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G.I & Nutrition > Normal/Abnormal Small Bowel/Colon IBD > Flashcards

Normal/Abnormal Small Bowel/Colon IBD Flashcards

1
Q

What are M cells?

A

antigen presenting cells aiding in immunosurveillance; location over lymphoid follicles –> rich in terminal ileum with peyer’s patches

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2
Q

In what layer of the bowel do inflammatory cells hang out?

A

lamina propria

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3
Q

An out-pouching of the distal small bowel containing all the layers (hence a true diverticulum) that occurs as a result of a “pulling” of this segment during retraction of the small bowel back into the abdominal cavity during fetal development.

A

Meckel’s Diverticulum

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4
Q

Failure of gut to retract back into peritoneal cavity; must be surgically placed back.

A

Omphalocele

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5
Q

What is atresia associated with?

A

trisomy 21

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6
Q

What is a common consequence of malrotation?

A

May cause subsequent “twisting” and ischemia.

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7
Q

Etiology of Hirschsprung’s

A

Failure of development of Meissner’s and Auerbach’s plexi; migration from cephalocaudal direction to normally reach fetal rectum by 12 weeks - migration problem

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8
Q

Hirschsprung’s Histology

A

lack of ganglion cells in distal portion rectum; may involve more proximal colon as well.

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9
Q

Presentation of Hirchsprung’s

A

Usually neonatal

  1. Failure to pass meconium
  2. Obstruction
  3. Proximal dilatation - i.e. affected segment relatively constricted.
  4. There is a rare, familial form associated with mutations in the RET oncogene.
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10
Q

Where do Meckel’s diverticula arise?

A

w/in 1 foot proximal of ileocecal valve

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11
Q

Presentation of Meckel’s diverticula?

A

bleeding + “appendicitis”

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12
Q

Are all layers present in a Meckel’s?

A

yes –> true diverticulum

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13
Q

Those changes which occur due to compromise of blood flow. These changes follow a sequence some parts of which are reversible and others not.

A

Ischemia

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14
Q

Clinical presentation of small bowel ischemia

A

severe, acute abdominal pain out of proportion to physical exam

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15
Q

Where do ischemic changes in the small bowel begin?

A

mucosa: most sensitive to ischemia

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16
Q

Features of acute small bowel ischemia

A

mucosal ulceration, neutrophils, edema/thumbprinting –> muscle necrosis and perforation

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17
Q

Features of chronic small bowel ischemia

A

fibrosis and stricture

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18
Q

Most common thrombotic source in small bowel ischemia

A

SMA > mesenteric vein

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19
Q

Causes of small bowel ischemia

A

thrombotic/emblic, voluvulus, adhesions, vasculitis, hypotension, vasospasm

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20
Q

Is there cross-feeding between arcades?

A

no –> not until reaching the marginal artery of drummond

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21
Q

Why is small bowel ischemia notable for sharp demarcations between injured/non-injured areas?

A

b/c of parallel arcades

22
Q

What is the major factor in determining area of ischemic damage in small bowel ischemia?

A

size of the occluded vessel correlates with area of damage

23
Q

What are thumbprints?

A

xray areas of edema associated with ischemia

24
Q

3 grades of small bowel ischemia?

A

mild, moderate, severe

25
Q

T/F mucosal erosions and ulcerations may be repaired after ischemia

A

T –> via reepithelialization

26
Q

Ulceration suggests what grade of ischemia?

A

moderate/severe

27
Q

What are the histologic features of mild small bowel ischemia?

A

edema, mild acute inflammatory infiltrate

28
Q

In which segment of the population do volvuli occur most often?

A

elderly

29
Q

After the gut re-enters the abdominal cavity, specific areas of the gut are “tacked” down to prevent free rotation of the gut. When these areas of “tacking down” occur in wrong areas, bands of fibrosis are formed termed ______

A

Ladd bands –> may aserve as a point of rotation for gut resulting in obstruction and ischemia

30
Q

Which of ulcerative colitis and crohn’s disease has a genetic component?

A

both do but different genetic components

31
Q

2 types of IBD

A

crohn’s and ulcerative colitis

32
Q

Among which population group is incidence of IBD highest?

A

white/jewish in canada/europe/us

33
Q

In which decade of life does IBD present?

A

2nd-4th

34
Q

Site of involvement: CD

A

any where from mouth to anus, all layers, can skip areas

35
Q

Site of involvement: UC

A

colon only, continuous w/o skipping, mucosa only

36
Q

This disease is geographically unlimited with respect to the GI tract and thus affects anywhere from mouth to anus and is transmural. The disease is noncontinuous and thus may have “skip” areas. Many investigators think of this disease (or at least a subset) as a granulomatous vasculitis.

A

Crohn’s

37
Q

Crohn’s pathology

A

transmural inflammation w/fibrosis/stricture/fistulae + cobblestone mucosa, linear/apthous/fissuring/knife like ulcers, creeping fat, thickened wall, non caseous granulomas, pyloric metaplasia

38
Q

Tx of Crohn’s

A

immunosuppression/surgery if severe

39
Q

Sequelae of Crohn’s

A

stricture/obstruction, GI cancer, malnutrition

40
Q

This is a geographically restricted inflammatory disease which is mucosally limited and continuous beginning from rectum and extending proximally. The small bowel and rest of the GI tract are not affected. Cause is not known.

A

Ulcerative colitis

41
Q

What causes stricture in Crohn’s?

A

muscle hypertrophy

42
Q

Ulcerative colitis pathology

A

crypt distortion, muscularis mucosa thickening, cryptitis, hemorrhage, pseudopolymps, no strictures, loss of haustra, no granulomas

43
Q

Sequelae of Ulcerative colitis

A

Cancer, primary sclerosing cholangitis of liver, pyoderma granulosa

44
Q

Tx of Ulcerative colitis

A

immunosuppression, j pouch for fecal continence, surgery cures, dysplasia surveillance

45
Q

Crohn’s 3 categories of pathogenesis and associated genes

A
  1. autophagy: atg16L1, IRGM, LRKK2
  2. intracellular bacterial sensing: NOD2
  3. ER stress: XBP1 and ORMDL3
46
Q

Consequences of NOD2 mutations in Crohn’s

A
  1. abnormal paneth granules = decreased killing of pathogens
  2. defective sensing and clearance of bacteria = increased load/inflammation
  3. prevents p38 phosphorylation of nuclear protein for IL10
  4. weakened tight junctions that increase permeability to pathogens
47
Q

What does NOD2 induce?

A

dimerizes, binds to rick –> activates NF-kB but not apoptosis

48
Q

What is tubular colon?

A

With remission of the active inflammatory component, the colonic mucosa regenerates and repairs ulcerated areas. This repair in conjunction with disruption and distortion of the muscularis mucosa may lead to a flat appearance of the colon as shown on the left. There is a relatively normal colon to the right for comparison. This appearance is also termed a “tubular colon.”

49
Q

Breach in epithelial integrity

A

crypt abscess

50
Q

The finding of _____ on a biopsy is a very powerful feature to help diagnose IBD

A

crypt distortion

51
Q

What must one do before making a dx of IBD?

A

rule out infection!

52
Q

Which of Crohn’s and UC are geographically limited?

A

UC is geographically limited

G.I & Nutrition (43 decks)

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