Nausea and Vomiting: Antiemetic Pharmacology
4th Year MBBS • GIT Module
Connect the vomiting pathways with their dominant receptors, antiemetic drug targets, clinical uses and important cautions for rapid revision. :contentReference[oaicite:0]{index=0}
1. The Topic in One Connected Flow
Vomiting can begin from the gastrointestinal tract, chemoreceptor trigger zone, vestibular system or higher brain centres. Each pathway uses characteristic neurotransmitters. Antiemetic therapy works best when the drug blocks the receptor or mechanism most important in that clinical setting.
2. Key Clinical Connections
Vestibular stimulation → H1 and M1 signalling → nausea and vomiting → H1 antihistamines or scopolamine reduce vestibular input.
Scopolamine → muscarinic blockade → benefit in prevention → dry mouth, blurred vision, urinary retention or confusion may occur.
Metoclopramide → D2 blockade + 5-HT4 stimulation → antiemesis + faster gastric emptying → useful when nausea accompanies delayed gastric emptying.
Central D2 blockade → extrapyramidal effects and prolactin rise; domperidone enters the CNS poorly → fewer motor adverse effects.
Acute serotonin release → 5-HT3 activation → ondansetron-class blockade; delayed substance P signalling → NK1 blockade with aprepitant.
Conditioned anxiety before treatment → higher-centre emetic response → benzodiazepine such as lorazepam acts as an adjunct.
3. AIM High-Yield Integration Review
⭐ Chemotherapy → intestinal serotonin release → 5-HT3 activation → ondansetron reduces acute emesis.
