Clinical meaning
Nausea and vomiting are mediated through multiple pathways, and the NP must match the antiemetic to the underlying mechanism. The vomiting center in the medulla receives input from: (1) Chemoreceptor trigger zone (CTZ) — area postrema outside the blood-brain barrier; senses circulating toxins, drugs, and metabolic derangements; D2, 5-HT3, NK1, and opioid receptors predominate; (2) Vestibular system — motion sickness, vertigo; H1 and muscarinic (M1) receptors predominate; (3) GI tract — vagal afferents from the gut; 5-HT3 receptors on vagal nerve terminals sense mucosal irritation, chemotherapy-induced serotonin release, and distension; (4) Higher cortical centers — anticipatory nausea, psychogenic vomiting; benzodiazepines and cannabinoids are effective. Antiemetic selection: chemotherapy-induced: ondansetron (5-HT3 antagonist) ± dexamethasone ± aprepitant (NK1 antagonist) — three-drug regimen for highly emetogenic chemotherapy; post-operative: ondansetron 4 mg IV; motion sickness: scopolamine patch or meclizine; gastroparesis: metoclopramide (D2 antagonist, 5-HT4 agonist — promotes gastric motility); pregnancy: pyridoxine (B6) + doxylamine first-line, then ondansetron. The NP avoids metoclopramide for >12 weeks (FDA black box warning for tardive dyskinesia) and avoids promethazine IV push (tissue necrosis risk — only IM or diluted IV...