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BB2 > Dementia > Flashcards

Dementia Flashcards

1
Q

Define dementia

A

Clinical syndrome characterised by a cluster of symptoms manifested by difficulties in memory, language, behavioural, psychological changes and impairments in daily living

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2
Q

What are the common symptoms of dementia?

A 
Memory loss
Confusion and disorientation
Difficulty with language
Changes in mood
Social withdrawal
Difficulty with day to day tasks
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3
Q

What are the main dementia screening methods?

A

MMSE - mini mental state exam
GPCOG - GP Assessment of Cognition
MoCA- montreal cognitive assessment

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4
Q

What are the features of the GPCOG?

A
  • Out of 9
  • Time orientation (ask date)
  • Clock drawing (visuospatial functioning) where you ask them to draw the numbers on a clock and draw a specific time, point for each
  • Information - can you tell me something that happened in the news recently
  • Recall - give name and address at start of test and ask to repeat at end which totals up to 5 points
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5
Q

What are the scores significant of in GPCOG?

A 
5-8 = mild impairment
<4 = cognitive impairment
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6
Q

What are the risk factor of dementia?

A

Non modifiable: age, genetic pre-disposition, family history, down syndrome
modifiable: vascular risk factors, cognitive inactivity, environment (head injury), depression

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7
Q

What are the types of dementia and which are more common?

A
  • Alzheimers is most common
  • Vascular
  • mixed
    Dementia with Lewy bodies
  • Parkinson’s and frontotemporal
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8
Q

What is the pathophysiology Alzheimer’s?

A
  • protein misfolding disease (plaque accumulation of protein in brain)
  • beta-amyloid plaque deposits = senile plaques form EC
  • Tau protein hyperphosphorylates = neurofibrillary tangles in cell bodies
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9
Q

Which genetic changes cause early-onset Alzheimer’s?

A
  • Amyloid Precursor Protein - APP (related to downs syndrome as extra APP = extra synthesis) (chromosome 21)
  • Presenilin 1 - PSEN1 (chromosome 14)
  • PSEN2 (chromosome 1)
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10
Q

Which genetic changes causing Alzheimer’s are most common?

A
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11
Q

What do neurofibrillary tangles and senile plaques cause?

A
  • neuritic dystrophy
  • synaptic loss
  • selective neuronal cell loss

= loss of cholinergic cells

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12
Q

What is the normal pathway of APPs?

A
  • protein expressed in neurons/glial cells/endothelial SM and is involved in neuron growth and repair
  • protein cleaved by secretase enzymes
  • protein becomes soluble so can be recycled
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13
Q

What are the features of the secretase protein which cleaves amyloid?

A

PSEN1 and PSEN2 subunits

mutations in these cause Alzheimer’s, PSEN1 most common

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14
Q

What is the diseased pathway of APPs?

A
  • protein is wrongly cleaved by beta and gamma secretases= non-soluble amyloid-beta peptides (most commonly of types 40 and 42)
  • peptides aggregate forming senile plaques
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15
Q

What do senile plaques do?

A
  • potentially get between neurons disrupting signalling so therefore impair memory
  • start an immune response causing microglia activation
  • amyloid angiopathy = haemorrhage risk increased as weakens walls
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16
Q

What is the normal function of the tau protein?

A
  • neurons held together by cytoskeleton which ships nutrients/molecules along the cell
  • Tau stabilises microtubules making up cytoskeleton by binding via kinases/phsophates
  • encoded by MAPT
17
Q

What can a mutation in MAPT cause?

A

MAPT encodes Tau

Mutation can cause fronto-temporal dementia

18
Q

What is the diseases pathway of Tau?

A
  • oxidative stress from amyloid plaques = dysregulation of kinase activity
  • Forms neurofibrillary tangles
  • Stop microtubules from signalling = apoptosis
19
Q

What does kinase do to Tau?

A

Binds phosphate to tau protein causing it to become tangled (hyperphosphorylation) = neurofibrillary tangles

20
Q

What genetic changes cause late onset Alzheimer’s?

A
  • associated with Apolipoprotein E

- important in cholesterol metabolism

21
Q

What are the isoforms of apolipoprotein E?

A
  • ApoE4 poses greatest risk @ chromosome 19

- ApoE2 has protective role

22
Q

What are the biomarkers of Alzheimer’s disease?

A
  • high amyloid beta peptide levels even before onset of symptoms
    in CSF:
  • decreased amyloid beta levels (as forms in plaques so would be less in CSF)
  • increased total tau levels
23
Q

What are the 2 cholinergic treatments for Alzheimers?

A
  • acetylcholinesterase inhibitors

- NMDA receptor antagonists

24
Q

What are some examples of acetylcholinesterase inhibitors?

A
  • donepezil
  • galantamine
  • rivastigmine
25
Q

What is the mechanism of action of acetylcholinesterase inhibitors?

A
  • cholinergic forebrain pathways (limbic and cortical structures) degenerate
  • by inhibiting acetylcholinesterase this increases failing cholinergic signal by breaking down acetylcholine
  • promotes healthy cognition
26
Q

When would acetylcholinesterase inhibitors be used for?

A

Mild to moderate cases

27
Q

What is an example of an NMDA receptor antagonist?

A

memantine

- nitromemantine is a derivative of memantine

28
Q

What is the mechanism of action of NMDA receptor antagonists?

A
  • Slow form of excitotoxicity and increased glutamate in Alzheimers
  • Blocking release of glutamate reduces this
29
Q

When would NMDA receptor antagonists be used?

A
  • moderate Alzheimer’s when patient intolerant to AChe inhibitors
  • severe cases
30
Q

What are some other symptomatic medication for AD?

A
  • antidepressants
  • antipsychotic
  • mood stabilisers
31
Q

What are some new therapeutic approaches/strategies?

A
  • aim is to block synthesis and aggregation of amyloid beta 42 or formation of neurofibrillary tangles of hyperphosphorylated tau protein:
  • inhibition/stimulation of secretases involved in APP metabolism
  • prevention of amyloid aggregation
  • anti-amyloid immunotherapy
  • anti-tau immunotherapy
  • tau phosphorylation and aggregation inhibition

BB2 (31 decks)

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