Dementia Flashcards

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1
Q

What are the likely presenting features of dementia?

A

Chronic confusion
Personality change
Amnesia

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2
Q

What neurological-functions are affected in dementia and which ones are NOT affected?

A

Affected - memory, ability to learn new info, judgement and thinking, processing information, emotional behaviour and social control, motivation

Not affected - Consciousness

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3
Q

How long do symptoms have to have persisted for before a diagnosis of dementia is given?

A

6 months or longer

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4
Q

What are some different types of dementia?

A
Alzheimer's disease 
Lewy body dementia 
Vascular dementia 
Parkinsonian dementia 
HIV dementia 
Fronto-temporal dementia
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5
Q

What are some differentials for dementia?

A
DEMENTIA 
Drugs/delirium
Emotional / depression
Metabolic disorders
Eye and ear disorders
Nutritional disorders
Trauma, toxins and tumours
Infections 
Alcohol, atherosclerosis
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6
Q

What neurotransmitter is lacking in AD and how does this shape the theory of treatment?

A

Acetycholine

First line pharmacological management is acetylcholinesterase inhibitors

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7
Q

What are some examples of first line drug treatment options in AD?

A

Rivastigmine, Neostigmine and Donepezil

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8
Q

In some severe cases of AD an additional drug is used, what is it?

A

Memantine

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9
Q

What are first line drug treatments in DLB?

A

Rivastigmine and Donepezil

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10
Q

Should anti-psychotics be given to patients with dementia?

A

They can sometimes be given but only if the patient is at risk of hurting themselves and/or is experiencing, BPSDs or symptoms of hallucinations/delusions and agitation

Give at low dose ask review every 6 weeks

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11
Q

What scans are recommended in vascular dementia?

A

MRI

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12
Q

What is the most common cause of dementia and what is the difference between early and late onset?

A

Alzheimer’s disease
Early onset <65
Late onset >65

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13
Q

What is the organic, neurological pathology in Alzheimer’s disease?

A

Deposition of Beta-Amyloid plaques
Implications of ApoE4 gene (involved in cholesterol metabolism)
Reduction in amount of Ach - due to reduction in number of cholinergic neurones at nucleus basalis
T21 at greater risk
3x greater risk with FH

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14
Q

What findings will be found upon imaging the brain?

A
Cerebral atrophy 
Plaque formation 
Senile plaques 
Neurofibrillary tangles 
Ach depletion 

***REVIEW IMAGES

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15
Q

What tests can be used to formally assess cognition in possible AD?

A

MoCA or Adenbrooks (ACE-III)

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16
Q

What are the clinical features of AD?

A
THE 5 As:
Aphasia 
Amnesia 
Agnosia 
Apraxia - loss of motor function
Associated behaviours (BPSDs)
17
Q

What are some examples of BPSDs in dementia?

A

Physical aggression, wandering, agitation, restless, screaming, crying, cursing

*it’s these symptoms which usually mean people end up in care

18
Q

Using the bio-psycho-social model how should AD be managed?

A

BIO - Rivastigmine add in memantine if not working. Consider a/ps if considerable BPSDs
PSYCHO - Supportive therapy, reminiscence therapy, cognitive rehab, treatment for comorbid conditions
SOCIAL - Carer support, OT input and social care interventions

19
Q

What are the risks associated with prescribing a/ps for BPSDs in elderly people?

A

Higher risk of stroke and cardiovascular disease
High risk of Parkinsonian effects
Higher risk of falls

20
Q

Some of the symptoms of dementia can be acutely exacerbated by organic disease, what are some causes?

A
PINCH ME 
P - pain 
I - Infection 
N - Nutritional depletion 
C - Constipation 
H - Hydration
M - Medication
E - Environment
21
Q

What is the characteristic disease pattern in vascular dementia?

A

STEPWISE DETERIORATION with every vascular event

Vascular dementia can arise from a single cortical infarct or as a sum of multiple smaller infarcts

22
Q

What are some risk factors for vascular dementia?

A

All the same as for vascular disease:
HTN, High cholesterol, diabetes, smoking, obese

***link of a dominant gene on chromosome 19

23
Q

What investigations should be done in a patient with suspected vascular dementia?

A

FBC, U&E, Ca, Glucose, TFTs
CT head
ECG
UTI - rule out delirium

24
Q

What is the management of vascular dementia?

A

BIO - treat reversible causes and consider anti-coagulation
PSYCHO - Emotional support, cognitive rehab and treatment for comorbid psych conditions (CBT for anxiety)
SOCIAL - carer support, OT input and social care interventions

25
Q

What management is NOT given in vascular dementia?

A

ACH-ESTERASE INHIBITORS

However the NMDA antagonist Memantine does seem to have some beneficial effect

26
Q

What is the second most common dementia in people under the age of 65 in the UK?

A

Fronto-Temporal dementia

27
Q

What are some different sub-types of FTD?

A

Behavioural variant
Progressive, non-fluent aphasia
Semantic

28
Q

What investigations should be done in a patient with suspected FTD?

A

Fluency assessment (word and categorical design)
Abstract thinking and metaphor interpretation
Sorting tasks (wisconsin sorting)
Stroop test (word orange is written in blue and have to say colour not word)
Hand position test
Copying task
Rhythm tapping task
Trail making tests
Cognitive assessment

29
Q

What would you see on an MRI scan of a patient with FTD?

A

Atrophy of the frontal and temporal lobes

30
Q

What are the three different histological types of FTD?

A

Microvaculoar (60%)
Pick’s type (25%)
Combined (15%)

31
Q

How should we treat FTDs?

A

Do NOT give Ach-esterase inhibs
SSRIs have shown some use
Treat symptoms

32
Q

What is different about some of the features of DLB?

A

There is FLUCTUATING COGNITION
A lot of people (70%) will experience PARKINSONIAN symptoms
Approx 70% will also experience VISUAL HALLUCINATIONS

33
Q

What are some other, less common, features of DLB?

A
Disorder in REM 
High neuroleptic sensitivity
Changes in PET scan 
Systematised delusions 
Depressive episodes 
Recurrent falls, syncope and LOC
34
Q

What should be done to treat DLB?

A

Treating the parkinsonism symptoms with L-DOPA is NOT effective and often appears to make things worse
ACh-esterase inhibitors appear to work and Rivastigmine often used
Psychological interventions VITAL

Treatment often not very effective