27. PEPTIC ULCER DISEASE

Introduction

Peptic ulcers are open sores that develop in the inner lining of the stomach, duodenum (first part of small intestine) or the lower part of esophagus. These ulcers occur when the protective lining is damaged by strong stomach acids and digestive enzymes (pepsin). Unlike simple erosions, peptic ulcers penetrate deeper into the tissues and cause more inflammation.

Common types of peptic ulcers include:

  • Gastric ulcer – ulcer in the stomach.
  • Duodenal ulcer – ulcer in the first part of small intestine.
  • Esophageal ulcer – ulcer in lower esophagus due to acid reflux.

Most peptic ulcers occur in the stomach or duodenum, with duodenal ulcers being more common (ratio 4:1). The most frequent cause of PUD is Helicobacter pylori infection.

Definition

Peptic Ulcer Disease (PUD) refers to circumscribed lesions in the mucosa of the upper gastrointestinal tract, especially in areas exposed to gastric acid and pepsin, such as the stomach and duodenum.

Epidemiology

PUD is more common in developing countries. H. pylori infection is strongly linked with poor hygiene and low socioeconomic status. According to recent WHO data, peptic ulcer deaths account for around 1.20% of total deaths in India, with an age-adjusted death rate of 12.37 per 100,000 population.

The overall mortality rate has significantly reduced in the past two decades due to better treatment.

Etiology (Causes)

1. Helicobacter pylori Infection

H. pylori is a gram-negative bacterium living in the stomach and duodenal mucosa. It breaks down urea into ammonia, increasing local pH and damaging the mucosa. Around 90% of duodenal ulcers and 70% of gastric ulcers are linked to H. pylori.

2. Excess Gastric Acid

HCl is produced by parietal cells. Excess acid production occurs due to:

  • Gastrin-secreting tumors (Zollinger–Ellison syndrome)
  • Increased number of parietal cells
  • Overstimulation of gastrin receptors

3. NSAIDs (Painkillers)

Medicines such as aspirin, ibuprofen and naproxen reduce protective mucus and irritate stomach lining, increasing ulcer risk—even with coated tablets.

4. Stress

Emotional stress does not directly cause ulcers but can worsen symptoms. Physical stress (burns, surgeries, trauma) can increase risk of gastric ulcers.

5. Genetic Factors

Family history increases risk. A rare genetic disorder, Zollinger-Ellison syndrome, causes high gastrin production and severe ulcers.

6. Smoking

Smokers have a higher chance of developing ulcers.

7. Alcohol

Heavy drinkers have increased risk due to irritation of stomach lining.

Other Factors Affecting HCl Secretion

Parietal cells are stimulated by vagus nerve, gastrin and histamine (from mast cells). Calcium, alcohol, coffee, high-fat food and increased acidity also stimulate HCl release.

Pathophysiology

Ulcers result from an imbalance between protective factors of the gastric mucosa and corrosive factors like acid and pepsin.

1. Protective Factors

  • Thick mucus barrier that prevents acid from reaching the lining.
  • Bicarbonate secretion neutralizes acid.
  • Pancreatic and biliary secretions that reduce acid entering the duodenum.
  • Intact mucosal blood flow that delivers nutrients and removes toxins.
  • Good cell renewal and repair mechanisms.

2. Corrosive Factors

  • Exposure to gastric acid and pepsin is essential for ulcer formation.
  • Damage occurs when mucosal barrier breaks, allowing back-diffusion of acid into deeper tissues.

3. Physiological Defects

Duodenal Ulcer Defects

  • Increased gastric acid secretion.
  • Higher number of parietal cells producing HCl.
  • Elevated serum pepsinogen I levels → higher pepsin activity.
  • Increased gastrin secretion after meals.
  • Failure to suppress acid secretion at low pH.
  • Faster gastric emptying → more acid reaches duodenum.

Gastric Ulcer Defects

  • Weak mucosal defense or direct mucosal injury.
  • High gastrin levels in some patients.
  • Decreased pyloric pressure.
  • Delayed gastric emptying.
  • Increased bile reflux.
  • Low prostaglandin levels in mucosa (restored after healing).

Signs & Symptoms

Small ulcers may be silent, but deeper ulcers produce noticeable symptoms.

Common Symptoms

  • Stomach pain (most common; often worse at night)
  • Pain relieved temporarily by food in some cases
  • Bloating
  • Heartburn
  • Nausea or vomiting

Severe Symptoms

  • Dark, black stools (bleeding ulcer)
  • Vomiting blood
  • Significant weight loss
  • Severe upper abdominal pain

Diagnosis

  • Physical exam: Epigastric tenderness noted between umbilicus and xiphoid region.
  • Laboratory tests: Hemoglobin, hematocrit and stool tests used to detect bleeding.
  • H. pylori testing: Urea breath test (preferred), stool antigen test or antibody test.
  • Endoscopy: Gold standard for diagnosis and direct visualization of ulcer crater.
  • Upper GI radiography: Alternative when endoscopy is not available.

Detailed Notes:

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