Peptic ulcer disease Study Guide

📖 Core Concepts Peptic ulcer disease (PUD) – breach of the gastric, duodenal, or lower esophageal mucosa that extends at least to the muscularis mucosae. Gastric vs. duodenal ulcer – gastric pain worsens with meals; duodenal pain improves with meals and often awakens the patient at night. Aggressive factors – gastric acid, pepsin, H. pylori–induced inflammation, NSAID‑induced mucosal injury. Defensive factors – mucus, bicarbonate, prostaglandins, adequate mucosal blood flow. Gold‑standard diagnosis – esophagogastroduodenoscopy (EGD) with visualization and biopsy. 📌 Must Remember Top etiologies: Helicobacter pylori infection (major) and NSAID use (4‑fold increased risk). Complication hierarchy: 1) GI bleeding (≈15 % of PUD) → most common; 2) perforation → acute peritonitis; 3) gastric outlet obstruction; 4) penetration; 5) malignancy risk (H. pylori ↑ gastric cancer 3‑6×). First‑line eradication regimen: PPI + clarithromycin + amoxicillin (7–14 days). When clarithromycin resistance >15 %: use bismuth‑based quadruple therapy (PPI + bismuth + tetracycline + metronidazole). Bleeding ulcer IV‑PPI protocol: 80 mg bolus then 8 mg/h infusion for 72 h. NSAID‑related ulcer prophylaxis: co‑prescribe a PPI, H2‑blocker, or misoprostol for chronic NSAID users. 🔄 Key Processes Ulcer formation Aggressive factor > defensive factor → mucosal breach → ulcer depth ≥ muscularis mucosae. H. pylori‑induced injury Colonization → urease → local alkalinization → CagA/PicB/VacA → inflammation → either ↓ acid (gastric ulcer) or ↑ acid (duodenal ulcer). NSAID mucosal damage COX‑1 inhibition → ↓ prostaglandins → ↓ mucus & bicarbonate + impaired blood flow → ulcer susceptibility. Management of a bleeding ulcer Resuscitate → maintain Hb > 7 g/dL → high‑dose IV PPI → endoscopic hemostasis (thermal, clips, epinephrine) → consider surgery/embolization if refractory. 🔍 Key Comparisons Duodenal ulcer vs. Gastric ulcer Pain: night‑time & improves with food vs. worsens with food. Weight change: gain (more eating) vs. loss. H. pylori‑related ulcer vs. NSAID ulcer Mechanism: inflammation altering acid balance vs. prostaglandin loss. Treatment focus: eradication therapy vs. NSAID cessation + PPI. PPI vs. H2‑receptor antagonist PPI: >90 % acid suppression, longer duration, first‑line. H2‑blocker: useful if PPI contraindicated, less potent. ⚠️ Common Misunderstandings “Stress causes ulcers.” – Only severe physiological stress (ICU patients) causes stress ulcers; chronic psychological stress is not a primary cause. “Spicy food and alcohol cause ulcers.” – They may aggravate symptoms but are not primary etiologic agents. “All ulcers need surgery.” – Most heal with medical therapy; surgery is reserved for perforation, uncontrolled bleeding, or refractory cases. 🧠 Mental Models / Intuition “Acid > Defense = Ulcer.” Visualize a seesaw: when the acid/pepsin side outweighs mucus‑prostaglandin side, the mucosa cracks. “Two‑hit model.” First hit = aggressive factor; second hit = impaired defense (NSAID, H. pylori inflammation). Both must be present for a full‑thickness ulcer. 🚩 Exceptions & Edge Cases COX‑2‑selective NSAIDs – fewer ulcers but can delay healing of existing lesions. Zollinger–Ellison syndrome – gastrin‑producing tumor → massive acid secretion → multiple refractory ulcers; consider serum gastrin testing. Clarithromycin resistance – regional rates >15 % → avoid triple therapy, jump to bismuth quadruple. 📍 When to Use Which Diagnose PUD: Red‑flag age > 45, weight loss, anemia, or bleeding → go straight to EGD. Uncomplicated dyspepsia without red flags → non‑invasive H. pylori test first. Choose eradication regimen: Low local clarithromycin resistance → triple therapy. High resistance or prior macrolide exposure → bismuth quadruple. Prophylaxis for chronic NSAID users: Age ≥ 65 or prior ulcer + NSAID → prescribe PPI. Low‑risk patient → consider H2‑blocker or misoprostol if PPI contraindicated. 👀 Patterns to Recognize Night‑time pain that improves after eating → think duodenal ulcer. Pain that worsens within 30 min of a meal → think gastric ulcer. Acute severe abdominal pain + free air on X‑ray → perforated ulcer. Melena or hematemesis + hemodynamic instability → bleeding ulcer; look for “visible vessel” or “active spurting” on endoscopy. 🗂️ Exam Traps “NSAID use doubles ulcer risk.” – Actually, NSAIDs increase risk four‑fold; aspirin specifically doubles risk. “All stress ulcers are caused by psychological stress.” – Only severe physiologic stress (critical illness) causes true stress ulcers. “H2‑blockers are as effective as PPIs for ulcer healing.” – PPIs are superior; H2‑blockers are second‑line. “If H. pylori test is negative, no eradication needed.” – False‑negative tests can occur; endoscopic biopsy with rapid urease or histology can confirm. --- Use this guide for a rapid, confidence‑building review before your exam. Focus on the core concepts, memorize the high‑yield facts, and practice the stepwise algorithms for diagnosis and management.