ULCERATIVE COLITIS diarrhoea by benbenzhou


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Ulcerative colitis is one of two main forms of inflammatory bowel disease, the other
being Crohn’s disease. Crohn’s disease can affect any part of the gastrointestinal
system from mouth to anus. Whereas ulcerative colitis affects the large bowel only.
Ulcerative colitis is a relapsing and remitting inflammatory disorder of the colonic
mucosa. It may affect just the rectum (proctitis) or extend proximally to affect part or
the entire colon (pancolitis).

The cause of ulcerative colitis is broadly speaking undnown, however it is likely that
environmental factors operative in an individual with a genetic predisposition. Many
papers have postulated that some insult to the intestinal epithelial integrity permits
bacteria and luminal antigens to trigger an aberrant immune response. The response is
thought to be Th-2 dominant with increased production of interleukin-5. Betis (Infect
Immun 71 1774) has proposed that ulcerative colitis may involve adhesin-expressing
strains of E.coli capable of inducing interleukin-8 production and transepithelial
migration of leukocytes.

Can be broadly divided into macroscopically and histologically. Affecting only the
large bowel it begins in the rectum and extends proximally in varying degrees with
continuous involvement. Mucosal inflammation causes a red mucosa which bleeds
easily, as well as ulcers and pseudopolyps (regenerating mucosa) in severe disease.
Ulcerative colitis is characterised by an absence of granulomata, however there goblet
cell depletion and crypt absecesses. The inflammatory response is predominantly Th-
2 mediated. Hyperaemic/haemorrhagic granular colonic mucosa +/- “pseudopolyps”
formed by inflammation. Punctate ulcers may extend deep into the lamina propria.

The purpose of investigations is to define the nature of the disease and the extent and
severity of bowel involvement.
FBC; anaemia is common in ulcerative colitis and is usually the normochromic,
normocytic anaemia of chronic disease, however iron deficiency anaemia may occur.
Platelet count, ESR and CRP are often raised in severe disease. U&ES and LFTs
should also be conducted as in severe disease the serum albumun may be low. Blood
cultures should also be taken to investigate infective agents.
Stool Microscopy Culture and Sensitivity (MC+S) and Clostridium Difficile
Toxin (CDT)
These tests should also be conducted to exclude infectious diarrhoea (Clostridium
difficile, Salmonella, Shigella, Campylobacter, E coli, amoebae).
A plain abdominal x-ray should be conducted during a severe attack of colitis to look
for toxic dilatation of the colon (>6cm) which can lead to perforation. In cases of
ulcerative colitis you would also expect to see mucosal thickening/islands and no
faecal shadowing.
Rigid or flexible sigmoidoscopy can establish a diagnosis of ulcerative colitis, during
this procedure a rectal biopsy can be conducted to examine the histology. A histology
showing inflammatory infiltrate, goblet cell depletion, glandular distortion, mucosal
ulcers crypt ulcers is highly suggestive of ulcerative colitis.
         Colonoscopy permits the exact extent and severity of colonic and terminal
ileal inflammation to be determined, and biopsies to be taken. A barium enema is
useful as an investigation showing loss of haustra, granular mucosa and a shortened
colon. It is important to note that a barium enema should never be conducted
following an acute attack of ulcerative colitis.

Management of ulcerative colitis is can be divided up according to whether the
intervention is medical or surgical and also depending upon the severity of the
ulcerative colitis.
Medical Interventions
Oral corticosteroids such as prednisolone are used to treat acute attacks and the dose
is tailed off as the symptoms improve. In severe attacks intravenous steroids are
necessary typically hydrocortisone 100mg/6h. Proctosigmoiditis can be treated locally
with steroid enemas and suppositories (mesalazine 250mg/8hr PR). Budesonide is a
topically acting steroid which is poorly absorbed from the gastrointestinal tract and
therefore had fewer systemic effects than other steroids. In severe cases blood
transfusions are considered (if Hb <10g/dL) as is the use of parenteral nutrition in
severe malnourishment. Intramuscular vitamins are also given.
         The 5-Aminosalicyclic acid (5-ASA) tablets (mesalazine, olsalazine,
balsalazine) are bowel-specific aminosalicylate drugs that are metabolized in the gut
having its predominant actions there, thereby having fewer systemic side effects. 5-
ASA exerts an anti-inflammatory action which induces remission in mild attacks of
ulcerative colitis. In lower doses they are useful as a maintenance treatment to reduce
the number of relapses, reducing the relapse rate from 80% to 20% at 1 year. 5-ASA
preparations can also be administered as an enema or suppository to treat
         Azathioprine is an immunomodulatory drug that suppresses the immune
system. It is a pro-drug, converted in the body to the active metabolites 6-
mercaptopurine and 6-thioinosinic acid. It is used in those patients who continue to
have frequent relapse despite taking an adequate dose of 5-ASAs. It is also indicated
as a steroid-sparing agent in those with steroid side-effects or those who relapse
quickly when steroids are reduced. Treatment is continued for several months at a
time during which FBC is monitored every 4-6 weeks.
         The novel therapy ciclosporin (=cyclosporin) can benefit patients with steroid
refractory ulcerative colitis, although there are reservations about its long-term
Surgical Interventions
Indications for surgery typically include perforation or massive haemorrhage – or
“toxic” dilatation of the colon. The other main indication is failure to respond to
medical interventions. The surgical procedures performed in ulcerative colitis are:
      Ileoanal anastomosis, in which the terminal ileum is used to form a reservoir,
         and the patient is continent with a few bowel motions per day. The pouch may
         become inflamed (“pouchitis”), leading to bloody diarrhoea which is treated
         initially withmetronidazole.
      Panproctocolectomy with ileostomy (the whole colon and rectum is removed
       and the ileum is brought out the abdominal wall as a stome).
      Colectomy with an ileorectal anastomosis (diseased rectum left in situ and
       diarrhoea may still occur).

Course and Prognosis
Ulcerative colitis presents with bloody diarrhoea, often containing blood and mucus.
The clinical course may be one of persistent diarrhoea, relapses and remissions, or
severe fulminating colitis. Progression of ulcerative colitis is highly variable. Only
10% of patients with procitits develop more extensive disease, but with severe
fulminant disease there is a risk of colonic perforation and death.
        Patients with extensive ulcerative colitis of more than 10 years’ duration are at
an increased risk of colorectal cancer (cumulative risk 12% after 25 years). These
patients are usually offered surveillance colonoscopy at intervals of 1-2 years.
Colectomy is recommended if high-grade dysplasia is discovered.

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