Step 1 topics → Gastrointestinal → Gastritis (Acute and Chronic A/B)

Gastritis (Acute and Chronic A/B)

USMLE Step 1 trap: Inverts the gastric locations of Type A vs Type B chronic gastritis. Type A autoimmune gastritis affects the fundus and body (targeting parietal cells), while Type B H. pylori gastritis begins in the antrum.

Gastritis covers a spectrum from acute mucosal injury to chronic atrophic destruction, and USMLE Step 1 tests it across all three angles: pure recall of causes, application of pathophysiology to clinical scenarios, and interpreting vignettes where the wrong diagnosis is tempting. The acute side is mostly about identifying the right trigger — NSAIDs, alcohol, stress ulcers in ICU patients — and knowing the mechanism, not just the list. The chronic side is where most students get burned, because Type A and Type B have mirror-image features that are easy to invert under pressure.

The chronic gastritis distinction is the highest-yield piece here. Type A is autoimmune, targets parietal cells in the fundus/body, causes achlorhydria, and drives compensatory hypergastrinemia — which then feeds ECL cell hyperplasia and carcinoid tumor risk. Type B is H. pylori, starts in the antrum, and is the bigger driver of peptic ulcer disease and adenocarcinoma. Students frequently swap the locations and the cancer risks, which is exactly what Step 1 exploits with answer choices that look almost identical.

Stress ulcers get tested as a clinical correlate where you have to match trigger to mechanism. Curling (burns) and Cushing (CNS injury) are reliably inverted by students who memorize the names without anchoring them to pathophysiology. The exam will give you a burn patient or a neurosurgical patient and ask what type of ulcer they're at risk for — knowing why each happens (ischemia vs. vagal hyperstimulation) is what locks in the right answer and makes it unforgettable.

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Common misconceptions

Common mistake
Wrong: Type A (autoimmune) gastritis affects the antrum and Type B (H. pylori) affects the fundus/body.
Right: Type A autoimmune gastritis affects the fundus and body (targeting parietal cells), while Type B H. pylori gastritis begins in the antrum.
Type A autoimmune gastritis targets parietal cells, which are concentrated in the fundus and body — that's where the destruction occurs. Type B H. pylori gastritis starts in the antrum because that's where the organism preferentially colonizes. The easiest anchor: 'A' for autoimmune, 'A' for anti-parietal cell antibodies, and parietal cells live in the body/fundus — not the antrum.
Common mistake
Wrong: Curling ulcers are caused by head injury and Cushing ulcers are caused by burns.
Right: Curling ulcers are caused by severe burns (decreased plasma volume → mucosal ischemia) and Cushing ulcers are caused by CNS injury (vagal stimulation → acid hypersecretion).
Common mistake
Wrong: Type A autoimmune gastritis carries no significant cancer risk because it is immune-mediated rather than infectious.
Right: Type A gastritis increases risk of gastric carcinoid tumors (from hypergastrinemia-driven ECL cell hyperplasia) and, to a lesser extent, gastric adenocarcinoma.
Type A gastritis destroys parietal cells, so acid output drops. The antrum senses low acid and keeps secreting gastrin in compensation — chronically elevated gastrin drives ECL cell hyperplasia in the fundus, which can progress to gastric carcinoid tumors. There is also an increased adenocarcinoma risk, though smaller than with H. pylori. Never call Type A 'low risk' just because it's autoimmune rather than infectious.
Common mistake
Wrong: NSAIDs cause acute gastritis primarily by direct topical irritation of the gastric mucosa.
Right: NSAIDs cause gastric mucosal injury primarily by inhibiting COX-1, reducing prostaglandin synthesis and thereby decreasing mucus and bicarbonate secretion.
NSAIDs taken orally do cause some local irritation, but that's not the primary mechanism of mucosal injury — and IV NSAIDs cause the same damage, which proves it. The real problem is systemic COX-1 inhibition: COX-1 is constitutively active in the gastric mucosa and drives prostaglandin E2 synthesis, which stimulates mucus and bicarbonate secretion and maintains mucosal blood flow. Block COX-1, lose those defenses, and the mucosa is exposed to normal acid levels it can no longer handle.
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What the exam tests

  1. Identify the causes of acute gastritis — including NSAIDs, alcohol, and stress states — and explain the actual mechanism of injury, not just the trigger list (e.g., NSAIDs work systemically via COX-1 inhibition, not topical irritation).
  2. Distinguish Type A (autoimmune) from Type B (H. pylori) chronic gastritis by location, associated lab findings (gastrin levels, parietal cell antibodies), and specific cancer risks including gastric carcinoid and adenocarcinoma.
  3. Match Curling ulcers to severe burns and Cushing ulcers to CNS injury, and explain the distinct mechanisms: mucosal ischemia from decreased plasma volume versus acid hypersecretion from vagal stimulation.

Can you avoid these mistakes?

A 58-year-old woman with autoimmune gastritis has a serum gastrin of 900 pg/mL (normal < 100). Her endoscopy shows atrophy of the fundus and body. What cancer type is she at highest risk for, and what is the cell of origin?
A patient with severe burns over 40% of his body develops hematemesis on day 3 of his ICU stay. What type of stress ulcer is this, and what is the underlying mechanism of mucosal injury?
You are told a patient has chronic gastritis with antral predominance, a positive urea breath test, and normal serum gastrin. Is this Type A or Type B? What would you expect if the gastritis were the other type instead?
A patient takes ibuprofen daily for arthritis and develops epigastric pain. Your attending says 'NSAIDs just irritate the stomach lining.' Why is this explanation incomplete, and what does misoprostol target to treat or prevent this complication?

Related topics

Gastric Secretion and Cell Types Gut Tube Regions and Blood Supply Midgut Rotation and Anomalies (Malrotation/Volvulus) Meckel Diverticulum Omphalocele vs Gastroschisis

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