Peptic Ulcer Disease: Etiology, Pathogenesis, and Mechanism of Ulcer Formation

Introduction

Peptic ulcer disease (PUD) is a common gastrointestinal condition characterized by mucosal erosions in the stomach and duodenum. It arises from an imbalance between aggressive factors like acid and pepsin and defensive mechanisms such as mucus and bicarbonate production.

Etiology and Risk Factors

• Helicobacter pylori infection - the leading cause
• Non-steroidal anti-inflammatory drugs (NSAIDs)
• Excess gastric acid secretion
• Smoking and alcohol consumption
• Genetic predisposition

Pathogenesis of Peptic Ulcers

The formation of peptic ulcers occurs due to various pathological processes:

• Helicobacter pylori-induced damage: H. pylori disrupts mucosal integrity by producing urease, leading to inflammation and increased acid secretion.
• NSAID-induced injury: NSAIDs inhibit prostaglandin synthesis, which weakens mucosal defense mechanisms.
• Gastric hyperacidity: Excess acid erodes the mucosal lining.
• Impaired mucosal repair: Reduced blood flow and cell regeneration contribute to ulcer persistence.

Clinical Features

• Epigastric pain: Burning sensation, aggravated by fasting and relieved by food.
• Nausea and vomiting: Due to altered gastric motility.
• Gastrointestinal bleeding: Presents as hematemesis or melena in severe cases.
• Complications: Perforation, gastric outlet obstruction, and malignancy risk.

Microbiology and Role of H. pylori

H. pylori is a Gram-negative bacterium responsible for persistent gastric inflammation, leading to ulcer formation. It colonizes the gastric epithelium, evading immune response while stimulating acid production.

Conclusion

Peptic ulcer disease is a multifactorial condition driven by infections, drug usage, and lifestyle choices. Early detection and appropriate management can significantly reduce morbidity.