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CPT > Neurological drugs > Flashcards

Neurological drugs Flashcards

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1
Q

What is the pathology of idiopathic Parkinson’s Disease (IPD)?

A
  • Neurodegeneration
  • Lewy bodies
  • Loss of pigment
  • Reduced
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2
Q

Outline the basal ganglia circuit

A
  1. Loss of dopaminergic neurones in substantia nigra results in reduced inhibition in neostriatum
  2. Loss of inhibition in neostriatum allows increased production of ACh (excitatory)
  3. Chain of abnormal signalling leads to impaired mobility
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3
Q

What are the features of Parkinsonism?

A
  • Tremor (low dopamine and disturbance of other neurotransmitter levels)
  • Rigidity (low dopamine and disturbance of other neurotransmitter levels)
  • Bradykinesia (low dopamine)
  • Postural instability
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4
Q

How do we make a diagnosis of IPD?

A
  • Clinical features
  • Exclude other causes of Parkinsonism
  • Response to treatment
  • Structural neuro imaging is normal
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5
Q

What are some non motor manifestations of IPD?

A
  • Mood changes
  • Hallucinations
  • Cognitive change
  • Sleep disorder
  • Restless legs
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6
Q

Outline catecholamine synthesis

A
  • Origin molecule is L-tyrosine
  • Gets converted to Levodopa (L-dopa)
  • L-dopa is converted to dopamine
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7
Q

What are the drug classes in IPD?

A
  • Levodopa (L-dopa)
  • Levodopa with COMT inhibitor
  • Dopamine receptor agonists
  • MAOI type B inhibitors
  • Anticholinergics
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8
Q

Why do we not just use dopamine as an IPD drug?

A
  • Dopamine cannot cross the blood brain barrier
  • Levodopa can cross by active transport
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9
Q

How does L-dopa work?

A
  • Must be taken up by dopaminergic cells in substantia nigra to be converted into dopamine
  • Fewer neurones are left in pts with IPD
  • Levodopa works less effectively as pt’s condition deteriorates
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10
Q

What are the pharmacokinetics of L-dopa?

A
  • Taken p.o.
  • Absorbed by active transport
  • 90% of drug inactivated in intestinal wall
  • Half life is 2 hours
  • 9% of drug is converted to dopamine in peripheral tissues
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11
Q

What does the short half life of L- dopa mean?

A
  • Short dose interval
  • Fluctuations in blood levels and symptoms
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12
Q

How is levodopa formulated?

A
  • Must be used in combination with peripheral dopa decarboxylase inhibitors
  • Because we don’t want drug to be broken down peripherally
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13
Q

Give some examples of Levadopa drugs

A
  • Co-careldopa e.g. Sinemet
  • Co-beneldopa e.g. Madopar
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14
Q

Why do we give levodopa alongside peripheral dopa decarboxylase inhibitors?

A
  • Reduce dose required
  • Reduce side effects
  • Increased levodopa reaching brain
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15
Q

What are the different formulations of Levodopa?

A
  • Tablet formulations only
  • Standard dosage - variable strengths
  • Controlled release preparations
  • Dispersible Madopar (not soluble)
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16
Q

What are the advantages of levodopa?

A
  • Highly efficacious
  • Low side effects
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17
Q

What are the disadvantages?

A
  • Precursor - needs enzyme conversion
  • Long term: loss of efficacy, involuntary movements, motor complications
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18
Q

What are the side effects of levodopa?

A
  • Nausea/anorexia
  • Hypotension (central and peripheral)
  • Psychosis
  • Tachycardia
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19
Q

What are the motor complications of levodopa?

A
  • On/off
  • Wearing off
  • Dyskinesias
  • Dystonia
  • Freezing
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20
Q

What are the interactions of levodopa?

A
  • Pyridoxine (vitamin B6) increases peripheral breakdown of levodopa
  • MAOIs risk hypertensive crisis
  • Many antipsychotic drugs block dopamine receptors and parkinsonism is a side effect
21
Q

Give some examples of Catechol-O-methyl transferase (COMT) inhibitors?

A
  • Entacapone
  • Opicapone
22
Q

How do we prescribe COMT inhibitors?

A
  • No therapeutic effect alone
  • Always use with levodopa (and dopa decarboxylase inhibitors)
  • Can use Stavelo (combination tablets)
23
Q

What is the mechanism of action of COMT inhibitors?

A
  • Reduce peripheral breakdown of levodopa to 3-O-methyldopa
  • Have a levodopa sparing effect
  • Prolongs motor response to levodopa
24
Q

Give some examples of dopamine receptor agonists

A
  • Non ergot: ropinirole and pramipexole
  • Patch (non-swallowing patients): Rotigotine
  • Subcutaneous (only used as a rescue drug): Apomorphine
25
Q

What are dopamine receptor agonists used for?

A
  • De Novo therapy
  • Add on therapy
  • Apomorphine is only used for patients with severe motor fluctuations
26
Q

What are the advantages of dopamine receptor agonists?

A
  • Direct acting
  • Less dyskinesias/motor complications
  • Possible neuroprotection
27
Q

What are the disadvantages of dopamine receptor agonists?

A
  • Less efficacy than levodopa
  • Impulse control disorders
  • More psychiatric side effects
  • Expensive
28
Q

Which impulse control disorders are caused by dopamine receptor agonists?

A
  • Pathological gambling
  • Hypersexuality
  • Compulsive shopping
  • Desire to increase dose
  • Punding
29
Q

Which impulse control disorders are caused by dopamine receptor agonists?

A
  • Pathological gambling
  • Hypersexuality
  • Compulsive shopping
  • Desire to increase dose
  • Punding
30
Q

What are the side effects of dopamine receptor agonists?

A
  • Sedation
  • Hallucinations
  • Confusion
  • Nausea
  • Hypotension
31
Q

How is apomorphine administered?

A
  • Bolus
  • Continuous infusion
32
Q

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

A
  • Metabolises dopamine
  • Predominates in dopamine containing regions in the brain
  • MAOB inhibitors enhance dopamine
33
Q

What are some examples of monoamine oxidase B inhibitors?

A
  • Rasagaline
  • Safinamide
34
Q

What are the positives of monoamine oxidase B inhibitors?

A
  • Can be used alone
  • Prolong action of levodopa
  • Smooths out motor response
35
Q

Give some examples of anticholinergics that can help treat patients with PD

A
  • Trihexyphenidyl
  • Orphenadrine
  • Procyclidine
36
Q

What are the advantages of anticholinergics?

A
  • Treat tremor
  • Not acting via dopamine systems
37
Q

What are the disadvantages of anticholinergics?

A
  • No effect on bradykinesia
  • Side effects include confusion and drowsiness
  • Minor role in treatment of PD
  • Hardly ever used
  • Always taken alongside other drugs
38
Q

What are the disadvantages of anticholinergics?

A
  • No effect on bradykinesia
  • Side effects include confusion and drowsiness
  • Minor role in treatment of PD
  • Hardly ever used
  • Always taken alongside other drugs
39
Q

What does myasthenia gravis cause?

A
  • Fluctuating, fatiguable weakness of skeletal muscle
40
Q

How does myasthenia gravis present?

A
  • Extraocular muscles - commonest presentation
  • Bulbar involvement - dysphagia, dysphonia, dysarthria
  • Limb weakness - proximal involvement
  • Respiratory muscle involvement
41
Q

Which drugs affecting neuromuscular transmission exacerbate Myasthenia Gravis?

A
  • Aminoglycosides
  • Beta-blockers, CCBs, quinidine, procainamide
  • Chloroquine, penicillamine
  • Succinylcholine
  • Magnesium
  • ACE inhibitors
42
Q

What are the complications of myasthenia gravis?

A
  • Acute exacerbation - myasthenic crisis
  • Overtreatment - leads to cholinergic crisis
43
Q

What are the symptoms of cholinergic crisis?

A
  • Caused by overtreatment
  • Get paralysis and muscle tiredness
  • Risk of respiratory arrest, DVT, swallowing difficulties
  • Need urgent treatment and protect airways
44
Q

What is the therapeutic management of Myasthenia gravis?

A
  • Acetylcholinesterase inhibitors
45
Q

What do acetylcholinesterase inhibitors do?

A
  • Enhance neuromuscular transmission
  • Skeletal and smooth muscle
  • Excess dose can cause depolarising block - cholinergic crisis
  • Muscarinic side effects
46
Q

Give some examples of ACh esterase inhibitors

A
  • Pyridostigmine - oral
  • Neostigmine - oral and IV preparations
  • Neostigmine has quicker action and duration up to 4 hours. Significant antimuscarinic side effects.
47
Q

Describe the actions of pyridostigmine

A
  • Prevents breakdown of ACh in NMJ
  • ACh more likely to engage with remaining receptors
  • Onset 30 mins
  • Peak 60-120 minutes
  • Duration 3-6 hours
  • Dose interval and timing is crucial
  • Muscarinic side effects
48
Q

What are the muscarinic side effects?

A
  • Salivation
  • Sweating
  • Lacrimation
  • Urinary incontinence
  • Diarrhoea
  • GI upset and hypermotility
  • Emesis

CPT (22 decks)

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