Flashcards in GI Deck (193)
Hormone responsible for gallbladder contraction? Where made?
Cholecystokinin (CKK), which is made in duodenum and jejunum in response to FA's and AA's
Defect of hepatic excretion of bilirubin glucuronides across canalicular membrane (MDR2 biliary transport protein); Chronic conjugated hyperbilirubinemia; black liver; histo with epi metabolites within lysosomes. Icterus, mostly asymtompatic; Benign = no tx
Extrahepatic biliary atresia
Obstruction of extra hepatic bile ducts. Jaundice by wk 3-4 w/ cholestatic picture (dark urine, echoic stools, and conjugated hyperbilirubinemia)
Liver bx = intrahepatic bile ductular proliferation, portal tract edema, fibrosis, parenchyma cholestasis
Middle-aged Caucasian males - diarrhea, wt loss, arthropathy, polyarthritis, psych, cardiac
Tropheryma whippeli - Gram + actinomycete. Only proliferates in macrophages = no inflammatory.
Bx - Enlarged FOAMY macrophages w/ rod-shaped bacilli and PAS-positive diastase-resistant granules
Tx = abx
Bile acid-binding resin names?
Cholestyramine, colestipol, colesevelam
What agents increase cholesterol content of bile?
Bile acid resins and fibrates
Mallory-Weiss v. Boerhaave
Mucosal tear v. transmural tear (esophageal air + fluid leak)
Where do H. pylori biopsy?
Prepyloric region of gastric antrum has highest yield.
Refers to abdominal radiograph with bluish, brittle, Ca-laden gallbladder wall that develops in some patients with chronic cholecystitis. 11-33%->gallbladder carcinoma = advise cholecystectomy
How does H. pylori lead to duodenal ulcers?
Chronic antral inflammation -> decrease in delta cells (somatostatin-producing cells) -> disinhibition of gastrin. High gastrin -> increased H+ secretion by parietal cells.
Pathogenesis of TPN-induced gallstones
Biliary stasis 2/2 to dec. cholecystokinin
Insulin secretion from pancreatic beta cells?
Glucose stimulates. Enters via GLUT-2 (fac.) then generates ATP. High ATP:ADP causes CLOSURE of K+ channels (KATP). Beta cells now depolarize b/c K+ not leaving the cell and building up inside --> opening of voltage dependent Ca2+ channel -> insulin release. Sulfonylureas bind to KATP --> channel closure -> insulin release.
Mild UDP glucuroyl transferase transferase defieincy. Uncojugated hyperbilirubinemia, usu. provoked by hemolysis, fasting, exertion, febrile illness, etc. No clinical consequence.
Bilirubin transported to liver w/ albumin. Uptaked. Conjugated by UDP-Glucuronyl transferase (absent in Crigler Najjar and low in Gilbert) -> Secreted (defetive in Rotor and Dubin-Johnson) as bilirubin glucuronide. Turned into urobilinogen in GI. Some go back thru portal system to liver/urine. Others go to feces (brown).
Varices = left gastric vein to esophageal vein. Hemorrhoids = superior rectal vein to middle/inferior rectal veins. Caput medusae = paraumbilical veins to superficial and inferior epigastric veins
Chronic mesenteric ischemia
Pt with atherosclerotic risk factors has pain after meals not responding to antacids and nothing on EGD. Due to atherosclerotic narrowing of celiac, SMA, IMA - not able to dilate in response to digestion.
Celiac disease pathology?
Atrophy of villi, flattening of mucosa, chronic inflammation of laminal propria. All reversible w/ gluten-free diet.
Foregut and blood supply
Esophagus, stomach, liver, gallbladder, pancreas, upper duodenum. Celiac
Midgut and blood supply
Lower duodenum, small intestine, ascending colon, proximal 2/3 of transverse colon. SMA
Hindgut and blood supply
Distal third of transverse, descending, sigmoid. IMA.
Midgut herniates through umbilical ring at wk 6 b/c slower growth of abdominal cavity. Return at wk 10 and completes 270 deg turn CCW around the SMA.
Failure of ventral and dorsal buds to fuse at wk 8. Asymptomatic.
How does pregnancy predispose to gallstone formation?
Estrogen-induced HMG-CoA reductase activity = cholesterol hypersecretion. Progesterone induces gallbladder hypomotility
Hirschsprung disease path
RECTAL biopsy. Failure of neural crest cells to migrate to intestinal wall. Submucosa will demonstrate absence of ganglionic cells (Meissner). Rectum always involved (wk 12), sigmoid 75%. Present will failure to pass meconium within 48 hrs, intestinal obstruction.
Final pathway of pancreatitis pathogenesis following acinar cell injury
Intra-acinar conversion of trypsinogen to active trypsin! This leads to other activation (elastase, chymotrypsin, phospholipase)). Proteases auto digest. Elastase leads to vascular dmg and hemorrhage. Lipase/phospholipase -> fast necrosis
Reflux esophagitis patho
Elongation of papillae, basal cell hypertrophy, intraepithelial eosinophils
Primary Biliary Cirrhosis
Chronic. Autoimmune destruction of INTRAhepatic bile ducts and CHOLESTASIS. Middle-aged women, insidious. PRURITIS (esp. night), fatigue. Hepatosplenomegaly, xanthomatous lesions. Jaundice, steatorrhea, portal HTN. Labs - elevated alkPhos, cholesterol, and serum IgM. Dx = anti-mitochondrial antibodies. Associated w/ Sjogren's, Raynaud's scleroderma, autoimmune thyroid, hypothyroidism, and celiac disease
Mutations in trypsinogen or SPINK1 (trypsin inhibitor). Mot common mut -> abnl trypsin that is not susceptible to inactivating cleavage by trypsin.
True vs. pseudodiverticulum
True diverticula contain mucosa, submucosa, AND muscular layers. e.g. Meckel's is failure of obliteration of vitelline duct (usu. wk 7). 2% of pop, 2 feet from ileocecal valve, 2 inches in length, 2% symptomatic, males 2x more affected. False diverticula DON'T contain muscularis (e.g. colonic and Zenker's)