Internal Diseases and Therapy · MU Sofia

94. Ulcerative colitis and Crohn’s disease

Compares ulcerative colitis with Crohn's disease, covering their distribution in the gut, morphology, genetic and immune causes, clinical features, extraintestinal manifestations and colonoscopic diagnosis. Treatment is set out in stepped tables by severity, with separate pathways for mild to moderate, moderate to severe and severe Crohn's, and for distal, extensive and fulminant colitis, followed by dietary advice.

Inside: 2 sections · 4 labelled pictures · 14 flashcards · 6 min

Topic 95 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 2 sections, about 918 words (6 min of reading), with 14 flashcards.

In this note

  1. Ulcerative colitis and Crohn's disease
  2. Treatment of Crohn’s

Ulcerative colitis and Crohn's disease

Ulcerative Colitis & Crohn's

Together these form IBD, inflammatory bowel disease. It is chronic and arises from inappropriate mucosal immune activation.

Ulcerative colitis is limited to the colon and rectum, extending only into the mucosa and submucosa. It’s progression is stepwise, not missing out sections. However Crohn's disease can affect any part of the GI tract, is frequently transmural and does skip, it doesn’t have to be continuous.

Crohn's is slightly more common in women (UC affects both sexes about equally), and both are more common in the west. The exact cause of IBD is uncertain, however mst believe it comes from errors in interaction between intestinal microbiota, intestinal epithelial dysfunction and aberrant mucosal immune responses. Primary factors we shall consider:

  • Genetics - risk is increased when family member has disease (NOD2 mutation increases susceptibility)
  • Mucosal immune response - immunosuppressors help with symptoms, suggesting the mucosal immune response is of central importance to the pathogenesis
  • Epithelial defects - defects in tight junctions present in Crohn's (NOD2 polymorphisms)
  • Microbiota - data suggests it’s important but we don’t know how

Morphology

  • Crohn's
  • Most common sites are terminal ileum, ileocecal valve and cecum
  • Disease limited to small intestine in 40% of cases
  • Presence of multiple, separate, delineated areas, known as skip lesions
  • Lesions do however coalesce into elongated serpentine ulcers along the axis of the bowel with fissures frequently developing and the formation of a cobblestone appearance
  • The intestinal wall thickens due to transmural edema, inflammation, fibrosis and hypertrophy of muscularis propria
  • Microscopic examination reveals clusters of neutrophils within a crypt known as crypt abscesses, ulceration is common, Paneth cell metaplasia may occur in left colon (where paneth cells are normally absent). Noncaseating granulomas are also found in 35% of patients
  • Ulcerative colitis
  • Always involves rectum and extends proximally continuously
  • Disease of the entire colon is pancolitis
  • Gross morphology shows broad-based ulcers with granular appearance
  • Regenerating mucosa often bulge into luman creating pseudopolyps
  • Mucosal atrophy may also develop
  • Unlike in Crohn's mural thickening is absent, serosal surface is normal and there are no strictures
  • Histologically, very similar to Crohn's

Image: “Severe ulcerative colitis” by Mikael Häggström , M.D. Author info - Reusing images - Conflicts of interest: None Mikael Häggström , M.D. Consent note , CC0, via Wikimedia Commons.

Clinical manifestations:

  • Crohn's
  • Abdominal pain (commonly in right lower quadrant)
  • Diarrhea
  • Hematochezia (fresh blood through anus on stool NOT melena)
  • Fatigue

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