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Gastric tumors

Gastric tumors

Gastric tumors

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Benign & Precursor Lesions - Tummy Bumps & Worries

Endoscopic view of gastric polyp with ulceration

  • Hyperplastic Polyps: Most common (~75%). Inflammatory proliferation, often with H. pylori gastritis. Low malignant potential.
  • Fundic Gland Polyps: Associated with PPI use; sporadic. Cystically dilated glands. No malignant potential.
  • Adenomatous Polyps: True neoplasms. Malignant potential ↑ with size (>2 cm) and villous features. Precursor to adenocarcinoma.
  • Chronic Gastritis: H. pylori drives progression: Atrophy → Intestinal Metaplasia → Dysplasia → Cancer.

⭐ Most intestinal-type gastric adenocarcinomas arise from precursor lesions, particularly adenomas and chronic gastritis-induced intestinal metaplasia.

Gastric Adenocarcinoma I - The Cancerous Crater

  • Most common stomach cancer, with high rates in East Asia. Major risk factors include chronic H. pylori infection, dietary nitrosamines (smoked foods), smoking, and Blood Type A.

Gastric adenocarcinoma with ulcerated crater

  • Lauren Classification:
FeatureIntestinal TypeDiffuse Type (Linitis Plastica)
AppearanceForms bulky, ulcerating masses; glandular.Infiltrates wall; signet ring cells. Thickened, leathery appearance.
PathogenesisLinked to H. pylori, intestinal metaplasia.Not associated with H. pylori; CDH1/E-cadherin mutation.
PrognosisBetter; hematogenous spread.Worse; early transmural/lymphatic spread.

Gastric Adenocarcinoma II - Spotting the Stomach Sneak

  • Morphology & Location
    • Linitis Plastica: Diffuse infiltration of the stomach wall, creating a rigid, leather bottle appearance. Poor prognosis.
    • Ulcerated: Large, irregular ulcer with heaped-up margins.
    • Most common on the lesser curvature of the antrum.

Linitis plastica gross specimen with thickened stomach wall

  • Clinical & Paraneoplastic Signs

    • Weight loss, abdominal pain, early satiety.
    • Acanthosis Nigricans: Velvety, hyperpigmented plaques in flexural areas.
    • Leser-Trélat Sign: Sudden eruption of multiple seborrheic keratoses.
  • Metastatic Spread

    • Virchow Node: Left supraclavicular node.
    • Sister Mary Joseph Nodule: Periumbilical subcutaneous nodule.
    • Krukenberg Tumor: Bilateral ovarian metastasis.

⭐ The Leser-Trélat sign, the abrupt appearance of numerous seborrheic keratoses, is a dramatic cutaneous marker strongly associated with an underlying gastric adenocarcinoma.

Other Gastric Tumors - The Stomach's Oddballs

GIST: Gross and Microscopic Pathology

TumorOrigin / CellKey Association / MutationTreatment
Gastric Lymphoma (MALToma)MALT tissue (B-cells)Chronic H. pylori infectionEradicate H. pylori (first-line)
GISTInterstitial Cells of Cajalc-KIT (CD117) gene mutationImatinib (tyrosine kinase inhibitor)
Carcinoid TumorNeuroendocrine (ECL) cellsChronic atrophic gastritis, hypergastrinemiaSurgical resection

High‑Yield Points - ⚡ Biggest Takeaways

  • H. pylori is the strongest risk factor for both gastric adenocarcinoma and MALT lymphoma.
  • Intestinal-type adenocarcinoma is common and gland-forming; diffuse-type has signet ring cells causing linitis plastica.
  • Metastatic signs: Virchow's node (supraclavicular), Krukenberg tumor (ovarian), and Sister Mary Joseph nodule (periumbilical).
  • Gastrointestinal Stromal Tumors (GISTs) arise from the interstitial cells of Cajal and are c-KIT (CD117) positive.
  • MALT lymphomas may regress completely with H. pylori eradication.

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