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DEATH OF THE
NEURON FOREST
An in depth look at AlzheimersDisease and it progression
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Presented by:
Kaila W illiams
Alexis Puente-Smith
Michelle Olive
Dave McCl ur e
Laur en Good man
Jason Card iff
Anjana Mitter
Dor i Nelsen
T erry Smiley
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We will cover
Stats and info
About the brain
Dementia
Alzheimers The stages of AD
Risk factors / Diagnosis
Treatment and Medications
Your Alzheimers patient
Wrap it up
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What is Alzheimers Disease?
Dementia is a syndromecharacterized bymultiple cognitive
deficits
AD is the most common
form of Dementia(estimated 60%-80% of
all cases)
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An estimated 5.4million Americanshave Alzheimersdisease
1 in every 8 peopleage 65 or older hasAlzheimers
Expected to be ashigh as 16 million by2050
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Estimated 3.5million formally
trained health care
professionals will
be needed by
2030 to meet the
needs of the
dementiapopulation alone
National Academy of Sciences, 2010
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Cerebrum
Involved in
remembering,
problem solving,
thinking, and feeling.It also controls
movement.Cerebellum
It controls
coordination and
balance.
Brain stem
It connects the brain to the
spinal cord and controls
automatic functions such as
breathing, digestion, heart rate
and blood pressure.
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Further divided into lobes that house the
various a
reas of function and cognition
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An adult brain contains about
100 billion nerve cells
(neurons) that connect at
more than 100 trillion points.
Signals traveling through
the neuron forest form the
basis of memories, thoughts,
and feelings.
Neurons are the chief type of
cell destroyed by Alzheimer's
disease.
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Signals move through anindividual nerve cell as a
electrical charge. Nerve cells connect at
synapses.
C
harge
reaches asynapse, triggering the
release of neurotransmitters.
Neurotransmitters travelacross the synapse,carrying signals to other cells (neurons).
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Dementia
A progressive,
irreversible decline in
mental function
The onset is slow and
can range f rom months
to years
Highest in those older
than 85 at 24-47%
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Early signs and symptoms
Mild memory loss
Forgetting words
or
names Difficulties in
± registration
± comprehension
± learning
± task execution
± language use
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Later terminal stage symptoms
Memory impairment,
Deficits in reasoning
and judgment,
Loss of ability in regard
to abstract thought
and clouding of
consciousness.
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AIDS,
Alzheimers
Vitamin B12deficiency
Carbon
monoxidepoisoning
Subdural
hematoma
and multiple
brain infarcts
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Dementia in regard to
Alzheimers is asymptom while
Alzheimers is the
disease causing the
condition.
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Alzheimer's disease leads to nerve cell death and
tissue loss throughout the brain.
Over time, the brain shrinks dramatically,
affecting nearly all its functions.
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The cortex shrivels
up, damaging areas
involved in thinking,
planning andremembering.
Shrinkage is
especially severe in
the hippocampus,an area of the
cortex that plays a
key role in
formation of new
memories.
Ventricles (fluid-
filled spaces within
the brain) grow
larger.
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Alzheimer's tissue has
fewer nerve cells and
synapses than a healthy
brain.
Plaques, abnormal clusters
of protein f
ragments, build
up between nerve cells.
Dead and dying nerve cells
contain tangles, which are
made up of twistedstrands of tau protein.
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Plaques form when protein
pieces called beta-amyloid
(BAY-tuh AM-uh-loyd) clumptogether.
Beta-amyloid is chemically
"sticky" and gradually builds
up into plaques.
The small clumps may block
cell-to-cell signaling at
synapses and may also
activate immune system cellsthat trigger inflammation
and devour disabled cells.
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In healthy areas:
The transport system is
organized in orderly
parallel strands
somewhat like railroad
tracks. Food molecules,
cell parts and other key
materials travel along
the "tracks."
A protein called tau
(rhymes with wow)
helps the tracks stay
straight.
In areas where tangles are forming:
Tau collapses into twisted strands calledtangles.
The tracks can no longer stay straight.
They fall apart and disintegrate.
Nutrients and other essential supplies
can no longer move through the cells,
which eventually die.
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Plaques and tangles (shown in the blue-shaded areas) tend to
spread through the cortex in a predictable pattern as
Alzheimer's disease progresses.
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Overview of
AD Staging
Original criteria created 1984
2011 recommendations provide for 3 major stages and consolidateprevious stages into one Dementia stage
Staging is difficult: AD is a continuous process and boundaries can bedifficult to define
Better diagnosis during Preclinical and Mild Clinical Impairment Stages
mayresult in lifetime savings of 50%
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Alzheimers Disease Stages
Based on 2011 NIA-AA Workgroups Recommendations
Disease
PhasesPreclinical MCI Alzheimer's Disease Dementia
Level of
Disability
Biomarkers
No clinical
ADLs
Unimpaired
Mild or
Stage I
Moderate
or Stage II
Severe or
Stage III
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Based on 2011 NIA-AA Workgroups Recommendations
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Preclinical Stage
Biomarkers appear an average of 10 years
before mild cognitive impairments
Amyloid- peptide accumulation proposed
as key early event
Neurodegeneration accelerates process,
resulting in subtle cognitive decline
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Mild Cognitive Impairment (MCI) Stage
Concern regarding a
change in cognition
Impairment in one
or more cognitivedomains
Preservation of
independence in
functional abilities
No dementia
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Alzheimers Dementia: Mild or Stage I
Difficulty with newlearning and makingnew memories.
Trouble finding
words. Easily loses way going
to familiar places.
Has trouble
organizing andthinking logically.
Loses judgmentabout money.
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Moderate or Stage II
Changes in behavior, concern
for appearance, hygiene, andsleep become morenoticeable.
Mixes up identity of people.
Has restless, repetitivemovements in late afternoonor evening.
Has trouble following written
notes or completing tasks.
Needs help finding the toilet,using the shower,remembering to drink, anddressing for the weather or
occasion.
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Severe or Stage III
Doesn'trecognize self or close family.
May refuse to eat,chokes, or forgets toswallow.
Loses control of boweland bladder.
Forgets how to walkor is too unsteady or
weak to stand alone.
Needs total assistancefor all activities of daily living.
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Risk Factors: Non-modifiable
Age is the greatest knownrisk factor
->65 years old
-doubles every 5 yrs
->85 years old, 50% chance
-woman live longer
Family history:
-close family member
-increases more if multiple
family members are affected.
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-Risk genes
apolipoprotein E-e4 (APOE-
e4) Found in 1993
-Deterministic genes
amyloid precursor protein
(APP), presenilin-1 (PS-1)
and presenilin-2 (PS-2).
Autosomal Dominant
Alzheimer
s Disease(ADAD) Will develop
around ages 40-50.
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Risk Factors: Modifiable
Heart Health Blood pressure
Heart disease
High cholesterol
Diabetes
Head Trauma Repeatedly or involves
loss of consciousness
Safety precautions
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Reducing your risk: ±Exercise
±Dont smoke ±Control blood pressure
±Control cholesterol
±Manage diabetes well ±Mental Stimulation
±Stay socially interactive
±Healthy weight
±Avoid excess alcohol
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Diagnostics
AssessmentPatient history
± Symptoms
Duration
Progression
Course
± Changes
Memory Forgetfulness
Behavior/Personality
Sense of smell
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Physical
assessment ± Changes in
cognition
Folsteins Mini-
mental exam
Set test
± Changes in mood
± Self-managementskills
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Laboratory
Tests No definitive diagnosing
lab test
Genetic testing
± Apolipoprotien E4 (Apo E4)
± Amyloid beta protein
precursor (soluble) (sBPP)
Other lab tests
± To rule out other causes of
dementia or
delir
ium CBC, Electrolytes, ETOH
screening, Thyroid and liver
function test, and Syphilis
screening
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Imaging and Other Diagnostics
Imaging
± CT
± PET
± SPECT
± MRI
Neuropsychological tests
± Showing progression of disease
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Treatment Goals for AD
± Slow the progressionof the disease
± Manage behavior problems, confusion,
sleep problems, andagitation
± Modify the homeenvironment
± Support familymembers and other caregivers
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Drug classes for treatment of Alzheimers
C
holinester
ase inhibitor
s Donepezil ( Aricept)
Galantamine(Reminyl)
Rivastigmine (Exelon)
Tacrine (Cognex)
NMDA( N-methyl-D-
aspartate) receptor antago
Memantine(Namenda)
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Antidepressants which are
not anticholinergics
Sertraline(Zoloft),
paroxentine(Paxil)
Psychotropic Drugs- Used
for behavioral problems
Risperdal (risperidone)
Quetiapine(Seroquel)
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Generic Brand Approved For Side Effects
donepezil Aricept All stages Nausea, vomiting, loss of
appetite and increased
f requency of bowel
movements.
galantamine Razadyne Mild to moderate Nausea, vomiting, loss of
appetite and increased
f requency of bowel
movements.
memantine Namenda Moderate to severe Headache, constipation,
confusion and dizziness.
rivastigmine Exelon Mild to moderate Nausea, vomiting, loss of
appetite and increased
f requency of bowelmovements.
tacrine Cognex Mild to moderate Possible liver damage,
nausea, and vomiting.
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Non-Phar macol ogic T her apy
For Alzheimer and Dementia Patients
Meaningful therapy CAN enrich patient &
caregivers lives
Consider patient interests and abilities
Boost patients self esteem & reduce stress
Instill sense of stability Keep it simple
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Music Therapy
Self Expression Improve mood, promote
relaxation
Decrease wandering and
restlessness
Slows decline in physical,
psychological and
cognitive processes
Stimulates recollection
of memories
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Animal Therapy
Stimulate social
interaction
Ease agitation
Companionship
Promote
physical activity
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Garden Therapy Connect patient tonature
Reduce stress;
Lowe
r Blood Pressure
Maintain circadiancycle (sleep/wake
cycle) Vitamin D = Healthy
Bones
Physical exercise
Most importantestablish a routine
Increase stability
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Improving Quality of life
Always consider patients interests and abilities Structure & routine is important
Encourage and give praise often
Compassion and patience a must
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Caring for your Alzheimers Pt.
Use simple
words
Speak slowly Show what you
are saying
Smile
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Activities of daily
living
Bathing
Dressing Eating
Safety
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Bathing Plan the bath or
shower for the
time of day whenthe person is mostcalm andagreeable.
Tell the personwhat you are goingto do, step by step,
and allow him or her to do as muchas possible.
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Try to have the person
get dressed at the
same time each day
Encourage the person
to dress himself or
herself to whatever degree possible.
Allow the person to
choose f rom a limitedselection of outfits.
Dressing
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Eating & Nutrition
View mealtimes as
opportunities for
social interaction
Aim for a quiet,
calm, reassuring
mealtime
atmosphere
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Safety
Identification or medical bracelet
Alzheimers Association Safe Return program
Environment
Plan ahead
± Notify neighbors and local authorities
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The biggest issue with AD Pts
Sundowners
Syndrome
E nd -o f-d ay
activit y
F atigue
Low light
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How to calm your pt
E stablish a routine
Monit or ing d iet
C ont rolling noise
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Caregivers
Family most
prominent
Respite Care
Understanding that
caring for themselves
is primary
Accepting the role as
caregiver
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Possible Nursing Diagnosis
Chronic confusion R/T disease progression (AD)
Risk for Injury R/T wandering, elder abuse or mistreatment
C
ompromised
Family coping and
Caregive
rRoleStrain R/T patients prolonged progression of
disability and increasing care needs
Self-care Deficit R/T cognitive deficit
Imbalance Nutrition
L
ess than BodyRequirements R/T self-care deficit and/or anorexia
Lets Review
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Let s Review What are plaques made of?
Beta amyloid polilopoprotiens
What are tangles made f rom?
Detached tau protiens
W
ho is most atrisk fo
rAlzheime
rs?
People over 65
What are the cognitive affected by Alzheimers?
Primary motor function, symantics vision and speech, establishment
of new memories, and regulation of unconscious muscle activity
Can neurons be regenerated?
NO
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Questions???
Thank you for your time and attention