Pathophysiology - The Gut's Acid Trip

- Core Imbalance: Aggressive factors (gastric acid, pepsin) overwhelm mucosal defenses (mucus, bicarbonate, prostaglandins, blood flow).
- Two Main Culprits:
- H. pylori: Most common. Produces urease to survive in acid. Toxins (CagA, VacA) incite inflammation, leading to mucosal damage.
- NSAIDs: Inhibit COX-1, decreasing protective prostaglandins ($PGE_2$), which reduces mucus, bicarbonate, and mucosal blood flow.
⭐ In duodenal ulcers, H. pylori in the antrum decreases somatostatin output, leading to unchecked gastrin release and ↑ total acid production.
Presentation & Diagnosis - Spotting the Ulcer
- Hallmark: Epigastric pain (dyspepsia), often gnawing or burning.
- Duodenal Ulcer (DU): Pain 2-5 hours post-meal, at night. Relieved by food/antacids.
- Gastric Ulcer (GU): Pain 15-30 mins post-meal. Worsened by food, causing anorexia/weight loss.
- Alarm Features: Age >60, unintentional weight loss, progressive dysphagia, persistent vomiting, iron deficiency anemia, GI bleeding (melena/hematemesis).

- Gold Standard: EGD (Endoscopy) for direct visualization & biopsy.
- Biopsy for histology & rapid urease test (H. pylori).
⭐ Exam Favorite: Any gastric ulcer found on imaging or endoscopy must be biopsied due to malignancy risk. Duodenal ulcers are almost never malignant.
Management - Dousing the Flames
- Core Goal: Heal existing ulcers & prevent recurrence.
- Acid Suppression: Proton Pump Inhibitors (PPIs) are first-line (e.g., Omeprazole). H2 blockers are second-line.
- H. pylori Eradication: Crucial if positive.
- Standard Triple Therapy: Clarithromycin + Amoxicillin + PPI for 14 days.
- Quadruple Therapy: (Used for macrolide resistance or treatment failure).
- 📌 Buy My Tasty Pepperoni: Bismuth subsalicylate + Metronidazole + Tetracycline + PPI.
- NSAID-Induced Ulcers: Discontinue NSAID if possible. If not, co-prescribe a PPI.
⭐ Warning: For gastric ulcers, always repeat endoscopy in 8-12 weeks after treatment to confirm healing and rule out underlying malignancy. Duodenal ulcers rarely harbor malignancy and do not require routine follow-up endoscopy.
Complications - When Ulcers Go Rogue
- Hemorrhage (Most Common): Presents as melena, hematemesis, or coffee-ground emesis. Endoscopy is crucial for diagnosis and hemostasis.
- Perforation: Acute, severe abdominal pain; a surgical emergency. Classic sign is free air under the diaphragm on upright chest X-ray.
- Gastric Outlet Obstruction (GOO): Caused by edema or scarring. Leads to early satiety, projectile non-bilious vomiting, and weight loss.
- Penetration: Ulcer erodes into an adjacent organ (e.g., pancreas), causing persistent, radiating back pain.
⭐ A posterior duodenal ulcer may perforate and erode the gastroduodenal artery, leading to massive hemorrhage.

High‑Yield Points - ⚡ Biggest Takeaways
- Most common causes: H. pylori infection and NSAID use.
- Classic symptom: Epigastric pain. Duodenal ulcers improve with food, while gastric ulcers worsen.
- Gold standard diagnosis: Upper endoscopy (EGD) with biopsy, especially for gastric ulcers to rule out malignancy.
- H. pylori treatment: Triple therapy (a PPI + clarithromycin + amoxicillin) is a standard regimen.
- Major complication: Perforation presents as sudden, severe abdominal pain and requires urgent surgery.
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