GI: IBD Flashcards
NEED TO ADD: CROHNS TREATMENT
A patient attends your clinic with suspected IBD. Their presenting complaint is having a change in bowel habit. What might you ask in your history to assess this change in bowel habit?
How often are they going to the toilet?
Has this changed from their usual?
Has the form of the stool changed?
Are they waking overnight to open their bowels?
Is there any blood in the motion?
Do they have tenesmus?
Do they have fecal urgency or incontinence?
Do the motions flush away easily?
What are the two conditions involved in IBD?
Chron’s disease and UC
What features distinguish Chron’s from UC?
Format for below: Chron’s vs UC
Affects anywhere from mouth to anus vs always affects rectum and extends proximally.
Skip lesions vs continuous
Transmural inflammation vs mucosa and submucosal inflammation only
Fissuring ulcers vs crypt absecesses
Increased incidence in smokers vs decreased incidence in smokers
Name two features specific to the microscopic appearance of Chron’s
Lymphoid and neutrophil aggregates
Non caseating granulomas
Define UC
An IBD characterised by diffuse inflammation of the colonic mucosa
Characteristically, where is UC found in bowel?
Rectum and extends proximally.
On endoscopy, what would you see in Chron’s?
Apthous ulcers
cobblestone appearance
On colonscopy , what would you see in UC?
- Ulcerative proctitis (look at pic in slides on BB on UC)
- loss of haustral markings
- psuedopolyps
In UC, the inflammation of mucosa can spread proximally by different amounts. What are the three main subcategories of this spread?
- distal (proctitis)
- left sided (inflammation up to the splenic flexure)
- can be extensive = beyond splenic flexure.
- (also have pancolitis = whole colon)
Who does UC usually affect?
two peak age groups:
* 15 to 25 years
* 55 to 65 years.
Patients can have a relapse of colitis. What is a common reason for this?
Pathogen causing gastroenteritis
What are cardinal symptoms of UC?
Bloody diarrhoea
Urgency (Including waking at night needing to open bowels)
Tenesmus
What investigations would you do for patient with suspected IBD?
Blood:
FBC (WCC - infection?, platelets - bleeding?), CRP (inflammation), U&E (may have hypokalaemia from diarrhoea)
LFTs- UC can have primary sclerosing cholangitis as a complication
Stool:
MC&S, C diff toxin
Radiological:
AXR - toxic megacolon, to see extent of inflammation, to see if they have proximal constipation (seen in left sided disease).
Endoscopic:
Flexible sigmoidoscopy, biopsy of bowel, colonoscopy at later date for bowel cancer.
Note - Dr Rogers said to give one from each group to ensure marks in exam. And even though it may say list investigations, justify why.
Name the three categories of extra-intestinal manifestations you would cover in a Hx of a pt with IBD
1) Those defo related to disease activity (present when bowels are bad)
2) Those usually related to disease activity
3) Those which are unrelated to disease activity (present regardless of bowel disease severity, can even present before diagnosis of IBD or after curative surgery)
What are extra-intestinal manifestations of IBD? 2 marks - so name 4!
1) Those defo related to disease activity
- erythema nodosum - usually on shins
- apathos ulcers
- episcleritis - one form of red eye
- acute arthropathy - a bit like RA but pain and stiffness which gets better when bowels get better
2) Those usually related to disease activity
- pyoderma gangrenous - ulcerative skin condition
- anterior uveitis - another form of red eye.
3) Those which are unrelated to disease activity
- sacroileitis - pain and inflammation in sacroiliac joint
- ankylosing spondylitis - bamboo spine
- primary sclerosing cholangitis - beaded appearance of bile ducts in imaging
If a patient has UC and PSC, why is it important to have bowel screening annually?
Both of these individually increase risk of bowel cancer. Together = further increase in bowel cancer risk!!! Can come about in between surveillances too.
What are aims of treatment for IBD?
Induce remission in acute disease
Maintain remission
Improve QofL
Decrease risk of colorectal cancer
Do IBD flares lead to an antithrombotic or prothrombotic state?
IBD patients are v v v PROTHROMBOTIC - some patients develop DVTs and PEs. Therefore pts should be on LWMH ! Prevents microvascular occlusions seen in IBD too so beneficial in more than one way
What must be given alongside steroids for IBD?
Bone protection - bisphosphonates, or calcium and vit d in younger pts.
Why is Mesalazine given as a topical preparation to apply PR or modified in treatment of UC?
Mesalazine is absorbed from the jejunum - not ideal when we want it to reach the colonic mucosa in UC.
Because of this property, it has to be applied PR or linked to a molecule that is enzymatically cleaved in the colon - to ensure it reaches there. Can also be given as suppositories or enema
What are side effects of mesalazine
These are uncommon but good to know:
- diarrhoea
- headache
- nausea
- rash
v rare: interstitial nephritis, nephritic syndrome
Why do U&Es need to be monitored in patients taking mesalazine?
Can cause interstitial nephritis and nephritic syndrome
A patient has UC. They are unable to take steroids as they are intolerant. What would you use to manage them?
Azathioprine - these are steroid sparing agents
What are ADRs of azathioprine?
Flu like symptoms, GI upset, leucopenia, hepatitis, pancreatitis, rash and infections
What is a disadvantage of Azathioprine?
Immunosuppresnts- so cause Flu like symptoms, GI upset, leucopenia, hepatitis, pancreatitis, rash and infections
Increase risk of skin cancer
Onset of action takes at least 6 weeks (Dr Rogers said usually 12 weeks)
A patient has a flare of UC but steroids do not seem to be helping. She still has severe bloody diarrhoea, tenesmus and urgency. This is termed Severe refractory colitis (where steroids and 5ASAs have failed to work in UC).
What might you do next in your management plan?
Ciclosporin. A salvage therapy in severe refractory colitis.
What are benefits of ciclosporin in severe refractory UC?
Rapid onset - starts IV then given orally.
A good drug to use while azathioprine is being taken but hasn’t reached onset of action (6 weeks)
Why do patients with UC need to have their proximal constipation relieved?
Necessary to allow for UC to improve, and induce remission - as once evacuated, no stool there to irritate already inflamed mucosa.
Why do patients with left sided UC have proximal constipation?
Colonic motility is affected by inflammation with rapid transit occurring in inflamed part of colon.
In left sided disease, distal transit is rapid, but the proximal transit is slowed (in non inflamed part of bowel) - this causes proximal constipation.
Note: This is a protective mecahanism by the body.
How is proximal constipation relieved in UC?
Give laxatives
When is emergency colectomy done in patients with PMH of UC?
They have toxic megacolon and acute colitis that isn’t responding to medical therapy
When may elective surgery be planned for a pt with PMH of UC?
When they:
- are steroid dependent
- want surgery
- have a high grade dysplasia or cancer found in screening
You see a 26M, 2wk Hx of bloody D-. Saw GP who gave him codeine and loperamide as well as ORT.
No one else at home has loose motions.
Feels tired and lethargic.
Most recent bloods show raised CRP.
What are Ddx?
UC - main differential
Chron’s
Infective colitis
What would you see on histology in UC?
Crypt abcesses and decreased goblet cells
Extra-intestinal features of IBD that are related to disease activity?
Arthritis - affects a few joints, asymmetrical
Erythema nodosum
Espiscleritis
Osteoporosis
Extra-intestinal features of IBD that are unrelated to disease activity?
Arthritis - polyarticular, symmetrical
Uveitis
Pyoderma gangrenosum
Clubbing
Primary sclerosing cholangitis
Presentation of PBC (primary biliary cirrhosis)?
Xanthoma, xanthelasma
Fatigue
Pruritis
GI disturbance, abdo pain
Jaundice
Pale, greasy stools
Signs of cirrhosis, liver failure —> ascites, hepatomegaly, splenomegaly, spider naevi
Investigations for PBC?
LFTs - ALP raised early on, ALT and bilirubin raised later.
Autoantibodies - Anti-mitochon (most specific), ANA
CRP, ESR, IgM
Liver biopsy to diagnose and stage
How is PBC treated?
Immunosuppresion - azathioprine or steriods
Liver transplant
Ursodeoxycholic acid = reduce intestinal absorption of cholesterol
Colestyramine = sequesters bile acid (bile acid = a cause of itching in PBC) so reduces this symptoms
Complications of PBC?
Advanced liver cirrhosis
Portal HTN
Fatigue - TATT
Distal renal tubular acidosis
HypoThyroidism
Osteoporosis
Hepatocellular carcinoma
Fatty, greasy stools = steatorrhea
RF for PSC? aka primary sclerosing cholangitis
Male
30-40
UC in PMH
FHx
Presentation of PSC?
Jaundice
Fatigue
Chronic RUQ pain
Pruritus
Hepatomegaly
Inv and corresponding results for PSC?
LFTs - ALP v high, raised bilirubin, ALT and AST also raised but more common as disease progresses
Autoantibody screen - p-ANCA, ANA and aCL
MRCP = gold standard for Dx!! - show bile duct lesions or strictures.
Complications of PSC?
Acute bacterial cholangitis
Cholangiocarcinoma
Colorectal cancer (relation to UC)
Cirrhosis, liver failure
Biliary strictures
Fat sol vitamin deficiency - ADEK
Management of PSC?
Liver transplant
ERCP to dilate and stent strictures
Ursodeoxycholic acid
Colestyramine
Monitor for complications - cirrhosis, cholangiocarcinoma, oesophageal varices
Imaging of choice in PSC?
ERCP/MRCP
How are flares classified in UC?
- Mild: < 4 bloody stools a day
- Moderate: 4-6 bloody stools a day
- Severe > 6 bloody stools a day
How to treat a mild- moderate flare of UC?
Oral steroids
How to treat a severe flare of UC?
Admit + IV steroids
How to maintain remission in a person with UC who has frequent relapses?
Following a severe relapse or >=2 exacerbations in the past year
* oral azathioprine or oral mercaptopurine
