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[AMS] Clinical Pharmacology & Therapeutics > S12) Neuropharmacology > Flashcards

S12) Neuropharmacology Flashcards

1
Q

Identify four clinical features of Parkinsonism

A
  • Tremor
  • Rigidity
  • Bradykinesia
  • Postural instability
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2
Q

What are the non-motor manifestations of Parkinson’s disease?

A
  • Mood changes
  • Pain
  • Cognitive change
  • Urinary symptoms
  • Sleep disorder
  • Sweating
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3
Q

After 15 years, what clinical features will patients with PD have during follow up?

A
  • Dyskinesia (94%)
  • Falls (81%)
  • Cognitive decline (84%)
  • Somnolence (80%)
  • Swallowing difficulties (50%)
  • Severe speech problems (27%)
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4
Q

How does one make a diagnosis of Idiopathic Parkinson’s Disease?

A
  • Clinical features
  • Exclude other causes of Parkinsonism
  • Response to treatment
  • Normal structural neuro-imaging
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5
Q

Describe the pathological features of IPD

A
  • Neurodegeneration
  • Lewy bodies synucleinopathy
  • Loss of pigment
  • Reduced dopamine
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6
Q

Describe three ways in which the basal ganglia circuitry is affected in IPD

A
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7
Q

Identify six different drug classes used to treat IPD

A
  • Levodopa (L-DOPA)
  • Dopamine receptor agonists
  • MAOI type B inhibitors
  • COMT inhibitors
  • Anticholinergics
  • Amantidine
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8
Q

Why is L-DOPA used to treat IPD instead of Dopamine?

A
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9
Q

How is Levodopa administered?

A

Oral administration

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10
Q

In five steps, describe the absorption of L-DOPA

A

⇒ Absorbed by active transport

⇒ Competes with amino acids

⇒ Taken up by dopaminergic cells in substantia nigra to be converted to dopamine

⇒ 90% inactivated in intestinal wall

⇒ Forms monoamine oxidase & DOPA decarboxylase

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11
Q

Which formulation of L-DOPA is used to increase the amount that gets to the brain?

A

L-DOPA is used in combination with a peripheral DOPA decarboxylase inhibitor – co-careldopa / co-beneldopa

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12
Q

What is the half life of L-DOPA?

A

T1/2 = 2 hours

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13
Q

What are the advantages of L-DOPA?

A
  • Highly efficacious
  • Low side effects e.g. nausea, vomiting, hypotension, tachycardia, psychosis
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14
Q

What are the disadvantages of L-DOPA?

A
  • Loss of efficacy (only effective in presence of dopaminergic neurones)
  • Needs enzyme conversion
  • Involuntary movements
  • Motor complications
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15
Q

Describe the drug-drug interactions of L-DOPA with the following:

  • Pyridoxine (Vitamin B6)
  • MAOIs
  • Antipsychotic drugs
A
  • Pyridoxine: increases peripheral breakdown of L-DOPA
  • MAOIs: risk hypertensive crisis
  • Antipsychotic drugs: lead to parkinsonism (block dopamine receptors)
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16
Q

Identify some different types of dopamine receptor agonists

A
  • Ergot derived
  • Non Ergot
  • Patch
  • Subcutaneous
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17
Q

Provide two examples of non ergot dopamine receptor agonists

A
  • Ropinirole
  • Pramipexole
18
Q

Provide an example of a patch dopamine receptor agonist

A

Rotigotine

19
Q

Provide an example of a subcutaneous dopamine receptor agonist

A

Apomorphine

20
Q

What are the advantages of dopamine receptor agonists?

A
  • Direct acting
  • Less dyskinesia / motor complications
  • Possible neuroprotection
21
Q

What are the disadvantages of dopamine receptor agonists?

A
  • Less efficacy than L-DOPA
  • Impulse control disorders
  • More psychiatric side effects
  • Expensive
22
Q

Provide five examples of impulse control disorders

A
  • Pathological gambling
  • Hypersexuality
  • Compulsive shopping
  • Desire to increase dosage
  • Punding
23
Q

What are the side effects of dopamine receptor agonists?

A
  • Sedation
  • Hallucinations
  • Confusion
  • Nausea
  • Hypotension
24
Q

Describe the mechanism of action of monoamine oxidase B inhibitors

A
  • Inhibits metabolism of dopamine by MAO
  • Prolongs action of L-DOPA
  • Smooths out motor response
25
Q

Provide two examples of monoamine oxidase B inhibitors

A
  • Selegiline
  • Rasagaline
26
Q

Describe the mechanism of action of Catechol-O-methyl Transferase (COMT) inhibitors

A
  • Reduce peripheral breakdown of L-DOPA to 3-O-methyldopa (3-O-methyldopa competes with L-DOPA for active transport into CNS)
  • Prolongs motor response to L-DOPA
27
Q

Provide an example of a COMT inhibitor

A

Entacapone (doesn’t cross BBB)

28
Q

Describe the use of anticholinergics in the treatment of PD

A
  • Acetyl choline may have antagonistics effects on dopamine
  • Minor role in treatment of PD
29
Q

Provide three examples of anticholinergics

A
  • Trihexyphenidydyl
  • Orphenadrine
  • Procyclidine
30
Q

What are the advantages of anticholinergics?

A
  • Treat tremor
  • Not acting via dopamine systems
31
Q

What are the disadvantages of anticholinergics?

A
  • No effect on bradykinesia
  • Several side effects
32
Q

What are the side effects of anticholinergics

A
  • Confusion
  • Drowsiness
33
Q

The mechanism action of amantadine is uncertain.

Provide some suggestions

A
  • Enhanced dopamine release
  • Anticholinergic NMDA inhibition
34
Q

What are the disadvantages of amantadine?

A
  • Poorly effective
  • Few side effects
  • Little effect on tremor
35
Q

Illustrate the differences in the post synaptic membrane of a normal neuromuscular junction with that of one in myasthenia gravis

A
36
Q

Describe the presentation of Myasthenia gravis

A
  • Extraocular muscles – commonest presentation
  • Bulbar involvement – dysphagia, dysphonia, dysarthria
  • Limb weakness – proximal symmetric
37
Q

Identify some drugs which affect the neuromuscular transmission and thus, exacerbate Myasthenia gravis

A
  • Aminoglycosides
  • Beta-blockers
  • CCBs
  • Quinidine
  • ACE inhibitors
38
Q

What are the complications of Myasthenia gravis?

A
  • Acute exacerbation – Myasthenic crisis
  • Overtreatment – cholinergic crisis
39
Q

What is the therapeutic management of Myasthenia gravis?

A

Acetylcholinesterase inhibitors – enhance neuromuscular transmission at skeletal and smooth muscle

40
Q

Provide two examples of acetylcholinesterase inhibitors

A
  • Pyridostigmine (oral)
  • Neostigmine (oral/IV)
41
Q

What are the antimuscarinic side effects of acetylcholinesterase inhibitors?

A
  • Miosis
  • SSLUDGE syndrome: salivation, sweating, lacrimation, urinary incontinence, diarrhea, GI upset and hypermotility, emesis

[AMS] Clinical Pharmacology & Therapeutics (29 decks)

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