Gastrointestinal Disorders: GERD & Gastritis

Reflux Esophagitis, Gastritis & Peptic Ulcer Disease

• Reflux disease is a common issue in the gastrointestinal tract
• Stomach acid and pepsin reflux into the lower esophagus
• This causes irritation, inflammation, and damage to the lower esophageal mucosa
• Can progress to intestinal metaplasia (Barrett's esophagus)

Barrett's Esophagus

• Chronic GERD complication
• Characterized by intestinal metaplasia of esophageal squamous mucosa
• Endoscopy shows red, velvety mucosa extending upwards

Pathogenesis of GERD

• Multifactorial
• Transient lower esophageal sphincter relaxation is a major cause
• Increased intra-abdominal pressure (e.g., pregnancy, old age, alcohol, tobacco)
• Hiatus hernia
• Delayed gastric emptying
• Defective esophageal mucosal resistance
• Increased gastric volume
• CNS depressants

Gastritis

• Inflammation of the gastric mucosa
• Can be acute (neutrophils) or chronic (lymphocytes and plasma cells) or mixed
• Acute gastritis is usually transient
• Severe erosive form can cause gastrointestinal bleeding
• Causes include NSAIDs, chemotherapy, excessive alcohol and smoking, stress, ischemia, shock, severe systemic infections (like salmonellosis), uraemia, acids and alkalis, mechanical trauma (e.g., nasogastric intubation), post-distal gastrectomy

Morphology

• Mucosal edema
• Vascular congestion
• Neutrophil infiltrate in the epithelial cells (signifies inflammation)
• Severe form: mucosal erosion & hemorrhage

Histology

• Neutrophils within the epithelial cells

Chronic Gastritis

• Chronic mucosal inflammatory changes leading to mucosal atrophy and epithelial metaplasia
• Can be a background to carcinoma development
• Etiology includes chronic infection by Helicobacter pylori (the most common cause), autoimmune conditions, toxins (alcohol, smoking), radiation, and chronic bile reflux (after gastroenterostomy)

Helicobacter pylori Associated Chronic Gastritis

• Most common cause (90%) is H. pylori
• Curved, gram-negative rod, transmitted fecal-oral
• Associated with poverty and overcrowding
• Usually acquired in childhood
• Pathogenesis involves bacterial virulence factors (flagella, urease, adhesins) and host factors (genetic polymorphisms affecting proinflammatory/anti-inflammatory cytokine expression).

Morphology (H. pylori Associated Chronic Gastritis)

• Predominantly affects the antrum
• Patients may have normal or increased acid production
• Organisms concentrate in surface mucosa over epithelial cells
• Inflammation (neutrophils, plasma cells, lymphoid aggregates)
• Can progress to patchy mucosal atrophy and intestinal metaplasia, leading to complications such as peptic ulcers, gastric adenocarcinoma, and MALT lymphoma.

Autoimmune Gastritis

• Less than 10% of chronic gastritis cases
• Involves body and fundus, spares antrum and cardia
• Autoimmune destruction of parietal cells
• Characterized by:
  • Antibodies to parietal cells and intrinsic factor
  • Decreased acid production (achlorhydria) and increased gastrin release
  • Vitamin B12 deficiency (pernicious anaemia)
  • Reduced serum pepsinogen I
• Often associated with other autoimmune diseases

Peptic Ulcer Disease

• Chronic mucosal ulceration in the duodenum or stomach
• Usually associated with H. pylori, NSAIDs or cigarette smoking
• Peptic ulcers are relapsing lesions, most commonly diagnosed in middle-aged to older adults
• Pathogenesis: imbalance between gastroduodenal mucosal defense mechanisms and damaging factors. PUD often develops on a background of chronic gastritis

Pathogenesis of Peptic Ulcer

• Aggressive forces (e.g., H. pylori, NSAIDs, aspirin, corticosteroids, smoking, alcohol)
• Imbalance between aggressive forces and mucosal defense mechanisms (e.g., surface mucus secretion, bicarbonate secretion, mucosal blood flow, epithelial regeneration, and prostaglandin elaboration)

Macroscopic Features (Peptic Ulcers)

• Usually solitary
• Sites include the first part of the duodenum, lesser curvature of the stomach, and the antrum
• Shallow or deep, various sizes (mm to cm)
• Round to oval lesions, relatively straight walls.
• Mucosal margin may overhang the base, which is clean
• Later, there is scarring and puckering of the surrounding tissue with folds radiating from the crater

Chronic Gastric Ulcer (Microscopy)

• Four zones:
  • Superficial necrotic debris and fibrin
  • Inflammatory cells (predominantly neutrophils) beneath the superficial layer
  • Granulation tissue in deeper layers
  • Collagenous/fibrous scar with thick-walled thrombosed vessels

Complications

• Chronic Gastric Ulcer and Peptic Ulcer:
  • Bleeding
  • Perforation
  • Obstruction (due to edema or scarring)
  • Malignant transformation (very rare)