Stomach Disorders: Gastritis and Peptic Ulcer Disease

Introduction

• Discussing stomach disorders, including gastritis and peptic ulcer disease (PUD).
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Gastritis

Overview

• Inflammation of the stomach lining (mucosa).
• Most commonly involves the antrum of the stomach.

Microscopic Level

• Layers of the alimentary canal involved: epithelium, lamina propria, muscularis mucosa.
• Characterized by small shallow erosions, not extending past the muscularis mucosa.
• Involves generalized mucosal inflammation and a thin mucus layer.

Symptoms

• Classic finding: epigastric abdominal pain.
• Pain relation to food: not significantly affected by eating.
• Suggestive of a patient with gastritis.
• Consider causes: NSAID use, ethanol consumption, H. pylori infection, stress-induced ulcers, autoimmune conditions.

Pathophysiology

Causes

1. NSAIDs and Ethanol:

   • Inhibit cyclooxygenase (COX) enzyme, reducing prostaglandin production.
   • Increase hydrochloric acid (HCl) production and decrease mucus production by parietal cells.

2. H. pylori Infection:

   • Increases gastrin production, stimulating HCl secretion.
   • Urease enzyme converts urea to ammonia, increasing stomach pH, and enabling H. pylori survival.
   • Causes cytotoxic damage via cagA and VacA toxins.

3. Stress-Induced Ulcers:

   • Curling ulcers from burns/sepsis causing hypovolemia and decreased tissue perfusion.
   • Cushing ulcers from brain injury/increased intracranial pressure, increasing vagus nerve activity leading to more HCl production.

4. Autoimmune Gastritis:

   • Antibodies attack parietal cells, reducing HCl and intrinsic factor production.
   • Primarily affects the fundus of the stomach, leading to atrophy.

Peptic Ulcer Disease (PUD)

Overview

• Can occur in the stomach antrum or more commonly in the duodenum.
• Characterized by deep ulcers extending beyond the mucosa into the submucosa.
• Classic finding: epigastric abdominal pain.
• Pain relation to food: Gastric ulcers worsen with food, duodenal ulcers improve initially.

Microscopic Level

• Presence of deep ulcers with significant inflammation.
• Thin mucus lining and injury to mucosal cells.

Pathophysiology

Causes

1. NSAIDs and Ethanol:

   • Same mechanism as for gastritis, with COX enzyme inhibition affecting prostaglandin production.

2. H. pylori Infection:

   • Increases gastrin production leading to HCl secretion.
   • Urease activity creating alkaline environment and cytotoxicity by cagA and VacA toxins.

3. Gastrinoma (Zollinger-Ellison Syndrome):

   • Tumor producing excessive gastrin, leading to refractory duodenal ulcers.
   • Indicated by high gastrin levels not suppressed by secretin.

Complications

• Upper GI Bleed: From erosion into gastric or duodenal arteries leading to hematemesis and melena.
• Perforation: Sasal erosion leading to pneumoperitonium and peritonitis.
• Gastric Outlet Obstruction: Antral fibrosis and edema causing gastric dilation, vomiting, and succussion splash.
• Cancer: Chronic inflammation leading to dysplasia and cancers like adenocarcinoma and MALT lymphoma.

Diagnosis

• HPylori Detection:
  • Stool antigen test, Urea breath test, and less commonly serology titers.
• Complication Identification:
  • Check for severe symptomatology indicating perforation or bleeding and perform appropriate imaging and endoscopy.
• Zollinger-Ellison Syndrome:
  • Measure serum gastrin levels and confirm with secretin stimulation test if necessary.
• EGD: For visualizing ulcers, biopsies for H. pylori or malignancy testing.

Treatment

• Acid Suppression: PPIs to reduce HCl production.
• Mucosal Protection: Sucralfate or misoprostol to increase mucus barrier.
• H. pylori Eradication: Clarithromycin, amoxicillin, and PPI (CAP therapy) or quadruple therapy with metronidazole for penicillin allergies.
• Management of Complications:
  • GI bleed treatment (e.g. endoscopic cauterization).
  • Surgical intervention for perforations (e.g. Graham patch).
  • Dilators for gastric outlet obstruction.

Conclusion

• Recap of causes, diagnosis, complications, and treatment approaches for gastritis and PUD.
• Importance of proper diagnosis and tailored treatment.