Term
| Acetaminophen toxicity results in extensive zone ____ hepatocellular necrosis because the hepatocytes in zone ___ contain enzymes that convert acetaminophen into a cytotoxic metabolite. |
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Definition
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Term
| What is the purpose of stellate cells in normal and injury? |
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Definition
| Vit A storage, fibroblasts to heal injury; this is also a cause of damge since most viruses have no cytopathic effect |
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Term
| The findings for drug induced and viral hepatitis are similar histologically, so then how are they deduced? |
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Definition
| Serology; autoimmune hep can have plasma cells in greater numbers |
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Term
| In addition it hep viruses, others cause acute mild hepatitis, which ones? |
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Definition
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Term
| Acute hepatitis is characterized by active hepatocellular damage and necrosis in the form of _______ or ________. There is no fibrosis or injury longer than 6 months. |
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Definition
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Term
| The inflammation in acute hepatitis is primarily in the _________, and is composed primarily of ________. There are fewer neutrophils, eosinophils or plasma cells. There are relatively few inflammatory cells in the portal tracts. __________ ________ hypertrophy results. |
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Definition
| Lobule, lymphocytes, kupfer cell |
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Term
| Hepatocellular regeneration occurs and one sees mitotic figures, binucleate cells and focally thickened hepatocellular plates. There may or may not be fatty change and there may or may not be canalicular cholestasis (bile within canaliculi). This is seen in what type of hepatits? |
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Definition
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Term
| persistent, often progressive inflammatory process characterized by lymphocytic inflammation in the portal tracts with varying degrees of parenchymal inflammation, hepatocellular injury and fibrosis. |
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Definition
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Term
| Acitivty of infiltrate and fibrosis are two criteria for staging chronic hep. How are they evaluated? |
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Definition
| Based on there distance from the portal tract; activity is infiltrate distance from the tract and crossing the limiting plate, and fibrosis is between the tracts |
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Term
| Gournd glass hepatocytes are seen in Hep B. Immunoperoxidase stains also let you see what 2 antigens? |
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Definition
| Surface, core; HBV, HCV, and cirrhosis can all cause hepatocellular carcinoma |
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Term
| The standard liver test for hepatocyte damage is AST, and ALT leakage from the cell. What are they from and which is greater in viral/alcohol induced hep? |
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Definition
| They are cytosolic and mitochondrial enzymes; viral ALT>AST, alcohol opposite |
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Term
| There are 3 tests for cholestasis. One is alk phos. What other two and describe where else alk phos comes from. |
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Definition
| GGT is microsomoal enzyme, Bilirubin; alk phos comes from bone, placenta, intestine, and small bile ducts |
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Term
| What are two standard tests for liver synthetic function? |
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Definition
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Term
| __________ is an autoimmune disease that results in destruction of small bile ducts. Biopsy specimens demonstrate mononuclear inflammatory lesions centered on the small bile ducts. Granulomas are often present. Portal tract scarring leads to bridging fibrosis and ultimately cirrhosis |
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Definition
| primary biliary cirrhosis |
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Term
| ____________ is progressive inflammatory disease that results in fibrosis of large intra and extrahepatic large bile ducts. Assoc with UC. cholangiogram shows strictures in the large duct(s). concentric fibrosis and ultimately fibrous obliteration of the bile duct. increased risk of developing cholangiocarcinoma. |
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Definition
| Primary sclerosing cholangitis |
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Term
| Other causes of large duct cholestasis include ________________(congenital cystic dilation of bile ducts), parasitic infestation and tumors. ___________ and _____________, (particularly tumors arising in the head of the pancreas) are the most common malignancies presenting with obstructive cholestasis. |
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Definition
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Term
| The major components of bile are bile salts, phospholipids (lecithin), and cholesterol. Gallstones are composed primarily of cholesterol, bilirubin, and calcium salts (bile salts). What are the two types of stones? |
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Definition
| >50% cholesterol is cholesterol stones, less than is pigment stones of black and brown |
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Term
| Excessive secretion of cholesterol into bile is the most common cause of cholesterol supersaturation. Why? |
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Definition
| High cholesterol concentration is toxic to the gall bladder decreasing motility and causing mucous hypersecretion. Decreased wall motility promotes crystal formation and thereby nucleation, or the formation of cholesterol aggregates. |
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Term
| Women in particular have an increased risk of gallstone formation. Why? |
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Definition
| Estrogen increases LDL uptake, ups HMB-CoA reductase which makes cholesterol, progesterone downs gall bladder motility |
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Term
| What is the pathophysiology of cholesterol stone formation in non-obese, Caucasian males with gallstones? |
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Definition
| Inadequate bile salt reduction results in lower concentrations of bile salts in bile and therefore elevated concentrations of cholesterol, i.e., supersaturation. |
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Term
| Pigment stones: Both black and brown pigment stones are due to an increased level of __________- bilirubin in bile. |
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Definition
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Term
| Brown pigment stones are from infection, black are from RBC breakdown. What is pathophys and which one does Crohn |
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Definition
| Infection, RBC breakdown interfere with conjugation in the liver; Crohn |
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Term
| __________ _________ results from occlusion of the neck of the neck of the gallbladder or the cystic duct by a gallstone. The subsequent increased intraluminal pressure causes dilation of the gallbladder. Histologically one sees edema and varying amounts of neutrophilic infiltration. |
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Definition
| Acute cholecystitis; acalculous chole is due post-surgical/trauma/infectious causes inducing ischemia; chronic is associated with repeated gall stones causing fiber depot |
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Term
| Both _________ steatohepatitis and NASH (caused by _________) are characterized by the presence of varying degrees of steatosis, inflammation, ballooning change, Mallory bodies and pericellular, lobular fibrosis. |
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Definition
| alcoholic ; T2DM, obesity, hyperlipid, |
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Term
| Two forms of steatosis are recognized, __________- in which the droplets of fat are generally larger than the nucleus and deform the cells, and __________ in which the cytoplasm appears foamy, having been replaced by a tiny vacuoles barely visible by light microscopy. Steatosis is thought to be a, non-progessive, reversible form of injury. |
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Definition
| macrovesicular , microvesicular |
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Term
| The inflammation in steatohepatitis is predominantly ______, with proportionally _____ inflammation in the portal tracts than is would be seen in chronic viral hepatitis. |
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Definition
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Term
| ________ increases the ratio of NADH: NAD, and NADPH: NADP which results in decreased fatty acid oxidation and increased lipid production. In _____ high insulin levels decrease fatty acid oxidation. Patients with ______- do not make adequate amounts apoproteins for the generation of VLDL, thereby decreasing export of fat form hepatocytes. |
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Definition
| Ethanol, T2dm, abetalipoproteinemia |
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Term
| pure macrovesicular steatosis is less frequently associated with other findings of ____________ than when there is a mixture of macro and micro vesicular steatosis. |
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Definition
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Term
| _________ __________results from impairment of mitochondrial beta-oxidation which results in decreased lipid oxidation (back up of the lipid breakdown pathway). Furthermore, the decreased availability of ATP causes a drop in gluconeogenesis. Both result in the accumulation of fatty acids and triglycerides. |
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Definition
| Microvesicular steatosis, which is rare to be pure and not include macro |
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Term
| ______________ is an enzyme deficiency, and a storage disorder depending upon the genotype. The clinical presentation is quite variable, and can result in neonatal cholestasis with progressive liver disease, or as cryptogenic cirrhosis in the adult. |
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Definition
| Alpha 1 antitrypsin disease |
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Term
| Liver disease from alpha 1 antitrypsin abnormalities is therefore a ______ disease, not an enzyme deficiency. In patients with |
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Definition
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Term
| The most characteristic finding of alpha 1 antitrypsin disorder is the presence of __________ cytoplasmic globules within the hepatocytes. These globules represent accumulated abnormal protein in the heptaocelluer ________. |
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Definition
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Term
| Hemochromatosis is the pathologic accumulation of iron in parenchymal cells of the liver and in other organs. What is diff btw primary and secondary? Men or women greater? |
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Definition
| Primary is hereditry, secondary is simple excess iron accum; men greater due to women mensing |
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Term
| Hemosiderin is an insoluble endstage product of ferritin degradation. _________ hemosiderin is derived primarily via hepatocellular receptor-mediated uptake from circulating transferrin and ferritin. This is the __________ form of hemosiderin deposition in genetic hemochromatosis. ___________ (Kupffer cell) hemosiderin is derived primarily from phagocytosis of senescent red blood cells. This is the primary form of hemosiderin in _________- hemochromatosis. |
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Definition
| Parenchymal , primary, Reticuloendothelial , secondary |
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Term
| Therefore in later stages of hemochromotosis the pattern of iron distribution does not necessarily indicate primary or secondary disease. What is the inheritance of primary? |
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Definition
| Auto rec; A mutant gene on chromosome 6 (HFE) results in increased iron absorption from the gastrointestinal tract. |
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Term
| What is the key diff btw phase one and two metabolismin liver? |
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Definition
| Phase one is to take lipophlic substance and introduce polar function via oxidation, hydrolysis, etc; P two is to coupl polar sub with polar compound like glucorinc acid, glycine, sulfate. |
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Term
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Definition
| CYP3A4; alcholo uses non-CYP |
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Term
| Rifampin, carbama, phenobarbit, pheny, st johns wort, and ethanol are all CYP __________. |
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Definition
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Term
| Cyclophosphamide and ifosfamide are CYP _____ ________. |
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Definition
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Term
| T or F, The majority of acetmino metab is glucorindation, then CYP. |
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Definition
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Term
| T or F, Chronic alcholo use can stim use of secondary metab via MEOS system and results in possible malnutrion vi amodified metabolism. |
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Definition
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Term
| How does alcholo protect against NAPQI formation? |
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Definition
| Stims CYP2E but occupies it; but once alcholo is gone the stimed CYP make more NAPQI |
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Term
| There are two theories of pruritis from jaundice what are they? |
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Definition
| Bile acids cause itchy, use bile acid meds; bile increases endogenous opiods, op antags work too |
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Term
| This disease is the most common liver disorder, source of up LFT, women=men, 5th and 6th decade, associated with obesity, t2dm (which can lead to HCC), hyperlipid, metabolic syndrome (due to up ROS) and anything else. |
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Definition
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Term
| To diagnose NAFLD you determine fatty infiltration and establish non-alcholic. What are the pros and cons of liver biopsy? |
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Definition
| Pro is histo staging is best prognostic indicator, PPV of noninvasive test is poor; con is findings don |
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Term
| 30% of people with NAFLD progress to HCC, what are management recommendations? |
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Definition
| Exercise, weight loss, diet, dontrol DM, hyperlipid, Vit E, thiazolidiones in DM patients, Bariatric surgery in those who fial the above |
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Term
| Acute pancreatitis is from autodigestino of the pancreas by enzymes. GET SMASHeD is the acronym for causes. Go. |
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Definition
| Gallstones, Etoh, Trauma, Steroids, Mumps, Autoimmune, Scorpion, Hypercalcemia/lipid, Drugs(sulfa) |
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Term
| The signs of acute pancreatitis are ab pain rad to the back, Nausea, vomit, eccymoses at flanks or peri-unbilicus. Sever cases can cause shock and organ failure. What are the tests and treatment? |
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Definition
| Elevated serum amylase, lipase, then ultrasound for gallstones or CT for fluid/calcifications; supportive care (bowel rest, hydration, electrolyt), antibiotics and drainage and debridement if infection (psuedocysts) or necrosis. |
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Term
| What are a few complications of acute pancreatitis? |
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Definition
| DIC, necrosis, infection, hypocalcemia/kalemia, ARDS, hemorrhage |
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Term
| The causes of chronic pancreatitis can be alchol, autoimmune, obstruction, CF, hyper triglyc, recurrent acute pancreatitis. What are the clinical findings? |
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Definition
| Patients present with persistent or intermittent abdominal pain similar to acute pancreatitis with or without changes in serum amylase/lipase. Steatorrhea, fat vitamin deficient, diabetes. |
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Term
| Testing for chronic panceratits, is CT and ultrasound as well as secretin/CCK secretion tests. What is the treat? |
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Definition
| Nutrional mange for exocrine insuffic - like modiefied fats, vitamins, enzxymes, calcium, b12; analgesia, drainage of cysts, endoscopy to dilate strictures; surgery reserved for complication because of high mobidity and mortality |
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Term
| What are the top causes for cirrhosis and portal hypertension? |
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Definition
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Term
| The most common cause of portal hypertesntion is up vascular resistance from cirrhosis and obstruction (budd-chiari). What are the complications? |
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Definition
| GI bleeding with esophogastric varices most important, ascites, hepatic encephalopathy, hepatorenal syndrome |
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Term
| T or f, Band ligation and TIPS are surgical techiniques to control esophogastric varices. |
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Definition
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Term
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Definition
| Peripheral vasodilation via NO and other mediators, reduced volume, reinin system, Na and water retention. |
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Term
| The treatment for hepatic encephalopathy is treat cuases, protect air, no sedation, and remove nitrogenous waste from gut via antibacterials and laxatives. What is cause? |
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Definition
| Disturbances in CNS functions due to hepatic insufficiency |
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Term
| T or f, The indications for orthotopic livert transplant are ESLD with hepatic encephalo, hyper bili, portal hyper, synthetic dysfunction. |
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Definition
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Term
| Name this - disease induced by cirhhotic liver probs that causes constricted renal vessels due dilation of splachnic vessels, rennin system activated but doesn |
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Definition
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