Dementia & Delirium Flashcards

1
Q

The most common cause of dementia in the UK is

A

Alzheimer’s disease

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2
Q

Vascular dementia makes up ___% of dementia cases in the UK?

A

20%

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3
Q

Lewy Body dementia makes up __% of dementias in the UK?

A

10-15%

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4
Q

Alzheimer’s makes up __% of dementias in the UK?

A

60-70%

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5
Q

MMSE stands for

A

mini-mental state examination

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6
Q

A MMSE score of ____ or less out of 30 suggests dementia

A

24

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7
Q

GPCOG test for cognition stands for

A

General practitioner assessment of cognition

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8
Q

AMTS test for dementia stand for

A

abbreviated mental test score

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9
Q

The AMT-4 test for dementia stands for

A

Abbreviated Mental Test- 4 questions

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10
Q

The 6CIT test for cognition stands for

A

Six-item Cognitive Impairment Test (6CIT)

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11
Q

The IQCODE test for dementia stands for

A

Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE)

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12
Q

Blood screen tests in primary care to rule out reversible causes of dementia

A

NICE recommend the following tests:
* FBC,
* U&E,
* LFTs,
* calcium,
* glucose,
* ESR/CRP,
* TFTs,
* vitamin B12 and folate levels. Patients are now commonly also referred on to old-age psychiatrists (sometimes working in ‘memory clinics’).

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13
Q

Reversible causes of dementia

A
  • Alcohol (thiamine def)
  • Drug abuse (barbituates)
  • Vitamin B12/ folate deficiency
  • Hypothyroidism
  • Addison’s
  • Infections such as HIV, Syphillis and UTIs
  • Tumors or haematomas that place pressure on the brain
  • Depression
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14
Q

In secondary care, it is essential to carry out _____ to rule out any other causes of reversible dementia and provide information of aetiology

A

Neuroimaging

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15
Q

Reversible causes of dementia that may be picked up on neuroimaging

A
  • Subdural haematoma,
  • normal pressure hydrocephalus
  • Tumour
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16
Q

Multi-infarct dementia is that which is caused by

A

Cerebrovascular disease (stroke)

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17
Q

Dementia secondary to stroke makes up ____% of strokes

A

10-20%

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18
Q

Rare causes of dementia (5%)

A
  • Huntington’s
  • CJD
  • Pick’s disease (atrophy of frontal and temporal lobes)
  • HIV (50% of AIDS patients)
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19
Q

Frontotemporal dementia is also known as

A

Pick’s disease

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20
Q

Risk factors for Alzheimer’s Disease

A
  • Increasing age
  • family history
  • Caucasian ethnicity
    Down’s syndrome
  • 5% of cases are inherited as an autosomal dominant trait
    mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
  • apoprotein E allele E4 - encodes a cholesterol transport protein
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21
Q

Macroscopic changes in Alzheimer’s (physical visual brain changes)

A

widespread cerebral atrophy, particularly involving the cortex and hippocampus

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22
Q

Microscopic changes in Alzheimer’s

A
  • Cortical plaques due to deposition of type A-Beta-amyloid protein and
  • **intraneuronal neurofibrillary tangles ** caused by abnormal aggregation of the tau protein

hyperphosphorylation of the tau protein has been linked to AD

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23
Q

Biochemical changes in Alzheimer’s

A

there is a deficit of acetylcholine from damage to an ascending forebrain projection

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24
Q

Describe what neurofibrillary tangles are:

A

They are paired helical filaments are partly made from a protein called tau
tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
in AD are tau proteins are excessively phosphorylated, impairing its function

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25
Q

Non-Pharmacological management of Alzheimer’s

A
  • NICE recommend offering ‘a range of activities to promote wellbeing that are tailored to the person’s preference’
  • NICE recommend offering group cognitive stimulation therapy for patients with mild and moderate dementia
  • other options to consider include group reminiscence therapy and cognitive rehabilitation
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26
Q

1st line pharmacological management of Alzheimer’s

A

the three acetylcholinesterase inhibitors :
donepezil
galantamine
and rivastigmine
to managing mild to moderate Alzheimer’s disease

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27
Q

2nd line pharmacological management of Alzheimer’s

A

**memantine (an NMDA receptor antagonist) **

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28
Q

Memantine, the 2nd line treatment of Alzheimer’s is recommended by NICE to be used in which circumstances?

A
  • moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
  • as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
  • monotherapy in severe Alzheimer’s
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29
Q

NICE does not recommend ___
for mild to moderate depression in patients with dementia

A

Antidepressants

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30
Q

antipsychotics should only be used for dementias patients when:

A

They are at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress

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31
Q

Donezepil is contraindicated in

A
  • bradycardia
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32
Q

Adverse effect of Donezepil

A

Insomnia

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33
Q

____ is the third most common type of cortical dementia after Alzheimer’s and Lewy body dementia.

A

Frontotemporal lobar degeneration (FTLD)

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34
Q

There are three recognised types of FTLD
(Frontotemporal Lobar Dementia)

A
  • Frontotemporal dementia (Pick’s disease)
  • Progressive non fluent aphasia (chronic progressive aphasia, CPA)
  • Semantic dementia
35
Q

The onset of frontotemporal lobar dementia is usually

A

before 65

36
Q

The nature of the onset of frontotemporal lobar dementia is an ____ one

A

insidious

37
Q

In frontotemporal lobar dementias, memory is relatively ____

A

preserved

38
Q

A classic feature of frontotemporal lobar dementia is

A

Personality change and social conduct problems

39
Q

The most common type of frontotemporal lobar dementia is

A

Pick’s Disease

40
Q

Pick’s Disease is characterised by:

A

personality change and impaired social conduct

41
Q

Features of Pick’s disease

A
  • personality change
  • impaired social conduct
  • hyperorality,
  • disinhibition,
  • increased appetite,
  • and perseveration behaviours.
42
Q

Features of Pick’s Disease present in the frontal and temporal lobes?

A

Focal gyral atrophy with a knife-blade appearance

43
Q

Macroscopic changes in Pick’s Disease

A

Atrophy of the frontal and temporal lobes

44
Q

Microscopic changes in Pick’s Disease

A
  • Pick bodies - spherical aggregations of tau protein (silver-staining)
  • Gliosis
  • Neurofibrillary tangles
  • Senile plaques
45
Q

NICE do not recommend that ____ or ____ are used in people with frontotemporal dementia (because they can make the symptoms worse)

A

AChE inhibitors or memantine

46
Q

CPA stands for

A

Progressive non fluent aphasia (chronic progressive aphasia, CPA)

47
Q

Characteristics of chronic progressive aphasia

A

Here the chief factor is non fluent speech. They make short utterances that are agrammatic. Comprehension is relatively preserved.

48
Q

Characteristics of Semantic Dementia

A

Here the patient has a 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.

49
Q

What actually are Lewy Bodies?

A

alpha-synuclein cytoplasmic inclusions

50
Q

What is a characteristic pathological feature of Lewy Body dementia?

A

alpha-synuclein cytoplasmic inclusions (Lewy bodies)

51
Q

Where are Lewy Bodies found in the brain in Lewy Body Dementia?

A

in the substantia nigra, paralimbic and neocortical areas.

52
Q

Features of Lewy Body Dementia

A
  • progressive cognitive impairment
    -occurs before parkinsonism
    -fluctuating cognition
    -in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
  • parkinsonism
  • visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
53
Q

Difference between Lewy body dementia parkinsonism and Parkinson’s with dementia?

A
  • Lewy body dementia typically occurs before parkinsonism
  • in contrast, in Parkinson’s disease, the motor symptoms typically present at least one year before cognitive symptoms (dementia)
54
Q

Diagnosis for Lewy Body dementia is usually ____

A

Clinical

55
Q

single-photon emission computed tomography (SPECT) is increasingly used in the diagnosis of ________ dementia

A

Lewy Body

56
Q

Drug treatment for Lewy Body Dementia

A

both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.

57
Q

____ should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism

A

neuroleptics

58
Q

Factors favouring delirium over dementia

A
  • acute onset
  • impairment of consciousness
  • fluctuation of symptoms: worse at night, periods of normality
  • abnormal perception (e.g. illusions and hallucinations)
  • agitation, fear
  • delusions
59
Q

____is the second most common form of dementia after Alzheimer disease

A

Vascular dementia (VD)

60
Q
A
61
Q

Vascular dementia is not a single disease but ____

A

It is not a single disease but a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease

62
Q

Stroke ____ the risk of developing dementia

A

Doubles

63
Q

There are 3 main subtypes of Vascular Dementia:

A
  • Stroke-related VD – multi-infarct or single-infarct dementia
  • Subcortical VD – caused by small vessel disease
  • Mixed dementia – the presence of both VD and Alzheimer’s disease
64
Q

Risk Factors for Vascular Dementia

A

-History of stroke or TIA
-Atrial fibrillation
-Hypertension
-Diabetes mellitus
-Hyperlipidaemia
-Smoking
-Obesity
-Coronary heart disease
-A family history of stroke or cardiovascular

65
Q

Rarely, VD can be inherited as in the case of ____

A

CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

66
Q

Classical presentation of Vascular Dementia

A

Several months or several years of a history of a sudden or **stepwise deterioration **of cognitive function.

67
Q

Symptoms of Vascular Dementia

A

-Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
-The difficulty with attention and concentration
-Seizures
-Memory disturbance
-Gait disturbance
-Speech disturbance
-Emotional disturbance

68
Q

Ways in which vascular dementia is diagnosed

A
  • A comprehensive history and physical examination
  • Formal screen for cognitive impairment
  • Medical review to exclude medication cause of cognitive decline
  • MRI scan – may show infarcts and extensive white matter changes
69
Q

General management of vascular dementia

A
  • Treatment is mainly symptomatic with the aim to address individual problems and provide support to the patient and carers
  • Important to detect and address cardiovascular risk factors – for slowing down the progression
70
Q

Is there any specific pharmacological management of vascular dementia?

A

No

70
Q

Non-pharmacological management of vascular dementia is tailored to the individual. This includes:

A

Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication

70
Q

When should AChE inhibitors or memantine only be considered for people with vascular dementia?

A

Only consider AChE inhibitors or memantine for people with vascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies.

71
Q

Acuet confusional state is also known as:

A

delirium or acute organic brain syndrome.

72
Q

Predisposing factors to delirium

A
  • age > 65 years
  • background of dementia
  • significant injury e.g. hip fracture
  • frailty or multimorbidity
  • polypharmacy
73
Q

Examples of possible causes of delirium

A
  • infection: particularly UTIs
  • metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration
  • change of environment
  • any significant cardiovascular, respiratory, neurological or endocrine condition
  • severe pain
  • alcohol withdrawal
  • constipation
74
Q

Features of delirium

A
  • memory disturbances (loss of short term > long term)
  • may be very agitated or withdrawn
  • disorientation
  • mood change
  • visual hallucinations
  • disturbed sleep cycle
  • poor attention
75
Q

There are 2 types of delirium

A
  1. Hyperactive
  2. Hypoactive
    (can also have mixed)
76
Q

Management of delirium

A
  • treatment of the underlying cause
  • modification of the environment
  • Consider drug treatment if other methods are not working
77
Q

What is the first-line sedative for delirium if needed?

A

haloperidol 0.5 mg as the first-line sedative

78
Q

When should a sedative be used to control delirium?

A

At a last resort, only when the patient is at risk to themselves or others

79
Q

Why can’t haloperidol be used to help with delirium in Parkinson’s?

A

antipsychotics can often worsen Parkinsonian symptoms

80
Q

What drug is used as a sedative against delirium in patients with Parkinson’s?

A

atypical antipsychotics quetiapine,clozapine and olanzapine are preferred

81
Q

What drug can’t be used to sedate delirium in Parkinson’s and why?

A

Haloperidol because it is a typical antipsychotic and that can worsen parkinsons symptoms