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41 Cards in this Set
- Front
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Etiology of extravascular hemolyis or ineffective hemolysis Lab findings Clinical features |
Patient produces high levels of UCB Increased UCB Dark urine due to increased urinbilinogen Increase risk for pigmented bilirubin (increased conjugated bilirubin in the bile) |
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Etiology of physiologic jaundice of the newborn Lab findings Clinical features |
Newborn liver has low UGT activity Increased UCB UCB is fat soluble, thus lodges in basal ganglia and causes kernicterus Treatment = phototherapy making UCB water soluble |
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Etiology of Gilbert syndrome Lab findings Clinical features |
AR genetically low UGT activity Increased UCB Jaundice DURING STRESS |
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Etiology of Crigler-Najjar syndrome Lab findings Clinical features |
Absence of UGT Increased UCB Kernicterus; usually fatal |
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Etiology of Dubin-Johnson syndrome Lab findings Clinical features Difference from Rotor syndrome |
Deficiency of canalicular transport protein Increased CB Not clinically significant, but liver is pitch dark Rotor syndrome lacks discoloration |
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Etiology of obstructive jaundice
Clinical features |
Gallstones, pancreatic carcinoma, cholangiocarcinoma, liver fluke block biliary tract Increased CB (from bile) Decreased urine urobilinogen Increased alk phos Pruritus from Increased bile acids (from bile) Increased cholesterol (from bile) Pale stool (no bile in bowel) Xanthomas (buildup of cholesterol) Steatorrhea (no bile in stool) |
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Etiology of hepatitis Lab findings Clinical features |
Inflammation disrupting hepatocytes and small bile ductules Increased CB (hepatocytes) Increased UCB (bile ductules) Dark urine due to increased urine bilirubin Urinobilinogen normal or decreased |
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Etiology of viral hepatitis |
Inflammation of liver parenchyma Usually due to hepatitis virus, but others caused by EBV and CMV May be acute or chronic |
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Acute hepatitis symptoms and labs |
Jaundice from mixed CB and UCB (bile ducts and hepatocytes) Dark urine (CB) Fever, malaise, anusea ALT > AST Symptoms < 6 months |
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Transmission of Hepatitis A and E |
Fecal oral HAV = travelers HEV = contaminated water or undercooked seafood |
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Similarities between Hep A and Hep E |
Acute hepatitis, no chronic state Anti-virus IGM during active, Anti-virus IgG protective HEV in pregnant causes fulminant hepatitis (liver failure) |
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Transmission of Hep B |
Parenteral (childbirth, unprotected sex, IV drug abuse) |
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Acute Hep B serology |
(+) HBsAG (+) HBeAG (envelope) and HBV DNA HBcAB IgM (-) HBsAB (-) |
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Window Hep B serology |
(-) HBsAG (-) HBeAG (envelope) and HBV DNA HBcAB IgM HBsAB (-) |
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Resolved Hep B serology |
(-) HBsAg (-) HBeAG (envelope) and HBV DNA HBcAB IgG HBsAB IgG (protective) |
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Chronic Hep B serology |
(+) HBsAG (>6mths) +/- HBeAG (envelope) and HBV (presence indicates infectivity) HBcAB IgG HBsAB (-) |
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Hep B immunization serology |
(-) HBsAG (-) HBeAG and HBV DNA (-) HBcAB HBsAB (+) |
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Hep C transmission |
Parenteral transmission (IVDA, unprotected sex, needles) |
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Progression of Hep C, labs to confirm |
Acute hepatitis, chronic disease in most cases HCV RNA tests confirms infection, persistence indicates chronic disease |
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Hep D progression |
Dependent on HBV for infection Superinfection = upon existing HBV Coinfection = infected at the same time |
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Definition of Cirrhosis |
End-stage liver damage Disruption of normal hepatic parenchyma with broad fibrosis and regenerative hepatocytes |
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What causes fibrosis in cirrhosis? |
Stellate cell beneath EC's in sinusoids produce TGF-β |
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Results of portal HTN |
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Results of decreased liver detoxification |
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Results of decreased protein synthesis |
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What causes damage in alcoholic hepatitis? |
Acetaldehyde
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Presentation of alcoholic hepatitis |
Painful hepatomegaly AST > ALT (AST is in the mitochondria) May result in death |
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Featrues of NAFLD |
Fatty change, hepatitis, cirrhoiss No exposure to alcohol Associated with obesity ALT > AST |
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Hemochromatosis pathophysiolgy, primary cause |
Excess body iron leading to deposition in tissues and organ damage Damage is mediated by generation of free radicals Enterocytes normally hold onto iron until it is needed in the blood. In primary hemochromatosis, all iron in the enterocyte gets put in the blood, which then gets poured into the tissues MUTATIONS IN HFE gene (C282Y) |
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Secondary hemochromatosis |
Complication of transfusions When iron in Hb is turned over, iron is recycled and eventually this builds up (hemosiderosis) and causes damage of hemochromatosis |
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Triad of hemochromatosis |
Also, cardiac arrhythmia and gonadal dysfunction |
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Lab results of hemochromatosis |
Increased ferritin Decreased TIBC Increased serum iron Increased % saturation |
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Genetic and pathophysiology of Wilson Disease |
AR defect in ATP-mediated hepatocyte copper transport Lack of copper transport in bile and lack of copper incorporation into ceruloplasmin Cu builds up in hepatocytes, leaks into serum, deposits in tissues Leads to free radicals |
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Clinical course of Wilson Disease and treatment |
Presents in childhood Cirrhosis Neurologic manifestations (parkinson/dementia/chorea) Kayser-Fleischer rings in cornea Increased HCC risk Treament = D-penacillamine (Cu-chelator) |
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Primary biliary cirrhosis pathophysiology and pathomnemonic lab finding |
Autoimmune granulomatous destruction of intrahepatic bile ducts Arises in women at 40 AMA IS PRESENT Obstructive jaundice, followed by sclerosis |
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Primary Sclerosing cholangitis pathophysiology |
Inflammation and fibrosis of intra and extra bile ducts Onion-skin appearance Uninvolved regions are dilated, leading to beaded string appearance |
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Clinical course and lab test for primary sclerosing cholangitis |
Cirrhosis is a late complication Increased risk of cholangiocarcinoma P-ANCA positive |
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Reye syndrome pathogenesis and presentation |
Aspirin to child Damage to mitochondria in hepatocytes
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Characterization of hepatic adenoma and drug relation |
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Risk factors for HCC and prognosis |
Chronic hepatitis Cirrhosis Aflatoxins from Aspergillus (p53 mutations) Tumors are often detected late because symptoms are masked by cirrhosis |
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Metastasis to the liver sources |
More common than primary Most common are colon, pancreas, lung, breast Multiple nodules, nodule free edge of the liver |
