IBD Flashcards
1
Q
In tayside there are 2500 patients with IBD. Do more have UC or crohn’s disease?
A
More have UC
2
Q
What are the risk factors for IBD?
A
Vitamin D deficiency (Vit D suppresses pro inflammatory mediators)
Low fibre diet (Fibre prevents release of proinflamatory cytokines)
Western diet and residual starch around the gut lining => inflammatory response
3
Q
What are the clinical features of Crohn’s disease?
A
Abdominal pain Diarrhoea Anorexia and weight loss Malaise and fever Fistulas and strictures are deeper in the mucosa and can effect anywhere from mouth to anus
4
Q
What are the clinical features of Ulcerative colitis?
A
Bloody diarrhoea, colicky abdominal pain
Urgency
Effects the lining of the gut and from the rectum upwards
5
Q
Why do most IBD patients have a protein energy malnutrition?
A
Catabollic effect increases protein and calorie requirements
Increased nutritional losses via symptoms eg vomiting
Poor absorption due to active disease and section of bowel affected
Often eat poorl to aviod symptoms and do not get adequate intake
6
Q
Crohn’s disease often effects the small bowel. What nutritional contents should you monitor?
A
Fat soluble vitamins, vitamin B12,
Iron
(VItamins D and B12 are only absorbed in the small bowel.
Folic acid
7
Q
UC affects the large bowel. What nutritional contents should be monitored?
A
Electrolytes and fluid status.
Iron deficiency
8
Q
Is there a therapeutic diet for IDB?
A
No the dietary advice is no different from the general population but patients can get an open appointment and its good to get in contact sooner rather than later
9
Q
What are the common high risk deficiencies in Crohn’s disease?
A
Anaemia- IV not oral replacement.
Osteoporosis (calcium and Vit D)
Fat soluble vitamins, zinc, iron and B12.
10
Q
Patients with crohn’s disease get a annual B 12 injection. T or F?
A
True
11
Q
Crohn’s disease: steroid therapy is more effective than Entral nutrition from inducing long term remission but when would EN be chosen over steroids?
A
Steroid intolerance
Patient refusal of steroids
EN with steroids for malnourished patients
Inflammatory stenosis of the small intestine
Paediatrics- first line
12
Q
Would EN be used in UC?
A
No
Exclusive EN for 3-6 weeks can be used as an alternative to steroids in active Crohn’s disease
13
Q
What is Modulen?
A
Nutritional supplement/replacement which contains a naturally occurring anti inflammatory factor. Used first line in children and considered in adults (poor compliance/response to medication)
14
Q
Preventing malnutrition is key to maintaining remission in IDB patients. T of F?
A
True
15
Q
When is Parentral nutrition used in IBD?
A
No evidence that PN helps to induce remission in CD or UC.
May be used Pre op to improve nutritional status.
PN or Home PN can be used in CD with intestinal failure due to short bowel syndrome
16
Q
When would you give total parentral nutrition in CD?
A
Extensive active disease in the small bowel Previous multiple surgeries Short bowel syndrome <1m Fistulas, strictures or obstructions All => Intestinal failure
17
Q
What is colitis?
A
Inflammation of the colon
18
Q
Why was crohn’s disease previously confused with TB?
A
They are both granulomatous diseases
19
Q
WHat is Crohn’s disease and where does it most commonly affect?
A
Chronic inflammatory ulcerating condition of the GI tract that can affect anywhere from the mouth to the anus.
Most common in the terminal ileum and colon
20
Q
Who is diagnosed with crohns disease?
A
Most people are in 20s and 30s
Slightly more common than males
21
Q
How does Crohn’’s disease present?
A
Ando pain Small bowel obstruction Diarrhoea Bleeding PR Anaemia Weight loss. (Similar symptoms to cancer but in a young person
22
Q
What is the clinical course of Crohns?
A
Chronic
Relapsing and remitting with an unpredictable response to therapy
23
Q
How is Crohns disease diagnosed?
A
Endoscopy and mucosal biopsy
24
Q
What is the endoscopic pattern of Crohns disease?
A
Patchy and segmental disease with Skip areas or lesions anywhere in the GI tract
Deep festering producing Cobblestonning and ulceration
Pseudopolyps may be seen but are uncommon
Fat wrapping
25
What are the histopathological appearances of crohn's disease?
Granuloma (non caseating) formation.
Patchy inflammation of the lamina propria
Crypts are irregular and infiltrated by inflammatory cells. (Cryptitis and crypt abscesses)
Transmural involvement of the bowel wall.
Sinus tracts (deep fissures
26
When are you most likely to see granulomas in Crohn's disease?
Young patients early in disease process.
27
What are the complications of chron's diease?
Malabsorbsion
- Hypoproteinaemia, Vit deficiency, Anaemia
- Iatrogenic small bowel syndrome due to repeated resections and recurrences.
- Gall stones as you do not reabsorb the bile salts
Fistulas
-Vesicocolic, enterocolic, gastrocolic, rectovaginal
- Tubovarian abscess
- Blind loop syndrome
Anal disease
- Sinuses, fissures, skin tags, abscess, perineum falls apart and effects genitalia
Intractable disease
Bowel obstruction. perforation, malignancy, Amyloids, rarely toxic megacolon
28
What genetic defects are associated with Chrons disease?
NOD2 on chromosome 16
Associated with HLA proteins
But it also has environmental triggers
29
What are the environmental triggers of Crohns disease?
Smoking increases risk
Infectious agents (viral mycobacterial)
Vasculitis could explain segmental distribution
Sterile environment
30
What happens to the immune system in Crohn's disease?
Autoimmune disease
Persistent activation of T cells and macrophages
Excess proinflamatory cytokine production
May be altered by changing bowel flora
31
What is Ulcerative colitis and where does it effect?
Chronic inflammatory disorder confined to the colon and rectum with mucosal and submucosal inflammation (superficial)
Begins in the rectum and proceeds continuously up the colon to where it stops
32
WHo gets UC?
30s and 40s.
Can occur in elderly and children
Slightly more ommon in males
33
What is the clinical presentation of UC?
```
Diarrhoea, mucus and blood PR.
Increased bowel frequency and urgency/incontinence.
Tenesmus
Night rising
Lower abdo pain LIF
Proctitis can cause constipation
```
34
What is the clinical course of UC?
Chronic
Relapsing and remitting.
Some people have one single attack but often its continuous low grade activity.
Acute fulminant colotis (toxic mega colon)
35
How is UC diagnoses?
Endoscopy and mucosal biopsy
36
What are the endoscopy findings in UC?
Red inflamed rectum which may spread continuously into the colon (can stop at the rectum or go all the way to caecum)
Ulcers and pseupopolyps are common
Loss of vessel pattern
Contact bleeding
37
What are the histopathologiacl findings in UC?
Diffuse mucosal chronic inflamation
Irregular shaped and branching crypts (Cryptitis and crypt abcesses) with loss of goblet cells
Superficial inflammation (except in toxic megacolon)
NO granulomas
38
What happens if te UC patient does not respond to therapy?
Sub total colectomy.
| You can remove the entire colon and preserve continence using as ileoanal anastamosis
39
What are the complications of UC?
Intractable disease
Flares may be due to enteric bacteria or CMV.
Toxic megacolon (surgical emergency- need to aviod perforation as this would lead to peritonitis)
Colorectal carcinoma (chronic inflammation => epithilial dysplasia and carcinoma)
Blood loss
Electrolyte disturbance
Anal fissures (uncommon)
40
When is the risk of colorectal carcinoma in chrons disease increased and when are patients surveyed?
Risk increased with pan colitis or disease longer then 10 years.
All UC patiets screened if disease longer than 10 years
41
What are the extra GI manifestations of UC?
Eyes: Uveitis, episcleritis
Mouth: Stomatitis, ulcers
Liver: Primary Sclerosing cholangitis, gallstones
Joints: Arthritis, Ankalosing spondylitis
SKin: Pyoderma gangrenosum, erythema nodosum
Kidneys: Stones, Hydronephrosis, Fistula, UTI
42
What is Primary Sclerosing cholangitis?
Autoimmune disease of the liver effecting the bile ducts. Development of strictures in the common and intrahepatic ducts.
Diagnosed by ERCP.
Cholestatic LFTs.
=> Liver transplant or 15% get cholangiocarcinoma
43
What are the genetic defects associated with UC?
NOD2 on chromosome 16
| HLA genes
44
WHat is the immune response in UC?
Persistent activation of T cells and macrophages
Autoantibodies produced eg ANCA
Excess pro inflammatory cytokine produced and bystander damage due to neutrophilic inflammation.
May be altered by microbiome
45
Is smoking associated with UC?
No
46
What are the main reasons for referral to gastroenterology from primary care?
Rectal bleeding
Altered bowel habbit
5% have colorectal cancer and 5% have IBD. ()% have something else
47
What is indeterminate colitis?
WHe you cannot decide if its UC or Crohns colitis
48
Where is IBD most common?
Developed world.
| The further north you live in the northern hemisphere the higher the incidence
49
What is the pathogenisis of IBD?
Genetic predisposition
Mucosal immune system
Environmental triggers
50
What are the greatest risk factors for developing iBD?
IBC in a first degree relative especially is early onset of disease
51
What is the link with IBD and NOD2?
20% of caucations with IBD have defects in this gene. If you are homozyous for the gene you are at greater risk than if you are heterozygous
NOD2 encodes a proteins involved in bacterial recognition
52
What is the role of the gut frola in IBD?
Altered bacterial flora can be seen in UC and antibiotics are effective in treating perianal crohn's disease so the gut flora is important.
53
Which T cells mediate crohns and UC?
```
Crohn's = Th1
UC = mixed Th1/2 and NK cells
```
54
Crohn's disease is associated with more/less bacteria in the gut?
More.
| UC is associated with less
55
Smoking increases stricturing and fibrosis in Crohn's disease but is protective in UC. T or F?
T
56
Patients with IBD must stop all NSAIDs. Why?
These pre-dispose to flare ups
57
What is Proctitis, left sided colitis and pancolitis?
Proctitis- Inflammation affecting the rectum only
Left sided colitis- extends to the splenic flecture
Pan colitis - effects the entire colon
58
What criteria is used to asses UC severity? What is severe UC?
Truelove and Witt criteria.
Severe = >6 bloody stools/day + 1 or more of:
Fever
Tachycardia
Anaemia
Elevated ESR (erythrocyte sedimentation rate)
This carries a 30% risk of colectomy
59
What other markers can be used to assess UC severity?
CRP (raised) and Albulmin (low)
60
Why do you do a sigmoindoscopy without bowel prep first line in suspected UC?
Bowel prep can lead to further irritation of the colon and complications including toxic megacolon and perforation
61
What are the signs of UC on a plain AXR?
Air within hte colon rather than stool
Mucosal oedenal/thumbprinting
Toxic megacolon
62
What defines toxic megacolon?
Transverse >5.5cm
| Caecum >9cm
63
Peri-anal disease is common in Crohn's disease. WHat is this?
Recurrent abscess formation in the anus => pain.
Can lead to a fistula with persistent leakage
Damages external and internal anal sphincters
64
Why would you check B12 and ferritin levels in someone with Crohn's disease?
These are absorbed in the terminal ileum and crohn's patients are likely to be deficient in them.
65
What are the most common tests to assess the small bowel?
Small bowel MRI with IV and oral contrast- Gold standard.
Barium follow through
Technetium labelled white cell scan
66
What is a Technetium labelled white cell scan?
Radiolabelled wihite cells will hone to the part of the bowel which is inflamed and light it up
67
What tool is used to assess Crohn's disease severity?
Crohn's disease activity index
68
What are the aims of IBD therapy?
Contraol inflammation and heal mucosa (gold standard)
Restore normal bowel habit (no night rising, 1 or 2 times a day with formed stool, no blood or mucus)
Improve QoL
Balance effects of disease with side effects of treatment
Aviod long term complications
69
What is the lifestyle advice given to IBD patients?
Stop smoking- Smoking leads to rapid recurrence of crohn's disease post surgery. 70% of smokers will have a relapse in 10 years whereas only 40% of non smokers will
Diet is not implicated in pathogenesis but can influence symptoms (eg strictures pre op may opt for a low fibre diet to reduce symptoms )
70
Smoking is the only independent predictor of clinical, endoscopic and surgical recurrence of Crohn's. T or F?
True
71
What is first line therapy for UC?
5ASA (5-Aminosalicylic acids)
| Mesalazine based
72
What is used to control acute flare ups of IBD?
Steriods- short courses. Not used long term.
73
What is the first line therapy in Crohn's management and an additional therapy in UC?
Immunosupressants
74
Anti-TNF therapy is used in both forms of IBD. WHen is it used?
When immunosupressants are not controlling the symptoms and inflamation
75
What is the action of 5 ASAs?
Topical effect or reducing mucosal inflammation.
| Reduces risk of colon cancer in long term
76
What are the side effects of 5ASAs?
Diarrhoea and idiosyncratic nephritis (monitor kidney function and assess for kindey damage before and after starting the drug
77
What are the different types of 5ASA drugs?
```
ORAL (Mesalazine based)
Mezavant- Prodrug (matrix carrier)
Asacol- pH dependent release
Pentasa- Delayed release
TOPICAL
Suppositories
Enemas
```
78
When would you give both oral and topical treatment with 5ASAs in UC?
During a flare up and then step down to just oral usually.
| Also oral medication is started on a high dose in flare ups and then step down to a half dose
79
When would pentasa be used as a drug of choce in UC?
UC backwash ileitis- where UC can effect the terminal ileum
80
The 5ASA tablets are massive, is there an alternative?
Granules to put on food or mix in
81
How which parts of the bowel do suppositories act on?
Distal 20cm.
| Better mucosal adherence than enemas though.
82
Less than 10% of enemas remain in the rectum. Most spread proximally to the sigmoid and descending colon. What mechanism causes this?
Reflex contraction towards the caecum
83
A foam enema of prednisalone is available. But why is oral budesonide preferred to oral prednisalone?
Oral prednisalone has many systemic effects. Budesonide has less systemic effects as it avoids some first pass metabolism
84
What is steroid treatment used for in management of IBD?
Induce remission during a flare up. Initially high dose reducing over 6-8 weeks
85
Why are steroids not used long term?
Side effects and 25% of people become steroid dependent
86
What are the side effects of steroids?
Metabolic = weight gain, diabetes, hypertension
Neuropsychiatric- manic, depression
Eyes = cataracts
GI ulceration (give a PPI too)
Skin = Acne and thinning
MSK = osteoporosis (give Acrete D3 too to improve bone health) avascular necrosis
Growth failure in children
87
When should steroids be taken?
First thing in the morning as if taken at night they can prevent sleep
88
What are the common immunosuppressants used in IBD?
Azathioprine/ mercaptopurine
| Methotrexate - infrequently
89
How is Azathioprine metabolised in the LIVER?
Azathioprine is the prodrug which is metabolised to 6MP.
6MP is then metabolised by HPRT to 6 TGN- the active drug which suppresses the bone marrow so fewer white cells are produced.
6MP is also naturally metabolised to 6MMP by TPMT (variants of this which metabolise 6MP at different rates). This effects the dosing as you don't want too much 6TGN as this will completely suppress the bone marrow.
6MP can also be metabolised to 6TU by Xanthine Oxidase (Do not administer a XO inhibator too as this will increase 6TGN concentration further suppressing bone marrow)
90
What is allopurinol?
An Xanthine oxidase inhibator.
| Do NOT co administer with azathioprine.
91
How long does it take azathioprine to act?
16 weeks (slow onset)
92
What are the side effects of azathioprine and what must you monitor?
Monitor bloods
Side effects = Pancreatitis, Leucopaenia, Hepatisis, small risk of lymphoma and skin cancer (use high factor suncream all year round
93
What are the targets for biological therapies in IBD?
TNF alpha (main- prevents proinflamatory cytokine release reducing WBCs)
MadCAM (prevents white cells adhering to enterocytes and migrating from the blood stream)
IL17 and 23
94
What is the most common monoclonal antibody used in IBD targeting TNF alpha?
Infliximab by IV infusion.
| This promotes apoptosis of activated T cells and has a rapid onset of action 24 hours
95
How is Infliximab used?
3 loading doses and then return for further IV infusion every 8 weeks.
You would also start azathioprine at the same time as it takes 16 weeks to take effect.
96
Why are monoclonal antibodies not used long term?
Some patients can develop antibodies against the monoclonal antibodies as they are recognised as non self.
Makes them useless.
Induces rapid remission in 30-40% of patients including mucosal healing.
97
WHat are the side effects of Infliximab?
Infusion reaction as some patients already have antibodies against the therapy (given low does hydrocortisomne to prevent this if possible)
Infection
Small risk of Lymphoma
98
Why must you check for TB before starting inflixamab?
Latent TB can be reactivated so it they have this then you must treat the B first before starting therapy
99
When is Inflixamab used?
Long term IBD stratery including immunosupression, surgery and supportive therapy
100
Inflixamab has just come off patent making it cheaper, what are the non brand alternatives?
Inflectra and Remsima
101
When is surgery required in IBD?
Emergency: first presentation and failure to respond to steroid therapy maybe with obstruction, abscess or fistulae. You can see if steroid response within 3 days.
Elective: failure to respond to medical therapy or dysplasia of colon mucosa. Planned and prepared, the patient is as fit as they can be and prepared for a stoma if required
102
What is an ileostomy?
Stoma at the terminal ileum as the colon has been removed.
103
WHat happens if a patient has had previous resection and then later develops another stricture?
You can try to repair the stricture rather than further resection
104
What is a Seton suture used to treat?
Perianal fistulae and abcesses- all the pus draines out and then healing begins from the proximal area
105
What are the options for surgery in UC?
Curative
1) Permanent ileostomy
2) Restorative proctoccolectomy and J pouch preserving continance (still need to toilet 4-5 times a day)
