Peptic Ulcer Disease Overview

Peptic Ulcer Disease (PUD)

• PUD is characterized by ulcers in the stomach lining, duodenum, or esophagus
• Ulcers form due to weakened mucosal barriers and the corrosive action of gastric acid and pepsin

Most Likely Causes

• Helicobacter pylori (H. pylori) infection: A common cause, especially when NSAID use is ruled out.
• Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): Inhibit cyclooxygenase (COX) enzymes, reducing prostaglandin production. Reduced prostaglandins lead to increased acidity and damage the lining.

Other Contributing Factors

• Excessive Gastric Acid Secretion: Increases acid exposure, potentially leading to erosion of the mucosal lining.
• Bile Salt Reflux: Duodenal bile reflux into the stomach can cause ulcer formation, especially gastric ulcers.

Pathophysiology of H. pylori-Associated PUD

• Colonization: H. pylori uses flagella to burrow into the gastric mucosa. Urease production creates ammonia and bicarbonate, creating an alkaline environment allowing survival in the stomach. Mucinase degrades the protective mucous layer.
• Immune Response: H. pylori triggers an immune response, attracting neutrophils and macrophages. These release cytotoxic substances, damaging epithelial cells and increasing local inflammation.
• Inflammatory Cytokines: Inflammatory cytokines (e.g., IL-1, IL-6, TNF-α) further enhance local acid production and impair the mucosal barrier.
• Epithelial Damage: The combined effect of proteolytic enzymes, ammonia, mucin degradation, and gastric acid exposure disrupts the mucosa, exposing epithelial cells to acid and pepsin. This results in ulceration.

Pathophysiology of NSAID-Associated PUD

• Prostaglandin Inhibition: NSAIDs inhibit COX-1 and COX-2 enzymes, thus reducing the production of prostaglandins. Prostaglandins are crucial in protecting the mucosal lining by stimulating bicarbonate and mucin production, while inhibiting acid secretion.
• Impaired Platelet Aggregation: NSAIDs reduce thromboxane A2 (TXA2) production, impacting platelet aggregation and hemostasis. This raises the risk of bleeding as ulcers erode into blood vessels.

Disease Transmission

• PUD itself is not contagious
• H. pylori can be transmitted through oral-oral or fecal-oral routes, often via contaminated food, water, or close contact.
• NSAID-related ulcers are caused by prolonged NSAID usage and are not transmitted.

Risk Factors

• Modifiable: H. pylori infection, NSAID use, alcohol consumption, smoking, dietary factors, and stress.
• Non-modifiable: Age, genetics, and chronic illnesses like liver, kidney, or respiratory diseases.

This quiz covers the essentials of Peptic Ulcer Disease (PUD), including its causes, pathophysiology, and contributing factors. Learn about the role of Helicobacter pylori, NSAIDs, and other elements that lead to ulcer formation. Test your understanding of the impacts on gastric health and treatment approaches.