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- 1. Pathology ofPathology of The Stomach - 2The Stomach - 2 Dr.CSBR.Prasad, M.D., May-2015-CSBRP
- 2. Gastric Polyps and Tumors • Polyps, nodules or masses that project above the level of the surrounding mucosa • Polyps may develop as a result of: – Epithelial or stromal cell hyperplasia – Inflammation – Ectopia or – Neoplasia May-2015-CSBRP
- 3. Gastric Polyps and Tumors • Most common are inflammatory or hyperplastic polyps (70%) • 50 and 60 years of age • In association with chronic gastritis Note: Because the risk of dysplasia correlates with size, polyps larger than 1.5 cm should be resected and examined histologically May-2015-CSBRP
- 4. Morphology Gross: • Less than 1 cm in diameter • Often multiple • Ovoid in shape and have a smooth surface Microscopically, polyps have: • Irregular, cystically dilated, and elongated foveolar glands • Lamina propria is typically edematous • Variable acute and chronic inflammation and • Surface ulceration may be present May-2015-CSBRP
- 5. FIGURE 17-16 Gastric polyps. A, Hyperplastic polyp containing corkscrew-shaped foveolar glands. B, Hyperplastic polyp with ulceration. C, Fundic gland polyp composed of cystically dilated glands lined by parietal, chief, and foveolar cells. D, Gastric adenoma recognized by the presence of epithelial dysplasia. Gastric polyps May-2015-CSBRP
- 6. FUNDIC GLAND POLYPS • Sporadic • FAP (familial adenomatous polyposis) • Secondary to proton pump inhibitor Tx • More common in females • CF: Nausea, Vomiting or Epigastric pain May-2015-CSBRP
- 7. ADENOMAS Definition (WHO): “A circumscribed benign neoplasm composed of tubular and / or villous structures lined by dysplastic epithelium" May-2015-CSBRP
- 8. ADENOMAS • Uncommon neoplasms in the stomach • Common in Japanese • They are almost always antral Background: – FAP syndrome – Sporadically, (chronic atrophic gastritis) Clinical Features: Asymptomatic - accidentally discovered during endoscopy May-2015-CSBRP
- 9. ADENOMAS Gross Findings: • Sessile / Pedunculated • Solitary / Multiple May-2015-CSBRP
- 11. ADENOMAS Microscopic Findings: • Arise within the surface and superficial pit epithelia • Abnormal neoplastic epithelium is usually confined to the superficial mucosa • The mid-mucosa contains cysts • Architectural classification (WHO): Patterns: – Tubular – Villous & – Tubulovillous May-2015-CSBRP
- 14. TUBULAR ADENOMA & VILLOUS ADENOMA May-2015-CSBRP
- 15. Dysplasias Two types of dysplastic epithelium: • The intestinal type • The gastric type Note: These types of dysplasias can occur in adenomas and also in the flat mucosa May-2015-CSBRP
- 16. INTESTINAL TYPE DYSPLASIA LOW GRADE / HIGH GRADE May-2015-CSBRP
- 17. GASTRIC TYPE DYSPLASIA LOW GRADE / HIGH GRADE May-2015-CSBRP
- 18. Malignant potential of Adenomas • Adenomas <1cm - no malignant potential • Adenomas >4cms - high malignant potential • Adenomas with prominent villous component – more malignant potential May-2015-CSBRP
- 19. CaseCase: Identify the abnormality. Give your differentials. Marcos Duarte Siosaki, M.D., and Ana Tarsila Souza, M.D. N Engl J Med 2013; 368:e7February 7, 2013 DOI: 10.1056/NEJMicm1204740
- 20. Diagnosis: • Supraclavicular mass - Virchow’s node • Gatric primary (Gastric carcinoma) May-2015-CSBRP
- 21. CaseCase: Identify the abnormality. Give your differentials. Marcos Duarte Siosaki, M.D., and Ana Tarsila Souza, M.D. N Engl J Med 2013; 368:e7February 7, 2013 DOI: 10.1056/NEJMicm1204740 Virchow's node or Troisier's node
- 23. Carcinoma of the stomach is one of the most common neoplasms in the world, and most are adenocarcinomas May-2015-CSBRP
- 24. Gastric Adenocarcinoma Def: Malignant epithelial tumor with glandular differentiation May-2015-CSBRP
- 25. Incidence • High in Japan (80 cases per 100,000), Costa Rica, Columbia, Chile, and Finland • Very low in Thailand and many parts of Africa May-2015-CSBRP
- 26. Pathogenesis Dietary Factors: – High salt consumption – Low intake of fresh fruits / vegetables – Smoking / Alcohol – Nitrosamines – Trace elements: selenium, zinc, copper, iron, and manganese (part of antioxidants) Genetic Factors • Blood group A • Gastric carcinomas display some of the same genetic alterations observed in other carcinomas May-2015-CSBRP
- 27. Pathogenesis Gastric carcinomas display some of the same genetic alterations observed in other carcinomas: – mutations in CDH1, which encodes E-cadherin (50% of sporadic cases) – BRCA2 mutations – Microsatellite instability – p53 mutations – hypermethylation of several genes: • TGFβRII • BAX • IGFRII and • p16/INK4a • Tumor invasion and metastasis: The synchronous expression of EGF, TGF-alpha and ras p21 • Poorly differentiated gastric carcinomas resulting in linitis plastica: overexpression of TGF-beta, IGF, and PDGF May-2015-CSBRP
- 28. May-2015-CSBRP
- 29. Pathogenesis Predisposing Conditions: • H. pylori infection • Atrophic gastritis • Subtotal gastrectomy with gastrojejunal anastomosis • Immunodeficiency syndromes • Chronic gastric ulcers and • Menetrier's disease Severe Atrophic Gastritis and Intestinal Metaplasia - by far the most important precursor lesions of gastric carcinoma May-2015-CSBRP
- 30. Pathogenesis - H. pylori infection May-2015-CSBRP
- 31. Pathogenesis - H. pylori infection • Cag genes (IL-8 - severe gastritis) • Vac A (epithelial cell damage) • fldA gene (MALTOMA) • H.pylori adhere to Lewis blood group antigen May-2015-CSBRP
- 32. Clinical features • Mean age of presentation is 55 years • M:F = 2:1 • Pain abdomen, unrelieved by food • Anorexia • Weight loss • Gastric outlet obstruction • Virchow's node • Sister Mary Joseph’s nodule May-2015-CSBRP
- 33. Gastric Adenocarcinoma Two major subtypes: 1. Early gastric cancer and 2. Advanced gastric cancer 1. Early gastric carcinoma - which is confined to the mucosa and submucosa, with / without lymph node metastases 2. Advanced gastric cancers - cancers that have invaded into or beyond the muscularis propria, with / without lymph node metastases May-2015-CSBRP
- 34. EARLY & ADVANCED GASTRIC CARCINOMA May-2015-CSBRP
- 40. May-2015-CSBRP
- 41. • Although overall incidence of gastric adenocarcinoma is falling, cancer of the gastric cardia is on the rise • This is probably related to: – Barrett esophagus, chronic GERD and – Obesity May-2015-CSBRP
- 42. Classifications for the gross appearance of gastric carcinoma • There are a number of classifications. The most widely adopted is that of Borrmann • Gastric carcinomas are subdivided into four types: – Type I for the well-circumscribed polypoid lesions – Type II for polypoid tumors with marked central ulceration – Type III for the ulcerated tumors with infiltrative margins and – Type IV for the linitis plastica • The main value of Borrmann's classification is that it eliminates the need of excessive verbal description of the gross appearance of the tumor May-2015-CSBRP
- 43. Gastric adenocarcinoma. A, Intestinal-type adenocarcinoma. B, Linitis plastica. May-2015-CSBRP
- 44. FIGURE 17-18 Gastric adenocarcinoma. A, Intestinal-type adenocarcinoma composed of columnar, gland-forming cells infiltrating through desmoplastic stroma. B, Signet-ring cells can be recognized by their large cytoplasmic mucin vacuoles and peripherally displaced, crescent-shaped nuclei. May-2015-CSBRP
- 45. Gastric carcinoma Prognostic indicators: • The depth of invasion and • The extent of nodal and distant metastasis • Virchow's node • Sister Mary Joseph’s nodule • Krukenberg’s tumor May-2015-CSBRP
- 46. Virchow's node Marcos Duarte Siosaki, M.D., and Ana Tarsila Souza, M.D. N Engl J Med 2013; 368:e7February 7, 2013 DOI: 10.1056/NEJMicm1204740 May-2015-CSBRP
- 47. Sister Mary Joseph’s nodule Sister Mary Joseph first noticed that a 'nodule' in the umbilicus was often associated with advanced malignancy May-2015-CSBRP
- 50. Complications • Bleeding / anemia • Perforation • Mets and associated complications May-2015-CSBRP
Editor's Notes
- FIGURE 17-16 Gastric polyps. A, Hyperplastic polyp containing corkscrew-shaped foveolar glands. B, Hyperplastic polyp with ulceration. C, Fundic gland polyp composed of cystically dilated glands lined by parietal, chief, and foveolar cells. D, Gastric adenoma recognized by the presence of epithelial dysplasia.
- Adenomas are uncommon neoplasms in the stomach, in contrast to the colon where they are frequent. Sporadically, especially in one of the forms of chronic atrophic gastritis. Adenomas are almost always antral; they rarely arise in the body mucosa, even when it is atrophic. Clinical Features: Adenomas, much like other gastric polyps, produce no symptoms - they are accidentally discovered during endoscopy
- SMALL SESSILE TUBULAR ADENOMA The superficial half of the mucosa is the adenoma, with its darkly staining dysplastic epithelium. The basal half is residual antral mucosa with a few cystic tubules. This adenoma was only slightly elevated above the surrounding nondysplastic mucosa.
- Small sessile tubular adenoma in which many of the tubules extend from surface to base and appear elongated.
- The villous pattern has elongated cores of attenuated lamina propria covered by dysplastic epithelium. n gastric villous adenomas, in contrast to those in the colon, the villi often have a papillary modification in which multiple branches arise from the surface villi.
- LARGE TUBULAR ADENOMA In contrast to figure 10-3, the tubules here appear mainly as cross sectional profiles. VILLOUS ADENOMA The mucosa has been converted into a series of parallel elongated structures or villi that are covered by dysplastic epithelium. Pure tubular adenomas tend to be broad sessile lesions, while villous and tubulovillous adenomas are more likely to be dome shaped or pedunculated. This is different from the colon where pure tubular adenomas are the most common pedunculated adenomas, while predominantly villous adenomas are usually sessile.
- INTESTINAL TYPE DYSPLASIA, LOW GRADE
- INTESTINAL TYPE DYSPLASIA, LOW GRADE : This epithelium is identical to that in many colorectal adenomas. The cells are elongated, as are their nuclei. The nuclei are stratified, but the stratification is mostly confined to the basal half of the cells. There is no nuclear pleomorphism. Small mucus vacuoles within dysplastic goblet cells are present in the luminal cytoplasm of many cells.
- GASTRIC OR FOVEOLAR CELL TYPE DYSPLASIA, LOW GRADE Top: The cells are columnar, but less so than in the intestinal type in figure 10-8. Many cells contain apical mucin vacuoles. The nuclei are oval to round, and many have small nuclei. Nuclear stratification is limited to the basal half of the epithelium. (Hematoxylin and eosin stain) Bottom: Many of the cells have small apical neutral mucin vacuoles that stain red with periodic acid- Schiff, but there is no staining with Alcian blue. (Alcian blue/ PAS stain)
- IMAGES IN CLINICAL MEDICINE Virchow&apos;s Node Marcos Duarte Siosaki, M.D., and Ana Tarsila Souza, M.D. N Engl J Med 2013; 368:e7February 7, 2013DOI: 10.1056/NEJMicm1204740 -------------------------------------------------------------------- A 64-year-old man presented with a 6-month history of epigastric pain, weight loss, and nausea. In the previous 3 months, he had lost 10 kg. On examination, he was noted to have a nontender, firm, fixed, left supraclavicular lymph node measuring 3.0 by 2.5 cm. Upper endoscopy revealed an adenocarcinoma of the gastric corpus. Computed tomography of the abdomen showed liver metastasis. Virchow&apos;s node, or Troisier&apos;s node, refers to carcinomatous involvement of the supraclavicular nodes at the junction of the thoracic duct and the left subclavian vein. Usually, nodal enlargement is caused by metastatic gastric carcinoma, although supraclavicular nodal involvement can also be seen in other gastrointestinal, thoracic, and pelvic cancers. Gastric cancers tend to metastasize to this region by means of migration of tumor emboli through the thoracic duct, where subdiaphragmatic lymphatic drainage enters the venous circulation in the left subclavian vein. Given the patient&apos;s low performance status, according to his Karnofsky performance-status score and his score on the Eastern Cooperative Oncology Group Performance Status scale, chemotherapy was contraindicated, and he was referred for palliative radiotherapy.
- IMAGES IN CLINICAL MEDICINE Virchow&apos;s Node Marcos Duarte Siosaki, M.D., and Ana Tarsila Souza, M.D. N Engl J Med 2013; 368:e7February 7, 2013DOI: 10.1056/NEJMicm1204740 -------------------------------------------------------------------- A 64-year-old man presented with a 6-month history of epigastric pain, weight loss, and nausea. In the previous 3 months, he had lost 10 kg. On examination, he was noted to have a nontender, firm, fixed, left supraclavicular lymph node measuring 3.0 by 2.5 cm. Upper endoscopy revealed an adenocarcinoma of the gastric corpus. Computed tomography of the abdomen showed liver metastasis. Virchow&apos;s node, or Troisier&apos;s node, refers to carcinomatous involvement of the supraclavicular nodes at the junction of the thoracic duct and the left subclavian vein. Usually, nodal enlargement is caused by metastatic gastric carcinoma, although supraclavicular nodal involvement can also be seen in other gastrointestinal, thoracic, and pelvic cancers. Gastric cancers tend to metastasize to this region by means of migration of tumor emboli through the thoracic duct, where subdiaphragmatic lymphatic drainage enters the venous circulation in the left subclavian vein. Given the patient&apos;s low performance status, according to his Karnofsky performance-status score and his score on the Eastern Cooperative Oncology Group Performance Status scale, chemotherapy was contraindicated, and he was referred for palliative radiotherapy.
- In contrast to diffuse gastric tumors, there is an increased risk of intestinal-type gastric cancer in individuals with FAP, particularly in Japan. This implies an interaction between host genetic background and environmental factors, since gastric cancer risk is less markedly elevated in individuals with FAP residing in areas of low gastric cancer incidence. Mutations in β-catenin, a protein that binds to both E-cadherin and adenomatous polyposis coli (APC), as well as microsatellite instability and hypermethylation of several genes including TGFβRII, BAX, IGFRII, and p16/INK4a have also been described in sporadic intestinal-type gastric cancer. Genetic variants of pro-inflammatory and immune response genes, including those that encode IL-1β, TNF, IL-10, IL-8, and Toll-like receptor 4 (TLR4), are associated with elevated risk of gastric cancer when accompanied by H. pylori infection, and p53 mutations are present in the majority of sporadic gastric cancers of both histologic types. Thus, although specific sequences of events have not been defined, it is clear that chronic inflammation promotes neoplastic progression. Amplification of ERBB2 seems to be an indicator of metastatic ability and overexpression of the EGF receptor system is a biologic marker for high malignancy. The synchronous expression of EGF, TGF-alpha and ras p21 is associated with tumor invasion and metastasis, and overexpression of TGF-beta, IGF, and PDGF is associated with collagen synthesis in poorly differentiated gastric carcinomas resulting in linitis plastica . However, further work is needed before the aforementioned findings can be applied to clinical practice.
- Gastric carcinomas display some of the same genetic alterations observed in other carcinomas. These changes include aberrant expression of bcl-2 protein; reduction or dysfunction of cadherin-e and K-sam amplification; point mutation of the ras oncogeneand the p53 tumor suppressor gene, gene amplification of epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), platelet derived growth factor (PDGF), insulin growth factor (IGF), and p185 (ERBB2) gene; and chromosomal loss of heterozygosity in chromosomes 7p, 17p, 1q, and 5q . Some of these genetic and oncogene changes may have prognostic implications. For example, loss of heterozygosity on chromosomes 5q and 17p is associated most commonly with well-differentiated carcinoma, whereas allele loss on chromosomes 1q and 7p may be involved in the progression to less well-differentiated adenocarcinoma. Amplification of ERBB2 seems to be an indicator of metastatic ability and overexpression of the EGF receptor system is a biologic marker for high malignancy. The synchronous expression of EGF, TGF-alpha and ras p21 is associated with tumor invasion and metastasis, and overexpression of TGF-beta, IGF, and PDGF is associated with collagen synthesis in poorly differentiated gastric carcinomas resulting in linitis plastica . However, further work is needed before the aforementioned findings can be applied to clinical practice.
- Gastric carcinomas display some of the same genetic alterations observed in other carcinomas. These changes include aberrant expression of bcl-2 protein; reduction or dysfunction of cadherin-e and K-sam amplification; point mutation of the ras oncogeneand the p53 tumor suppressor gene, gene amplification of epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), platelet derived growth factor (PDGF), insulin growth factor (IGF), and p185 (ERBB2) gene; and chromosomal loss of heterozygosity in chromosomes 7p, 17p, 1q, and 5q . Some of these genetic and oncogene changes may have prognostic implications. For example, loss of heterozygosity on chromosomes 5q and 17p is associated most commonly with well-differentiated carcinoma, whereas allele loss on chromosomes 1q and 7p may be involved in the progression to less well-differentiated adenocarcinoma. Amplification of ERBB2 seems to be an indicator of metastatic ability and overexpression of the EGF receptor system is a biologic marker for high malignancy. The synchronous expression of EGF, TGF-alpha and ras p21 is associated with tumor invasion and metastasis, and overexpression of TGF-beta, IGF, and PDGF is associated with collagen synthesis in poorly differentiated gastric carcinomas resulting in linitis plastica . However, further work is needed before the aforementioned findings can be applied to clinical practice.
- Cag genes are a groups of genes, their products act thru NF-K beta pathway, elaboration of IL-8 by the epithelial cells. Vac A (vacuolating cytotoxin) induces epithelial cell damage
- Early gastric carcinoma is defined as an invasive gastric carcinoma which is confined to the mucosa and submucosa, irrespective of whether lymph node metastases are present. This corresponds to T1 of the TNM classification. Advanced gastric cancers are defined as cancers that have invaded the stomach into or beyond the muscularis propria, irrespective of whether lymph node metastases are present. This corresponds to T2 to T4 of the TNM classification. Growth is usually very slow: it has been estimated that the doubling time is from 555 to 3076 days. However, once the tumor increases in size and invades the submucosa doubling time accelerates to 17 to 90 days. Still, it may take up to 6 years for a tumor of several millimeters to develop. The time interval for early gastric carcinoma to transform into advanced carcinoma is also long but variable, ranging from 6 months to 21 years.
- EARLY GASTRIC CARCINOMA: Scanning power view of histologic section illustrating the thickened elevated mucosa.
- EARLY GASTRIC CARCINOMA: Low- power view of gastric mucosa showing high-grade dysplasia (on the left) adjacent to intramucosal carcinoma. Note the diffuse infiltration of the lamina propria by atypical glandular profiles.
- FIGURE 17-17 Gastric adenocarcinoma. A, Intestinal-type adenocarcinoma consisting of an elevated mass with heaped-up borders and central ulceration. Compare to the peptic ulcer in Figure 17-14A . B, Linitis plastica. The gastric wall is markedly thickened, and rugal folds are partially lost.
- FIGURE 17-18 Gastric adenocarcinoma. A, Intestinal-type adenocarcinoma composed of columnar, gland-forming cells infiltrating through desmoplastic stroma. B, Signet-ring cells can be recognized by their large cytoplasmic mucin vacuoles and peripherally displaced, crescent-shaped nuclei.
- IMAGES IN CLINICAL MEDICINE Virchow&apos;s Node Marcos Duarte Siosaki, M.D., and Ana Tarsila Souza, M.D. N Engl J Med 2013; 368:e7February 7, 2013DOI: 10.1056/NEJMicm1204740 -------------------------------------------------------------------- A 64-year-old man presented with a 6-month history of epigastric pain, weight loss, and nausea. In the previous 3 months, he had lost 10 kg. On examination, he was noted to have a nontender, firm, fixed, left supraclavicular lymph node measuring 3.0 by 2.5 cm. Upper endoscopy revealed an adenocarcinoma of the gastric corpus. Computed tomography of the abdomen showed liver metastasis. Virchow&apos;s node, or Troisier&apos;s node, refers to carcinomatous involvement of the supraclavicular nodes at the junction of the thoracic duct and the left subclavian vein. Usually, nodal enlargement is caused by metastatic gastric carcinoma, although supraclavicular nodal involvement can also be seen in other gastrointestinal, thoracic, and pelvic cancers. Gastric cancers tend to metastasize to this region by means of migration of tumor emboli through the thoracic duct, where subdiaphragmatic lymphatic drainage enters the venous circulation in the left subclavian vein. Given the patient&apos;s low performance status, according to his Karnofsky performance-status score and his score on the Eastern Cooperative Oncology Group Performance Status scale, chemotherapy was contraindicated, and he was referred for palliative radiotherapy.
- Sister Mary Joseph first noticed that a &apos;nodule&apos; in the umbilicus was often associated with advanced malignancy. She drew William James Mayo’s attention to this sign and he published an article about it in 1928, referring to is as the &quot;pants button umbilicus&quot;. In 1949 the English surgeon Hamilton Bailey (1894-1961), in his famous textbook &quot;Physical Signs in Clinical Surgery&quot;, in 1949 coined the term &quot;Sister Joseph&apos;s nodule&quot; for an umbilical metastasis.