Intro to IBS - Stein Flashcards
Describe and contrast the epidemiologies of Ulcerative Colitis and Crohn’s disease.
Both are “western” diseases with high prevalence in North America and Western Europe.
About 1mil cases in the US; half UC, half CD.
Note: Most cases are sporadic.
Between UC and CD, which feature:
Mouth-to-anus involvement?
Superficial inflammation?
Patchy areas of involvement?
Mouth-to-anus: Crohn’s disease.
Superficial: Ulcerative colitis
Patchy involvement: Crohn’s disease.
Compare and contrast the clinical presentations of UC and CD.
Both feature: Abdominal pain, weight loss (and growth stunting), fever, fatigue, urgency, and bloody diarrhea.
Ulcerative colitis often features tenesmus (eg passing of mucus)
Crohn’s may feature vomiting.
Describe the appearance of ulcerative colitis on endoscopy
Erythema, edema, and loss of the usual vascular pattern.
Granularity & friability of the mucosa.
Erosions, ulcers, and bleeding.
Pseudopolyps, cecal patch, and backwash ileitis (pan-colitis only)
What is the most severe variant of ulcerative colitis?
How common is it?
Fulminant UC; features systemic signs (fever, elevated WBC) and high risk of perforation.
About 9% of patients feature this on initial rpesentation. Can develop at any course of the disease…
Which parts of the GI tract are (USUALLY) affected by Crohn’s disease?
Usually both the small and large intestine are affected by CD. However, it can affect anywhere “mouth to anus”
What are the three “major” endoscopic findings in Crohn’s disease?
Aphthous ulcers, cobblestoning, discontinuous (“skip”) lesions.
(also seen: strictures, fistulae)
Do each of the following features hint at Crohn’s or UC more?
Rectal sparing
Loss of normal vasculature
Involvement of terminal ileum but not cecum
Granulomas on biopsy
Rectal sparing: CD
Loss of normal vasculature: UC
Involvement of terminal ileum but not cecum: CD
Granulomas on biopsy: CD
Try to recall 6-7 extra-intestinal manifestations of IBDs.
Acute arthropathy
Erythema Nodosum (and pyoderma gangrenosum)
Choledocholithiasis and nephrolithiasis
Ocular complications (scleritis, uveitis)
Sacroillitis and ankylosing spondylitis
Primary sclerosing cholangitis
Describe the pathogenesis of inflammatory bowel diseases. Broad strokes.
Defects at the GI lining (NOD2, Th17, tight junctions) as well as microbiota disturbances facilitate an exaggerated immune response.
What is the desired outcome of IBS?
What is the worst outcome?
Remission of symptoms (“patient feels fine”)
Development of penetrating fistulas.
What treatment options are available for IBD (categories, not specifics)
Steroids
Immunomodulators
“Biologics” (eg mAbs)
Name four biologic treatments of IBS and their mechanism of action.
Infliximab: Anti-TNF mAb
Certolizumab pegol: Anti-TNF Fab fragment
Adalimumab: Anti-TNF mAb
Natalizumab: Anti-a4 integrin mAb
Which of the four biologics is no longer indicated due to increased incidence of brain infections?
Why are biologics the best choice of treatment for those with IBS?
Natalizumab
Good efficacy (high rate of remissions and mucosal repair) and allows weaning of glucocorticoids.
(low-yield slide) What were the findings of each of the following Anti-TNF trials?
CHARM
PRECiSE
SONIC
CHARM: Adalimumab (anti-TNF antibody) improves remissions in IBD.
PRECiSE: Certolizumab pegol improves remissions in IBD.
SONIC: Infliximab (and azathioprine) improve remission & mucosal healing and work better if given early in the disease course.
