IBD Flashcards
What is the key basic science underlying pathology in IBD?
IBD represents a defect in the innate immune system leading to constant up-regulation of the adaptive immune system. Always on and responding to normal antigens. TH1 and TH2 cells are pro-inflammatory. Dominant cytokines are TNF and IL-12
What is IBD?
a pattern of tissue injury to the gut caused by appropriately overactive adaptive immune system and an inappropriately overactive innate immune system. It is mediated by genetic predisposition and personalized gut bacterial populations
What are the genetics of IBD?
there are genetic factors, but it’s not all about the genetics. Even in MZ twins, there is only about a 50% concordance for Chron’s and a 5-14% concordance for ulcerative colitis
What are the most important environmental factors in IBD?
bacteria. IBD mostly occurs in regions of greatest bacterial conc., and fecal stream diversion treats and prevents disease, while restream causes disease flares.
* * ppl with IBD have a gut microbiome fingerprint with significant reductions in protective, non-inflammatory bacteria (like lactobacillus. this class is called firmicutes).
Epidemiology of ppl with IBD: geography, smoking, age
geography: places with overly good hygiene
smoking: protective for ulcerative colitis; promotes Chron’s disease, young ppl. may also be associated with altered flora (abx diet); or altered barrier function (acute infections, NSAIDs)
Features of ulcerative colitis: specimen
colon only, starts at rectum and works its way proximally
mucosal inflammation
continuous distributions,
rectal involvement
Clinical features of ulcerative colitis
bloody stools/rectal discharge unformed loose stools frequent stools urgency/tenesmus (urge to poop but no relief after they try) if severe, pain, vomiting, and fever.
Chron’s disease: specimen features
may be in many different locations: most offten in ileocolic, frequently in small bowel and colon, rarely in stomach, esochagus, etc. Rectal sparing. May have transmural involvement.
microscopically may form granuloma. skip lesions, cobblestoning.
May see inflammation, obstructions/strictures, microperforation, and fistulization
20-30 % of pts don’t have bloody diarrhea
Chron’s disease inflammation: sx
pain, tenderness, diarrhea, low grade fever, weight loss due to loss of appetitie (esp. in small intestine). May see skip lesions, bear claw lesions, omental creeping fat
Chron’s disease: obstruction sx
post-prandial cramps, distention, borborygmi (audible bowel sounds), vomiting, weight loss from food avoidance
Chron’s disease: fistulizations:
many locations: enteroenteric, enterovesical (recurrent UTIs, retroperitoneal (psoas abscess signs, including straight leg raise sign), enterocutaneous, perianal, rectovaginal. can get perianal abscesses
What are some complications of both Crohn’s and UC?
increased risk of colorectal cancer. Early on, the risk is higher in UC than Crohn’s
osteopenia, either from chronic inflammatory or from steroid treatments.
What factors increase the risk of colorectal cancer in pts with IBD?
long duration of IBD
extensive involvement of the colon
primary sclerosing cholangitis
family hx
Ulcerative colitis systemic complications
peripheral arthritis: usually monoarticular, asymmetric, large jts > small jts, w/o synovial destruction, subcutaneous nodules, and with seronegativity for RA
also see anklyosing spondylitis
also see erythema nodosu, and pyoderma gangrenosum
(uveitis may also be seen)
associated with PSC
Chron’s disease: systemic complications
uveitis more likely
erythema nodosum more likely (than in UC)
incr. risk of kidney stones (and UTIs if fistula)
bile salt wasting
malabsorption
