Inflammatory Bowel Disease (IBD) encompasses Crohn's Disease (CD) and Ulcerative Colitis (UC). UC is confined to the colon, affecting only the mucosa, and always starts rectally. CD can affect any part of the GI tract transmurally, with 'skip lesions'. Both are chronic, relapsing conditions presenting with diarrhoea, abdominal pain, and systemic symptoms. Management involves corticosteroids for flares and immunosuppressants/biologics for maintenance.
📋 Overview
IBD represents chronic, idiopathic inflammatory conditions of the GI tract. Understanding the key differences between UC and CD is crucial for finals. UC always begins in the rectum and extends proximally in a continuous fashion (proctitis, left-sided colitis, pan-colitis), affecting only the mucosa. Histologically, expect crypt abscesses and goblet cell depletion. CD involves transmural inflammation and can affect any part of the gut from mouth to anus, with the terminal ileum and proximal colon being most common. CD is characterised by 'skip lesions' (areas of normal bowel between inflamed sections) and non-caseating granulomas. Clinically, UC often presents with bloody diarrhoea and tenesmus, while CD presents with abdominal pain (often RIF), chronic non-bloody diarrhoea, weight loss, and perianal disease. Both have significant extra-intestinal manifestations (EIMs) like erythema nodosum, pyoderma gangrenosum, episcleritis, uveitis, and large-joint arthritis. UC has a unique association with Primary Sclerosing Cholangitis (PSC). Diagnosis relies on clinical suspicion, elevated faecal calprotectin, and definitive colonoscopy with biopsies. Management aims for remission induction during flares and maintenance to prevent relapse and long-term complications, including colorectal cancer.
🔬 Basic Science
IBD results from a dysregulated immune response to gut microbiota in genetically predisposed individuals. In CD, a Th1/Th17-mediated response predominates, while UC is often linked to a Th2-like response. Genetic factors, notably NOD2 mutations, are strongly associated with ileal CD. Histologically, UC shows inflammation limited to the mucosa and submucosa, with crypt distortion and 'crypt abscesses' (neutrophils within crypt lumina). CD exhibits transmural inflammation (all layers of the bowel wall), leading to characteristic complications like strictures and fistulae. Non-caseating granulomas are pathognomonic for CD but are only found in 50-70% of biopsies. The 'cobblestone' appearance in CD is due to deep longitudinal ulcers separated by oedematous mucosa.
🏥 Clinical Relevance
UC typically presents with frequent, small-volume bloody diarrhoea, urgency, and tenesmus. CD has a more variable presentation: chronic abdominal pain (often right iliac fossa, mimicking appendicitis), chronic non-bloody diarrhoea, weight loss, and growth failure in children. Perianal disease (fissures, skin tags, complex fistulae, abscesses) is a strong indicator of CD. On examination, look for oral aphthous ulcers, abdominal masses (inflammatory masses/abscesses in CD), or signs of EIMs (e.g., uveitis, erythema nodosum, joint effusions). Acute severe UC (Truelove & Witts criteria: >6 bloody stools/day PLUS fever >37.8°C, tachycardia >90 bpm, Hb <10.5 g/dL, ESR >30 mm/hr, or CRP >30 mg/L) is a medical emergency requiring immediate hospitalisation and IV steroids due to the high risk of toxic megacolon and perforation.
🧪 Investigations
Bedside: Stool culture and C. difficile toxin to rule out infective causes. Bloods: FBC (anaemia of chronic disease, iron deficiency anaemia, thrombocytosis), CRP/ESR (inflammatory markers), U&Es, LFTs (low albumin in severe disease, elevated ALP/GGT in PSC). Special Tests: Faecal calprotectin is highly sensitive for intestinal inflammation and useful for screening and monitoring. Imaging: Colonoscopy with multiple biopsies from all segments of the colon is the gold standard for diagnosis and differentiation. In CD, MRI or CT Enterography is essential to assess small bowel involvement and complications (strictures, fistulae). Small bowel capsule endoscopy can be considered if CD is suspected but OGD/colonoscopy are negative.
💊 Management
Acute flares: UC (mild-moderate): Topical or oral aminosalicylates (5-ASA, e.g., Mesalazine). Severe UC: IV corticosteroids (Hydrocortisone), with rescue therapy (e.g., Infliximab, Ciclosporin) if no response. CD: Oral corticosteroids (Prednisolone) for induction. Enteral nutrition can be used in children. Maintenance: UC: Oral 5-ASA is first-line. CD: Immunomodulators (Azathioprine, Mercaptopurine) are first-line. Biologics (e.g., Infliximab, Adalimumab, Vedolizumab, Ustekinumab) are used for moderate-severe disease unresponsive to conventional therapy. Surgery: Proctocolectomy is curative for UC. In CD, surgery is reserved for complications (e.g., obstruction, fistulae, abscesses) and is NOT curative, as disease can recur.