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MRCP Part 1 > Geriatric Medicine > Flashcards

Geriatric Medicine Flashcards

1
Q

What is the STOPP-START Criteria (Gallagher et al., 2008)?

A

Medications we should consider withdrawing in the elderly

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2
Q

Most common causes of dementia in the UK?

A
  1. Alzheimer’s
  2. Vascular Dementia
  3. Lewy Body Dementia
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3
Q

Assessment tools for dementia recommended by NICE for diagnosis of dementia?

A
  1. 10-point cognitive screener (10-CS)

2. 6-item cognitive impairment test (6CIT)

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4
Q

Primary care investigations for diagnosis of dementia?

A
  1. Bloods for reversible conditions = FBC, U&E, LFTs, Calcium, Glucose, TFTs, Vitamin B12, Folate
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5
Q

Secondary care investigations for dementia?

A
  1. Neuroimaging for reversible conditions = subdural haematoma, normal pressure hydrocephalus
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6
Q

What is essential in the investigation of dementia in 2011 NICE guidelines?

A

Structural imaging

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7
Q

What are 3 acetylcholinesterase inhibitors?

A
  1. Donepezil
  2. Rivastigmine
  3. Galantamine
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8
Q

Most important possible side effect of acetylcholinesterase inhibitors?

A

Bradycardia (or SA block/AV block)

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9
Q

What medications are contraindications/cautions for acetylcholinesterase inhibitors being started?

A
  1. Beta blockers
  2. Rate limiting calcium channel blockers
  3. Digoxin
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10
Q

Side effects of acetylcholinesterase inhibitors?

A
  1. Heart = Bradycardia, Syncope
  2. GI
  3. Neuro = Agitation, Hallucinations, EPSEs
  4. GU = urinary retention
  5. Neuroleptic malignant syndrome
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11
Q

Parkinsonian gentleman with post-op delirium, what medication is contraindicated?

A

Haloperidol

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12
Q

MOA of haloperidol?

A

Dopamine antagonist

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13
Q

MOA of domperidone?

A

Dopamine antagonist

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14
Q

Why is domperidone safe for treating GI symptoms in Parkinsons?

A

Despite being a dopamine antagonist, it does not easily cross the BBB and so risk of developing EPSEs is minimal

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15
Q

Is lorazepam safe to use in PD?

A

Yes

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16
Q

Is Olanzapine safe to use in PD?

A

Yes

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17
Q

Is Ondansetron safe to use in PD?

A

Yes

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18
Q

What percentage of elderly patients admitted to hospital experience delirium?

A

30%

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19
Q

Predisposing factors for delirium?

A
  1. Age > 65 y/o
  2. B/G Dementia
  3. Significant injury e.g. #NOF
  4. Frailty/multimorbidity
  5. Polypharmacy
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20
Q

Precipitating events for delirium?

A

IMCA PACUH

  1. Infection e.g. UTI
  2. Metabolic e.g. hypercalcaemia, hypo/hyperglycaemia, dehydration or Medication e.g. opioids
  3. Change of environment
  4. Any significant cardio/resp/neuro/endo condition
  5. Pain
  6. Alcohol withdrawal
  7. Constipation
  8. Urinary Retention
  9. Hypoxia
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21
Q

Features of delirium?

A
  1. Memory disturbance (short term > long term)
  2. Agitated/withdrawn
  3. Disorientation
  4. Mood Changes
  5. Visual hallucinations
  6. Disturbed sleep cycle
  7. Poor attention
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22
Q

First line sedative for delirium?

A

Haloperidol 0.5mg

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23
Q

Management of delirium?

A
  1. Treatment of underlying cause
  2. Modification of environment
  3. Haloperidol 0.5mg
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24
Q

Management of delirium in Parkinsons?

A
  1. Careful reduction of Parkinson medication
  2. Lorazepam
  3. Urgent symptom treatment = atypical antipsychotics e.g. quetiapine and clozapine, only be used for patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress
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25
Q

What is mixed state delirium?

A

Switching between states of hyperactive and hypoactive delirium

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26
Q

Theories as to pathophysiology of delirium?

A
  1. Overall level of neurotransmitters = ACh, DA, NA, Glutamade
  2. Neuronal membrane not depolarising correctly
  3. Inflammatory cytokines
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27
Q

How many more times likely are delirious patients likely to fall?

A

6 times

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28
Q

What doesnt NICE guidelines support for the management of mild dementia?

A

Memantine

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29
Q

Why may rivastigmine be started?

A

It comes in a patch form so is good for those unable to swallow

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30
Q

When is memantine indicated?

A

Moderate and severe Alzheimer’s disease

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31
Q

How can you classify management of dementia?

A
  1. Non-pharmacological
  2. Pharmacological
  3. Non-cognitive symptoms
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32
Q

Non-pharmacological management of Alzheimer’s?

A
  1. Offering a range of activities to promote wellbeing that are tailored to the person’s preference
  2. Offering Group Cognitive Stimulation Therapy for patients with mild to moderate dementia
  3. Consider group reminiscence therapy and cognitive rehabilitation
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33
Q

Pharmacological management of Alzheimer’s?

A
  1. Mild to moderate = ACh inhibitors (donepezil, galantamine, rivastigmine)
  2. Second line = memantine
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34
Q

MOA of memantine?

A

NMDA receptor antagonist

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35
Q

When is memantine indicated?

A
  1. Moderate Alzheimers intolerant to/have contraindication to ACh inhibitors
  2. Add on drug to ACh inhibitors for pts with moderate or severe Alzheimer’s
  3. Monotherapy in severe Alzheimer’s
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36
Q

Management of non-cognitive symptoms of Alzheimer’s?

A
  1. Antidepressants for mild to moderate depression NOT indicated
  2. Antipsychotics should only be used for pts at risk of harming themselves/others, or when the agitation, hallucinations or delusions are causing them severe distress
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37
Q

3 hypotheses for pathophysiology of Alzheimer’s?

A
  1. Cholinergic hypothesis
  2. Amyloid hypothesis
  3. Tau hypothesis
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38
Q

What is the cholinergic hypothesis?

A

Loss of central cholinergic neurones with subsequent reduction in acetylcholine

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39
Q

What is the amyloid hypothesis?

A

Accumulation of beta amyloid plaques causing neuroinflammation and disrupting communication between neurones

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40
Q

What is the tau hypothesis?

A

Abnormal aggregation of tau protein leading to tau tangles, leading to microtubule disruption and malfunction in biochemical processes in neurones

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41
Q

MOA of NMDA receptor antagonist?

A
  1. NMDA receptors mediate most excitatory transmission in the brain, playing an important role in learning and memory formation
  2. Beta amyloid proteins may cause abnormal rise in glutamate by inhibiting glutamate uptake or triggering glutamate release from glial cells
  3. Binding of glutamate to NMDA receptors leads to calcium influx and impulse transmisison
  4. Overstimulation of NMDA receptors by excess glutamate can lead to excessive influx of calcium, causing cell rupture and death
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42
Q

Lewy body dementia accounts for what percentage of dementia?

A

20%

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43
Q

Pathology of Lewy body dementia?

A

Alpha synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas

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44
Q

What percentage of Alzheimer’s pts have Lewy Bodies?

A

40%

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45
Q

Features of Lewy Body Dementia?

A
  1. Progressive Cognitive Impairment
  2. Parkinsonism
  3. Visual hallucinations (also delusions and non-visual hallucination)
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46
Q

Features of progressive cognitive impairment in Lewy Body dementia?

A
  1. In contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
  2. Cognition may be fluctuating
  3. Usually develops before Parkinsonism
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47
Q

Diagnosis of Lewy Body dementia?

A
  1. Usually clinical

2. SPECT, known commercially as DaTScan

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48
Q

Sensitivity and specificity of DaT scan for Lewy Body Dementia?

A
  1. Sensitivity = 90%

2. Specificity = 100%

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49
Q

Management of Lewy Body Dementia?

A
  1. Motor symptoms = levodopa

2. Cognitive symptoms = Acetycholinesterase inhibitors and Memantine

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50
Q

What should be avoided in LBD?

A

Neuroleptics as pts may develop irreversible parkinsonism

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51
Q

Who is Lewy Body dementia named after?

A

Frederic Lewy, German born American neurologist

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52
Q

What famous person had Lewy Body dementia?

A

Robin Williams

53
Q

What is required to diagnose dementia?

A

Neuroimaging

54
Q

What drug used for Alzheimer’s is associated with insomnia?

A

Donepezil

55
Q

What scale is used for risk of pressure sore development?

A

Waterlow scale

56
Q

Potential score range of Waterlow scale? What do scores indicate?

A

1-64

  1. > 10 increased risk
  2. > 15 high risk
  3. > 20 very high risk
57
Q

What is the Townsend scale?

A

Indicator of deprivation

58
Q

What is the Rankin scale?

A

Degree of disability in patients post-stroke

59
Q

Risk factors for pressure ulcers?

A

LIMP

  1. Lack of mobility
  2. Incontinence
  3. Malnourishment
  4. Pain (leads to reduction in mobility)
60
Q

Where do pressure ulcers appear?

A

Over bony prominences such as the sacrum or heel

61
Q

Grading of Pressure Ulcers?

A

Grade 1 - 4

62
Q

Grade 1 Pressure Ulcer?

A
  1. Non-blanchable erythema of intact skin. 2. Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin
63
Q

Grade 2 Pressure Ulcer?

A
  1. Partial thickness skin loss involving epidermis or dermis, or both.
  2. The ulcer is superficial and presents clinically as an abrasion or blister
64
Q

Grade 3 Pressure Ulcer?

A
  1. Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.
65
Q

Grade 4 Pressure Ulcer?

A

Extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures with or without full thickness skin loss

66
Q

Management of pressure ulcer?

A
  1. A moist wound environment encourages ulcer healing, hydrocolloid dressing and hydrogels may facilitate this. Soap should be discouraged to avoid drying the wound
  2. Wound swabs should not be routinely done as the vast majority of pressure ulcers are colonised with bacteria, the decision to use systemic antibiotics should be taken on a clinical basis (e.g. evidence of surrounding cellulitis)
  3. Referral to TVN
  4. Surgical debridement may be beneficial for selected wounds
67
Q

What 2 enzymes are actually inhibitied by ACH esterase inhibitors?

A

Acetylcholinesterase and butyrylcholinesterase

68
Q

Definition of delirium according to CAM?

A

Acute onset of change in mental state from the patient’s baseline with inattention, in addition to either disorganised thinking or altered consciousness. Sleep wake cycle is often reversed.

69
Q

Important side effect of ondanseteron?

A

Constipation

70
Q

What is the only dementia subtype where MRI is superior to CT?

A

Vascular dementia = cortical and subcortical ischaemic lesions are better demonstrated, and some vascular pathologies such as micro-bleeds may otherwise be missed

71
Q

Initial haloperidol dose for delirium?

A

0.5mg haloperidol oral, and IM if needed

72
Q

Alternative delirium management if haloperidol is C/I due to PD/LBD?

A

Lorazepam

73
Q

MOA and use of oxybutinin and tolterodine?

A

Anti-muscarinic medications used in treatment of urge incontinence

74
Q

In whom should immediate release oxybutinin be avoided?

A

Frail older women

75
Q

MOA of rotigotine?

A

Dopamine agonist

76
Q

Uses of rotigotine?

A

Parkinson’s disease and restless legs syndrome

77
Q

5 factors favouring delirium over dementia?

A
  1. Impairment of consciousness
  2. Fluctuation of symptoms = worse at night, periods of normality
  3. Abnormal perception e.g. illusions and hallucinations
  4. Agitation, fear
  5. Delusions
78
Q

What is the role of cholinesterase inhibitors in dementia?

A

Improve some cognitive function and improvement in ADls

79
Q

Genetics of Alzheimer’s disease?

A
  1. Most cases are sporadic
  2. 5% are Autosomal Dominant
  3. Apoprotein E allele E4 = encodes a cholesterol transporting protei
  4. Risk factor = Down’s syndrome
80
Q

Autosomal dominant mutations responsible for Alzheimer’s?

A
  1. Amyloid precursor protein (Chromosome 21)
  2. Presenilin 1 (Chromosome 14)
  3. Presenilin 2 (Chromosome 1)
81
Q

Classification of pathological changes in Alzheimer’s?

A
  1. Macroscopic
  2. Microscopic
  3. Biochemical
82
Q

Macroscopic changes of Alzheimer’s?

A

Widespread cerebral atrophy, particularly involving the cortex and hippocampus

83
Q

Microscopic changes of Alzheimer’s?

A
  1. Cortical plaques due to deposition of Type A beta amyloid protein
  2. Intraneuronal neurofibrillary tangles caused by abnormal aggregation of tau protein
84
Q

Biochemical changes of Alzheimer’s?

A

Deficit of acetylcholine from damage to an ascending forebrain projection?

85
Q

What are neurofibrillary tangles?

A
  1. Paired helical filaments are partly made from a protein called tau
  2. tau is a protein that interacts with tubulin to stabilise microtubules and promote tubulin assembly into microtubules
  3. In AD tau proteins are excessively phosphorylated, impairing function
86
Q

What is Korsakoff’s syndrome?

A

An amnesic disorder caused by thiamine deficiency associated with prolonged ingestion of alcohol

87
Q

Main symptoms of Korsakoff’s?

A
  1. Amnesia
  2. Confabulation
  3. Minimal content in conversation
  4. Lack of insight and apath
88
Q

Triad of Wernicke’s?

A
  1. Confusion
  2. Ataxia
  3. Ophthalmoplegia
89
Q

Patient who has deteriorated following the introduction of an antipsychotic agent?

A

Lewy Body Dementia

90
Q

CJD EEG?

A

Disease-typical periodic sharp wave complexes

91
Q

When is FDG-PET used for dementia?

A

If there is diagnostic uncertainty and if classifying a subtype of dementia would change management

92
Q

Features of frontotemporal dementia?

A
  1. Predominant behaviour and personality changes
  2. Executive function difficulties
  3. Younger age of onset (45-65) with memory loss occurring later in the disease course
93
Q

Findings in CSF that would support a diagnosis of Alzheimer’s?

A
  1. Total tau
  2. Phosphorylated Tau 181
  3. Amyloid Beta 1-42
  4. Amyloid Beta 1-40
94
Q

What is the function of COMT inhibitors?

A

Stop peripheral breakdown of levodopa increasing the levels that cross the BBB

95
Q

COMT stands for?

A

Catechol-O-methyltransferase

96
Q

Examples of COMT inhibitors?

A

Entecapone and Tolcapone

97
Q

What are 3 monoamines?

A
  1. Serotonin
  2. Dopamine
  3. Noradrenaline
98
Q

MAO inhibitors used for?

A

Depression and panic disorder

99
Q

Most common types of cortical dementia?

A
  1. AD
  2. LBD
  3. FTLD
100
Q

FTLD?

A

Frontotemporal lobar degeneration

101
Q

3 types of FTLD?

A
  1. Frontotemporal dementia (Pick’s disease)
  2. Progressive non-fluent aphasia (chronic progressive aphasia, CPA)
  3. Semantic dementia
102
Q

Features of FTLD?

A
  1. Onset before 65
  2. Insidious onset
  3. Relatively preserved memory and visuospatial skills
  4. Personality change and social conduct problems
103
Q

Most common type of FTLD?

A

Pick’s disease

104
Q

Features of Pick’s diease?

A
  1. Personality change and impaired social conduct (main)
  2. Hyperorality
  3. Disinhibition
  4. Increased appetite
  5. Perseveration behaviours
105
Q

Classification of pathology of Pick’s Disease?

A

Macroscopic and Microscopic

106
Q

Macroscopic changes in Pick’s disease?

A
  1. Focal gyral atrophy with a knife blade appearance

2. Atrophy of the frontal and temporal lobes

107
Q

Microscopic changes of Pick’s disease?

A
  1. Pick bodies
  2. Gliosis
  3. Neurofibrillary tangles
  4. Senile plaques
108
Q

What are Pick bodies?

A

Spherical aggregations of tau protein (silver-staining)

109
Q

Management of Pick’s disease?

A

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

110
Q

Main features of progressive non-fluent aphasia?

A

Non fluent speech, they make short utterances that are agrammatic, comprehension is relatively conserved

111
Q

Features of semantic dementia?

A
  1. Fluent progressive aphasia
  2. Speech is fluent but empty and conveys very little meaning
  3. Unlike in Alzheimer’s, memory is better for recent rather than remote events
112
Q

When does delirium tremens typically occur?

A

3 days into cessation

113
Q

What is vascular dementia?

A

A group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease

114
Q

Vascular dementia accounts for what percentage of dementia?

A

17%

115
Q

Stroke increases risk of dementia by how much?

A

2x

116
Q

3 main types of vascular dementia?

A
  1. Stroke-related VD (multi-infarct or single-infarct dementia)
  2. Subcortical VD (caused by small vessel disease)
  3. Mixed dementia (presence of both VD and Alzheimer’s disease)
117
Q

Inherited caused of Vascular Dementia?

A

CADASIL

118
Q

What does CADASIL stand for?

A

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

119
Q

Buzzword for Vascular dementia?

A

Stepwise deterioration

120
Q

Diagnosis of vascular dementia?

A

NINDS-AIREN criteria for probable vascular dementia

  1. Presence of cognitive decline that interferes with ADLs, not due to secondary effects of cerebrovascular event
  2. Cerebrovascular disease defined by neurological signs and/or brain imaging
    3a. A relationship between the above two disorders inferred by: onset of dementia within 3 months following a recognised stroke
    b. An abrupt deterioration in cognitive functions
    c. Fluctuating, stepwise progression of cognitive deficits
121
Q

Classification of management of vascular dementia?

A
  1. General
  2. Pharmacological
  3. Non-pharmacological
122
Q

General management of Vascular dementia?

A

Cardiovascular risk factors

123
Q

Non-pharmacological management of vascular dementia?

A
  1. Cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal assisted therapy
  2. Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
124
Q

Pharmacological management of dementia?

A

No specific pharm treatment approved for cognitive symptoms

125
Q

When do you consider AChE inhibitors or memantine for VD?

A

If they have comorbid Alzheimers/PD Dementia/LBD

126
Q

Any evidence that aspirin is effective in treating pts with a diagnosis of vascular dementia?

A

No

127
Q

Any randomised trials evaluating statins for vascular dementia?

A

No

128
Q

What is Pramipexole?

A

A dopamine agonist used to treat PD and restless legs syndrome

MRCP Part 1 (4 decks)

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