Peptic Ulcer Disease Thomas Rosenzweig, MD

Acute Gastritis (has neutrophils) Acute (Active) Gastritis neutrophils are present above the basement membrane in direct contact with epithelial cells Erosion loss of the epithelium → no mucus Seen with mucosal neutrophils and a fibrin- containing purulent exudate in the lumen Ulcers – deep erosions Hemorrhage cause dark punctae in hyperemic mucosa Acute erosive hemorrhagic gastritis BOTH Erosion and Hemorrhage

Acute Gastritis (has neutrophils) Normal Protection Gastritis Risk (NSAIDs) inhibit cyclooxygenase- (COX) dependent synthesis of prostaglandins E2 and I2 Stops normal defense mechanisms Uremic patients and those infected with urease-secreting H. pylori Stops bicarbonate transporters via ammonium ions Chemicals Direct cellular damage Excessive alcohol consumption, NSAIDs, radiation therapy, and chemotherapy Foveolar cells Secretes Mucin Neutral pH from Bicarbonate Epithelial cells Secretes Bicarbonate Forms a physical barrier beneath mucus Stops back diffusion of acid and leakage of other luminal materials (including pepsin) into the lamina propria

Stress-Related Mucosal Disease occurs in patients with severe physiologic stress due to local ischemia Ex. Critically ill pt. Stress ulcers seen with shock, sepsis, or trauma Curling ulcers Seen with burns or trauma In the proximal duodenum Cushing ulcers Seen with intracranial disease Risk of perforation

Peptic Ulcer Disease chronic mucosal ulceration affecting the stomach or duodenum ↓ mucosal defense and ↑ chronic gastritis risk factors Main risks: H. pylori infection Most common ↑ gastric acid and ↓ duodenal bicarbonate NSAIDs Over 60 years old Smoking ↓ mucosal blood flow, oxygenation, and healing

Peptic Ulcer Disease Round to oval, sharply punched-out defect Risk of death from bleeding Symptoms: Burning or aching 1-3 hours after a meal (worse at night) Better with alkali or food Peptic ulcers Proximal duodenum Within a few centimeters of the pyloric valve Involve the anterior duodenal wall Gastric Peptic ulcers Along the lesser curvature Near the interface of the body and antrum

Hypertrophic Gastropathies Ex. Ménétrier disease Ex. Zollinger-Ellison syndrome Giant “cerebriform” enlargement of the rugal folds from epithelial hyperplasia without inflammation ↑ growth factor release uncommon diseases

Ménétrier Disease ↑ factor-α (TGF-α) Irregular enlargement of the gastric rugae Enlarged rugae are present in the body and fundus antrum is spared Hyperplasia of foveolar mucous cells Elongated glands with a corkscrew-like appearance Treatment: intravenous albumin

Zollinger-Ellison Syndrome Caused by gastrin-secreting tumors Most are malignant 75% are sporadic and solitary 25% multiple endocrine neoplasia type I (MEN I) Doubled oxyntic mucosal thickness in the stomach due to a 5x ↑ of parietal cells found in the small intestine or pancreas Seen with duodenal ulcers or chronic diarrhea Treat with proton pump inhibitors

Key Concepts