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UPPER GI BLEEDING: COLON CANCER

UPPER GI BLEEDING: COLON CANCER. GROUP A BGD February 1, 2010. Clinical Manifestations. Cecum and ascending colon May become quite large without resulting in any obstructive symptoms or noticeable alterations in bowel habits Lesions of the right colon

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UPPER GI BLEEDING: COLON CANCER

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  1. UPPER GI BLEEDING: COLON CANCER GROUP A BGD February 1, 2010

  2. Clinical Manifestations • Cecum and ascending colon • May become quite large without resulting in any obstructive symptoms or noticeable alterations in bowel habits • Lesions of the right colon • Commonly ulcerate, leading to chronic, insidious blood loss without a change in the appearance of the stool • Tumors of the ascending colon • Fatigue, palpitations, angina pectoris • Hypochromic, microcyticanemia indicative of iron deficiency

  3. Clinical Manifestations • Transverse and descending colon • Tend to impede the passage of stool • Abdominal cramping, occasional obstruction, perforation • Rectosigmoid • Hematochezia, tenesmus, narrowing of the caliber of stool • Anemia is an infrequent finding • Random fecal occult blood test may be negative • Cancer may bleed intermittently • Radiographs of the abdomen often reveal characteristic annular, constricting lesions ("apple-core" or "napkin-ring")

  4. Clinical Manifestations • Patient Correlation • Hematochezia • Chief complaint • 6 hours PTA passed out half a tsp of blood after defecation • 4 hours PTA 1 tbsp of blood • 30 minutes PTA 2 cups of fresh blood • Rectal exam showed fresh blood on examining finger

  5. Clinical Manifestations • Patient Correlation • Impeded passage of stool • Constipation for several years • Palpitations • Sitting HR 110 beats/min • Supine HR 90 beats/min • Felt dizzy, had cold clammy perspiration

  6. Pathophysiology • Most colorectal cancers, regardless of etiology, arise from adenomatous polyps. • Polyp - a grossly visible protrusion from the mucosal surface • Non-neoplastichamartoma (juvenile polyp) • Hyperplastic mucosal proliferation (hyperplastic polyp) • Adenomatous polyp – premalignant • Only a minority of such lesions becomes cancer

  7. Pathophysiology • Molecular changes • Mutational activation of an oncogene followed by and coupled with the loss of genes that normally suppress tumorigenesis • Point mutations in the K-rasprotooncogene • Hypomethylation of DNA, leading to gene activation • Loss of DNA (allelic loss) at the site of a tumor-suppressor gene [the adenomatouspolyposis coli (APC) gene] on the long arm of chromosome 5 (5q21) • Allelic loss at the site of a tumor-suppressor gene located on chromosome 18q [the deleted in colorectal cancer (DCC) gene] • Allelic loss at chromosome 17p, associated with mutations in the p53 tumor-suppressor gene

  8. Pathophysiology

  9. Pathophysiology • Clinically, the probability of an adenomatous polyp becoming a cancer depends on: • Gross appearance of the lesion • Histologic features • Size • Adenomatous polyps: • Pedunculated (stalked) • Sessile (flat-based) • Cancers develop more frequently in sessile polyps

  10. Pathophysiology • Histologically, adenomatous polyps may be: • Tubular • Villous (i.e. Papillary) • Most are sessile- become malignant more than three times as often as tubular adenomas • Tubulovillous

  11. RiskFactors • Advanced age • Diet: animal fat • History of cancer • Polyps, particularly adenomatous polyps • Hereditary syndromes • Polyposis coli • Non-polyposis syndrome (Lynch syndrome) • Inflammatoryboweldisease • Infection (viral exposure, Streptococcusbovisbacteremia) • Uterosigmoidoscopy • Physicalinactivity • Smoking/tobacco use • Alcohol • Exogenous hormones • Environmentalfactors • Present in the patient • Advanced age (78 years old) • Smoking (19 pack years)

  12. RiskFactors • Diet • Upper socioeconomic populations • Japan: increased incidence of colorectal cancer since they adopted a “western” diet • Animal fats • Red meats and processed meat increased proportion of anaerobes in the gut microflora conversion of normal bile acids into carcinogens • Insulin resistance • “Western” diets, physical inactivity- higher prevalence of obesity • Obese persons • Insulin resistance increased circulating levels of insulin higher circulating concentrations of insulin-like growth factor type I stimulate proliferation of the intestinal mucosa

  13. RiskFactorsHereditable (Autosomal Dominant) Gastrointestinal Syndromes

  14. Diagnostic Procedures • Screening • Goal: earlier detection of localized, superficial cancers in asymptomatic individuals to increase the surgical cure rate • Candidates: • 50 years old • Family history of the disease in first-degree relatives

  15. Diagnostic Procedures • Digital rectal examination • Part of any routine physical evaluation in adults older than age 40 • An inexpensive maneuver for the detection of masses in the rectum

  16. Diagnostic Procedures • Hemoccult blood test • Detects occult fecal blood • Colonoscopy • Superior to double-contrast barium enema • has a higher sensitivity for detecting villous or dysplastic adenomas or cancers than the strategy employing occult fecal blood testing and flexible sigmoidoscopy

  17. Diagnostic Procedures • Biopsy • During a colonoscopy, several biopsies (each at different locations in the colon and rectum) may be taken • Used to diagnose cancer or estimate how far cancer has spread • Used to obtain bits of tissue to be checked in the laboratory for signs of cancer or other diseases

  18. Diagnostic Procedures • Proctosigmoidoscopy • Based on the observation that 60% of early lesions are located in the rectosigmoid • Flexible, fiberopticsigmoidoscopes • To visualize the colon for up to 60 cm, which enhances the capability for cancer detection

  19. Diagnostic Procedures • Virtual colonoscopy • Computed tomography colography • A method under study to examine the colon by taking a series of x-rays and using a high-powered computer to reconstruct 2-D and 3-D pictures of the interior surfaces of the colon from these x-rays • Pictures can be saved, manipulated to better viewing angles, and reviewed after the procedure, even years later

  20. Diagnostic Procedures • Air-contrast barium enema • Highly sensitive for detecting polyps greater than 1 cm in diameter • After the barium passes through the intestine, air will then be pumped into it • Using the barium, the technician is able to get a clear picture of the lining of the intestine from multiple angles

  21. Diagnostic Procedures • Endoscopic ultrasound • To evaluate the gastrointestinal tract  • Improves tumor characterization, and enables more precise TNM staging

  22. Diagnostic Procedures • Pre-operative elevation of the plasma carcinoembryonic antigen (CEA) level predicts eventual tumor recurrence

  23. Management • Lower GI bleeding • Stable patients may undergo appropriate diagnostic procedures to determine the source of bleeding • Unstable patients • Appropriate fluid and electrolytes • Once stable, determine the source of bleeding for appropriate management • Colon cancer treatment options depends on: • Stage of the cancer • Whether the cancer has recurred • General health status of the patient

  24. Management

  25. Management

  26. Management • Surgery Pre-operative Procedures

  27. Management • Surgery Intraoperative Procedures

  28. Management • Surgery Post-operative Procedures

  29. Management • Surgery Post-operative Procedures

  30. Management • Chemotherapy • 5-FU • Partial response in 15-20% of patients • Backbone of treatment • IV or oral (capecitabine)- similar efficacy • 5-FU + folinic acid (leucovirin) • Improves efficacy; three-fold improvement in partial response • Enhances binding to thymidylatesynthase

  31. Management • Chemotherapy • 5-FU + LV + Irinotecan (FOLFIRI regimen) • Topoisomerase 1 inhibitor • Improves response rates and survival of patients with metastatic disease • Adverse effect: diarrhea • 5-FU + LV + Oxiplatin (FOLFOX regimen) • Platinum analogue • Improves response rate • Adverse effect: dose-dependent neuropathy, resolves following cessation of therapy • FOLFIRI = FOLFOX

  32. Management • Chemotherapy • Monoclonal antibodies • Effective for advanced colorecatal cancer • Cetuximab and Panitumumab- directed against EGFR • Bevacizumab- directed against VEGF; anti-angiogenesis

  33. Management • Radiotherapy • Not effective in the primary treatment of colon cancer • May be recommended for prevention of regional recurrences after surgical resections (stage 2 or 3) • Pre-operatively: may be indicated for potentially large, unresectabletumors (to shrink them) and permit subsequent surgical removal

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