Inflammatory Bowel Disease Flashcards

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1
Q

Where does Crohn’s Disease affect, ,what causes it and how does it fluctuate?

A
  • Anywhere on the GI tract
  • Cause is unknown
  • Exacerbations and remission
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2
Q

How does the inflammation in Crohn’s differ from UC and how is it caused?

A
  • Crohn’s:
    Transmural inflammation (throughout wall of GI tract)
    Caused by dense infiltration of lymphocytes and macrophages
  • Ulcerative Colitis:
    Inflammation of mucosal layer ONLY
    Caused by an infiltration of inflammatory cells into mucosa
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3
Q

What are the differences in consequences of inflammation in Crohn’s vs. UC?

A

Crohn’s:

  • Fissuring ulceration (eating away at wall of tract leads to fistulae)
  • Submucosal fibrosis (scar tissue formation between epithelial + smooth muscle leading to strictures)

UC:

  • Loss of goblet cells (inflammation affects mucosal layer)
  • Presence of ulcerations
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4
Q

What are the symptoms of Crohn’s?

A
  • Diarrhoea
  • Pain
  • Narrowing of the gut lumen leading to strictures (narrowed lumen) and bowel obstruction
  • Abscess formation
  • Fistulization to skin and internal organs
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5
Q

How do strictures form and how do they affect you?

A
  • Inflammation (from infiltration of lymphocytes/macrophages) leads to scar tissue formation
  • This leads to narrowing of the lumen and then obstruction
  • Risk of rupture as pressure builds at narrow lumen/obstruction
  • Resulting in pain/cramp/bloating
  • Scar tissue = poor absorption of food/drug
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6
Q

How do fistulae form and where are they found?

A
  • Via ulcers; inflammation leads to ulcers
  • These develop into tunnelst = fistulae
  • Go between areas of GIT, between organs (to bladder etc) or to skin (anal fistula)
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7
Q

What are the consequences of Crohn’s?

A
  • Weight loss
  • Macronutrient/micronutrient deficiency (when inflamed/exacerbated)
  • Fatigue
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8
Q

What are the differences in how nutrition is affected between Crohn’s and UC?

A

Crohn’s:

  • Protein-energy malnutrition in 20-80% of patients
  • Weight loss from macro/micronutrient deficiency

UC:
- Less severe nutritional consequences (inflammation of the colon only : none observed aside from in severe diarrhoea with electrolyte/fluid loss, and GI pain can affect appetite)

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9
Q

What are the symptoms of ulcerative colitis?

A
  • Severe diarrhoea (electrolyte/fluid loss)
  • Blood loss (via ulcers; lowers blood pressure)
  • Loss of peristaltic function leading to rigid colonic tube > potentially leading to toxic megacolon in severe cases
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10
Q

What is toxic megacolon?

A

Distension of the colon resulting in perforation and systemic toxicity in the form of sepsis; colonic bacteria enter bloodstream

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11
Q

How does taking loperamide affect UC?

A

Patients unwittingly take loperamide to stop severe diarrhoea but ends up contributing to the loss of peristaltic function (and potentially leading to toxic megacolon)

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12
Q

Where can extra-intestinal inflammation occur and for which IBD?

A
  • In joints/eyes/skin/mouth/liver
  • In Crohn’s and IBD
    (systemic disease)
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13
Q

What is the mode of action of 5-aminosalicylate (mesalazine) and what does it treat?

A
  • It inhibits leukotriene & prostanoid synthesis, scavenges free radicals and decreases neutrophil chemotaxis (movement/activity from chemical stimulus - changes in gene transcription of PPAR(gamma) receptor)
  • Sulfasalazine is metabolised to mesalazine (requires colonic bacteria)
  • Effects observed in UC/questionable use in Crohn’s
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14
Q

What issues with absorption could arise from sulfasalazine to treat UC?

A

Sulfasalazine is a pro-drug; required to be metabolised by colonic bacteria in to the active drug mesalazine; may have insufficient time for metabolism w/severe diarrhoea

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15
Q

How are steroids used in IBD?

A

For their anti-inflammatory and immunosuppressive effect:

  • Corticosteroids
    E.g. budesonide; poorly absorbed thus far fewer systemic side effects
    -Used to induce remission (particularly in severe disease)
    -Enemas used for more distal or rectal inflammation e.g. Predfoam
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16
Q

What immunosuppressants are used in IBD and how do they work?

A

Azathioprine (1st choice; converted to active mercaptopurine) and methotrexate; inhibit purine synthesis and thus DNA, reducing inflammatory cell proliferation.

Cyclosporine (used when no response to above/steroid-sparing); inhibiting IL-2 (interleukin 2) induced gene expression

17
Q

What are the potential dangers with using azathioprine?

A
  • Azathioprine converted to active form mercaptopurine which is then metabolised via multiple pathways incl. TPMT (thiopurine methyltransferase; inactivation) and HGPRT (therapeutic)
  • Some patients have little to no TPMT activity; thus mercaptopurine all metabolised by HGPRT which normally gives rise to desired immunosuppression via cytotoxic nucleotide analogues
  • But w/o TPMT to ‘deal’ with some mercaptopurine too there’s too much of the toxic analogue; bone marrow toxicity
    DO TPMT TEST TO DETERMINE POSSIBLE TOXICITY
18
Q

What is the mode of action for infliximab (infusion) and adlimumab (injection) and what do they treat?

A
  • They neutralise the inflammatory cytokine TNF-a(lpha)
    (however associated w/risk of TB)
  • Monocolonal antibodies for severe, active Crohn’s
19
Q

How are elemental feeds beneficial for Crohn’s?

A

They can induce remission; ingesting basic amino acids/lipids (elements) that don’t have to be digested.

20
Q

Why would small bowel removal occur in Crohn’s and what are the consequences?

A
  • V shitty stricture-y/narrow/scarred part
  • Resulting in a shortened bowel, meaning reduced absorption of food/drug
  • Requiring nutritional support
  • Parenteral nutrition may be required generally to prevent undernutrition
21
Q

How are probiotics beneficial in UC?

A

UC potentially caused by pathogenic colonic bacteria; add ‘friendly bacteria’ such as Yakult

22
Q

What is the treatment tree of Crohn’s for remission?

A

1.) Monotherapy - Conventional steroid (prednisolone etc)
[alternative = budesonide/5-ASA)
2.) Add-on therapy:
First line: Azathioprine or mercaptopurine
Second line: Methotrexate (if patient has low TPMP enzyme)
3.) Severe active Crohn’s:
Infliximab or adlimumabb.

23
Q

What counselling points are there with oral steroids?

A
  • Best taken as single dose in morning after food
  • Avoid contact with people who have shingles/chickenpox/measles
  • Carry steroid treatment card if taking oral corticosteroids for