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Block 5; Week 5 > Dementia > Flashcards

Flashcards in Dementia Deck (73)
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1
Q

What is the prevalence of dementia at 85+ years of age?

A

40%

2
Q

T/F Our population is getting older & therefore our population of demented patients is getting larger.

A

Yeah, true.

3
Q

What is dementia?

A

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

4
Q

Do patients with Down’s Syndrome have dementia?

A

No. It must be acquired. Those with congenital mental & developmental delays do not have dementia.

5
Q

T/F Delirium & dementia are the same.

A

False. They are different. one of the main distinguishing characteristics of dementia is that it is persistent. Delirium is not.

6
Q

If you have amnesia or aphasia & nothing else—>do you have dementia?

A

No. b/c dementia does not consist of isolated deficits, but of multiple deficits. A syndrome.

7
Q

The diagnosis of dementia requires diminishment in 3 or more domains of mental capacity. What are some options for domains?

A
**there are 9 domains
memory
language: receptive & expressive
perception
praxis
calculations
semantic knowledge: conceptual knowledge
executive functions
personality
emotional expression/awareness
8
Q

What is praxis?

A

knowledge of how to do things–>use a screwdriver

9
Q

Name 4 common dementia syndromes.

A

Alzheimer’s Disease
Dementia with Lewy Bodies
Vascular Dementia
Frontotemporal Dementia

10
Q

What is the usual age of onset of Alzheimer’s disease? Which deficit usu occurs first? What are the other losses that often happen?

A

usual age of onset–>age 65
usu memory goes first.
slowly progressive decline in recent memory, language, visuospatial impairment, executive dysfunction

11
Q

Describe what happens in dementia with lewy bodies.

A

fluctuating course
dementia followed by spontaneous parkinsonism
visual hallucinosis and/or psychosis
neuroleptic sensitivity

12
Q

What are the signs of vascular dementia?

A

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

13
Q

What is the usual age of onset for frontotemporal dementia? What are the beginning losses? What is eventually lost?

A

age of onset less than age 65
prominent impairment of behavior, social conduct, judgment
early disturbance of language, progressive aphasia
begins with language loss or behavioral control loss or loss of concepts.

14
Q

What is the difference b/w dementia & mild cognitive impairment?

A

Dementia: memory loss & loss of at least 2 cognitive domains; diminished ADL
Mild Cognitive Impairment: memory loss but persevered condition & ADL

15
Q

T/F If you can do activities of daily living–you are NOT demented.

A

True.

16
Q

Does mild cognitive impairment ever progress to dementia?

A

Yes-1/3 of the time
1/3 of the time you remain at mild cognitive impairment
1/3 of the time you get better! yay!

17
Q

What is the onset, duration, and course of delirium like?

A

acute onset.
duration of hours–days
fluctuating course

18
Q

What is the onset, duration, and course of dementia like?

A

can’t really notice when it starts (insidious)
duration of months to years
usually a constant course

19
Q

What is the arousal, attention, and memory like for patients with delirium?

A

Arousal: lethargic–agitated
Attention: prominent distractibility
Memory: impaired by inattention

20
Q

What is the arousal, attention, and memory like for patients with dementia?

A

Arousal: normal
Attention: normal or mildly abnormal
Memory: amnesia present, but attentional function intact

21
Q

What is speech/language, perception & affect like for patients with delirium?

A

Language: dysarthric, incoherent, dysgraphia prominent
Perception: frequent misperceptions
Affect: fearful or suspicious

22
Q

What is speech/language, perception & affect like for patients with delirium?

A

Language: dysnomic, aphasia
Perception: normal or mildly abnormal
Affect: normal or mildly abnormal

23
Q

What are the motor signs of delirium? What does the EEG show?

A

postural tremor
myoclonus-occurs late in the game
maybe asterixis (tremor of hand when wrist extended)
EEG: diffusely slow

24
Q

What are the motor signs of dementia? What does the EEG show?

A

usually none until late progression of dementia

EEG: normal or mildly slow

25
Q

When old people get lost while driving should you report them? Is this a motor problem or memory problem?

A

usu a memory problem

only if it is a motor problem are they really endangering other people & needed to be reported to the DMV

26
Q

What does normal aging look like?

A

of cognitive and behavioral changes
Most consistently manifests as a generalized slowing of both intellectual and physical performance
preserved crystalline intelligence (old solutions)
decreased fluid intelligence
stable verbal IQ
decreased working memory

27
Q

What is praxis?

A

Integration and performance of learned, complex motor act

28
Q

What is a normal median score for the MMSE for a person with these stats?
>85 years and >12 years of education

A

28

29
Q

What is a normal median score for the MMSE for a person with these stats?
70-74 and >12 years of education

A

29

30
Q

What is a normal median score for the MMSE for a person with these stats?
65-69 and 0-4 years of education

A

22

31
Q

What is the animal naming test? What is this a highly sensitive test for?

A

name as many animals as you can in 1 minute.
highly sensitive for alzheimer’s disease-these people can often only name 12
average normal is 18.

32
Q

Which things count as activities of daily living?

A
Bathing
Dressing
Toileting
Transfer
Continence
Feeding
Independent
Assistance
Dependent
33
Q

Which things count as instrumental activities of daily living?

A
Traveling
Telephone
Shopping
Preparing meals
Housework
Medication
Money
Independent, Assistance, or Dependent
34
Q

Which is a better 3 year predictor of incidence of dementia: ADL or IADL impairment?

A

IADL is a better predictor

35
Q

What are the 2 categories of dementia?

A

subacute & chronic

36
Q

Describe subacute dementia.

A

duration is less than 6 mo

can be caused by prions, tumors or auto-immune

37
Q

What are some tumors that can cause subacute dementia?

A

primary tumors
metastatic tumors
lymphoma

38
Q

What are some autoimmune conditions that can cause subacute dementia?

A

Hashimoto’s Disease
K channel antibodies
Paraneoplastic process

39
Q

What are some neurodegenerative diseases that are caused by normal proteins gone bad?

A

Alzheimer’s Disease
Frontal Temporal Lobe Dementia
DLD?
Creutzfeld-Jakob Disease

40
Q

Which protein is messed up in Alzheimer’s?

A

Amyloid (Abeta42)

Tau

41
Q

Which protein is messed up in Frontal Temporal Lobe Dementia?

A

Tau

42
Q

Which protein is messed up in DLD?

A

Synuclein

43
Q

T/F CJ disease includes prions.

A

True.

44
Q

What are some tauopathies?

A
CTE: chronic trauma encephalopathy
PSP: progressive supranuclear palsy
AD: Alzheimer's
FTLD: Frontal Temporal Lobe Dementia
CBD: Chronic Basal Ganglionic Degeneration
45
Q

What are some amyloidopathies?

A

AD: Alzheimer’s

46
Q

What are some synucleinopathies?

A

MSA: multiple system atrophy
DLB: Dementia with Lewy bodies
PD: Parkinson’s Disease

47
Q

Describe the idea behind protein recycling.

A

old or abnormal protein has a signal on it…ubiquitin attaches to it & it gets put in the trash
proteases (which use ATP) degrade the abnormal protein.

48
Q

What is kuru?

A

seen in people of New Guinea who practiced cannibalism as a part of funeral ritual
women & children ate brain & were most affected
**get an instead gait & dysarthria–eventually get ataxia & uncontrollable laughter
incubation period of 14 yrs…

49
Q

Describe the onset & symptoms of Creutzfeld-Jakob disease.

A

onset-late middle age
usu sporadic
progressive dementia & myoclonic jerks

50
Q

Describe the onset & symptoms of familial fatal insomnia.

A

onset: late middle age
see progressive insomnia & dementia
see spongiform changes in the brain w/o inflammation (spongiform encephalopathy)
death in months following symptoms

51
Q

A lot of these prion disorders started in animals. Describe the deal with scarpie-prion disorder of sheep.

A
onset is 3-4 years
caused by altered prion protein
get intense itching, ataxia, death
shows spongiform encephalopathy
transmitted into the environment thru urine & milk
52
Q

A lot of these prion disorders started in animals. Describe the deal with Mad Cow Disease.

A

affects cows at 4-5 yo
experience weakness, ataxia, spongiform encephalopathy
people can get it when they eat bad cow meat

53
Q

What was the variant of CJD that affect young people in Britain?

A

looked like a psychiatric disorder
due to ingestion of beef that had spongiform encephalopathy
long duration of illness (14 mo)

54
Q

T/F Prions are protease resistant & insoluble.

A

True.

55
Q

Describe prion conversion.

A
normal protein changes & enucleates
starts stacking into beta sheets
it elongates & a piece breaks off
autocatalytic process by which one bad protein starts making a bunch of other proteins bad too
fast progression of disease
56
Q

What is a good test to pick up dead brain tissue from a stroke within an hour of onset?

A

diffusion weight axial CT

57
Q

How do prions spread from cell to cell?

A

Misfolded protein kills the cell-cell membrane damage, excessive energy usage etc
Dead cell releases misfolded protein
Remaining cells engulf the abnormal protein and transport it by axonal transport to synapse

58
Q

Describe how tau protein can undergo prion conversion with head trauma. Which condition does this describe?

A
  • *head trauma can cause micro-hemorrhages
  • *tau holds things together with axonal transport from soma to synapse.
  • *when tau is released b/c of trauma->it is picked up by another cell & misfolds into fibrillar form
  • *this is what happens in chronic traumatic encephalopathy
59
Q

What is the end result of CTE?

A

atrophy of frontal & temporal lobes

tau deposition in these lobes & in the basal ganglia

60
Q

Cortico-basal-ganglionic degeneration is a pure tauopathy. Which things fall into this category?

A

Parkinson’s
Alien Hand
Apraxia-disorder of motor planning
Aphasia-language problem

61
Q

Progressive supra-nuclear palsy is a pure tauopathy. Which things fall into this category?

A
Axial rigidity
messed up ocular movements
dementia
dysphasia
dysarthria
62
Q

20% of Pre-Senile Alzheimer’s is ______.

80% of Dementia is _______.

A

Frontal Temporal Lobar Dementia

Alzheimer’s

63
Q

What are some of the pathological things that observed upon autopsy of Alzheimer’s patients?

A

amyloid plaques

tau & neurofibrillary tangles

64
Q

What is the amyloid precursor protein?

A

transmembrane protein
involved in cell adhesion
has a G protein

65
Q

Why can the amyloid precursor protein turn evil?

A

secretases will eat the APP up & spit out external & internal portions of it.
they will leave a beta amyloid peptide (40-42AA)
Beta amyloid can misfold & aggregate

66
Q

Which area of the brain is first targeted by Alzheimer’s?

A

medial temporal lobe is the first to go!

67
Q

T/F Parkinson’s is a systemic disease, not a brain disease.

A

True…

68
Q

Describe Braak’s staging of Lewy bodies.

A

the protein that is evil gets into the brainstem
then it gets into the basal ganglia
then it moves to the cortex

69
Q

What are the symptoms of stage 1 of Braak? Which structures are damaged during this stage?

A

constipation & dysautonomia & orthostatic hypotension
anosmia-b/c the protein is found in the nasal epithelium
**DMX & Olfactory nucleus are damaged during this stage.

70
Q

What are Lewy bodies?

A

eosinophilic & intracytoplasmic inclusions

they are particularly numerous in the substantia nigra pars compacta

71
Q

Which structures are damaged during stages 3 & 4? What are the symptoms of this?

A

Structures: locus ceruleus, raphe nucleus, amygdala, limbic cortex–>Symptoms: depression, anxiety
Structures: nucleus subceruleus, peduculopontine nucleus, thalamus, hypothalamus–>symptoms: Sleep Rem disturbance
**substantia nigra is also damaged in stage 4

72
Q

Which structures are damaged in stage 6? What are the symptoms of this stage?

A
thalamus & neocortex compromised.
get hallucinatory experiences.
impaired concentrations. 
personality changes
**dementia
73
Q

A cholinergic deficit can often be seen in which 2 separate disorders? What is the treatment for this?

A

Parkinson’s Disease (Lewy bodies in cholinergic basal forebrain)
Alzheimer’s Disease (neurofibrillary tangles in cholinergic basal forebrain)
**use cholinesterases