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MSRA > Geriatric Medicine > Flashcards

Geriatric Medicine Flashcards

1
Q

Lewy body dementia mushkies?

A
  1. 20% dementia
  2. Characteristic pathological feature is alpha synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas
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2
Q

What percentage of pts with Alzheimers have Lewy bodies?

A

40%

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3
Q

Lewy Body dementia features?

A
  1. Progressive cognitive impairment = in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss, cognition may be fluctuating, usually develops before parkinsonism
  2. Parkinsonism
  3. Visual hallucinations (delusions and non-visual hallucinations may also be seen)
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4
Q

Lewy body dementia Dx?

A
  1. Usually clinical
  2. DATSCAN (SPECT), 90% sensitivity and 100^% specificity
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5
Q

Lewy Body dementia RX?

A
  1. Acetylcholinesterase inhibitors (donepezil, rivastigmine) and memantine
  2. Avoid neuroleptics as may develop irreversible parkinsonism
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6
Q

What is included by Lewy Body Dementia?

A
  1. Dementia with Lewy Bodies (DLB)
  2. Parkinson’s disease dementia (cardinal features before dementia)
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7
Q

DLB sleep problems?

A

REM sleep disorder = violently acting out their dreams as many as 40 years before the onset of dementia symptoms

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8
Q

Alzheimer’s disease risk factors?

A
  1. Age
  2. FHx
  3. AD = 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
  4. Apoprotein E allele E4 (encodes cholesterol transport protein)
  5. Caucasian
  6. Down’s syndrome
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9
Q

Alzheimer’s pathology?

A
  1. Macroscopic = widespread cerebral atrophy, particularly involving hippocampus and cortex
  2. Microscopic = Type A Beta Amyloid Plaques, Tau neurofibrillary tangless, hyperphosphorylated Tae
  3. Biochecmical = deficit of acetylcholine from damage to an ascending forebrain projection
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10
Q

Neurofibrillary tangles mushkies?

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 its function
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11
Q

Alzheimer’s management?

A
  1. Non pharmacological
  2. Pharmacological
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12
Q

AD Non-pharmacological management?

A
  1. Range of activities to promote wellbeing
  2. Cognitive stimulation therapy for mild and moderate
  3. Consider group reminiscence therapy and cognitive rehabilitation
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13
Q

AD Pharmacological management?

A
  1. Acetylcholinesterase inhibitors 1st line for mild to moderate (Donepezil, Rivastigmine, Galantamine)
  2. Memantine (NMDA receptor antagonist) 2nd line
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14
Q

Memantine AD indications?

A
  1. Moderate Alzheimer’s intolerant/contraindicated to acetylcholinesterase inhibitors
  2. Add on drug for moderate or severe Alzheimer’s
  3. Monotherapy in severe Alzheimer’s
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15
Q

AD non-cognitive symptoms Rx?

A
  1. Dont recommend antidepressants
  2. Antipsychotic only used if risk of harm to self or others, or if in severe distress
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16
Q

Donepezil s/e?

A
  1. Bradycardia –> relative contraindication (as may cause bradycardia and AVN block)
  2. Adverse effects include insomnia
17
Q

Vascular dementia mushkies?

A

The second most common form of dementia after Alzheimer disease. 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.

18
Q

Vascular dementia epidemiology?

A
  1. 17% Dementia in UK
  2. Prevalence of dementia following a first stroke varies depending on location and size of the infarct, definition of dementia, interval after stroke and age among other variables. Overall, stroke doubles the risk of developing dementia
  3. Incidence increases with age
19
Q

Main subtypes of VD?

A
  1. Stroke-related = multi-infarct or single-infarct
  2. Subcortical = small vessel disease
  3. Mixed = AD + VD
20
Q

Inherited cause of VD?

A

CADASIL

21
Q

VD presentation?

A

Stepwise deterioration

22
Q

VD Dx?

A
  1. Hx and Ex (NINDS-AIREN criteria for probable vascular dementia)
  2. Formal screen for cognitive impairment
  3. Medical review to exclude medication cause
  4. MRI (may show infarcts and extensive white matter changes)
23
Q

NINDS-AIREN criteria for probably vascular dementai?

A
  1. Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event = clinical exam and neuropsychological testing
  2. Cerebrovascular disease = defined by neurological signs and/or brain disease
  3. A relationship between the above two disorders inferred by: the onset of dementia within 3m following a stroke, an abrupt deterioration in cognitive functions, fluctuating + stepwise progression of cognitive deficits
24
Q

VD Rx?

A

Non-pharmacological and pharmacological

25
Q

VD Non-pharmacological Rx?

A
  1. CST, multisensory stimulation, music and art therapy, animal-assisted therapy
  2. Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
26
Q

VD pharmacological management?

A
  1. No specific treatment approved for cognitive symptoms
  2. 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
  3. No evidence that aspirin is effective
27
Q

Dementia assessment tools recommended by NICR?

A
  1. 10-point cognitive screener (10-CS)
  2. 6-item cognitive impairment test (6CIT)
28
Q

Dementia primary care Ix?

A
  1. Blood screen is usually sent to exclude reversible causes (e.g. Hypothyroidism). NICE recommend the following tests: FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels. Patients are now commonly referred on to old-age psychiatrists (sometimes working in ‘memory clinics’)
29
Q

Dementia secondary care Ix?

A

Neuroimaging is performed to exclude other reversible conditions (e.g. Subdural haematoma, normal pressure hydrocephalus) and help provide information on aetiology to guide prognosis and management

30
Q

1st line sedative for delirium in elderly?

A

0.5mg haloperidol

31
Q

Delirium in parkinsons?

A
  1. Careful reduction of Parkinsons medication may be helpful
  2. If symptoms require urgent treatment then atypical antipsychotics quetiapine and clozapine are preferred
32
Q

Frontotemporal lobar degeneration types (FTLD)?

A
  1. Frontotemporal dementia (Pick’s disease)
  2. Progressive non-fluent aphasia (chronic progressive aphasia, CPA)
  3. Semantic dementia
33
Q

Common features of frontotemporal dementias?

A
  1. Onset before 65
  2. Insidious
  3. Relatively preserved memory and visuospatial skills
  4. Personality change and social conduct problems
34
Q

Pick’s disease features?

A

Personality change and impaired social conduct. Other common features include hyperorality, disinhibition, increased appetite, and perseveration behaviours

35
Q

Pick’s disease pathology?

A
  1. Macroscopic
  2. Microscopic
36
Q

Macroscopic Pick’s changes?

A
  1. Focal gyral atrophy with a knife-blade appearance
  2. Atrophy of the frontal and temporal lobes
37
Q

Microscopic Pick’s changes?

A
  1. Pick bodies = spherical aggregations of tau protein (silver-staining)
  2. Gliosis
  3. Neurofibrillary tangles
  4. Senile plaques
38
Q

CPA (chronic progressive aphasia) features?

A
  1. Non-fluent speech = utterances that are agrammatic
  2. Comprehension is relatively preserved
39
Q

Semantic dementia mushkies?

A
  1. Speech is fluent but empty and conveys little meaning
  2. Unlike Alzheimer’s, memory is better for recent rather than remote events

MSRA (25 decks)

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