Dementia Flashcards

1
Q

Most decline skill

A
Speed processing (digit symbol, letter, patten comparison)
Working memory (reading, computation, etc)
Long term memory
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2
Q

Last to decline

A

World knowledge (vocab)

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3
Q

What is dementia?

A

Declines in cognitive, function, and behaviour?

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4
Q

Most common cause of dementia?

A

Alzheimers

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5
Q

Cause of Alzheimers Disease?

A

Unknown.

Risk factor is age.

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6
Q

Life expentancy of A.D.

A

3-20yrs post diagnose.

8yrs average

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7
Q

Diagnosis of A.D.

A
History taking.
Cognitive Ax (mini mental, etc)
Neurological Ax
Meds review
Blood tests.
Amyloid imaging.
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8
Q

Symptoms of A.D.

A

Changes in memory.
Atrophy of brain.
Declining amyloid-beta protein.

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9
Q

Atrophy of brain

A

Widening of sulci and enlargement of ventricles.

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10
Q

Most affected lobes in brain atrophy

A

Frontal, temporal, and parietal.

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11
Q

Pre clinical A.D.

A

First noticed in Entorhinal cortex, then proceed to hippocampus.

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12
Q

First sign of A.D.

A

Memory loss (misplace item, forget recent events, get lost easily)

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13
Q

Mild to moderate A.D.

A

Cerebral cortex begins to shrink

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14
Q

Mild AD signs

A

memory loss, confusion, trouble handling money, mood changes, increased anxiety.

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15
Q

Moderate AD signs

A

increase memory loss, problems recognising people, difficulty with language and thoughts, restlessness, agitation, wandering, etc

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16
Q

Sundowning behaviour

A

behavioural problems tend to begin or worsen in late PM/evening.

17
Q

Severe AD

A

Extreme shrinkage in brain occur. Dependant on others for care.

18
Q

Severe AD signs

A

weight loss, seizure, skin infection, groaning, moaning, grunting, incontinence.

19
Q

Death in AD is commonly due to

A

Aspiration pneumonia, or other infections.

20
Q

? Hypothesis of AD

A

Reduced choline uptake and acetylcholine release.

Loss of cholinergic neurons from basal forebrain.

21
Q

Enzyme responsible for synthesis of acethycholine?

A

Choline acetyltransferase.

22
Q

Treatment for AD

A

Acetylcholinesterase inhibitors.

23
Q

Pathology of AD

A

Increased levels of amyloid beta peptide.
Increased levels of hyperphosphory-lated tau (p-tau).
Widespread loss of neurons and synapses.

24
Q

What is p-tau??

A

a microtubule assembly protein that accumulates intracellularly as neurofibrillary tangles (NFTs).

25
Q

Non AD pathway

A

Alpha cleavage to gamma cleavage

26
Q

AD pathway

A

Beta cleavage to gamma cleavage.

27
Q

What happens when APP is cleaved by B and Y secretase enzymes??

A

neurotoxic AB peptides are released.

28
Q

Accumulation of AB can lead to

A

Axonal damage.

Synaptic damage, excitotoxicity, mitochondrial dysfunction, lysosomal failure, damage to signalling pathways.