GI and Nutrition UWorld Flashcards
Retroperitoneal abdominal structures
"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
Ligaments that make up the lesser omentum
Hepatoduodenal ligament and hepatogastric ligament
Chemotactic factors for neutrophils
IL-8
Leukotriene B4
5-HETE
C5a
How does secretory IgA differ from serum IgA
It has a J chain that holds two IgA molecules together and a secretory component that allows it to enter the G.I. lumen
Why is the rectum always involved in hirschsprung’s disease?
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
What cells are present in the different layers of the stomach mucosa?
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.
Why does shigella cause bloody diarrhea
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
First line defense cell in the intestine
Paneth cells. They are found in small groups at the base of intestinal crypts and secrete lysozyme and defensins that help protect against infection.
Genetic mutations associated with Lynch Syndrome
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.
How does nucleotide base excision repair occur?
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.
Coarse pigmented granules found within hepatocytes of a patient with jaundice
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.
What drugs are most effective for motion sickness and why?
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.
Why does the urease breath test work for diagnosis of H. pylori infection?
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.
Polycistronic mRNA
Like the Lac operon, multiple proteins are synthesized from the single mRNA (rare in eukaryotes, common in prokaryotes)
What happens to pancreatic fluid content as flow increases and there is increased release of secretin?
HCO3- increases and Cl- decreases
Frequent source of retroperitoneal bleeding after blunt abdominal trauma
Pancreatic contusion
Common etiology for true esophageal diverticula
Traction diverticula from mediastinal masses
Toxin produced by E. coli that do not ferment sorbitol on MacConkey’s agar or produce glucuronidase
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.
Bacteria that produce toxins capable of activating adenylyl cyclase
"CCCAPE" Campylobacter Cereus Cholera Anthrax (edema factor) Pertussis (pertussis toxin) ETEC (heat labile toxin)
Bacteria that produce toxins capable of activating guanylyl cyclase
ETEC (heat stable toxin)
Yersinia
Bacteria that produce toxins capable of inactivating EF-2
Diphtheria Pseudomonas (exotoxin A)
C. difficile toxin
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
Site of secretion and action: Gastrin Somatostatin CCK Secretin GIP Motilin VIP
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
Pathophysiology of ulcers that develop second to H. pylori infection
H. pylori destroys somatostatin-secreting D cells, disinhibiting gastrin release from G cells
Function of apolipoproteins: A-I B-48 B-100 C-II E3 & E4
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
Mechanism of action of medications you give for hepatic encephalopathy
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
Colon cancer that may present as high volume, mucus-containing diarrhea
Villous adenomas
Origin of the round acidophilic Councilman bodies seen on biopsy of patients with hepatitis
These are apoptotic hepatocytes
2 main watershed areas of the colon
Splenic flexure (SMA -> IMA) Distal sigmoid colon (IMA -> hypogastric arteries)
Most common mutation associated with Crohn’s disease
NOD2 -> NF-kB inactivation -> impaired innate immunity (less mucus secretion, less antimicrobial peptide synthesis) -> lumenal bacteria penetrate submucosal tissue -> exaggerated adaptive immune response
Difference between acute interstitial pancreatitis and acute necrotizing pancreatitis?
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
Linkage disequilibrium
A pair of alleles in the same gamete (haplotype) are inherited more or less often than you would expect by random chance.
Why do nitrites cause cancer?
They promote deamination of C, A and G residues to uracil, hypoxanthine and xanthine, respectively
What is the normal cytokine response when a macrophage is infected by mycobacterium tuberculosis?
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
Medications that can raise uric acid levels and precipitate gout flare
Niacin
HCTZ
Cyclosporine
Pyrazinamide
Hepatic encephalopathy precipitating factors
Drugs (sedatives, narcotics) Hypovolemia (diarrhea, vomiting) Excess nitrogen load (bleeding, constipation) Infection Portosystemic shunting
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
1) parvovirus B19
2) adenovirus, herpesvirus and poxvirus
3) HBV
4) poliovirus
5) HIV
6) influenza, measles and rabies
What does the cystic artery branch off of?
Right hepatic artery
Sequence of mutations in adenomatous colorectal carcinoma
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)
N-myc
Oncogene seen in neuroblastoma
Unique histologic appearance of hepatocytes in hepatitis B infection? Hep C?
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
Leptin
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.
Why do fibrates increase risk for gallstones
They inhibit the rate limiting step of bile acid synthesis (cholesterol 7-alpha hydroxylase), resulting in increased ratio of cholesterol to bile.
Pathogenesis of cholesterol gallstones
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.
How are bile acids made?
Free cholesterol -> cholic and chenodeoxycholic acids -> conjugation with glycine or taurine
Enzyme that activates trypsinogen. Why is trypsinogen so important?
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.
Why do patients taking aspirin have a lower incidence of colorectal cancer
Elevated activity of COX-2 plays a role in the adenoma-carcinoma sequence.
How does colitis-associated carcinoma differ from sporadic colorectal carcinoma?
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.
Associations with hepatic angiosarcomas
Vinyl chloride, arsenic and Thorotrast
Result of adenosine deaminase deficiency
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).
How are dietary lipids absorbed in the small intestine?
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.
