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Neuro (M2) > Alzheimer's Disease > Flashcards

Alzheimer's Disease Flashcards

1
Q

Other term for dementia

Description

A
  • Major neurocognitive disorder
  • Decline in 1+ cognitive domains, decrease in ADL’s, +/- behavioral disturbance
  • Decline in cognition includes: impaired memory, disturbed language, visuospatial abnormalities (difficulty driving), decreased problem solving / executive function (including sequencing [pants on before shoes]), reduced attention, apraxia, agnosia
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2
Q

Minor neurocognitive disorder

A

Modest decline in 1+ cognitive domains, ADLs intact but require increased effort, +/- behavioral disturbance.
Usually occurs 2-3 years before dementia.

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3
Q

Avg age of AD
Life expectancy
How long do drugs delay progression?

A

75-85
Avg life expectancy is 6-12 years from diagnosis
Drugs delay progression by 6-12 months.

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4
Q

What percentage of Parkinson’s pxs get dementia?

A

50%

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5
Q

What part of brain is involved in memory storage?

A

Association cortices

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6
Q

What part of brain is involved in memory retrieval?

A

Frontal cortex. Need to come up w/ strategy to recall something.

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7
Q

What part of brain is involved in declarative memories?

A

Hippocampus and temporal lobe?

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8
Q

Episodic memory

A

Type of declarative memory in which you remember the context in which a fact took place

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9
Q

Semantic memory

A

Type of declarative memory that is not associated w/ a specific episode in the past

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10
Q

How does PFC lesion affect LTM vs STM?

A
  • LTM – PFC lesion may inhibit source-related information from being encoded / retrieved leading to poor recall.
  • STM – PFC lesion may cause failure of attention and /or impulse control
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11
Q

What is long term potentiation?
Where does it take place?
How does it work?

A
  • Activity-dependent strengthening of synaptic connectivity that underlies memory. One type of plasticity.
  • Occurs in hippocampus and cortex.
  • LTP involves a complex cascade of phosphorylation, protein insertion / removal, protein synthesis, etc.
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12
Q

What brain structure is important for consolidation of info into LTM?

A

Hippocampus

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13
Q

Which NTs are altered in AD?

A

Deficits in Ach and somatostatin, possibly due to loss of neurons. Ach involved in RAS and memory formation.

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14
Q

How does cortical atrophy progress in AD?

A

Usually begins in the hippocampus and medial temporal lobe, then parietal cortex, then the remainder of neocortex.

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15
Q

Hydrocephalus ex vacuo

A

Enlargement of ventricles w/o increased spinal CSF pressure.

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16
Q

What are senile plaques made of?
How do they form?
What do they do?
What stain is used to see plaques?

A
  • EXTRACELLULAR deposition of fibrillar amyloid-β (Aβ) results in amyloid (senile) plaques. Made of amyloid, dystrophic neurites, proinflammatory cytokines, MAC (C5-9), Apo E, aluminum, and microglia
  • Aβ peptides are produced from amyloid precursor protein (APP) by combination cleavages with β-secretase and γ-secretase.
  • Aβ triggers oxidation, excitotoxicity, plaque formation, inflammation, and tau hyperphosphorylation, all of which kill neurons.
  • Amyloid is visualized w/ Congo Red stain or immunohistochemical stains
17
Q

What are neurofibrillary tangles?

How are they visualized?

A

Intraneuronal inclusion bodies made of paired helical filaments of hyperphosphorylated tau.
Tau is visualized w/ silver stain or immunohistochemistry.

18
Q

Microglial activation

A

Initially, microglia function normally and help clear plaques by phagocytosis, but they cannot adequately clear all the plaques and may actually contribute to pathology. Over time, microglia lose their ability to take up / degrade Aβ, and instead show increased expression of inflammatory cytokines.

19
Q

Amyloid angiopathy
How common?
Which parts of brain are affected?

A

Amyloid gets into plaques / vessels. Vessels may become brittle and hemorrhage. Cerebral amyloid angiopathy occurs in 90% of AD pxs. Occipital lobes are most commonly and severely affected.

20
Q

DSM Criteria for MND due to AD (3 main things)

A
  • Criteria met for major neurocognitive disorder
  • Insidious onset and gradual progression of impairment
  • Disturbance not due to cerebrovascular disease
21
Q

AD risk factors

A

Aging (most important), head trauma, education (higher education is protective), female gender (may just be b/c women live longer), Al / NO toxicity, inflammation (including plaques), late life depression, CV risk factors (HTN, dyslipidemia, A fib, obesity, smoking).

22
Q

Which proteins are detrimental in AD? Beneficial?

A
  • Apo E4 is risk factor.
  • Presenilin 1 / 2 mutations. Precursor to gamma secretase protein.
  • Apo E2 is protective.
23
Q

How is familial AD inherited?

A

Autosomal dominant

24
Q

Early ADL functional impairment vs late functional impairment.

A
  • Early on (Instrumental ADL’s): driving, meal prep, shopping, financial management.
  • Later problems (Basic ADL’s): DEATH: dressing, eating, ambulating, toileting, and hygiene
25
Q

What percentage of AD pxs live at home?

A

70%

26
Q

How common are emotional / psychological disturbances in AD?

Which sxs?

A

Emotional / psychological disturbances affect 90% of pxs w/ AD.
Most common are depression, anxiety, irritability, apathy, insomnia, paranoid delusions, visual hallucinations, restlessness, yelling, swearing, and physical aggression.

27
Q

What percentage of caregivers get depression?

A

33%

28
Q

AD Treatment (4 main things)

A
  • Cognitive enhancing meds – donepezil, galantamine, rivastigmine, or memantine. Approved for AD; Some benefit for vascular dementia and LBD; Not useful for frontotemporal dementia.
  • Behavioral interventions – distraction techniques, use of soothing music, redirecting px
  • SSRI’s, and atypical antispychotics may be used if behavioral interventions fail or if behavior is dangerous. Antipsychotics have black box warning for increased mortality in elders.
29
Q 
Vascular Dementia
Caused by?
Characterized by?
Avg age
Risk factors
Prognosis
A

Due to strokes
Step-wise decline
Avg age = 65-75 y/o
Vascular risk factors - high cholesterol and HTN
Irreversible, but may slow progression via cognitive enhancing meds and by addressing vascular risk factors.

30
Q

Parkinson’s Disease Dementia
Description
Cause
Tx

A

Onset of cognitive symptoms at least one year after the onset of motor symptoms. Classic parkinsonian symptoms (rigidity, tremor, bradykinesia) predominate, and are superimposed with cognitive symptoms such as memory loss, slowed processing speed, and inattention.
Cognitive impairment is due to the development of Lewy bodies throughout subcortical regions.
Tx w/ antiparkinsonian meds +/- cognitive enhancers. Antipsychotics are avoided due to exacerbating Parkinson sxs.

31
Q

Dementia w/ Lewy Bodies (DLB)
4 main characteristics
Pathology
Tx

A

(1) fluctuating symptoms, (2) visual hallucinations, (3) cognitive impairment and (4) less severe parkinsonian symptoms than in Parkinson’s disease.
Lewy bodies are found in cerebral cortex. DLB often coexists with Alzheimer’s disease.
Tx w/ antiparkinsonian meds +/- cognitive enhancers. Antipsychotics are avoided due to exacerbating Parkinson sxs.

32
Q 
Frontotemporal Dementia (FTD)
Pathology
Sxs
Avg age / prognosis
Tx
A
  • Presence of tau inclusion bodies w/ lobar degeneration of frontal / temporal lobe. May have family hx of early dementia.
  • Behavioral disturbance / aphasia. May be hypersexual or hyper-oral.
  • Early FTD may be misdiagnosed as major depression due to sxs of apathy, amotivation, and anergia. May be misdiagnosed as mania due to disinhibition, impulsivity, and irritability.
  • Psychosis may be an early sign of fronto-temporal dementia. Psychosis is a late sign of AD.
  • Onset is usually b/w 50-65. Death usually occurs w/in 5 years.
  • Cognitive enhancing meds are NOT helpful.
33
Q

Psychosis in AD vs frontotemporal dementia

A

Psychosis is an early sign of fronto-temporal dementia. Psychosis is a late sign of AD.

34
Q

In what condition is confabulation common?

A

Alcoholic dementia

35
Q

What is the 2nd most common form of dementia behind AD?

A

Mixed dementia.

50% of pxs w/ VD and DLB also have AD.

36
Q

Reversible causes of dementia (5)

A

Depression (pseudodementia), hypothyroidism, B12 deficiency, normal pressure hydrocephalus, and subdural hematoma.

Neuro (M2) (34 decks)

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