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
What is the mechanism of toxin B of C diff?
Induces actin depolymerization, leading to mucsoal cell death, bowel wall necrosis, pseudomembrane formation
26
What is the mechanism of shiga toxin?
ADP ribosylation; disables 60s ribosomal subunit by removing adenine form rRNA; leading to intestinal epithelial cell death and diarrhea
27
What strain of E coli does not ferment sorbitol overnight?
EHEC O157:H7
28
What is the mechanism of shiga-like toxin?
Inactivates 60s ribosomal subunit
29
What is the characteristic pathology seen in primary biliary cholangitis?
Lymphocytic infiltrates and destruction of small and mid-sized intrahepatic bile ducts; can see granulomas
30
In GVHD, what organs are most commonly affected?
Skin, liver, gastrointestinal
31
What is seen histologically in GVHD?
Lymphocytic infiltration and destruction of small intrahepatic bile ducts
32
What pathology is seen in acetaminophen OD?
Liver failure with centrilobular necrosis
33
What pathology is seen in alcoholic hepatitis?
Hepatocellular swelling and necrosis, mallory bodies, and neutrophilic infiltration and fibrosis
34
What are the endoscopic findings on HSV-1 esophagitis?
Small vesicles resulting in punched-out ulcers
35
What endoscopic findings are seen in CMV esophagitis?
Linear ulcerations
36
What are the endoscopic findings of candida albicans esophagitis?
Patches of adherent, grey/white pseudomembranes on erythematous mucosa
37
What is the most common cause of duodenal PUD?
H pylori
38
Wht is Kehr sign?
Shoulder pain representing referred pain de to peritoneal irritation
39
What is the sensory innervation of internal hemorrhoids?
Autonomic from the inferior hypogastric plexus
40
What is the innervation of external hemorrhoids?
Branches of pudendal nerves
41
Where is iron absorbed in the GI tract?
Duodenum and proximal jejunum