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CPT > Neurology > Flashcards

Neurology Flashcards

1
Q

What is used in idiopathic Parkinson’s disease to improve motor symptoms?

A

Levodopa

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2
Q

Outline the pathology of idiopathic Parkinson’s disease

A
  • Neurodegeneration
  • Lewy bodies
  • Loss of pigment due to increased turnover
  • Reduced dopamine
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3
Q

Clinical features of Parkinsonism

A

Tremor
Rigidity
Brradykinesia
Postural instability

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4
Q

Diagnosis of idiopathic Parkinson’s disease

A
  • clinical features
  • exclude other causes of Parkinsonism
  • response to levodopa
  • structural neuro imaging is normal
  • must have bradykinesia
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5
Q

What is idiopathic Parkinson’s disease?

A

Progressive neurodegenerative disorder due to loss of substantia nigra dopamine neurones

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6
Q

At what point of loss of pigment in idiopathic Parkinson’s disease do symptoms present?

A

> 50% loss

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7
Q

Non motor manifestations of idiopathic Parkinson’s disease

A
  • mood changes
  • hallucinations
  • sleep disorder
  • fatigue
  • urinary symptoms
  • hypotension
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8
Q

Describe Parkinsonian tremor

A

Low frequency
Pillrolling
At rest
Stops with movement

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9
Q

Describe Parkinsonian rigidity

A

Lead pipe
Tension all the way through flexion

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10
Q

Describe Parkinsonian gait

A
  • short shuffling steps
  • struggle to initiate + stop
  • turning on block
  • asymmetric arm swing
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11
Q

What enzyme converts levodopa to dopamine?

A

Dopa decarboxylase

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12
Q

Outline catecholamines synthesis

A

L tyrosine > levodopa > dopamine > noradrenaline > adrenaline

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13
Q

Why is levodopa used instead of dopamine to treat idiopathic Parkinson’s disease?

A

Levodopa crosses the blood brain barrier but dopamine cannot

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14
Q

Pharmacokinetics of levodopa

A
  • oral administration
  • absorbed by active transport
  • t1/2 2 hours
  • 90% inactivated in intestinal wall
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15
Q

How is levodopa converted to dopamine?

A
  • Cross BBB
  • Taken up by axons within substantia nigra
  • Converted into dopamine in the cell
  • Catalysed by dopa decarboxylase
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16
Q

Describe the formulation of levodopa

A
  • used in combination with peripheral dopa decarboxylase inhibiotr
  • co-careldopa: levodopa + carbidopa
  • co-beneldopa: levodopa + benserazide
  • tablet only P.O.
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17
Q

Why is levodopa given in combination with peripheral dopa decarboxylase inhibitor?

A
  • Reduces conversion in peripheral tissue
  • Reduces dose required
  • Reduces side effects
  • Increased levodopa reaching brain
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18
Q

Advantages + disadvantages of levodopa

A

Advantages:
- high efficacy
- low side effects
.
Disadvantages:
- loss of efficacy long term due to degeneration of axons
- needs enzyme conversion
- motor complications long term

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19
Q

Side effects of levodopa

A
  • Nausea + anorexia
  • hypotension
  • psychosis (schizophrenia like effects)
  • hallucination
  • tachycardia
20
Q

Motor complications of long term levodopa

A
  • wearing off
  • dyskinesias
  • dystonia
  • freezing
21
Q

Important drug drug interactions with levodopa

A
  • pyridoxine increased peripheral breakdown
  • monoamine oxidase inhibitors increase risk of hypertensive crisis
  • antipsychotic drugs block dopamine receptors
22
Q

What drugs are used in treatment of idiopathic Parkinson’s disease

A
  • levodopa
  • levodopa with COMT inhibitor
  • dopamine receptor agonists
  • anticholinergics
  • amantadine
23
Q

Why do COMT inhibitor have no therapeutic effect alone?

A

Do not cross BBB

24
Q

What is stalevo?

A

Combination tablets of COMT inhibitor, levodopa + peripheral dopa decarboxylase inhibitor

25
Q

Mechanism of action of COMT inhibitors

A
  • Reduces peripheral breakdwon of levodopa to 3-O-methyldopa by COMT
  • 3-O-methydopa competes with levodopa active transport into CNS
  • prolongs motor response to levodopa (reduces symptoms of wearing off)
26
Q

Examples of COMT inhibitors

A

Entacapone
Opicapone

27
Q

Examples of dopamine receptors agonists + their administration

A
  • non ergot: ropinirole + pramipexole
  • patch: rotigotine
  • s.c.: apomorphine
28
Q

Advantages + disadvantages of dopamine receptor agonists

A

advantages:
- direct acting
- less dyskinesia/motor complications
- possible neuroprotection
.
disadvantages:
- less efficacy than levodopa
- impulse control disorders
- more psychiatric side effects
- expensive

29
Q

Examples of impulse control disorders

A
  • pathological gambling
  • hypersexulaltiy
  • compulsive shopping
  • desire to increase dose
  • punding
30
Q

What is punding?

A

Compulsive performance of repetitive, mechanical tasks such as collecting + sorting

31
Q

Side effects of dopamine receptor agonists

A
  • sedation
  • hallucinations
  • confusion
  • nausea
  • hypotension
32
Q

What is used in patients with severe motor fluctuations

A

S.c. Apomorphine bolus

33
Q

What is the action of monoamine oxidase B?

A

Metabolises dopamine

34
Q

What is the mechanism of action of monoamine oxidase B inhibitors?

A

Inhibits monoamine oxidase B > reduces metabolism of dopamine

35
Q

Examples of monoamine oxidases B inhibitors

A

Selegiline
Rasagaline
Safinamide

36
Q

Advantages + disadvantages of anticholinergics in IPD treatment

A

advantages:
- treat tremor
- not acting via dopamine system
.
disadvantages:
- no effect on bradykinesia
- confusion + drowsiness

37
Q

Why may meds be missed in hospital admissions?

A
  • confused patients
  • meds not known
  • delays in writing up drug
  • delays in acquiring drug on ward
  • set times for drug round
38
Q

Consequences of missed Parkinson’s disease meds on hospital admission

A
  • worsening symptoms
  • increased fall risk
  • dopamine agonist withdrawal syndrome
39
Q

Symptoms of dopmaine agonist withdrawal syndrome

A
  • agitation
  • panic
  • anxiety
  • depression
  • fatigue
  • hypotension
40
Q

Solutions of missed Parkinson’s disease meds due to hosptial admission

A
  • education for ward staff
  • prioritise prescription, acquisition + administration of meds
  • self administration if appropriate
  • rotigotine patches or s.c. Apomorphine if oral cannot be taken
  • incident report for missed dose
41
Q

What is fatiguability?

A

A muscle that is in use gets weaker as you use it
Strengthens with rest

42
Q

Presentation of myasthenia gravis

A
  • fatiguability
  • dysphagia, dysphonia, dysarthria
  • fluctuating weakness
  • ptosis
  • double vision
43
Q

Management of myasthenia gravis

A

Acetylcholinesterase inhibitors
- enhances neuromuscular transmission

44
Q

Examples of acteylcholinesterase inhibitors

A

Pyridostigmine
Neostigmine

45
Q

What is the onset + duration of pyridostigmine?

A

30min onset
3-6hour duration

46
Q

Side effects of pyridostigmine

A
  • miosis
  • SSLUDGE syndrome:
  • salivation
  • sweating
  • L acrimation
  • urinary incontience
  • diarrhoea
  • GI upset
  • emesis
47
Q

How does the onset of pyridostigmine affect its administration?

A

Given 40-60 mins before meals to optimise swallow

CPT (28 decks)

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