McHugh: Dementia Flashcards

1
Q

At what age does the prevalence of dementia begin to double every 5 yrs?

A

after age 65

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

What’s this?

syndrome of acquired, persistent intellectual impairment that is due to brain dysfunction

A

dementia

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

What does it mean that dementia is persistent?

A

it does not get better or worse…

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

Operationally, dementia implies impairment in three or more of the following domains of mental capacity:

A
memory
language
perception
praxis (knowing how to do things)
calculations
semantic knowledge
executive function
personality
emotional expression or awareness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What’s this?
onset after 65
slowly progressive decline in recent memory, language, visuospatial impairment, executive dysfunction

A

Alzheimer’s disease

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

What’s this?
fluctuating course
dementia followed by spontaneous parkinsonism
visual hallucinosis and/or psychosis neuroleptic sensitivity

A

dementia w Lewy Bodies

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

abrupt cognitive loss, stepwise decline Infarcts and/or vascular disease by imagingfocal neurologic signs

A

vascular dementia

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

onset before 65
prominent impairment of behavior, social conduct, judgment
early disturbance of language, progressive aphasia

A

frontotemporal dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Is dementia a global impairment of intellectual function?

A

no, not global

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

Does dementia always impair memory?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Does dementia always impair insight?

A

no; pts are usu aware of their dementai

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

Is dementia only a cognitive disorder and never primarily a behavioral disorder?

A

no, can be behavioral, too

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

Is dementia inevitable and synonymous w senility? Is it = to Alzheimer’s disease?

A

no!

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

Can dementia have an acute onset?

A

yes

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

Is dementia treatable?

A

it is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
What's this?
memory loss
preserved cognition
preserved ADL (activities of daily living)
not demented
A

mild cognitive impairment

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

What’s this?
memory loss
at least 2 cognitive domains
diminished ADL

A

dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
What's this?
acute onset
lasts hrs to days
fluctuating course
lethargy upon arousal
prominent distractability
memory impaired by inattention
dysarthric speech
frequent misperceptions
fearful, suspicious aspect
A

delirium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
What's this?
Onset most often insidious
Lasts months to years
Usually constant
Normal arousal and memory
dysnomic or aphasia
no misperceptions
A

dementia

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

What are these associated w?
Decreased complex or sustained attention
Interference from redundant or irrelevant material
Preserved crystallized intelligence (old solutions)
Decreased fluid intelligence (new information for novel solutions)
Relatively stable verbal IQ
Decline in performance IQ
Decreased working memory
Slowed retrieval of stored memory

A

normal aging

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

can distinguish the intellectual changes of dementia from those associated to delirium, isolated cognitive deficits, normal aging and other conditions
Identifies patterns and profiles of neurobehavioral dysfunction which suggest specific dementing diseases
Establishes and communicates severity of dementia and follow course of patients over time

A

mental status assessment

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

What MMSE score is appropriate for those ages 85+ w more than 12 years of education?

A

28

23
Q

What MMSE score is appropriate for those ages 70-74 w more than 12 years of education?

A

29

24
Q

What MMSE score is appropriate for those ages 65-69 w 0-4 years of education?

A

22

25
Q

What test is looking at temporal lobe semantic storage, and assessing category fluency?

A

animal naming test

26
Q

How do you perform the animal naming test? What is the animal naming test highly sensitive to?

A

1 min to name as many animals as you can - you get 1 pt for each animal named w/i the minute, avg performance is 18/minute; Alzheimer’s disease

27
Q

At 3 yrs, impairment of instrumental activities of daily living is a predictor of the incidence of (blank)

A

dementia

28
Q

Dementia can be sub-acute or chronic. Over what duration is it sub-acute?

A

less than 6mo

29
Q

What are 3 causes of sub-acute dementia?

A
  1. tumors
  2. auto-immune disease
  3. prions
30
Q
What's this?
Prion disorder of sheep
Onset 3-4 years
Intense itching
Ataxia and death
Altered prion protein 
Spongiform encephalopathy
Transmitted by milk, urine through enviornment
A

scrapie

31
Q
What's this?
Prion disorder of cows and other ungulates
Affects cows 4-5 years of age
Weakness and ataxia
Spongiform encephalopathy
Sporadic vs. enviornment/diet
A

mad cow disease

32
Q

progressive dememtia and myoclonic jerks. Onset late middle age, most cases sporadic, rarely familial

A

CJ disease

33
Q

progressive insommnia and dementia

A

familial fatal insomnia

34
Q
What prion form is this?
209 AA, Alpha Helix
Copper binding
Soluable
Protease digestible
A

normal cellular

35
Q
What prion form is this?
209 AA beta sheet
Function if any unknown
Insoluable
Protease resistant
A

abnormal form

36
Q

How does the prion model work?

A

Normal cellular protein misfolds
Misfolded protein cannot be cleared
It becomes the template to cause other proteins to misfold
Misfolded protein kills the cell
Dead cell releases misfolded protein
Remaining cell engulfs the abnormal protein & transports it by axonal transport to synapse

37
Q

What is this?
Closed head injury causes tau protein to be released into CSF
It is converted to a fibrillar form which is taken up by nearby cells and transported along axons
It acts as a template to misform normal tau
Aggregates cross synaptic space to cortical neurons

A

chronic traumatic encephalopathy

38
Q

Chronic traumatic encephalopathy occurs when there is atrophy of the frontal and temporal lobes. (blank) deposits in those lobes and in the basal ganglia, causing dementia (decreased memory, executive function, depression, and aggressive behavior.

A

TAU

39
Q

What are the pure tauopathies?

A

CBD: cortico-basal ganglionic degeneration
PSP: progressive supra-nuclear palsy
FTLD: fronto-temporal lobar degeneration

40
Q
What are these symptoms of?
Parkinson’s
	Alien hand
	Apraxia
	Aphasia
4 repeat Tau and overlaps with PSP
A

CBD

41
Q

What are these symptoms of?
Axial rigidity
Loss of vertical and terminally all EOM
Dementia/dysphagia/dysarthia 4repeat Tau

A

PSP

42
Q

What the heck is this?
Behavioral variant-loss of executive function, apathy
Primary progressive aphasia
Semantic variant-loss of concepts with preserved vocabulary
Many but not all due to mutation on Tau gene on chromosome 17 Pick’s disease
3repeat Tauopathy

A

FTLD

43
Q

20% of pre-senile Alzheimer’s are (blank)

A

FTLD

44
Q

Alzheimer’s disease doubles in prevalence every 5 yrs after age (blank)

A

65

45
Q

What is the major amyloidopathy?

A

Alzheimer’s disease

46
Q

In what portion of the brain will amyloid first build up in Alzheimer’s?

A

medial temporal lobes

47
Q

What is this?

LEWY BODY FORMATION IN THE BRAIN FOLLOWS CAUDAL-ROSTRAL PATH

PHENOTYPE FOLLOWS STAGES

DEFINITE STAGES ARE DEFINED

A

Braak hypothesis

*protein spreads from medulla to pons to basal ganglia to cortex

48
Q

Eosinophilc, round intracytoplasmic inclusions, particularly numerous in the substantia nigra pars compacta

A

lewy bodies

49
Q

In the Braak stages 1 and 2, what two things are most affected?

A

olfactory neurons *nose

motor nucleus of the vagus *gut

50
Q

What symptom of Parkinson’s precedes the onset of motor disease by 10 years?

A

constipation

*death to neurons in myenteric plexus

51
Q

Pre-motor symptoms in Parkinson’s disease?

A

olfactory loss - stage 1 Braak
dysautonomia (gastroparesis, constipation, urinary urgency, erectile dysfuntion) - stage 1 Braak
depression/anxiety - stage 2 Braak
REM sleep behavior - stage 2

52
Q

By Braak stage 6, what structures are affected? What does this lead to?

A

thalamus, neocortex; cognitive loss

53
Q
SUB-CORTICAL DEMENTIA
IMPAIRED CONCENTRATION
SLOWED RESPONSES
PERSONALITY CHANGE
VARIABLE COGNITIVE LOSS
AUDITORY-BANGS, KNOCKS, OCC. VAGUE VOICES
TACTILE-ANIMAL CONTACT
VISUAL ILLUSIONS-INANIMATE SEEN AS LIVING
PASSAGE –BRIEF, PASSING BY PATIENT
SENSE OF PRESENCE
A

BRAAK STAGE 6

54
Q

Both Parkinson’s disease and Alzheimer’s have a common (blank) deficit

A

cholinergic