Alzehimers Flashcards by Kelsey Con

what is dementia

decline in mental ability servere enough to interfere with daily activities
a SYMPTOM

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brain changes usually start in the hippocampus so the first symptom that presents is

selective memory impairment

then progresses to other parts of the brain and get sensory and motor impairment

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what are the hallmark brain changes

diffuse neuritic plaques
plaques display marked amyloid beta deposition
neurofibillary tangles made up of phosphorylated tau protein

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risk factors

age - over 65 
hyperlipidemia 
hypertension 
CVB
genetic - for rare early onset 
physically inactive 
brain trauma 
obese
diabetes
reduced brain capacity

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way to distinguish cognitive decline due to normal aging from dememntia

dementia forget more recent events
normally aging you are worried about your memory, in dementia the relative are worried but you are not
dementia can forget a family member name

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3 essential things neurons must do

communicate with each other, carry out metabolism , repair themselves

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issues with caregivers for these peopl

takes a huge physical and psychological toll on the person caring for someone with alzheimers

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when does the pathological processes begin

decades before symptoms present

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does severity of disease correlate to the plaque burden

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some brain changes that occur

NFT and amyloid plaque accumulation 
decrease in functing synapses
reducting in accetylcholine
cell death brain atrophy 
vascular dysfuncton....

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neurogeneration due to accumulation of

neurofibrillary tangles

amyloid plaques

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hallmarks of alzheimers

neuritic plaques

neurofibrillary tangles

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what are the plaques

formed from protein pieces that stick together

block cll to cell siignaling at the synaps

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what are nuerofibrillary tangles

collapsed and twisters fibers of protein called tau that build up insde the nerve cell
tau normally helps to stabalize the transport system for essential materials
wihtout this the nerve cell will die

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neurotransmitter changes

reduced activity of choline acetyltransferase which makes acetylcholine
loss of certain nicotinic receptor subtypes which reuptake ach
reduced number of cholinergic neurons

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symptoms of alz

poor recall 
aphasia - language loss 
decreased motivation 
anosognosia - reduced self awareness
irritable 
wandering 
psychosis 
sleep disturbance
seizure
motor disturbance

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other possible causes of cognitive decline

drugs
neurologic disease - stroke
illness - anemia, thyroid, get a blood test to rule out 
surgery 
environment

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what are some red flags that require neuroimaging to rule out other things

<60o 
new onset 
rapid progression 
head trauma 
cancer histoyr 
anticoagulant use
early incontinence and gait disorde

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anticholinergics that contribute to cognitive decline

antihistamines
antipsychotics
tricyclic antidepressants
antiemetics
oxybutynin
ranitidine

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psychoactive drugs that cause cognitive decline

alcohol 
anticonvulsants
antidepressant 
antiparkinsons
muscle relaxant
antipsychotic
opioids
sedative hypnotics
anything that causes cns depression

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other drugs that cause cognitive decline

ciprofloxacin
clarithromycin 
antiarrythmics
digoxin 
nsaids
corticosteroids

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commnly used cognitive test

mini mental state exam

used to estimate severity and monitor change incognitive impairment during therapy

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what is required for anticholinesterase coverage

MMSE 10-26

mild-mod

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normal vs agressive drop in MMSE score

normal to drop 1-2 points a year

>3 bad

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what is sundowning

rapid decline in function in hte evening

mild dementia

learning and memory impairment language difficulty inability to form purposeful movements

moderate dementia

``` long term memory loss inability to recognise close relatives aimless wandering emotional change urinary incontinence ```

severe dementia

complete loss of speech severe apathy and exhaustion bedriden death

secondary prevention measures

``` mediterranean diet statin? treat hypertension exercise and cognitive training cognitive reserve from higher education ```

is there a cure for alzheimers

how do cholinesterase inhibitors help

stabilize/slow disease may help with some symptoms doesnt fix the problem inhibit anticholinesterase so less ach breakdown

side effect of cholinesterase inhibtors

urinary incontinence stimulating GI fall risk

drugs for mild - mod

cholinesterase inhibtors

examples of cholinesterase inhibitors

donepazil rivastigmine galantamine

drugs for mod-severe disease

add anti glutamatergic or alone | memantine

which cholinesterase inhibitor can be used in severe disease

donepazil

should take cholinesterase inhibitors with

food

is one cholinesterase better than the other

no trials to demonstrate this

efficacy of ChEI

benefit for about 6-9 months then graduall decline | limited data on relevant outcomes adn there is no delay in institutionalization

side effects of ChEI

dose depended GI - vomit, diarrhea, anorexia insomnia likely to occur at start of treatment of dose escalation prevent by longer titration and taking wiht foo d

contradindications for ChEI based on conditions affected by increasing cholinergic tone

cardiac conduction abnormalities , bradycardia active PUD - cheis increase gastric acid secretion asthma/copd

when discontinuing ChEIs taper by

25-50% every week to min rebound constipation

memantine MOA

blocks the sustained activation of NMDA receptors cause by abnormal glutaminergic activity NMDA antagonist

memantine indication

moderate to severe | not mild

problems with memantine

BID dosing not covered by pharmacare many DI not recommended in severe liver impairment

memantine side effects

``` dizzy constipation confusion headache hypertension ```

cautions of memantine

seizures and CV disease

how do you mnage sleep disturbances

suggest non pharms first and look for causes | trazadone or zoplicone but not benzos or OTCs

what are some behavioural and psychological symptoms of dementia

depression anxiety psychosis agitation

causes of BPSD

``` poor sleep physical confitions sensory overload disruption of routine sensory deficits.... ```

what does PIECES stand for in the causes of dementia

``` physical intellectual emotional cultural environmental social ```

non drug measures for BPSD

``` ABC charting - note of cuases reduce noise avoid changes in surroundings schedule activities lots of physical activity discourage naps caregiver education critical ```

when might antopsychoics be potentially appropriate

hallucinations delusions aggressive behaviour

when are psychotics appropriate

if the symptom presents danger significant decline in function persistent distress

when are antipsychotics inappropriate

``` wandering, incooperative unsociability mild anxiety impaired memory doesnt represent a danger ```

AE associated with anitpsychotics in alzehiemers

``` death stroke weight gain hyperlipidemia/glycemia sedation, falls anticholinergic* urinary infection ```

does BPSD resolve

usually spontaneously resolves or responds to psychosocial intervention

causes of delirium

metabolic disorders - thyroid, diabetes illness drug and drug witjdrawal street drugs

delirium vs dementiia

delirium is more acute and abrupt with a fluctuating course affects alertness and vitals as well attention impaired

are estrogen or nsaids recommended

observational studies prospective trials dont show benefit not recommended

are statins recommended

only if patient has other indications for statin use

are vit E and gingko biloba recommended

no get NV, diarrhea vit e can cause death

is polyphenol recommended

no recommendation

estimation of severity based on MMSE score

mild: 20-26 mod: 10-19 severe: <10

dosing and timing of antipsychotics for BPSD

start low go slow time based on behavior pattern titrate up every 1-2 weeks

which is the only antipsychotic officially labelled for use in BPSD

risperidone

reasons to discontinue ChEIs

rapid progression - MMSE decrease 2 or more in 12 months symptoms deteriorate in 3-6 months of therapy persistant side effects poor adherence