GI and Nutrition UWorld

Question 1

Retroperitoneal abdominal structures

Answer 1

"SAD PUCKER"
S: Suprarenal (adrenals)
A: Aorta + IVC
D: Duodenum parts 2-4
P: Pancreas, except for its tail
U: Ureters
C: Colon, descending + ascending parts
K: Kidneys
E: Esophagus, thoracic part
R: Rectum

Question 2

Ligaments that make up the lesser omentum

Answer 2

Hepatoduodenal ligament and hepatogastric ligament

Question 3

Chemotactic factors for neutrophils

Answer 3

IL-8
Leukotriene B4
5-HETE
C5a

Question 4

How does secretory IgA differ from serum IgA

Answer 4

It has a J chain that holds two IgA molecules together and a secretory component that allows it to enter the G.I. lumen

Question 5

Why is the rectum always involved in hirschsprung’s disease?

Answer 5

The neural crest cells migrate caudally during embryogenesis and the rectum is narrow because it cannot relax due to the absence of Auerbach and Meissner plexuses

Question 6

What cells are present in the different layers of the stomach mucosa?

Answer 6

The uppermost layer is composed of simple columnar epithelial cells that secrete mucus.

The next layer is the upper glandular layer and it contains oxyntic (pink) parietal cells that secrete gastric acid and intrinsic factor.

The next layer down is the deep aspect of the gastric glands. It contains basophilic chief cells that secrete pepsinogen.

The next layer down is the muscularis mucosa, separating the lamina propria from the submucosa.

Question 7

Why does shigella cause bloody diarrhea

Answer 7

It first infects M-cells in the Peyer’s patches of the ileum and spreads laterally to other M-cells and secretes its toxin. This causes all of the superficial mucosa to slough off and present with bloody mucus-containing stool

Question 8

First line defense cell in the intestine

Answer 8

Paneth cells. They are found in small groups at the base of intestinal crypts and secrete lysozyme and defensins that help protect against infection.

Question 9

Genetic mutations associated with Lynch Syndrome

Answer 9

MSH2 and MLH1 that code for MutS (mismatch repair enzyme that detects mismatches and recruits MutL). MutL and MutS form a complex that recruits exonuclease I to cut out the mismatched DNA. DNA polymerase delta refills the degraded daughter strand and DNA ligase seals the correction.

Question 10

How does nucleotide base excision repair occur?

Answer 10

Glycosylases detect the abnormal base, remove it and leave an empty sugar phosphate in its place. Endonuclease cleaves the 5’ end and lyase cleaves the 3’ end. The normal base is then placed there by DNA polymerase and it is sealed by ligase.

Question 11

Coarse pigmented granules found within hepatocytes of a patient with jaundice

Answer 11

Dubin-Johnson. This is due to AR mutation in a canalicular membrane transport protein that prevents excretion of conjugated bilirubin into bile canliculi. The granules are black due to accumulation of epinephrine metabolites in lysosomes.

Question 12

What drugs are most effective for motion sickness and why?

Answer 12

Motion sickness occurs when there is incongruent stimulus occurring between the visual, vestibular and somatosensory systems. Integration of these sensory pathways occurs at the vestibular nuclei via M1 and H1 receptors. Consequently scopolamine (anti-muscarinic) and anti-histamines (diphenhydramine, meclizine and promethazine) are first line for motion sickness.

Question 13

Why does the urease breath test work for diagnosis of H. pylori infection?

Answer 13

H. pylori has urease, which converts urea to CO2 and NH3. You can give a patient radiolabeled 13C and measure the amount of labeled CO2 expired for diagnosis.

Question 14

Polycistronic mRNA

Answer 14

Like the Lac operon, multiple proteins are synthesized from the single mRNA (rare in eukaryotes, common in prokaryotes)

Question 15

What happens to pancreatic fluid content as flow increases and there is increased release of secretin?

Answer 15

HCO3- increases and Cl- decreases

Question 16

Frequent source of retroperitoneal bleeding after blunt abdominal trauma

Answer 16

Pancreatic contusion

Question 17

Common etiology for true esophageal diverticula

Answer 17

Traction diverticula from mediastinal masses

Question 18

Toxin produced by E. coli that do not ferment sorbitol on MacConkey’s agar or produce glucuronidase

Answer 18

E. coli O157:H7 produces shiga-like toxin that has a B binding domain for M-cells and an A toxin that inhibits the 60S ribosomal subunit by deleting an adenosine residue and preventing tRNA linkage to the 60S subunit.

Question 19

Bacteria that produce toxins capable of activating adenylyl cyclase

Answer 19

"CCCAPE"
Campylobacter 
Cereus
Cholera
Anthrax (edema factor)
Pertussis (pertussis toxin)
ETEC (heat labile toxin)

Question 20

Bacteria that produce toxins capable of activating guanylyl cyclase

Answer 20

ETEC (heat stable toxin)

Yersinia

Question 21

Bacteria that produce toxins capable of inactivating EF-2

Answer 21

Diphtheria
Pseudomonas (exotoxin A)

Question 22

C. difficile toxin

Answer 22

Toxin A is enterotoxic and causes inflammation and fluid secretion

Toxin B inactivates Rho-regulatory proteins, resulting in depolymerization of actin and causes cell death via membrane disruption

Question 23

Site of secretion and action:
Gastrin
Somatostatin
CCK
Secretin
GIP
Motilin
VIP

Answer 23

Gastrin - G cells - increases HCl release
Somatostatin - pancreatic D cells - decreases secretion of most GI hormones
CCK - I cells - increases pancreatic enzyme and HCO3- secretion
Secretin - S cells - increases HCO3- secretion and decreases HCl release
GIP - K cells - decrease HCl and increase insulin release
Motilin - M cells - increase GI motility
VIP - pancreas - increases HCO3- secretion, stimulates intestinal water secretion and counteracts gastrin in the stomach

Question 24

Pathophysiology of ulcers that develop second to H. pylori infection

Answer 24

H. pylori destroys somatostatin-secreting D cells, disinhibiting gastrin release from G cells

Question 25

Function of apolipoproteins:
A-I
B-48
B-100
C-II
E3 & E4

Answer 25

A-I: activates LCAT, which esterifies cholesterol (deficiency results in low HDL cholesterol and increased circulating free cholesterol)

B-48: chylomicron assembly and intestinal secretion
B-100: LDL uptake by extra hepatic cells
C-II: lipoprotein lipase activation (deficiency results in type 1 hyperlipoproteinemia with hyperchylomicronemia)
E3 & E4: VLDL and chylomicron remnant uptake by hepatocytes

Question 26

Mechanism of action of medications you give for hepatic encephalopathy

Answer 26

Rifamixin: non-absorbable antibiotic that reduces bacteria in the gut that generate NH3

Lactulose: catabolized to short-chain fatty acid in gut by bacteria, lowers gut pH and generates non-absorbable NH4+ from NH3

Question 27

Colon cancer that may present as high volume, mucus-containing diarrhea

Answer 27

Villous adenomas

Question 28

Origin of the round acidophilic Councilman bodies seen on biopsy of patients with hepatitis

Answer 28

These are apoptotic hepatocytes

Question 29

2 main watershed areas of the colon

Answer 29

Splenic flexure (SMA -> IMA)
Distal sigmoid colon (IMA -> hypogastric arteries)

Question 30

Most common mutation associated with Crohn’s disease

Answer 30

NOD2 -> NF-kB inactivation -> impaired innate immunity (less mucus secretion, less antimicrobial peptide synthesis) -> lumenal bacteria penetrate submucosal tissue -> exaggerated adaptive immune response

Question 31

Difference between acute interstitial pancreatitis and acute necrotizing pancreatitis?

Answer 31

Interstitial: inflammatory process stops at localized edema and saponification of fatty acids with calcium

Necrotizing: inflammatory process proceeds, edema blocks blood supply to acini, trypsin is activated and activates other pancreatic enzymes leading to auto digestion of the pancreas

Question 32

Linkage disequilibrium

Answer 32

A pair of alleles in the same gamete (haplotype) are inherited more or less often than you would expect by random chance.

Question 33

Why do nitrites cause cancer?

Answer 33

They promote deamination of C, A and G residues to uracil, hypoxanthine and xanthine, respectively

Question 34

What is the normal cytokine response when a macrophage is infected by mycobacterium tuberculosis?

Answer 34

Macrophages secrete IL-12 -> IL-12 stimulates Th1 cells and NK cells to produce IFN-gamma -> IFN-gamma binds to its receptor on macrophages, which dimerizes and activates Janus kinases 1 and 2 -> STAT1 goes to the nucleus and activates transcription of proteins that will enhance macrophages intracellular killing of Tb

Question 35

Medications that can raise uric acid levels and precipitate gout flare

Answer 35

Niacin
HCTZ
Cyclosporine
Pyrazinamide

Question 36

Hepatic encephalopathy precipitating factors

Answer 36

Drugs (sedatives, narcotics)
Hypovolemia (diarrhea, vomiting)
Excess nitrogen load (bleeding, constipation)
Infection
Portosystemic shunting

Question 37

Identify the virus with the following replicative sequence

1) ssDNA -> dsDNA template -> ssDNA progeny
2) dsDNA -> ds DNA template -> dsDNA progeny
3) dsDNA -> +ssRNA template -> dsDNA progeny
4) +ssRNA -> -ssRNA template -> +ssRNA progeny
5) +ssRNA -> dsDNA template -> +ssRNA progeny
6) -ssRNA -> +ssRNA template -> -ssRNA progeny

Answer 37

1) parvovirus B19
2) adenovirus, herpesvirus and poxvirus
3) HBV
4) poliovirus
5) HIV
6) influenza, measles and rabies

Question 38

What does the cystic artery branch off of?

Answer 38

Right hepatic artery

Question 39

Sequence of mutations in adenomatous colorectal carcinoma

Answer 39

APC mutation on chromosome 5p (loss of cellular adhesion, increased replication and small poly formation) -> K-RAS (increased intracellular signaling and unregulated growth leads to polyp enlargement) -> p53 + DCC (failed tumor suppression)

Question 40

N-myc

Answer 40

Oncogene seen in neuroblastoma

Question 41

Unique histologic appearance of hepatocytes in hepatitis B infection? Hep C?

Answer 41

Ground glass appearance due to HbSAg accumulation in hepatocytes that appear as fine, granular and homogenous inclusions.

Hep C presents with lymphoid aggregates in the portal tracts and macrovesicular steatosis

Question 42

Leptin

Answer 42

Decreases appetite by decreasing production of NPY, a potent appetite stimulant in the arcuate nucleus of the hypothalamus.

Increases formation of POMC, which is cleaved to form alpha-MSH, which also decreases appetite in the arcuate nucleus.

Question 43

Why do fibrates increase risk for gallstones

Answer 43

They inhibit the rate limiting step of bile acid synthesis (cholesterol 7-alpha hydroxylase), resulting in increased ratio of cholesterol to bile.

Question 44

Pathogenesis of cholesterol gallstones

Answer 44

Increased cholesterol, decreased bile acid and decreased phosphatidylcholine result in supersaturation of biliary micelles and vesicles with cholesterol. Mucus hyper secretion from infection, calcium salts and hypo motility result in precipitation of gallstones.

Question 45

How are bile acids made?

Answer 45

Free cholesterol -> cholic and chenodeoxycholic acids -> conjugation with glycine or taurine

Question 46

Enzyme that activates trypsinogen. Why is trypsinogen so important?

Answer 46

Enteropeptidase. Trypsin degrades the initial breakdown job from pepsin to dipeptides and amino acids. It also activates chymotrypsin, elastase and carboxypeptidase that are necessary for complete breakdown of proteins.

Question 47

Why do patients taking aspirin have a lower incidence of colorectal cancer

Answer 47

Elevated activity of COX-2 plays a role in the adenoma-carcinoma sequence.

Question 48

How does colitis-associated carcinoma differ from sporadic colorectal carcinoma?

Answer 48

Colitis associated carcinoma has early p53 and late APC mutations, opposite the sporadic type. They are also multifocal instead of solitary and they often arise from flat, polypoid lesions.

Question 49

Associations with hepatic angiosarcomas

Answer 49

Vinyl chloride, arsenic and Thorotrast

Question 50

Result of adenosine deaminase deficiency

Answer 50

Accumulation of adenosine in B and T cells is toxic and results in widespread cell death -> SCID. It is the second most common cause of SCID (to X-linked).

Question 51

How are dietary lipids absorbed in the small intestine?

Answer 51

They are digested by pancreatic enzymes in the duodenum (lipase, phospholipase A2 and cholesterol esterase).

Micelles come into close contact with the jejunum and fatty acids, monoglycerides and cholesterol are absorbed across the brush border.

Triglycerides, phospholipids and cholesterol esters are reconstructed with apoproteins to form chylomicrons that get released into intestinal lymphatics.