Tumors of the colon & rectum
Polyps & Polyposis syndrome: Non-neoplastic: Hamartoma , Metaplastic , inflammatory. Colorectal adenoma 50% over 60 years. Histology: Tubular , villous or tubulovillous.Nearly all forms of colorectal carcinoma develop from adenomatous polyps over 5-10 years. Risk for malignancy in polyp: -Large size > 2cm. -Multiple polyps. -Villous architecture. -Dysplasia.
Clinical presentation
Usually asymptomatic GI bleeding. Anemia. Villous adenoma some times secrete large amount of mucus lead to diarrhea & hypokalaemia. Carcinoma transformation.Treatment: Polypectomy followed by surveillance colonoscopy at 3-5year intervals. Very large or sessile polyps can sometimes be removed safely by Endoscopic Mucosal Resection ( EMR) & if not by surgery. Between10-20% of polyps show histological evidence of malignancy. When cancer cells seen within 2mm of the resection margin of the polyp , when the polyp cancer is poorly differentiated or when lymphatic invasion is present segmental colonic resection is recommended.
Familial Adenomatous Polyposis(FAP)
AD Extra intestinal features: Subcutaneous epidermoid cysts. Lipoma. Benign osteoma. Desmoid tumour. Dental abnormality. Congenital hypertrophy of the retinal epithelium.Clinical syndromes
Gardner ,s syndrome. Turcot ,s syndrome. Attenuated FAP. Diagnosis: Genetic analysis for 1st degree relatives Colonoscopy. Treatment: Colectomy& ileal pouch anal anastamosisPeutz-Jeghers syndrome
Is characterized by multiple hamartomatous polyps in small intestine & colon , as well as melanin pigmentation of the lips , mouth & digits. Most cases are asymptomatic, although chronic bleeding , anemia or intussusception can be seen.
There is increased risk of carcinoma of small intestine & colonic adenocarcinoma and carcinoma of the pancreas , lung, ovary ,breast and endometrium. It is autosomal dominant. Diagnosis required 2 of the following: Small bowel polyposis. Mucucutanous pigmentation. Family history suggesting autosomal dominant inheritance.
Colorectal cancer
Etiology: Environmental: Dietary: Increased risk: Red meat. Saturated animal fat. Decreased risk: dietary fiber. fruits & vegetables. Ca Folic acid. Omega 3 fatty acids.Non dietary
Medical conditions: --Colorectal adenoma. --Long lasting extensive UC or Crohns especially when associated with Primary Sclerosing Cholangitis. --Acromegaly. -- pelvic radiotherapy. --UretrosigmoidostomyOthers: --Obesity& sedentary life style -- Alcohol & Tobacco. --Cholycystectomy --Type 2 DM --Use of aspirin NSAIDs (COX-2 inhibitor),Statins associated with reduced risk Genetic factors: FAP 1% 10% +ve FH. HNPCC (Lynch ,s syndrome) AD
Criteria for diagnosis of HNPCC
3 or more relatives with Ca colon. Colorectal cancer in 2 or more generations At least one member affected < 50y. Exclusion of FAP. Management: Pedigree assessment. Genetic testing. ColonoscopyPathology
Polypoidal & fungating. Annular & constricting. >65 % in recto-sigmoid. 15% in Caecum & ascending colon.Clinical features:
Left sided colonic tumours: Intestinal obstruction Bleeding per rectum.Right sided colonic tumours: Anaemia & occult GI bleeding. Altered bowel habits. 10% Fe deficiency anaemia & weight loss.
On Examination
Palpable mass. Signs of anaemia. Hepatomegaly ( secondaries ). PR: Palpable rectal tumourInvestigations
Colonoscopy. Endo anal U/S. Pelvic MRI. CT Colography ( Virtual Colonoscopy ). CEA.Modified Dukes classification: A-T confined to bowel wall 5y survival is >90%. B-T extend through bowel wall 5y survival is >65%. C-T involving LN ,5ys is 30-35%. D-Distant metastasis , 5ys is < 5%.
Management
Surgery followed by colonoscopy every 6-12 months. Chemotherapy:5FU+Folonic acid for Duke C. Radiotherapy: preoperative for large fixed rectal tumour , Dukes B &C rectal T postoperatively to decrease recurrence.Prevention:
Chemoprevention: Aspirin. Calcium. Folic acid. Selective Cox.2 inhibitors. Secondary prevention: Fecal occult blood :annually after 50y. Colonoscopy. Sigmoidoscopy: every 5y for those > 50y. Molecular genetic analysis.Acute colonic Ischemia
Splenic flexure & descending colon (Water shade areas ). Pathology: Reversible colopathy. Transient colitis. Colonic stricture. Gangrene & fulminant pan colitis Etiology: Arterial thromboembolism. Decreased BP. Colonic Volvulus. Strangulated hernia. Hypercoagulable state.