Pharmacology - IBD Flashcards

1
Q

Crohn’s disease where

A

-anywhere in GIT from mouth to anus

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2
Q

Crohn’s cause

A

unknown

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3
Q

Crohn’s pattern

A

exacerbations and remission

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4
Q

Crohn’s disease what and how

A
  • transmural (through wall) inflammation
  • dense infiltration of lymphocytes and macrophages –> eating all way through wall –> fissuring ulceration –> submucosal fibrosis
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5
Q

Ulcerative colitis

A
  • inflammation of mucosal layer only
  • infiltration of inflammatory cells into mucus
  • loss of goblet cells
  • ulcerations
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6
Q

Crohn’s vs ulcerative colitis severity

A

Crohn’s more severe, colitis more superficial

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7
Q

Crohn’s symptoms

A
  • diarrhoea
  • pain
  • fibrosis –> narrowing of gut lumen –? strictures, bowel obstruction
  • abcess formation
  • fistulisation to skin and internal organs
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8
Q

Stricutres

A

inflammation –> scar tissue formation –> narrowing of lumen –> pain, cramping, bloating –> risk of rupture

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9
Q

Fistulae

A

-inflammation –> ulcers –> develop into tunnels –> go between organs or to skin

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10
Q

Crohn’s disease consequences

A
  • weight loss
  • micro/macro nutrients
  • fatigue
  • protein-energy malnutrition in 20-80% paients
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11
Q

Ulcerative colitis symptoms

A
  • severe diarrhoea, change in electrolytes
  • blood loss
  • loss of peristalic function
  • toxic megacolon –> distension of colon, perforation, sepsis
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12
Q

Extra-intestinal inflammation

A
  • joints, eyes, skin, mouth and liver

- forms of IBD

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13
Q

IBD treatment

A

5-aminosalicylate:

  • questionable in Crohn’s
  • some effect in ulcerative colitis

Steroids:
ex: oral prenisolone, budenoside (poor absorption, less systemic effects)

Immunosuppressants:
MTX
Azathioprine –> mercaptopurine (inhibit purine synthesis)
Cyclosporin (inhibit IL-2 induce gene expression)

TNF-α blockers:
neutralise inflammatory sytokine TNF-α implicated in Crohn’s
infliximab-infusion
adalimumab-injection

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14
Q

5-aminosalicylate:

A
  • inhibit LT & prostanoid synthesis, scavenge free radicals & decrease neutrophil chemotaxis effects on PPARγ receptors
  • produg: sulfasalazine adn bacteria in colon–> mesalazine
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15
Q

TPMT enzyme consideration with azathioprine

A
  • metabolise mercaptopurine
  • great inter-patient variability in activity –> test for enzyme before treatment
  • no activity: toxicity
  • high activity: risk of resistance
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16
Q

Crohn’s nutrition considerations

A

elemental feeds: induce remission –> reduced steroid use

may require parenteral support

small bowel removal –> reduced absorption–> combination of methods for nutritional support

17
Q

Probiotics effective?

A

-could be effective in ulcerative colitis (suggestion UC caused by pathogenic colonic bacteria)

18
Q

Crohn’s treatment

A

Monotherapy:
-conventional steroid or alt. budenoside / 5-ASA

After remission induced….

Add-on therapy:

  • first line: azathiopurine/mercaptopurine directly
  • second line: MTX

Severe active Crohn’s:
-infliximab / adalimumab

19
Q

Oral steroids counselling

A
  • best as single dose in morning, after food
  • always carry steroid treatment card if taking for >3 weeks
  • do not stop abruptly, wean off
  • adequate Ca2+ intake and good nutrition
  • normal body weight
  • smoking cessation
  • moderate alcohol consumption
  • physical exercise
20
Q

5-ASA counselling

A
  • report any bleeding, bruising, fever etc.
  • swallow enteric-coated whole
  • may colour tears yellow and urine orange, normal
  • may stain soft contact lenses, use glasses
21
Q

azathiopurine/mercaptopurine counselling

A
  • test TMPT levels before therapy

- seek help if any symptoms (sore throat, vomiting, dark urine, abdominal pain etc.)