Dementia Flashcards

1
Q

What is dementia?

A

A neurodegenerative syndrome with progressive decline in several cognitive domains.

The initial presentation is usually memory loss.

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2
Q

How is a diagnosis of dementia made?

A

History from the patient. It is important to exclude any illness causing temporary confusion!

Ask about the timeline of decline and the domains affected, there might be non-cognitive symptoms such as agitation, aggression or apathy. These indicate late disease.

Do cognitive testing.

Examination to identify a physical cause, risk factors such as for vascular dementia and parkinsonism.

Do a medication review to see if any drugs might ellicit symptoms.

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3
Q

Explain cognitive testing in dementia.

A

Dementia screen such as AMTS.

+

Short tests of executive function and language.

Carry out a mental state exmination to identify anxiety, depression or hallucinations

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4
Q

Explain the AMTS.

A

Abbreviated Mental Test Score

1 - 42 west street

2 - Age

3 - Time

4 - Year

5 - Date of birth

6 - Date of 1st/2nd world war

7 - Queen

8 - Where are you?

9 - Recognise 2 people

10 - Count backwards 20-1

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5
Q

Investigations of dementia.

A

Look for reversible causes such as;
TFT, B12, Folate, Thiamine, Ca2+ def.

Check MSU, FBC, ESR, U&Es, LFTs, Glucose.

MRI to identify reversible pathologies.

Functional imaging - FDG, PET, SPECT

Consider EEG

Check antibodies for syphilis, HIV, CJD or other rare causes if indicated.

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6
Q

When should you consider EEG in dementia?

A

Suspected delirium

Frontotemporal Dementia

CJD

Seizure disorder

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7
Q

Subtypes of dementia

A

Alzheimer’s disease (most common)

Vascular dementia (25%)

Lewy Body’s dementia (15-25%)

Fronto-temporal dementia

Pick’s disease

HIV related dementia

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8
Q

Other causes of dementia.

A

Alcohol and drug abuse

Repeated head trauma

Pellagra

Whipple’s disease

Huntington’s

CJD

Parkinson’s

HIV

Cryptococcis

Familial autosomal dominant AD

CADASIL

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9
Q

Explain Vascualr dementia.

A

Cumulative effect of many small strokes. There is sudden onset and stepwise deterioration.

Look for any evidence of arteriopathy such as increased BP, past strokes and focal CNS signs.

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10
Q

Management of vascular dementia.

A

Treat any underlying cause such as strokes, hyperlipidaemia, HTN etc…

Haloperidol can be used if patient is agitated.

Alzheimer’s disease medicines, such as donepezil (Aricept), galantamine (Reminyl), rivastigmine (Exelon) or memantine are not used to treat vascular dementia, but may be used in people who have a combination of vascular dementia and Alzheimer’s disease.

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11
Q

What is Lewy body dementia?

A

Fluctuating cognitive impairment, detailed visual hallucinations and later parkinsonism.

Histology is characterised by Lewy Bodies in brainstem and neocortex.

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12
Q

Treatment of Lewy Body dementia.

A

Acetylcholinesterase (AChE) inhibitors, such as donepezil (Aricept), rivastigmine (Exelon) and galantamine (Reminyl), may help improve hallucinations, confusion and sleepiness in some people.

Memantine - NMDA antagonist

Levodopa can be given, it may make it worse as well.

Avoid antipsychotics in Lewy Body Dementia. It can lead to neuroleptic malignant syndrome.

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13
Q

Explain fronto-temporal dementia.

A

Front and temporal atrophy with loss of over 70% of spindle neurons.

Patients display executive impairment, behavioural and personality cahnges, disinhibtion, hyperorality, sterotype behaviour and emotional unconcern.

Episodic memory and spatial orentation are preserved until later stages.

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14
Q

Other considerations to make in dementia.

A

Depression can mimic dementia.

Try and SSRI or if severe mirtazapine.

CBT can help as well.

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15
Q

Cause of AD.

A

Environmental and genetic factors both play roles.

Accumulation of beta-amyloid peptide - a degradation product of amyloid precursor protein results in progressive neuronal damage. Neurofibrillary tnagles and increased number of amyloid plaques and loss of the neurotransmitter acetylcholine.

Neuronal loss is selective . the hippocampus, amygdala, temporal neocortex and subcortical nuclei are most vulnerable.

Vascular effects are also important as 95% of AD patients show evidence of vascular dementia as well.

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16
Q

Risk factors of AD.

A

1st degree relative with AD.

Down’s syndrome

Homozygosity for apoE

Vascular risk factors like HTN, diabetes, dyslipidaemia, AF etc..

Decrease physical and cognitive activity

Depression

Loneliness

17
Q

E.g. of pharmacological treatment of cognitive decline.

A

Acetylcholinesterase inhibitors - Donepezil, rivastigmine, galantamine.

Antiglutamatergic treatment - Memantine

Antipsychotics - In severe non-cognitive symptoms only. There is a possible increased risk of stroke/TIA. Avoid in mild to moderate Lewy body dementia, AD and vascular dementia.

Vitamin supplementation