Gastritis

Gastritis = inflammation of the mucosal lining of the stomach

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A) Acute Gastritis

• Usually transient acute mucosal inflammation; may involve hemorrhage into mucosa or erosions of epithelium

Pathogenesis (associated with):

• Heavy NSAIDs use (especially aspirin)
• Excessive alcohol consumption
• Stress situations (trauma, burns, hypothermia)
• H. pylori infection
• Heavy smoking

Morphology

• Hemorrhagic-erosive inflammation of gastric mucosa
• Pangastritis (entire stomach) or antral gastritis
• Mucosal hyperemia, punctate hemorrhages, multiple erosions
• Acute ulcers: anywhere in stomach, <1 cm; usually do not penetrate muscularis propria
• May disappear within days or complete mucosal restitution

Clinical

• Epigastric pain, nausea, vomiting
• Occasionally: hematemesis + melena → hemorrhagic shock (major cause of hematemesis in alcoholics)

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B) Chronic Gastritis (most common form)

• Chronic inflammatory changes → mucosal atrophy + epithelial dysplasia

Type A (Autoimmune Gastritis)

• Auto-antibodies against parietal cells (acid-producing cells)
• Injury → gland destruction + mucosal atrophy → loss of acid production + intrinsic factor → pernicious anemia (vitamin B12 deficiency)
• Most common in Scandinavia; associated with other autoimmune disorders (Hashimoto thyroiditis, Addison disease)

Type B (Bacterial Gastritis — H. pylori)

• H. pylori colonizes gastric mucosal surface; protected from acid by urease + ammonium production (neutralizes H⁺ ions)
• Two patterns of gastritis after H. pylori infection:
  1. Antral type: high acid production → higher risk of duodenal ulcers
  2. Pangastritis: multifocal mucosal atrophy + low acid secretion → increased risk for adenocarcinoma
• H. pylori induces: duodenal peptic ulcer, gastric adenocarcinoma, MALT lymphoma

Type C (Chemical Gastritis)

• Chemicals irritate mucosal lining → mucosal atrophy
• Seen in chronic alcoholics and NSAID users

Morphology (chronic gastritis — all types)

• Lymphocytic and plasma cell infiltration of the lamina propria
• Variable gland loss + mucosal atrophy
• Intestinal metaplasia: replacement of glandular epithelium by columnar absorptive cells → dysplasia → carcinoma

Clinical

• Usually asymptomatic or mild (abdominal discomfort, nausea, vomiting)
• Autoimmune gastritis → hypochlorhydria or achlorhydria
• H. pylori → duodenal peptic ulcers, gastric adenocarcinoma, MALT lymphoma

💡 High-yield: Acute gastritis = NSAIDs/alcohol/stress/H. pylori; erosions <1 cm; hematemesis in alcoholics. Type A chronic = parietal cell antibodies → pernicious anemia; Scandinavia. Type B = H. pylori; urease; antral type → duodenal ulcers; pangastritis → adenocarcinoma + MALT lymphoma. Type C = chemicals/NSAIDs. Intestinal metaplasia is precancerous.