Transcript Ulcerative Colitis - Ipswich-Year2-Med-PBL-Gp-2

Ulcerative Colitis
Which of the following would not be
associated with UC
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Toxic megacolon
Granulomas
Pseudopolyps
Primary sclerosing cholangitis
Pathogenesis of IBD
• Genetic susceptibility
• Failure of immune regulation
• Triggering by microbial flora
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
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
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
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)
What distinctive features of UC are
present?
Which is Normal Colon? Why?
What is the most serious complication
of UC