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Geriatrics > Dementia > Flashcards

Dementia Flashcards

1
Q

What is the rate per year of someone with mild cog impairment converting to Alzheimers disease?

A

5-10% (compared with 1-2% normal)

Need to have significant cog decline from previous level in one or more domain but the deficits do NOT interfere with the capacity for independence in every day activities (i.e. compensatory strategies for complex ADLs)

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2
Q

True or false- can get prominent parkinsonian features in vascular dementia?

A

True

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3
Q

What are the synucleopathies and why are they called that?

A

DLB
MSA
Parkinson’s disease

See accumulation of alpha synuclein

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4
Q

What are the tauopathies and why are they called that?

A

Alzheimer’s disease
PSNP
Frontotemporal dementia

Tau protein is deposited within neurons in the form of neurofibrillary tangles (NFTs)

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5
Q

What do you see on SPECT and PET in DLB?

A

Occipital hypoperfusion

On MRI the mesio temporal region is spared.

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6
Q

What is the classic presentation in vascular dementia?

A

Memory loss can be spared early improve by prompting; not rapid forgetters
Poor attention
Gait affected- looks like PD but more apraxic
Language usually ok, just some dysarthria
Executive dysfunction may be prominent

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7
Q

What are the three core features and what are some other features suggestive of DLB?

A
  1. Fluctuating cognitiosn
  2. Recurrent visual hallucinations
  3. Spontaneous features of parkinsonism a year post onset (truncal, slowed gait, less tremor, less L dopa response)

Suggestive:
REM sleep behaviour
Severe neuroleptic sensitivity- Quetiapine if must fFTD
Low DA uptake in basal ganglia on SPECT or PET
Falls, autonomic dysfunction
Depressions
Executive dysfunction
Unexplained black outs
RELATIVELY PRESERVED MEMORY
Marked attention and visuospatial difficulties

OFTEN RESPOND VERY WELL TO CHOLINESTERASE INHIBITORS- but can lead to worse tremor and drooling

Rapid onset with progressive decline compared with AD

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8
Q

What areas to cholinesterase inhibitors improve?

donepezil
galantamine
rivastigmine

A

Attention, concentration, anxiety, apathy, depression

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9
Q

MOA Donepeil

A

Prevent breakdown of Acetylcholine by inhibiting acetylcholinesterase

Note slows or prevents decline with NNT of 10 but not disease modifying. May improve adverse behavious and delay onset of adverse behavior. Might delay admission to nursing home. Retain ADLs

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10
Q

MOA glantamine

A

Allosteric potentiator of human nicotinic ACh receptors

Also weak body wide reversible cholinesterase inhibitors

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11
Q

MOA rivastigmine

A

Inhibits butylcholinesterase

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12
Q

Doneepezil side effect profile

A 
GI upset
AV block
Syncope OR 1.5
Asthma
Peptic ulcer disease
Insomnia with vivid dreams 
Increase frequency urination
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13
Q

Memantine MOA

A

In AD there is increased glutamate with XS activation of NMDA with increased intracellular calcium

Memantine is an NMDA antagonist

Benefits on agitation and aggression
Used in mod-severe AD and VD
Can use with donepezil

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14
Q

When people talk about “cortical” features of dementia, what do they mean?

A

Apraxia
Aphasia
Amnesia
Agnosia

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15
Q

Where is amyloid?

A

between cells

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16
Q

Where is tau?

A

inside cells

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17
Q

What are the main risk factors for AD (hint unmodifiable)

A

Female
Age
Family history
APOE4

18
Q

What is thought to be the defect in Alzhimers disease familial?

A 
AD in under 1%
Associated mutations: 
-APP
-presenilin  1
-presenilin 2

Presinilin proteins make up part of gamma secretase which cleave APP to give amyloidogenic Amyloid beta protein 42. (alpha secretase is ok)

19
Q

What is the role of amyloid precursor protein?

A

Cleaved pathologically by secretase–>increase in beta amyloid. APOE4 interacts with beta amyloid in some way.

20
Q

What does functional imaging and imaging in general show in FTD?

A

Asymmetrical frontal/temporal atrophy but can be bilateral

Hypometabolism and hypoperfusion in same areas

21
Q

What are the motor syndromes associated with FTD?

A

Motor neuron disease (upper and lower limbs, but more prominent bulbar dysfunction- facial, tongue weakness, dysphagia)

Corticobasal degeneration

PSNP

22
Q

Corticobasal degeneration clin picture

A

Asymmetric parkinsonism, apraxia, myoclonus, dystonia, alien limb syndrome

HypER reflexic
Axial rigidity
abnormal eye movement- slow pursuit, saccadic

23
Q

What do you see pathologically in DLB?

A

Lewy bodies- eosinophilic intracytoplasmic accumulations of alpha-synuclein revealed by ubiquitin and alpha synuclein staining techniques

24
Q

Treatment of DLB?

A

Levodopa for falls risk
Cholinesterase inhibitors work
For psych symptoms use agents that do not block dopamine receptors- eg clozapine

25
Q

Most common dementia?

A

AD or AD/VaD

26
Q

Prevalence of AD as per age?

A

1-2% in 65-74
25% over 85

doubles every 5 years

27
Q

DSM 5 defining dementia now called MAJOR NEUROCOGNITIVE DISORDER

A

Evidence of significant cognitive decline from prev level performatnce

One or more areas:
learning and memory
language
exec dysfunction
complex attention
social cognition
perceptual-motor

not exclusively during delirium

Not better explained by another mental disorder

28
Q

What are the limitations of MMSE?

A

Not sensitive for AD - but specific
not good for frontal or executive dysfunction
depend on age, language, education level
not good for tracking change over time

29
Q

Strongest RF for AD?

A

Age

Also FH, female, head injury, MCI, vascular disease, low B12 or folate, apolipoprotein E e4 allele, Down’s

30
Q

4 types of AD

A

amnestic (usual type)

logopenic aphasia - early non fluent aphasia

posterior cortical atrophy with aprasxia, prominent visuospatial deficits

Frontal varient looks like FTD with early behavioural sx

31
Q

What possibly reduces risk AD?

A

Physical exercise current (not in youth)

32
Q

How does aplipoprotein E on chromosome 19 predispose to AD?

A

controversial

E4 allele is strong RF for AD, especially with head injury - mean onset in 60s rather than 80s
>50% late sporadic AD have E4
Around 20% have at least one E4

DO NOT check someones ApoE4

33
Q

Types of FTD?

A

Behavioural
Semantic dementia (fluent but jibberish)
Primary progressive aphasia (nonfluent- stuttering)
Motor subtypes (MDN, CBD, PSNP)

MND is associated with chromosome 17

Recent progranulin mutation identified
Also TDP 43

34
Q

Does FTD run in family?

A

About half have FH

35
Q

What are the neuropathologies that you see in AD?

A

Tau–>tangles- inside cells
Lewy bodies –>alpha synuclein
Plaques (amyloid) -outside cells

36
Q

How is PET useful in AD?

A

useful to rule IN AD

37
Q

What CSF biomarkers do you see?

A

Amyloid beta 42 decreased
p-tau increased

in AD

38
Q

MRI findings in AD

A

generalised atrophy
volume loss hippocampi

PET shows hypometabolism of precuneus and lateral parietotemporal cortex

39
Q

Mainstay of treatment of behavioural disturbance in dementia?

A

behavioural mx
carer education/support
Otherwise, evidence for risperidone in aggressive or psychotic nursing home patients
Evidence for olanzapine
No evidence for quetiapine or newer agents

40
Q

What increases risk of MCI converting?

A 
FH AD
Imaging changes consistent with AD (pet shows amyloid)
CSF biomarkers
increase age
rapid forgetting on neuropsych testing
41
Q

lewy body imaging

A

occipital hypoperfusion on SPECT and PET

MRI shows mesiotemporal SPARING!

Geriatrics (8 decks)

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