Small Bowel and Colon: Non-neoplastic diseases Flashcards
3 categories of causes of inflammation of the small bowel and colon?
Ischemia
Idiopathic Inflammatory Bowel Disease (IBD)
Infectious
4 ways that ischemia can happen?
Thrombosis/emboli
Mechanical (volvulus, adhesions)
Vasculitis
Hypotension
What determines how large a swath of bowel is taken out with a thromboembolus?
How early in the branching architecture the vessel is occluded.
What does a “thumbprinting” pattern on radiology of the small bowel correspond to?
Edema caused by ischemia.
Which layer(s) is most sensitive to ischemia?
The muscosa -it’s most metabolically active.
of the mucosa, the epithelium, as it’s furthest from the blood supply
What have adhesions got to do with ischemia?
They can cause initiation points for volvulus.
2 major types of IBD?
Ulcerative colitis (UC) Crohn's disease (CD)
4 factors contributing to the pathogenesis of IBD?
Immune system
Genetics
Environment
Gut flora
Where does Crohn’s (CD) affect? Does it progress in a particular direction?
Can affect anywhere from mouth to anus - with “relative sparing” of the rectum.
No, the lesions can skip around discontinuously.
Where does ulcerative colitis (UC) affect?
Does it progress in a particular direction?
UC only affects the colon (hence the name).
Yes, it tends to start distally and progress proximally.
What term is used to describe the GI layers that are affected by CD?
What can this lead to?
Transmural inflammation.
This can cause fistulae and strictures.
Does CD or UC have more extra-intestinal manifestations?
CD has more extra-intestinal manifestations.
3 microscopic features of CD? (which is pathognomonic?)
Granulomas (not pathognomonic, more common in CD but not always present)
Fibrosis
Cryptitis, knife ulceration
What layers does UC affect?
Mucosa only.
Is CD or UC associated with primary sclerosing cholangitis?
UC
3 microscopic features of UC?
Crypt distortion*
Muscularis mucosa thickening
Cryptitis
(*Is this the name of a GI-metal band? No. Should it be? I think so.)
3 cellular processes affected by genetic abnormalities associated with CD?
Autophagy
Intracellular bacterial sensing (NOD2)
ER stress
What cell do NOD2 mutations affect? What goes wrong?
Paneth cells (and… probably other epithelial cells…)
Lumenal pathogens aren’t killed as well.
Intracellular bacteria aren’t sensed/cleared -> inflammation.
Decreased IL-10 (anti-inflammatory) synthesis.
What areas of the NOD2 gene are often disrupted in CD? What does this do?
The leucine rich repeats (LRRs).
This area is important for binding LPS (and thus sensing intracellular bacteria.
Fine detail: What happens downstream of NOD2 binding LPS?
RICK (kinase) -> NF-kB activation
What’s the model for CD involving pathogens, epithelial cells, and host immune cells?
Pathogens (eg. AIEC) aren’t cleared well in lumen or from epithelial cells.
Immune cells see pathogens, but don’t make IL-10 well, so they’re more inflammatory than they should be - and make lots of TNF.
Cobble stones, skip lesions, serpendigenous ulcers, fistulae, strictures, and creeping fat are all gross pathology buzzwords for which type of IBD?
CD
What does quiescent, healed UC look like?
Flat mucosa.
What must you rule out before diagnosing IBD?
Infectious causes (and probably other things)
