Neurocognitive Flashcards

1
Q

dementia

A

slow onset, progressive, chronic

not better explained by different disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how is delirium different from dementia

A

acute onset of reversible mental status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

dementia is characterized by

A

significant and progressive decline in cognition involving one more more cognitive domains that affect independence in everyday activities

can’t be exclusively during delirium and not better explained by another disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

symptoms of dementia

difficulty…

A

retaining new information

handling complex tasks

reasoning

spatial ability/orientation

language

behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

behavioral disturbances

A

common in dementia

associated with adverse outcomes, increased disability, caregiver stress, earlier institutionalization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

behavioral assessment should asses which disturbances

A

agitation/aggression

hallucinations

delusions/paranoia

sundowning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

mCI

A

presence of memory difficulty and objective memory impairment BUT preserved ability to function in daily life

increased dementia risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

10 warning signs of dementia

A
  1. memory loss
  2. difficulty preforming everyday tasks
  3. problems with language
  4. disorientation to time and place
  5. poor or decreased judgement
  6. problems with abstract thinking
  7. misplacing things in unusual places
  8. changes in mood/behavior
  9. Changes in personality
  10. loss of initiative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

dementia detection

A

minimental status exam

orientation, registration, language, recall

max score is 30, less than 24 Is abnormal

best if done serial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

subtypes of dementia

A
  1. Alzheimer’s dz
  2. vascular multi infarct dementia
  3. dementia with Lewey bodies
  4. frontotemporal dementia
  5. Parkinson disease w/dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MC cause of all dementia

A

alzheimer

rare autosomal dominant but MAJORITY OF CASES are sporadic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

histological findings of AD

A

extracellular amyloid plaques (senile plaques)

intraneuronal protein tau in neurofibrally tangles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

AD pathophysiology

A

development of progressive atrophy and gloss

first to hippocampus then moves into areas of brain controlling thinking and decision making

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

AD risk factors

A

increasing age
family history

HTN, depression, insulin resistance, down’s head trauma

MC in women, African Americans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

genetic disposition for AD

A

mutation accounts for <5% of AD but all early onset AD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

when to consider AD

A

insidious and progressive memory loss

significant impairment in language, visuospatial dysfunction ,executive function and behavior changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

AD work up

A

should rule out other causes

physical exam, MME

Blood work (LFT, B12, TSH, CBC, RPR)

Imaging (non contrast CT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

staging of AD

pre clinical

A

no changes in judgment or impairment of daily activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

staging of AD

mild AD

A

pts get lost in familiar places, lose ability to handle money

increased dependence on the caregiver,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

staging of AD

moderate AD

A

pt can’t make sense of world around and relies on caregivers

agitation, wandering, tearfulness (esp. @ night)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

staging of AD

severe AD

A

completely unable to communicate

bed bound with loss of bowel/bladder = infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

mc cause of death in AD

A

infection (aspiration, PNA, UTI, skin infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

general AD tx

A

symptomatic (cholinesterase, NMDA)

psychotropic drugs to change behavior and mood disturbance

24
Q

cholinesterase inhibitors

A

benefit on cognitive fxn and ADLs, help non cognitive symptoms (personality changes)

used in all stages

25
Q

cholinesterase inhibitors ADRs

A

weight loss, n/v/d and dizziness

bradycardia, AV block, syncope, falls

SJS

26
Q

cholinesterase inhibitors used inAD

A

Donepezil (Aricept)
Rivastigmine (Exelon)
Galantmine (Razadyne)

27
Q

Donepezil brand + indications + ADR+ formulation

A

(Aricept) AD tx

tablets or ODT

decreased drug interactions but cholinergic side effects common

OK in liver/renal

28
Q

Rivastigmine brand + formulations + ADR + indication

A

(Exelon) mild-mod AD

tablet, patch

reiterate if d/c > 3 days

cholinergic SE, meals with food, no dose adjustment in CKD but in liver DZ

29
Q

galantamine brand + indications + ADR+ formulation

A

Razadyne

suspension (can be mixed in non-EtOH)

mild - mod dementia

dose adjust in CKD + Liver dz

30
Q

partial NMDA antagonist used in AD

A

Memantine (Namenda)

31
Q

AD and NMDA receptor

A

excessive stimulation due excessive glutamate causing increased CA and disruption of information processing

32
Q

memantine MOA

A

NMDA antagonist

improves glutamate transmission and lessening overstimulation = slowed death

33
Q

Namenda indications

A

memantine/NMDA antagonist

mod-severe AD (+/- cholinesterase)

34
Q

what can you do to slow progression or reduce risk of AD

A

reducing brain inflammation (I.e. NSAIDs)

Good diet and exercise (may slow progression, limited alcohol use)

35
Q

vascular dementia

A

multi-vascular dz that causes dementia

Vascular dementia and AD often co exist

36
Q

types of vascular dementia

A

multiple cortical infarcts
single infarct
small vessel disease

37
Q

multiple infarct dementia

A

combined effects of different infarcts produces cognitive decline

38
Q

single infarct dementia

A

one large infarct causes severe impairment

39
Q

small vessel dementia is divided into two types

A

no big step off instead over time

subcortical leukoencepholopathy (white matter)

numerous lacunae (small vessel occlusions)

40
Q

mild vascular cognitive impairment

A

cognitive decline worse than expected for age and edu. BUT effects don’t meet criteria for dementia

memory issue but functional skills are within normal limits

41
Q

vascular dementia epidemiology

A

MC in men , asians

more rapidly fatal due to increased likelihood of other CV risks

HTN is main risk factor

42
Q

vascular dementia presentation

A

acute cognitive impairment after a neurologic event (single infarct)

may develop subacute impairment of stepwise progression

progressive motor and cognitive, mood changes over years

depression and intellectual defects occur = disoriented with memory deficits inattention and vague inability to focus

43
Q

how to differentiate vascular dementia and AD

A

vascular: greater deficits of frontal executive fxn (balancing check book), PATCHY* neuro deficits

AD: long term memory defects (what did I eat for breakfast?), global neuro deficits

apathy early on = VD

44
Q

tx of vascular dementia

A

prevention of NEW strokes

Antiplatelet drugs, statins, controlling vascular risk factors

45
Q

DLB

A

dementia that is 2/2 disruption of neuronal flow from frontal lobe to other areas of brain

46
Q

DLB epidemiology

A

older age, more common in men, all ethnicities

may be with PD and AD

47
Q

presenting clinical features of DLB

A

PRESENTS with dementia (AD -= memory loss)

early impairment in attention, executive and visuospatial fxn

severe sensitivity to neuroleptics, hypersomnia, orthostatic HoTN

48
Q

4 core clinical features of DLB

A

Must have 2 of 4

  1. fluctuation in cognition and alertness (good days and bad days)
  2. visual hallucinations (v uncommon in AD)
  3. Parkinsonism (less severe than PD)
  4. REM sleep behavior disorder (dream enactment)
49
Q

DLB testing

A

MMSE shows impaired figure copying, clock drawing, spelling world backwards (executive functioning)

AD pts have trouble with recall and orientation

50
Q

clues to DLB diagnosis

A

fluctuations in cognitive functions, naps > 2 hrs, unresponsiveness, orthostatic HotN, hallucinations, delusions, parkonsonians

etc.

51
Q

diagnostic work up of DLB + tx

A

neuropsychological testing

cholinesterase inhibitors (tx apathy, anxiety, hallucinations, delusions)

Parkinsonism meds

SSRI

atypical neuroleptics

52
Q

what class of drugs is C/I’d in DLB

A

HALDOL (first gen antipsychotics)

53
Q

dementia characterized by focal degeneration of frontal and temporal lobes

A

frontotemporal dementia

umbrella term for multiple different types

54
Q

FTD epidemiology

A

patients in late 50s and early 60s

men > female

55
Q

s/s FTD (9)

A
  1. personality/social behavior/language changes progressing to dementia affecting cognition
  2. extrapyramidal or motor neuron involvement
  3. difficulty with speech
  4. disinhibition, impulsiveness, giddiness, apathetic
  5. neglect of personal hygiene, mental rigidity, stereotyped behavior
  6. loss of social awareness, empathy
  7. hyperorality, inappropriate sexuality, binging, carb craving, EtOH and tobacco excess
  8. compulsions
  9. utilization behavior
56
Q

FTD on exam

A

speech: non-fluent, difficulty finding words

behavior changes

visual and spatial functions and constructional tasks

memory is preserved

new artistic or musical talents

57
Q

tx of FTD

A

symptomatic management

SSRI (Zoloft, Paxil)

trazodone (sleep and behavior changes)

neurotransmitter therapies don’t work

progresses more rapidly than AD (8-10 yr survival)