Neuropharmacology Flashcards

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1
Q

Describe the pathophysiology of Parkinson’s

A
  • Loss of Dopaminergic neurones in Substantia Nigra
  • Results in reduced inhibition in Neostriatum
  • Allows increased ACh production
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2
Q

List 5 drug classes used to treat the motor symptoms of Parkinson’s

A
  • L-Dopa (Levodopa)
  • Dopamine receptor agonists
  • MAO-B Inhibitors
  • COMT Inhibitors
  • Anticholinergics
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3
Q

Describe the effectiveness of L-Dopa

L-Dopa can cross the BBB in contrast to Dopamine

A
  • Taken up by dopminergic cells in Substantia Nigra, then converted to Dopamine
  • As disease progresses there are fewer cells left to do this, so reduced effectiveness
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4
Q

Why is L-Dopa given with DOPA Decarboxylase Inhibitors?

A

Prevents conversion of L-Dopa to Dopamine in peripheral tissues therefore;

  • Reduced dose required
  • Reduced side effects
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5
Q

What’s the importance of the fact that L-Dopa is absorbed via Active Transport

A

Competes with Amino Acids, so caution with high protein meals eaten within an hour of medication

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6
Q

List 2 preparations of L-Dopa and their contents, including the Peripheral DOPA Decarboxylase inhibitor

A

Sinemet/ Co-careldopa;
- Levodopa + Carbidopa

Madopar/ Co-beneldopa;
- Levodopa + Benserazide

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7
Q

List ADRs of L-DOPA

A
  • Nausea + Vomiting
  • Hypotension
  • Psychosis (hallucinations, delusions)
  • Tachycardia
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8
Q

List 3 DDIs of L-Dopa

A
  • Vitamin B6 increases peripheral breakdown of L-DOPA
  • Antipsychotics (D2 antagonists)
  • Risk of Hypertensive Crisis with Monoamine Oxidase Inhibitors/ MAOIs (not MAO-B Inhibitors at normal dose)
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9
Q

Why are Ergot derived Dopamine receptor agonists now avoided in favour of Non-Ergot derived agonists?

A

They had retroperitoneal fibrotic side effects

(Ergot derived: Bromocryptine, Pergolide, Cabergoline)

(Non-ergot derived: Ropinerole, Pramipexole)

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10
Q

Suggest 2 advantages and 3 disadvantages of using Dopamine agonists over L-Dopa?

A

Advantages;

  • Direct acting
  • Less motor complications

Disadvantages;

  • Less efficacy
  • More psychiatric side effects
  • Can develop impulse control disorders (Gambling, hypersexuality, compulsive shopping)
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11
Q

List 5 ADRs of Dopamine Agonists

A
  • Sedation
  • Hallucinations
  • Nausea
  • Confusion
  • Hypotension
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12
Q

What class of drug are Selegiline, Rasagaline and Safinamide?

How do these work?

A
  • Monoamine Oxidase B/ MAO-B Inhibitors

- Inhibit MAO-B, which metabolises Dopamine

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13
Q

What class of drugs are Opicapone and Entacapone?

Do these have any therapeutic effect on their own?
How do they work?

A
  • COMT Inhibitors

- No, they reduce the peripheral breakdown of L-DOPA

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14
Q

Procyclidine and Orphenadrine are Anticholinergics used in Parkinson’s.

List advantages and disadvantages of using Anticholinergics for this

A

Advantages;

  • Treat tremor
  • Not acting via Dopamine systems

Disadvantages;

  • No effect on Bradykinesia
  • ADRs: Confusion, Drowsiness, Usual anticholinergic ones
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15
Q

How does Amantidine work? (Used in improving Dyskinesia)

A
  • NMDA receptor inhibition

- Dopamine receptor agonism

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16
Q

What are 3 criteria for surgical treatment of Parkinson’s?

Suggest 2 types of surgery

A
  • Dopamine responsive
  • Significant side effects with L-DOPA
  • No psychiatric illness
  • Deep Brain Stimulation of STN
  • Destructive lesion (Thalamus, GPi)
17
Q

List 5 treatment options for Myasthenia Gravis

A
  • AChEsterase Inhibitors
  • Corticosteroids (reduced immune response)
  • Azathioprine
  • Plasmapheresis (short term improvement)
  • IV Immunoglobulin
18
Q

What can an excessively high dose of an AChEsterase Inhibitor lead to?

A

A Cholinergic Crisis- Depolarising block-> Muscle weakness

19
Q

Neostigmine and Pyridostigmine are AChEsterase Inhibitors.

Compare their administration

A

Neostigmine: Oral and IV
Pyridostigmine: Oral

20
Q

State the Onset, Peak and Duration of Pyridostigmine

A

Onset: 30 mins
Peak: 60-120 mins
Duration: 3-6 hours

(Neostigmine: Quicker action, duration up to 4hrs)