Antiemetics and prokinetics: receptor-based pharmacology
The inputs to the vomiting reflex and their receptors, how D2, 5-HT3, NK1, H1 and muscarinic antagonists, corticosteroids and olanzapine map onto them, the prokinetics (metoclopramide, domperidone, erythromycin, prucalopride), and the interactions and adverse effects that follow from each mechanism.
Tier 1Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Vomiting is coordinated in the brainstem (nucleus tractus solitarius and a central pattern generator). Four inputs feed it, each with its own receptors: the chemoreceptor trigger zone, vagal afferents from the gut, the vestibular system, and the cortex.
- Good antiemetic prescribing means identifying the input and blocking its receptor: D2, 5-HT3, NK1, H1 or muscarinic.
- Prokinetics act on 5-HT4 (metoclopramide, prucalopride), peripheral D2 (domperidone) or motilin (erythromycin) receptors.
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Sources
- 2023 MASCC and ESMO guideline update for the prevention of chemotherapy- and radiotherapy-induced nausea and vomitingESMO Open (Herrstedt et al., 2024;9:102195), 2023
- Therapeutic Guidelines: Palliative CareAU/NZTherapeutic Guidelines Ltd, 2024
- Therapeutic Guidelines: GastrointestinalAU/NZTherapeutic Guidelines Ltd, 2023
- eviQ: prevention of anti-cancer therapy induced nausea and vomitingAU/NZCancer Institute NSW, 2025
- Australian Medicines HandbookAU/NZAustralian Medicines Handbook Pty Ltd, 2026
- Last updated
- 14 November 2026
What changed
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