Inflammatory Bowel Disease Flashcards
A good bowel history.
How often are they going to the toilet?
Changed from usual?
Has the form changed?
Are they waking overnight to go to the bathroom?
Is there any blood in stools?
Do they have tenesmus?
Do they have faecal urgency?
To they have faecal incontinence?
Is it foul smelling/float/does it easily flush?
Two main types of IBD.
Ulcerative colitis
Crohn’s
Investigations in IBD.
Bloods - FBC, U&Es and CRP
Stools - Cultures (exclude infective colitis) and Faecal calprotectin (usually raised in active disease and negative in remission)
Simple imaging like AXR is not commonly done anymore, however if there is suspicion of toxic megacolon it can be done.
Endoscopy
Cross-sectional imaging
Colonoscopy with biopsy is gold standard but not done in acute setting due to risk of perforation.
Explain endoscopy in IBD.
Flexible sigmoidoscopy is the safest test in bloody diarrhoea
Colonoscopy is done if you need to look for more proximal disease.
Capsule endoscopy is useful to view the small bowel mucosa.
Explain cross-sectional imaging in IBD.
CT abdomen when looking for acute complications
MRI enterography when looking for small bowel Crohn’s, fistulas or to map the extent of small bowel Crohn’s.
MRI rectum to image perianal Crohn’s
What is Ulcerative colitis?
A relapsing and remitting inflammatory disorder of the colonic mucosa.
It may just affect the rectum (proctitis), or extend to involve part of the colon (left-sided colitis) or the entire colon (pancolitis).
It should never (although it on rare occassions does) spread proximal to the ileocaecal valve.
It does not commonly involve perianal disease (such as Crohn’s can).
Cause of ulcerative colitis.
Inappropriate immune response against colonic flora in genetically susceptible individuals.
Pathology of UC.
Hyperaemic/haemorrhagic colonic mucosa +/- pseudo polyps formed by inflammation.
Punctate ulcers may extend deep into the lamina propria, but the inflammation is not transmural.
Continuous inflammation limited to the mucosa differentiates UC from Crohns.
Epidemiology of UC.
100-200/100000 in prevalence.
It typicall presents in 20-40 yo.
It is 3 times more common in non-smokers (and the opposite is true for Crohn’s) and symptoms may even relapse on stopping smoking.
Symptoms of UC.
Episodic or chronic diarrhoea with or without blood and mucus.
Crampy abdominal discomfort
Bowel frequency related to severity of disease
Urgency/tenesmus (proctitis)
Systemic symtpoms in attacks such as fever, malaise, anorexia, weight loss and fatigue.
Signs of UC.
May be none
In acute severe UC there may be fever, tachycardia and tender, distended abdomen.
Extraintestinal signs as well.
Extraintestinal signs of UC.
Clubbing
Skin - Aphthous oral ulcers (pic), Erythema nodosum, Pyoderma gangrenosum
Eyes - Conjunctivitis, Episcleritis, Iritis
Joint - Large joint arthritis, sacroiliitis, ankylosing spondylitis
PSC
Nutritional deficits.
Investigations in UC.
Bloods- FBC, ESR, CRP, U&Es, LFT and blood culture
Stool MC&S (culture and sensititivty) and CDT (C. diff toxin). This is to exclude Campylobacter, C. diff, Salmonella, Shigella, E. coli and amoebae.
Faecal calprotectin
AXR
Lower GI endoscopy
Findings on AXR in UC.
No faecal shadows
Mucosal thickening/islands.
Mural thickening
Thumbprinting (not only seen in UC)
Possible lead pipe colon on enema.
Explain lower GI endoscopy in UC.
Limited flexible sigmoidoscopy if acute to assess and biopsy.
Full colonoscopy once controlled to define disease extent.
Histology of UC.
Expansion of chronic inflammation in the mucosa and, in active cases, the presence of acute inflammation.
In mildly active cases, there is an acute cryptitis that progresses to crypt abscesses in moderately active cases.
In severe cases, mucosal ulcers develop as a result of the ongoing acute inflammatory process. Areas of relatively preserved mucosa between ulcerated areas may have a polypoid appearance grossly and are referred to as “pseudopolyps.” (This is mainly seen macroscopically)
Reduced goblet cells
Non-granulomatous
In cases of many years’ duration, dysplasia of the large bowel mucosa may develop and signifies an increased risk for the development of colorectal adenocarcinoma.
How is the severity of UC assessed?
Acute complications of UC.
Toxic dilatation of colon with risk of perforation
Venous thromboembolism (give prophylaxis to all in-patents regardless of rectal bleeding)
Hypokalaemia
Chronic complications in UC.
Colonic cancer
Lead pipe colon
Treatment of mild UC.
Remission/induction/maintenance = 5-ASA such as Mesalazine. This is given PR for distal disease or PO for more extensive disease.
Treatment of moderate UC.
If 4-6 motions a day but otherwise well induce remission with oral prednisolone 40mg OD for 1 weak and then taper by 5mg/week overfollowing 7 weeks.
Then go for 5-ASA like Mesalazine for maintenance.
Side-effects of 5-ASA.
Rash
Haemolysis
Hepatitis
Pancreatitis
Paradoxical worsening of colitis
What do all immunosuppressant medications require monitoring of?
FBC
U&Es
LFTs.