Alzehimers Flashcards
what is dementia
decline in mental ability servere enough to interfere with daily activities
a SYMPTOM
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
what are the hallmark brain changes
diffuse neuritic plaques
plaques display marked amyloid beta deposition
neurofibillary tangles made up of phosphorylated tau protein
risk factors
age - over 65 hyperlipidemia hypertension CVB genetic - for rare early onset physically inactive brain trauma obese diabetes reduced brain capacity
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
3 essential things neurons must do
communicate with each other, carry out metabolism , repair themselves
issues with caregivers for these peopl
takes a huge physical and psychological toll on the person caring for someone with alzheimers
when does the pathological processes begin
decades before symptoms present
does severity of disease correlate to the plaque burden
no
some brain changes that occur
NFT and amyloid plaque accumulation decrease in functing synapses reducting in accetylcholine cell death brain atrophy vascular dysfuncton....
neurogeneration due to accumulation of
neurofibrillary tangles
amyloid plaques
hallmarks of alzheimers
neuritic plaques
neurofibrillary tangles
what are the plaques
formed from protein pieces that stick together
block cll to cell siignaling at the synaps
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
neurotransmitter changes
reduced activity of choline acetyltransferase which makes acetylcholine
loss of certain nicotinic receptor subtypes which reuptake ach
reduced number of cholinergic neurons
symptoms of alz
poor recall aphasia - language loss decreased motivation anosognosia - reduced self awareness irritable wandering psychosis sleep disturbance seizure motor disturbance
other possible causes of cognitive decline
drugs neurologic disease - stroke illness - anemia, thyroid, get a blood test to rule out surgery environment
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
anticholinergics that contribute to cognitive decline
antihistamines antipsychotics tricyclic antidepressants antiemetics oxybutynin ranitidine
psychoactive drugs that cause cognitive decline
alcohol anticonvulsants antidepressant antiparkinsons muscle relaxant antipsychotic opioids sedative hypnotics anything that causes cns depression
other drugs that cause cognitive decline
ciprofloxacin clarithromycin antiarrythmics digoxin nsaids corticosteroids
commnly used cognitive test
mini mental state exam
used to estimate severity and monitor change incognitive impairment during therapy
what is required for anticholinesterase coverage
MMSE 10-26
mild-mod
normal vs agressive drop in MMSE score
normal to drop 1-2 points a year
>3 bad
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
no
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
