ALZHEIMER’S DISEASE:
A Study of Alzheimer’s Disease
Pathology and Nursing
Management of Unmet Needs

By Jennifer Krueger, RN, BSN
Alverno College, MSN 621
April 29, 2010
TUTORIAL INSTRUCTIONS
To navigate throughout this tutorial:
Click on the icon in the lower left corner of
each slide to return to the Table of Contents
page at any time.
Table
of
Contents
Only use the left or right arrows located
in the upper right hand corner of each
slide, to progress to the next slide or return
to the previous slide.
(Unless specifically indicated, images were obtained from Microsoft Clipart, 2011)
CASE STUDY--Rosie
Meet, Rosie! Rosie is 84 years old and lives with
her daughter, son-in-law, and two grandchildren.
She moved in with her daughter six months ago,
after her husband passed away. While Rosie is in
excellent physical health, her family has noticed
some changes in her personality and decisionmaking skills.
Throughout this tutorial, you will answer questions
about Rosie as they relate to each section. When
you come to a slide with Rosie’s picture, answer
the question. Then click the forward arrow in the
upper right corner of the slide to continue.
LEARNING OBJECTIVES:
 Explain the basic pathology of Alzheimer’s Disease
including the influence of stress, inflammation,
aging and genetics.
 Recognize challenging behavior as communication
of unmet needs.
 Identify nursing interventions that will
influence/reduce challenging behaviors in patients
with Alzheimer’s Disease.
TABLE OF CONTENTS
Click on a box to find out more about
each topic…
JUST THE FACTS
DidYou Know?
•Alzheimer’s Disease is the most common cause of dementia in older adults;
60-80% of all cases. (Omnicare, 2010)
•Approximately 13% of all persons older than 65 years old have Alzheimer’s
Disease. (Omnicare, 2010)
•In 2008 5.2 million people were affected by Alzheimer’s Disease. (Omnicare, 2010)
•The risk of developing the disease increases with age, and approximately 50% of
all people over the age 85 have Alzheimer’s Disease. (Porth and Maftin, 2009)
•Currently, there are no specific diagnostic tests to diagnose Alzheimer’s Disease;
diagnosis is made by excluding other possible causes of dementia symptoms.
(Porth and Maftin, 2009)
JUST THE FACTS
DidYou Know?
There are normal a changes in the brain, associated with
aging…
Weight of brain decreases.
Neuron loss, mostly in the cortex in the superior temporal area.
Neurons atrophy with changes in neurotransmission.
Despite changes, cognitive abilities remain intact.
Changes in personality or cognitive deficits are considered not normal in
the older adult.
Many times, plaques and tangles associated with Alzheimer’s Disease are
found in older adults with no cognitive impairment.
(Porth and Maftin, 2009)
JUST THE FACTS
What Is Alzheimer’s Disease?
A disease involving neuropathic and neurotransmitter changes.
A disease causing cortical atrophy with loss of neurons particularly in the parietal and
temporal lobes of the brain.
A progressive disease leading to death within 8 to 10 years after diagnosis.
Ranges in stages of very mild cognitive decline to very severe cognitive decline.
(Porth and Maftin, 2009)
(Alzheimer’s Association, 2011)
(Image credit : Jannis Productions, Stacy Jannis. Picture used
with permission from the Alzheimer’s Association)
JUST THE FACTS
Stages Of Alzheimer’s Disease
Click on each stage to learn more…. (Stages are as defined by the Alzheimer’s Association)
No Impairment. Person does not show any signs and symptoms to a
medical professional or family members.
Very Mild Cognitive Decline. Patient may feel like they have memory
lapses, forgetting familiar words or objects. Family, friends and medical
professionals do not detect any signs or symptoms.
Mild Cognitive Decline (Early-stage). Family and friends may start noticing
problems with name-finding, planning or organizing. A medical professional
may detect problems with memory or concentration.
Moderate Cognitive Decline (Mild or early-stage). A careful medical
interview should be able to detect problems in several areas including,
knowledge of current events, impaired ability to perform challenging
mental arithmetic (counting backward from 75 by 7s), managing
finances, memory of personal history, may be moody and withdrawn.
(Alzheimer’s Association, 2011)
(Porth and Maftin, 2009)
JUST THE FACTS
Stages Of Alzheimer’s Disease
Click on each stage to learn more….(Stages are as stated by the Alzheimer’s Association)
Moderately Severe Cognitive Decline (Moderate or mid-stage). Major gaps
in memory and cognitive function. Will need some assistance with day to day
activities. Will not remember address or phone numbers. Able to remember
significant details about self and is usually able to use the toilet and feed self.
Severe Cognitive Decline (Moderately severe or mid-stage). Memory
continues to worsen. Significant changes in personality may emerge. Will
need help with dressing, toileting; may be incontinent. Tends to wander or
get lost.
Very Severe Cognitive Decline (Severe or late-stage). Final stage of
disease. Loses all ability to respond to their environment, including the
ability to speak and control movement.
(Alzheimer’s Association, 2011)
(Porth and Maftin, 2009)
JUST THE FACTS
Let’s Review!
Two years ago, Rosie started to feel like she was forgetting
simple things; birthdays, phone numbers and names of friends.
Since moving in with her daughter, Rosie has been choosing
inappropriate clothing for the season and is refusing to participate
in her normal social activities. She seems moody at times and has
been forgetting to take her daily medications.
Rosie is most likely in what stage of Alzheimer’s Disease:
Click on the correct shape below!
Sorry, try again!
Rosie’s cognitive
ability is affected.
Stage 1, is “No,
Impairment”.
You’re Correct!
Rosie is most likely
in the early stages of
Alzheimer’s Disease.
Sorry, try again!
Sorry, try again! Rosie’s
Rosie’s impairment is not impairment is not as severe
as severe as Stage 5.
as Stage 7.
PATHOPHYSIOLOGY
Anatomy 101: The Brain
What area does what?
(Image credit: Alzheimer’s Disease Education and Referral Center,
NIA. Picture used with permission from the Alzheimer’s Association)
Roll Over Each Lobe To Find Out!
(Porth and Maftin, 2009)
PATHOPHYSIOLOGY
Anatomy 101: A Brain Cell
Neuron: A brain cell affected by Alzheimer’s Disease
Click on a box to label
the parts of a neuron!
The three main parts of a neuron:
Axon: The extension from the neuron cell body that takes information away from
the cell body.
Cell Body (S0ma): The part of the cell that contains the nucleus.
Dendrite: Extensions from the neuron cell body that takes information to the cell
body.
(Porth and Maftin , 2009)
PATHOPHYSIOLOGY
Pathological Aspects
The major pathological features of Alzheimer’s Disease are the presence of
neuritic plaques, neurofibrillary tangles, and amyloid angiopathy .
Click on a box to learn about each feature contributing to the progression
of Alzheimer’s Disease.
(Porth and Maftin, 2009)
PATHOPHYSIOLOGY
Pathological Aspects
Neuritic plaques are clusters of protein fragments, arranged around a central amyloid core.
The most common type of deposits have fragment residues of 40-42 amino acids in length.
Plaques are associated with degeneration of neurons at the synaptic junction,
affecting cell to cell communication.
As Alzheimer’s Disease progresses, plaque formation
increases.
(Porth and Maftin, 2009)
(Wippolid, Carins, Vo, Holtzmann and Morris, 2007)
PATHOPHYSIOLOGY
Pathological Aspects
Are primarily composed of a protein called Tau wound around each other in a helical fashion.
They are resistant to chemical or enzymatic breakdown and remain in brain tissue after the
neuron dies.
Tangles destroy cell transport systems leading to neuron death.
Tangles have also been identified in other forms of dementia, although usually without
plaque formation, as found in Alzheimer’s Disease.
The relationship between tangles and plaques is not completely
understood.
(Alzheimer’s Association, 2011)
(Lippens, Sillen, Landrieu, Amniai, Sibille, Babier,
Leroy, Hanoulle & Wiersuzeski, 2007)
(Wippolid, Garins, Vo, Holtzmann and
Morris, 2007)
(Porth and Maftin, 2009)
PATHOPHYSIOLOGY
What About Tau?
Tau protein is important in the structural stabilization of nerve cells, allowing transport of
necessary proteins and enzyme-containing vesicles essential for cell maintenance
and function.
Tau is only present in neurons.
Too much or too little Tau leads to neuronal dysfunction.
If Tau collapses, as it does in Alzheimer’s Disease, it twists into helical strands becoming
neruofibillary tangles.
When tangles form, cells begin to die.
(Alzheimer’s Association, 2011)
(Lippens et al, 2007)
(Wippolid et al, 2007)
PATHOPHYSIOLOGY
Pathological Aspects
There are many types of amyloid proteins present in the body; B-amyloid is unique to the
brain.
B-amyloid is a protein fragment that is snipped from a larger protein called Amyloid
Precursor Protein (APP) which is associated with the cell membrane.
APP processing can follow two pathways, benign and harmful. As the harmful pathway
progresses, B-amyloid protein fragments start sticking together forming oligomers.
Oligomers start to grow larger becoming protofibrils and fibrils; eventually other proteins
and material are added forming neuritic plaques.
Click on each arrow below to progress the amyloid pathway to neuron death!
(Menon and Lutsep, 2010)
(Porth and Maftin, 2010)
PATHOPHYSIOLOGY
Pathological Aspects
Click on the video to learn more !
"
(Retrieved from YouTube, 2011 and embedded with permission of
the Alzheimer's Disease Education and Referral Center, a service of
the National Institute on Aging, 2008).
PATHOPHYSIOLOGY
Pathological Aspects
What does this all mean?
As plaques and tangles accumulate, neurons die. The cortex of the brain atrophies,
initially damaging areas involved in thinking, planning and remembering.
As the disease progresses, the parietal and temporal lobes of the brain are particularly
affected; these areas are related to communication and interpretation of sensory input.
Eventually, plaques and tangles spread to large portions of the brain causing severe atrophy
and cortical damage .
(Alzheimer’s Association, 2011)
(Porth and Maftin, 2009)
Tangle and plaque involvement are
represented by shaded blue areas. Images credit: Alzheimer’s Disease Education and Referral Center,
NIA. Picture used with permission from the Alzheimer’s Association.)
PATHOPHYSIOLOGY
Let’s Review!
Rosie has Stage 4 Alzheimer’s Disease. What three major factors
contribute to the progression of her symptoms?
A. Neurofibrillary tangles, confusion and dehydration.
B. Neuritic plaques, neuron repair and synapse junctions.
C. Neuritic plaques, neurofibrillary tangles and
amyloid processing.
D. Amyloid angiopathy, neuritic plaques and a history of
falling.
Sorry, try again!
Sorry, try again!
You’re Correct!
Sorry, try again!
Confusion is a symptom
of AD. Dehydration is not
a major factor
contributing to the
progression of AD.
Of these three,
only neuritic plaques
is a factor
contributing to AD.
Neuritic plaques, neurofibrillary
tangles and amyloid processing
are the 3 major factors contributing
to Alzheimer’s Disease.
Falling is not a major
factor contributing
to the progression
of a AD.
PATHOPHYSIOLOGY
Let’s Review!
Inside Rosie’s brain, neurofibillary tangles are forming. Which
protein fragment may be snipped from the larger APP,
eventually leading to the formation of oligomers?
A. Neuritic plaques
B. Amyloid Precursor Protein
C. A-amyloid
D. B-amyloid
Sorry, try again!
Neuritic plaques are
formed from clusters
of protein fragments.
Sorry, try again! Amyloid
Precursor Protein is APP.
Sorry, try again!
Alpha amyloid is
Not correct.
You’re Correct!
B-amyloid fragments
may form oligomers that
eventually form
neuritic plaques, in
people with AD.
IMMUNE AND STRESS RESPONSE
Alzheimer’s Disease and the IMMUNE RESPONSE…
What is the IMMUNE RESPONSE?
“The collective response of cells and molecules of the Immune System” (Porth and Maftin, 2009).
The Immune System includes:
1. Innate and Adaptive immunity (barriers to microbes/antigen recognition).
2. Cells ( Leukocytes, Lymphocytes, and Dendritic Cells).
3. Cytokines (Proteins that stimulate cells of the immune system to respond).
(Porth and Maftin, 2009)
IMMUNE AND STRESS RESPONSE
Alzheimer’s Disease and the IMMUNE RESPONSE
An activated IMMUNE RESPONSE will begin the INFLAMMATORY PROCESS.
There are two types of inflammatory process:
Acute: Short in duration. Characterized by exudate seeping into tissues, heat,
swelling, pain.
Chronic : Long in duration, lasting days to years. Presence of WBC’s, fibrosis and
tissue necrosis.
Inflammatory Response
(Porth and Maftin, 2009)
IMMUNE AND STRESS RESPONSE
Alzheimer’s Disease and the IMMUNE RESPONSE….
The exact role the IMMUNE RESPONSE plays in AD is still uncertain;
however it has been attracting attention in research in four ways:
1. As a first responder to initial pathological AD events.
2. Assisting in clearing of the toxic by-products of APP processing.
3. Provider of protection to neurons.
4. As a possible target for treatment strategies.
(Cohen, 2009)
IMMUNE AND STRESS RESPONSE
Alzheimer’s Disease and the IMMUNE RESPONSE
Facts about “Microglia”; the first responders to initial Central Nervous System
damage….
Microglia are immune cells of the Central Nervous System (CNS). They are considered
to be in a “resting state” until activated.
Upon CNS injury, microglia are triggered from the
substances released from the damaged tissue.
Activated microglia release growth factors,
anti-inflammatory factors, and protective
substances (cytokines) to restore
damaged tissue.
(University of Washington, 2008)
IMMUNE AND STRESS RESPONSE
Alzheimer’s Disease and the IMMUNE RESPONSE
Microglia and Alzheimer’s Disease…
•Microglia immune response contributes to the progression of Alzheimer’s Disease,
although exact contributions are not really known.
•In people with Alzheimer’s disease microglia
are found in close association with B-amyloid.
•Microglia respond to abnormal APP
processing by assisting in the clearing of toxic
by-products.
•Their role in the CNS may be far more complex
than previously appreciated.
(Cohen, 2009)
(Mandrekar-Colucci and Landreth, 2010)
IMMUNE AND STRESS RESPONSE
Alzheimer’s Disease and the STRESS RESPONSE
What is the STRESS RESPONSE?
Stress is a state of symptoms arising from the “coordinated activation of the
neuroendocrine and immune system”(Porth and Maftin, 2009). It was first described by Hans Selye, an
endocrinologist in the 1930’s. He called it the General Adaptation Syndrome (GAS).
(Porth and Maftin, 2009)
Activating the GAS releases hormones and neurotransmitters alerting the body
to stressors. Adaptations are made within the body to return it to a
balanced state.
(Porth and Maftin, 2009)
IMMUNE AND STRESS RESPONSE
Let’s Review!
Which type of cell inside Rosie’s Central Nervous System clear
toxic by-products of APP processing?
A. Neurons
B. B-amyloid
C. Monocyte
D. Microglia
Sorry, try again!
Neurons are brain
cells.
Sorry, try again!
B-amyloid is a
protein fragment.
Sorry, try again!
Monocytes are white
blood cells related to
Microglia.
You’re Correct!
Microglia clear
toxic by-products of
APP processing.
IMMUNE AND STRESS RESPONSE
Let’s Review!
Inside Rosie two complementary systems are triggered in the
pathology of AD. Which two systems are involved?
A. Immune and Stress
B. Digestive and Immune
C. Skeletal and Stress
D. Neurological and Respiratory
You’re Correct!
Although how, is
not exactly known!
Sorry, try again!
This is not correct.
Sorry, try again!
This is not correct.
Sorry, try again!
This is not correct.
GENETICALLY SPEAKING
Alzheimer’s and Genetics
There are two types of Alzheimer’s Disease, early-onset and late
onset; both have genetic links:
Late-Onset
Early-Onset

Rare; only 5% of all people who have AD.

Most cases of AD are Late-Onset.

Develops in people ages 30-60 years old.

Develops after age 60.

Some cases of early-onset AD are inherited; they are
called Familial AD (FAD).

Gene mutations found in early-onset are not
found in late-onset.

FAD is caused by gene mutations on specific
chromosomes 21, 14, and 1.

A specific gene for late-onset has not been
identified.

These mutations form abnormal amyloid precursor
protein (APP), causing increased amounts of Bamyloid.

A pre-disposing genetic risk does exist related
to, apolipoprotein E (APOE) gene, found on
chromosome 19.

If a person inherits either chromosomes, 21,14, or 1
they will almost always develop AD.
(National Institute of Aging, 2008)
GENETICALLY SPEAKING
Genetic Research and Alzheimer’s Disease
•Research in AD genetics has intensified regarding questions related to “What makes
the disease process begin?” and “What role do AD risk-factor genes interacting with other
genes, lifestyle and/or environmental factors affect the risk of developing AD?”
•Focuses on prevention and treatments.
•Scientist believe four to seven more AD risk-factor genes exist and are working to discover
them.
•A major goal is to develop accurate reliable screening tests; however they may never be
able to predict with 100% accuracy.
(National Institute of Aging, 2008)
GENETICALLY SPEAKING
Let’s Review!
Rosie has late-onset Alzheimer’s Disease. What predisposing risk
factor gene may have interacted with lifestyle and environmental factors
increasing Rosie’s chances of developing Alzheimer’s Disease?
A. Chromosome 21.
B. APOE gene.
C. Amyloid Precursor Protein (APP).
D. Chromosome 1.
Sorry, try again!
Chromosome 21 is
related to early-onset
AD.
You’re Correct!
APOE gene has
been identified as a
risk factor gene related
to late-onset AD.
Sorry, try again!
APP is related to the
formation of tangles
found in both late &
early-onset AD.
Sorry, try again!
Chromosome 1
is related to
early-onset AD.
WHAT ARE CHALLENGING
BEHAVIORS?
“People only see what they are prepared to see….” (Ralph Waldo Emerson
ThinkExist.com, 2011)
Rosie’s has progressed to Stage 6 of Alzheimer’s Disease. She started to wander
from home and became very verbally abusive. Her family was no longer able to care for
her at home and placed her in a long-term care facility. Nursing staff has reported Rosie
to be verbally abusive, fearful, and combative with bathing. She also continually calls out
“ I want to go home!”.
Problem
Behaviors
Challenging
Behaviors
What Do You See?
WHAT ARE CHALLENGING
BEHAVIORS?
What are typical CHALLENGING BEHAVIORS exhibited by people
who have Alzheimer’s Disease?
(Alzheimer’s Association,2011)
WHAT ARE CHALLENGING
BEHAVIORS?
In long-term care settings CHALLENGING BEHAVIORS might
be exhibited…
(Alzheimer’s Association,2011)
WHAT ARE CHALLENGING
BEHAVIORS?
Why do CHALLENGING BEHAVIORS occur?
May be related to deterioration of brain due to disease pathology in areas that regulate
impulse control, emotions and sensory processing.
May be related to pain that can be felt, but not articulated or specifically identified.
May be related to an underlying medical condition, like a urinary tract infection or pneumonia.
May be related to side effects of medications.
May be triggered by environmental conditions, for example lighting, noise or agitated
behaviors of others.
Click on the picture to find out!
(Alzheimer’s Challenging Behavior Task Force, 2010)
WHAT ARE CHALLENGING
BEHAVIORS?
Whatever the source, a caregiver’s response may improve or
make the behavior worse. In this way, “behaviors are best
seen as a dynamic interaction between the person with
dementia, the caregiver and the specific environment.”
(Alzheimer’s Challenging Behavior Task Force, 2010)
(Alzheimer’s Challenging Behavior Task Force, 2010)
WHAT ARE CHALLENGING
BEHAVIORS?
Let’s Review!
Since moving into the long-term care facility, Rosie’s challenging behavior
of yelling and resisting bathing has worsened. What factors may be
affecting her behavior?
A. Caregiver’s response to the bathing experience.
B. Progression of AD affecting Rosie’s Parietal and Temporal lobes
of her brain.
C. Environment of shower room, including lighting, sounds and
temperature.
D. All of the above.
Sorry, try again!
This could be a
contributing factor.
Sorry, try again!
This could be a
contributing factor.
Sorry, try again! You’re Correct! All of these
This could be a
factors could be influencing
contributing factor.
Rosie’s behavior.
NURSING MANAGEMENT OF
UNMET NEEDS
What are unmet needs?
Physical Needs: Pain, illness, hunger, thirst, constipation, fatigue, response to
incontinence, side effects related to medications, impaired vision or hearing.
Affective Needs: Intolerance of environmental stressors (overstimulation from
noise, lighting, etc.), boredom, loneliness, balance of sensory-stimulating verses
sensory-calming activities, meaningful human interaction.
(Alzheimer’s Association, 2011)
(Alzheimer’s Challenging Behaviors Task Force, 2010)
(Kovach, C., Logan, B., Noonan, P., Schlidt, A.,
Smierz, J., Simpson, M., & Wells, T., 2006)
“When behavioral symptoms are unnoticed, dismissed or not understood as symptoms of
unmet needs, the needs of the older person with dementia are missed…” (Kovach et al, 2006).
NURSING MANAGEMENT OF
UNMET NEEDS
What is YOUR response?
Do you CONSISTENTLY DO A COMPLETE PHYSICAL ASSESSSMENT with anyone
experiencing behavioral problems, especially when symptoms appear suddenly?
Do you DISMISS BEHAVIOR SYMPTOMS, as “typical or normal behavior” for that person?
Do you CONSIDER ENVIRONMENTAL STRESSORS OR PHYSICAL NEEDS WITH anyone
experiencing behavior problems?
Do you CONSIDER PERSONAL PREFERENCES with every activity? (What did the person
enjoy/like prior to be moved to the facility?
(Alzheimer’s Challenging
Behavior Task Force, 2010)
(Alzheimer’s Association, 2011)
(Kovach et al, 2006)
“….failure to recognize behavior as symptoms leads to the under treatment of many
needs.” (Kovach et al, 2006).
NURSING MANAGEMENT OF
UNMET NEEDS
Possible BARRIERS….
(Alzheimer’s Challenging Behavior Task Force, 2010)
(Simpson, Stevens, & Kovach, 2007)
NURSING MANAGEMENT OF
UNMET NEEDS
To manage a CHALLENGING BEHAVIOR….
Assess for physical needs and intervene as necessary:
 Pain
Thirst
Physical illness
Hunger
Constipation
Incontinence
Vision
Hearing
(Kovach et al, 2006)
“It takes an average of 23 minutes to manage disruptive behaviors. Agitated
behaviors are contagious, so it is advantageous to get them under control as soon as
possible” (Alzheimer’s Challenging Behavior Task Force, 2010).
NURSING MANAGEMENT OF
UNMET NEEDS
To manage a CHALLENGING BEHAVIOR….
Assess for affective needs and intervene as necessary:
Environment (lighting, noise level, movement)
Overstimulation/Understimulation
Boredom
Loneliness
Need for human contact
Fear
New or different staff
(Kovach et al, 2006)
“It takes an average of 23 minutes to manage disruptive behaviors. Agitated
behaviors are contagious, so it is advantageous to get them under control as soon as
possible” (Alzheimer’s Challenging Behavior Task Force, 2010).
NURSING MANAGEMENT OF
UNMET NEEDS
To manage a CHALLENGING BEHAVIOR….adapt YOUR
response:
Stop the activity that could be contributing to the behavior.
Try to distract with something enjoyable.
Stay calm.
Don’t argue.
Respond to the emotions underlying the behavioral need.
Ask yourself, “If safety is not an issue, can the behavior be accepted?”
“It takes an average of 23 minutes to manage disruptive behaviors. Agitated
behaviors are contagious, so it is advantageous to get them under control as soon as
possible” (Alzheimer’s Challenging Behavior Task Force, 2010).
(Alzheimer’s Association, 2011)
(Kovach et al, 2006)
NURSING MANAGEMENT OF
UNMET NEEDS
To manage a CHALLENGING BEHAVIOR….
Person-Centered Care:
“Care provided according the residents’ needs, desires and preferences”
(Alzheimer’s Challenging Behaviors Task Force, 2010).
Adapting the environment by encouraging “a continuous process of listening,
trying new things, seeing how they work and changing in an effort to
individualize care”(Alzheimer’s Challenging Behaviors Task Force, 2010).
“Person-Centered care seeks to maximize choice and autonomy, and thus can
reduce the presence of challenging behaviors”(Alzheimer’s Challenging Behaviors Task Force, 2010).
Likes to go to bed 22:30pm.
Prefers waking up at 9:30.
Does not like showers, baths only.
Coffee, black, 2 sugars.
Likes gardening, and quilting.
NURSING MANAGEMENT OF
UNMET NEEDS
Let’s Review!
The next time Rosie becomes verbally abusive at her care-givers while
being given a shower, the nurse should…
A. Ensure Rosie’s showering routine is designed around her preferences.
B. Assess Rosie for physical needs, specifically pain.
C. Stop the shower and stay calm.
D. All of the above.
Sorry, try again!
Sorry, try again!
Sorry, try again!
You’re Correct!
Assessing for pain,
stopping the shower,
staying calm and being
person-centered may
meet Rosie’s unmet
needs.
NURSING MANAGEMENT OF
UNMET NEEDS
Let’s Review!
As Rosie’s nurse, what can you do to affect Rosie’s possibility of
exhibiting future, challenging behaviors?
A. Call Rosie’s physician and ask them to increase the dosage of Rosie’s
scheduled anti-psychotic.
B. Plan to dismiss Rosie’s behavior as normal.
C. Identify Rosie’s challenging behavior as an unmet need and be
prepared to assess both physical and affective stressors.
D. Insist with Rosie she needs to stop behaving this way.
Sorry, try again!
This should not be your
first choice.
Sorry, try again!
By dismissing Rosie’s
behavior as normal, you
may miss an unmet
need.
You’re Correct!
Rosie’s challenging
behavior may be
related to an unmet
need, like pain.
Sorry, try again!
Arguing with
Rosie may make
the situation
worse.
REFERENCES
Alzheimer’s Association. (2011). The challenging behaviors of Alzheimer’s disease. Portland, OR:
Author.
Alzheimer’s Association. (2011). Stages of Alzheimer’s disease. Retrieved from
http://www.alz.org/alzheimers_disease_stages_of_alzheimers.asp
Alzheimer’s Association. (2011). Inside the brain: An interactive tour. Retrieved from
http://www.alz.org/alzheimers_disease_4719.asp
Alzheimer’s Challenging Behaviors Task Force (2010). Handcuffed. Milwaukee, WI: Author.
Cohen, R. (2009). The role of the immune system in Alzheimer’s disease. Focus, The Journal of
Lifelong Learning in Psychiatry, 7 (1), 28-35.
Kovach, C., Logan, B., Noonan, P., Schlidt, A., Smierz, J., Simpson, M., & Wells, T., (2006).
Effects of the serial trial intervention on discomfort and behavior of nursing
home residents with dementia. American Journal of Alzheimer’s Disease and
Other Dementias, 21 (3), 147-155.
Lippens, G., Sillen, A., Landreau, I., Amniai, L., Sibille, N., Barbier, P., Leroy, A., Hanoulle, X.,
& Wieruszeski, J., ( 2007). Tau aggregation in Alzheimer’s disease. Prion, 1 (1), 21-25.
Mandrekar-Colucci, S., Landreth, G., (2010). Microglia and inflammation in Alzheimer’s
disease. CNS & Neurological Disorders Drug Targets, 9. Retrieved from
http://www.biomedsearch.com/nih/Microglia-Inflammation-in-Alzheimers-Disease
/20205644.html
REFERENCES
Menon, R. and Lutsep, H. (2011). Cerebral amyloid angiopathy. Retrieved from http://
emedicine.medscape.com/article/1162720-overview.
National Institute on Aging. (2008). Alzheimer’s disease genetics fact sheet (NIH Publication
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