GI Drugs Cheat Sheet
Advanced Pharmacology — Comprehensive Quick Reference
PART I: PEPTIC ULCER DISEASE & GERD
1. PUD/GERD OVERVIEW
• Peptic Ulcer Disease (PUD): Two main causes — H. pylori infection and NSAIDs
• GERD: Chronic reflux of gastric acid into esophagus
• Treatment goals: Eradicate H. pylori, reduce/neutralize acid, protect gastric mucosa
2. H. PYLORI ERADICATION REGIMENS
Regimen Components Key Points
Quadruple Therapy (Regimen Pepto-Bismol + Flagyl (Metronidazole) + >90% eradication rate; used when Clarithromycin
of Choice) Tetracycline + PPI resistance is a concern
Triple Therapy PPI + Amoxicillin or Flagyl + Biaxin (Clarithromycin) Used when Clarithromycin resistance is low (<15%)
3. H2 RECEPTOR BLOCKERS
• MOA: Competitive antagonists at H2 receptors on parietal cells; reduce acid secretion by ~70%
Drug (Generic) Brand Key Points / ADEs
Cimetidine Tagamet CYP450 inhibitor (many drug interactions); ADEs: gynecomastia, galactorrhea, confusion
in elderly
Famotidine Pepcid Most commonly used H2B; fewer drug interactions than Cimetidine
Nizatidine Axid Similar efficacy; no CYP450 interactions
Ranitidine Zantac Withdrawn from US market (NDMA contamination concern)
4. PROTON PUMP INHIBITORS (PPIS)
• MOA: Prodrugs that irreversibly bind H+/K+-ATPase (proton pump) on parietal cells; reduce acid secretion >90%
• Administration: Take 30-60 minutes before meals (need acidic environment for activation)
Drug (Generic) Brand
Lansoprazole Prevacid
Dexlansoprazole Dexilant
Omeprazole Prilosec
Esomeprazole Nexium
Pantoprazole Protonix
Rabeprazole Aciphex
PPI ADEs (Chronic Use)
• Fracture risk (use >1 year) — decreased Ca++ absorption
• Low B12, Low Mg++ — decreased absorption
• C. difficile infection and community-acquired pneumonia
• Use Ca++ citrate (not carbonate) with PPIs — citrate does not need acid for absorption
GI Drugs Cheat Sheet Page 1
, ■ Omeprazole (Prilosec) and Esomeprazole (Nexium) inhibit CYP2C19 — decrease effectiveness of Clopidogrel (Plavix). Avoid
combination.
5. PROSTAGLANDINS
Drug Brand MOA Use ADEs / Warnings
Misoprostol Cytotec PGE1 analog; replaces Prevention of Diarrhea (dose-limiting);
protective prostaglandins NSAID-induced ulcers contraindicated in pregnancy
(abortifacient)
6. ANTACIDS
• MOA: Neutralize gastric acid (increase gastric pH); do NOT inhibit secretion
• Administration: Give after meals
Agent Key Effect / Notes
Aluminum hydroxide Causes constipation
Magnesium hydroxide Causes diarrhea
CaCO3 (Tums) Calcium supplement; can cause constipation and rebound acid secretion
NaHCO3 (baking soda) Not recommended — can cause metabolic alkalosis; high sodium load
7. MUCOSAL PROTECTIVE AGENTS
Drug Brand MOA Key Points
Sucralfate Carafate Forms gel barrier over ulcer crater in acidic Needs acidic environment — do NOT give with
pH PPIs or H2Bs; give on empty stomach
Bismuth subsalicylate Pepto-Bismol Coating/protective action + antimicrobial Part of quadruple therapy for H. pylori; ADEs: black
tongue and stools; avoid in children <12 (salicylate)
GI Drugs Cheat Sheet Page 2
Advanced Pharmacology — Comprehensive Quick Reference
PART I: PEPTIC ULCER DISEASE & GERD
1. PUD/GERD OVERVIEW
• Peptic Ulcer Disease (PUD): Two main causes — H. pylori infection and NSAIDs
• GERD: Chronic reflux of gastric acid into esophagus
• Treatment goals: Eradicate H. pylori, reduce/neutralize acid, protect gastric mucosa
2. H. PYLORI ERADICATION REGIMENS
Regimen Components Key Points
Quadruple Therapy (Regimen Pepto-Bismol + Flagyl (Metronidazole) + >90% eradication rate; used when Clarithromycin
of Choice) Tetracycline + PPI resistance is a concern
Triple Therapy PPI + Amoxicillin or Flagyl + Biaxin (Clarithromycin) Used when Clarithromycin resistance is low (<15%)
3. H2 RECEPTOR BLOCKERS
• MOA: Competitive antagonists at H2 receptors on parietal cells; reduce acid secretion by ~70%
Drug (Generic) Brand Key Points / ADEs
Cimetidine Tagamet CYP450 inhibitor (many drug interactions); ADEs: gynecomastia, galactorrhea, confusion
in elderly
Famotidine Pepcid Most commonly used H2B; fewer drug interactions than Cimetidine
Nizatidine Axid Similar efficacy; no CYP450 interactions
Ranitidine Zantac Withdrawn from US market (NDMA contamination concern)
4. PROTON PUMP INHIBITORS (PPIS)
• MOA: Prodrugs that irreversibly bind H+/K+-ATPase (proton pump) on parietal cells; reduce acid secretion >90%
• Administration: Take 30-60 minutes before meals (need acidic environment for activation)
Drug (Generic) Brand
Lansoprazole Prevacid
Dexlansoprazole Dexilant
Omeprazole Prilosec
Esomeprazole Nexium
Pantoprazole Protonix
Rabeprazole Aciphex
PPI ADEs (Chronic Use)
• Fracture risk (use >1 year) — decreased Ca++ absorption
• Low B12, Low Mg++ — decreased absorption
• C. difficile infection and community-acquired pneumonia
• Use Ca++ citrate (not carbonate) with PPIs — citrate does not need acid for absorption
GI Drugs Cheat Sheet Page 1
, ■ Omeprazole (Prilosec) and Esomeprazole (Nexium) inhibit CYP2C19 — decrease effectiveness of Clopidogrel (Plavix). Avoid
combination.
5. PROSTAGLANDINS
Drug Brand MOA Use ADEs / Warnings
Misoprostol Cytotec PGE1 analog; replaces Prevention of Diarrhea (dose-limiting);
protective prostaglandins NSAID-induced ulcers contraindicated in pregnancy
(abortifacient)
6. ANTACIDS
• MOA: Neutralize gastric acid (increase gastric pH); do NOT inhibit secretion
• Administration: Give after meals
Agent Key Effect / Notes
Aluminum hydroxide Causes constipation
Magnesium hydroxide Causes diarrhea
CaCO3 (Tums) Calcium supplement; can cause constipation and rebound acid secretion
NaHCO3 (baking soda) Not recommended — can cause metabolic alkalosis; high sodium load
7. MUCOSAL PROTECTIVE AGENTS
Drug Brand MOA Key Points
Sucralfate Carafate Forms gel barrier over ulcer crater in acidic Needs acidic environment — do NOT give with
pH PPIs or H2Bs; give on empty stomach
Bismuth subsalicylate Pepto-Bismol Coating/protective action + antimicrobial Part of quadruple therapy for H. pylori; ADEs: black
tongue and stools; avoid in children <12 (salicylate)
GI Drugs Cheat Sheet Page 2
