## Chronic Atrophic Gastritis and Achlorhydria ### Pathophysiology of Autoimmune Atrophic Gastritis: **Key Point:** Autoimmune atrophic gastritis involves autoantibodies against parietal cell antigens (H⁺/K⁺-ATPase, intrinsic factor) leading to chronic inflammation, glandular atrophy, and loss of acid-secreting capacity. ### The Cascade: 1. **Autoimmune attack:** Antibodies against parietal cell H⁺/K⁺-ATPase and intrinsic factor 2. **Chronic inflammation:** T-cell infiltration and destruction of gastric glands 3. **Glandular atrophy:** Progressive loss of parietal cells and chief cells 4. **Result:** Loss of acid-secreting cells → achlorhydria (pH >6.0) 5. **Secondary effect:** Loss of intrinsic factor → vitamin B12 malabsorption → pernicious anemia ### Why This Is Different from Other Causes of Hypochlorhydria: - **Not a regulatory problem:** The remaining parietal cells cannot be stimulated to secrete acid because there are insufficient cells - **Permanent loss:** Unlike H2 blockers or PPIs, the damage is irreversible - **Associated findings:** Elevated serum gastrin (due to loss of acid feedback), megaloblastic anemia, neurologic symptoms from B12 deficiency **Clinical Pearl:** Achlorhydria in atrophic gastritis is accompanied by elevated fasting serum gastrin (>1000 pg/mL) because the loss of acid feedback removes the inhibition on gastrin secretion. This is the opposite of Zollinger-Ellison syndrome (high acid + high gastrin). **High-Yield:** Atrophic gastritis = Autoimmune parietal cell destruction = Achlorhydria + High gastrin + B12 deficiency
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