jdlevenson's version from 2015-06-20 04:06


2015-05-27 to 29 GI


130 questions; 38 incorrect


16 (DONE); 20 (DONE), 44 (16/44; 10 incorrects), 20 (??; 6 incorrects), 44 (??; 10 incorrects), 20 (??; 5 incorrects), 30 (12/30; 7 incorrects)


Question Answer
Protein or carb, 1 gram =4 calories
Fat, 1 gram =9 calories
Ethanol, 1 gram =7 calories


Question Answer
Meckel’s rule of 2s2% of population, 2 types of tissue (most often gastric but sometimes pancreatic, colonic, endometrial), 2 ft prox to ileocecal valve (it is connected to ileum), 2 inches long, presents in first 2 years of life
Meckel’s is formed fromIncomplete obliteration of tube from yolk sac to midgut lumen (omphalomesenteric duct)
Primitive gut tube fromlateral and cephalic flexion of embryo
Foregut supplied byCeliac (esophagus to upper duodenum as well as liver and gall bladder and pancreas)
Midgut supplied bySMA. Lower duodenum, SI and ascending colon and proximal 2/3 of transverse.
At 6th week of embryonic development, what herniates outMidgut, through umbilical ring , to allow for rapid growth of intestine and liver despite slower growth of the abdominal cavity. Returns at week 10 and then completes a 270 degree counterclockwise turn around the SMA to allow for proper placement. Hindgut descent along IMA happens after midgut returns.
If midgut rotation goes awry, presentation?Cecum in RUQ fixed with fibrous bands/ Ladd’s bands to the second portion of the duodenum with entire midgut fixed to SMA leading to intestinal obstruction at birth and bilious vomiting.
If midgut rotation goes awry, complication?Intestinal obstruction and Midgut volvulus with intestinal gangrene and perforation
Abrnomal migration of neural crest cellsHirschsprung. Absence of parasympathetic ganglion in a segment of the colon. Narrowed denervated area. Symptoms of intestinal obstruction.
Hirschsprung ALWAYS affects?Rectum. Neural crest cells migrate caudally and Hirsch is a result of arrest of migration. Areas with absent ganglion cells cannot relax.
Neural crest cells present in proximal colon by 8th week and rectum by12 week.
MESODERMMuscle (skeletal, cardiac, smooth), Mesothelium (serosal linings); Endothelium of blood vessels; Spleen; Osseous tissue, ovaries, outer layer of suprarenal gland; Dura/ Ducts of genital system; Endothelium of lymphatic vessels; Renal; Microglia/ Male gonads ADD TO ANKI
Marked intrahepatic bile ductile proliferation, portal tract edema and fibrosis, parenchymal cholestasis in newborn/ 3 week oldExtrahepatic biliary atresia. Leads to total obstruction by 3rd week with signs such as light stools, dark urine, firm enlarged liver and increased bilirubin, Alk phos and gamma-glutamyl transferase. If drainage not restored, will lead to biliary cirrhosis by 6 months of life.


Question Answer
Crohn’s pathogenesisincreased activity of TH1 helper T cells -> increased production of IL-2, IFN gamma, TNF, causing subsequent intestinal injury.
Crohns, TH1 or TH2?TH1. Produce TNF, IL2, IFN gamma.
UC, TH1 or TH2?TH2. IL-4, 5, 6, 10.
Crohn’s most commonly affectsTerminal ileum.


Question Answer
Ischemic colitis presentationAbdominal pain and bloody diarrhea. Splenic flexure and distal sigmoid colon.


Question Answer
Linkage disequilibriumWhen 2 allele loci are inherited more or less often together within a gamete than would be expected based on random chance; can occur even if on different chromosomes
HeteroplasmyPresence of different organelle genomes within a single cell. MITOCHONDRIAL.
PleiotropyOccurrence of multiple phenotypes often in different organ systems from a single gene
Hemochromatosis what chromosome6; HFE gene; HLA-A3 (Class I) that appears to increase iron absorption; usually missense that leads to cysteine to tyrosine


Lipid lowering drugs*
Question Answer
Most effective treatment for hypertriglyceridemiaFibrates. May also use statins, niacin and fish oil/ omega 3 fatty acid supplements.
Fibrates MOAActivate PPAR-gamma which increases lipoprotein lipase activity.
Fibrates A/E?Muscle toxicity and gallstones
5-aminosalicylates (sulfasalazine, mesalamine) treat IBD such as Crohn’s and UC. Inhibit cytokines, prostaglandins, and leukotriene synthesis during inflammation.
CN and NRTIs have mitochondrial toxicity
Question Answer
What lipid lowering drug can INCREASE triglyceridesBile acid-binding resins like cholestyramine. Also can cause decreased absorption of other drugs and fat soluble vitamins as well as upset GI. SO DO NOT USE IN PATIENTS WHO HAVE BOTH HYPERCHOLESTEROLEMIA AND HYPERTRIGLYCERIDEMIA.
Bile acid resins + statins as therapy, what considerationAdministered together they can interfere with statin absorption so need to allow 4 hours between
Most effective at increasing HDL?Niacin/ Vitamin B3. Recall, it inhibits lipolysis in adipose tissue and reduces hepatic VLDL synthesis.
sulfacauses HTN.
Question Answer
CN poisoningAmyl nitrite – forms methemoglobin that binds CN ions preventing CN from binding to mitochondrial enzymes.
Acute lead or mercury poisoningCaNa2EDTA; forms complexes with mono, di, or trivalent ions.
Which hyperlipidemia drugs increase cholesterol content of bile and have increased risk of gallstonesFibrates and bile acid-binding resins. Use with caution in people with preexisting gallbladder disease. Both increase hepatic synthesis of cholesterol.


Question Answer
Sensitivity and specificity are or are not affected by disease prevalenceAre not*
Positive predictive value is greater in a situation where there is a higher or lower prevalence of that diseasePPV is greater in a situation with higher disease prevalence/ more likely to be a true positive
Positive predictive value would be lower in a population...Where that disease is relatively uncommon/ more likely to be a false positive


Question Answer
Pancreas tail lies inSplenorenal ligament.
Pancreas is retroperitoneal or notHead neck body are retroperitoneal but the tail is not
Pancreas makes contact withDuodenum (where it overlies L2); body (overlies L1 and L2 vertebrae and makes contact posteriorly with the aorta, super mesenteric vessels and left kidney) and tail courses within the splenorenal ligament
Brunner’s glands are only located where? What do they do?Only in duodenum. Deep in submucosa. Secrete alkaline mucus into ducts that track upwards through muscularis mucosa to crpyts of Lieberkuhn for release into lumen.
Villi are covered by whatSimple columnar epithelium with a brush border (surface absorptive cells) interspersed with goblet cells. Deep to them are crypts of lieberkuhn what are simple tubular glands on top of muscular mucosa that deliver secretions into intervillar spaces.
Fundic stomach liningGastric pits (simple columnar) of glands of parietal cells and chief cells (pepsinogen -> pepsin in presence of acid)
Peyer’s patches are specific toIleum. Clumps of lymphoid tissue (whereas duodenum -> brunner’s).
Clon vs intestine and stomachNO PITS OR VILLI.
Jejunum surfaceVilli with more goblet cells than duodenum; it also has crypts of lieberkuhn.
Portal vein is anterior or posterior to IVC?Anterior.
Lesser omentum is made ofHepatoduodenal ligament and hepatogastric ligament. Double layer of peritoneum extends from liver to lesser curvature of stomach and beginning of duodenum. Between layers of omentum – hepatic artery, common bile duct, portal vein, lymphatics and hepatic plexus.
Adjustable gastric banding procedure goal is toSlow passage of food, increasing satiety and limiting amount of food consumed. To encircle the upper stomach, the gastric band must pass through the lesser omentum.
Round ligament, remnant of fetal umbilical vein, is contained inFalciform ligament.
Greater omentum is made ofVisceral peritoneum from greater curvature of stomach, inferiorly over small intestine, and then ascends to encmpass transverse colon before reaching posterior abdominal wall. Gastrocolic ligament included; anterior wall of lesser sac as well.
GI watershed areasSplenic flexure and distal sigmoid colon
Short gastric arteries or gastroepiploic arteries have poor anastomoses?Short gastric; more vulnerable to ischemic injury.
Pancreatic arteriesPancreatic, short gastric and left gastroepiploic


Question Answer
Majority of ulcers are on greater or lesser curvature of stomachLesser, so affect left and right gastric arteries.
Location of ulcers in stomachBorder between body (acid secreting epithelium via parietal cells and HCl and IF) and antrum (gastrin producing via G cells).
Definitive test for H. PyloriBiopsy. But can also use urease breath test (bacteria has a urease that will break urea into nitrogen and C02 that will eventually be breathed out, 30 minutes after or so).
H. Pylori most frequently colonizes what portion of GIPrepyloric antrum of stomach. H. Pylori does not commonly colonize duodenum since it needs gastric tissue.
Duodenal bulb ulcers, anterior prone to? Posterior prone to?Anterior – perforation. Posterior – hemorrhage.
Ulcer that penetrates posterior duodenal bulb will affectGastroduodenal artery.
Which ulcers can be malignant, duodenal or gastricGastric. MALT or gastric adenocarcinoma.
Ulcers that are not in duodenal bulb but instead in distal duodenum or atypical location suggestsZE syndrome. Also suspicious – multiple ulcers, ulcers refractory to therapy and recurrence after acid reducing surgery.
ZE tumors usually inPancreas but also may be in duodenum, stomach or other organs.
ZE syndrome presentationHypersecretion of gastrin -> peptic ulcers + diarrhea from inactivation of enzymes by excess acid