Gastritis, Gastric Cancers, and Submucosal Tumors

• Audio chapter
  Single-voice audio, listen on the commute.
• ABIM-format MCQs
  5-option vignettes with full wrong-answer teaching.
• Study guide
  Tables, decision trees, primary sources.
• AI tutor
  Chapter-grounded, answers the question you're stuck on.

What this chapter covers

• Section 7.1: Autoimmune atrophic gastritis and pernicious anemia

  Autoimmune atrophic gastritis is the prototype of chronic non-H. pylori gastritis, and the entire phenotype falls out of one sentence about anatomy: autoimmune destruction of parietal cells is corpus-predominant and antral-sparing, and every downstream manifestation tracks the location of the lesion.

• Section 7.2: H. pylori cancer precursor cascade and Menetrier disease

  Chronic gastritis from H. pylori does not become gastric cancer overnight.

• Section 7.3: Zollinger-Ellison syndrome

  Zollinger-Ellison syndrome is the gastrin-driven ulcer disease that masquerades as refractory peptic ulcer disease.

• Section 7.4: Gastric adenocarcinoma

  The Lauren classification divides gastric adenocarcinoma into two histologic types.

• Section 7.5: MALT lymphoma and gastric DLBCL

  Gastric lymphoma accounts for less than 5 percent of gastric neoplasms, and the two main types are managed very differently from the first decision.

• Section 7.6: Gastric NETs (carcinoid)

  Gastric neuroendocrine tumors arise from enterochromaffin-like (ECL) cells in the body and fundus or from enterochromaffin cells.

• Section 7.7: GIST

  Gastrointestinal stromal tumor is the GI cancer where the driver mutation determines drug selection.

Podcast episodes

1. 01

   Gastritis and Gastric Cancers: Acid and Atrophy

   Every patient here is read through what has happened to acid. Autoimmune gastritis destroys body parietal cells and spares the antrum, so iron deficiency comes before B12 deficiency, gastrin runs high, and type one neuroendocrine tumors can form. Separately labeled antral and body biopsies, antibodies, and H. pylori testing confirm it, and B12 and iron are replaced. Intestinal metaplasia after H. pylori is eradicated, staged with OLGIM, and surveyed by stage and risk modifiers. Zollinger-Ellison syndrome is proven by gastrin with pH, then localized and treated, with MEN1 changing the plan. Menetrier disease ends the episode with giant folds and low acid.

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2. 02

   Gastric Tumors: Diagnosis and Drug Choice

   Every gastric tumor in this episode is sorted by one feature that sets its treatment. For adenocarcinoma it is the Lauren type, signs of spread, and the molecular profile that picks the drug. For lymphoma it is MALT versus large cell, and the t(11;18) result that predicts whether H. pylori eradication will work. For neuroendocrine tumors it is the gastrin and gastric pH that define type one, two, or three. For GIST it is endoscopic ultrasound, risk by size, mitoses, site, and rupture, and the mutation that chooses imatinib or another drug. The episode closes with the traps the boards set.

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Key topics

• ·Autoimmune atrophic gastritis and pernicious anemia
• ·Why iron deficiency precedes B12 deficiency
• ·Sydney protocol biopsies and serologic markers
• ·B12 and iron replacement and type one gastric NETs
• ·H. pylori and the path to intestinal-type cancer
• ·Eradication and test of cure
• ·OLGA and OLGIM staging and surveillance
• ·Zollinger-Ellison syndrome and the secretin test
• ·Gastrinoma localization and MEN1
• ·Menetrier disease
• ·Intestinal versus diffuse gastric adenocarcinoma
• ·Signs of metastatic spread on exam
• ·Staging with endoscopic ultrasound, CT, and laparoscopy
• ·Molecular profiling for HER2, PD-L1, MMR, and claudin
• ·Endoscopic, perioperative, and surgical management
• ·Linitis plastica and CDH1 testing
• ·Gastric MALT lymphoma and H. pylori eradication
• ·Diffuse large B-cell lymphoma and R-CHOP
• ·Gastric neuroendocrine tumor types by gastrin and pH
• ·GIST diagnosis, risk, and mutation-directed therapy