Inflammatory bowel disease (Ulcerative Colitis [UC] and Crohn’s Disease [CD])

06/05/2013 by admin | Gastroenterology

Ulcerative colitis:

  1. Idiopathic inflammatory bowel disease
  2. Genetic factors thought to play a role – 15% of cases have a clear FH
  3. Smoking is protective in UC for unknown reasons
  4. Presentation: 2/1000, white jewish population at 2-4 fold risk. 25-45yo age group
  5. Pathophysiology of UC:
    1. o Inflammation is always present in rectum
    2. o Extends a variable distance proximally to colon
    3. o Inflammation is continuous and diffuse
    4. o Inflammation is limited to mucosa of the bowel
  6. Distribution of inflammation:
    1. o 15% – pancolitis: presents with chronic diarrhoea, and constitutional upset
    2. o 40% – distal and L-sided colitis: presents with rectal bleeding associated with urge and tenesmus.
    3. o 45% – proctitis: presents with rectal bleeding associated with urge and tenesmus.
  7. All presentations have common extra-intestinal manifestations:
    1. o Eye inflammation = Uveitis
    2. o Organ involvement = Hepatitis/gallstones/primary biliary cirrhosis
    3. o Skin lesions = Pyoderma gangrenosum and erythema nodosum
    4. o Arthralgia = Sacroiilitis/monoarthritis/ankylosing spondylitis
  1. Ix:
    1. o Recognise severe colitis early and tx aggressively (use Truelove-Witts criteria):
    2. o Stool frequency >6/d
    3. o Temp >38c
    4. o Pulse >90
    5. o Hb <10.5g/dl
    6. o ESR >30mm/h
    7. o Rectal biopsy: may differentiate a short lived infective colitis
    8. o Flexi-sigmoidoscopy/colonoscopy: yearly surveillance indicated after 8 years of active disease because longstanding total colitis = increased risk of colonic carcinoma
    9. o Abdo XR: inflamed bowel will be empty. Exclude ‘toxic mega-colon’ (massive dilatation at high risk of perforation).
    10. o Stool culture: exclude infective diarrhoea
  2. Mx:
    1. o 5-aminosalicylic acid (5-ASA) compounds = sulphasalazine / mesalazine – effective in mild attacks – reduce rsik of subsequent flare ups
    2. o Steroids: severe acute flare ups require admission and IV steroids. Less severe attacks require oral/topical steroids
    3. o Cyclosporine: used for severe acute colitis that fails to responds to initial tx
    4. o Azathioprine: used in those experiencing frequent relapses
    5. o Surgery: if colon is life-threatening (perforated/cancer/sever dysplasia), hemi-/full colectomy and stoma.
  3. Complications: toxic mega-colon and severe haemorrhage is more common in 1st attack. After 30 years – there is a 20% risk of CRC. Also risks of hypokalaemia/hypoalbuminaemia/anaemia
  4. Prognosis: after 1st attack, 5% die <1 year, 10% have continually active disease and 15% spontaneously remit, and 75% have intermittent disease.


Crohn’s Disease:

  1. Chronic granulomatous inflammatory disease, affecting small areas of deep ulceration in the small and large bowel, characterized by ‘skip lesions’, and fistulae/stricture formation
  2. Uncommon, 5/100,000
  3. Clinical features: diarrhoea (80%), abdo pain (50%), weight loss (70%), fever (40%)
  4. State of condition is based on:
    1. o The site of disease: small bowel is more likely to present with malabsorption, and features of small bowel obstruction than colonic disease which causes diarrhoea
    2. o The extent and severity of inflammation
    3. o Secondary complications: abscesses, strictures, fistulae
    4. o Extra-intestinal manifestations: aphthous ulcerations, erythema nodosum, acute arthropathy, eye complications.
  5. Differential diagnosis should include Yersinia infection and intestinal TB
  6. Ix:
    1. o Systemic markers of inflammation: ESR, CRP – good markers of disease progression and activity
    1. o Barium contrast radiology: small bowel Crohn’s can be demonstrated on a small bowel enema or follow-through study – gives important info about extent of disease and intestinal obstruction
    2. o Endoscopy: diagnostic biopsy
    3. o USS/CT of abdo: useful to exclude abscess formation in sick patients with palpable abdo mass. MRI useful for ix of perianal and pelvic disease
  1. Mx:
    1. o 5-aminosalicylic acid (5-ASA) compounds = sulphasalazine / mesalazine – effective in mild attacks – reduce risk of subsequent flare ups
    2. o Steroids: severe acute flare ups require admission and IV steroids (pred or IV hydrocortisone). In isolated distal colonic disease can give local prep.
    3. o Azathioprine and methotrexate are effective maintenance tx and can be used if frequent or sever relapse. Also antibodies to TNF-alpha have been licensed.
    4. o Surgery: given patchy and recurrent nature of CD, surgery tends to be conservative and reserved for disease not responding to medical therapy and complications (abscesses/fistulae)
    5. o Nutrition: high metabolic demand of acute inflammation and small intestinal dysfunction – elemental liquid diets work well.
  2. Prognosis: incurable, remitting/relapsing course, 15% mortality rate. 70% of patients will have surgery at some stage.



  1. Suspect if chronic diarrhoea and weight loss despite preservation of appetite
  2. Thyrotoxicosis can also produce these symptoms
  3. Causes of malabsorption:
    1. o Common: coeliac disease (as described later), pancreatic exocrine deficiency (CF, chronic pancreatitis with post-prandial pain and steatorhhoea leading to weight loss), Crohn’s Disease (described above in IBD)
    2. o Uncommon: hypolactasia (genetic – 90% African/Asian adults, or acquired – GI infection), small bowel bacterial overgrowth (hypo or achlorhydria, duodenal jejunal and diverticula, strictures fistulae and blind loops, slow transit time and autonomic neuropathy caused by DM/systemic sclerosis, Ig deficiency states, bacterial deconjugate bile saltssteatorrhoea and mild B12 deficiency) , giardiasis (acute or chronic), HIV
    3. o Rare: tropical sprue, Whipple’s disease, amyloidosis
  4. Clinical features:
    1. o Weight loss, general fatigue, diarrhoea, steatorrhoea
    2. o If caused by pancreatic failure = Hx of excessive alcohol, or CF
    3. o If caused by GI infection = travel history
  5. O/e:
    1. o Objective evidence of weight loss
    2. o Markers of general malnutrition: leukonychia, glossitis, cheilitis (=inflammation of the lips), anaemia (folate/vit b12/protein)
    3. o Markers of specific deficiencies: scurvy (vit C), koilonychia (iron), osteomalacia (vit D and calcium), bruising (vit K)
    4. o Signs of thyrotoxicosis: tremor, tachycardia, exophthalmos
    5. o LN’s: Virchow’s node
    6. o Abdo exam: mass maybe palpable in ileal Crohn’s disease.
    7. o PR: stool is pale, offensive, oily
  6. Ix:
    1. o Faecal microscopy: fat globules in stool = steatorrhoea
    2. o Bloods: FBC, LFTs, albumin, INR, calcium, magnesium, zinc, vit B12, folate, TSH and T4 (rule out thyrotoxicosis), ESR and CRP (raised in Crohn’s), endomesial antibody (seen in coeliac disease)
    3. o Endoscopy an duodenal biopsy: to exclude coeliac disease
    4. o Small bowel imaging (enema and enteroscopy): in used when non-coeliac small bowel disease is suspected
    5. o Tests of small bowel function:
    6. o Hydrogen breath test: H2 appears when lactose (=hypolactasia) or lactulose (=small bowel overgrowth) are given
    7. o 14C-labelled triolene breath test: measure ability of small bowel to absorb fat. Triolene is not absorbed in pancreatic exocrine failure
    8. o Pancreatic imaging: USS, CT, and endoscopic retrograde cholangiopancreatography are indicated when chronic pancreatitis is suspected to underlie pancreatic exocrine failure
    9. o Tests of pancreatic function:
    10. o Pancraolauryl test: fluoresceine dilaurate is ingested and if pancreatic exocrine enzymes are present – fluorosceine is split off absorbed and passed into urine where it can be detected
    11. o Faecal elastase: not found in stool in moderate-severe pancreatic exocrine failure
  1. Mx:
    1. o Dietary advice and supplementation: vit and nutrient replacement may be indicated (folate, vit B12, iron)
    2. o Protect the bones: aim to avoid osteopenenia 
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