Small Bowel and Colon: Non-neoplastic diseases

Question 1

3 categories of causes of inflammation of the small bowel and colon?

Answer 1

Ischemia
Idiopathic Inflammatory Bowel Disease (IBD)
Infectious

Question 2

4 ways that ischemia can happen?

Answer 2

Thrombosis/emboli
Mechanical (volvulus, adhesions)
Vasculitis
Hypotension

Question 3

What determines how large a swath of bowel is taken out with a thromboembolus?

Answer 3

How early in the branching architecture the vessel is occluded.

Question 4

What does a “thumbprinting” pattern on radiology of the small bowel correspond to?

Answer 4

Edema caused by ischemia.

Question 5

Which layer(s) is most sensitive to ischemia?

Answer 5

The muscosa -it’s most metabolically active.

of the mucosa, the epithelium, as it’s furthest from the blood supply

Question 6

What have adhesions got to do with ischemia?

Answer 6

They can cause initiation points for volvulus.

Question 7

2 major types of IBD?

Answer 7

Ulcerative colitis (UC)
Crohn's disease (CD)

Question 8

4 factors contributing to the pathogenesis of IBD?

Answer 8

Immune system
Genetics
Environment
Gut flora

Question 9

Where does Crohn’s (CD) affect? Does it progress in a particular direction?

Answer 9

Can affect anywhere from mouth to anus - with “relative sparing” of the rectum.
No, the lesions can skip around discontinuously.

Question 10

Where does ulcerative colitis (UC) affect?

Does it progress in a particular direction?

Answer 10

UC only affects the colon (hence the name).

Yes, it tends to start distally and progress proximally.

Question 11

What term is used to describe the GI layers that are affected by CD?
What can this lead to?

Answer 11

Transmural inflammation.

This can cause fistulae and strictures.

Question 12

Does CD or UC have more extra-intestinal manifestations?

Answer 12

CD has more extra-intestinal manifestations.

Question 13

3 microscopic features of CD? (which is pathognomonic?)

Answer 13

Granulomas (not pathognomonic, more common in CD but not always present)
Fibrosis
Cryptitis, knife ulceration

Question 14

What layers does UC affect?

Answer 14

Mucosa only.

Question 15

Is CD or UC associated with primary sclerosing cholangitis?

Answer 15

UC

Question 16

3 microscopic features of UC?

Answer 16

Crypt distortion*
Muscularis mucosa thickening
Cryptitis
(*Is this the name of a GI-metal band? No. Should it be? I think so.)

Question 17

3 cellular processes affected by genetic abnormalities associated with CD?

Answer 17

Autophagy
Intracellular bacterial sensing (NOD2)
ER stress

Question 18

What cell do NOD2 mutations affect? What goes wrong?

Answer 18

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.

Question 19

What areas of the NOD2 gene are often disrupted in CD? What does this do?

Answer 19

The leucine rich repeats (LRRs).

This area is important for binding LPS (and thus sensing intracellular bacteria.

Question 20

Fine detail: What happens downstream of NOD2 binding LPS?

Answer 20

RICK (kinase) -> NF-kB activation

Question 21

What’s the model for CD involving pathogens, epithelial cells, and host immune cells?

Answer 21

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.

Question 22

Cobble stones, skip lesions, serpendigenous ulcers, fistulae, strictures, and creeping fat are all gross pathology buzzwords for which type of IBD?

Answer 22

CD

Question 23

What does quiescent, healed UC look like?

Answer 23

Flat mucosa.

Question 24

What must you rule out before diagnosing IBD?

Answer 24

Infectious causes (and probably other things)