Ulcerative Colitis Flashcards
Summarise ulcerative colitis
Ulcerative colitis is a type of inflammatory bowel disease characterised by diffuse inflammation of the colonic mucosa and a relapsing, remitting course.
Patients commonly experience bloody diarrhoea, chronic diarrhoea (or both), lower abdominal pain, faecal urgency, and extraintestinal manifestations, particularly those related to activity of the colitis.
Diagnosis requires endoscopy with biopsy and negative stool culture.
Relapses are often associated with pathogens; therefore, stool should be obtained for culture in all cases of disease flare-up.
Treatment aims to induce and maintain remission. Drug choice and formulation depends on the severity and extent of disease.
Toxic megacolon can occur with associated risk of perforation. Bowel adenocarcinoma is a complication in 3% to 5% of patients.
Define ulcerative colitis
Ulcerative colitis (UC) is a type of inflammatory bowel disease that characteristically involves the rectum and extends proximally to affect a variable length of the colon. It is recognised as a multifactorial polygenic disease, as the exact aetiology is still unknown. Included in the aetiological theories are environmental factors, immune dysfunction, and a likely genetic predisposition
Describe the epidemiology of ulcerative colitis
In the Western world the incidence rate ranges from 1 to 24 cases per 100,000 person-years, with the highest incidence rates seen in Scandinavia and Northern Europe.[8] Prevalence is approximately 1 per 1000. Geographically, UC is more common in the western and northern hemispheres, and has a low incidence in Asia and the Far East, although this has been reported to be increasing.[8][9] While the incidence has remained stable, the prevalence seems to have increased in the past few decades, in part due to advances in diagnosis and treatment. It is slightly more common in men than in women. Most patients are aged 20 to 40 years at diagnosis. Another peak occurs at age 60 years. UC is uncommon in children <10 years of age
Describe the aetiology of ulcerative colitis
The cause of inflammatory bowel disease (IBD) in general and of UC in particular is unclear, but it seems to occur in genetically susceptible people in response to environmental triggers. Epidemiological studies have highlighted genetic predisposition factors for IBD. Among relatives with Crohn’s disease (CD) and UC, the odds ratio to develop IBD is in the range of 15 to 42 over the normal population for CD and 7 to 17 for UC.[10][11][12][13][14] UC is probably an autoimmune disease initiated by an inflammatory response to colonic bacteria. Immune dysfunction has been postulated as a cause, with limited evidence. UC might also be linked to diet, although diet is thought to play a secondary role. Food or bacterial antigens might affect the already damaged mucosal lining, which has increased permeability.
Describe the macroscopic pathophysiology of ulcerative colitis
Macroscopically, most cases of UC arise in the rectum, with some patients developing terminal ileitis (i.e., extending up to 30 cm) due to an incompetent ileocaecal valve or backwash ileitis. The bowel wall is thin or of normal thickness, but the presence of oedema, the accumulation of fat, and hypertrophy of the muscle layer may give the impression of a thickened bowel wall. The term ‘proctitis’ is used when the inflammation is limited to the rectum.
Describe the microscopic pathophysiology of ulcerative colitis
Microscopically, UC usually involves only the mucosa, with the formation of crypt abscesses and a coexisting depletion of goblet cell mucin. In severe cases, the submucosa can be involved, and in some cases, the deeper muscular layers of the colonic wall can also be affected. Further microscopic changes include inflammation of the crypts of Lieberkuhn and abscesses. Ulcerated areas are soon covered by granulation tissue. The undermining of mucosa and the excesses of granulation tissue form polypoidal mucosal excrescences, known as inflammatory polyps or pseudopolyps
Describe the early disease manifestations of ulcerative colitis
Early disease manifests as bleeding, petechial haemorrhages, and haemorrhagic inflammation with loss of the normal vascular pattern. Oedema is present, and large areas become denuded of mucosa. Undermining of the mucosa leads to the formation of crypt abscesses, which are the hallmark of the disease.
Describe active severe colitis
Acute severe colitis can result in a fulminant colitis or toxic megacolon, which is characterised by a thin-walled, dilated colon that can eventually become perforated.
Describe pseudopolyps
Pseudopolyps form in 15% to 20% of chronic cases. Chronic and severe cases can exhibit areas of precancerous changes, such as carcinoma in situ or dysplasia.
Describe the general classification of ulcerative colitis
Left-sided colitis: inflammation up to the splenic flexure.
Extensive colitis: inflammation beyond the splenic flexure.
These categories are useful when formulating treatment options and planning the timing of surveillance colonoscopy, which is used to detect and prevent colorectal carcinoma
Describe the Montreal classification
The Montreal classification proposes the maximal extent of involvement as the critical parameter:
E1 (ulcerative proctitis): involvement limited to the rectum (proximal extent of inflammation is distal to the rectosigmoid junction)
E2 (left-sided UC, also called distal UC): involvement limited to a portion of the colorectum distal to the splenic flexure
E3 (extensive UC, also called pancolitis): involvement extends proximal to the splenic flexure.
Describe a drawback of the Montreal classification
A major drawback of the extent-based classification is the instability of disease extent over time. Progression and regression have been well identified and accepted. Approximately one third of patients with E1 or E2 disease will experience proximal disease extension, predominantly in the first 10 years from diagnosis.[5] Disease extent may regress over time, with regression rates estimated from a crude rate of 1.6% to an actual rate of 71% after 10 years
Describe how we can classify ulcerative colitis by severity
In addition to extent of disease, UC is classified by severity:
S0: clinical remission (asymptomatic)
S1 (mild UC): passage of ≤4 stools per day (with or without blood), absence of any systemic illness, and normal levels of inflammatory markers (erythrocyte sedimentation rate [ESR])
S2 (moderate UC): passage of >4 stools per day but with minimal signs of systemic toxicity
S3 (severe UC): passage of ≥6 bloody stools daily, pulse rate of at least 90 bpm, temperature of at least 37.5°C (99.5°F), haemoglobin level of <105g/L (10.5 g/dL), and ESR of at least 30 mm/hour.
Fulminant disease correlates with >10 bowel movements daily, continuous bleeding, toxicity, abdominal tenderness and distension, blood transfusion requirement, and colonic dilation (expansion).
Describe a typical case history for ulcerative colitis
A 27-year-old man with a 3-month history of rectal bleeding and diarrhoea is referred for evaluation. Laboratory tests show mild anaemia, a slightly elevated sedimentation rate, and the presence of white blood cells in stool. Stool culture is negative. Colonoscopy shows continuous active inflammation with loss of vascular pattern and friability from the anal verge up to 35 cm, with a sharp cut-off. The colonic mucosa above 35 cm appears normal, as does the terminal ileum. Biopsy specimens show active chronic colitis.
Describe the other presentations of ulcerative colitis
Less common presentations include mild distal colitis, in which rectal bleeding may be absent. This can mimic irritable bowel syndrome. Colicky lower abdominal pain may occur, but severe pain is usually limited to severe colitis. Many patients with proctitis present with constipation. A small proportion (5%) of children have growth failure as their only presenting complaint.
Describe the extra intestinal manifestations of ulcerative colitis
There are several extraintestinal manifestations. Those that are associated with the activity of the colitis include erythema nodosum (2% to 4%), aphthous ulcers (10%), episcleritis, peripheral arthropathy (5% to 10%), and anterior uveitis (1%). Those that are independent of the colitis activity include pyoderma gangrenosum (1% to 2%), sacroiliitis (12% to 15%), ankylosing spondylitis (1% to 2%), and primary sclerosing cholangitis (3% to 7%).
When should you suspect iBD
Inflammatory bowel disease (IBD) should be suspected in patients who have bloody diarrhoea and/or diarrhoea with signs of systemic inflammation for >3 weeks. Diagnosis requires, at a minimum, negative stool culture and some form of sigmoidoscopy or colonoscopy.
Summarise the history and examination
In addition to the presence of bloody diarrhoea, a history of lower abdominal pain, faecal urgency, tenesmus (a feeling of needing to pass a stool even though the colon is empty), and the presence of extraintestinal manifestations, particularly those related to disease activity, such as erythema nodosum and acute arthropathy, are further suggestive clinical features. UC should be suspected in patients with primary sclerosing cholangitis, as up to 70% have underlying UC.
Summarise the initial work-up
The initial work-up for all patients should include basic laboratory tests (full blood count [FBC], metabolic panel, inflammatory markers), stool studies, and either a colonoscopy or flexible sigmoidoscopy to visualise the mucosa and obtain a biopsy. An abdominal x-ray is indicated for any patients on their first presentation or during any acute relapse. If there is any uncertainty about which type of inflammatory bowel disease the patient may have, an upper gastrointestinal (GI) work-up should be carried out to assess for Crohn’s disease present in the upper GI tract.
Summarise the stool studies for ulcerative colitis
Between 20% and 50% of relapses of UC are associated with infection, so stool studies should be obtained, including comprehensive culture and Clostridium difficile toxin assessment, even in patients with a relapse of known UC. White blood cells may be present in the stool with negative stool culture.
Of all the stool inflammatory tests available, faecal calprotectin is recommended. It is elevated when there is bowel inflammation and correlates with endoscopic and histological gradings of disease severity. It is useful in supporting clinicians when considering inflammatory bowel disease in the differential diagnosis of irritable bowel syndrome. It can help determine which patients require urgent endoscopy and can prevent unnecessary referrals for colonoscopy (>60% in younger patients presenting with lower GI symptoms, the majority of whom will not have inflammatory bowel disease).[21] In those with an established diagnosis of IBD this test can be useful to assess for ongoing bowel inflammation
Summarise the lab studies for ulcerative colitis
FBC may show leukocytosis, thrombocytosis, and anaemia. Inflammatory markers (erythrocyte sedimentation rate and C-reactive protein) may be raised. Metabolic abnormalities can include hypokalaemic metabolic acidosis secondary to diarrhoea; elevated sodium and urea secondary to dehydration; elevated alkaline phosphatase, bilirubin, aspartate aminotransferase, and alanine aminotransferase in patients with concomitant primary sclerosing cholangitis; and hypoalbuminaemia secondary to malnourishment or as an acute-phase reactant.
Summarise sigmoidoscopy and biopsy
Flexible sigmoidoscopy can be performed in the endoscopy unit without sedation or full bowel prep but can visualise only the distal colon. Full bowel prep and colonoscopy is required if disease is suspected to extend beyond the distal bowel on the basis of x-ray. Endoscopic evaluation with histological confirmation is the key to diagnosis, but histological features overlap considerably between UC, Crohn’s disease, and infectious colitis; hence, the diagnosis is based on the combination of history, endoscopic findings, histology, and microbiology, rather than on any single modality. During acute flares endoscopic examination should be limited to flexible sigmoidoscopy without bowel prep, due to the increased risk of perforation.
For a reliable diagnosis of IBD, ileocolonoscopy should be performed. A minimum of two biopsies from at least five sites along the colon, including the rectum and terminal ileum, should be obtained
