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69 Cards in this Set
- Front
- Back
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Pathologic states of the liver
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-hepatocellular disease (DAMNIT)
-Biliary disease (inflammation, neoplasm, toxin) -Hepatic insufficiency (dec. functional hepatocytes) |
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Cholestasis
-definition |
-stoppage or suppression of bile flow
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Anemia
-hepatic lesion suggested |
-hepatitis
-decreased functional mass |
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Codocytosis
-hepatic lesion suggested |
-decreased functional mass
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Decreased UN
-hepatic lesion suggested |
-decreased functional mass
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Hyperammonemia
-hepatic lesion suggested |
-decreased functional mass
-portosystemic shunt |
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Hyperbilirubinemia
-hepatic lesion suggested |
-cholestasis
-decreased Bc transport |
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Hypercholesterolnemia
-hepatic lesion suggested |
-cholestasis
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Hypoalbuminemia
-hepatic lesion suggested |
-decreased functional mass
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Hypoproteinemia
-hepatic lesion suggested |
-decreased functional mass
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Inc. ALT, AST, ID, LD
-hepatic lesion suggested |
-damaged hepatocytes
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Inc. ALP
-hepatic lesion suggested |
-cholestasis
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Inc. GGT
-hepatic lesion suggested |
-biliary hyperplasia
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Ammonium biurate crysalluria
-hepatic lesion suggested -pathogenesis |
-dec. functional mass
-inadequate fixing of NH4 into urea and decreased conversion of uric acid to allantoin |
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Bilirubinuria
-hepatic lesion suggested |
-cholestasis
-decreased Bc transport |
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Hyposthenuria or Isosthenuria
-hepatic lesion suggested -pathogenesis |
-dec. functional mass
-decreased medullary tonicity due to decreased urea concentration -inc. NH4+ excretion may inhibit concentrating mechanism |
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Inc. PTT or PT
-hepatic lesion suggested -pathogenesis |
-cholestasis
-dec. functional mass -dec. vitamin K-dependent coagulation factors due to impaired intestinal absorption of vitamin K -dec. clearance of inhibitors of coagulation factors such as FDP -dec. production of most coagulation factors |
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Transudate
-hepatic lesion suggested -pathogenesis |
-dec. functional mass
-cirrhosis -inc. Na+ and H2O retention -dec. plasma oncotic pressure -portal hypertension -dec. lymph drainage |
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Bilirubin factors that are able to be excreted in urine
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-conjugated bilirubin (Bc)
-urobilinogen (Ub) -Bu/Alb cannot pass through the filtration barrier |
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Bilirubin remains associated with albumin until
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-uptake by hepatocytes
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Once taken in by hepatocytes, what happens to bilirubin
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-becomes associated with y & z proteins which inhibit bilirubins ability to exit the hepatocyte and re-enter the blood
-becomes conjugated and enters bile canuliculi -bile secreted into intestine -Bc degraded into Ub in intestines -Ub can be excreted either in bile, urine, or feces |
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Urobilinogen that is excreted in feces is converted to
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-Stercobilinogen
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delta bilirubin
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-degraded bilirubin that binds to albumin
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How to measure:
-[Bt] -[Bd] -[Bi] |
-[Bt] = [Bu + Bc + Bdelta] (total bilirubin)
-[Bd] = [Bc + Bdelta] (all forms except unconjugated) -[Bi] = [Bt] - [Bd] = [Bu] (indirect bilirubin) |
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Forms of Bilirubin measured by HPLC that correlate to the different types of bilirubin
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-Bu = Balpha
-Bc = Bbeta & By -Bdelta |
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Hyperbilirubinemia
-causes |
-increased Bu Production (hemolytic disorder; extravascular)
-Decreased Bu uptake by hepatocytes (fasting/anorexia in horses) -Decreased Bc excretion in Bile (obstructive cholestasis; hepatic/post-hepatic) |
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Is icterus seen in a congenital portosystemic shunt case?
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-Never
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Hemolytic Hyperbilirubinemia
-expected bilirubin values |
-inc. [Bt]
-[Bu] >>> [Bc] -[Bi] >> [Bd] |
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Hemolytic hyperbilirubinemia
-pathogenesis |
Extravascular hemolysis of erythrocytes
-increased rate of formation of bilirubin --incomplete removal of bilirubin by hepatocytes ---inc. [Bt] due to inc. [Bu] --inc. conjugation of bilirubin in hepatocytes ---rate of Bc formation exceeds Bc excretion into Bile ----Bc regurgitated into plasma -----inc. [Bt] due to inc. [Bc] |
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Hemolytic hyperbilirubinemia
-expected bilirubin values with time or liver disease |
-Bu =/< Bc
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Fasting hyperbilirubinemia
-pathogenesis |
Conversion of stored truglycerides to fatty acids
-inc. FA delivery to hepatocytes --FAs bind to Z-protein ---dec. ligands available for binding Bu ----dec. uptake of Bu by hepatocytes -----inc. [Bt] due to inc. [Bu] |
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Fasting hyperbilirubinemia
-expected bilirubin values |
-[Bu] > [Bc]
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How quickly will horse [Bt] increase after being off feed?
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-12-15 hrs
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Hyperbilirubinemia due to obstructive cholestasis
-pathogenesis |
Impaired bile flow in canaliculi, bile ducts, gall bladder
-Bc accumulated in bile canaliculi --Bc returns to the plasma ---inc. [Bt] due to inc. [Bc] ----inc. [Bc] interferes with Bu uptake -----inc. [Bt] due to increased [Bu] ----if persistent inc. [Bc] ---> formation of Bdelta -----Inc. [Bt] due to inc. [Bdelta] |
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Ways Bc can return to the plasma in hyperbilirubinemia due to obstructive cholestasis
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-leakage to the space of Disse or Central Vein
-Hepatic necrosis & Bc picked up by sinusoidal blood -Bile acids inhibit Bc excretion ---> Bc regurgitated |
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Functional cholestasis
-aka |
-Sepsis-associated cholestasis
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Functional cholestasis
-due to |
-TNFalpha interfering with Bile Acid secretion
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Functional cholestasis
-expected bilirubin values |
-[Bc] > [Bu]
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Relative normal Bilirubin concentrations of Biliary Bilirubin vs. Plasma Bilirubin
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-Bile 2x Plasma Bilirubin
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Bile effusion into peritoneal cavity
-pathogenesis |
Bile leakage into peritoneal fluid
-Inc. [Bilirubin] in peritoneal fluid --Inc. Bilirubin diffusion to plasma and/or lymph ---Inc. [Bilirubin] in plasma/serum |
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Bile acids
-definition |
-cholesterol-derived anionic acids and associated anions
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Primary bile acids
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-cholic acid
-chenodeoxycholic acid |
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Secondary Bile Acids
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-Deoxycholic acid
-Lithocholic acid |
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Bile Acid assays
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-Spectrophometric assay = total [BA]
-RIA, EIA = Conjugated [BA] |
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What are conjugated bile acids conjugated with
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-taurine
-glycine |
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Bile Salt
-function |
-needed for the digestion of dietary lipids
-emulsify fats |
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Bile Acid
-locations in health |
-normally within enterohepatic circulation returned to the liver via intestinal absorption and portal blood flow
-very little in systemic blood |
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Primary BAc
-3 possible fates |
-absorption by the intestinal mucosa and entrance into portal blood
-deconjugation by enteric bacteria to a Primary BA then absorbed by intestinal mucosa -degeneration to Secondary BA which can either be excreted in feces or reabsorbed into portal blood |
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Hypercholemia
-defintion |
-Inc. Bile Acid concentration in blood
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Hypercholemia
-due to |
-Decreased bile acid excretion into bile
-Decreased bile acid clearance from portal blood |
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Hypercholemia due to obstructive cholestasis
-pathogenesis |
Hepatic or Posthepatic lesion that impairs bile flow
-dec. bile acid excretion into bile --bile acids accumulate in hepatocytes ---bile acids regurgitated into blood ----hypercholemia |
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Hypercholemia due to functional cholestasis
-pathogenesis |
Inflammatory disease causing the release of TNFalpha
-Inc. TNFalpha causes dec. transport of BA into canaliculi --Dec. bile acid excretion into bile ---bile acids accumulate in hepatocytes ----bile acids regurgitated into blood -----hypercholemia |
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Reasons for decreased bile acid excretion into bile
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-obstructive cholestasis
-functinoal cholestasis |
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Reasons for decreased bile acid clearance from portal blood
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-Portosystemic shunt
-Dec. liver functional mass |
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Hypercholemia due to portosystemic shunt
-pathogenesis |
Congenital or aquired portosystemic shunt
-dec. bile acid delivery to hepatocyte via portal blood --dec. removal of bile acids from portal blood ---hypercholemia |
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Hypercholemia due to Dec. liver functional mass
-pathogenesis |
Progressive liver disease or hepatic atrophy (from shunt)
-too few hepatocytes to remove BA from portal blood --BA pass through liver to central vein ---hypercholemia |
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Reasons why dogs with Canine Hepatic Cirrhosis have hypercholemia
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-obstructive cholestasis
-dec. liver functional mass -acquired portosystemic shunts |
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Bile Acid Challenge Test
-main concept |
-challenges the systems ability to remove BAs from portal blood
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Bile Acid Challenge Test
-how to perform |
-fast for 12 hrs
-collect blood sample for fasting [BA] -feed small meal to stimulate Gall Bladder contraction -collect blood sample 2 hrs after the meal (postprandial [BA]) |
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In what animals is the Bile Acid Challenge Test not done on?
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-icteric animals
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Ammonium
-sources |
-digestion of dietary proteins by intestinal bacteria
-peripheral tissues |
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What happens with ammonium after it enters the liver?
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-enters hepatocytes
-used for the synthesis of urea, amino acids, proteins -urea diffuses to sinusoidal blood or bile canaliculi |
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How can urea be excreted?
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-kidneys
-intestines (bile) but can also be reabsorbed via enterohepatic circulation |
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How can NH4+ be excreted?
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-urine
-fixed into urea -fixed into glutamine in renal tubular cells (deaminated during acidemia --> excretion) |
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Causes for false increases in ammonium
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-hemolysis
-delayed sample analysis -serum and not plasma is measured (higher conc. in plasma) |
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Causes for false decreases in ammonium
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-exposure to (conversion to NH3 then lost to air)
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Hyperammonemia
-causes |
-portosystemic shunt
-decreased functional mass -Urea cycle defect -Increased NH4+ production |
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Reasons for increased NH4+ production
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-postprandial
-urea toxicosis in cattle -strenuous exercise -equine intestinal disease |
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Reasons urea cycle defects cause increase NH4+
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-dec. enzymes
-deficiency in arginine, ornithine, or citrulline |
