1. Ulcerative Colitis

2. Which of the following would not be associated with UC Toxic megacolon Granulomas Pseudopolyps Primary sclerosing cholangitis

3. Pathogenesis of IBD Genetic susceptibility Failure of immune regulation Triggering by microbial flora

4. Epidemiology of UC and Genetic Susceptibility UC more common than Crohn’s Peak incidence between 20-25 YO Higher prevalence in western countries among white population First degree relatives have 3 to 20x greater risk of developing IBD 20% of UC patients have affected relatives

5. Pathogenesis of IBD IBD is a Th cell mediated disease Associated with abnormal MHC antigens. Specifically, UC is associated with HLA-DRB1 Mouse studies have found a CD4+ variant secreting IL17 to be a culprit Support for the hygiene hypothesis – Mice infected with Helminths are protected from IBD – Germ-free mice don’t develop IBD – Mice deficient in IL 2 and IL 10 (regulatory cytokines) develop IBD

6. What type of diarrhoea is present in IBD Malabsorptive because of damage and eventual destruction of absorptive epithelium Further loss of function occurs when ulcerations are filled with granulation tissue, fibrosis occurs within the submucosa and resulting disarray of the epithelium

7. Morphology Continuous inflammation with no skip lesions of the rectum and sigmoid colon May involve the entire colon Pancolitis (proximal involvement) is rare but possible Broad based pale ulcerations form and can coalesce Islands of regenerating mucosa form pseudopolyps Collections of neutrophils in the epithelium forms crypt abscesses which burst causing foreign body reaction within the exposed submucosa Exposure of the neural plexus to faeces (toxins) results in shutdown of contraction. The colon distends and can rupture (toxic megacolon)

8. What distinctive features of UC are present?

9. Which is Normal Colon? Why?

10. What is the most serious complication of UC