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.
Treatment of severe UC.
If unwell and 6 or more motions a day admit the patient.
IV hydration/electrolyte replacement.
IV steroids such as hydrocortisone 100mg/6h or methylprednisolone 40mg/12h.
Thromboembolism prophylaxis
Exclude infection.
Monitoring of severe UC.
Monitor temp, pulse and BP, record stool charts
Twice-daily exam of abdomen, distension, bowel sounds and tenderness.
Daily FBC, ESR, CRP, U&Es +/- AXR. Consider blood transfusion if anaemic and Hb <80g/L
Indications of rescue therapy in UC.
If on day 3-5 and CRP is still > 45 or > 6 stools a day.
Rescue therapy of UC.
Ciclosporin
Infliximab
or
Surgery.
If severe UC is improving, how should treatment be altered?
Transfer to oral prednisolone 40mg OD.
Schedule maintenance infliximab if used for rescue, or azathioprine if ciclosporin is used for rescue.
If treatment fails (even rescue therapy) what should be done?
Urgent colectomy by day 7-10.
Indications for immunomodulation in UC.
Patients falre on steroid tapering or require 2 or more courses of steroids a year.
Azathioprine is used.
Indications for biologic therapy in UC.
For patients intolerant of immunomodulation or develop symptoms despite an immunomodulator.
Infliximab, adalimumab and golimumab might be used (anti-TNFalpha)
Or adhesion molecules involved in gut lymphocyte trafficking such as vedolizumab.
Indications for surgery in UC.
This is needed at some tage in 20% of patients.
If there is failure of medical therapy or fulminant colitis with toxic dilation/perforation.
Different surgeries in UC.
Subtotal colectomy + terminal ileostomy
Completion proctectomy
Ileo-anal anastomosis (J-pouch)
What is Crohn’s disease?
A chronic inflammatory disease characterised by transmural granulomatous inflammation affecting any part of the gut from mouth to anus. Especially the terminal ileum.
Unlike UC there is unaffected bowel between areas of active disease called skip lesions.
Epidemiology of Crohn’s.
Prevalence = 100-200/100000
Incidence = 10-20/100000/yr
Typically presents in 20-40 yo
Smoking increases the risk and NSAIDs may exacerbate disease.
Symptoms of Crohn’s.
Diarrhoea
Abdo pain
Weight loss
Failure to thrive
Systemic symptoms such as fatigue, fever, malaise and anorexia.
Signs of Crohn’s disease.
Bowel ulceration
Abdominal tenderness/mass
Perianal abscess/fistuale/skin tags
Anal strictures
Extra-intestinal signs of Crohn’s.
These are ranked commonest to least common.
MSK
Arthritis: colitic type, ankylosing spondylitis, isolated joint involvement
Hypertrophic osteoarthropathy: clubbing, periostitis
Skin
Reactive lesions: erythema nodosum, pyoderma gangrenosum, aphthous ulcers, necrotizingvasculitis
Specific lesions: fissures, fistulas, oral Crohn’s disease, drug rashes
Nutritional deficiencies: acrodermatitis enteropathica, purpura, glossitis, hair loss, brittle nails
Hepatopancreatobiliary system
Primary sclerosing cholangitis, bile-duct carcinoma
Associated inflammation: autoimmune chronic active hepatitis, pericholangitis, portal fibrosis, cirrhosis, granulomatous disease
Metabolic manifestations: fatty liver, gallstones associated with ileal Crohn’s disease
Ocular system
Uveitis/iritis, episcleritis, scleromalacia, corneal ulcers, retinal vascular disease
Investigations in Crohn’s.
Bloods - FBC, ESR, CRP, U&Es, LFTs, INR, Ferritin, TIBC, B12, Folate
Stool - MC&S and CDT. Faecal calprotectin.
Colonoscopy and biopsy
Capsule endoscopy for small bowel
MRI - to assess pelvic disease and fistulae, small bowel dsiease and strictures.
Enema
Histology of Crohn’s
The characteristic pattern of inflammation in Crohn disease is a transmural involvement of the bowel wall by lymphoid infiltrates that contains sarcoidlike granulomas in about half of the cases (most commonly in the submucosa).
Paneth cell hyperplasia is frequent and areas of pyloric metaplasia may be seen.
In full-blown cases, long and deep fissure like ulcers form.
Non-pharma treatment of Crohn’s.
Help quit smoking.
Optimise nutrition
Assess severity by pulse, temp, ESR, WCC, CRP and decreased albumin.
This will guide further treatment.
Treatment of mild-moderate Crohn’s.
Symptomatic but systemically well.
Prednisolone 40mg OD PO for 1w.
Taper by 5mg every week for next 7w.
Then plan maintenance therapy.
Treatment of severe Crohn’s.
Admit.
IV hydration/electrolyte replacement
IV steroids e.g. hydrocortisone 100mg/6h or methylprednisolone 40mg/12h.
Thromboembolism prophylaxis
Exclude infection.
Monitoring of severe Crohn’s.
Temp, pulse, BP and record stool chart.
Physical examination daily.
Daily FBC, ESR, CRP, U&Es and plain AXR.
Consider need for blood transfusion (<80g/L) and nutritional support.
Management of severe Crohn’s once improving.
Switch to oral prednisolone 40mg OD.
Rescue therapy for Crohn’s if things are not improving in severe Crohn’s.
Biologics.
Surgery.
Different therapies in Crohn’s disease.
Azathioprine
Biologics
Nutrition
Surgery
Maintenance therapy in Crohn’s.
Azathioprine and biologics.
Azathioprine is indicated if refractory to steriods, relapsing on steroid taper or requiring 2+ steroid courses in a year.
Remember to montior FBC, U&Es, LFTs weekly for 4 weeks then every 4 wks for 3 months.
After this at least 3-monthly.
Alternative immunomodulators to azathioprine in Crohn’s.
6-mercaptopurine
Methotrexate
Biologics used in Crohn’s.
Anti-TNFalphas like infliximab and adalimumab - should be avoid in underlying malignancy and TB.
Anti-integrins such as vedolizumab.
Anti-IL12/23 such as ustekinumab.
Explain nutrition treatment in Crohn’s.
Enteral is preferred but consider TPN as a last resort.
Elemtal diets containing amino acids can give remission.
Low residue diets can help symptoms in those with active disease or strictures.
Indications for surgery in Crohn’s.
Drug failure
GI obstruction from strictures, perforation, fistulae or abscess.
Perianal disease
Growth failure in young people
Surgical aims in Crohn’s.
Resection of affected areas
Control perianal or fistulising disease
Defunction distal disease with a temporary ileostomy e.g.
Explain perianal disease in Crohn’s (does not happen in UC)
Occurs in about 50%.
MRI and examination under anaesthetic are an important part of assessment.
Treatment of perianal disease in Crohn’s.
Oral antibiotics
Immunosuppressant therapy +/- anti-TNFalpha
Local surgery +/- seton insertion.
What is the first line of choice medication wise in perianal or fistulating Crohn’s?
Biologics
Differences between Crohn’s and UC.
Crohn’s can affect anywhere from mouth to anus where as UC always affects the rectum and extends proximally.
Crohn’s have skip lesions where as UC is continuous.
Crohn’s has transmural inflammation where as UC has mucosa and submucosal inflammation only.
Crohn’s have fissuring ulcers and non-caseating granulomas where as UC has crypt abscesses.
Crohn’s have lymphoid and neutrophil aggregates as well as cobble-stone appearance.
Crohn’s have perianal disease.
Crohn’s is increased in smokers, UC is decrease in smokers.
