia, immunocompromise, or malignancy concern.

Progression and follow-up: Follow ulcer-free intervals, healing time, nutrition/hydration, triggers, medication adverse effects, systemic clues, and biopsy results for persistent lesions.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oral Medicine and Dentistry Interface

Oral lichen planus

Pathophysiology: Oral lichen planus is a chronic T-cell mediated mucocutaneous inflammatory disorder with reticular white striae, erythematous, erosive, or ulcerative lesions; mimics include lichenoid drug reaction, graft-versus-host disease, lupus, candidiasis, leukoplakia, and dysplasia.

How Oral Medicine and Dentistry Interface assesses it: Assess pain/burning, reticular versus erosive pattern, bilateral buccal mucosa/tongue/gingiva involvement, skin/genital/nail lesions, hepatitis C risk, dental amalgam/contact allergens, medications such as NSAIDs/ACE inhibitors/thiazides, tobacco/alcohol, and dysplasia risk factors.

Diagnosis: Classic bilateral reticular lesions may be clinical, but erosive, unilateral, indurated, persistent, or changing lesions need biopsy with histopathology and sometimes direct immunofluorescence. Screen/treat candidiasis if superinfection suspected. Biopsy is essential if leukoplakia or squamous cell carcinoma cannot be excluded.

First-line treatment: Manage symptoms with meticulous oral hygiene, avoid irritants, treat candidiasis, and use high-potency topical corticosteroids such as clobetasol gel or fluocinonide gel, or dexamethasone rinse; triamcinolone dental paste can help focal lesions.

Second-line treatment: Refractory erosive disease may need topical tacrolimus/pimecrolimus with specialist oversight, intralesional steroids, short systemic corticosteroids, or systemic immunomodulators. Review and substitute possible lichenoid-trigger medications when medically safe.

Third-line / advanced care: Refer oral medicine/oral surgery/dermatology for biopsy, severe erosive disease, dysplasia, nonhealing ulcer, suspected malignancy, or need for systemic immunosuppression.

Progression and follow-up: Follow pain, eating ability, candidiasis from steroids, lesion map/photos, dysplasia/cancer surveillance, medication triggers, and biopsy changes over time.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oral Medicine and Dentistry Interface

Temporomandibular disorder

Pathophysiology: Temporomandibular disorder includes masticatory muscle pain, TMJ internal derangement/disc displacement, arthralgia/arthritis, parafunction/bruxism, trauma, hypermobility, and pain sensitization; most cases are benign and improve with conservative care.

How Oral Medicine and Dentistry Interface assesses it: Assess jaw pain location, clicking/locking, mouth opening limitation, bruxism/clenching, headache/ear symptoms, trauma, dental occlusion changes, inflammatory arthritis, sleep/stress, chewing gum habits, neurologic deficits, fever, and red flags such as cancer, infection, or giant cell arteritis symptoms.

Diagnosis: Clinical exam: jaw range of motion, deviation, joint sounds, muscle tenderness, bite/occlusion, cranial nerves, teeth wear, and cervical contribution. Imaging is not routine; panoramic X-ray rules dental/bony disease, MRI evaluates disc/internal derangement, CT/CBCT evaluates bony change/trauma/ankylosis when indicated.

First-line treatment: Conservative care: soft diet, avoid wide opening/gum, heat/ice, jaw relaxation, NSAID such as naproxen (Aleve/Naprosyn) or ibuprofen (Advil/Motrin) if safe, acetaminophen, physical therapy, stress/sleep management, and dentist-fitted occlusal splint/night guard for bruxism.

Second-line treatment: Short-term muscle relaxant such as cyclobenzaprine (Flexeril) at night may help muscle spasm; trigger point therapy, behavioral therapy, and treatment of sleep bruxism/OSA can help. Avoid irreversible occlusal adjustment or extensive dental reconstruction for routine TMD.

Third-line / advanced care: Refer oral maxillofacial surgery/orofacial pain/rheumatology for closed lock, persistent severe limitation, inflammatory arthritis, trauma/fracture, suspected infection/tumor, refractory pain, or need for arthrocentesis/injection/surgical evaluation.

Progression and follow-up: Follow pain, mouth opening, diet, function, medication adverse effects, splint use, headaches, sleep/bruxism, and transition to chronic pain strategy if central sensitization emerges.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oral Medicine and Dentistry Interface

Oral cancer screening

Pathophysiology: Oral cavity and oropharyngeal cancers are usually squamous cell carcinomas linked to tobacco, alcohol, betel nut, immunosuppression, and HPV for oropharynx; potentially malignant disorders include leukoplakia, erythroplakia, erythroleukoplakia, oral submucous fibrosis, and dysplasia.

How Oral Medicine and Dentistry Interface assesses it: Assess nonhealing ulcer, red/white patch, induration, mass, dysphagia, odynophagia, otalgia, hoarseness, neck mass, weight loss, tobacco/alcohol/betel use, HPV risk/vaccination, dentures/trauma, immunosuppression, and lesion duration over 2 weeks.

Diagnosis: Perform conventional visual and tactile intraoral/extraoral exam including tongue borders, floor of mouth, palate, buccal mucosa, gingiva, oropharynx, salivary glands, and neck nodes. ADA guidance: suspicious lesions need immediate biopsy or specialist referral; salivary/light-based adjuncts are not recommended to decide malignancy.

First-line treatment: Remove obvious trauma and reassess only briefly when lesion clearly traumatic; otherwise biopsy or refer to oral surgery/ENT/oral medicine. Counsel tobacco cessation, alcohol reduction, HPV vaccination when age-eligible, and denture adjustment if traumatic.

Second-line treatment: Imaging such as CT/MRI neck or PET/CT is staging after diagnosis or for deep mass/neck node, not a replacement for biopsy. Pathology guides surgery, radiation, chemotherapy, or immunotherapy decisions.

Third-line / advanced care: Urgent referral for indurated ulcer, erythroplakia, unexplained neck mass, tongue/floor-of-mouth lesion, cranial nerve deficit, airway/swallow compromise, or persistent lesion beyond 2-3 weeks.

Progression and follow-up: Follow biopsy completion, pathology, staging, dental clearance before radiation, nutrition/swallowing, xerostomia/osteoradionecrosis risk, tobacco/alcohol cessation, and surveillance for recurrence/second primaries.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oral Medicine and Dentistry Interface

Bisphosphonate jaw osteonecrosis risk

Pathophysiology: Medication-related osteonecrosis of the jaw (MRONJ) is exposed/probeable jaw bone that persists in patients exposed to antiresorptive or antiangiogenic drugs without jaw radiation/metastasis, driven by impaired bone remodeling, infection, trauma, angiogenesis changes, and cancer-dose therapy risk.

How Oral Medicine and Dentistry Interface assesses it: Assess drug and dose: oral alendronate (Fosamax), risedronate (Actonel), ibandronate (Boniva), IV zoledronic acid (Reclast/Zometa), pamidronate, denosumab (Prolia/Xgeva), romosozumab (Evenity), bevacizumab (Avastin), sunitinib (Sutent), cancer versus osteoporosis indication, duration, steroids, diabetes, smoking, dentures, periodontal disease, planned extraction/implant, pain, exposed bone, fistula, or numbness.

Diagnosis: Diagnosis is clinical with dental/oral surgery exam; panoramic imaging or CT/CBCT evaluates sequestrum, osteolysis, fracture, sinus involvement, or dental infection. Rule out osteoradionecrosis, metastatic disease, osteomyelitis, periodontal abscess, and trauma. Do not use CTX blood testing to predict risk.

First-line treatment: Prevention is best: dental optimization before high-dose cancer antiresorptives when possible, treat periodontal/dental infection, excellent oral hygiene, regular dental care, and conservative/restorative choices when feasible. For osteoporosis-dose therapy, routine dental care usually continues with individualized risk discussion.

Second-line treatment: Established MRONJ management depends on stage: chlorhexidine (Peridex) rinses, analgesia, antibiotics such as amoxicillin-clavulanate (Augmentin) only for secondary infection, smoothing sharp bone, and oral surgery-directed debridement/resection for progressive or symptomatic disease. Drug holidays are individualized with prescriber because fracture/cancer skeletal-event risks may outweigh uncertain jaw benefit.

Third-line / advanced care: Refer oral maxillofacial surgery/oral medicine and the prescribing oncology/endocrine team for exposed bone, fistula, pathologic fracture, extraoral fistula, sinus involvement, severe pain/infection, or need for extraction while on high-dose therapy.

Progression and follow-up: Follow exposed bone size, pain, infection, imaging changes, nutrition, dental trauma sources, antiresorptive plan, cancer/fracture risk, and surgical healing.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oral Medicine and Dentistry Interface

Odontogenic sinusitis

Pathophysiology: Odontogenic sinusitis arises when maxillary dental infection, periodontal disease, periapical pathology, extraction, implant, oroantral fistula, or foreign material seeds the maxillary sinus; it is often unilateral and anaerobe-predominant compared with routine viral rhinosinusitis.

How Oral Medicine and Dentistry Interface assesses it: Assess unilateral foul nasal drainage, maxillary pressure, dental pain, recent extraction/root canal/implant/sinus lift, oroantral communication, fever, facial swelling, immune status, and failure of usual sinusitis therapy.

Diagnosis: Dental exam plus nasal exam; CT sinus/maxillofacial shows unilateral maxillary sinus opacification, periapical lucency, oroantral fistula, implant protrusion, or foreign body. Dental periapical/panoramic imaging helps identify source. Culture is considered for refractory/surgical cases.

First-line treatment: Treat the dental source: endodontic therapy, extraction, periodontal therapy, closure of oroantral fistula, or implant/foreign-body management. Adjuncts include saline irrigation, intranasal corticosteroid such as fluticasone (Flonase), analgesia, and antibiotics when bacterial infection is significant or surgery delayed.

Second-line treatment: Antibiotics often need anaerobic oral flora coverage, such as amoxicillin-clavulanate (Augmentin); alternatives depend on allergy/local resistance and may require ENT/dental guidance. Persistent disease may need endoscopic sinus surgery plus dental source control.

Third-line / advanced care: Urgent ENT/oral surgery/ED for orbital symptoms, vision changes, severe facial swelling, neurologic signs, high fever/sepsis, invasive fungal concern, or deep space infection.

Progression and follow-up: Follow resolution of unilateral drainage/odor, dental source completion, CT/endoscopy if persistent, oroantral fistula closure, implant complications, and recurrence.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oral Medicine and Dentistry Interface

Trigeminal neuralgia dental mimic

Pathophysiology: Trigeminal neuralgia causes brief electric shock-like unilateral facial pain in trigeminal distributions from neurovascular compression or secondary causes such as multiple sclerosis, tumor, or postherpetic neuropathy; it is often mistaken for tooth pain, leading to unnecessary dental procedures.

How Oral Medicine and Dentistry Interface assesses it: Assess paroxysmal seconds-to-minutes pain, trigger zones, brushing/chewing/talking triggers, refractory period, distribution V2/V3, sensory loss, bilateral symptoms, age under 40, MS symptoms, shingles history, dental pathology, and continuous background pain.

Diagnosis: Diagnosis is clinical but requires dental exam to exclude odontogenic disease. MRI brain/trigeminal protocol with and without contrast is used to evaluate neurovascular compression and secondary causes, especially atypical features, sensory deficits, young age, or bilateral symptoms.

First-line treatment: First-line medication is carbamazepine (Tegretol/Carbatrol) or oxcarbazepine (Trileptal) with CBC, sodium, liver monitoring and drug-interaction review. Avoid extraction/root canal unless objective dental disease explains pain.

Second-line treatment: Alternatives/add-ons include baclofen (Lioresal), lamotrigine (Lamictal), gabapentin (Neurontin), pregabalin (Lyrica), or botulinum toxin in specialist care. Treat postherpetic neuralgia differently with gabapentinoids, TCAs, topical lidocaine, or other neuropathic pain strategies.

Third-line / advanced care: Refer neurology/neurosurgery for medication intolerance, refractory pain, diagnostic uncertainty, sensory deficit, MS/tumor concern, or procedures such as microvascular decompression, stereotactic radiosurgery, or percutaneous rhizotomy.

Progression and follow-up: Follow attack frequency, triggers, medication adverse effects including hyponatremia/rash/blood dyscrasia, dental procedure avoidance, nutrition/weight loss, mood/suicide risk during severe pain, and MRI findings.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Oral Medicine and Dentistry Interface

Dental prophylaxis questions

Pathophysiology: Dental antibiotic prophylaxis aims to prevent rare but serious infective endocarditis in the highest-risk cardiac patients; routine prophylaxis for prosthetic joints is generally not recommended because harms and resistance usually outweigh benefits.

How Oral Medicine and Dentistry Interface assesses it: Assess planned dental procedure, whether it manipulates gingival tissue/periapical region or perforates oral mucosa, cardiac history, prosthetic valve/valve repair material, prior infective endocarditis, select congenital heart disease, transplant valvulopathy, prosthetic joint complications, allergy history, C. difficile history, and current antibiotics.

Diagnosis: No lab test decides prophylaxis. Confirm cardiac indication from records/cardiology when uncertain. Highest-risk IE indications include prosthetic cardiac valve or prosthetic valve-repair material, prior infective endocarditis, unrepaired cyanotic congenital heart disease or repaired CHD with residual shunt/regurgitation near prosthetic material, and cardiac transplant with valvular regurgitation.

First-line treatment: When IE prophylaxis is indicated, typical adult regimen is amoxicillin (Amoxil) 2 g orally 30-60 minutes before the procedure. Good daily oral hygiene and regular dental care reduce bacteremia burden more than repeated antibiotics for low-risk patients.

Second-line treatment: For penicillin allergy, current AHA/ADA alternatives include cephalexin (Keflex), azithromycin (Zithromax), clarithromycin (Biaxin), or doxycycline; avoid cephalosporins with anaphylaxis/angioedema/urticaria history to penicillin/ampicillin. Clindamycin is no longer preferred for IE prophylaxis because of more severe adverse reactions including C. difficile.

Third-line / advanced care: For prosthetic joints, prophylaxis is generally not recommended; consider only after consultation with orthopedics for prior joint-surgery complications or unusual high-risk circumstances. Refer cardiology/orthopedics/dentistry if indication is unclear rather than prescribing by habit.

Progression and follow-up: Document indication, procedure, antibiotic/dose/time, allergy rationale, adverse reactions, and update the plan as cardiac/joint status changes.

Built from the app's uploaded pharmacology/pathophysiology modules and source library where available, then cross-checked against Mayo Clinic, MedlinePlus, Merck Manual Professional, CDC/USPSTF guidance, specialty guidelines, and DailyMed labels for named drugs.

Reputable Sources Used for This Module

Use these maintained medical libraries and US guideline sources to verify current recommendations.

Mayo Clinic Diseases and ConditionsMedlinePlus Health TopicsMedlinePlus All Health TopicsMerck Manual Professional TopicsAmerican Board of Medical SpecialtiesCDC Clinical Guidance and GuidelinesUSPSTF RecommendationsFDA DailyMed Drug LabelsIDSA Practice GuidelinesADA Standards of Care