LECOM Ch 18 Liver hepatic path robbins
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| Causes of Pre-hepatic portal HTN (3) | obstructive thrombus, narrowing of portal vein, massive splenomegaly
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| Most common causes of Intrahepatic portal HTN | cirrhosis
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| Causes of post-hepatic portal HTN (3) | R sided heart failure, constrictive pericarditis, hepatic vein outflow obstruction
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| Bile is used to excrete 3 things: | bilirubin, cholesterol, xenobiotics
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| Neo-nate w/ normal looking liver, super high unconjugated bili, colorless bile. Dies. Disease and genetic defect | AD: Crigler-Nijar Type 1. Absent UGT1A1. Kernicterous
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| Only monoglucoronidated bilirubin, yellow skin. Cause and name of Dsx | AR: Mild UGT1A1 activity, Crigler-Najjar type 2
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| Mild fluctuating uconjugated hyperbilirubinemia, with stress, no hemolysis or liver disease Name and inheiritance | Gilbert Syndrome AR; Decreased UGT1A1
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| Chronic conjugated hyperbilirubinemia, dark pigmented hepatocyte cytoplasm. Name and genetic defect | AR; Dubin-Johnson syndrome, MDRP-2 loss
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| Chronic conjugated hyperbilirubinemia, normal liver. Dx | Rotor Syndrome
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| Green-brown plugs in dilated bile canaliculi | Cholestasis
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| BUZZ: “Feathery degeneration” | cholestasis, bile droplets in hepatocytes
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| Bile lakes filled with cellular debris and pigment in addition to feathery degeneration points to | chronic or prolonged cholestasis
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| With cholestasis what enzyme is characteristically elevated? | GGT
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| GGT levels in PFIC-1, 2, and 3 | Normal; normal; High
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| Infantile cholestasis, normal GGT, pruritis, high serum bile acid levels, not ductal proliferation, liver failure by adulthood. Disease and faulty gene | PFIC-1, ATP8B1
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| Infant cholestasis, normal GGT, pruritis, growth failure, cirrhosis by age 10. Dx and mutation | PFIC-2 and ABCB11
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| Cholestatis, HIGH GGT, toxic destruction of hepatic epithelia. Dx and mutation | PFIC-3; ABCB4
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| necrosis with portal bridging | chronic hepatitis
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| which type of hepatitis is associated with focal, lobular macrovesicular steatosis | HCV
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| which type of hepatitis is associated with highest incidence of chronic hepatitis | HCV
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| focal hepatocyte necrosis, giant cell transformation, cholestasis, portal mononuclear cell infiltrate, extramedullary hematopoiesis | hepatitis
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| persistence of HBsAg in serum >6mo | carrier state
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| Name this viral hepatitis: - enveloped ds DNA | HBV
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| Name this viral hepatitis:- fecal-oral transmission | HAV
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| Name this viral hepatitis:- water borne | HEV
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| Name this viral hepatitis:- long incubation period | HCV; HBV
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| Name this viral hepatitis:- no carrier state | HAV
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| Name this viral hepatitis: - no chronic hepatitis | HAV; HEV
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| Which phase of viral hepatitis is this? (prodrome, jaundice, recovery) - fever, painful hepatomegaly - increase serum transaminase - atypical lymphocytosis | prodrome
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| Which phase of viral hepatitis is this? (prodrome, jaundice, recovery) - increased urine bilirubin and urobiliniogen - IgM antibodies | jaundice
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| Which phase of viral hepatitis is this? (prodrome, jaundice, recovery) - IgG antibodies | recovery
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| Which viral hepatitis is this? - DNA polymerase with reverse transcriptase activity | HBV
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| Major causes of fulminant hepatitis. | - drugs: acetominophen, isoniazid, MAOI, halothane, methyldopa
- toxins: mushroom
- HBV
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| What is the most important prognostic factor of chronic hepatitis? | etiology
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| Name some organisms that cause hepatocellular carcinoma. | - HBV
- Aflatoxin from food spoilage mold
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| Hepatocytes with speres and tubules in cytoplasm, “ground glass” hepatocytes. Which virus? | HBV
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| shrunken liver with a wrinkled capsular surface and microscopically shows massive irregular areas of necrosis | acute fulminant hepatitis
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| Clusters of plasma cells in portal tract/hepatic lobule interface is character istic of what | autoimmune hepatitis
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| Hepatitis w/ elevated serum IgG, gamma globulin, and ANA, SMA, AAA, or anti-SLA/LP | Autoimmune hepatitis type 1
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| Hepatitis w/ elevated serum IgG, gamma globulin, and ALKM-1, ALC-1 | Autoimmune hepatitis type 2
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| Most common cause of fulminant hepatitis in the USA | drug induced
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| Mallory bodies are present with :(6) | alcoholic hepatitis, NAFLD, PBC, Wilson disease, chronic cholestatic syndromes, and hepatocellular tumors
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| Most common cause of chronic liver disease in the USA? | NAFLD
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| Steatohepatitis is suspected. Macro/micro vesicular steatosis, multifocal parenchymal inflammation, Mallory bodies, sinusoidal fibrosis, neutrophils, AST/ALT=1 Dx | NASH
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| AST > ALT | AST is present in mitochondria: AST>ALT indicates alcohol hepatitis since alcohol damages mitochondria
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| ALT>AST | viral hepatitis
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| portal fibrosis and cirrhosis liver cells filled with blue granules on Prussian blue stain | Hereditary hemochromatosis
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| What is this liver condition? - micronodular cirrhosis - DM - slate gray skin - hepatomegaly - arrhythmias - atypical arthritis - hypogonadism | hemochromatosis - destruction of pancreatic islet cell (DM)
- iron deposit in myocardium, pituitary gland, adrenal gland, thyroid, parathyroid, joints, skin.
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| What is the treatment for Wilson's disease? | Cu chelator (D-penicillamine)
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| What is this disease? - behavioral change - psychosis - parkinson like syndrome - Kayser Fleischer ring | Wilson's disease
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| What is this disease? - decreased serum ceruloplasmin - increase hepatic Cu - increased urinary Cu secretion - mutated ATP7B gene (CH13) | Wilson's disease
- mutated transmembrane Cu transporting ATPase on canaliculi membrane
- Cu spill over around age 5
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| liver is diffusely nodular with small, uniform nodules and microscopically shows diffuse fibrosis encircling regenerative nodules; liver cells contain PAS-pos globular cytoplasmic inclusions | alpha1 anti-trypsin deficiency
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| What is the most sensitive test for recent alcohol intake and is used to monitor those in treatment for abuse? | GGT
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| What is this liver condition? Morphology - fatty change: micro and macrovesicular - fibrosis - mallory body | alcoholic liver disease
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| What is this condition? - cause neonatal hepatitis with cholestatic jaundice - PAS positive cytoplasmic globular inclusions - emphysema | alpha-1-AT deficiency
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| What is this condition? - neonates with jaundice, dark urine, light and acholic stool - panlobular giant cell transformation (rossettes) | neonatal cholestasis
- 50% idiopathic
- 20% biliary atresia
- 15% alpha-1-AT deficiency
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| lg liver, yellow and greasy; preservation of architecture and marked fatty change | alcoholic fatty liver
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| liver fluke Clonorchis sinensis predisposes to ____ carcinoma | bile duct
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| granulomatous bile duct destruction | primary biliary cirrhosis
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| antimitochondrial Ab | primary biliary cirrhosis
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| obstructive jaundice, granulomatous destruction of bile ducts | primary biliary cirrhosis
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| concentric bile duct fibrosis “onion-skin fibrosis” | sclerosing cholangitis often associated with inflammatory bowel
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| Pathogenesis of secondary biliary cirrhosis. | biliary obstruction -> secondary infection -> periportal fibrosis -> hepatic scarring, nodular formation -> bridging fibrosis -> cirrhosis
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| Pathogenesis of primary biliary cirrhosis. | - aberrant MHCII on bile duct epithelial cells -> autoreactive T cells -> hyperagammaglobulinemia with complication activation and circulating immune complexes (IgM)
- anti-mitochondrial antibodies
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| Etiology of secondary biliary cirrhosis. | - gallstones
- tumors of biliary tree and head of pancreas
- stricture
- in children: biliary atresia, CF, choledochal cysts, paucity of bile duct
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| What is this disease? - gross: fine granular appearance - micro: portal edema with neutrophils, periductal fibrosis, mononuclear infiltrate | secondary biliary cirrhosis
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| Name a complication of secondary biliary cirrhosis. | ascending cholangitis
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| What is the strongest indicator for prognosis in primary biliary cirrhosis? | degree of fibrosis
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| What is this disease? - hyperagammaglobulinemia - increased circualting immune complex (IgM) Morphology - early: portal mononuclear inflammation with granulomatous response - late: fibrosis | primary biliary cirrhosis
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| What is this disease? Morphology - bile duct with onion skin periductal fibrosis and mononuclear infiltrate Cholangiography: - beaded bile ducts with strictures | Primary sclerosing cholangitis
- chronic disease with inflammation, obliterative fibrosis, segmental constriction of intra- and extra- hepatic bile ducts
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| MCC ascending cholangitis | E.coli; MC risk factor is obstruction from lithiasis
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| centrilobular necrosis | hepatic congestion with R-sided CHF
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| MCC Budd-Chiari syndrome | Polycythemia vera
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| Gross appearance of a liver of an individual with cor pulmonale | nutmeg caused by chronic passive congestion from right-sided heart failure
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| liver is diffusely nodular, green w/ small, uniform nodules; fibrous bridging between portal areas | biliary cirrhosis
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| 30yo pregnant female previously on oral contraceptives presents with severe abdominal pain. US shows well-circumscribed subcapsular hepatic mass | hepatic adenoma
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| Pathogenesis of hepatocellular carcinoma. | repeated cycle of liver cell death and regeneration -> more opportunity for gene mutation
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| Which of the following class of hepatocellular carcinoma has the best prognosis? - well differentiated - moderately differentiated - poorly differentiated - fibrolamellar variant - fibrolamellar variant | well differentiated cell separated by dense collagen
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| What is this malignancy? - moderately differentiated adenocarcinoma - distorted ducts with prominent sclerotic stroma - primary mass with numerous intrahepatic satellite tumors | bile duct carcinoma
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| Complication of liver adenoma. | rupture of subcapsular tumor (especially pregnancy) -> intraperitoneal hemorrhage
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| What is this neoplasm? - highly vascular - well circumscribed - can't see bile ducts, central vein - thickened plates (1-2 cell layers) | liver adenoma
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| What is this neoplasm? gross: - yellow nodule with a central scarr micro:- central fibrous scar | focal nodular hyperplasia- 85% female
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| What is this neoplasm? - gross: spongy, red-purple mass with hemorrhage and fibrosis - micro: dialted vessels lined by single layer endothelial cells. | Hemangioma
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| What is this neoplasm? - diffuse spherical nodules of regenerating hepatocytes, arising in non-cirrhotic liver - nodules not separated by fibrous septae | nodular regenerative hyperplasia
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| Which condition exhibit both macro- and micro-vesicular steatosis? | alcoholic fatty liver
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| Which condition would you think of if you see periportal necrosis? | eclampsia
- periportal sinusoids contain fibrin deposits with hemorrhage into space of Disse
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| How to treat eclampsia? | Termination of pregnancy
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| What intrahepatic biliary architectual anomaly is associated with AD PKD? | polycystic liver disease
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| What intrahepatic biliary architectual anomaly is associated with AR PKD? | congenital hepatic fibrosis - abdominal pain on stooping
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| What is this intrahepatic biliary architectual anomaly? - clusters of dilated bile ducts in/near portal tract- no clinical significance | von meyenburg complexes
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| What is this intrahepatic biliary architectual anomaly? - multiple diffuse cysts detached drom biliary tree - abdominal pain on stooping - associated with AD PKD | polycystic liver disease
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| What is this intrahepatic biliary architectual anomaly? - extensive fibrosis with abnormally shaped bile ducts - associated with AR PKD - complication: portal HTN, bleeding varices | congenital hepatic fibrosis
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| What is this intrahepatic biliary architectual anomaly? - larger bile ducts segmentally dilated with inspissated bile - often seen with congenital hepatic fibrosis - complication: gallstones, cholangitis, hepatic abscess, portal HTN | Caroli disease
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| Which circulatory disorder of the liver is this? - portal HTN with esophageal varices - splenomegaly - ascites - infarction of intestines | portal vein thrombosis
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