32. Deterioration of intellect Flashcards

1
Q

what is dementia

A

An acquired global impairment of intellect memory and personality without impairment of consciousness, that is usually (but not always) progressive and usually irreversible

Presentation: Progressive IMPairment of Intellect, Memory and Personality resulting in impairment in the activities of daily living.

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2
Q

approach to ?cognitive decline

A
  1. rule out reversible causes = PINCH ME, mood, agitation, bleed, hearing loss
    - examination: CN, neuro Ul, LL, hearing, cardiovascular (vascular dementia)
    - bloods: confusion screen
    - imaging: CT head ?bleed
  2. Assess cognitive decline severity eg MMSE
  3. Get imaging during the work up eg CT or MRI
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3
Q

What assessment tools for dementia are recommended for the NON-specialist setting

A

10-point cognitive screener (10-CS),

6-Item cognitive impairment test (6CIT)

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4
Q

interpretation of MMSE

A

<24 = could be dementia

<10 severe dementia

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5
Q

presentation alzhimers

A

insidious onset, Loss of ability to learn, process and retain new info, memory loss especially for names and recent events, language deficits, rapid forgetting, normal gait and neuro exam early

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6
Q

imaging results alzhimers

A

generalised atrophy (esp medial temporal and parietal later), beta amyloid plaques amyloid plaques and neurofibrillary (tangles tau protein tangles within brain cells)

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7
Q

management alzhimers

A

non-pharma
- activities to promote wellbeing

pharma
1. acetylcholinesterase inhibitor eg donepezil, galantamine and rivastigmine)

  1. memantine (an NMDA receptor antagonist)
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8
Q

what investgation should you do before prescribing acetylcholinesterase inhibitors ?

A

ECG

Unsafe if have QT prolongation, third degree heart block, sinus bradycardia - always check ECG before prescribing.

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9
Q

adverse effects acetylcholinesterase inhibitors

A

cholinergic side effects such as diarrhoea, nausea and vomiting, bradycardia, increased salivary production and urinary incontinence.

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10
Q

SE acetylcholinesterase inhibitors

A

diarrhoea

donezapil - insomnia

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11
Q

SE memantine

A

constipation

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12
Q

presentation vascualr dementia

A

abrupt or gradual onset, focal neurological signs, signs of vascular disease, stepwise deterioration in someone with previous cardiovascular illness or events.

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13
Q

pathology/imaging findings vascualr dementia

A

strokes, lunacar infarcts, white matter lesions, vulnerable to CVS events

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14
Q

what imaging is best for vascualr dementia

A

MRI

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15
Q

what may be used to help make a diagnosis of vascualr dementia

A

NINDS-AIREN criteria

  • presence of cog decline that interferes with ADLs, not due to secondary effects of CVS event
  • cerebrovascular disease as shown by neuro signs and/or imaging
  • relationship between the above, inferred by
    the onset of dementia within three months following a recognised stroke
    an abrupt deterioration in cognitive functions
    fluctuating, stepwise progression of cognitive deficits
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16
Q

management of vascualr dementia

A
  1. manage CVS risk
    eg Antiplatelet therapy (aspirin, clopidogrel), Carotid angioplasty/stenting, BP control, glycaemic control, statins

+ supportive and social prescribing

17
Q

presentation frontotemporal dementia/picks disease

A

insidious onset, 50-60yo, rapid progression, sibinhibition, socially inappropriate, poor judgement, apathy, poor executive function, impulsivity.

No movement abnormalities

18
Q

pathology/imaging frontotemporal dementia

A

MRI shows significant atrophy of the frontal and temporal lobes. Pick cells and pick bodies in cortex

19
Q

management of picks disease

A

supportive care, benzos, antipsychotics

NICE do not recommend that AChE inhibitors or memantine are used in people with frontotemporal dementia

20
Q

what is Semantic dementia

A

a type of frontotemporal lobar degeneration

fluent progressive aphasia. The speech is fluent but empty and conveys little meaning. Unlike in Alzheimer’s memory is better for recent rather than remote events.

21
Q

common features of the frontotemporal lobar dementias

A

Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems

22
Q

triad in pellagra? other fetaures>

A

Dementia, Dermatitis, Diarrhoea

Other features include hair loss, sunlight sensitivity and glossitis.

23
Q

cause of pellagra? risk factors?

A

Caused by vitamin B3 (niacin) deficiency.

Alcoholism and crohn’s are risk factors for pellagra due to malnutrition/malabsorption. Pellagra may occur as a consequence of isoniazid therapy (isoniazid inhibits the conversion of tryptophan to niacin).

24
Q

tetrad of wernike’s

A

ataxia, ophthalmoplegia, nystagmus and acute confusional state

25
Q

where are the lesions in wernikes

A

mamillary bodies and ventricle walls

26
Q

which b vitamin is thiamine

A

B1

27
Q

what is korsakoffs

A

irreversible damage and haemorrhage to the mammillary bodies of the hypothalamus and the medial thalamus

28
Q

features korsakoffs

A

anterograde amnesia: inability to acquire new memories
retrograde amnesia
confabulation