pathology of the stomach-part 2 · gastric adenocarcinoma u 90% of all gastric cancers. u early...
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Pathology of the stomach-part 2
Manar Hajeer, md, FRCPath
University of Jordan, School of medicine
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Peptic Ulcer Diseaseu Most often is associated with H. pylori infection or NSAID useu Imbalance between mucosal defenses and damaging forces.
u In USA, NSAID is becoming the most common cause of gastric ulcers: as H.pylori infection is falling and increased use of low-dose aspirin in aged population.
u Any portion of the GIT exposed to acidic gastric juicesu Most common in gastric antrum, first part of duodenum.u Esophagus in (GERD) or ectopic gastric mucosa (Meckel
diverticulum)
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Pathogenesisu More than 70% of PUD cases are associated with H. pylori infection
u Only 5 -10% of H. pylori–infected individuals develop ulcers.
u Gastric acid is fundamental in pathogenesis.
u Cofactors: smoking, chronic NSAIDs, high-dose corticosteroids, alcoholic cirrhosis, COPD, CRF, hyperparathyroidism.
u Hyperacidity is caused by:
u H. pylori.
u Parietal cell hyperplasia.
u Excessive secretory response (vagal)
u Hypergastrinemia as in Zollinger-Ellison syndrome
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Zollinger-Ellison syndrome
u Multiple peptic ulcerationsu Stomach , duodenum, even jejunumu Caused by uncontrolled release of gastrin by a tumor
(gastrinoma) and the resulting massive acid production.
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MORPHOLOGY
u 4:1, proximal duodenum : stomach.u Anterior duodenal wallu >80% solitary.u Round to oval, sharply punched-out defectu Base of ulcers is smooth and cleanu Granulation tissue.u Hemorrhage & Perforation are complications.
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Robbins Basic Pathology 10th edition
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Duodenal ulcer
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Clinical Features
u Epigastric burning or aching painu Pain 1 to 3 hours after meals at daytimeu Worse at night, relieved by alkali or foodu Nausea, vomiting, bloating, bletching.u Iron deficiency anemia, frank hemorrhage, or perforation.
u Current therapies are aimed at H.pylori eradication.u Surgery reserved for complications.
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GASTRIC POLYPS AND TUMORSu Gastric Polyps:u Inflammatory and Hyperplastic Polyps
u Gastric Adenoma
u Gastric Adenocarcinomau intestinal and diffuse types
u Lymphomau MALToma.
u Neuroendocrine (Carcinoid) Tumoru Gastrointestinal Stromal Tumor
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Gastric polyps
u Polyps: masses projecting above the level of adjacent mucosau Epithelial or stromal cell hyperplasia, inflammation, ectopia, or
neoplasia.
u Inflammatory and Hyperplastic Polypsu 75% of all polyps.u Arise in a background of chronic gastritisu Regress after H.pylori eradication.u Risk of dysplasia if size > 1.5 cm.
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Gastric Adenoma
u 10% of all polyps.
u Increase with age.u M:F = 3:1u Background of chronic gastritis, atrophy and intestinal metaplasia.
u Dysplasia in all cases, low- or high-grade.u Risk of adenocarcinoma related to the size ( greatest if > 2cm).
u Risk of carcinoma higher than colonic adenoma.u 30% have concurrent CA.
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Gastric adenoma
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Gastric Adenocarcinoma
u 90% of all gastric cancers.
u Early symptoms mimic gastritis >>> late diagnosis.
u Rates vary markedly with geography (Japan, Costa Rica, Chile).
u Screening >> early detection.
u Background of mucosal atrophy and intestinal metaplasia.
u PUD does not increase risk, except after surgery
u In USA rates dropped > 85%, BUT increased rate of cardia cancer due to GERD & obesity.
u Two main types: intestinal and diffuse.
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Pathogenesis
u Genetic alterations due to H.pylori associated chronic gastritis , lesser extent EBV (10%).
u Most cases are sporadic.
u Familial cases: mutations in CDH1 (E-cadherin) >> diffuse type.
u Sporadic diffuse type Ca: CDH1 mutation in 50%.
u FAP: APC gene mutation, intestinal type cancer.
u Sporadic intestinal-type Ca: B catenin mutation
u P53 mutation in sporadic cancer of both types.
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MORPHOLOGY
u Lauren classification: separates gastric cancers into intestinal and diffuse types.
u Intestinal type:
u Bulky.
u Exophytic mass or ulcer.
u Form glands.
u Diffuse gastric cancers
u Infiltrative growth pattern
u Discohesive cells (signet ring cells)
u Desmoplastic reaction (thick wall, linitis plastic).
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Intestinal type
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Intestinal type
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Linitis plastica
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Signet ring cells:large mucin vacuoles that expand the cytoplasm and push the nucleusto the periphery,
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Diffuse type, signet ring cells
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Clinical Features
u Intestinal-type gastric cancer
u High-risk areas
u Develops from precursor (adenoma, dysplasia)
u Mean age 55 yrs.
u M:F 2:1
u Diffuse type gastric cancer:
u Incidence uniform across countries.
u No precursor lesion.
u M:F 1:1
u Younger age.
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u The drop in gastric cancer incidence applies only to the intestinal type.
u Incidences of intestinal and diffuse types are now similar in some regions.
u Most powerful prognostic factors: depth of invasion & extent of nodal and distant metastasis at the time of diagnosis
u Most cases Dx at advanced stage.
u 5 year survival 90% to 20% for early and advanced tumors, respectively.
u Tx: surgery, chemotherapy, targeted Tx (anti HER2)
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Lymphoma
u Stomach is the most common site of extranodallymphoma.
u 5% of all gastric malignancies.
u Most common type : indolent extranodal marginal zone B-cell lymphomas (MALToma)
u Second most common lymphoma: diffuse large B cell lymphoma
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Neuroendocrine (Carcinoid) Tumor
u Tumors arising from neuroendocrine-differentiated gastrointestinal epithelia (e.g., G cells).
u > 40% occur in the small intestine.
u Associated with endocrine cell hyperplasia, chronic atrophic gastritis, and Zollinger- Ellison syndrome
u Slower growing than carcinomas.
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Intramural or submucosal masses (small polypoid lesions)
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Islands, trabeculae, strands, glands, or sheets of uniformcells with scant, pink granular cytoplasm and salt and pepper chromatin.
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carcinoid syndrome
u Due to vasoactive substances
u Seen in 10% of cases.
u strongly associated with metastatic disease.
u Cutaneous flushing, sweating, bronchospasm, colicky abdominal pain, diarrhea, and right-sided cardiac valvular fibrosis