Cognitive Impairment Flashcards
define cognition
the operation of the mind by which we become aware of objects of thought or perception- includes all aspects of perceiving, thinking, and remembering
define delirium
a clinical state characterized by fluctuating disturbance in cognition, mood, attention, arousal, and self awareness, which arises acutely either without prior intellectual impairment or superimposed on chronic intellectual impairment
define dementia
a deterioration of intellectual function and other cognitive skills, leading to a decline in the ability to perform ADL
what is the msot common type of dementia
alzheimer’s
dementia impacts
1. memory
2. function
3. thinking
4. al of the above and more
4
what is the new term in the DSM used for cognitive impairment
neurocognitive disorder
what is pseudodementia
dementia is mimicked by functional psychiatric illness
Alzheimer’s has
1. increased worldwide
2. only increased in wealthier countries
3. more effect on men
4. all of the above
1
what are some medications that directly cause cognitive impairment`
Anticholinergics
Psychotropic: BZDs, neuroleptics
Ethanol
Opioids
what are some medications that indirectly cause cognitive impairment
Diuretics (ex- electrolyte abnormalities)- most common
Withdrawal of medications
what are the 5As of cognitive changes
aphasia
apraxia
agnosia
abstraction
ADL
difficulty finding the right word is called
aphasia
not having purposeful movement patterns is called
apraxia
the inability to recognize and identify objects or people is called
agnosia
difficulty in realizing and formulating a plan to achieve goals is called
abstraction (lack of)
describe 2 cognitive screening tests
clock drawing test
MMSE
MoCA
SLUMS, RUDAS
watermelon seeds
Alzheimer’s is a progressive disease of the brain of _____ etiology characterized by diffuse atrophy throughout the _______ with distinct histopathologic changes termed ________ and ________
unknown
cerebral cortex
senile plaques
neurofibrillary tangles
name the 6 etiologies of alzheimers
genetics- chromosomes 1, 14, 21- ApoE presence
deposition of foreign bodies
dysreg of NT
inflam
environmental agents
vascular RFs
what are some modifiable RFs for alzheimers
Smoking
Diabetes
Diet - high trans saturated fats
Obesity- midlife vs late life
Hyperlipidemia
hypertension
early life RF for alzheimers is
less education
name 3 ways to decrease risk for alzheimers
Nutrition- fruits and veg, lower saturated fats
Physical exercise
Hearing- address and assess sx
Sleep- addressing OSA< avoiding deprivation
Cognitive training, stimulation- individual or group based
Social engagement and education
Poverty reduction, social engagement
Early life educational attainment
Frailty- manage early
Medications- avoid exposure to anticholinergics
Address modifiable health conditions
name 3 things that are protective against alzheimers
Periodic and low amongst of alcohol (binge drinking increases risk)
Cognitive reserve- higher education
Physical activity/ exercise
Other
Diet (mediterranean)- low red meat, olive oil, fish, etc
Multilingualism
Marriage
Social activity/ engagement
describe the characteristics of early alzheimers
Insight retained
Word loss
Minor forgetfulness/ decreased STM
describe characteristics of intermediate stage AZD
Loss of insight
Behavioral disturbances
describe the characteristics of late stage AZH
Nonresponsive
Loss of language
what is retrogenesis
forgets memories in reverse
Forgets retirement → children → marriage → spouses name → etc
what is the prognosis of alzheimer’s
up to 20yrs
how are alzheimer’s diagnosis made
interview of family/caregivers, neuro and physical exam, CT/MRI head, neuropsychological testing, CXR, ECG, EEG, blood work (CBC, electrolytes, Ca, Mg, etc), review of medications, assessment of substance use
research criteria of AD is
focus on biomarkers and PET
what is a definite AD dx
All criteria for probable AD + histopathologic evidence (brain sample)
what is a probable AD dx
Prog impared memory, cognitive function, multiple domains affected, onset >40yrs
No biopsy taken- no NFT or plaques to confirm, but everything else consistent
what is a possible AD dx
Atypical, gradually progressive decline, one domain affected
what is a major neurodegenerative disorder
Evidence of cognitive decline from previous level of performance (ex- used to be a chief and now can’t cook an egg)
Interferes with independence in everyday activity
Insidious onset and gradual progression of impairment
T or F: there is no cure for AD
T
what are 2 sx tx for AD
Cholinesterase inhibitors
memantine
what are 2 potentially disease modifying AD tx
aducanumab, lecabenab
name the 3 ACh increasing medicatiosn
donepezil
rivastigmine
galantamine
which ACh med is for mild-severe AD
donepezil
donepezil elimination in the
liver
SEs of ACh increasing meds include
N/V, bradycardia, insomnia, muscle cramps, fatigue, urgency, asthma exacerbation
CIs for ACh meds (6)
active PUD
anorexia
bradycardia
asthma
QT prolongation
seizures
how effective are AChE-i
med- effect of ~1 point difference which is not v detectable
expectations for AChEi in AD
stabilization and maintenance of cog fxn over time
stabilize decline
improve caregiver burden
how long should AChEi be trialed
3-6mths
is one AChEi superior to another
no
when should AChEi be dosed?
Better adherence in morning, but if GI effects or dizziness = PM to sleep through the nausea and SEs + don’t avoid eating all day resulting in more weight loss
T or F: AChEi requires titration
T- initial dose will be subtherapeutic
when is washout necessary for AChEi
if SEs (washout for <7d) and switching to another drug
is you want to switch from donepezil to rivastigmine and pt has no SEs, is washout necessary?
no- just switch to eq dose immediately
what is the bottom line on AChEi effectiveness
Benefit is modest, early initiation is beneficial, SEs often poorly tolerated by older adults
memantine is a
NMDA receptor antagonist
memantine MOA
prevents calcium influx, dysregulation, and cell death from ↑ GLU of AD
can memantine be used with CI
yes- different MOA
memantine indications
Mod-severe AD (can use this after pt progresses on CI)
Monotx or as adjunct with CI
mementine is eliminated in the _______ and is _____ dependent
urine
pH dependent
SEs of mementine
In first mth, pts may actually have increased confusion, that usually resolves and pt improves- generally well tolerated
Increased BP, corneal ADD
which med should AD pts with asthma and bradycardia use
mementine
memantine 20mg saw slight improvements in AD pts in
cog fxn
ADL
behaviour and mood
what may be used instead of AP in AD pts to manage behaviours
memantine
what is mild cognitive impairment
predementia- not necessarily progressing
day to day activities not yet impacted
how should predementia be treated
nonpharm only- exercise, cog training, planning, smoking cessation
AChEi harmful
what is the most common type of nonAD dementia
vascular dementia
vascular dementia onset is
sudden or gradual
VaD progression, neuro findings, and memory
progression = slow and stepwise
neuro = evidence of focal deficits
memory = mildly affected
vascular dementia executive function impairment is
early and severe
vascular dementia type is _________ while AD is ________
subcortical
cortical
vascular dementia effect on gait vs AD
vasc = disturbed early
AD = normal
describe Lewy body dementia, parkinson disease dementia
If lewy bodies seen first then movement disorder = Lewy body dementia
If movement issues seen first, then lewy bodies = PD dementia
Brains look the same after few years, even if different start
pathophys of If lewy bodies dementia/ PK dementia
lewy bodies deposited = disruption in substantia nigra + cerebral cortex = Neurotransmitter alterations
how to differentiate between lewy body dementia and PK
duration of PK in relation to dementia
3 core features of Lewy body dementia, parkinson disease dementia
fluctuations in cognition, visual hallucinations, parkinsonism
how to treat Lewy body dementia, parkinson disease dementia
rivastigmine, other CIs
Lewy body dementia, parkinson disease dementia is sensitive to ___________ and should be avoided
neuroleptics
what is frontal dementia
just the frontal lobe affected = personality, emotions, itneractions changed
which has earlier onset: frontal or lewy/ PK dementia
frontal
the main pathophys of frontal dementia is
deficits in 5HT
disinhibition and personality changes describes
1. AD
2. lewy body dementia
3. vascular dementia
4. frontal dementia
4
how to treat frontal dementia (choose all that apply)
1. AChEi
2. memantine
3. caregiver support
4. SSRIs
SSRIs + caregiver support
5 classifications of BPSD
depression
agitation
aggression
apathy
psychosis
how should BPSD be targeted
ABCs to find trigger for behaviour, then change environment
what is the only pharmacotx for BPSD
risperidone
PRN trazodone and lorazepam fro agitation
