Yr4 Geriatrics - Study Points Flashcards

1
Q

What is Dementia?
- 7 Subtypes?
- Epidemiology?

A

Epidemiology of Dementia Subtypes
- >90 years – mixed dementias more common.
- <65 years – greater relative incidence FTD, less vascular dementia.
- Any rapidly progressive dementia (over months) – refer to a neurological service with access to LP/EEG to examine for rarer conditions such as CJD.

  • DLB = Dementia with Lewy body
  • FTD = Frontotemporal dementia
  • PDD = Parkinson’s disease dementia
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2
Q

What is the difference between a Mild Cognitive Impairment and Dementia?
- How do we make a diagnosis of dementia?

A

MCI or Dementia?
- Difference between mild cognitive impairment and dementia = dysfunction in ADLs
- Evidence of ‘cognitive impairment’ - subjective and objective.
- Amnestic (memory) or non-amnestic (language, attention).
- Does not affect activities of daily living.
- About 10-15% of people with MCI will develop dementia (per annum), compared to 1-2% of the older population.
- Some people with MCI will improve.
- Some people with MCI will remain static.

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3
Q

What are 6 Aims of a Dementia Assessment?
- Why is it important to diagnose Dementia? (6 reasons)

A

Aims of Dementia Assessment
1. Establish if a person has dementia.
2. Exclude other conditions that have a similar presentation, especially potentially reversible causes of cognitive impairment.
3. Establish dementia sub-type.
4. Evaluate the impact - what is the severity and extent of disability?
5. Evaluate family and social support, and the physical environment.
6. Evaluate any comorbidity.

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4
Q
  • What are 10 common symptoms that might suggest an underlying dementia?
  • 6 Cognitive Symptoms?
  • 6 Psychiatric and Behavioural Symptoms?
  • Dysfunction in ADL?
A

Common symptoms that might suggest an underlying dementia
1. Memory loss (often the first feature if Alzheimer’s dementia) – e.g., repeatedly lose items, miss appointments.
2. Confusion.
3. Repetitiveness.
4. Becoming lost in a familiar area.
5. Personality change (more irritable, inappropriate, hoarding, indifference, ritualistic behaviours).
6. Apathy and withdrawal - can be diagnosed with depression.
7. Forgetting how to use familiar household appliances or objects (suggests apraxia).
8. Not recognising objects for what they are (suggests agnosia).
9. Impaired language skills (struggle to find the right word to use, vocabulary limited and grammar poor).
10. Loss of ability to undertake everyday tasks (driving, cooking, shopping, banking, reading) - suggests a disorder of executive function.

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5
Q

List 10 Potentially reversible causes of cognitive impairment.

A

Potentially reversible causes of cognitive impairment
1. Delirium.
2. Psychiatric disease - depression, anxiety.
3. Alcohol/other substance abuse.
4. Medication - side effects (e.g., BZD, anticholinergics, psychotropics, narcotics, antiepileptics, antidepressants).
5. Neurological disease - tumours, chronic subdural.
6. Normal pressure hydrocephalus (NPH) – triad: dementia, gait disturbance, urinary incontinence
7. “Classics” - B12/folate deficiency, hypothyroid, hypercalcaemia.
8. Infections - neurosyphilis, HIV.
9. Collagen vascular disease - cerebral vasculitis.
10. Obstructive sleep apnoea.

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6
Q

Diagnosis of Dementia
- What history will you take?
- Collateral?
- IQCODE?
- Assessing Functional State and the Environment?
- ADLs?

A

Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE)
When taking a collateral history (from someone who knows the person with suspected dementia), consider supplementing with a structured
instrument, such as the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE).

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7
Q

What will you look for on Physical Examination when making a diagnosis of Dementia?

A
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8
Q

“Memory Complaints” - 4 Differential Diagnoses?

A
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9
Q

How do we distinguish between the 3D’s: Delirium, Dementia, & Depression?

A
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10
Q

Are we usually using Cognitive Screening Tests as true Screening tests?
- Screening vs. Case Finding?
- List 10 Examples of cognitive screening tests?

A

Cognitive Screening Tests - Not “True” Screening Tests
- Screening = detection of disease amongst ‘healthy’ community members of (unsuspected) disorders or risk factors. The ideal screening test is sensitive, specific, valid, easy to administer, minimally time-consuming.
- Case Finding = Detection of cognitive impairment where there is a high probability of disease in a particular population or setting. We are usually ‘case finding’ with cognitive screening tests.

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11
Q

List 9 Limitations of cognitive screening tests?
- When might the results be skewed?
- MoCA versus the MMSE?

A
  1. Scores must be interpreted considering age, literacy, and education achievement.
  2. Intellectual and physical disabilities will affect the reading and writing components.
  3. Depression, anxiety and impaired concentration will also influence the score.
  4. Sensory impairments, language and cultural bias.
  5. Detect cognitive impairment from any cause.
  6. They are not designed to provide a comprehensive cognitive assessment.
  7. Do not make a definitive diagnosis of ‘dementia’ per se.
  8. A ‘normal’ score does not exclude the possibility of early cognitive decline.
  9. A ‘normal’ MMSE score can occur in FTD and DLB.
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12
Q

What are the Diagnostic capability of MMSE cognitive screening test?
- Would a score of 30/30 rule out dementia?
- Would a score of ≤ 24/30 confirm a
diagnosis of dementia?

A

Diagnostic capability of MMSE cognitive screening test
- Comparison with normative values may not detect mild decline in high functioning individuals (or falsely detect dementia in individuals with life-long poor cognitive function).
- Can be poor at detecting mild dementia.
- A score on an MMSE may vary by a few points between assessors, times of day, locations. Small differences are considered insignificant.

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13
Q
  • When might you consider Neuropsychological Testing for Dementia Diagnosis?
  • What are the indications for a Psychiatry Review (Psychogeriatrician) when making a dementia diagnosis?
A

Neuropsychological Testing - Not required in all cases.
1. When diagnosis is uncertain or there are atypical features.
2. Especially in younger onset.
3. Especially if possibility of depression (or similar).
4. Can form a baseline for monitoring.
5. Formal extensive cognitive testing of multiple domains.
6. Can help establish subtype if unclear.

BPSD = Behaviours and psychological symptoms of dementia

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14
Q

Dementia Work-up
- 10 Laboratory Tests?
- Role of Neuroimaging? 3 characteristic changes?
- 4 Additional Investigations?

A
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15
Q

Dementia Work-up: Neuroimaging
- Structural Neuroimaging (CT/MRI): Shape, Position, Volume of Brain Tissue? Patterns of shrinkage?
- Functional and Metabolic Neuroimaging? Examples?

A
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16
Q

How would you go about Informing a Diagnosis of Dementia?

A
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17
Q

What are the DSM-5 Diagnostic Criteria (2013) for a Major and Minor Neurocognitive Disorder (NCD)?
- 6 Cognitive Domains described in the DSM-5?

A

DSM-5 Diagnostic Criteria (2013)
Minor NCD - Deficits do not interfere with ADLs (equivalent to MCI, prodromal dementia)
- IADLs (referring to more complex tasks, such as paying bills or managing medications) are preserved, but greater effort, or compensatory strategies, or accommodation may be required to maintain independence.

Major NCD- Deficits sufficient to interfere with ADLs. (equivalent to dementia)
- Requires (at least) minimal assistance with IADLs.

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18
Q

9 Dementia Subtypes/Causes of Neurocognitive disorder according to DSM-5?

A
  1. Alzheimer’s disease (AD)
  2. Vascular neurocognitive disorder
  3. Frontotemporal (FTD) neurocognitive disorder
  4. Neurocognitive disorder due to Traumatic brain injury (TBI)
  5. Lewy body dementia (DLB),
  6. Parkinson’s disease (PDD)
  7. HIV infection
  8. Substance-induced neurocognitive disorder
  9. Neurocognitive disorder due to Huntington’s disease (HD), Prion disease (CJD), or to another medical condition; and neurocognitive disorder not elsewhere classified
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19
Q

Alzheimer’s Dementia
- Incidence?
- Life expectancy?
- Contributing Factors?
- Characteristics of Early stages?
- Characteristics of Later stages?
- Cognitive deficits?
- Natural History and associated MMSE score?

A
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20
Q

Outline the pathology of Alzheimer’s Dementia.

A
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21
Q

Vascular Dementia
- Incidence?
- Symptoms?
- When is the term used?
- Course?
- What is diagnosis based on?
- 2 Subtypes?

A
  • The term ‘Vascular dementia’ is used when cognitive deficits are severe enough to interfere with daily activities and function.
  • Cognitive deterioration can occur ‘step wise’ (with repeated larger vessel occlusions) or gradually (likely multiple small vessel occlusions which are lacunes or WM lesions).
  • Do not diagnose Vascular Dementia purely based on vascular imaging burden.
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22
Q

What 11 thing might make you suspect a diagnosis of Vascular Dementia vs. Alzheimer’s Dementia?

A
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23
Q

Dementia with Lewy Bodies (DLB)
- Course?
- Symptoms?
- Pathology?
- Vs. Alzheimer’s Dementia?
- Which meds to avoid? What to use to treat distressing hallucinations?

A
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24
Q

Fronto-Temporal Dementia
- Incidence?
- Symptoms?
- Age groups?
- Pathology?

A
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25
Q

Parkinson’s Disease Dementia
- Clinical features?
- Meds?

Normal Pressure Hydrocephalus
- Triad?
- Findings: CT brain? MRI brain?
- Gait Apraxia? Opening pressure on LP?

A

Normal Pressure Hydrocephalus - “Gait Apraxia”
- Impaired initiation.
- Magnetic (feet appear as if ‘stuck’ to the floor)
- May improve markedly after a few steps.
- Slow, shuffling, wide-based, poor turning.
- Can perform gait-related leg movements when lying in bed (i.e. it is an apraxia – motor is ok)
- Normal opening pressure on LP.

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26
Q

What are the General Principles of Management of Dementia?

A
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27
Q

Pharmacotherapy for Alzheimer’s Dementia
- 3 Treatment Targets?
- 2 Options for Cognitive Symptoms?

Role of Cholinesterase Inhibitors in Dementia
- How do they work?
- Main side effects?
- Contraindications?
- Evidence in different subtypes?

A

Pharmacotherapy for Alzheimer’s Dementia - Treatment Targets
1. Underlying Disease (none yet).
2. Cognitive symptoms
* Cholinesterase inhibitors
* Memantine (NMDA receptor antagonist)
3. Non-cognitive symptoms (e.g.
behavioural and psychological symptoms).

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28
Q

Pharmacological Treaments of Dementia: Memantine (Ebixa)
- MOA?
- Side effects?
- Efficacy?

A
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29
Q

What are the Behavioural and Psychological Symptoms of Dementia (BPSD)? (10)
- General Management Principles of BPSD?

A

BPSD - Non-cognitive symptoms of dementia
- Tend to occur late
- Common, may be very distressing.
1. Agitation
2. Aggression
3. Delusions
4. Hallucinations
5. Shouting
6. Touching
7. Wandering
8. Pacing
9. Insomnia
10. Withdrawal

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30
Q

Pharmacotherapy for BPSD
- First-line?
- Risks vs. Benefits?
- 6 Key Messages?
- Which agents? Dosing?

A
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31
Q

Functions of the Brain: Linking anatomy with pathology
- Frontal Lobe?
- Temporal Lobe?
- Parietal Lobe?
- Occipital Lobe?

A
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32
Q

Memory
- Definition?
- Which parts of the brain control memory?
- What is Registration?
- What is Short term memory? How to test it?
- What is Long-term memory? 2 Types and how to test them each?
- What is Episodic memory? Examples? How do we test it?

A

Memory
- Definition: Process of learning involving the registration of information, storage of that information, and the retrieval of the information at a later time.
- Memory is a mesial temporal lobe and hippocampal function.

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33
Q

Memory Impairment in Dementia
- What type is usually affected first?
- Changes to memory in Vascular Dementia vs. Alzheimer’s Dementia?

A

Memory Impairment in Dementia
* Impairment of memory tends to be the first feature of Alzheimer’s disease.
* Memory impairment may follow general intellectual decline in Vascular Dementia.
* People with Alzheimer’s dementia: Learn slower, learn less, Recognise poorly, Forget more quickly.
* Anterograde Memory (new learning) is affected first, often with better preservation of Retrograde Memory (memory for past events). i.e. can remember the past well but cannot remember three words after a few minutes (poor recall).
* Impairment of episodic memory commonly seen in Alzheimer’s disease (also MCI, PDD, depression).

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34
Q

Parkinson’s Disease
- Epidemiology: Incidence? Mean age at diagnosis? Prevalence? Mortality?
- Risk factors: 7 Increased? 5 Decreased?

A

Epidemiology
- Second most common neurodegenerative disorder after Alzheimers.
- Incidence increases rapidly after 60 years of age.
- Mean age at diagnosis 70.5 years.
- Prevalence 0.3% general population, 1% over 65 years of age.
- Mortality 2-5 x higher than age-matched controls.

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35
Q

Parkinson’s Disease: Pathophysiology
- Basal Ganglia Circuits?

A

Pathophysiology
- Lewy (1912) – presence of cytoplasmic inclusion bodies in neurons in various brain region
- Tretiakoff (1919) – loss of neurons in substantia nigra
- 1950s – dopamine depletion in basal ganglia
- Idiopathic
- Genetics– mostly sporadic, first-degree relatives 2.3 times higher risk (ask family history)

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36
Q

Clinical Features of Parkinson’s Disease
- 4 Motor?
- 4 Non-Motor?

A

Clinical Features
Motor
1. Tremor (typically resting) - Unilateral tremor is the most common presenting symptom and sign.
3. Rigidity (may be cogwheel or lead-pipe).
4. Bradykinesia - Prior symptoms may include difficulties writing, doing up buttons, a feeling of stiffness or slowness, voice fluctuations.
5. Postural instability.

Non-Motor: Sensory, autonomic, neuropsychiatric, sleep.

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37
Q

Describe the Parkinsonian Gait - 5 Features?

A

Parkinsonian Gait
1. Difficulty getting up from chair/bed.
2. Initial apraxia/freezing.
3. Stooped posture, reduced arm swing.
4. Short and rapid steps – festination.
5. Difficulty stopping and turning around.

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38
Q

Motor features of Parkinson’s Disease
- 4 Cardinal manifestations?
- 5 Craniofacial?
- 5 Visual?
- 5 MSK?
- Gait?

A
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39
Q

What are the Non-Motor Symptoms of Parkinson’s Disease?
- 2 Sensory?
- 4 Autonomic Dysfunction?
- 6 Neuropsychiatric?
- 5 Sleep Disorders?

A

Non-Motor Symptoms (NMS)
- Very common, about 97% of patient in a multicentre study reported NMS.
- Each patient experiencing average of eight NMS.
- Often affect QOL more than motor symptoms.

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40
Q

Neuropsychiatric Symptoms of Parkinson’s Disease
- 1) Depression?
- 2) Anxiety?
- 3) Apathy?
- 4) Cognitive Impairment?
- 5) Psychosis and Hallucinations?

A
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41
Q

Sleep Disorders in Parkinson’s Disease
- 1) Excessive Daytime Sleepiness (EDS)?
- 2) Restless Leg Syndrome (RLS)?
- 3) REM sleep Behaviour Disorder (RBD)?

A

Sleep Disorders in Parkinson’s Disease
- Sleep difficulty – most common NMS as reported by PD patients.
- Significant effect on QOL.
- Most common sleep disturbance reported by patients is Sleep Fragmentation and Early Morning Awakening.
- Causes - nocturia, difficulty turning over in bed, cramps, vivid dreams, pain, dystonia and depression.
- ‘Sleep disorders’ include:

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42
Q

4 Symptoms of Autonomic Dysfunction in Parkinson’s Disease?
- Natural History of PD?

A

Autonomic Dysfunction in PD
1. Postural Hypotension – in up to 60% of patients. Could be due to drugs. Increases risk of falls
2. Urinary problems – frequency, nocturia, urgency and urge incontinence – reduced bladder capacity due to involuntary detrusor contraction.
3. Constipation– slow colonic transit, very common and important as it interferes with drug absorption.
4. Sexual Dysfunction – decreased interest and low drive due to depression, fatigue, bradykinesia and rigidity. Excessive sexual drive can be associated with medications.

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43
Q

Diagnosing Parkinson’s Disease
- Diagnostic Criteria?
- 4 Supportive Criteria?
- 9 Absolute Exclusion Criteria?
- 9 Red Flags?

A

Absolute Exclusion Criteria
1. Cerebellar abnormalities.
2. Gaze palsy.
3. Diagnosis of probable behavioural variant FTD or PPA.
4. Lower limb parkinsonism for more than three years.
5. Treatment with a dopamine antagonist.
6. Absence of observable response to high-dose levodopa.
7. Unequivocal cortical sensory loss, clear limb ideomotor apraxia, or progressive aphasia.
8. Normal functional neuroimaging of the presynaptic dopaminergic system.
9. Documentation of an alternative condition known to produce
parkinsonism.

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44
Q
  • Which investigations would you consider in the diagnosis of PD?
  • When is idiopathic PD unlikely? (11 points)
A

Investigations
1. Cranial Imaging done to exclude specific structural abnormalities (eg, hydrocephalus, tumour, or lacunar infarcts).
2. DaTscan – Dopamine Transporter Scan (diagnostic method to look for loss of dopaminergic neurons in the striatum). Parkinsonism vs ET but cannot differentiate PD vs Parkinson’s-plus.
3. MIBG scan – tests cardiac sympathetic denervation. Relatively sensitive and specific in differentiating PD vs. Parkinson’s-plus.

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45
Q

What is the Unified Parkinson’s Disease Rating Scale (UPDRS)?
- 6 Components?
- Motor Staging – Hoen and Yahr?

A
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46
Q

Management of PD
- 5 Medications? MOA?
- Surgical?
- MDT?
- Principles of Initiating Therapy?

A

Management of PD
Medications
1. Levodopa
2. Dopamine Agonists
3. MAO-B inhibitors
4. Anticholinergics
5. Catechol-O-methyl transferase (COMT) inhibitors

Surgical - DBS

PD Multidisciplinary team management
- PT, OT, Nurse, Doctor, Speech Pathologist, Dietician, Social
Work, Clinical Psychologist

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47
Q

Pharmacological Treatment of PD: Levodopa
- Which symptoms is it most helpful for?
- What is it usually combined with?
- Adverse effects?
- Motor Fluctations?

A

Levodopa
- Most effective drug therapy.
- Very effective for bradykinesia, helps with rigidity and tremors (not so much for postural instability).
- Usually combined with a peripheral decarboxylase inhibitor (Carbidopa/benserazide) to block conversion to dopamine in the systemic circulation and liver (before it crosses the blood-brain barrier)..
- Available as immediate release or controlled release.

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48
Q

Pharmacological Treatment of PD: Dopamine Agonists
- 3 Examples?
- Useful for?
- Adverse Effects?
- Dopamine Dysregulation Syndrome?

Pharmacological Treatment of PD: MOA-B Inhibitors
- 2 Examples?
- Drug interactions?

A

Dopamine Agonists - Adverse Effects:
1. Nausea, vomiting, somnolence, postural hypotension, confusion, hallucinations, psychosis.
2. Excessive sleepiness and “sleep attacks”
3. Impulse control disorders (gambling, shopping) – warn.
4. Dopamine Dysregulation Syndrome
- Compulsive use of dopaminergic drugs despite dyskinesias.
- More common younger onset, male.
- Dopaminergic agents cause mood elevation with withdrawal effects with lower doses.
- Impulse control disorder may accompany DDS.
- DA > levodopa

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49
Q

Pharmacological Treatment of PD: COMT Inhibitors
- 2 Examples?
- MOA?
- Adverse Effects?
- 2 Other Medications?

A
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50
Q

Advanced Therapies for PD
- 4 Indications?
- 2 Options?
- 2 Options for Continuous dopaminergic drug delivery?
- 5 Indications for DBS in PD?

A

Advanced Therapies
Indications
1. Severe Disease
2. Pronounced motor fluctuations
3. Dyskinesias
4. Nocturnal Akinesia

Options
1. Continuous dopaminergic drug delivery
* Apomorphine Injection/Infusion
* Levodopa/Carbidopa intestinal Gel (Duodopa)
2. Deep Brain Stimulation (DBS)

51
Q

Management of Non-Motor Symptoms in PD
- Postural Hypotension? (7)
- Constipation? (5)
- Psychosis and Hallucinations? (6)

A

Constipation
1. Adequate fluid and dietary fibre intake.
2. Most patients need laxatives/stool softeners.
3. Movicol.
4. Coloxyl and Senna.
5. More severe cases needs regular
suppositories/ enemas.

52
Q

Management of Non-Motor Symptoms in PD
- Depression & Anxiety? (6)
- Drooling of Saliva? (5)
- Overactive Bladder Syndrome? (5)
- REM Sleep Behaviour Disorder (RBD)? (4)
- Excessive Day-time Sleepiness (EDS)? (4)

A

Drooling of Saliva
1. Conscious swallowing
2. Chewing sugar free gum
3. Atropine eye drops orally
4. Botox injection to parotids – often lasts for 3-6 months

Overactive bladder syndrome
1. Rule out UTI/BPH in males/medications like diuretics
2. Bladder diary
3. Anticholinergics
4. Beta 3 agonist – mirabegron – promising results
5. Botox injection in severe cases

53
Q

Non-Pharmacological Therapies in the Management of PD
- 7 Allied Health?

A

Non-Pharmacological Therapies in PD
- Mainly includes the support of the multidisciplinary PD team.
- Increasingly important as the disease progresses.
- Evidence supports the MDT model.

54
Q

List 8 Differential Diagnoses of Parkinson’s Disease?

A
55
Q

List 7 Medications that can cause Drug-induced Parkinsonism?

A

Drug-induced Parkinsonism
1. Typical anti-psychotics (haloperidol, chlorpromazine, phenothiazine)
2. Atypical anti-psychotics (risperidone, olanzapine, aripiprazole)
3. Anti-emetics (metoclopramide, prochlorperazine)
4. Calcium channel blockers (amlodipine)
5. Mood stabiliser (lithium)
6. Anticonvulsant (sodium valproate)
7. Antidepressant (SSRI - fluoxetine, citalopram, paroxetine, sertraline)

56
Q

Differentials for Parkinson’s Disease: Progressive Supranuclear Palsy
- Which protein?
- Symptoms?
- How does it differ from PD?

A

Progressive Supranuclear Palsy
- Progressive supranuclear palsy (PSP), also known as Steele Richardson Olszewski syndrome.
- Tau protein.
- Vertical supranuclear palsy with downward gaze abnormalities.
- Postural instability with early unexplained falls.
- Bradykinesia and rigidity are typically symmetrical in onset.
- Apathy, disinhibition, dysphoria, and anxiety are common.
- Typical resting tremor of PD is rare in PSP.

57
Q

Differentials for Parkinson’s Disease: Multiple System Atrophy
- What is it?
- Characteristic symptoms?
- Which protein?
- 8 Common Symptoms?

A

Multiple System Atrophy (MSA)
1. Parkinsonism – akinesia/ bradykinesia, rigidity, postural instability, tremor (irregular jerky postural and action tremor in arms), resting tremor in 1/3. Poor L-dopa response. Early postural instability and falls (within 3 years of onset). Rapid progression regardless of dopaminergic therapy.
2. Pyramidal signs (including extensor plantar responses).
3. Cerebellar– ataxia, dysarthria, nystagmus.
4. Dysautonomia- MSA-C and MSA-P, early. Urinary dysfunction (urgency, incontinence, voiding difficulty, nocturia), postural hypotension, decreased sweating (anhidrosis in 50%), erectile dysfunction in men.
5. Dysphagia common.

58
Q

Differentials for Parkinson’s Disease: Corticobasal Degeneration (CBD)
- Which protein?
- Symptoms?
- Symmetry?
- 6 Symtoms?

A

Corticobasal Degeneration (CBD)
- Clinical features heterogenous.
- Tau protein
- Symptoms initially affect one limb (upper or lower).
- Asymmetric parkinsonism including akinesia/ bradykinesia, rigidity, and postural instability and falls.
- Cortical dysfunction.
- Hyperreflexia, Axial rigidity, Tremor (jerky and irregular), Dystonia (hand or foot), Myoclonus, Speech (dysarthria, apraxia).
- Oculomotor dysfunction (pursuit eye movements slow and saccadic - this is an oculomotor apraxia)

59
Q

Differentials for Parkinson’s Disease: Dementia with Lewy Bodies (DLB)
- Pathophysiology?
- Symptoms?

A

Dementia with Lewy Bodies (DLB)
- Neurolept sensitivity (avoid typical antipsychotics, risperidone and olanzapine, maxolon and stemetil). Use quetiapine to treat distressing hallucinations.
- Pathologically: loss of dopaminergic neurons in substantia nigra and cingulate gyrus. Lewy bodies (containing protein alpha synuclein found in these affected areas).

60
Q
A
61
Q

Falls
- Definition?
- Epidemiology?
- Approach to the patient who has fallen? (4)

A

What is a fall?
- An event which results in a person coming to rest inadvertently on the ground or floor or other lower level.
- This includes collapse and syncope but not seizure.
- 30% of adults aged over 65 will fall annually.
- Global disease burden of nearly 17 million years of life lost in 2017.
- Falls-related expenditure close to 1% of healthcare costs.
- Prevalence of falls will increase due to increase in older adults numbers and increase in multimorbidity, polypharmacy and frailty.

62
Q

Falls
- 10 Key Questions to Ask a patient who has fallen?
- 3 Intrinsic Falls Risk Factors?
- 3 Extrinsic Falls Risk Factors?
- 9 Medical Conditions which increase falls risk?
- 9 Medications which increase falls risk?

A

Intrinsic Falls Risk Factors
1. Medical Co-morbidities
2. IMpaired Vision & Hearing - Multifocal glasses increases risk of falls – looking at the floor (bottom part) – not in focus (for reading)
3. Age related changes in neuromuscular function, gait & postural reflexes

Extrinsic Falls Risk Factors
1. Medications?
2. Improper use of assistive devises for ambulation
3. Environmental hazards

“Mechanical” fall = nothing term & causes early closure & bias

63
Q

Falls
- Examination?
- Investigations?

A

Examination
- General state - frailty
- Cognition - AMT4, 4AT
- Postural BP and HR
- Full neurological and cardiovascular examination
- Mobility - Assess transfers out of chair/bed
- Gait assessment

64
Q

Differences in A to E with Geriatric Patients?

A

Can have a lot bigger subdural bleed before neuro is affected as there is more space to bleed into.

65
Q

Trauma in Geriatrics following Falls
- Head injuries: how do they present? Guidelines re: CT scanning? Increased risk with which meds?
- C-spine injuries: increased risk of what? CT scanning guidelines? Associated harms with patients remaining in C-spine precautions?
- Chest Injuries: Mx? Complications?
- Upper Limb: Most common fractures? Which sling?
- Pelvic Fractures?
- Lower Limb: Most common fractures? Mx?

A

Chest Injuries
* Age is the strongest predictor of mortality and mortality increased proportionally with number of rib fractures (OR 1.19)
* Surrogate markers of polytrauma
* Plain XR may miss up to 50% of fractures.
* Early Pain Control: Multi-modal and regional analgesia
* Early Mobilisation and Physiotherapy
* Complications: 34% develop pneumonia, respiratory failure, pain leading to agitation and delirum

66
Q

MDT & Multi-interventional response for Falls in the Geriatric Population? (5)

A
67
Q

Elder Abuse
- Prevalence?
- 6 Risk factors for victims?
- 4 Risk factors for perpetrators?

A

Elder Abuse
- Prevalence is roughly 6%
- Maintain a high index of suspicion for elder abuse, especially in the elderly trauma patient presenting with usual patterns and inconsistent history

Risk factors for victims:
1. Female gender
2. Poor physical health
3. Cognitive impairment, particularly with disruptive behaviours
5. Poor future planning
6. Dysfunctional family setting

Risk factors for Perpetrators:
1. Drug and alcohol dependence
2. Mental illness
3. Financial dependence on the victim
4. Carer stress

68
Q

Cognitive Impairment
- Delirium vs. Dementia vs. Depression?

A

Delirium is an acute deterioration of cognition.
- Inattention, Disorganised Thinking, Altered Conscious State

Dementia is progressive deterioration of cognition.
- Apraxia (loss of function/ability to use tools), Aphasia, Agnosia (inability to recognise or name objects), Loss of Executive Functioning

Depression
- Less likely to express sadness
- Somatic, psychomotor retardation

69
Q

Delirium
- Why does it matter?
- List 10 Risk Factors.
- 6 Prevention strategies?

A

Why does Delirium matter?
- It may be the only sign of a medical illness
- 20% patients aged over 70 admitted to hospital have a CI
- 10% of older patients admitted with delirium
- 8% develop delirium during their hospital stay
- Increases morbidity and mortality
- 11% of healthcare associated complications in SMHS were due to delirium

70
Q

Delirium
- Assessment?
- 4 Components of the 4AT?
- Causes: DELIRIUM?
- 8 Investigations?

A

Delirium - Assessment
- History from patient, nursing staff and family
- Examination for signs of infection or pain
- Medication review
- Review charts – fluid balance, bowel chart, sleep and behaviour chart
- Check previous blood tests

71
Q

Management of Delirium
- Non-pharmacological? (10)
- Pharmacological? (6)

A
72
Q

Geriatric Presentations to the ED
- Vague Symptoms?
- Abdominal Pain?

A
73
Q

Falls
- Definition?
- Causes?

A

Definition of a Fall
‘A fall is an event which results in a person coming to rest inadvertently on the ground or floor or other lower level.’

74
Q

Epidemiology of Falls
- Incidences in different settings?
- Frequency at different ages?
- Burden of disease?
- Costs: Individual? Community?

A

Epidemiology of Falls
- 30% community dwellers >65 years
- 40% hospitalised (rehabilitation/ subacute) patients
- 50% of residents in long term care facilities (one or more falls in 12 months)
- People living in residential care settings at higher risk of falls and falls related injuries than those living in the community.

Costs
- Individual: loss of function and diminished QOL; fear of falling (increases risk of future falls).
- Community: Health costs attributable to falls-related injury. Hospital bed-days. Additional residential care beds required.

75
Q
  • 8 Consequences of Falls?
  • Injury Rates?
  • Incidence of Falls in Hospital?
A

Injury Rates
* Roughly:
* 1 in every 3 falls results in an injury.
* 1 in every 30 falls results in fracture.
(Rates are higher or lower, depending on the study)

76
Q

Falls
- Precipitating Events? Examples?
- What is an Intrinsic/Extrinsic Risk Factor?
- Examples of Environmental hazards?
- 16 Examples Intrinsic Risk Factors?

A

Precipitating Event
Older people fall because these intrinsic and extrinsic risk factors …..then interact with a precipitating event.
1. Changes in medications
2. Slips and trips
3. Hazardous activities (e.g., climbing a ladder …)
4. Acute medical illness: Pain, Weakness, Syncope/hypotension, Seizure, Delirium, Dizziness/poor balance/ gait disturbance

Risk factors
- Extrinsic = Related to a person’s environment or their interaction with the environment.
- Intrinsic = Related to a person’s behaviour or condition.

77
Q

Outline the Risk Factors for Falls.

A

Falls usually occur when a threat to the normal homeostatic mechanisms that maintain postural stability (e.g., acute illness, environmental stress, unsafe walking surface, medications) is superimposed on age-related declines in balance, ambulation and cardiovascular function.

A person’s risk of falling increases as their number of risk factors accumulates.

78
Q

How does Age-Related Functional Decline contribute to Falls Risk?
- Vision?
- Cognition?

A

Age-Related Functional Decline
Sensory changes:
- Visual
- Proprioceptive
- Vestibular

Physical changes
- BP regulation
- Central processing
- Gait
- Neuromotor function
- Postural control

Cognitive changes

79
Q

List the Diseases associated with functional decline?
- How might Environment contribute to falls risk?
- Risk ratios for falls?

A

Environment
- A significant interaction exists between environment and intrinsic factors. i.e., often multifactorial.
- Visual impairment + unfamiliar surrounds (+ dim light at night)
- Urinary incontinence + toilet far away…
- Restraints + delirium…
- E.g., One study (Donald 2000) found that carpet flooring, compared to vinyl flooring, was associated with a statistically significant increased rate of falling. (Rate ratio 14.73, 95% CI 1.88 to 115.35)

80
Q

Which Medications and Toxins may contribute to falls?

A
81
Q
  • What are the 4 Key risk factors for falling in hospital?
  • 5 Considerations for Falls prevention in hospital?
  • Role of education in falls prevention for in-patients?
A

Key risk factors for falling in hospital:
1. Age
2. A history of falls
3. Impaired cognition and
4. Impaired mobility

Falls Prevention - Considerations:
1. Strength and balance
2. Education
3. Medications
4. Environmental modifications
5. Prevent Complications

Good evidence for multifactorial interventions (individual fall-risk assessments followed by tailored interventions and referrals to address identified risks)

82
Q

Outline the 12 Standard Falls-Prevention Strategies in Hospitalised Patients?

A
83
Q

Outline 8 Standard Falls-Prevention Strategies in Community Dwelling Older Persons?

A
84
Q

Outline an Approach to Falls Evaluation.
- History?

A

Falls Evaluation
- History (especially of the fall, medical history, medications, environment, consequences of fall etc.)
- Examination
- Investigations
- Targeted to history.

Falls History - Circumstances of the fall:
- Activity at time of fall
- Location
- Use of walking aid (or not)
- Footwear
- Time of day (night versus day)
- Lighting
- Eyewear (e.g., glasses - bifocals, multifocal)

85
Q

What is an important question to ask regarding falls history?
- 3 Major Causes of Syncope?

A

Major Causes of Syncope
1. Orthostatic (postural hypotension) – meds, fluid, GI losses, autonomic (diabetes, PD) etc.
2. Cardiac arrhythmias (tachy/brady) or Structural cardiopulmonary disease (AS, HOCM, PE, severe PHT). No warning – be suspicious for a cardiac cause.
3. Reflex syncope (vasovagal– typical triggers include emotion,
pain, prolonged standing; situational– cough, strain, micturition; carotid sinus). Pre-syncopal symptoms typically associated with reflex syncope.

86
Q

Falls Evaluation
- Examination?
- Investigations post-fall?

A

Medical assessment post-fall
- Neurological observations and assessments, including Glasgow Coma Scale (especially if head strike).
- Identify: Delirium, new/increasing confusion, headache, clinical deterioration, amnesia, vomiting, change in conscious level.

Investigations post-fall
Consequences
- X-ray and/or CT (i.e., hips, spine, pelvis, wrist, head etcetera)

Causes
- Consider further investigation re cause of fall (depends on history and examination).

87
Q

3 Indications for Urgent CT head post-fall?
- Canadian CT Head Rules?
- Anticoagulation & Falls?

A

Indications for Urgent CT head
1. Suspect a head injury - Altered level of consciousness or a headache, or amnesia or vomiting. Note GCS (may decline later with serial review)
2. Patient hit head and coagulopathic (DOAC, warfarin, clexane, aspirin or clopidogrel)
3. Canadian CT Head Rules

88
Q

Outline the WA Falls Action Plan.

A

A range of services are available in WA to deliver falls prevention interventions. The WA Falls Action Plan represents an overarching approach to falls prevention in different settings.
- The red items demonstrate population health strategies, the orange items are services involved in screening, referring and assessing and the green items are the types of available interventions and where they are delivered.
- Multicoloured items are an indication of the dual role of these behaviours or services i.e. exercise can be promoted as both a general population health strategy and also an individualised intervention for people at risk of falls.

89
Q

Outline the Post-Fall Multidisciplinary Management Guidelines for Western Australian Health Care Settings (2018)
- Immediate Post-fall procedure?
- Immediate Actions?
- Medical assessment post-fall?

A

Immediate Actions
1) Assess for physical injury:
* Neck pain/ injury indicate the neck should be immobilised.
* Head injury, hip or other fracture and/ or soft tissue injury following a fall dictates specific action.
* Medical review as soon as possible for assessment and investigations (imaging such as XR or CT).

Bedside investigations:
1. Vital signs observations (including BSL).
2. Neurological observations and assessments, including Glasgow Coma Scale.
3. Cognitive assessment using AMT4/4AT/CAM.

Identify: Delirium, new/increasing confusion, headache, clinical deterioration, amnesia, vomiting, change in conscious level.

90
Q

Post-Fall Multidisciplinary Management Guidelines for Western Australian Health Care Settings (2018)
- Type of fall and ongoing 48-hour observations?

A
91
Q

Outline the Syncopal Causes of Falls.
- What is Syncope?
- What are the 8 Classic Prodromal Symptoms of Imminent syncope/ presyncope?

A

Syncope
- Clinical syndrome in which transient loss of consciousness (TLOC) is caused by a period of inadequate cerebral blood flow and oxygenation.
- Usually of brief duration (by definition, syncope is self-limited).
- Initial evaluation relies heavily on a comprehensive history, physical examination, ECG, assessing the heart for structural heart disease (ECHO).
- Can experience pre-syncope (near syncope) symptoms alone, or pre-syncopal symptoms prior to a syncopal episode.
- Be suspicious for a cardiac cause if no warning.

92
Q

4 Major Causes of Syncope?

A

Major Causes of Syncope
1. Orthostatic syncope
2. Cardiac arrhythmias
3. Structural cardiopulmonary disease
4. Reflex syncope

93
Q

List 8 Considerations for medication use in older persons?

A
94
Q

Outline the Pharmacological Changes with Ageing - Pharmacokinetic and Pharmacodynamic
- 3 Changes occur in Drug Absorption, Distribution, Metabolism, Excretion?
- 4 Pharmacodynamic examples?
- Implications of Frailty?

A

Implications of Frailty
- Increased body fat + decreased lean body mass (affecting Vd) = ‘sarcopenia’.
- Greater age-related reduction in albumin.
- Total drug levels of albumin-bound drugs can be unreliable- e.g., valproate, phenytoin. Can be ‘toxic’ at apparently ‘therapeutic’ drug levels.
- Prescribers need to take extra care in the setting of frailty– there is an increased risk of adverse outcomes, including adverse drug effects.

95
Q

What are the Implications of pharmacodynamic and pharmacokinetic changes with ageing?

A

= Periodically review long-term medications
- Effects on drug pharmacodynamics and pharmacokinetics change with ageing may alter the effectiveness and safety of long-standing medications over time with ageing.
- Prescription doses may need to change with time (due to physiological changes that occur with ageing).

96
Q

Case - Prescribing in the Elderly

A

Examination
- HR 54bpm, Afebrile, BP 110/50, SaO2 98% RA
- BSL 4.8.
- Chest clear.
- Cardiovascular - dual heart sounds, no murmurs. AF.
- Peripheral oedema to ankle. JVP not elevated.
- Abdomen - unremarkable.
- Neuro - peripheral and cranial nerves intact.

Medication Issues to Consider in this case - 6 Practical considerations? 6 Specific drug considerations?

97
Q

5 Potential medication-related causes of collapse in an elderly patient on the following medications?

A
98
Q

How might Treatment Priorities need to be adjusted in the elderly population?

A
99
Q

What is Iatrogenesis?
- Most common example?
- ADR in Older Persons - Why?
- 5 Most common meds?
- 4 Other examples of Individual Drug ADR Occurring More Commonly in Older People?

A

Iatrogenesis
- Definition: Refers to any unintended and untoward consequence of a well-intended healthcare intervention.
- An adverse reaction to a medication is the most common example of iatrogenesis in healthcare.
- Iatrogenesis is often preventable.
- Iatrogenesis is associated with increased length of hospital stay, increased patient mortality and morbidity, and increased cost.

ADR in Older Persons – Why?
* Drug-drug interactions
- More drugs to interact.
* Individual drug adverse effects
- More common in older persons.

100
Q

Polypharmacy
- Definition?
- Why is it hard to avoid?
- 5 Risk Factors?

A

Polypharmacy = Defined as simultaneous use of ≥ 5 medications.

Risk Factors
1. Older age
2. Female gender
3. Increasing number of diagnoses
4. Hospitalisation
5. Depression

101
Q

What considerations need to be made when applying clinical guidelines to older persons?

A

Common Exclusion Criteria for Clinical Trials That Do Include Older Persons
1. Presence of co-morbid diseases
2. Multiple Medications
3. Residents of aged-care facilities
4. Cognitive Impairment
5. Need for Interpreter

102
Q

What is the Prescribing Cascade Phenomenon?
- 5 Examples?

A

Prescribing Cascade - Occurs when a new medication is prescribed to treat symptoms that have arisen from an unrecognised adverse drug effect that is the result of an existing therapy.

103
Q

What are Prescribing Omissions?
- 3 Common Examples?

What are Potentially Inappropriate Medications (PIMS)?
- Name 5 Prescribing Tools used to identify PIMS?

A

Prescribing Omissions
- Also known as under-prescribing.
- Failure to prescribe a medication for which there is a clinical indication and which, for the patient, is appropriate to prescribe.

Common Examples:
1. Anticoagulation for stroke prevention in AF.
2. ACEI/ARB for patient with heart failure.
3. Bone protection for patient on long-term steroid therapy.

Potentially Inappropriate Medications (PIMS)
- Definition: Medications where the risk of adverse events from the drug outweighs the clinical benefit.
- 20 - 40% of community-living people.
- 30 - 50% in residential care.

104
Q

What are the High Risk Medications in Older People?

A
105
Q

List 4 Factors Impacting Adherence to Medications in the Elderly?
- 4 Ways to improve this?

A
  1. Polypharmacy - Complicated treatment regimes
  2. Cognition (memory)
  3. Social factors - Education, finances etc.
  4. Physical Factors may also affect compliance
    - Dexterity (affected by arthritis or PD) e.g., unable to open bottle or packets.
    - Swallowing difficulties - difficult to take tablets

Improving Adherence
1. Simplify regimes
2. Use dispensing aids
3. Supervise medications
4. Involve carers.

106
Q

DEPRESCRIBING
- Definition?
- 4 Benefits of Deprescribing?
- The Steps to Deprescribing?
- Principles of Deprescribing?

A

DEPRESCRIBING = The process of withdrawal of an inappropriate medication, supervised by a healthcare professional with the goal of improving outcomes.
- Should occur as part of a medication review.
- Steps to Deprescribing: 1) Prioritize medications for discontinuation based on risk-benefit and ease of discontinuation & 2) Discuss the recommendations with the patient, provide information, allow shared decision making.

Benefits of Deprescribing
1. Resolve related adverse drug effects.
2. Improve patient satisfaction and QOL.
3. Improve physical and cognitive function.
4. Reduce financial cost to patient and community.

107
Q

List 10 possible indications for a Home Medicines Review by a Pharmacist?
- 9 Steps?

A
108
Q

Epilepsy in the Elderly - Case Study

A

History - The son tells you he was staring blankly for 5 minutes whilst in the GP’s office, then mentions he had a similar episode a year ago. On both occasions it took him about 24 hours to “come right”. MRI brain reveals a right parietal cortical infarct (old) as well as the internal capsule infarct on the left.

109
Q

Prevalence & Causation of Epilepsy in the Elderly?

A

Introduction
* The prevalence and incidence of epilepsy are highest in later life with almost 25% of new cases occurring in older patients.
* The relationship between age and incidence of epilepsy is bimodal.
Causation
* Seizures in elderly patients are nearly exclusively partial in onset and complex partial seizures are the most common seizures in this age group.
* Cerebrovascular disease is the single most common pathological factor underlying epilepsy in the elderly.

110
Q

Definitions: Seizure Aetiology
- Idiopathic?
- Remote Symptomatic?
- Provoked?

A

Definitions: Seizure Aetiology
- Idiopathic: No obvious cause
- Remote Symptomatic: Due to previous but not acute cerebral insult
- Provoked: Seizure(s) occurring in close temporal association with an acute systemic, metabolic, or toxic insult or in association with an acute CNS insult (within 7 days).

111
Q

Provoked or Acute Symptomatic Seizures - What are the important clinical features?

A
112
Q

Provoked or Acute Symptomatic Seizures - 2 ICAUSES

A
113
Q

Provoked or Acute Symptomatic Seizures - 5 INFECTIVE CAUSES?

A
114
Q

Provoked or Acute Symptomatic Seizures - 1 INFLAMMATORY CAUSE?

A

Immune Mediated Encephalopathies: NMDA receptor antibody encephalitis causes rapidly progressive encephalopathy, neuropsychiatric features, dyskinesias and autonomic disturbance. Seizures occur in about 75%. It is more common in women and is associated with underlying malignancy, usually ovarian teratoma, and is treatable with IVIG. Limbic encephalitis occurs in association with anti-voltage gated potassium channel Abs and presents with a more indolent cognitive decline, neuropsychiatric features and partial-onset seizures that may secondarily generalize. Treatment is with immunosuppression.

115
Q

Provoked or Acute Symptomatic Seizures – 2 VASCULAR CAUSES?

A

VASCULAR CAUSES
1. Arterial Infarction: Stroke causes both acute symptomatic seizures and epilepsy. 2.5-5 % of patients develop early seizures, and these suggest a worse prognosis. Seizure risk is higher with larger infarcts, especially if it involves the cortex; seizures are less likely with deep white matter ischemic lesions.
2. Venous Infarction: Cerebral venous sinus thrombosis is an uncommon cause of cortical infarction and intracerebral haemorrhage. It is slightly more common in women. It presents with headache (either non-specific or with raised pressure features), encephalopathy, focal neurological symptoms, or seizures and papilledema in some cases.

116
Q

Provoked or Acute Symptomatic Seizures in the Elderly:
- 5 Metabolic Causes?
- 10 Drugs reported to cause seizures?
- Seizures in the elderly from other Pathologies? (2)

A

Metabolic Causes:
1. Hyper and hypoglycaemia
2. Hyponatremia
3. Hypomagnesemia
4. Hypo and hypercalcemia
5. Liver failure and hepatic encephalopathy

Seizures from other Pathologies
- Alzheimer’s patients have a 20% risk of developing seizures by the 5th year of their illness. Recurrent seizures (ie epilepsy) is common.
- Although seizures may occur early after SAH, the risk of these patients developing epilepsy is low.

117
Q
  • Clinical Manifestations of Epilepsy in the Elderly?
  • Steps in Diagnosis?
  • Investigations and Diagnosis of Epilepsy in the Elderly?
A

Clinical Manifestations of Epilepsy in the Elderly
- The most common clinical manifestations of CPS - confusion, disorientation and unresponsive staring - may be both subtle and quite prolonged.
- Some ictal behaviours such as orofacial automatisms, rubbing, tapping, stroking, disrobing and wandering may not be recognised as possible seizure activity by carers and clinicians, especially in those with dementia.
- Altered mental state/memory lapses have many other possible explanations in the elderly, and as a consequence delays in diagnosis are common.

118
Q

Pharmacotherapy for Epilepsy - Prescribing for the Elderly: 4 Issues?

A
119
Q

7 Features of ideal AEDs?

A

The ideal AED should be: DOESN’T EXIST
1. completely absorbed
2. undergo linear pharmacokinetics
3. have a clearance unaffected by renal impairment
4. not induce or inhibit hepatic enzymes
5. not produce neurotoxic side effects
6. achieve its target dose without titration
7. come in a range of formulations

120
Q

Commonly used AEDs
Carbamazepine
- Use?
- Dosing?
- Pharmacokinetic SE?
- Other SE in elderly?

Phenytoin
- Use?
- Dosing?
- Routes of administration?
- Pharmacokinetic SE?
- Other SE in elderly?

A

Carbamazepine
- Effective against partial and generalised TCS in all age groups.
- Controlled release formulation allows bd dosing.
- 100 mg nocte, then after 2 weeks 100 mg bd, increasing to 200 mg bd after a month.
- Induces metabolism of other lipid-soluble drugs.
- Rash (5%) more common in later life.
- NOT found to impair psychomotor activity in old age, but dose related nausea, headache, dizziness, diplopia and ataxia occurs.
- May be assoc. with osteomalacia/ osteoporosis.

121
Q

Commonly used AEDs
Sodium Valproate
- Use?
- Dosing?
- Pharmacokinetic SE?
- Interaction?

Lamotrigine
- Use?
- Dosing?
- Routes of administration?
- Pharmacokinetic SE?
- Other SE in elderly?

A
122
Q

Commonly used AEDs
Topiramate
- Efficacy & tolerability?
- SE?
- Use in pregnancy?

Lamotrigine
- Use?
- SE in elderly?
- Drug interactions?
- Pharmacokinetics?
- Dosing?

A
123
Q

Epilepsy in the Elderly
- Counselling & Education?
- Sequelae?

A

Counselling and Education
- Seizures, medication
- Epilepsy is controlled but not cured by these medicines
- Treatment may be needed life-long
- Minimise possible seizure-inducing factors: fatigue, sleep-wake cycle, alcohol and substance abuse/withdrawal
- Activities of Daily Living - Safety issues
- First aid/help at hand in case of a seizure
- Driving restrictions

124
Q

Monitoring of AEDs in epileptic elderly patients?

A

Appropriate Monitoring
* CLINICAL = the most important
* MONITORING BLOOD LEVELS
- Can be overvalued and even abused.
- The lower limit = meaningless
- The upper limit = ill-defined (except PHT)
* Do not alter AED’s on the basis of blood levels alone!