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Block 8 Week 5 > Aziz: Dementia > Flashcards

Aziz: Dementia Flashcards

1
Q

Which structures in the brain are involved in the circuitry of cognition?

A 
cortex
basal ganglia
cerebellum
thalamus
pons
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2
Q

What are the cognitive domains that need to be assessed in a patient with dementia?

A 
memory
attention
executive function
language
visuospatial abilities
behavior
functional status
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3
Q

What is the best screening test for patients with dementia?

A

MMSE

**can also use MOCA, mini cog, or clock drawing

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4
Q

What is mild cognitive impairment?

A

cognitive impairment that doesn’t interfere with activities of daily living and is not severe enough to meet criteria for dementia

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5
Q

T/F: Mild cognitive impairment can affect a single domain or multiple domains

A

True

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6
Q

What percentage of patients with mild cognitive impairment eventually convert to dementia in 6 years?

A

80%

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7
Q

3 risk factors for the progression of mild cognitive impairment to dementia?

A
  1. apolipoprotein allele carrier
  2. poor performance on semantic cueing memory test
  3. reduced hippocampal volumes
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8
Q

What is dementia? What causes it?

A

progressive deterioration of cognitive function that results in impairment of social and occupational functioning; caused by relentless brain tissue (neuron) degeneration

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9
Q

List a few types of dementia that we spoke about

A 
Alzheimer dementia
dementia with Lewy bodies
frontotemporal dementia
vascular dementia
Parkinson disease dementia
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10
Q

What are some risk factors for Alzheimer dementia?

A 
age 
female sex
low level of education
down syndrome
head trauma
apoE
genetics
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11
Q

What might you notice histologically about the neurons in a patient with dementia?

A

formation of plaques in the interstitial space between neurons
neuronal cells are unhealthy and plump

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12
Q

What happens to the cortex in patients with Alzheimer’s disease?

A

cortical atrophy

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13
Q

Symptoms of Alzheimer disease?

A

memory loss that disrupts daily life +
at least one of the following:
aphasia, apraxia, agnosia, disurbed executive function

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14
Q

In Alzheimer’s, the cognitive abnormalities must represent a change from a previous higher level of function, be (blank), & impair (blank)
Gradual onset and continued decline
Not present exclusively during a period of (blank).

A

progressive; functioning; delirium

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15
Q

What tests should be done on a patient with dementia?

A 
CBC
glucose, electrolytes, BUN/creatinine, liver functioning
serum vit B12
thyroid function tests
noncontrast CT or MRI
depression screening
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16
Q

Tests that should not be performed routinely on patients with dementia?

A 
syphilis screening
EEG
lumbar puncture
linear or volumetric MRI or CT
SPECT
APOe genotyping
17
Q

T/F: ApoE-e4 testing does not add substantially to the diagnosis of Alzheimer’s, and is not recommended as a part of routine screening

A

True

18
Q

3 stages of Alzheimer disease?

A

pre-symptomatic phase
symptomatic, pre-dementia phase
dementia phase **insidious onset over months to years with a progressive history of cognitive decline

19
Q

What will the CSF AB1-42 be like if a patient has Alzheimer’s? Wht will phosphorylated tau and total tau be like?

A

CSF AB1-42 will be low (being used up in the formation of neurotic plaques)
tau will be high, because with neuronal atrophy, tau will leak out and will be high

20
Q

What are some aspects of the total care for patients with dementia?

A 
home care
institutionalized care
hospital care
clinic care
community care
21
Q

Dementia complications?

A 
inadequate nutrition
reduced hygiene
difficulty taking meds
deteriorating emotional health
difficulty communicating
delusions and hallucinations
sleep difficulties
22
Q

How do we treat Alzheimer’s dementia?

A

AChE inhibitors like Rivastigamine and Donepezil and Galantamine

OR

Memantine which is an NMDA antagonist (blocks activation of these receptors to avoid excitotoxicity and too much neuron death)

23
Q

What is the cholinergic theory of AD?

A

Alzheimer’s dementia is associated with decreased cholinergic activity
AChE inhibitors slow the breakdown of ACh to keep it present in the synapses longer!

24
Q

What is the glutamate hypothesis of AD?

A

glutamate is released in large amounts in dead or dying neurons; increased extracellular glutamate increases NMDA receptor activity and can lead to excitotoxicity and death in downstream neurons

25
Q

So what does memantine do for patients with Alzheimers? What are the side effects?

A

blocks NMDA receptors to prevent glutamate excitotoxicity; dizziness, confusion, headache, constipation

26
Q

How can we prevent dementia?

A 
treat it early
diet
physical exercise
intellectual activities
manage CV risk factors!!
27
Q

This is probably the best prevention for dementia…

A

view the brain as a highly vascular organ and take measures to stay healthy cardiovascularly; exercise, eat fish, low sat fat diet, green tea, red wine, mediterranean diet

28
Q

What is the prognosis of Alzheimer’s disease? Like from diagnosis to death?

A

~4.5 years survival from incident dementia to death

29
Q

What are three subtypes of frontotemporal degeneration?

A

behavioral variant: irritability, disinhibition, lack of empathy

semantic variant: word finding difficulty, loss of meaning of words

progressive nonfluent aphasia:

30
Q

Which type of frontotemporal dementia is this?

lack of insight, hyperorality, apathy, irritability, disinhibition, lack of empathy, rudeness

A

behavioral variant

31
Q

What type of frontotemporal dementia is this?

fluent, effortless, and grammatically correct, but word finding difficulty = empty speech, naming deficits and loss of word knowledge.

A

semantic variant

32
Q

What type of frontotemporal dementia is this?

agrammatism, speech apraxia, word finding difficulties, speech effortful, slow

A

progressive nonfluent aphasia

33
Q

What genes are involved in frontoremporal dementia?

A

chromosome 17 *associated with tauopathy

chromosome 9 *associated with TDP-43 proteinopathy

34
Q

Dementia caused by an accumulation of small lesions in the vasculature; could be due to a single strategic infarct, cerebral hemorrhage, extensive microvascular disease

A

vascular dementia

**this is why you need to keep your heart/vessels in shape!

35
Q

Core features:
Fluctuating cognition or alertness
Recurrent visual hallucinations
Spontaneous motor symptoms of parkinsonism
Supportive features: repeated falls, syncope or transient LOC, delusions, neuroleptic sensitivity, hallucinations of other modalities, REM sleep behavior disorders, depression
MRI: Normal or whole brain atrophy
Pathology: Lewy Bodies.

A

dementia with lewy bodies

36
Q

What are some characteristic features of dementia with Lewy bodies?

A 
fluctuating cognition or alertness
recurrent visual hallucinations
spontaneous motor symptoms of parkinsonism
repeated falls
syncope
delusions
hallucinations

Block 8 Week 5 (13 decks)

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