ca gall bladder ; adenoca stomach

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  • 1.CARCINOMA OF THEGALLBLADDER

2. INTRO Most common malignancy of the extrahepaticbiliary tract Slightly more common in women Occurs most frequently in the seventh decade oflife Mean 5-year survival rate has remained for manyyears at about 5% to 12% despite surgicalintervention 3. The most common sites of involvement are thefundus and the neck; about 20% involve the lateralwalls. 4. ETIOLOGY The most important risk factor associated withgallbladder carcinoma is gallstones (cholelithiasis),which are present in 95% of cases However, it should be noted that only 0.5% ofpatients with gallstones develop gallbladder cancerafter twenty or more years 5. Carcinogenic derivatives of bile acids are believedto play a role. Genetic factors Previous surgery on the biliary tract IBD 6. MORPHOLOGY Carcinomas of the gallbladder show two patterns ofgrowth: infiltrating and exophytic 7. The infiltrating pattern is more common and usuallyappears as a poorly defined area of diffuse thickeningand induration of the gallbladder wall that may coverseveral square centimeters or may involve the entiregallbladder. Deep ulceration can cause direct penetration of thegallbladder wall or fistula formation to adjacent viscerainto which the neoplasm has grown. These tumors are scirrhous and have a very firmconsistency 8. The exophytic pattern grows into the lumen as anirregular, cauliflower mass but at the same timeinvades the underlying wall. The luminal portion may be necrotic, hemorrhagic,and ulcerated 9. The opened gallbladder contains a large, exophytic tumorthat virtually fills the lumen 10. HISTOLOGY Most carcinomas of the gallbladder areadenocarcinomas. Some of the carcinomas are papillary inarchitecture and are well to moderatelydifferentiated; others are infiltrative and poorlydifferentiated to undifferentiated About 5% are squamous cell carcinomas or haveadenosquamous differentiation 11. NORMAL ADENOCARCINOMA 12. Malignant glandular structures Papillary patternare present within a denselyfibrotic gallbladder wall. 13. By the time these neoplasms are discovered, mosthave invaded the liver centrifugally, and manyhave extended to the cystic duct and adjacent bileducts and portal-hepatic lymph nodes. The peritoneum, gastrointestinal tract, and lungsare common sites of seeding. 14. GASTRIC ADENOCARCINOMA 15. INTRO Adenocarcinoma is the most common malignancyof the stomach, comprising over 90% of all gastriccancers Early symptoms resemble those of chronic gastritis.As a result, these tumors are often discovered atadvanced stages, 16. EPIDEMIOLOGY Gastric cancer incidence varies markedly withgeography The cause of the overall reduction in gastric canceris unknown. 17. One possible explanation is the decreasedconsumption of dietary carcinogens, such as N-nitroso compounds and benzopyrene, because ofreduced use of salt and smoking for foodpreservation and the widespread availability offood refrigeration. Conversely, intake of green, leafy vegetables andcitrus fruits, which contain antioxidants such asvitamin C, vitamin E, and beta-carotene, and iscorrelated with reduced risk of gastric cancers,may have increased as a result of improved foodtransportation networks. 18. Gastric cancer is more common in lowersocioeconomic groups and in individuals withmultifocal mucosal atrophy and intestinalmetaplasia. PUD does not impart an increased risk of gastriccancer, but patients who have had partialgastrectomies for PUD have a slightly higher risk ofdeveloping cancer in the residual gastric stump asa result of hypochlorhydria, bile reflux, and chronicgastritis. 19. Although overall incidence of gastricadenocarcinoma is falling, cancer of the gastriccardia is on the rise. This is probably related to Barrett esophagus andmay reflect the increasing incidence of chronicGERD and obesity. 20. ETIOPATHOGENESIS Helicobacter Pylori Infection: Chronic H. pylori infection is the most important cause ofdistal gastric adenocarcinoma It commonly generates chronic gastritis, and over severaldecades may induce mucosal atrophy, which in somepatients precedes the development of cancer . Bacterial virulence factors, such as CagA and Vac A(vacuolating enzyme), play an important role in the severityof gastritis and intestinal metaplasia 21. Dietary and Lifestyle Factors: Smoking and dietary habits (high intake of salt-preservedand/or smoked foods) also play a role in increasing cancerrisk, either individually or by compounding the role of H.pylori infection Genetic Susceptibility Some individuals are at increased risk of developing gastriccancer, as well as other malignancies, because ofdominantly inherited cancer predisposition syndromes, suchas FAP, Lynch syndrome, and Li-Fraumeni syndrome .Patients with Peutz-Jeghers are also at risk for developinggastric cancers 22. Hereditary Diffuse Gastric Cancer (HDGC): Familial diffuse gastric cancer with autosomal dominantinheritance, caused by germline mutation of E-cadherin(CDH1), is a recently reported syndrome Precursor Lesions Whether in H. pylori-associated chronic gastritis orautoimmune gastritis, atrophy followed by intestinalmetaplasia develops over time, beginning a sequence ofevents that may culminate in neoplasia, particularlyadenocarcinoma of tubular type. 23. Gastric Polyps: Various polypoid lesions have thepotential to develop into adenocarcinoma Adenomatous Polyps: The risk of malignant transformation isrelated to size (>2 cm) and the presence of high-gradeintraepithelial neoplasia/dysplasia Non-neoplastic Polyps: Hyperplastic polyps and raresyndromic examples, as well as hamartomatous polyps thatgenerally occur as part of hereditary polyposis syndromes(Peutz-Jeghers polyp, juvenile polyp, Cronkhite-Canadasyndrome-associated polyp), also may undergo malignanttransformation 24. MORPHOLOGY Most gastric adenocarcinomas involve the gastricantrum; the lesser curvature is involved more oftenthan the greater curvature Gastric tumors with an intestinal morphology tend toform bulky tumors composed of glandularstructures , while cancers with a diffuse infiltrativegrowth pattern are more often composed of signet-ring cells 25. Gastric adenocarcinoma. Intestinal-type adenocarcinomaconsisting of an elevated mass with heaped-up borders andcentral ulceration. 26. NORMAL HISTOLOGY 27. Gastric adenocarcinoma. Intestinal-type adenocarcinomacomposed of columnar, gland-forming cells infiltrating throughdesmoplastic stroma. 28. When there are large areas of infitration, diffuserugal flattening and a rigid, thickened wall mayimpart a leather bottle appearance termed linitisplastica Breast and lung cancers that metastasize to thestomach may also create a linitis plasticalikeappearance. 29. Linitis plastica. The gastric wall is markedly thickened, andrugal folds are partially lost. 30. Signet-ring cells can be recognized by their largecytoplasmic mucin vacuoles and peripherally displaced,crescent-shaped nuclei. 31. CLINICAL FEATURES Intestinal-type gastric cancer predominates in high-risk areas and develops from precursor lesionsincluding flat dysplasia and adenomas. The meanage of presentation is 55 years, and the male-to-female ratio is 2 : 1. In contrast, the incidence of diffuse gastric cancer isrelatively uniform across countries, there are noidentified precursor lesions, and the disease occursat similar frequencies in males and females. 32. The depth of invasion and the extent of nodal anddistant metastasis at the time of diagnosis remainthe most powerful prognostic indicators for gastriccancer 33. In advanced cases gastric carcinoma may first bedetected as metastases to the supraclavicularsentinel lymph node, also called Virchows node. Gastric tumors can also metastasize to theperiumbilical region to form a subcutaneousnodule, termed a Sister Mary Joseph nodule, afterthe nurse who first noted this lesion as a marker ofmetastatic carcinoma. 34. Local invasion into the duodenum, pancreas, andretroperitoneum is also characteristic. In such casesefforts are usually focused on chemotherapy orradiation therapy and palliative care 35. Surgical resection remains the preferred treatmentfor gastric adenocarcinoma. After surgical resection, the 5-year survival rate ofearly gastric cancer can exceed 90%, even iflymph node metastases are present. In contrast, the5-year survival rate for advanced gastric cancerremains below 20% 36. THANK YOU ..