Case 5 wrap up Flashcards

1
Q

long term memory can be split into?

A

declarative (explicit) memory
non-declarative (implicit) memory

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2
Q

declarative (explicit) memory can be split into?

A

episodic (personal episodes in time and space)
semantic (facts, meaning, concepts and knowledge about the external world)

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3
Q

non declarative (implicit) memory splits into 4 types, which are?

A

procedural (skills and habits)
priming and perceptual learning
simple classical conditioning
non-associative learning

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4
Q

memory systems can be split into?

A

long term memory
short term memory (working memory)

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5
Q

what regions of the brain are involved in episodic memory?

A

hippocampus, medial temporal lobe, neocortex

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6
Q

what regions of the brain are involved in semantic memory?

A

lateral and anterior temporal cortex, prefrontal cortex

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7
Q

what regions of the brain are involved in procedural (skills and habit) memory?

A

striatum, cerebellum, motor cortex

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8
Q

what regions of the brain are involved in priming and perceptual learning?

A

neocortex

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9
Q

what regions of the brain are involved in simple classical conditioning?

A

amygdala and cerebellum

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10
Q

what regions of the brain are involved in non-associative learning?

A

reflex pathways

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11
Q

21/30 on MoCA (Montreal Cognitive Assessment) suggests what

A

Suggests Mild Cognitive Impairment (MCI)

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12
Q

what is dementia

A
  • An acquired syndrome of decline in memory
    and/or other cognitive functions sufficient to
    affect daily life in an alert patient
  • Progressive and disabling
  • NOT an inherent aspect of ageing
  • Different from normal cognitive lapses
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13
Q

common causes (aetiology) of dementia

A
  • Alzheimer
  • Vascular
  • Mixed
  • Fronto-temporal
    dementia (FTD)
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14
Q

less common and rare causes (aetiology) of dementia

A
  • Parkinson’s
  • Levy Body Dementia
  • Huntingtons
  • Creuzfelt-Jacob disease
  • etc.
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15
Q

how can mild cognitive impairment be described as? (you don’t need to list all bullet points)

A

A ‘predementia’ syndrome ….
* Subjective and objective cognitive deficit
* No major impairment of ADL (activities of daily living)
* Not inevitably progressive to dementia, but when it is it’s usually Alzheimer’s

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16
Q

neuropathology of Alzheimer’s disease (2 bullet points)

A
  • Starts entorhinal cortex and hippocampus
  • Spreads to most of the cortex except the occipital cortex
17
Q

In Alzheimer’s disease, there is marked atrophy in?

A

In Alzheimer’s disease, there is marked atrophy in superior and lateral regions, with sparing of the occipital lobe

18
Q

pathological features of Alzheimer’s (2 bullet points)

A
  • Extracellular amyloid deposition (plaques)
  • Intraneuronal neurofibrillary tangles (NFT)
19
Q

what about amyloid in AD (3 or 4 bullet points)

A
  • Deposition of insoluble protein fragments
  • Amyloid protein coded for by APP gene
  • APP mutations can cause AD
  • But most cases of amyloid depositions are sporadic (scattered/isolated/ occurs at irregular intervals or only in a few places)
20
Q

what about Neurofibrillary tangles (NFTs) in AD? (3 bullet points)

A
  • Polymerised tau (hyperphosphorylated)
  • Tau forms paired helical filaments
  • Cytosolic (inside neurons)