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3. Senior Block- Integrated Care > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

Give 5 risk factors for Parkinson’s Disease

A 
>60 years old 
Family history 
Hx of brain trauma 
Male 
Obesity 
Low vitamin D
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2
Q

Give the 3 main causes of parkinsonism

A

Idiopathic Parkinson’s Disease

Medication- induced- antipsychotics, metoclopramide, valproate, lithium, amiodarone

Vascular Parkinson’s- series of small strokes can reduce blood flow to the brain and cause Parkinson’s

Parkinson plus syndromes 
wilson's disease
Essential tremor
Huntington's disease 
CJD
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3
Q

What is the pathophysiology of Parkinson’s disease?

A

Progressive dopaminergic neuron degeneration in the substantia nigra (in basal ganglia). Less dopamine at the receptors of the stratum so transmission to the thalamus and motor cortex is reduced which results in the symptoms of Parkinson’s.

Build up of Lewy bodies in the basal ganglia, cortex and brainstem

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4
Q

What are the 3 core features of Parkinson’s Disease?

A

Extrapyramidal triad:

Tremor- pill rolling, unilateral
Hypertonia- rigidity, stiff muscles
Bradykinesia- slow movements

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5
Q

Give 5 examples of motor symptoms in Parkinson’s Disease

A

Stooped posture
Bradykinesia- slow to move, slow to initiate movement
Reduced arm swing
Mask like face
Pill rolling tremor- increases with stress, decreased with voluntary movement
Micrographia
Rigid arms- cogwheel rigidity/lead pipe
Postural instability
Gait: festinant, shuffling, quick and short steps, slow to initiate movement, need multiple steps to turn.

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6
Q

Give 4 psychological symptoms of Parkinson’s disease

A

Depression
Anxiety
Mild cognitive impairment
Dementia- severe memory problems, behavioural changes

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7
Q

Give 3 examples of autonomic dysfunction in Parkinson’s Disease

A 
Urinary frequency 
Constipation 
Postural hypotension 
Erectile dysfunction 
Excessive saliva production
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8
Q

How is Parkinson’s Disease diagnosed?

A

Clinical diagnosis- Need all 3 core features

Levodopa challenge- if symptoms are relieved by Levodopa then highly suggestive of Parkinson’s Disease

Can do Head CT/MRI to rule out other diagnoses

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9
Q

Who is involved in the Parkinson’s Disease MDT?

A 
Specialist Parkinson's Disease nurse
GP
PT
OT
SALT
Palliative care nurse
Support groups 
DVLA
Voluntary section 
CPN
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10
Q

When is Levodopa given in Parkinson’s Disease?

A

When symptoms of Parkinson’s Disease interfere with daily living

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11
Q

What kind of drug is levodopa?

A

Dopamine precursor

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12
Q

Which drug is commonly prescribed alongside Levodopa and why?

A

Dopa-decarboxylase inhibitor- eg. Carbidopa

Inhibits peripheral breakdown of levodopa so more can enter CNS

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13
Q

Give 4 side effects of Levodopa

A 
Hallucinations 
Insomnia 
Psychotic symptoms 
Hypokinesia
Dyskinesia 
N+V
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14
Q

What is the on-off phenomenon experience with levodopa?

A

Symptoms will be completely cured when drugs is working but as it wears off the symptoms return. Off periods tend to get longer and occur quicker after taking levodopa over time

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15
Q

What is an akinetic crisis?

A

Sudden withdrawal of L-DOPA results in complete inability to move and requires ITU treatment

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16
Q

Give 3 examples of Dopamine agonists

A

Pramipexole, Ropinirole, Rotigotine, Apomorphine, Bromocriptine

17
Q

Give 4 side effects of dopamine agonists

A 
Risk of heart problems 
Fatigue 
Dizziness
Nausea 
Constipation 
Hypotension 
Headaches 
Hallucinations 
Movement problems
18
Q

Give an example of a Monoamine oxidase-B inhibitor (MAO-B)

A

Selegiline

Rasagiline

19
Q

When is a Monoamine oxidase-B inhibitor used to treat Parkinson’s Disease?

A

Alternative to Levodopa for treating early Parkinson’s. Often used alongside levodopa when more control is needed.

20
Q

What is the mechanism of action of Monoamine oxidase-B inhibitors?

A

Block Monoamine oxidase-B which is an enzyme that breaks down dopamine.

21
Q

Give 3 side effects of Monoamine oxidase-B inhibitors

A 
Nausea
Headache 
Abdominal pain 
Postural hypotension 
Atrial fibrillation 
Depression
22
Q

Give an example of a Catechol-O-methyltransferase (COMT) inhibitor

A

Entacapone

23
Q

How do Catechol-O-methyltransferase (COMT) inhibitors work?

A

Stop the breakdown of levodopa so used alongside levodopa to increase its effectivity

24
Q

Give 3 side effects of Catechol-O-methyltransferase (COMT) inhibitors?

A 
Risk of liver damage
Sleeping problems 
Fainting 
Headaches 
Dizziness 
Hallucinations
25
Q

What is Apomorphine used for in Parkinson’s Disease management?

A

Subcutaneous injection/infusions of a DA agonist to reduce ‘off’ spells

26
Q

What is a Parkinson’s Plus Syndrome?

A

A group of neurodegenerative diseases which present with Parkinsonism but are not Parkinson’s Disease. Usually have a worse prognosis

27
Q

What signs may be present which suggest a Parkinson’s Plus Syndrome rather than Parkinson’s Disease?

A

Poor response to levodopa
Rapid progression of dementia
Early onset of postural instability and falls
Early involvement of autonomic nervous system

28
Q

What is the pathophysiology of Lewy Body Dementia?

A

Cerebral atrophy especially of the frontal lobe with deposition of Lewy Bodies in glia cells. The Lewy bodies cause myelin and glial dysfunction and subsequent neuronal degeneration.

29
Q

What are the clinical features of Lewy body dementia?

A

Dementia
Extrapyramidal motor symptoms
Visual hallucinations
Paranoia
Frequent falls
Rapid eye movement sleep behaviour disorder
Increased sensitivity to neuroleptic medication

30
Q

How is Lewy body dementia managed?

A

Supportive therapy
Physiotherapy
Parkinson’s medications can be effective

31
Q

What is Multiple System Atrophy?

A

Rare, adult onset neurodegenerative disease characterised by neuronal degeneration in the substantia nigra and Ley body formation.

32
Q

Give 4 clinical features of Multiple System Atrophy

A

Parkinsonism
Cerebellar features- ataxia, tremor, dysarthria
Autonomic dysfunction- incontinence, dysphagia, dizziness
Neuropsychiatric disorders

33
Q

How is Multiple System Atrophy managed?

A

Supportive

Will have no response to dopamine

34
Q

What is Progressive Supranuclear Palsy?

A

Brain is damages as a result of a buildup of the protein tau. As the tau builds up in the brain, the symptoms get worse.

35
Q

Give 4 clinical features of Progressive Supranuclear Palsy

A 
Frequent falls 
Frontal lobe abnormalities- apathy, impaired reasoning, disinhibition 
Vertical gaze palsy 
Bradykinesia
Dysphagia
36
Q

What is corticobasal degeneration?

A

Build up of tau damages the cortex and basal ganglia.

37
Q

Give 3 clinical features of corticobasal degeneration

A

Unilateral limb failure
Alien limb phenomenon- do not recognise limb as their own
Dementia
Muscle stiffness

38
Q

How is corticobasal degeneration managed?

A

Symptom control
Cognitive stimulation
Physiotherapy
SALT

3. Senior Block- Integrated Care (7 decks)

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