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Ca esophagus
Risk factors- Alcohol, tobacco, smoking Dietary-low intake of vitamin A&C riboflavin, fresh fruits and vegetables China-pickled vegetables Barretts esophagus Incidence-10% of all GI cancers 80% -SCC 20%-adenoCa Site: Located in the middle 1/3 rd or distal esophagus.
Early eso. Ca-A tumor that has not extended beyond thesubmucosa With no metastases to lymph nodes, good prognosis. Advanced eso. Ca-extension beyond the submucosa
GROSS APPEARANCE
Fungating- protruding into the lumen of the esophagus. Ulcerative-undermining ulcer with raised edges Scirrhous-infiltrating tumor leading to stenosis or obstruction
Microscopic appearance
Barretts esophagus
Complication of long standing gastroesophageal reflux Risk factor for esophageal adenocarcinoma Classified as Long >3cm short<3 cm
Barrett esophagus
Diagnosis based on: 1)Endoscopic evidence of columnar lining above the GE junction 2)Histologic evidence of intestinal metaplasia
Stomach tumors
Epithelial tumors Intraepithelial neoplasia: Adenoma Adenocarcinoma Small cell carcinoma Neuroectodermal tumor Non epithelial Leiomyoma schwannoma Malignant Lymphoma
Ca Stomach
Second most common tumor in the world. Incidence: Japan ,chile ,Costa rica Common in lower socioeconomic groups M:F-2:1
Risk factors
Environmental factors: Infection by H.pylori Diet-Nitrites derived from nitrates smoked food lack of fresh fruits,vegetables Cigarette smoking Host factors: Chronic gastritis Reflux
Contd..
Gastric adenomas Barrett esophagus Genetic factors: Increased risk with blood group A Family history of gastric cancer HNPCC Familial gastric carcinoma syndrome
Carcinoma of stomach:proliferative
Microscopic appearance
Gastric Lymphoma/MALT Lymphoma 5% of malignancies Stomach is commonest site for extranodal lymphoma.
Morphology
Gross-May be solitary or multiple extend either into the serosa or the lumen C/S tan ,firm to soft,hemorrhagic changes seen.necrosis or cystic changes seen
Microscopy
Cellular tumours Exhibit spindle cells,plump epitheloid cells
Colon cancer
Ascending colon Transverse colon Descending colon Sigmoid colon Rectum Anal canal
Chronic inflammationIBDs-ulcerative colitis- 8 to 10 years,early onset, pan-colitis Crohns disease-3 fold increase, early onset,long duration Therapeutic pelvic irradiation Adenomas-precursor lesions-defined by presence of intra-epithelial neoplasiahypercellularity with enlarged hyperchromatic nuclei Villous adenomas, high-grade dysplasia Familial adenomatous polyposis-100 colorectal polyps
FAP
Uncommon autosomal dominant disorders Gene present on 5q21 chromosome (APC) Classified into classic,attenuated,gardner,turcot syndrome Minimum 100 polyps necessary for diagnosis(majority are tubular adenomas)
Contd..
Cancer preventive measures include Early detection and prophylactic colectomy in first degree relatives.
HNPCC-autosomal dominant ,familial syndrome (described by Lynch)/Lynch syndrome defect in gene repair and microsateelite instability.Increased risk of colon cancer and extra
Adenomas
Types Tubular adenomas Tubulo villous adenomas Villous adenomas
Villous adenoma
Right colon: Ascending colon Fluid feces can pass the mass-present late. Exophytic mass- fungating with intraluminal growth Left colon Transverse & Descending colon Solid feces- constipation, abdominal distension Present earlier due to obstructionannular growth Endophytic-ulcerative growth with predominant intra-mural growth.
Gross appearance
CARCINOMA Epithelium More common Middle & old age Lymph node metastases Slow growth Blood borne metastases late Radio-sensitive
SARCOMA Connective tissue Less common Young Uncommon Rapid growth Early Radio-resistant