alzheimers pres

8/3/2019 Alzheimers Pres

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DEATH OF THE

NEURON FOREST

An in depth look at AlzheimersDisease and it progression



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



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



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)



An estimated 5.4million Americanshave Alzheimersdisease

1 in every 8 peopleage 65 or older hasAlzheimers

Expected to be ashigh as 16 million by2050



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



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.



Further divided into lobes that house the

various a

reas of function and cognition



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.



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).



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%



Early signs and symptoms

Mild memory loss

Forgetting words

or

names Difficulties in

± registration

± comprehension

± learning

± task execution

± language use



Later terminal stage symptoms

Memory impairment,

Deficits in reasoning

and judgment,

Loss of ability in regard

to abstract thought

and clouding of

consciousness.



AIDS,

Alzheimers

Vitamin B12deficiency

Carbon

monoxidepoisoning

Subdural

hematoma

and multiple

brain infarcts



Dementia in regard to

Alzheimers is asymptom while

Alzheimers is the

disease causing the

condition.



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.



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.



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.



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.



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.



Plaques and tangles (shown in the blue-shaded areas) tend to

spread through the cortex in a predictable pattern as

Alzheimer's disease progresses.



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%



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



Based on 2011 NIA-AA Workgroups Recommendations



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



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



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.



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.



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.



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.



-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.



Risk Factors: Modifiable

Heart Health Blood pressure

Heart disease

High cholesterol

Diabetes

Head Trauma Repeatedly or involves

loss of consciousness

Safety precautions



Reducing your risk: ±Exercise

±Dont smoke ±Control blood pressure

±Control cholesterol

±Manage diabetes well ±Mental Stimulation

±Stay socially interactive

±Healthy weight

±Avoid excess alcohol



Diagnostics

AssessmentPatient history

± Symptoms

Duration

Progression

Course

± Changes

Memory Forgetfulness

Behavior/Personality

Sense of smell



Physical

assessment ± Changes in

cognition

Folsteins Mini-

mental exam

Set test

± Changes in mood

± Self-managementskills



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



Imaging and Other Diagnostics

Imaging

± CT

± PET

± SPECT

± MRI

Neuropsychological tests

± Showing progression of disease



Treatment Goals for AD

± Slow the progressionof the disease

± Manage behavior problems, confusion,

sleep problems, andagitation

± Modify the homeenvironment

± Support familymembers and other caregivers



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)



Antidepressants which are

not anticholinergics

Sertraline(Zoloft),

paroxentine(Paxil)

Psychotropic Drugs- Used

for behavioral problems

Risperdal (risperidone)

Quetiapine(Seroquel)



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


f requency of bowel

movements.

memantine Namenda Moderate to severe Headache, constipation,

confusion and dizziness.

rivastigmine Exelon Mild to moderate Nausea, vomiting, loss of


f requency of bowelmovements.

tacrine Cognex Mild to moderate Possible liver damage,

nausea, and vomiting.



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



Music Therapy

Self Expression Improve mood, promote

relaxation

Decrease wandering and

restlessness

Slows decline in physical,

psychological and

cognitive processes

Stimulates recollection

of memories



Animal Therapy

Stimulate social

interaction

Ease agitation

Companionship

Promote

physical activity



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



Improving Quality of life

Always consider patients interests and abilities Structure & routine is important

Encourage and give praise often

Compassion and patience a must



Caring for your Alzheimers Pt.

Use simple

words

Speak slowly Show what you

are saying

Smile



Activities of daily

living

Bathing

Dressing Eating

Safety



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.



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



Eating & Nutrition

View mealtimes as

opportunities for

social interaction

Aim for a quiet,

calm, reassuring

mealtime

atmosphere



Safety

Identification or medical bracelet

Alzheimers Association Safe Return program

Environment

Plan ahead

± Notify neighbors and local authorities



The biggest issue with AD Pts

Sundowners

Syndrome

E nd -o f-d ay

activit y

F atigue

Low light



How to calm your pt

E stablish a routine

Monit or ing d iet

C ont rolling noise



Caregivers

Family most

prominent

Respite Care

Understanding that

caring for themselves

is primary

Accepting the role as

caregiver



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



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



Questions???

Thank you for your time and attention

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