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Block 5 Week 5 Dani > Dementia and Prion-related Diseases > Flashcards

Dementia and Prion-related Diseases Flashcards

1
Q

Every 4 years after the age of 65-69, SDAT prevalence increase by how much?

A

it doubles (starting at 2% for ages 65-69)

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2
Q

The populations of numerous countries has a higher percentage of people that are getting (blank) than past years

A

older

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3
Q

(blank) is a syndrome of acquired, persistent intellectual impairment that is due to brain dysfunction.

A

dementia

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4
Q

What kind of dementia is this:

conenital mental retadation, and developmental delay

A

acquired dementia

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5
Q

What kidn of dementia is this:

delirium

A

persistent dementia

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6
Q 
What kind of dementia is this:
isolated deficiets (amnesia or aphasia)
A

multiple deficits dementia

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7
Q 
Operationally, dementia implies impairment in (blank) or more of the following domains of mental capacity:  
Memory 	Praxis			Executive Functions
Language   	
Calculations		
Personality
Perception 	
Semantic Knowledge	
Emotional Expression
Awareness
A

three

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8
Q

How can you figure out if someone has dementia?

A

mental status assessment, clinical rating scales, neuropsychological testing

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9
Q

When do you get alzeheimers?

A

after 65

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10
Q

What is this:

slowly progressive decline in recent memory, language, visuospatial impairment, executive dysfunction

A

alzheimers

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11
Q 
What is this:
fluctuating course
dementia followed by spontaneous parkinsonism
visual hallucinosis and/or psychosis
neuroleptic sensitivity
A

dementia with lewy bodies

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12
Q

What is this:
abrupt cognitive loss, stepwise decline
Infarcts and/or vascular disease by imaging
focal neurologic signs

A

vascular dementia

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13
Q

Dementia is abrupt or insiduous?

A

insiduous

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14
Q

Is delirium constant or fluctuating?

A

fluctuating

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15
Q

What is this:
onset BEFORE 65
prominent impairment of behavior, social conduct, judgement
early disturbance of lanuage, progressive aphasia

A

frontotemporal dementia

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16
Q

T/F

dementia is a global impairment of intellectual function

A

F

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17
Q

T/F

dementia always impairs memory?

A

F

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18
Q

T/F

dementia always impairs insight; patients aware of their deficits dont have dementia

A

F

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19
Q

T/F dementia is a cognitive disorder and never primarily a behavioral disorder

A

F

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20
Q

Dementia is synonymous with alzheimers disease

T/F

A

F

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21
Q

Dementia can have an acute onset

A

T

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22
Q

Can you treat dementia?

A

no, but you can treat the symptoms

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23
Q 
Is this dementia or mild cognitive impairment:
memory loss
preserved cognition
preseved ADL
not demented
A

mild cognitive impairment

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24
Q

Is this dementia or not:
memory loss
at least 2 cognitive domains
diminished ADL

A

dementia

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25
Q 
Is this delirium or dementia:
Onset is acute
duration is hours to days
course is fluctuating
arousal is lethargic to agitated
distracted
memory impaired by inattention
dysarthric, incoherent speech and language
frequent misperceptions
fearful
postural tremor
myoclonus or asterixis
EEG is slow
A

delirium

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26
Q

What is this:
most often insidious, last months to years, usually is constant, normal arousal and attnetion but abnormal amnesic memory, aphasia an dysnomic speech and language skills, mormal perception and fine motor skills until later in life and a normal EEG

A

dementia

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27
Q

What is this:
Learning is slower
Learned material is retained
Language, math, visual-spatial ability is preserved
Problem solving using shifting strategy is impaired, but experience aids

A

normal aging :)

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28
Q

(blanK) 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 exam

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29
Q

Alzheimers is associated with what protein gone bad?

A

amyloids

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30
Q

What are the elements you test in mental status evaluation?

A 
arousal and attention
language
memory
perception and construction
personality and emotion
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31
Q

Median scores based on age and educational level for MMSE are what:
>85 years and >12 years of education = (blank)
70-74 and >12 years of education = (blank)
65-69 and 0-4 years of education = (blank)

A

28
29
22

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32
Q

what is the mini cog?

When are you considered demented on this exam?

A

combines 3 item recall w/ clock drawing test

if you get a 0/3 on recall or if you get a 1 or 2/3 and mess up clock drawing

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33
Q

memories are not stored in the (blank), it is just a pointer to the neural populations that are engaged during the memory phenomenon.

A

hippocampus

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34
Q

is it normal when you’re older to get interference form redundant or irrelevant material?

A

yes

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35
Q

What is preserved as you age, crystallized or fluid intelligence?

A

crystalllized

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36
Q

What are the categories of Katz index of ADLs? How do you rank each category?

A 
bathing
dressing
toileting
transfer
continence
feeding
independent, assistance, dependent
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37
Q 
What are these:
Traveling
Telephone
Shopping
Preparing meals
Housework
Medication
Money
A

instrumental activites of daily living

38
Q

At 3 years, instrumental activites of daily living impairment is a predictor of incidence of (blank).

A

dementia

greater the impairment, the greater the likelihood of dementia

39
Q

What is the amount of time that is considered subacute dementia?

A

less than 6 months

40
Q

What can cause sub-acute dementia?

A

prions, tumors, autoimmune

41
Q

What are these:
Prions, Tumors, Auto-immune
Tumors- primary, metastatic and lymphomas
Auto-immune-Hashimoto’s, K channels antibodies, paraneoplastic
Prions –Hereditary, Acquired, Iatrogenic

A

causes of sub acute dementia

42
Q

What is the cellular protein that goes bad in SDAT (alzheimers)?

A

amyoloid (abeta 42) and Tau

43
Q

What is the cellular protein that goes bad in FTLD (frontal temporal lobe dementia)?

A

Tau

44
Q

What protein goes bad in parkinsons disease dementia with lewy bodies (DLD)?

A

synuclein

45
Q

What protein goes badin creutzfeld jakob disease (CJD)?

A

prions

46
Q

What kind of neurogenerative diseases are these:
Multiple system atrophy
Parkinsons’ Disease
Dementia with lewy bodies

A

synucleinopathies

47
Q

What kind of neurodegenerative disease does alzheimers belong to?

A

amyloidopathies

48
Q

What kind of neurogenerative diseases are these:
Alzheimers disease, progressive supranuclear palsy, chronic traumatic encephalopathy, frontotemporal dementia, corticobasal degeneration

A

Tauopathies

49
Q

How does normal protein degredation happen?

A

with ubiquitination and proteases

50
Q

What is Kuru?

A

a neurodegenerative brain disease caused by cannabilizing brain tissue

51
Q

What disease is this:

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

A

CJ disease

52
Q

What is this:

progressive insomnia and dementia

A

familial fatal insomnia (FFI)

53
Q

How long does it take for a person to pass away from CJ disease or familial fatal insomnia?

A

6-12 months following symptoms

54
Q 
What is this:
Onset 3-4 years
Intense itching
Ataxia and death
Altered prion protein 
Spongiform encephalopathy
Transmitted by milk, urine through enviornment
A

scrapie-prion disorder of sheep

55
Q 
What is 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

56
Q

What is this:
Young people in Britain-prion disorder
Presents as a psychiatric disorder
Due to ingestion of beef affected by bovine spongiform encephalopathy
Relatively long duration of illness(14 months)
No new cases since control of bovine disease

A

variant CJD

57
Q

What is the abnormal form of PrPC and what does it make?

A

PrPsc

209 beta sheet insoluble, protease resistant, prion

58
Q

How do you get rid of a prion?

A

you have to burn it (cant autoclave it and is protease resistant)

59
Q

How does a prion work?

A

normal protein undergoes change and forms beta sheets that elongate and trigger normal proteins to misfold-> kills cell membranes

60
Q

Tau is a microtubular (Blank) protein. So when these get messed up and aggregate its bad.

A

stabilizing

61
Q

What is chronic traumatic encephalopathy (CTE)?

A

closed head injury disrupts fiber tract and you get tau protein release that misfolds proteins

62
Q

Whats scary about concussions?

A

if you get one and dont let it heal properly you cant get misfolded proteins!

63
Q 
What is this:
can cause parkinsons
alien hand
apraxia
aphasia
4 repeat tau and overlaps with PSP
A

CBD (cortio-basal ganlgionic degeneration)

64
Q 
What is this:
Axial rigidity
	Loss of vertical and terminally all EOM 
	Dementia/dysphagia/dysarthia 
4repeat Tau
A

PSP (progressive supra-nuclear palsy)

65
Q

What 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
20% of pre-senile Alzheimer’s are due to this
3 repeat Tauopathy

A

FTLD (fronto-temporal lobar degeneration)

66
Q

The amyloid precursor protein has a (blank) function with (blank) control and cell binding

A

G protein

calcium

67
Q

Beta amyloid peptide can misfold into (blank) and (Blank)

A

fibril

aggregate

68
Q

B amyloid fibrils can travel in (blank) to neighboring cells forming template for further misfolding

A

axons

69
Q

where does degenearation first occur in the brain with alzeheimers?

A

medial temporal lobe and then travels to pairetal lobe and temporal lobe

70
Q

Is parkinson a systemic disease or a local disease?

A

systemic disease

71
Q

lewy body fromation follows what kind of path?

A

a caudal - rostral path

72
Q

What is the Braak staging of lewy bodies?

A

asymptomatic phase, presymptomatic phase

73
Q

What is this:
Eosinophilc, round intracytoplasmic inclusions
Described in 1912 by a German neuropathologist
Inclusions particularly numerous in the substantia nigra pars compacta.

A

lewy bodies

74
Q

what do you find in parkinsons and dementia?

What do you find in alzheimers disease

A

synuclein and lewy bodies

amyloid plaque cores

75
Q

What is affected in BRAAK stage 1 and 2?

A

(olfactory neurons and motor nucleus of vagus)
DMN-X- MOTOR FUNCTION TO PHARYNX, GUT
SENSORY FUNCTION FROM PALATE , PHARYNX, GUT
HYPOPHONIA, CONSTIPATION PRECEED OTHER MOTOR SYMPTOMS BY YEARS
CARDIAC SYMPATHETIC DENERVATION
ie. think nose and gut!!!!

76
Q

if you have alot of amyloid you probably have what?

A

alzeheimers

if you dont have any, you have some form of dementia

77
Q

when you are in stage one of braak, why do you have olfactory loss?

A

because you have damage to the olfactory bulb, and ant. olf. nerve, and amygdala is damaged

78
Q

When you are in stage one of braak stage. why do you have dysautomonia-gastroparesis, constipation, urinary urgency, erectile dysfunction?

A

because you have damage to dorsal motor nucleus of vagus, symp. ganglia, enteric plexu, intermed/later column cord

79
Q

When you are in stage 2,3 of braak stage why do you have depression/anxiety?

A

your locus ceruleus, raphe nucleus, amygdala, limbic cortex

80
Q

Why do you have disorganized Rem sleep behvaior when stage 2 of braak stage?

A

nucleus subcerules, peduculopontine nucleus, thalamus, hypothalamus are affected

81
Q

What are the three components that contribute to the overlapping nature of parasomnias?

A

sleep phenomena, seizures, psychogenic

82
Q

What kind of parasomnias are these:
PTSD
nocturnal panic
dissociative disorders

A

psychogenic

83
Q

What kind of parasomnias are these:
confusional arousals
sleepwalking
sleep terrors

A

NREM

84
Q

What kind of parasomnias are these:
hypnagogic hallucinations
sleep paralysis

A

REM disorders

85
Q

Parkinson is associated with what kind of disorder?

A

affective disorder

86
Q 
What BRAAK stage is this:
SUB-CORTICAL DEMENTIA
IMPAIRED CONCENTRATION
SLOWED RESPONSES
PERSONALITY CHANGE
VARIABLE COGNITIVE LOSS
A

BRAAK stage 6

87
Q

What stage of BRAAK is this:
Hallucinations of…..
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

88
Q

What are 2 distinct disorders with a common cholinergic deficit?

A

PDD and AD

89
Q

How can you differentiate between PDD and AD?

A

PDD:
lewy body pathology in cholinergic basal forebrain and brainstem PPT
AD: neurofibrillary tangles in cholinergic basal forebrain and brainstem PPT

90
Q

When you have parkinsons disease, what happens to your blood pressure as you stand up?

A

it goes down

Block 5 Week 5 Dani (9 decks)

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