Cognitive Impairment Flashcards

1
Q

define cognition

A

the operation of the mind by which we become aware of objects of thought or perception- includes all aspects of perceiving, thinking, and remembering

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2
Q

define delirium

A

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

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3
Q

define dementia

A

a deterioration of intellectual function and other cognitive skills, leading to a decline in the ability to perform ADL

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4
Q

what is the msot common type of dementia

A

alzheimer’s

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5
Q

dementia impacts
1. memory
2. function
3. thinking
4. al of the above and more

A

4

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6
Q

what is the new term in the DSM used for cognitive impairment

A

neurocognitive disorder

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7
Q

what is pseudodementia

A

dementia is mimicked by functional psychiatric illness

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8
Q

Alzheimer’s has
1. increased worldwide
2. only increased in wealthier countries
3. more effect on men
4. all of the above

A

1

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9
Q

what are some medications that directly cause cognitive impairment`

A

Anticholinergics
Psychotropic: BZDs, neuroleptics
Ethanol
Opioids

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10
Q

what are some medications that indirectly cause cognitive impairment

A

Diuretics (ex- electrolyte abnormalities)- most common
Withdrawal of medications

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11
Q

what are the 5As of cognitive changes

A

aphasia
apraxia
agnosia
abstraction
ADL

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12
Q

difficulty finding the right word is called

A

aphasia

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13
Q

not having purposeful movement patterns is called

A

apraxia

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14
Q

the inability to recognize and identify objects or people is called

A

agnosia

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15
Q

difficulty in realizing and formulating a plan to achieve goals is called

A

abstraction (lack of)

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16
Q

describe 2 cognitive screening tests

A

clock drawing test
MMSE
MoCA
SLUMS, RUDAS
watermelon seeds

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17
Q

Alzheimer’s is a progressive disease of the brain of _____ etiology characterized by diffuse atrophy throughout the _______ with distinct histopathologic changes termed ________ and ________

A

unknown
cerebral cortex
senile plaques
neurofibrillary tangles

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18
Q

name the 6 etiologies of alzheimers

A

genetics- chromosomes 1, 14, 21- ApoE presence
deposition of foreign bodies
dysreg of NT
inflam
environmental agents
vascular RFs

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19
Q

what are some modifiable RFs for alzheimers

A

Smoking
Diabetes
Diet - high trans saturated fats
Obesity- midlife vs late life
Hyperlipidemia
hypertension

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20
Q

early life RF for alzheimers is

A

less education

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21
Q

name 3 ways to decrease risk for alzheimers

A

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

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22
Q

name 3 things that are protective against alzheimers

A

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

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23
Q

describe the characteristics of early alzheimers

A

Insight retained
Word loss
Minor forgetfulness/ decreased STM

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24
Q

describe characteristics of intermediate stage AZD

A

Loss of insight
Behavioral disturbances

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25
describe the characteristics of late stage AZH
Nonresponsive Loss of language
26
what is retrogenesis
forgets memories in reverse Forgets retirement → children → marriage → spouses name → etc
27
what is the prognosis of alzheimer's
up to 20yrs
28
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
29
research criteria of AD is
focus on biomarkers and PET
30
what is a definite AD dx
All criteria for probable AD + histopathologic evidence (brain sample)
31
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
32
what is a possible AD dx
Atypical, gradually progressive decline, one domain affected
33
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
34
T or F: there is no cure for AD
T
35
what are 2 sx tx for AD
Cholinesterase inhibitors memantine
36
what are 2 potentially disease modifying AD tx
aducanumab, lecabenab
37
name the 3 ACh increasing medicatiosn
donepezil rivastigmine galantamine
38
which ACh med is for mild-severe AD
donepezil
39
donepezil elimination in the
liver
40
SEs of ACh increasing meds include
N/V, bradycardia, insomnia, muscle cramps, fatigue, urgency, asthma exacerbation
41
CIs for ACh meds (6)
active PUD anorexia bradycardia asthma QT prolongation seizures
42
how effective are AChE-i
med- effect of ~1 point difference which is not v detectable
43
expectations for AChEi in AD
stabilization and maintenance of cog fxn over time stabilize decline improve caregiver burden
44
how long should AChEi be trialed
3-6mths
45
is one AChEi superior to another
no
46
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
47
T or F: AChEi requires titration
T- initial dose will be subtherapeutic
48
when is washout necessary for AChEi
if SEs (washout for <7d) and switching to another drug
49
is you want to switch from donepezil to rivastigmine and pt has no SEs, is washout necessary?
no- just switch to eq dose immediately
50
what is the bottom line on AChEi effectiveness
Benefit is modest, early initiation is beneficial, SEs often poorly tolerated by older adults
51
memantine is a
NMDA receptor antagonist
52
memantine MOA
prevents calcium influx, dysregulation, and cell death from ↑ GLU of AD
53
can memantine be used with CI
yes- different MOA
54
memantine indications
Mod-severe AD (can use this after pt progresses on CI) Monotx or as adjunct with CI
55
mementine is eliminated in the _______ and is _____ dependent
urine pH dependent
56
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
57
which med should AD pts with asthma and bradycardia use
mementine
58
memantine 20mg saw slight improvements in AD pts in
cog fxn ADL behaviour and mood
59
what may be used instead of AP in AD pts to manage behaviours
memantine
60
what is mild cognitive impairment
predementia- not necessarily progressing day to day activities not yet impacted
61
how should predementia be treated
nonpharm only- exercise, cog training, planning, smoking cessation AChEi harmful
62
what is the most common type of nonAD dementia
vascular dementia
63
vascular dementia onset is
sudden or gradual
64
VaD progression, neuro findings, and memory
progression = slow and stepwise neuro = evidence of focal deficits memory = mildly affected
65
vascular dementia executive function impairment is
early and severe
66
vascular dementia type is _________ while AD is ________
subcortical cortical
67
vascular dementia effect on gait vs AD
vasc = disturbed early AD = normal
68
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
69
pathophys of If lewy bodies dementia/ PK dementia
lewy bodies deposited = disruption in substantia nigra + cerebral cortex = Neurotransmitter alterations
70
how to differentiate between lewy body dementia and PK
duration of PK in relation to dementia
71
3 core features of Lewy body dementia, parkinson disease dementia
fluctuations in cognition, visual hallucinations, parkinsonism
72
how to treat Lewy body dementia, parkinson disease dementia
rivastigmine, other CIs
73
Lewy body dementia, parkinson disease dementia is sensitive to ___________ and should be avoided
neuroleptics
74
what is frontal dementia
just the frontal lobe affected = personality, emotions, itneractions changed
75
which has earlier onset: frontal or lewy/ PK dementia
frontal
76
the main pathophys of frontal dementia is
deficits in 5HT
77
disinhibition and personality changes describes 1. AD 2. lewy body dementia 3. vascular dementia 4. frontal dementia
4
78
how to treat frontal dementia (choose all that apply) 1. AChEi 2. memantine 3. caregiver support 4. SSRIs
SSRIs + caregiver support
79
5 classifications of BPSD
depression agitation aggression apathy psychosis
80
how should BPSD be targeted
ABCs to find trigger for behaviour, then change environment
81
what is the only pharmacotx for BPSD
risperidone PRN trazodone and lorazepam fro agitation