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444-Oncology and Neurology > Cognitive Impairment > Flashcards

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
Q

describe the characteristics of late stage AZH

A

Nonresponsive
Loss of language

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26
Q

what is retrogenesis

A

forgets memories in reverse
Forgets retirement → children → marriage → spouses name → etc

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27
Q

what is the prognosis of alzheimer’s

A

up to 20yrs

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28
Q

how are alzheimer’s diagnosis made

A

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

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29
Q

research criteria of AD is

A

focus on biomarkers and PET

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30
Q

what is a definite AD dx

A

All criteria for probable AD + histopathologic evidence (brain sample)

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31
Q

what is a probable AD dx

A

Prog impared memory, cognitive function, multiple domains affected, onset >40yrs
No biopsy taken- no NFT or plaques to confirm, but everything else consistent

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32
Q

what is a possible AD dx

A

Atypical, gradually progressive decline, one domain affected

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33
Q

what is a major neurodegenerative disorder

A

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
Q

T or F: there is no cure for AD

A

T

35
Q

what are 2 sx tx for AD

A

Cholinesterase inhibitors
memantine

36
Q

what are 2 potentially disease modifying AD tx

A

aducanumab, lecabenab

37
Q

name the 3 ACh increasing medicatiosn

A

donepezil
rivastigmine
galantamine

38
Q

which ACh med is for mild-severe AD

A

donepezil

39
Q

donepezil elimination in the

A

liver

40
Q

SEs of ACh increasing meds include

A

N/V, bradycardia, insomnia, muscle cramps, fatigue, urgency, asthma exacerbation

41
Q

CIs for ACh meds (6)

A

active PUD
anorexia
bradycardia
asthma
QT prolongation
seizures

42
Q

how effective are AChE-i

A

med- effect of ~1 point difference which is not v detectable

43
Q

expectations for AChEi in AD

A

stabilization and maintenance of cog fxn over time
stabilize decline
improve caregiver burden

44
Q

how long should AChEi be trialed

A

3-6mths

45
Q

is one AChEi superior to another

A

no

46
Q

when should AChEi be dosed?

A

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
Q

T or F: AChEi requires titration

A

T- initial dose will be subtherapeutic

48
Q

when is washout necessary for AChEi

A

if SEs (washout for <7d) and switching to another drug

49
Q

is you want to switch from donepezil to rivastigmine and pt has no SEs, is washout necessary?

A

no- just switch to eq dose immediately

50
Q

what is the bottom line on AChEi effectiveness

A

Benefit is modest, early initiation is beneficial, SEs often poorly tolerated by older adults

51
Q

memantine is a

A

NMDA receptor antagonist

52
Q

memantine MOA

A

prevents calcium influx, dysregulation, and cell death from ↑ GLU of AD

53
Q

can memantine be used with CI

A

yes- different MOA

54
Q

memantine indications

A

Mod-severe AD (can use this after pt progresses on CI)
Monotx or as adjunct with CI

55
Q

mementine is eliminated in the _______ and is _____ dependent

A

urine
pH dependent

56
Q

SEs of mementine

A

In first mth, pts may actually have increased confusion, that usually resolves and pt improves- generally well tolerated
Increased BP, corneal ADD

57
Q

which med should AD pts with asthma and bradycardia use

A

mementine

58
Q

memantine 20mg saw slight improvements in AD pts in

A

cog fxn
ADL
behaviour and mood

59
Q

what may be used instead of AP in AD pts to manage behaviours

A

memantine

60
Q

what is mild cognitive impairment

A

predementia- not necessarily progressing
day to day activities not yet impacted

61
Q

how should predementia be treated

A

nonpharm only- exercise, cog training, planning, smoking cessation
AChEi harmful

62
Q

what is the most common type of nonAD dementia

A

vascular dementia

63
Q

vascular dementia onset is

A

sudden or gradual

64
Q

VaD progression, neuro findings, and memory

A

progression = slow and stepwise
neuro = evidence of focal deficits
memory = mildly affected

65
Q

vascular dementia executive function impairment is

A

early and severe

66
Q

vascular dementia type is _________ while AD is ________

A

subcortical
cortical

67
Q

vascular dementia effect on gait vs AD

A

vasc = disturbed early
AD = normal

68
Q

describe Lewy body dementia, parkinson disease dementia

A

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
Q

pathophys of If lewy bodies dementia/ PK dementia

A

lewy bodies deposited = disruption in substantia nigra + cerebral cortex = Neurotransmitter alterations

70
Q

how to differentiate between lewy body dementia and PK

A

duration of PK in relation to dementia

71
Q

3 core features of Lewy body dementia, parkinson disease dementia

A

fluctuations in cognition, visual hallucinations, parkinsonism

72
Q

how to treat Lewy body dementia, parkinson disease dementia

A

rivastigmine, other CIs

73
Q

Lewy body dementia, parkinson disease dementia is sensitive to ___________ and should be avoided

A

neuroleptics

74
Q

what is frontal dementia

A

just the frontal lobe affected = personality, emotions, itneractions changed

75
Q

which has earlier onset: frontal or lewy/ PK dementia

A

frontal

76
Q

the main pathophys of frontal dementia is

A

deficits in 5HT

77
Q

disinhibition and personality changes describes
1. AD
2. lewy body dementia
3. vascular dementia
4. frontal dementia

A

4

78
Q

how to treat frontal dementia (choose all that apply)
1. AChEi
2. memantine
3. caregiver support
4. SSRIs

A

SSRIs + caregiver support

79
Q

5 classifications of BPSD

A

depression
agitation
aggression
apathy
psychosis

80
Q

how should BPSD be targeted

A

ABCs to find trigger for behaviour, then change environment

81
Q

what is the only pharmacotx for BPSD

A

risperidone
PRN trazodone and lorazepam fro agitation

444-Oncology and Neurology (22 decks)

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