alzheimer's disease- systems and disease III

alzheimer's is the most common form of?

progressive degenerative brain disease

clinically alzhiemers is characterized by

slow decline in memory, language, cognition, visuospatial skills and impaired judgment

alzheimer's causes changes in which lobes?

temporal and prefrontal cortex

T/F individual with diabetes will have faster rate of progressive of alzhimer's

true

T/F the rate of progression of alzheimer's is the same for everyone

false

this disease alone or in combo with other pathologies accounts for up to ___% of dementia in the USA

90

prevelance of AD among ppl aged 65 or older is ______% and above 80 it ranges from ______%

8-10%
30-45%

risk factors of AD

increasing age
family hx
female gender (b/c females live longer and lower estrogren after menopause)
brain trauma
down syndrome
cerebrovascular disease
head trauma
long-term HTN
exposure to electromagnetic fields

give me pathophysiology of AD

synaptic dysfunction and loss
senile or neuritic plaque: dying neurons, glial cells and beta-amyloid protein
neurofibrillary tangles
decreased or loss acetylcholine
decreased monosamines (dopamine and norepinephrine)

first area that is affected in AD

hippocampus (medial temporal lobe)

main functions of temporal and frontal lobes

frontal: motor, intelligence, judgement, behavior, and language
temporal: memory and language

why does brain size decrease with AD?

atrophy of brain; volume of grat and white matter decrease
more prominent sulci and ventricles
CSF fills spaces

in coronal cut of AD brain, what will we see?

increased size of ventricles

within or outside neuron? plaques and neurofibrillary tangles

plaques: outside neuron
neurofibrillary tangles: within neuron

first symptom of AD

memory dysfunction

TMA cognitive deficits of AD

difficult to learn new info

factual info usually intact

loss of semantic knowledge (word meanings)

decreased generic knowledge (how many days in year)

difficult comprehension

difficulty completing sentences

severe memory loss in late stage

disorientation

language disturbances

apraxia: develops later in disease and may results in decrease in ability to dress and eat (can't carry out purposeful mvmt)

TMA language disturbances in AD

they can have long pauses in speech due to difficulties in word finding (anomia)
simpler speech patterns and vocabulary

TMA visual and spatial difficulties those with AD face

frequently get lose while driving

inability to recognize friends and family members

problems with reading or depth perception

wandering

drawing is abnormal

cannot draw 3-D object

AD S/S non-cognitive

denial

unawareness of illness (anosognosia)--> NO, NO i do not have

lack of motivation

reduced affection

periods of depression

aggression, agitation, anxiety

loss of inhibitions (check)

physical S/S AD

impaired mvmt
rigidity
mm twitch
seizures
dragging feet
poor sleep patterns

stages of AD

1: no cognitive impairment

2: very mild decline

3: mild decline--> word or name finding problems (agnosia), misplaces valuable objects, sucks at planning

4: moderate cognitive decline--> decreased knowledge on recent events, impaired ability to perform arithmetic

5: moderately severe decline--> unable to recall important details such as address, phone number, college/school, confused on date, need help getting dressed

6: severe decline--> disruption of sleep/wake cycle, repetitive behaviors, hallucinations/aggressiveness, need help getting dressed/going potty

7: severe decline--> lose ability to walk, need a lot of help with ADL's, lose ability to smile, mm rigid

T/F we can diagnose AD with MRI and size of ventricles

false; there is no definitive test for AD, a true diagnosis can only be made after a person dies and an autopsy is performed on brain

tests that may aid in diagnosis

psychological test: for memory and attn span
EEG (electroencephalography): brave-wave activity
blood test: Apo E4 gene
CT
MRI
PET

T/F in early stages of AD we will see decrease in brain size

false; we cannot see this until later stages

common screening test for patient with AD

draw clock test; pts with AD will not be able to draw clock face with hands at quarter to two

Is there any effective tx for AD to stop the nerve cell death?

no but there's medication that targets to stop the breakdown of ACH in brain and alleviate symptoms of depression, anxiety, and delusions

three medications used to improve intellectual function in pts with mild to moderate AD up to 18 months

cognex, aricept, and exelon

what does cognex, aricept, and exelon do?

breakdown Ach in brain and thereby increasing the brains level of Ach which helps restore communication in brain cells

aricept and tacrine facts

aricept= most effective earlier in AD and has fewer side affects
tacrine= modest benefits and not good for those who carry ApoE4 gene

what is the only drug approved for tx of moderate to severe AD

namenda

treats withdrawal and apathy

methylphenidate

anti seizure drug and used to treat agitation

carbamazepine

treats depression

SSRIs

T/F estrogen pills worsen AD

nah they may lower the rates of AD (in postmenopausal)

T/F those who regularly take aspirin will reduce risk of AD

true

vitamin thought to delay AD

vitamin D

average live of patient with AD

8 years

most common cause of death of a patient

AD is infxn (pneumonia)

PT implications of AD

stretching
endurance activities
strengthening activities
aerobic activities
exercise with music