SAQPharmacologyAntiemetics2021 · Metoclopramide

Question bank · 2021 · Pharmacology

More than 60% of candidates
missed part (b) — the disadvantages, not the pathophysiology.

Show the model answerAttempt it first — that is what makes it stick
A

4 marks

Drugs used for aspiration prophylaxis

Antacids, H2 antagonists and drugs that increase gastric motility — not antiemetics.

What earns the markspart (a)

Read the questionAspiration prophylaxis — NOT antiemetics
The classesAntacid, H2 antagonist, prokinetic
For eachExample, mechanism, and what it does not do
ClassExampleDoseMechanism
Non-particulate antacidSodium citrate0.3 M, 30 mL orallyNeutralises existing gastric acid without leaving particulate matter that itself worsens aspiration pneumonitis
H2 receptor antagonistRanitidine50 mg IVSpecific, competitive antagonism at gastric parietal cell H2 receptors — reduces acid volume and acidity, with no effect on gastric emptying or lower oesophageal sphincter tone
ProkineticMetoclopramide10 mg IVD2 antagonism increases gastric emptying and lower oesophageal sphincter tone, coordinating gastric–pyloric–small intestinal motility

Commonly lost: Part (a) asks about acid aspiration prophylaxis, not antiemetics. Many answered it as an antiemetics question and lost the marks.

B

6 marks — only 13% scored 6.0 or more

Disadvantages of metoclopramide as a sole antiemetic

Efficacy, the CNS effects that follow from crossing the blood–brain barrier, cardiovascular effects, and the less commonly recalled systemic effects.

What earns the markspart (b)

Disadvantages = side effectsPlus why it is not first-line
By systemExtrapyramidal, cardiovascular, endocrine, haematological
Not the pathophysiologyOf nausea and vomiting — no marks

Every disadvantage below traces back to two facts about metoclopramide’s pharmacology. First, its antiemetic action works through dopamine (D2) receptor antagonism at the CTZ — a single mechanism against a reflex with several converging inputs (dopamine, serotonin, histamine, acetylcholine, substance P), so it does nothing against the stimuli that arrive through the other pathways, which is the pharmacological reason roughly half of clinical trials find it no better than placebo. Second, unlike domperidone — which shares the same D2-antagonist mechanism but does not cross the blood–brain barrier — metoclopramide readily crosses the blood–brain barrier, which is what lets it act directly on the CTZ but is also the direct cause of essentially every central disadvantage below.

CategoryDisadvantage
EfficacyDoes not antagonise the multiple stimuli that drive nausea and vomiting — roughly half of clinical studies found it no better than placebo
Central nervous systemCrosses the blood–brain barrier: sedation, agitation, dry mouth, extrapyramidal side effects, neuroleptic malignant syndrome
CardiovascularHypotension, tachy- or bradyarrhythmias after rapid IV bolus administration
GastrointestinalAbdominal cramps; delayed healing of intestinal anastomosis
Endocrine / metabolicRaised plasma prolactin; hypokalaemia and sodium retention; may precipitate intermittent porphyria
OtherInhibits plasma cholinesterase; urticaria and angioedema; interacts with antidepressants, antipsychotics and CYP450 inhibitors

Commonly lost: More than 60% described the pathophysiology of nausea and vomiting instead of answering the question. No marks were given for it.

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If this came up in the viva

Viva points

The blood–brain barrier is the thread that runs through this whole answer.
  1. Metoclopramide and domperidone are both D2 antagonists. Why does only one of them cause extrapyramidal effects?

    Answer

    Metoclopramide crosses the blood–brain barrier and acts directly on central D2 receptors — the same property that produces its extrapyramidal and sedative effects. Domperidone shares the same D2-antagonist mechanism but does not cross the blood–brain barrier, so it is far less likely to cause them.

  2. Metoclopramide is widely available, but it isn’t a first-line antiemetic. Why?

    Answer

    Its antiemetic efficacy is modest — a trial of 30 studies found systemic metoclopramide 10 mg reduced 24-hour PONV against placebo with a number needed to treat of 7.8, and roughly half of clinical studies found it no better than placebo. Set against that modest benefit are its extrapyramidal risk, sedation, and the other problems that follow from crossing the blood–brain barrier.

Every viva on this topic, with answers

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