Iflammatory Bowel Disease (IBD)

  1. What is the epidemiology for IBD?
    • Ulcerative colitis: 2-6/100,000 people per year
    • Crohn's disease: 5-10/100,000 people per year
  2. What is the clinical presentation of Ulcerative colitis?
    • Diffused inflammation limited to the surface of the colon
    • Distal (confined to descending colon/sigmoideum) or Extensive (can include the transverse and ascending colon)
    • Persistent bloody diarrhea
    • Urgency
    • Tenesmus (urgency accompanied by pain, cramping and involuntary straining efforts)
    • Extra-gastrointestinal manifestations (joints, eyes, skin, etc)
    • Growth failure/retardation and malnutrition (kids)
  3. What is the clinical presentation of Crohn's disease?
    • Patchy, transmural inflammation in any part of the GI tract, including small intestines (30%) and stomach (5%)
    • Classified by location and pattern (inflammatory, fistulating, stricturing)
    • Intestinal obstruction (stricturing)
    • Fistula (often perianal)
    • Fissures (fistula from gut to other organs)
    • Malnourished
    • Malaise
    • Anorexia
    • Fever
    • Extra-gastrointestinal manifestations (joints, eyes, skin, etc)
    • Growth failure/retardation and malnutrition (kids)
  4. What is the etiology of IBD?
    • Unknown
    • Genetics play a role
    • Luminal flora of the gut
    • Smoking:
    • increases risk of Crohn's
    • decreases risk of ulcerative colitis
  5. What is the pathophysiology of IBD?
    • Microflora in the GI tract inappropriately stimulate the immune system and trigger the inflammatory process
    • Eventually T-cells are activated
    • This process occurs both inside and outside the GI tract
  6. What are the risk factors/exacerbating factors for IBD?
    • Smoking (Crohn's only)
    • Infections (pulmonary or enteric)
    • Use of NSAIDs
    • Change in diet
    • Psychological stress
  7. What ar the complications of IBD?
    • Ulcerative colitis:
    • fulminant colitis
    • perforation of the colon
    • toxic megacolon
    • Crohn's:
    • abscess formation
    • intestinal obstruction
    • fistulas
    • strictures
    • small intestinal bacterial overgrowth (SIBO)
    • Others:
    • arthrits/osteoporosis
    • venothromboembolism (DVT, PE, clots)
    • oral lesions (autoimmune mediated)
    • anemia
    • liver and pancreatic diseases
    • eye disease (uveitis)
    • erythema nodosum (tender, red bumps, usually on lower legs)
    • pyoderma gangrenosum (ulceration of skin, usuall on lower legs)
    • colorectal cancer
    • toxic megacolon
  8. What is the non-pharmacologic therapy for IBD?
    • Nutrition - maintain a steady diet void of triggers for exacerbation
    • Surgery (colectomy) - for pts who fail or intolerant to drug therapy, or with toxic megacolon
    • Aggressive fluid replacement
  9. What are the pharmacotherapies for IBD?
    • Cipro + Metronidazole (Crohn's induction)
    • 5-ASA and related (induction and maintenance - oral only if Crohn's)
    • Oral corticosteroids (induction, except Budesonide for maintenance of mild-moderate Crohn's)
    • IV corticosteroids (induction)
    • Cyclosporine (Induction)
    • Thiopurines (Maintenance)
    • Methotrexate (Induction and Maintenance)
  10. What are the biologic agents used in IBD?
    • Infliximab (Induction and Maintenance)
    • Adalimumab (Induction and Maintenance of Crohn's)
    • Certolizumab pegol (Induction and Maintenance of Crohn's)
    • Natalizumab (Induction and Maintenance of Crohn's)
  11. What is the MOA of Metronidazole and Ciprofloxacin in IBD (Crohn's only)?
    • Antibacterial (inhibition of bacterial DNA/RNA; Inhibition of Topo II DNA gyrase)
    • Anti-inflammatory
  12. What are the SE of Metronidazole and Ciprofloxacin?
    • NVD
    • Disulfiram reaction
    • Photosensitivity
    • Furry tongue/metallic taste
    • Urine discoloration
    • Peripheral neuropathy
    • Carcinogenic
    • Pregnancy cat C
    • Tendonitis/tendon rupture
    • QT prolongation
    • Dysglycemia
  13. What is the MOA of 5-ASA and related compounds in IBD?
    Anti-inflammatory (exact mechanism unknown)
  14. What are the 5-ASA drugs used in IBD?
    • Sulfasalazine
    • Mesalamine, 5-ASA
    • Olsalazine
    • Balsalazide
  15. What are the SE of Sulfasalazine?
    • Yellow/brown urine
    • Photosensitivity
    • Oligospermia
    • NVD
  16. What are the special considerations for Sulfasalazine?
    • Pro-drug converted to 5-ASA by bacteria in the gut
    • Avoid in patients with hepatic insufficiency or G6PD
  17. What are the SE of Mesalamine, 5-ASA?
    • Abdominal pain
    • NVD
  18. What are the special considerations for Mesalamine, 5-ASA?
    • Many oral and topical formulations
    • Different sites of action
  19. What are the SE of Olsalazine and Balsalazide?
    • Abdominal pain
    • NVD
  20. What are the special considerations for Olasalazine and Balsalazide?
    Pro-drugs converted to 5-ASA by bacteria in the gut
  21. What are the DI of 5-ASA?
    • Thiopurines concurrent use increases risk of myelosuppression
    • Warfarin - increases prothrombin time and INR
  22. Why can budesonide be used for maintenance therapy in IBD, unlike other corticosteroids?
    It has high topical activity and a high rate of first-pass metabolism
  23. Which thiopurine is preferred d/t less hepatotoxicity?
  24. Why are thiopurines only used for maintenance of IBD and not induction?
    Typically takes several weeks, and up to 6 months, for onset
  25. Which Calcineurin inhibitor is used in IBD?
    Cyclosporine (Induction only)
Card Set
Iflammatory Bowel Disease (IBD)
Iflammatory Bowel Disease (IBD)