Dementia Flashcards

1
Q

core clinical criteria for dementia

A

cognitive/behavioral symptoms that:

  1. interfere with the ability to function at work
  2. represent decline from previous levels of functioning
  3. not explained by delirium or major psychiatric disorder
  4. cognitive impairment is detected and diagnosed through history taking and objective cognitive assessment
  5. involves >/= 2 domains
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2
Q

domains in core clinical criteria

A
  1. impaired ability to acquire and remember new information
  2. impaired reasoning and handling of complex tasks, poor judgment
  3. impaired visuospatial abilities
  4. impaired language functions
  5. changes in personality, behavior, or comportment
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3
Q

normal aging vs dementia

A

table 2

9 items

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4
Q

potentially reversible causes of dementia

A
drugs
endocrinopathies
metabolic disorders
emotional depression
nutritional deficiencies
tumor/trauma
infection/infirmities of the senses
arteriosclerosis
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5
Q

most frequent dementing disease

A

cerebral atrophy maiinly alzheimer but including lewy-body, parkinison, frontotemporal, and pick disease

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6
Q

what is mild cognitive impairment

A

aka pre-dementia

  • memory complaints that are mild and do not interfere with daily functioning but still disproportionate to patient’s age and education
  • normal process of aging
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7
Q

treatment for pre-dementia

A

observe, cholinesterase inhibitors

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8
Q

definition of alzheimer’s disease

A

neurodegenerative disease characterized by a clinical dementia with prominent memory impairment and specific microscopic pathology including senile plaques and neurofibrillary tangles

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9
Q

treatment for alzheimer’s disease

A

cholinesterase inhibitors for mild, moderate, and severe AD

memantine for moderate and severe AD

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10
Q

NIA-AA cirteria: probable ad dementia

A

insidious onset, gradual

clear cut history of worsening condition

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11
Q

NIA-AA criteria: probably ad dementia categories

A
amnestic presentation (most common, learning and recall impairment)
non-amnestic presentation (language, word finding)
visuospatial presentation (spatial cognition)
executive dysfunction (impaired reasoning, judgment, and problem solving)
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12
Q

NIA-AA criteria: probable ad dementia with increased level of certainty

A

probable ad dementia with documented decline on subsequent evaluations
probably ad dementia in a carrier of causative ad genetic mutation

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13
Q

NIA-AA criteria: possible ad dementia

A

atypical course: meets the core clinical criteria, sudden onset or insufficient historical detail

etiologically mixed presentation: meets all core criteria but has (1) cerebrovascular disease (2) dementia with lewy bodies ( 3) other neurological disease/medication

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14
Q

DSM 5 criteria for AD

A
  • meet criteria for major or minor neurocognitive disorder
  • insidious onset
  • not explained by other diseases
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15
Q

DSM 5 criteria for major neurocognitive disorder

A

probable AD: 2 present, possible AD: 1 present

1 evidence of a causative ad genetic mutation
2a clear decline in memory and learning
2b steadily progressive, gradual decline in cognition
2c no evidence of mixed etiology

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16
Q

DSM 5 criteria for mild neurocognitive disorder

A

probable ad: evidence of causative ad genetic mutation
possible ad: no evidence of a causative ad mutation and ALL 3 PRESENT
- clear evidence of decline in memory and learning
- progressive, gradual decline
- no evidence of mixed etiology

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17
Q

features of familial alzheimer

A
earlier onset (<65 yo)
associated with asynchronous myoclonus, epilepsy, aphasia, paratonia
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18
Q

genetic defect in familial alzheimer

A

amyloid precursor protein
presenilin 1
presenilin 2

19
Q

main pathology of AD

A

amyloid neurotoxicity

20
Q

factors related to amyloid neurotoxicity

A

apo e: modifies formation of plaques (apo e2 is PROTECTIVE)
apo e4: elevated serum ldl, results in inadequate clearance of ab 42 promoting amyloid toxicity
tau protein: promotes microtubule assembly and structure

21
Q

typical locations of reduced brain weight

A

bilateral hippocampal or medial temporal lobes

22
Q

patho hallmarks of AD

A

neurofibrillary tangles and neuritic plaques in parietal lobe

granulovacular degeneration of neurons (pyramidal layer)

23
Q

what are neurofibrillary tangles

A

helical filaments composed of hyperphosphorylated microtubular protein (tau)

24
Q

what are neuritic plaques

A

spherical deposits composed of amyloid (B amyloid) surrounded by degenerating nerve terminals

25
Q

cholinergic therapies available

A

choline, lecithin
muscarininc cholinergic agonist drugs
cholinesterase inhibitors

26
Q

cholinesterase inhibitors availbale

A

donepezil, rivastigmine, galantamine

GI side effects are most common

27
Q

nmda receptor antagonists

A

moa: vs glutamic acid

memantine

28
Q

current recommended practice for AD treatement

A

mid/early stage: cholinesterase inhibitor
mild to mod stage: cholinesterase inihibitor or nmda antagonist or both
severe late stage: both

29
Q

definition of vascular dementia

A

cognitive decline in the setting of cerebrovascular disease

- cognitive impairment is early with deficits in executive dysfunction

30
Q

proposed mechanism critically located single infarcts

A

MCA: severe aphasia with additional cognitive impairment
PCA: amnesia with bilateral inferomedial temporal or thalamic damage
ACA: abulia, memory impairment or language disturbance
MCA: acute confusion or psychosis with non-language dominant parietal lobe damage

31
Q

symptoms of binswanger disease

A
abulia
abnormal behavior
pseudobulbar palsy
pyramidal signs
disturbed gait
urinary incontinence
32
Q

features of lewy body dementia

A

dementia, visual hallucinations, parkinsonism, and rem sleep behavior disorder

33
Q

treatment for lewy body dementia

A

cholinesterase inhibitors

34
Q

most common differential diagnoses for lewy body dementia

A

alzheimer’s disease and mixed dementia

35
Q

dementia with lewy bodies vs parkinson’s disease dementia

A

DLB: cognitive impairments are coincident with or appear within 1 year of the motor signs
PDD: cognitive decline occurs in the course of well established parkinson disease

36
Q

core features of dementia with lewy bodies

A

fluctuating cognition
visual hallucinations
spontaneous features of parkinsonism

37
Q

suggestive features of dementia with lewy bodies

A

REM sleep behavior disorder
sever neuroleptic sensitivity
low dopamine transporter uptake in basal ganglia (SPECT/PET)

38
Q

probably and possible dementia with lewy bodies

A

probable: >/= 1 suggestive + core feature
possible: >/=1 suggestive

39
Q

patho in dementia with lewy bodies

A
  • (neuron loss) neurodegeneration associated with abnormal a-synuclein metabolism + formation of lewy bodies
  • neuronal loss in substantia nigra (dopamine) and nucleus basalis of meynert (acetylcholine)
40
Q

treatment for dementia with lewy bodies

A
cholinesterase inhibitors (rivastigmine, donepezil)
memantine (namenda)
SSRI (sertaline and escitalopram)
dopaminergic agents (levodopa/carbidopa)
atypical antipsychotics (quetiapine)
41
Q

definition of frontotemporal dementia

A

progressive neurodegenerative disorder with

  • behavioral or frontal variant frontotemporal dementia*
  • semantic variant primary progressive aphasia
  • non-fluent/agrammatic variant primary progressive aphasia
42
Q

symptoms of behavioral variant frontotemporal dementia

A

at least 3

  • early behavioral dishibition
  • early apathy or inertia
  • early loss of sympathy or empathy
  • early perservative, stereotypes, or compulsive/ritualistic behavior
  • hyperorality and dietary changes
  • executive or generation deficits with relative sparing of memory and visuospatial functions
43
Q

seven pathologies of frontotemporal dementia

A

pick’s disease (tau- and ubiquitin positive spherical inclusions)
familial ftd with tau positive inclusions
argyrophilic grain disease
ubiquitin positive inclusions
tdp-43 immunoreactive inclusions
neuronal filament inclusions

44
Q

treatment of frontotemporal dementia

A

management of symptoms

SSRIs (sertaline, citaloprams, escitalopram) and atypical antipsychotics