STEPTRACKERGASTROINTESTINAL | PATHOLOGY + MICROBIOLOGY | HIGH-YIELD REVIEW

Stomach I — Gastritis

Acute mucosal injury from lost protection, and the two chronic gastritides that sit at opposite ends of the stomach.

FOCUS ON
Acute gastritis = protective barrier fails (NSAIDs, alcohol, burns, CNS injury, shock). H pylori = antrum, most common chronic gastritis, ulcers, adenocarcinoma, MALT lymphoma. Autoimmune = body/fundus, parietal cell destruction → achlorhydria, ↑ gastrin, B12 deficiency, carcinoid and cancer risk.
DISORDER
MECHANISM
FEATURES
CLUE
Acute erosive gastritis
Imbalance between acid and mucosal defense (mucus, HCO₃⁻, blood flow, prostaglandins)
Erosions (mucosa only); dyspepsia, hematemesis, melena
NSAIDs (↓ PGE₂), alcohol, chemo, uremia
Curling ulcer
Severe burns → hypovolemia → mucosal ischemia
Acute stress ulcers in stomach/duodenum
"Burned by the Curling iron"
Cushing ulcer
Brain injury → ↑ vagal tone → ↑ ACh → ↑ acid
Stress ulcers after head trauma, tumor, surgery
"Always Cushion the brain"
Stress-related mucosal disease
Shock, sepsis, mechanical ventilation, coagulopathy → ischemia
Multiple superficial erosions, GI bleeding in ICU
PPI prophylaxis in high-risk ICU patients
H pylori gastritis
most common chronic
Gram⁻ curved rod, urease → NH₃ buffers acid and injures mucosa; flagella, CagA, VacA
Starts in antrum; lymphoid follicles, neutrophils; may spread (pangastritis)
Peptic ulcers, intestinal-type adenocarcinoma, MALT lymphoma
Autoimmune gastritis
CD4 T-cell (type IV) attack on parietal cells; anti-parietal cell (H⁺/K⁺-ATPase) and anti-intrinsic factor antibodies
Body/fundus atrophy; achlorhydria; ↑↑ gastrin; G-cell hyperplasia (antrum spared)
Pernicious anemia; other autoimmune disease (thyroid, T1DM, vitiligo)
Chemical (reactive) gastropathy
Bile reflux (post-gastrectomy), NSAIDs, alcohol
Foveolar hyperplasia, few inflammatory cells
Injury without much inflammation
Ménétrier disease
↑ TGF-α / EGFR signaling → foveolar (mucous) cell hyperplasia
Giant rugal folds in body/fundus; parietal cell atrophy; protein-losing → hypoalbuminemia, edema
Precancerous; can mimic Zollinger-Ellison on imaging
Gastric MALT lymphoma
Chronic H pylori antigen drives B cells; t(11;18) resists eradication therapy
Marginal zone B-cell lymphoma
Early disease regresses after H pylori eradication
Gastric carcinoid (type 1)
Autoimmune gastritis → chronic hypergastrinemia → ECL cell hyperplasia
Small, multiple, usually indolent neuroendocrine tumors
Gastrin is trophic to ECL cells

Mechanism — two chronic gastritides

H pylori in antrum
→
↓ D cells (somatostatin)
→
↑ Gastrin, ↑ acid
→
Duodenal ulcer
Anti-parietal T cellsBody/fundus
→
No acid, no IF
→
↑↑ GastrinECL hyperplasia → carcinoid
B12 deficiencyMegaloblastic anemia, SCD

Long-standing pangastritis → atrophy → intestinal metaplasia → dysplasia → intestinal-type adenocarcinoma.

H pylori vs autoimmune gastritis

FEATURE
H PYLORI
AUTOIMMUNE
Location
Antrum (first)
Body + fundus
Acid
↑ (antral) or ↓ (pangastritis)
↓↓ achlorhydria
Gastrin
Normal or ↑
↑↑
B12
Usually normal
↓ (no IF)
Risks
Ulcer, adenocarcinoma, MALT
Adenocarcinoma, carcinoid
Diagnosis
Urea breath test, stool antigen, biopsy
Antibodies, ↑ gastrin, low B12
Treat H pylori
PPI + clarithromycin + amoxicillin (metronidazole if penicillin-allergic) · or bismuth quadruple therapy · confirm eradication with breath test or stool antigen.

How it's tested

COMMON CONFUSIONCurling = burns (hypovolemia, ischemia). Cushing = brain injury (vagal stimulation, more acid). Both are stress ulcers.
THE TRAPVery high gastrin doesn't always mean a gastrinoma. With low acid (autoimmune gastritis, PPIs), gastrin rises as a normal response. Check gastric pH.
YOUR APPROACHLocation (antrum vs body) + acid level + gastrin + B12 + antibodies separate the chronic gastritides. Then name the complication.

If you see… think…

Long-term ibuprofen, coffee-ground emesis → acute erosive gastritis (↓ PGE₂)
Upper GI bleeding three days after major burns → Curling ulcer
Bleeding gastric ulcer after a head injury → Cushing ulcer
Antral gastritis with lymphoid follicles and curved rods → H pylori
Positive urea breath test → active H pylori infection
Achlorhydria, ↑ gastrin, anti-IF antibodies, glossitis → autoimmune gastritis
Autoimmune gastritis + small multiple gastric nodules → ECL-cell carcinoid
Giant rugal folds + hypoalbuminemia + edema → Ménétrier disease
Gastric lymphoma that regresses after antibiotics → MALT lymphoma
Bile-stained gastric mucosa after Billroth II → chemical (reflux) gastropathy