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bHCE > Dementia > Flashcards

Dementia Flashcards

1
Q

What is mild cognitive impairment (MCI)?

A

early memory decline on formal memory tests (e.g. MMSE) (i.e. it cannot just be subjective) without clinical evidence of the other features of dementia

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2
Q

What can mild memory problems indicate in elderly people?

A

Dementia

Depression

Anxiety

Stress

Physical problem

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3
Q

What are the ways dementia can be classified?

A

Cortical

Subcortical

Progressive

1ry or 2ry

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4
Q

What is cortical dementia?

A

dementias causing problems with: memory, language, thinking and social skills

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5
Q

What is subcortical dementia?

A

dementias causing problems with: memory, emotions and movements

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6
Q

What is progressive dementia?

A

Dementia that deteriorates over time

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7
Q

What is the difference between 1ry and 2ry dementia?

A

1ry dementia has no alternative cause

2ry dementia occurs as a result of: physical disease or injury

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8
Q

How is Alzheimer’s dementia classified?

A

It is a: primary progressive cortical dementia

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9
Q

What are the types of dementia (with prevelances)?

A

7 types:

Alzheimer’s dementia (62%)

Vascular dementia (17%)

Mixed dementia (10%)

Dementia with Lewy bodies (4%)

Other causes (3%)

Parkinsons disease dementia (2%)

Frontotemporal dementia (2%)

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10
Q

How many people are affected at any one time by Alzheimer’s dementia (AD)?

A

500,000

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11
Q

Over what age are 98% of AD pts?

A

98% are over 65

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12
Q

What are the three types AD? (with their rarities)

A

Early onset (less than 10%)

Late onset (85%)

Familial (5%)

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13
Q

What is early onset AD associated with?

A

Myoclonus

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14
Q

What is the age at which early and late AD are split?

A

65

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15
Q

How much of the familial subtype of AD is inherited?

A

100%

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16
Q

At what age does familial AD normally onset?

A

in the 40’s

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17
Q

How does vascular dementia (VD) normally progress?

A

In a stepwise manner

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18
Q

What is mixed in mixed dementia?

A

A mix of AD and VD

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19
Q

How many people in the UK are affected by dementia with Lewy bodies (DLB)?

A

25,000

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20
Q

The symptoms of DLB are most similar to what type of dementia?

A

AD

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21
Q

Pt’s with DLB often show features of what?

A

Parkinsonism hallucinations

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22
Q

What are the causes of dementia under the umbrella term “Other causes” of dementia?

A

Creuztfeldt-Jakob disease

Huntington’s disease

Dementias due to high alcohol intake: Korsakoff’s syndrome AND alcohol-related dementia

Dementia related to reversible conditions: B12 deficiency AND hypothyroidism

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23
Q

What is Creuztfeldt-Jakob disease?

A

human form of mad cow disease caused by prions

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24
Q

What is Korsakoff’s syndrome?

A

Dementia due to lack of lack of thiamine (Vit B1)

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25
Q

What proportion of Parkinson’s disease pts are affected by dementia?

A

30% of parkinsons pts have dementia

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26
Q

What are the signs and symptoms of parkinson’s disease dementia most similar to?

A

DLB

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27
Q

For how long must a pt have had Parkinson’s before they can be diagnosed with Parkinson’s disease dementia?

A

The pt must have had Parkinson’s for 2 years before developing dementia to be diagnosed with Parkinson’s disease dementia

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28
Q

What is frontotemporal dementia?

A

It describes a range of dementias including picks disease

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29
Q

What age group + gender is frontotemporal dementia more common in?

A

Over 65’s

Equal in M + F

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30
Q

What are the early signs of frontotemporal dementia? (as opposed to)

A

Personality and behaviour changes (as opposed to memory decline)

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31
Q

What proportion of pts with mild cognitive impairment (MCI) develop dementia each year?

A

15%

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32
Q

How many people are their with dementia in the UK?

A

820,000

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33
Q

How much roughly does dementia cost the NHS each year?

A

£20 billion

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34
Q

What proportion of over 95’s have dementia?

A

1/3

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35
Q

What is the m:f split of dementia?

A

2/3 of dementia pts are female

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36
Q

Worldwide roughly how many people are affected by dementia?

A

20 million

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37
Q

How many over 65 year olds have dementia?

A

5%

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38
Q

How many over 80 y/o’s have dementia?

A

20%

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39
Q

Which dementias are more common in men than women?

A

VD

DLB

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40
Q

If your parent has dementia what is the likelyhood you will develop it?

A

Uncertain you will inherit it

If you do it is unlikely to present in the same way

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41
Q

What three genes are implicated in early onset AD? (and on what chromosomes are these on)

A

Amyloid precursor protein (APP) (chromosome 21)

Presenilin gene 1 (PSEN-1) (chromosome 14)

Presenilin gene 2 (PSEN-2) (chromosome 1)

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42
Q

What is the inheritance pattern of early onset AD?

A

Autosomal dominant

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43
Q

When should you screen someone for early onset AD?

A

If 2 or more relatives develop AD under the age of 60

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44
Q

To what is late onset AD linked to?

A

apolipoprotein E4 (APO-E4)

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45
Q

What are the respective risk increases of developing late onset AD if you have APO-E4?

A

If 1 copy = x4 risk of AD

If 2 copies = x10 risk of AD

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46
Q

What proportion of the population have 2 copies of late onset APO-E3?

A

60%

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47
Q

What proportion of pt’s who are homozygous APO-E3 will develop late onset AD?

A

50% by 80yrs

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48
Q

Which apolipoprotein (APO) is slightly protective for late onset AD?

A

APO-E2

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49
Q

What is the distribution of APO-E2 within the population?

A

1 copy - 11%

2 copies - 0.5%

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50
Q

What are the genetic sybtypes of VD and how common are they?

A

They are all rare

Cerebral Autosomal-Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)

Hereditary Cerebral Hemorrhage With Amyloidosis (HCHWA)

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51
Q

Which gene is linked to CADASIL?

A

Notch 3

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52
Q

Which gene is linked to HCHWA?

A

APP gene

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53
Q

How is Down’s syndrome linked to AD?

A

As the Amyloid precursor protein is located on chromosome 21 and it is linked to AD via APO-E4 downs have a trisomy of chromosome 21

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54
Q

What is the increase in risk of AD in Down’s syndrome?

A

50% of 50-60 y/o’s

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55
Q

What is the inheritance pattern of Huntington’s disease?

A

Autosomal domiant

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56
Q

When do pts with Huntington’s disease typically develop dementia?

A

Earlier on than a normal person

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57
Q

How heritable is frontotemporal dementia and which gene is implicated?

A

Very heritable

Faults on the: Tau gene

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58
Q

What characterises AD?

A

loss of neurons and synapses from the cerebral cortex

and certain subcortical regions

causing gross atrophy

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59
Q

Which areas of the brain are mainly affected in AD?

A

temporal lobe (especially the hippocampus)

parietal lobe

parts of the frontal cortex

cingulate gyrus

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60
Q

What area is affected earliest in AD?

A

The hippocampus

61
Q

What are the two abnormal structures found in AD? (inside or outside cells)

A

Amyloid plaques (outside cells)

Neurofibrillary tangles (inside cells)

62
Q

How are amyloid plaques thought to cause cause cell death?

A

block cell-to-cell signalling

or

activate immune system responses that trigger inflammation and cell death within the brain

63
Q

What form the amyloid plaques?

A

amyloid precursor protein abnormally forms Beta-amyloid which stick and clump together

64
Q

How are neurofibrillary tangles thought to cause cell death in AD?

A

Tau usually helps the strands of the transport system link together

so when faulty the transport system can no longer do its job

thus the cells dies

65
Q

Are amyloid plaques and neurofibrillary tangles pathognomonic for Alzheimer’s disease?

A

No they also occur as a normal part of ageing

66
Q

What is the frontal lobe responsible for?

A

Voluntary motor activity

Speaking ability

Complex thought

Personality

67
Q

What will a deficit in the frontal lobe cause?

A

Problems with:

Initiating action (due to problems with voluntary motor activity(

Complex thought

Inhibition (due to changes in personality)

68
Q

What is the parietal lobe responsible for?

A

Processes sensory information

Sequence of actions

Proprioception

Calculation and construction

69
Q

What will a deficit in the parietal lobe cause?

A

Problems recognising faces and objects (as processes sensory information)

difficulty in carrying out a sequence of actions (as parietal lobe sequences actions)

70
Q

What is the temporal lobe responsible for?

A

Attention

Recording and storing verbal and visual memory

Learning of information

71
Q

What will a deficit in the temporal lobe cause?

A

diminished attention

difficulty with short term memory

difficulty producing speech

72
Q

What are the functions which experience progressive decline in dementia?

A

Memory

Cognitive function

Awareness of the environment

Decline in emotional control

73
Q

How long should symptoms be present for before dementia should be diagnosed?

A

6 months

74
Q

What are the early signs of dementia?

A

1) Short term memory loss (the earliest symptom)
2) Repetition of questions
3) Difficulty embracing change

75
Q

How long do the early signs of dementia usually last for?

A

3-4 years

76
Q

What are the levels of functioning in the varying degrees of dementia progression?

A

Early - independent

Middle - achieves some ADLs

Late - dependant

77
Q

What are the middle signs of dementia?

A

1) Failure to recognise people
2) Difficulty with daily tasks
3) Needs prompting

78
Q

What are the late signs of dementia?

A

1) Incontinence
2) Aggression
3) Decline in speech
4) Weight loss

79
Q

How long do patients typically last in the late stage of AD?

A

1-2 yrs

80
Q

What is the mean life expectancy following a diagnosis of AD?

A

7yrs

81
Q

How similar are the symptoms between pts with AD?

A

They vary quite a lot

82
Q

What is the common cause of death of AD pts? (what is a big contributing factor)

A

Pneumonia (malnutrition due to AD)

83
Q

Which has a worse prognosis; AD or VD?

A

VD

84
Q

What are the types of VD?

A

1) Post-stroke dementia
2) Multi-infarct dementia
3) Subcortical vascular dementia
4) Mixed cortical and subcortical dementia.

85
Q

How much higher is the risk of VD in those that have had a stroke?

A

9x

86
Q

A year after a stroke what % of pts develop dementia?

A

25%

87
Q

How does multi-infarct VD progress?

A

in a step wise decline following a series of small strokes in the cerebral cortex (cortical vascular dementia)

88
Q

Which type of dementia is more typically of pts with HTN?

A

Subcortical vascular dementia

89
Q

What causes subcortical vascular dementia? (if widespread what is this called)

A

Ischaemic damage causes demyelination of nerve sheaths i.e. white matter (Binswanger’s disease)

90
Q

What are the two typical symptoms in VD?

A

Memory problems less apparent earlier on

‘Step wise’ progression

91
Q

What is the diagnostic criteria for VD called?

A

NINDS-AIREN

92
Q

What are the diagnostic criteria for VD?

A

1) Memory impairment and impairment in a further cognitive domain (as for AD)
2) Deficits should be causing limitation with Activities of Daily Living (ADLs) not due to the physical effects of stroke alone
3) Evidence of cerebrovascular disease on clinical examination and imaging

93
Q

What is the core criteria for diganosing AD?

A

1) Evidence of impairment of memory + at least one of:
- Language impairment
- Apraxia
- Agnosia
2) Present for >6 months

94
Q

What is the curative treatment for DLB? (what treatments can be used at all)

A

There is none (NICE recommend a trial of AChEi’s)

95
Q

What is the average and range of life expectancies for DLB?

A

Average = 5-7 yrs

Range = 2-20 yrs

96
Q

What is the management of DLB focused on?

A

managing neuropsychiatric disturbances and movement disorders

97
Q

What are Lewy bodies made up of?

A

the protein: alpha synuclein

98
Q

How do Lewy bodies disrupt the brain?

A

They interrupt the action of ACh and dopamine at the nuronal synapses.

99
Q

What are the two domains that Lewy bodies are found in? (what are they called)

A

The substantia nigra (classical Lewy bodies)

In the cortex (cortical Lewy bodies)

100
Q

Where are Lewy bodies found in Parkinson’s disease?

A

In the substantia nigra thus they are classical Lewy bodies

101
Q

Which areas of the cortex shrink in DLB?

A

parietal lobes

temporal lobes

cingulate gyrus

102
Q

What causes the formation of Lewy bodies?

A

Its unknown

103
Q

What are the core features of DLB?

A

1) Fluctuating cognition (although this does get progressively worse)
2) Features of parkinsonism
3) Visual hallucinations

104
Q

How can the fluctuating cognition in DLB confuse clinicians?

A

It can be as extreme as to cause stupor which can lead to clinicians hunting for a different explanation than that of DLB?

105
Q

Describe the nature of visual hallucinations in DLB?

A

Complex and detailed

not always destressing

106
Q

What normally accompany visual hallucinations in DLB?

A

delusions

107
Q

What are common supportive features of DLB?

A

Sensitivity to neuroleptics (antipsychotics) inducing parkinsonism

REM sleep behaciour disorder (RBD)

108
Q

What is the worst case scenario in giving pts with DLB neuroleptics?

A

A fatal neuroleptic malignant syndrome

109
Q

What is REM sleep behaviour disorder?

A

During REM sleep pt will: move gesture and/or speak

110
Q

What is an early sign/risk factor for DLB?

A

REM sleep behaviour disorder (RBD)

111
Q

How many ADLs should be affected before diagnosing DLB?

A

2 ADLs

112
Q

How many people does frontotemporal dementia affect?

A

1 in 5000

113
Q

What is the youngest age group frontotemporal dementia (FTD) can affect?

A

Although rare it can affect 20-30 y/o’s

114
Q

What is the length of survival of pts with FTD?

A

10-15 years

115
Q

What is the curative treatment for FTD?

A

There is none

116
Q

How should behavioral symptoms be medically managed in FTD?

A

antidepressants and

consideration for atypical neuroleptics

117
Q

Which medications should not be used in FTD + why?

A

Acetylcholinesterase inhibitor drugs used in Alzheimer’s, such as donepezil

may worsen the condition

118
Q

What is the underlying pathological process in FTD?

A

Abnormal Tau protein aggregation

119
Q

What are the typical changes in FTD (how may this manifest)?

A

Changes in:

1) personality and behaviour (person becoming increasingly more extrovert and disinhibited)
2) Language problems (reduced speech)
3) Pt’s overindulge (Hyperphagia)

120
Q

What are the neurological signs seen in FTD?

A

Primitive reflexes may develop:

  1. Palmar grasp relex
  2. Rooting reflex (Move face towards a stimulus, for breast feeding)
121
Q

What is the standard criteria used for FTD diagnosis called?

A

Lund-Manchester criteria

122
Q

How is Parksinsons disease dementia (PDD) and Dementia with Lewy bodies (DLB) differentiated?

A

PDD - few years of unilateral parkinsons before dementia symptoms

DLB - A year of bilateral signs and cognitive decline before parkinsons symptoms

123
Q

What is the issue trying to treat PDD and LBD (with subsequent Parkinson’s)?

A

L-DOPA (the treatment for parkinsons) can exacerbate dementia symptoms /psychotic symptoms

The antipsychotics can exacerbate the Parkinson’s symptoms

124
Q

Which medications should especially be avoided in PDD?

A

Haloperidol

chlorpromazine

sulpiride (an antipsychotic)

125
Q

What are the two management principles for medications in AD?

A

1) Treatment to enhance cognitive function
2) Treatment of behavioural and psychological symptoms of dementia (BPSD)

126
Q

What are the two types of medication licensed for AD? (and what do they help with)

A
  1. Acetylcholinesterase inhibitor
  2. NMDA receptor antagonist (May help slow cognitive decline and control symptoms)
127
Q

What are the three acetylcholinesterase inhibitors currently available?

A

Donepezil (Aricept)

Galantamine (Reminyl)

Rivastigmine (Exelon)

128
Q

How do acetylcholinesterase inhibitors work?

A

They inhibit the breakdown of acetylcholine which is important in cognitive processes

129
Q

What is the name of the NMDA receptor antagonist licensed for AD?

A

Memantine

130
Q

Where does memantine have its affect and how does it work?

A

It blocks the NMDA glutamate receptors

At normal levels, glutamate aids in memory and learning

but if levels are too high (as in dementia), it leads to overstimulation of nerve cells resulting in degeneration

131
Q

What are the behavioural/mental mimics of dementia?

A
  1. delirium
  2. learning disability
  3. depression
    (4. Diogenes syndrome)
132
Q

What are the groups of physiological mimics of dementia?

A

1) Medications s/e’s
2) Metabolic
3) Nutritional
4) Infections
5) Subdural haematomas
6) Poisoning
7) Tumours
8) Normal pressure hydrocephalus

133
Q

What are the metabolic mimics of dementia?

A

Hypothroidism

134
Q

What are the nutritional mimics of dementia?

A

Vit B12 deficiency

Thiamine deficiency (Vit B1) due to alcoholism.

Pellegra (Vit B6 deficiency) can cause confusion mimics dementia

135
Q

What are the infectious mimics of dementia?

A

Syphillis + AIDs can cause dementia

Lyme disease can cause memory loss

136
Q

What are the poisonous mimics of dementia? (do these resolve)

A

Lead + other heavy metals

Recreational drugs

Alcohol

(All may persist, substances can cause “substance induced persisting dementia”)

137
Q

How can tumours lead to dementia?

A

Due to direct damage and

from release of toxins

138
Q

What are the classic symptoms see in normal pressure hydrocephalus?

A

There is a classic triad:

Worsening confusion

Abnormal gait

Urinary incontinence

139
Q

For what stages of AD are the three acetylcholinesterase (AChE) inhibitors indicated?

A

Mild to moderate AD

140
Q

For which AD pts is memantine indicated for?

A

Pt’s with moderate AD who cannot take AChE inhibitors

OR

Pt’s with severe AD

141
Q

Which AD medications should GP’s start pt’s on?

A

Should only be a specialist who starts AD medications

142
Q

What is the mainstay of treatment for behavioural + psychological symptoms of dementia (BPSD)?

A

Non-pharmacological treatment

143
Q

What is the best antipsychotic for BPSD generally?

A

Respiradone

144
Q

Which type of dementia should care be taken in when prescribing antipsychotics?

A

DLB

PDD

145
Q

What do antipsychotics increase the risk of in dementia pts?

A

Sedation

falls

parkinsonism

Stroke x3 (even higher if >80)

146
Q

In DLB what can be used to treat BPSD?

A

Rivastigmine (a parasympathomimetic)

147
Q

What is the issue with using TCA’s in dementia?

A

They can affect cognition

148
Q

Who should prescribe antipsychotics to elderly pts?

A

Geriatricians

or

Old age psychiatrists

bHCE (18 decks)

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