Lower GI & Nutrition Integrative Cases Flashcards

1
Q

What lab findings are seen in celiac disease?

What is one of the worst possible sequelae?

A

Positive antibodies (IgA, IgG) against gliadin, tTG, and endomysium.

Non-hodgkin’s lymphoma.

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2
Q

What symptoms do patients with celiac (presumably classic) present with?

Why might a microcytic anemia be seen?

A

Diarrhea, gas, fatigue, weight loss / failure to thrive.

As celiac disease damages the villous lining of the GI tract, it can cause malabsorption resulting in deficiencies of iron and other nutrients.

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3
Q

Give three histological findings seen in a biopsy of tissue affected by celiac disease.

A

Villous atrophy

Crypt hyperplasia (note mitoses)

Plasma cell expansion in the lamina propria.

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4
Q

Crohn’s and ulcerative colitis can be distinguished by the expansion of different T cell populations. What are they?

A

Crohns - Th1

Ulcerative Colitis - Th2

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5
Q

Here is a series of epidemiologic traits, pathological findings, or extraintestinal signs & complications. Specify if one is found in UC or CD.

  1. Creeping fat
  2. History of smoking
  3. Malabsorption and steatorrhea
  4. Toxic megacolon
  5. Primary sclerosing cholangitis
A
  1. CD (no creeping fat seen in UC)
  2. CD (smoking may be slightly protective from UC)
  3. CD (UC doesn’t affect small bowel, thus no malabsorption)
  4. UC (generally; can be seen in Crohn’s)
  5. UC
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6
Q

Here is a series of epidemiologic traits, pathological findings, or extraintestinal signs & complications. Specify if one is found in UC, CD, or both.

  1. Erythema nodosum
  2. Increased risk of cancer
  3. “Apple-core sign”
  4. Aphthous ulcers
  5. Mucosal erosions
A
  1. CD (also beware Pyroderma gangrenosum)
  2. Mainly UC, but also CD if involving the colon
  3. CD (due to wall thickening)
  4. CD
  5. UC (as opposed to transmural)
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7
Q

What is the “pseudomembrane” is pseudomembranous colitis?

What progression of this requires surgical intervention?

A

Fibrinopurulent debris generated from a C. Diff infection and response.

Toxic megacolon.

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8
Q

What is diverticulitis?

Where does it occur?

A

Inflammation of an existing diverticulum.

Diverticula tend to occur in the lower colon, especially at the sites of vasa recta entry.

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9
Q

What is the defect observed in FAP?

How is it treated?

A

Autosomal dominant mutation of APC gene on chromosome 5.

Prophylactic colectomy

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10
Q

What does ischemic injury look like on histology?

Distinguish between the causes of mucosal and tramural ischemia.

A

Coagulative necrosis results in “ghosting” of the intestinal villi (villi affected before crypts)

Mucosal usually due to hypoperfusion, transmural due to occlusion (thrombus, embolism)

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11
Q

In the context of ischemic injury, are watershed areas more or less susceptible?

A

It depends on the cause of ischemia. Since watershed areas are at the border of two vascular supplies, they resist occlusive ischemia but are more susceptible to hypoperfusive ischemia.

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12
Q

Name 4 physical forms of bowel obstruction

A

Herniation

Volvulus

Adhesion

Intussusception

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13
Q

What is required for fat absorption?

A

Bile salts, pancreatic lipase, colipases.

Phospholipases and cholesterol esterases are also helpful.

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14
Q

Why might patients on RNY gastric bypass experience iron deficiency anemia?

A

Duodenal bypass means reduced absorptive surface for iron.

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15
Q

What vitamin deficiencies are steatorrheic patients apt to develop?

A

ADEK

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