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FRACP CME > Geriatrics > Flashcards

Geriatrics Flashcards

1
Q

Sensitivity and specificity of diagnosis of dementia depending on following cut offs for ACE-III

88
82

A

88 - Sn 1.00, Sp 0.96

82 - Sn 0.93, Sp 1.00

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2
Q

Absolute contraindications for anticholinesterase inhibitor therapy (4)

A
  1. Cardiac conduction issues
    - Bradycardia, sick sinus syndrome, QTc prolongation, heart block
  2. Significant airway obstruction
  3. Active peptic ulcer
  4. known hypersensitivity
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3
Q

Absolute contraindication for NMDA antagonist

A
  1. History of seizures

2. Known hypersensitivity

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4
Q

Difference between depression and bereavement

A

Bereavement has diurnal variation (gets worse as the day goes by)

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5
Q

4 major risk factors for cognitive impairment in PD

A
  1. Older age
  2. Age of onset of PD >60 years
  3. Duration of PD
  4. Severity of parkinsonism
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6
Q

How does cognitive features of PD dementia differ from AD?

A

Predominantly executive and visuospatial dysfunction

Less prominent memory deficits and relatively preserved language function

Apraxia, aphasia, and severe memory loss are usually absent in PDD (common in AD)

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7
Q

Which parkinsonian meds can exacerbate visual hallucinations in PD?

A

Amantadine
Anticholinergics
Dopaminergic agents

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8
Q

Which core motor features of PD are associated with cognitive impairment?

A

Gait and postural instability

Tremor predominant PD are less likely to develop cognitive impairment

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9
Q

Clinically distinguishing features between DLB vs PDD

A

DLB have following clinical features

  1. Faster clinical decline
  2. Earlier onset of hallucinations and delusions
  3. Reduced levodopa responsibility
  4. Significant fluctuations in cognition

PDD are more likely to have

  • Tremors
  • Asymmetrical parkinsonism and more severe
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10
Q

Why should MMSE not be relied upon to detect disabling cognitive impairment in PDD?

A

MMSE is not very sensitive to executive dysfunction, which is a key feature of PDD

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11
Q

Side effect of SSRI

A

GI - nausea, diarrhoea
Neuro - insomnia, drowsiness, tremor, headache, sexual dysfunction

Other - dizziness, sweating, anxiety

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12
Q

Risk associated with antipsychotic use in BPSD

  • Absolute mortality risk
  • NNH over 12 weeks/12 months
  • Stroke risk
A

Absolute mortality icnrease of 1% over 10-12 week treatment

NNH of 100 over 12 weeks, 20 over 12 months

3.5x increased risk of stroke

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13
Q

3 CYP1A2 inhibitor

Name 3 important substrates

A
  1. Amiodarone
  2. Ciprofloxacin
  3. Cimetidine

Substrates include caffeine, clozapine, theophylline

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14
Q

CYP1A2 substrates - 3

A

Caffeine
Clozapine
Theophylline

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15
Q

Name 4 CYP2C9 inhibitors

A
  1. Amiodarone
  2. Fluconazole
  3. Fluoxetine
  4. Cotrimoxazole
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16
Q

CYP2C9 substrates

A

Carvedilol
Glipizide
NSAIDS - ibuprofen and celecoxib
Losartan

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17
Q

CYP2D6 inhibitors

A

Amiodarone
Fluoxetine
Paroxetine

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18
Q

CYP2D6 substrates

A

Most relevant for geriatrics - CHART-D

Carvedilol
Haloperidol
Amitriptyline
Risperidone
Tramadol
Donepezil
19
Q

What are the potent inducers of CYP1A2, 2C9 and 2C19?

A

Carbamazepine, phenytoin, and rifampin

20
Q

What happens when omeprazole is given in context of CYP2C19 inducers such as carbamazepine, phenytoin and rifampin?

A

Omeprazole is the substrate for 2C19 - reduced efficacy

21
Q

Which CYP enzymes do amiodarone inhibit?

A

CYP1A2, 2C9, 2D6

22
Q

Which CYP enzymes do fluoxetine inhibit?

A

CYP2C9, 2D6

23
Q

CYP3A4 and 3A5 inhibitors

A
  1. Clarithromycin
  2. Erythromycin
  3. Diltiazem
  4. Verapamil
24
Q

CYP3A4 and 3A5 substrates

A
  1. Amlodipine
  2. Atorvastatin/Simvastatin
  3. Cyclosporine
  4. Diazepam
  5. Verapamil
  6. Sildenafil
25
Q

Role of memantine in BPSD

A

Effective in treatment of irritability, agitation, aggression and psychosis over 3-6 months in AD, modest benefit in BPSD in vascular dementia but not in DLB.

26
Q

Medications to be used in behavioural emergencies

A

IM route - olanzapine 2.5mg per dose upto 7.5mg

Oral route

  • Benzodiazepines 5-1.25mg per dose upto 7.5mg
  • Risperidone 0.5-1mg per dose upto 4mg
  • Olanzapine wafer 2.5mg per dose upto 10mg
27
Q

Pharmacokinetic changes in older adults

A

Think ADME.

1. Absorption – depend on absorptive surface, gastric pH, splanchnic blood flow, and GI motility, which are mostly unaffected with ageing

2. Distribution
• Increased fat to lean body mass ratio
• Decreased total body water
• Sometimes decreased serum albumin

Consequence is:
• Increased Vd for hydrophobic meds (such as diazepam), and decreased Vd for hydrophilic meds such as digoxin, resulting in higher serum level

3. Metabolism
• Age related decline in phase 1 activity due to reduced hepatic blood flow and liver size
• Phase II hepatic metabolism (conjugation) is not affected by age
  1. Excretion
    Renal function decreases with age, therefore estimation of CrCl/GFR is essential
28
Q

Time to benefit in pharmacotherapy of older adults in relation to:

  1. Glycaemic control
  2. Prevention of fracture
  3. Use of statins for CV events
A

Glycaemic control: at least 3 years for macrovascular complications, 7 years for microvascular complications
Bisphosphonates: 1.5 years for fractures
Statins: 1-2 years for CV events, more than 3 years to prevent strokes

29
Q

Function of non-dominant parietal lobe

Suggestive history and how to test

A

Visuospatial perception

History:

- Losing objects
- Getting lost
- Difficulty navigating familiar/unfamiliar terrains

Assessment - needs to assess both perceptual and constructional abilities, typically includes copy/drawing tasks such as clock drawing and cubes

30
Q

Function of dominant parietal lobe

Suggestive history and how to test

A

Praxis, referring to the ability of executing learned motor movements in the absence of primary deficits in motor and spatial abilities

Typically presenting with dressing apraxia, issues with feeding or bathing, not clearly explained by motor deficits

31
Q

Two types of praxis

A
  1. Ideomotor praxis - ability to perform learned motor movements (eg: ask the patient to demostrate the use of an object with/without objects in the hand)
  2. Ideational praxis (step-wise series of coordinated tasks such as taking the piece of paper, fold it in half and put it in the envelope)

They test the dominant parietal lobe.

32
Q

How would you test executive function/frontal lobe?

A

○ Mental flexibility (eg: trail-making test B)
○ Verbal fluency, especially letter fluency (rather than category fluency)
○ Luria’s fist edge palm test (may show perseveration)
○ Response inhibition - go/no go test
Abstract reasoning

33
Q

Mechanism of action of memantine in AD

A

NMDA receptor antagonist
Glutamate is the primary excitatory neurotransmitter in the cortical and hippocampal neurons
Excessive NMDA activation by glutamate is thought to cause damage

34
Q

Biomarkers predicting risk of conversion from MCI to AD

A
  1. Hippocampal volume on MRI
    a. 25th percentile 2-3x likely to develop AD compared to 75th percentile
    b. CSF - low AB42, high total tau and phospho-tau
    c. APOE4 allele
    d. Temporal-parietal hypometabolism of FDG-PET
    E. Amyloid deposition on AB PET imaging
35
Q

Why is the diagnosis of MCI important?

A

Important to diagnose MCI as risk of dementia is much higher.

General population - 1-2%
MCI - 10-15% annual risk

36
Q

4 core clinical features of DLB (on top of essential feature of dementia)

A
  1. Fluctuating cognition
  2. REM sleep disturbance
  3. Visual hallucination
  4. Parkinsonism
37
Q

Indicative biomarker of DLB

A
  1. Reduced dopamine transporter uptake in basal ganglia via SPECT or PET
  2. Abnormal (low uptake) 123-iodine MIBG myocardial scintigraphy
  3. Polysomnographic confirmation of REM sleep without atonia
38
Q

3 key clues towards idiopathic parkinsons disease

A
  1. Asymmetry
  2. Look out for atypical features (such as cerebellar deficits, long tract signs etc)
  3. Response to levodopa
39
Q

MDS diagnostic criteria of clinically established PD

A
  1. Absence of absolute exclusion criteria
  2. At least two supportive criteria
  3. No red flags
40
Q

MDS diagnostic criteria of clinically probable PD

A
  1. Absence of exclusion criteria
  2. Presence of any red flags are counterbalanced by supportive criteria
    No more than 2 red flags are allowed
41
Q

4 Supportive criteria for PD under MDS

A
  1. Clear and dramatic beneficial response to dopaminergic therapy
  2. Levodopa induced dyskinesia
  3. Rest tremor of a limb
  4. Presence of olfactory loss or cardiac sympathetic denervation on MIBG scintigraphy
42
Q

MDS absolute exclusion criteria for PD (9)

A

9 features

  1. Cerebellar deficits
  2. Presence of supranuclear palsy
  3. Diagnosis of FTD within 5 years
  4. Lower limb predominant parkinsonism >3 years
  5. Drug induced parkinsonism
  6. Nil response to high dose levodopa
  7. Cortical sensory loss, clear limb ideomotor apraxia or progressive aphasia
  8. Normal DaT scan
  9. Documentation of alternative condition known to produce parkinsonism or if alternative is felt more likely to be than PD
43
Q

10 Red flag features to look out for in PD

A
  1. Rapidly progressive gait abnormality requiring wheelchair use within 5 years
  2. Complete absence of progression of motor symptoms/signs for 5 or more years (unless it is due to treatment)
  3. Early bulbar dysfunction
  4. Inspiratory respiratory dysfunction - diurnal or nocturnal inspiratory stridor or frequent inspiratory sighs
  5. Severe autonomic failure in the first 5 years
  6. Recurrent falls due to impaired balance within 3 years
  7. Disproportionate anterocollis or contractures of hand or feet within 10 years
  8. No NMS-PD despite 5 years of duration
  9. Pyramidal tract signs
  10. Bilateral symmetric parkinsonism
44
Q

6 predictive factors for delirium above 70 years of age

A
  1. Prior cognitive impairment (delirium/dementia)
  2. Sleep deprivation
  3. Immobility
  4. Visual impairment
  5. Hearing impairment
  6. Dehydration

FRACP CME (8 decks)

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