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Abbey MSII Unit 3 > Behav. Sci. Dementia > Flashcards

Flashcards in Behav. Sci. Dementia Deck (49):
1

what are age-associated cognitive changes?

-difficulty retrieving words and names
-slower processing speed
-difficulty sustaining attention when faced with competing environmental stimuli
-learning something new takes a bigger effort
-no functional impairment

2

how does dementia occur?

on a continuum (normal aging, followed by mild cognitive impairment, followed by dementia)

3

mild cognitive impairment definition

-memory complaint corroborated by an informant
-objective memory impairment for age and education
-preserved general cognition
-normal activities of daily living can still be done
-not demented

4

amnestic MCI

-memory loss not meeting the criteria for dementia
-progresses to AD at rate of 10%-15% per year vs. 1%-3% incidence in the general population
-may be the earliest phase of AD
-clinical diagnosis because no "MCI test"

5

DSM-IV diagnostic criteria for dementia

memory decline/impairment and at least one of the following:
aphasia (language decline)
impaired executive function
apraxia (inability to do certain actions)
agnosia (inability to interpret sensations)
-cognitive deficits must impact social/occupational function

6

early-onset AD

occurs btw 30-60
rare; familial in most cases

7

what are the gene mutations present in early-onset AD?

1,14,21
1 - presenilin 2 mutation
14- presenilin 1 mutation
21 - abnormal amyloid precursor protein

8

late-onset AD

MC
develops after 60
combination of factors

9

which gene is implicated in late-onset AD?

chromosome 19 - apolipoprotein E4 gene

10

what is present in the brain of someone with AD?

amyloid plaques (alpha beta) both extracellular and in arteries (amyloid angiopathy)
neurofibrillary tangles (intracellular inclusions of tau)

11

what is disproportionately atrophied in AD?

hippocampus (memory!)

12

what does silver stain show?

neuritic plaques and neurofibrillary tangles in AD brain

13

congo red shows what?!

amyloid in plaques

14

what are the cleave sites on APP?

40 and 42 - 42 is worse

15

mutations in which gene is responsible for the large majority of cases of autosomal dominant alzheimer's?

presenilin

16

how does a neuritic plaque appear?

dense central core of compact amyloid surrounded by a clear zone and a peripheral corona or halo

17

what is the patient at risk for when they have amyloid angiopathy?

hemorrhage

18

why does the body have difficulty clearing neurofibrillary tangles?

insoluble - body can't clear

19

how do neurofibrillary tangles appear?

flame shape (form shape of neuron)

20

what are the neurofibrillary tangles?

hyperphosphorylated tau (microtubule-associated protein)

21

frontotemporal lobar degeneration gene

FTLD-tau (can also have TDP or FUS associated)
earlier onset than AD
affects anterior frontal and superior temporal lobes, spares occipital and parietal
knife edge

22

what protein is associated with frontotemporal lobar degeneration?

pick bodies (tau) - rounded

23

AD risk factors

increasing age, females, family history, less education, depression, head injury, low folate and vit B12, presence of apolipoprotein E4 allele, alcohol abuse

24

what are the 3 key features of AD?

impaired cognition, impaired function, and behavioral disturbances

25

how to tell the difference between depression vs dementia

1. depression will demonstrate less motivation during cognitive testing
2. express cognitive complaints that exceed measured deficits
3. maintain language and motor skills

26

frontotemporal dementia (pick's disease) vs alzheimer's

Pick's has insidious onset, gradual progression
early decline in social interpersonal conduct
early impairment in regulation of personal conduct with loss of insight
early emotional blunting
characterized by behavioral abnormalities
memory loss occurs later

27

treatment for frontotemporal dementia

no role for cholinesterase inhibitors
careful use of atypical antipsychotics (quetiapine, risperdol)
divalproex for behavior control
SSRIs for irritability, depression, impulsiveness

28

pharmacotherapy of alzheimer's

cholinergic (donepazil - ACE inhibitor)
NMDA receptor antagonists

29

what is the most used class of drugs for AD right now?

neurotransmitter replacement

30

why do anticholinesterases work?

AD results in degeneration of basal nucleus causing acetylcholine deficiency which contributes to the memory deficits

31

what are the anticholinesterases used in AD?

donepezil, rivastigmine, galantamine

32

what is memantine?

glutamate NMDA receptor blocker used in AD

33

what are the options for treating neuropsychiatric disturbances in AD patients?

1. counseling! look for the triggers - behavioral approach
2. antipsychotics (risperidone and haloperidol)
3. antidepressants (sertraline and venlafaxine)
4. anxiolytics (buspirone and lorazepam)

34

vascular dementia

multi-infarct dementia
cerebral amyloid angiopathy (can be in association with alzheimer's)
hypertension-related small vessel disease

35

what is present in the brain of vascular dementia?

lacunar infarcts
subcortical dementia (cognitive slowing, impaired problem solving, visuospatial abnormalities, disturbances of mood/affect)

36

vascular dementia clinical appearance

"step wise progression" abrupt after CVA, seen with cardiovascular risks
"mixed" dementia with AD or Lewy Body not unusual
emotional lability

37

treatment of vascular dementia

focus on controlling cardiovascular risk factors
also: cholinesterase inhibitors (donepezil, galantamine, rivastigmine)

38

Lewy body dementia

characterized by intracellular, fibriller deposits of presynaptic terminal protein alpha-synuclein (lewy bodies)

39

what are the lewy body disorders

1. parkinson's
2. dementia with lewy bodies

40

parkinson's disease

MCC parkinsonism (tremor, postural instability, impaired voluntary movement)
dopaminergic deficit (responsive to L-dopa)

41

lewy body dementia vs parkinsons

lewy body: onset of dementia within 12 months of parkinsonism

parkinson's: onset of dementia more than 12 months AFTER diagnosis of PD

42

what is needed to make diagnosis of parkinsons'

pallor of substantia nigra AND lewy bodies

43

dementia with Lewy bodies

-memory less affected than AD,
-frontal and subcortical features (deficits in attention and alertness),
-pronounced fluctuations and variations in symptoms
-have vivid visual hallucinations and delusions (including dreams - REM sleep disorder)

44

where are lewy bodies more present in dementia with lewy bodies?

cortical - amygdala and cingulate gyrus most common

45

how do lewy bodies appear?

dark core and pale corona - stain positive for alpha-synuclein

46

Mini Mental Status Exam

used for screening
normal 30-27
mild 30-20
moderate 20-10
severe 10 or lower

47

MoCA (montreal cognitive assessment)

normal more than 26
mild 18-26
moderate 10-17
severe less than 10

48

functional assessment: ADLs

activities of daily living: DEATH
dressing, eating, ambulating, toilet, hygiene

49

functional assessment: IADLs

instrumental ADLs: SHAFT
Shopping, Housekeeping, Accounting, Food prep, Transport