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GI Disorders
MOAs & DDIs
| Drug | Drug Target | MOA | Drug Interactions |
|---|---|---|---|
| Cimetidine | H2 receptor on parietal cells | Selective, reversible, competitive H2 receptor blockade (full antagonist) | Increases toxicity of narrow therapeutic index drugs; decreases activation of clopidogrel; AR, estradiol decrease; increases prolactin |
| Famotidine | H2 receptor on parietal cells | Selective, reversible, competitive H2 receptor blockade (full antagonist) | |
| Nizatidine | H2 receptor on parietal cells | Selective, reversible, competitive H2 receptor blockade (full antagonist) | |
| Ranitidine (Zantac) | H2 receptor on parietal cells | Selective, reversible, competitive H2 receptor blockade (full antagonist) | |
| Omeprazole | H+/K+/ATPase (parietal cell) | Prodrug; activated; irreversibly inactivates pump → profound acid suppression | clopidogrel interaction; pantoprazole preferred with clopidogrel; CYP2C19/3A4 competition: warfarin, phenytoin, diazepam, cyclosporine |
| Esomeprazole | H+/K+/ATPase (parietal cell) | Irreversible (covalent) pump inhibition via disulfide bridges | CYP2C19/3A4 competition: warfarin, phenytoin, diazepam, cyclosporine |
| Lansoprazole | H+/K+/ATPase (parietal cell) | Irreversible (covalent) pump inhibition via disulfide bridges | CYP2C19/3A4 competition: warfarin, phenytoin, diazepam, cyclosporine |
| Dexlansoprazole | H+/K+/ATPase (parietal cell) | Irreversible (covalent) pump inhibition via disulfide bridges | CYP2C19/3A4 competition: warfarin, phenytoin, diazepam, cyclosporine |
| Pantoprazole | H+/K+/ATPase (parietal cell) | Irreversible (covalent) pump inhibition via disulfide bridges | preferred if also taking clopidogrel; CYP2C19/3A4 competition: warfarin, phenytoin, diazepam, cyclosporine |
| Rabeprazole | H+/K+/ATPase (parietal cell) | Irreversible (covalent) pump inhibition via disulfide bridges | CYP2C19/3A4 competition: warfarin, phenytoin, diazepam, cyclosporine |
| Vonoprazan | H+/K+/ATPase (K+ site) | Reversible (ionic) dose-dependent inhibition via competition with K+ on the pump | |
| Calcium carbonate | Neutralize (reduce) intra-gastric acidity | can cause toxic accumulation of weakly basic drugs and make weakly acidic drugs less effective | |
| Sodium bicarbonate | Neutralize (reduce) intra-gastric acidity | can cause toxic accumulation of weakly basic drugs and make weakly acidic drugs less effective | |
| Aluminum hydroxide | Neutralize (reduce) intra-gastric acidity | can cause toxic accumulation of weakly basic drugs and make weakly acidic drugs less effective | |
| Magnesium hydroxide | Neutralize (reduce) intra-gastric acidity | can cause toxic accumulation of weakly basic drugs and make weakly acidic drugs less effective | |
| Bismuth subsalicylate | Mucosal proteins; H. pylori | Forms protective layer on erosions/ulcers; inhibits H. pylori growth | Salicylate; avoid in pregnancy/pediatrics |
| Sucralfate | Positively charged proteins at ulcer base | Sucrose sulfate + Al(OH)3 polymerizes to form a barrier; reacts with gastric HCl to form viscous, paste-like barrier; binds albumin/fibrinogen on ulcers; prevents back-diffusion of H+; adsorbs pepsin and bile acids | reduces absorption of fluoroquinolones, warfarin, phenytoin, theophylline, quinidine etc. |
| Metoclopramide | D2 receptors (CTZ; enteric) | Block dopamine receptors centrally in CTZ, increases lower esophageal sphincter tone, aids gastric emptying, accelerates transit through small bowel (prokinetic) | hypertensive agents, QTc prolonging agents |
| Ondansetron | 5HT3 receptor | block serotonin receptors in the sensory vagal fibers in gut wall and CTZ | QT prolonging agents; serotonin syndrome when combined with other serotonergic agents |
| Granisetron | 5HT3 receptor | block serotonin receptors in the sensory vagal fibers in gut wall and CTZ | QT prolonging agents; serotonin syndrome when combined with other serotonergic agents |
| Dolasetron | 5HT3 receptor | block serotonin receptors in the sensory vagal fibers in gut wall and CTZ | QT prolonging agents; serotonin syndrome when combined with other serotonergic agents |
| Palonosetron | 5HT3 receptor | block serotonin receptors in the sensory vagal fibers in gut wall and CTZ | QT prolonging agents; serotonin syndrome when combined with other serotonergic agents |
| Aprepitant | NK1 receptors (area postrema/brainstem) | blockade of substance P at NK1 receptor – substance P involved in both acute and delayed phase of CINV | Many CYP3A4/2C9 interactions |
| Fosaprepitant (IV) | NK1 receptors (area postrema/brainstem) | blockade of substance P at NK1 receptor – substance P involved in both acute and delayed phase of CINV | Many CYP3A4/2C9 interactions |
| Rolapitant | NK1 receptors (area postrema/brainstem) | blockade of substance P at NK1 receptor – substance P involved in both acute and delayed phase of CINV | Many CYP2D6 interactions |
| Netupitant | NK1 receptors (area postrema/brainstem) | blockade of substance P at NK1 receptor – substance P involved in both acute and delayed phase of CINV | Many CYP3A4 interactions |
| Dexamethasone | Glucocorticoid receptor (nuclear) | Enhances efficacy of 5HT3 antagonists; anti-inflammatory | High doses typically required |
| Methylprednisolone | Glucocorticoid receptor | Antiemetic adjunct | — |
| Cyclizine | H1 (vestibular, CNS) | Competitive, reversible H1 receptor antagonism (or inverse agonism) | CNS depressants, QTc prolonging drugs |
| Diphenhydramine | H1 (vestibular, CNS) | Competitive, reversible H1 receptor antagonism (or inverse agonism) | CNS depressants, QTc prolonging drugs |
| Dimenhydrinate | H1 (vestibular, CNS) | Competitive, reversible H1 receptor antagonism (or inverse agonism) | CNS depressants, QTc prolonging drugs |
| Hydroxyzine | H1 (vestibular, CNS) | Competitive, reversible H1 receptor antagonism (or inverse agonism) | CNS depressants, QTc prolonging drugs |
| Meclizine | H1 (vestibular, CNS) | Competitive, reversible H1 receptor antagonism (or inverse agonism) | CNS depressants, QTc prolonging drugs |
| Promethazine | H1 (vestibular, CNS) | Antihistamine with antimuscarinic/antidopaminergic actions | hypertensive agents, QTc prolonging agents |
| Scopolamine (Hyoscine) | M1 (vestibular pathways) | Blocks muscarinic signaling → anti-motion sickness | Anticholinergic AEs |
| Doxylamine | H1 (vestibular, CNS) | Competitive, reversible H1 receptor antagonism (or inverse agonism) | CNS depressants, QTc prolonging drugs |
| Dronabinol | CB1, CB2 | synthetic analogs of delta-9-tetrahydrocannabinol (THC), act at cannabinoid receptor 1 (CB1) in CNS | CNS depressants (alcohol, benzodiazepines, barbiturates) Hypotensive agents |
| Nabilone | CB1 | CB1 agonism → antiemetic | CNS depressants (alcohol, benzodiazepines, barbiturates) Hypotensive agents |
| Prochlorperazine | D2 receptors in CTZ (central) | Blocks dopamine receptors in CNS including CTZ | hypertensive agents, QTc prolonging agents |
| Chlorpromazine | D2 receptors in CTZ (central) | Blocks dopamine receptors in CNS including CTZ | hypertensive agents, QTc prolonging agents |
| Droperidol | D2 receptors in CTZ (central) | Blocks dopaminergic stimulation of CTZ | hypertensive agents, QTc prolonging agents |
| Haloperidol | D2 receptors in CTZ (central) | Blocks dopaminergic stimulation of CTZ | hypertensive agents, QTc prolonging agents |
| Olanzapine | D2, 5-HT2/3, adrenergic, histamine, muscarinic | Block dopamine receptors centrally in CTZ, increases lower esophageal sphincter tone, aids gastric emptying, accelerates transit through small bowel (prokinetic) | hypertensive agents, QTc prolonging agents |
| Amisulpride | D2/D3 in CTZ | Dopamine receptor antagonism reduces emetic signaling | QTc prolongation risk (class); EPS possible |
| Midazolam | GABA-A receptor (positive allosteric modulator) | Anxiolysis and sedation helpful in anticipatory/adjunct NV management | Sedation; respiratory depression risk with other CNS depressants |
| Trimethobenzamide | Chemoreceptor Trigger Zone (exact mechanism unclear) | Suppresses CTZ to reduce emesis | Oral or IM; typically 300 mg TID–QID (dosing per lecture table) |
| Fosnetupitant (IV) | NK1 receptors (area postrema/brainstem) | blockade of substance P at NK1 receptor – substance P involved in both acute and delayed phase of CINV | Many CYP3A4 interactions |
| Pyridoxine (Vitamin B6) | — | Mechanism for antiemesis not fully defined; vitamin replacement | Usual 12.5–25 mg PO TID–QID; high doses long-term may cause peripheral neuropathy |
| Ginger | — | Proposed 5-HT3 modulation and gastric motility effects (not established in lecture) | 250 mg–2 g/day divided; may have anticoagulant and hypotensive effects—consider interactions |
| Misoprostol | Inhibits acid secretion; stimulate mucus, bicarbonate secretion | ||
| Clarithromycin | 50S ribosomal elongation complex | Bacteriostatic; binds rRNA to block elongation; leads to protein synthesis arrest | |
| Metronidazole | Prodrug activated under anaerobic conditions by nitro reduction → reactive species | Disulfiram-like effect with alcohol |
Created by:
CaristW