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Gastroenterology > Inflammatory bowel disease > Flashcards

Inflammatory bowel disease Flashcards

1
Q

What is Crohn’s disease?

A

Disorder of unknown aetiology characterised by transmural inflammation of the GIT.

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2
Q

Where does Crohn’s disease usually affect?

A

May involve any part of the entire GIT: mouth –> perianal. Usually seen in terminal ileal and perianal locations.

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3
Q

What is Crohn’s disease characterised by?

A

-Skip lesions (normal bowel mucosa found between diseased areas).

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4
Q

What are the complications of Crohn’s disease?

A
  • Transmural inflammation –> fibrosis –> intestinal obstruction
  • Inflammation –> sinus tracts –> penetration of serosa –> perforations and fistulae.
  • Malnutrition (damaged mucosa, poor absorption).
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5
Q

Where is the incidence of Crohn’s disease highest?

A

Highest incidence in northern climates and developed countries; lowest in southern climates and less developed countries.

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6
Q

When is the peak age of onset of CD?

A

15 - 40 years.

Smaller second peak 60 - 80 years.

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7
Q

Are women or men more affected by CD?

A

Equally affected.

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8
Q

What is the aetiology of Crohn’s disease?

A

Unclear: genetic, environmental factors + host immune response.

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9
Q

How does the initial CD lesion begin?

A

Inflammatory infiltrate around intestinal crypts–> ulceration of the superficial mucosa. Inflammation progresses to involve deeper layers and forms non-caseating granulomas. Granulomas involve all layers of intestinal wall, mesentery and regional lymph nodes.

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10
Q

What are the early endoscopic findings of CD?

A

Hyperaemia and oedema of inflammed mucosa. Progresses to discrete superficial ulcers separated by healthy tissue (skip lesions).

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11
Q

Why are individuals with CD prone to oxalate kidney stone formation?

A

CD involving terminal ileum interferes with bile acid resorption –> steatorrhoea –> excessive fat in stool binds calcium increasing oxalate absorption.

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12
Q

What are the extra intestinal manifestations of CD?

A

Skin, joints, mouth, eyes, liver and bile ducts.

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13
Q

How is CD classified?

A

Vienna classification:

1) Age at Diagnosis (A1, A2)
2) Location (L1-4)
3) Behaviour (B1- B3)

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14
Q

CD secondary prevention?

A

Smoking cessation only lifestyle modification shown to effect recurrence.
-CRC screening colonoscopy every 1-2y, 8y post diagnosis.

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15
Q

What are the key diagnostic factors for CD?

A

-Presence of RFx
-Abdo pain
-Prolonged diarrhoea
-Perianal lesions
+/- bowel obstruction, blood in stools, fatigue, weight loss.

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16
Q

What are the RFx for CD?

A
  • White ancestry
  • Age 15 - 40, or 60 - 80y
  • FHx of CD
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17
Q

What tests should be ordered investigating CD?

A

FBE (anaemia, leukocytosis); iron studies (normal, or iron deficiency); B12 (normal or low); serum folate (normal or low); CRP (elevated).
Plain abdo films (small or large bowel dilation, calcification), barium meal (skip lesions, thickening, ulceration, fistulae) CT abdo.

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18
Q

What barium meal/CT findings indicative of CD?

A

Skip lesions, bowel wall thickening, surrounding inflammation, abscess, fistulae.

19
Q

What endoscopy/colonoscopy findings indicative of CD?

A
  • Aphthous ulcers
  • hyperaemia, oedema,
  • cobblestoning,
  • skip lesions.
20
Q

DDx for CD?

A

UC (colonoscopy differentiates - rectal and contiguous)); infectious colitis (Hx sick contacts and travel); pseudomembranous colitis (recent Ab use).

21
Q

How does Crohn’s disease usually present?

A

Acute: RIF pain and tenderness (may mimic appendicitis). Or fx of low SBO.
Chronic: weight loss, colicky abdo pain and diarrhoea.

22
Q

How should CD be managed?

A

Smoking cessation, diet (fluid during exacerbation, supplementation), antidiarrhoeals, 5-ASA, Antibiotics, corticosteroids, immunosuppressives, biologicals, surgical treatment.

23
Q

Considerations regarding antidiarrhoeals in CD?

A

Loperamide drug of choice.

Caution if colitis is severe (risk of toxic megacolon).

24
Q

What is 5-ASA?

A

Sulfasalazine.
Chemically similar to aspirin==> 5-ASA bound to sulfapyradine to prevent absorption by stomach. Bacteria hydrolyse to release 5-ASA.

25
Q

What are the features of Crohn’s disease?

A 
CHRISTMAS:
Cobblestones (Radiology appearance)
High temperature
Reduced lumen
Intestinal fistulae, Infliximab
Skip lesions
Transmural (all layers, may ulcerate)
Malabsorption
Abdominal pain
Submucosal fibrosis
26
Q

What is the role of immunosuppressives in Crohn’s disease management?

A

6-mercaptopurine, azathioprine, methotrexate.

Maintain remission rather than treat active.

27
Q

What are the side effects of immunosuppressives used in Crohn’s disease?

A

Vomiting, pancreatitis, bone marrow suppression, increased risk of malignancy.

28
Q

What are the biologicals used to treat Crohn’s disease?

A

Infliximab IV or adalimumab ==> antibody to TNFa.
Proven effective for treatment of fistulae.
Improves immunosuppressives activity.

29
Q

What is the role of surgery in CD?

A

Complications (fistulae, obstruction, abscess, perforation, bleeding); failure to thrive in children; intolerance of medical therapy.
If risk of short bowel syndrome.

30
Q

What are the complications of ileal resection?

A 
watery diarrhoea (impaired bile salt absorption). Rx = cholestyramine, loperamide.
>100cm resected --> steatorrhoea  (reduced SA, bile salt deficiency). Rx = fat restriction.
31
Q

What is UC?

A

Inflammatory disease affecting colonic mucosa from rectum to caecum. RECTUM ALWAYS INVOLVED.

32
Q

Describe epidemiology of UC.

A
  • Prevalence 35-100/100,000.
  • 2/3 onset by 30y
  • M=F
  • Risk less in smokers
33
Q

Describe the inflammation of UC.

A

Diffuse, continuous and confined to mucosa.

34
Q

What are the clinical features of UC?

A
  • Chronic disease characterised by diarrhoea and rectal bleeding, +/- cramps.
  • Tenesmus, urgency, incontinence
  • Systemic: fever, anorexia, LoW, fatigue
  • Extra-intestinal manifestationss
  • Characteristic exacerbations and remissions.
35
Q

Ix in UC?

A
  • Sigmoidoscopy/colonoscopy (contraindicated in severe exacerbation)
  • Stool culture, microscopy (exclude C diff)
36
Q

Rx of UC?

A
  • 5-ASA (topical, oral)
  • Corticosteroids (remit acute disease e.g. methylprednisolone 30mg IV q12h).
  • Immunosuppresants (cyclosporine, infliximab; azathioprine)
  • Surgical Rx - aim for cure with colectomy
37
Q

First step UC flare management?

A

Admission for IV steroids: hydrocortisone 400mg daily or methylprednisolone 60mg daily.
Reevaluate after 3d.

38
Q

3d assessment during UC flare up management?

A

Adequate response = transition to oral red 40mg. Add azathioprine pre discharge.
Inadequate = >8 stools/day or 3-8 + CRP >45. Contingency planning with surg.

39
Q

What are the complications of UC?

A

Similar to CD +:

  • More liver problems (esp primary sclerosing cholangitis)
  • Increased CRC risk
  • Toxic megacolon
40
Q

How can the severity of UC be assessed?

A

Truelove and Witt’s Classification of severity.

6+ bowel motions per day associated with one other severe criterion (temperature, HR, Hb, CRP).

41
Q

What are the indications for surgery in ulcerative colitis?

A
  • Severe exacerbation
  • toxic colon
  • chronic colitis
  • dysplasia/neoplasia
42
Q

What are the surgical options to manage UC?

A
  • Proctocolectomy with permanent ileostomy
  • Ileorectal anastomosis after colectomy
  • Continent ileostomy
43
Q

What is proctocolectomy with permanent ileostomy?

A

Surgical removal of the rectum and all or part of the colon. Most widely accepted for UC and FAP. End of ileum brought through abdo wall to form a stoma.

44
Q

Describe the process of iliorectal anastomosis after colectomy in UC.

A

In pts with less severe rectal disease, ileorectal anastomosis may be possible. Risk of subsequent carcinoma/recurrence of inflammation in the rectum.

Gastroenterology (54 decks)

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