Alzheimer's Flashcards

1
Q

What are the clinical signs of Alzheimer’s?

A

The 5 As: Amnesia, Anomia, Apraxia, Agnosia, Aphasia

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2
Q

What are the clinical signs of vascular dementia?

A

Step-wise decline, personality changes, history of vascular disease.

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3
Q

What are the clinical signs of dementia with Lewy bodies?

A

Slow, stiff movements, tremor, hallucinations, sleep problems

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4
Q

What are the clinical signs of Frontotemporal Dementia?

A

Inappropriate behaviour, love of sweet food, younger onset (50)

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5
Q

What are the pathology results of Alzheimer’s?

A

Amyloid-beta plaques
Neurofibrillary tangles (tau)
Loss of brain volume

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6
Q

What are the pathology results of vascular dementia?

A

Multiple mini-infarcts

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7
Q

What are the pathology results of dementia with Lewy bodies?

A

Lewy bodies of alpha-synuclein

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8
Q

What are the pathology results of frontotemporal dementia?

A

“Pick bodies” of tau in frontal lobe

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9
Q

Who are in MDT for this?

A

GP
Neurologist
(Radiologist, Pathologist)

Physiotherapist
Occupational Health Therapist
Psychologist

Support Groups
Family/Carer

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10
Q

What is difference between definition of mild cognitive impairment and dementia?

A

The extent to which it impacts activities of daily living

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11
Q

What are the 5As?

A

Amnesia: loss of memory
Anomia: inability to name objects
Apraxia: loss of dexterity e.g. in dressing
Agnosia: inability to recognise things (including people) – different from anomia, in which the understanding of the object’s role/function is preserved.
Aphasia: inability to talk

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12
Q

What is the pathophysiology in AD?

A

-Amyloid precursor protein [APP] = transmembrane protein
-Normal =  and γ secretase → normal degradation product
-AD = by  and γ secretase → abnormal product resistant to degradation → A
-A accumulates outside the cell to form amyloid plaques
-A accumulates outside the cell to form amyloid plaques
-Interferes with neuronal communication (+ inflammation) → dementia
-Tau tangles
Inside the neuron
-Tau = protein that supports microfilaments within the neuron

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13
Q

What does Abeta do?

A

A triggers phosphorylation of tau, causing it to disassociate from the MF and accumulate into neurofibrillary tangles
Tangles + weakened microfilaments → ↓neuronal function and apoptosis → atrophy
↓ACh
Cortex
Pathological changes → degeneration of cholinergic nuclei → ↓ cortical ACh

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14
Q

What are key phrases for AD pathophysiology?

A
  • β Amyloid → extracellular plaques
  • Hyperphosphorylated tau → neurofibrillary tangles
  • Neuronal and synaptic loss
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15
Q

Where does Memory retrieval/long-term memory in the brain?

A

posterior cingulate cortex

hippocampus

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16
Q

Where is short term memory in brain?

A

Anterior thalamus

17
Q

Which two enzymes are amyloid plaques produced by?

A

Beta and gamma secretase

18
Q

Which neurotransmitter is deficient in Alzheimers?

A

acetylcholine

19
Q

What does the MCA say?

A

assume a person has the capacity to make a decision themselves, unless it’s proved otherwise
wherever possible, help people to make their own decisions
don’t treat a person as lacking the capacity to make a decision just because they make an unwise decision
if you make a decision for someone who doesn’t have capacity, it must be in their best interests
treatment and care provided to someone who lacks capacity should be the least restrictive of their basic rights and freedoms

20
Q

What is capacity?

A

-The person must be able to:
-understand the information relevant to the decision
-retain that information
-use or weigh up that information as part of the process of making the decision
-Capacity is decision and time-specific
E.g. may have capacity to choose tea or coffee but may not have capacity to decide whether or not they require help in ADLs.
E.g. may not have capacity today due to fever but may next week when recovered

21
Q

Who decides best interest?

A

Technically, you as the medical professional.

BUT must take into account
The patient
Those caring for the patient
/Family
Independent advocates/ Lasting power of attorneys/court-appointed guides.
22
Q

What was the patient?

A

Patient with memory problems
6-CIT
Diagnosed with probable Alzheimer’s
Clinical communication and ethical challenges

23
Q

What is dementia?

A

Umbrella term for cognitive decline
Insidious onset
Progressive
Interfering with activities of daily life

Not situational stress; clear consciousness​
Deficits: behaviour, attention, memory,language, visuospatial function

8 or above on the 6-CIT

24
Q

What is mild cognitive impairment?

A

Still cognitive decline
Worse than would normally be expected for a healthy person of their age
But NOT interfering with activities of daily life
10-15% progress to dementia per year
6-8 on the 6-CIT

25
Q

What is normal ageing?

A

Key differentiators:
Normal aging preserves temporal orientation, visuospatial skills and insight.

Dementia/MCI tend to lose these.

Both tend to lose verbal recall, mental flexibility and sustained attention