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Qbank > GI Qbank > Flashcards

GI Qbank Flashcards

1
Q

What does urease convert urea to?

A

Carbon dioxide and ammonia, causing pH increase

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2
Q

What supplements are used in breastfed infants?

A

Vitamin D and iron (in preterm/lower bw)

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3
Q

What is seen on biopsy in celiac disease?

A

Villous atrophy, crypt hyperplasia, and intraepithelial lymphocyte infiltration

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4
Q

What is the classic histologic finding in Whipple disease?

A

Small intestinal mucosa containing enlarged foamy macrophages packed with both rod shaped bacilli and PAS-positive, diastase resistant granules

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5
Q

What is the most common clinical presentation of Whipple disease?

A

Middle-aged white males presenting as malabsorption with diarrhea and weight loss

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6
Q

What is the gram stain of tropheryma whippelii?

A

Gram positive

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7
Q

What cells produce secretin? Secretin is released in response to what?

A

Produces by duodenal S cells; released in response to increased duodena H+ concentrations

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8
Q

What is the function of secretin?

A

Increase bicarb pancreatic secretion

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9
Q

What is the embryological origin of the spleen?

A

Dorsal mesentery (mesoderm)

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10
Q

What is the sudan III stain of the stool?

A

Qualitative assay that can identify unabsorbed fat and confirm malabsortion

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11
Q

What is the rate limiting step of glycolysis?

A

PFK-1

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12
Q

Cholesterol gallstones can be caused by inhibition of what enzyme?

A

7alpha hydroxylase

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13
Q

Brown pigmented gallstones can be caused by what enzyme?

A

Beta-glucuronidase

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14
Q

Brown pigmented gallstones are seen when?

A

Infection - esp E coli, A lumbricoides, C sinensis

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15
Q

What are the different types of gallstones? When do you see each?

A

Pigmented (brown = infection; black = hemolysis); cholesterol

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16
Q

What are pigmented gallstones composed of?

A

Calcium salts of uncojugated bilirubin

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17
Q

What is the function of beta-glucuronidase?

A

Released by injured hepatocytes and bacteria in pigmented gallstones; hydrolyzes bilirubin glucuronides and increased amount of unconjugated bilirubin

18
Q

What toxin is associated with bacillus anthracis? Factors?

A

Anthrax exotoxin - edema factor and lethal factor

19
Q

What is the mechanism of edema factor seen in B anthracis?

A

Acts as adenylyl cyclase and increased cAMP

20
Q

What is the mechanism of lethal factor in B anthracis?

A

Protease that inhibits protein kinase signaling, causing apoptosis

21
Q

What is the mechanism of pertussis toxin?

A

ADP ribosylation of Gi, disinhibiting adneylate cyclase, increasing cAMP levels, causing edema and phagocyte dysfunction

22
Q

What is the mechanism of botulinum toxin?

A

Blocks presynaptic release ACh resulting in flaccid paralysis

23
Q

What toxins does C diff have?

A

Toxin A and toxin B

24
Q

What is the mechanism of toxin A seen in C. Diff?

A

Recruits and activates neutrophils, leading to release of cytokines that cause mucosal inflammation and fluid loss, diarrhea

25
Q

What is the mechanism of toxin B of C diff?

A

Induces actin depolymerization, leading to mucsoal cell death, bowel wall necrosis, pseudomembrane formation

26
Q

What is the mechanism of shiga toxin?

A

ADP ribosylation; disables 60s ribosomal subunit by removing adenine form rRNA; leading to intestinal epithelial cell death and diarrhea

27
Q

What strain of E coli does not ferment sorbitol overnight?

A

EHEC O157:H7

28
Q

What is the mechanism of shiga-like toxin?

A

Inactivates 60s ribosomal subunit

29
Q

What is the characteristic pathology seen in primary biliary cholangitis?

A

Lymphocytic infiltrates and destruction of small and mid-sized intrahepatic bile ducts; can see granulomas

30
Q

In GVHD, what organs are most commonly affected?

A

Skin, liver, gastrointestinal

31
Q

What is seen histologically in GVHD?

A

Lymphocytic infiltration and destruction of small intrahepatic bile ducts

32
Q

What pathology is seen in acetaminophen OD?

A

Liver failure with centrilobular necrosis

33
Q

What pathology is seen in alcoholic hepatitis?

A

Hepatocellular swelling and necrosis, mallory bodies, and neutrophilic infiltration and fibrosis

34
Q

What are the endoscopic findings on HSV-1 esophagitis?

A

Small vesicles resulting in punched-out ulcers

35
Q

What endoscopic findings are seen in CMV esophagitis?

A

Linear ulcerations

36
Q

What are the endoscopic findings of candida albicans esophagitis?

A

Patches of adherent, grey/white pseudomembranes on erythematous mucosa

37
Q

What is the most common cause of duodenal PUD?

A

H pylori

38
Q

Wht is Kehr sign?

A

Shoulder pain representing referred pain de to peritoneal irritation

39
Q

What is the sensory innervation of internal hemorrhoids?

A

Autonomic from the inferior hypogastric plexus

40
Q

What is the innervation of external hemorrhoids?

A

Branches of pudendal nerves

41
Q

Where is iron absorbed in the GI tract?

A

Duodenum and proximal jejunum

Qbank (33 decks)

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