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CONTACT HOURS
When
Alzheimer disease
 strikes early
Alzheimer disease is generally seen in individuals
age 65 and older; however, in approximately 5% of
cases, it occurs in those younger than age 65.
By Amanda Perkins, MSN, RN
A progressive, degenerative disease affecting the cerebral cortex-the site at
which the highest level of neural processing takes place-Alzheimer disease
in individuals younger than age 65 is termed early-onset. Typically affecting
people between ages 40 and 50, early-onset Alzheimer disease may be seen
in individuals as young as age 30.
Two types
There are two types of early-onset Alzheimer disease: common and genetic.
Common Alzheimer disease is the type that occurs in most cases, whereas
the genetic form of the disease is extremely rare. With genetic Alzheimer
disease, signs and symptoms typically develop between ages 30 and 50.
The cause of common early-onset Alzheimer disease is unknown, whereas
the genetic type is associated with a mutation in one of three genes located
on three different chromosomes: 1, 14, and 21 (see Genetics and early-onset
Alzheimer disease). The mutations seen on the chromosomes are as follows:
-  chromosome 1-presenilin 2 (PSEN2)
-  chromosome 14-presenilin 1 (PSEN1)
-  chromosome 21-amyloid precursor protein (APP).
Presenilin proteins are linked to early-onset Alzheimer disease. The
genes that code for them are found on chromosomes 1 and 2. Of the three
mutations, PSEN1 and PSEN2 account for the majority of genetic early-
onset Alzheimer disease cases (see Mutant presenilin). These genetic
mutations shouldn't be confused with the apolipoprotein, or APOE, gene,
which increases the overall risk of Alzheimer disease.
Research related to the correlation of Alzheimer disease with health,
environment, and lifestyle factors is ongoing. It's believed that the disease
may be linked with vascular conditions, such as heart disease, stroke, and
ILLUSTRATION BY WILD PIXLE / ISTOCK (c)
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hypertension, as well as metabolic
conditions, such as diabetes and obesity.
Changes in the brain
Alzheimer disease is characterized by beta
amyloid plaques, neurofibrillary tangles,
neuronal degeneration, and diffuse atrophy
of the cerebral cortex.
Beta-amyloid plaques occur as the result
of accumulation of beta-amyloid-a small
fibrillary peptide that builds up in the
Genetics and early-onset Alzheimer disease
Let's delve deeper into chromosomes and the abnormal genes found on
chromosomes 1, 14, and 21. A chromosome is a structure found within
cells; specifically, within the cell nucleus. Chromosomes are made up of
tightly coiled strands of genes that are the blueprint for each individual
person. We receive 23 chromosomes from each parent, for a total of 46
chromosomes. Mutations of the genes found on these chromosomes can
lead to various diseases such as Alzheimer disease. Defects in the genes
found on chromosomes 1, 14, and 21 have been associated with early-
onset Alzheimer disease.
Chromosome 1
The gene mutation that occurs with chromosome 1 is found in the gene
STM2, which codes for PSEN2. This abnormality is rare and seen most
commonly in descendants of Germans who immigrated to Russia in the
18th century and then to the United States in the 20th century.
Chromosome 14
The gene mutation that occurs with chromosome 14 is found in the
gene S182, which codes for PSEN1. This gene mutation is much more
common, accounting for approximately 80% of all cases of inherited
Alzheimer disease.
Chromosome 21
This chromosome is the smallest in the entire genome. The mutation
that occurs with chromosome 21 is found in APP. Abnormalities in APP
are also linked to Down syndrome. Research has shown that most
individuals with Down syndrome will develop Alzheimer disease by
age 60.
Mutations found within the genes described above appear to
accelerate the formation of beta-amyloid and lead to the development
of plaques. Additionally, the presenilins associated with chromosomes 1
and 14 appear to cause apoptosis, a natural process in which cells are
programmed to self-destruct (sometimes referred to as cellular suicide).
Normally, apoptosis is beneficial to the body, eliminating unnecessary cells
and targeting cancer cells so that healthy tissue can be maintained. With
Alzheimer disease, apoptosis eliminates cells that the body needs.
spaces around synapses, the communication
points between neurons. Beta-amyloid is a
normal finding in healthy individuals.
Under normal conditions, the beta-amyloid
that's in the brain dissolves and is removed
by the body.
In patients with Alzheimer disease,
there's too much beta-amyloid present and
the body isn't able to remove it, resulting in
an accumulation of the peptide. The beta
amyloid accumulates into fibrils that clump
together and form plaques that effectively
kill brain cells, which causes a disruption in
brain functioning. Although it's known that
beta-amyloid causes brain cell death, it's
unknown how this process occurs. Unlike
other cells found in the body, brain cells
can't be replaced once they die. As more
brain cells die in the patient with Alzheimer
disease, symptoms become increasingly
pronounced.
It's believed that APP-the parent pro
tein for beta-amyloid-plays a role in
beta-amyloid plaque formation. APP is a
large protein found in the brain, heart,
kidneys, lungs, spleen, and intestines. It
protrudes through the neuronal mem
brane, with a portion of the protein found
within the cell and the remainder on the
outside of the cell. Enzymes cut APP into
two fragments, leaving a beta-amyloid
fragment within the brain. It's known that
once cut, the APP fragments clump togeth
er; however, it's unknown what exactly
happens within the body to cause the
clumping.
Neurofibrillary tangles are abnormal
clumps of proteins, in some cases tau.
Helping maintain nerve cell structure and
making it possible for the cells to carry
nutrients from the cell body to the axons,
tau plays a critical role in the brain. In
patients with Alzheimer disease, tau pro
tein abnormally twists, causing axons to
tangle and leading to the development of
neurofibrillary tangles in neuronal cell bod
ies. The plaques and tangles that develop
in the brain are found in areas important
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for memory and intellectual functions.
Additionally, a loss of connections occurs
between neurons-the brain cells responsi
ble for not only communicating with differ
ent parts of the brain, but also from the
brain to the body.
Damage in the brain may start in the hip
pocampus-the area responsible for memo
ry formation. It's believed that this damage
begins a decade before signs and symptoms
develop. Healthy neurons stop functioning
and, eventually, connections are lost, neu
rons are unable to communicate with one
another, and neuronal death occurs. As neu
rons continue to die and connections are
lost, new areas of the brain become affected
until there's widespread damage and
atrophy.
Research has indicated that individuals
with early-onset Alzheimer disease may
decline at a faster rate than those who
develop Alzheimer disease after age 65.
However, specific brain changes that occur
before the development of symptoms
haven't been demonstrated. The National
Institute on Aging is currently conducting a
study on early-onset Alzheimer disease. It's
hoped that this study will be able to identi
fy changes that occur before symptom
development.
Signs and symptoms
The symptoms associated with early-onset
Alzheimer disease are similar and overlap
with those seen in other forms of the dis
ease, including:
-  early symptoms
-forgetfulness, especially with new
information
-repeatedly asking the same questions
-difficulty solving basic problems
-losing track of the date and/or time of year
-losing track of location and how the per
son arrived at the location
-problems with depth perception
-difficulty with conversations
-difficulty with word finding
-difficulty concentrating
SCIENCE SOURCE (c)
Mutant presenilin
Mutations in the presenilin proteins (PSEN1 and PSEN2) and APP can be
found in patients with early-onset Alzheimer disease (autosomal dominant
hereditary). An important part of the disease process is the accumulation of
beta-amyloid. To form it, APP must be cut by two enzymes: beta secretase
and gamma secretase. Presenilin is the subcomponent of gamma secretase
that's responsible for cutting APP.
-misplacing items
-increasingly poor judgment
-withdrawal from work and/or social
situations
-change in mood and personality
-increasing difficulty completing familiar
tasks
-repeating stories
-forgetting names of familiar people
-wandering, especially at night
-  late symptoms
-depression
-severe mood swings and behavior
changes
-increasing agitation and irritability
-increasing confusion about time, place,
and events
-suspicions about family and friends
-disinhibition
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-difficulty speaking, swallowing, and
walking
-severe memory loss
-psychosis
-incapacity for self-care.
Alzheimer disease is characterized by
three different stages: mild, moderate, and
severe. In the mild stage, the patient begins
to have memory loss and cognitive difficul
ties. The patient and/or family members
may report wandering, getting lost, having
difficulty with money/paying bills, repeat
ing questions, increasing difficulty with
daily tasks, and personality and behavioral
changes.
In the moderate stage, damage in the
brain has spread to the areas responsible for
language, sensory processes, conscious
thought, and reasoning. In this stage, the
patient may have increased memory loss
and confusion, along with difficulty recog
nizing friends and family, learning new
things, and performing complex tasks. The
patient may also experience problems cop
ing with new situations, hallucinations,
delusions, paranoia, and impulsive
behaviors.
In the severe stage, plaques and tangles
are spread throughout the brain and brain
atrophy is present. The patient will be bed
ridden and unable to communicate; the
body will eventually shut down.
The progression of Alzheimer disease
affects each individual differently. In
some cases, the patient with early-onset
did you know?
Of the top 10 diseases causing death in the United States, Alzheimer
disease is the only one that can't be prevented, cured, or slowed,
according to the Alzheimer's Association. Occurring more commonly
in female patients (two-thirds of those diagnosed), Alzheimer disease
is very costly for patients, families, and the nation. According to the
Alzheimer's Association, it's estimated that in 2015, the national cost
of Alzheimer disease, as well as other dementias, was $226 billion.
Additionally, it's estimated that without a cure or improved treatments,
the cost will increase to $1.1 trillion by 2050.
Alzheimer disease may move through
the stages more quickly. However, it's
important to remember that each
patient will progress through the stages at
different speeds.
Diagnosis
The diagnosis of early-onset Alzheimer
disease can be challenging, with misdi
agnosis occurring more commonly than
with other types of the disease. Defini
tive diagnosis of Alzheimer disease can
only be made after death when an au
topsy can be completed. Diagnosis is
based on a history and physical; signs
and symptoms; cognitive tests; blood,
urine, and spinal fluid analysis; and
computed tomography (CT) or magnetic
resonance imaging (MRI).
The cognitive tests conducted are used
to assess memory, problem solving, and
other mental skills. Many of these tests are
performed serially so that changes in cog
nition and memory can be assessed. In
addition, the patient's family and/or care
givers are asked about changes they've
noticed. In many cases, the family and/or
caregivers may be able to detect changes
in the patient early on. CT and/or MRI
may be utilized to assess damaged areas
in the brain.
The usefulness of biologic markers,
such as proteins and genes, is being
researched. It's hoped that current
research will lead to markers that can
detect Alzheimer disease. If discovered,
biomarkers specific to Alzheimer disease
can be used to not only aid in diagnosis,
but also predict future disease. At this
time, CT and MRI are being researched as
potential biomarkers for Alzheimer dis
ease. These scans may prove useful by
detecting brain shrinkage and slowed
brain metabolism and blood flow.
At this time, individuals can be tested for
the genetic mutations associated with
Alzheimer disease, but this testing is typical
ly limited to those with a family history.
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Complications
Most of the complications seen with Al
zheimer disease are those that arise from
immobility, including:
-  aspiration
-  pneumonia and other infections
-  falls
-  fractures
-  skin breakdown, such as pressure ulcers
-  malnutrition and dehydration.
Aspiration occurs when patients inhale
food and/or fluids into their lungs. As
Alzheimer disease progresses, patients have
increasing difficulty coordinating swallow
ing and breathing, leading to aspiration risk.
If aspiration occurs, the patient may develop
an infection, most commonly pneumonia.
The patient with Alzheimer disease has a
high risk of falls due to increasing immobili
ty, wandering, and poor safety awareness.
Falls may raise the risk of fractures, which
can be particularly dangerous for patients
with Alzheimer disease because of the com
plications associated with immobility.
Patients with Alzheimer disease are also
at risk for skin breakdown, specifically pres
sure ulcers, which lead to ischemia and
potential tissue necrosis. As the patient
becomes increasingly immobile, the risk of
pressure ulcer development is higher.
In the advanced stages of Alzheimer dis
ease, patients have increasing difficulty eat
ing and drinking, leading to malnutrition
and dehydration. Many patients don't die as
a result of Alzheimer disease; rather, they
die from pneumonia or other complications
of immobility.
Although the complications associated
with early-onset Alzheimer disease are the
same as those seen in other Alzheimer
patients, it's important to be aware that
these complications can be particularly chal
lenging for patients who develop the disease
early, at a time in their life when they would
normally be able to care for themselves and
others. Family members may find it particu
larly difficult when a young spouse or par
ent is unable to eat independently, falls
consider this
A 45-year old female patient arrives at the physician's office with complaints
of increasing forgetfulness. She states that she started to have problems
recalling names and dates approximately 6 months ago. She also reports
that she has been having difficulty with word finding, concentrating, finding
common household objects, and sleeping, along with mood swings. She
tells you that she's concerned because her grandmother developed demen
tia at an early age.
frequently, or experiences nighttime
wandering.
Management
Alzheimer disease is a progressive disease
that has no cure. Current treatment is
aimed at helping patients maintain mental
and physical function, control behavior, im
prove quality of life, and slow disease pro
gression. Although treatment hasn't been
shown to dramatically slow the progression
of the disease, it's beneficial in controlling
agitation, anxiety, behavioral problems,
sleep disturbances, and depression. Treat
ment is most effective when started early.
It's important to be aware that, in most
cases, medication is ineffective as the disease
progresses. Medications, such as donepezil,
rivastigmine, and memantine, may help
slow the progression of the disease, but may
only be beneficial for a few months to a few
years.
Used to treat all stages of Alzheimer
disease, donepezil works by increasing
acetylcholine levels in the brain. For some
patients, this medication improves think
ing, overall function, and behavior. It isn't
curative but, in some patients, it may slow
disease progression. Donepezil is most
effective when started early and becomes
less effective as the disease progresses.
Used to treat mild-to-moderate
Alzheimer disease, rivastigmine increases
acetylcholine in the brain by blocking the
enzymes that break it down. For some
patients, this medication may improve
thinking, remembering, the ability to
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perform activities of daily living (ADLs),
and overall functioning.
When administering donepezil or riva
stigmine, monitor the patient closely for
inter actions with other medications, such as
antipsychotics, antiarrhythmics, beta-blockers,
digoxin, and nonsteroidal anti-inflammatory
drugs (NSAIDs). When given with antipsy
chotics, these medications can increase the
risk of Parkinson-like symptoms. When
given with antiarrhythmics, beta-blockers,
and/or digoxin, they can cause bradycardia
or other cardiac conduction problems. When
given with NSAIDs, these medications can
increase the risk of stomach ulcer develop
ment. Donepezil and rivastigmine are both
cholinesterase inhibitors, meaning that they
interfere with the breakdown of acetylcho
line. They lose effectiveness as an increasing
number of acetylcholine-producing cells die.
Memantine is a glutamate receptor-
blocking agent used to treat moderate-to
severe Alzheimer disease. This medication
regulates glutamate by blocking its action at
receptors, which is important because these
receptors are overstimulated in patients
with Alzheimer disease. It may slow the
progression of the disease, improve cogni
tive and psychomotor function, and
improve the patient's ability to carry out
ADLs. Memantine and the cholinesterase
inhibitors act differently in the body and, as
a result, can be administered together.
In addition to medications, the following
may help delay disease progression:
-  physical activity
-  cardiovascular treatment
-  diabetes treatment
did you know?
Medications selected for the treatment of Alzheimer disease include those
that prevent the breakdown of acetylcholine, a chemical important for
memory and thinking, and those that regulate glutamate, a brain chemical
that can cause cell death when produced in large amounts. These
medications are utilized because destruction occurring in the brain leads
to decreased levels of acetylcholine and increased levels of glutamate,
which can be neurotoxic and intensify signs and symptoms.
-  antioxidants
-  cognitive training.
Research on the effectiveness of alterna
tive treatments, such as light therapy, music
therapy, pet therapy, and aromatherapy, is
being conducted. Nonpharmacologic
approaches are sought because they may be
more cost effective and potentially decrease
the amount of medications needed.
The treatment of early-onset Alzheimer
disease mirrors that of other patients with
Alzheimer disease. Treatment is aimed at
slowing disease progression and allowing
the patient to maintain independence for as
long as possible. In some instances, the
patient with early-onset Alzheimer disease
may choose to participate in clinical trials.
Your role
Alzheimer disease can be a devastating di
agnosis for your patients and they may
need a great deal of emotional support.
When caring for those with early-onset Al
zheimer disease, be aware of your patients'
stress levels and help them cope effectively.
Always maintain a positive attitude when
working with these patients and let them
know that they aren't alone.
Provide education to patients and their
families about the disease; legal documents,
such as advance directives and living wills;
and therapeutic interventions, including
pharmacologic and nonpharmacologic
approaches to care. If patients or their fami
lies are considering nonpharmacologic
interventions, give them evidence-based
information and encourage them to check
with the healthcare provider before trying
anything that they've seen on TV or
researched on the Internet.
Encourage patients to stay mentally
engaged and physically active for as long as
they can. You'll also want to encourage them
to plan ahead. Finances can be of particular
concern because patients may need to stop
working earlier than planned and experi
ence a loss of income as a result. Additional
ly, the patient's spouse may need to quit his
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or her job, or cut back on hours to take on
the caregiver role.
When caring for patients with Alzheimer
disease, remember that these patients are
sensitive to external stimuli and have a ten
dency to become easily agitated. Additional
ly, nighttime awakening is very common,
which can create safety risks for the patient
and cause caregiver strain. In many cases,
individuals with early-onset Alzheimer dis
ease will be living at home with family. Fre
quent awakenings and wandering at night
can put stress on family members.
It's important to keep the patient's envi
ronment familiar and free of clutter, with
minimal stimulation, good lighting, and an
appropriate temperature. To create a familiar
environment when the patient isn't at home,
pictures and personal effects from home can
be brought to the care facility. It may also be
beneficial to provide consistent caregivers
whenever possible and maintain a routine.
Alzheimer disease doesn't just affect an
individual; rather, it changes the entire fami
ly dynamic and affects the family as a
whole. Caregivers undergo great emotional
stress, with 60% of people caring for patients
with Alzheimer disease rating their stress
levels as high to very high, according to the
Alzheimer's Association. In addition to high
stress levels, 40% of caregivers report that
they experience depression. Many caregiv
ers become stressed due to lack of support,
minimal knowledge of available support
services, and feeling unprepared for the care
that needs to be provided.
This diagnosis can be particularly devas
tating for children who may have to take on
the role of caregiver for a young parent and
also be concerned about the possibility of
developing early-onset Alzheimer disease
themselves. Educate the children of patients
with early-onset Alzheimer disease about
genetic testing, but stress that it's a choice
requiring careful consideration. Also be
aware that this diagnosis can be very diffi
cult for spouses who have to change their
expectations of the future and take on a
on the web
Alzheimer's Association:
www.alz.org/alzheimers_disease_early_onset.
asp
John's Hopkins Medicine:
www.hopkinsmedicine.org/healthlibrary/
conditions/nervous_system_disorders/early
onset_alzheimers_disease_134,63/
Mayo Clinic:
www.mayoclinic.org/alzheimers/art-20048356
National Institute on Aging:
https://www.nia.nih.gov/alzheimers/early-onset
alzheimers-disease-resource-list
caregiving role for the person with whom
they're sharing their life.
If family members are in the caregiver
role, assess their well-being and coping
strategies. Educate them about available
support groups. Keep in mind that many
support groups developed for Alzheimer
disease are geared toward individuals over
age 65. You may need to research support
groups in your area for patients with early-
onset Alzheimer disease.
Additionally, educate the family about
how to deal with difficult behaviors, avoid
triggers, administer medication safely, and
monitor for adverse reactions. Stress the
importance of maintaining a consistent rou
tine. Caregivers need to be prepared for hal
lucinations, delusions, paranoia, resisting
care, and, in the later stages, anger and
potential physical abuse. Caring for a person
with Alzheimer disease can be frustrating
and exhausting because there's no end in
sight and their loved one will continue to
deteriorate. Another stressor for family
members is that their loved one will eventu
ally forget them and all memories associated
with them. In many cases, these family care
givers will be responsible for their loved one
24 hours a day with no breaks. However,
with proper education, you can increase the
quality of life for both your patients and
their caregivers.
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Keeping up to date
To provide appropriate care and education
for your patients and their families, it's es
sential that you stay on top of current re
search in the area of early-onset Alzheimer
disease. A variety of research studies are
being conducted on early-onset Alzheimer
disease and it's hoped that this research
will shed light on changes that occur in the
brain before and after the development of
symptoms, leading to innovative treatments
and disease prevention. 
REFERENCES
Alzheimer's Association. 2015 Alzheimer's disease
facts and figures. www.alz.org/facts/downloads/facts_
figures_2015.pdf.
Ashwell K. The Brain Book. New York, NY: Firefly Books; 2012.
Davis NJ, Hendrix CC, Superville JG. Supportive
approaches for Alzheimer disease. Nurse Pract.
2011;36(8):22-29.
Johns Hopkins Medicine. Early-onset Alzheimer's disease.
www.hopkinsmedicine.org/healthlibrary/conditions/
nervous_system_disorders/early-onset_alzheimers_
disease_134,63/.
Mayo Clinic. Alzheimer's disease. www.mayoclinic.
org/diseases-conditions/alzheimers-disease/home/
ovc-20167098.
Mayo Clinic. Early-onset Alzheimer's: when symptoms
begin before age 65. www.mayoclinic.org/alzheimers/
art-20048356.
McNair T. Early intervention for caregivers of
patients with Alzheimer's disease. Home Healthc Now.
2015;33(8):425-430.
National Institute on Aging. Alzheimer's disease fact
sheet. www.nia.nih.gov/alzheimers/publication/alzheim
ers-disease-fact-sheet.
Uriri-Glover J, McCarthy M, Cesarotti E. Solving the puz
zle of Alzheimer disease. Nurse Pract. 2012;37(9):20-27.
Amanda Perkins is an  of Nursing at Vermont
Tech in Randolph Center, Vt.
The author and planners have disclosed no potential conflicts of
interest, financial or otherwise.
DOI-10.1097/01.NME.0000489901.70466.65
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