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.

 

Malabsorption

  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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