Acute and Chronic Gastritis: Pathogenesis and clinical findings

Acute and Chronic Gastritis: Pathogenesis and clinical findings
Author: Oswald Chen
Reviewers: Vina Fan, Ben Campbell, Eldon Shaffer* * MD at time of publication
Helicobacter pylori (most common)
NSAIDs, alcohol, gastric reflux
Critical illness, trauma
Gastric ulceration (see Peptic Ulcer Disease slide)
↓ Gastric mucosal defense
(↓ secretion of prostaglandins and mucus)
Acid erodes gastric mucosa
Inflammatory cells (primarily neutrophils) infiltrate site of injury
Acute Gastritis
Acute inflammation of gastric mucosa
Inflammatory cells (primarily lymphocytes and plasma cells) accumulate in gastric mucosa
Autoimmune Metaplastic Environmental Metaplastic Atrophic Gastritis (AMAG) Atrophic Gastritis (EMAG)
Atrophic Gastritis
Chronic inflammation of gastric mucosa
Inflammatory cells destroy gastric glandular epithelial cells
Gastric mucosal atrophy and metaplasia (replacement of gastric mucosal cells with intestinal epithelial cells, commonly goblet cells)
(parietal cell loss → ↓ hydrochloric acid secretion)
↓ Iron absorption
Iron deficiency anemia
(see Iron Deficiency Anemia slide)
Activation of chemoreceptors and mechanoreceptors
of visceral nociceptors
Visceral afferents stimulate chemoreceptor trigger zone of medulla
Nausea/ vomiting
Associated with human leukocyte antigens HLA-B8 and HLA-DR3, which are proteins expressed on immune cell surface
Antibodies destroy parietal cells and intrinsic factor in gastric body and fundus
Epigastric pain (typically burning or gnawing) Dyspepsia (abdominal discomfort after
eating, often with early satiety and bloating)
Parietal cell loss →
↓ intrinsic factor →
↓ vitamin B12 absorption
Vitamin B12 deficiency
(see Vitamin B12 Deficiency slide)
Macrocytic Peripheral anemia neuropathy
↓ Gastric acidity leads to ↓ inhibition of G cells in antrum Hypergastrinemia (↑ gastrin release from G cells)
Gastrin binds to cholecystokinin-B (CCK-B) receptors on parietal and enterochromaffin-like (ECL) cells of gastric body
↑ CCK-B signaling leads to ↑ cell proliferation and ↓ cell death (↓ apoptotic activity)
Hyperplasia (↑ number of cells)
Low-grade dysplasia (disordered growth of epithelium) High-grade dysplasia
Carcinoid tumor (0.7% of cases) Malignancy arising from ECL cells
Gastric adenocarcinoma (0.3% of cases) Malignancy arising from gastric epithelial cells
Sign/Symptom/Lab Finding
Published November 15, 2022 on