Inflammatory Bowel Disease Flashcards

1
Q

What is inflammatory bowel disease?

A

Umbrella term for 2 idiopathic chronic inflammatory diseases:
Ulcerative colitis
Crohn’s disease

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2
Q

What is indeterminate colitis?

A

Diagnosed when it is not clear if inflammation is due to Crohn’s or UC

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3
Q

3 factors involved with pathogenesis of IBD?

A

Genetic predisposition
Problems with mucosal immune system
Environmental triggers

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4
Q

3 facts about genetics of IBD, if a patient is diagnosed with it?

A

IBD risk in first degree relatives is increased

With monocygotic twins, the risk is higher in Crohn’s disease for the other twin, that in UC

Early onset may have strongest genetic links

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5
Q

What is the best established risk factor for IBD development?

A

Positive family history

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6
Q

What is an important mutation in Crohn’s patients?

A

NOD2 is a disease susceptibility gene, of which a mutated form is found in some Crohn’2 patients

Homozygotes have a higher risk of getting the disease than heterozygotes

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7
Q

How does NOD2 contribute to development of Crohn’s?

A

Encodes a protein involved in bacterial recognition and, when mutated, this is lost

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8
Q

2 reasons why gut flora is important in IBD?

A

Antibiotics are effective in treating perianal Crohn’s disease

There is an altered bacterial flora in the colon of patients with UC

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9
Q

What is the normal immune system meant to do?

A

Tolerate dietary antigens and commensal flora

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10
Q

4 components of the innate immune system in the GI tract?

A

Tight junctions regulate epithelial permeability

Hydrophobic mucus protects the epithelial cell layer

Defensins (cationic anti-microbial peptides) can be activated constitutively or in response to bacterial components

NOD2 contributes to normal mucosal defences

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11
Q

Differences between mediation of Crohn’s and UC?

A

Crohn’s - Th1 mediated disease

UC - mixed Th1, Th2 mediated disease/natural killer T cells

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12
Q

4 theories of IBD pathogenesis?

A
  1. Pathogenic bacteria can produce toxins that cause bacterial resistance to killing by macrophages; the bacteria begin to invade the mucosa and an immune response is stimulated
  2. Abnormal microbial composition
  3. Defective host containment of commensal bacteria
  4. Defective host immunoregulation alters tolerance there is altered antigen presentation function
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13
Q

Changes in activity in Crohn’s and UC?

A

Anti-microbial activity in Crohn’s is reduced

There is too much bacterial killing in UC

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14
Q

Smoking impact on Crohn’s and UC?

A

Aggravates Crohn’s disease

Protects against UC

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15
Q

NSAIDs effect on IBD?

A

Aggravate

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16
Q

What is UC?

A

Inflammation of the colon of unknown aetiology that has a relapsing course

17
Q

Compare and contract UC and Crohn’s disease?

A

ADD TABLE

18
Q

Determining the severity of UC?

A

> 6 bloody stools every 24 hours

AND

1 or more of:
Fever 
Tachycardia
Anaemia 
Elevated CRP
19
Q

Investigations for UC?

A

CRP and albumin (negative acute phase reactant - severe inflammation will decrease this)

Plain AXR, endoscopy and histopathology

20
Q

2 signs of UC on AXR?

A

Stool will be absent in an inflamed colon

Thumb-printing sign indicates mucosal oedema

Toxin megacolon if transverse colon is greater than 5.5 cm or caecum is greater than 9 cm

21
Q

What is a toxin megacolon?

A

Massive distension that can lead to perforation

22
Q

What to ask in a UC history?

A
Recent travel
Antibiotics
NSAID’s
Family history
Smoking
Skin, eyes, joints