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Laboratory evaluation of hepatic disease

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Abstract

The recognition and diagnosis of hepatobiliary diseases can be challenging. The associated clinical signs are varied and often quite vague and non-specific, and while there is a wide range of laboratory tests of both hepatic damage and function, there is rarely a single test that definitively identifies the disease. This chapter considers the disgnostic approach to liver disease, serum biochemistry, routine haematology, urinalysis, liver function tests, genetic testing, liver biopsy, pattern recognition in liver disease and prognostic indices. Case examples are included.

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Figures

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12.3 Mechanism of hepatic enzyme release. (a) Hepatocellular damage: (i) Mild damage causes release of cytosolic ALT and a small amount of aspartate aminotransferase (AST) through increased cell membrane permeability; (ii) Hepatocyte necrosis causes liberation of more ALT and mitochondrial AST is also released. (b) Intra- and extrahepatic cholestasis: (i) ALP is normally secreted in bile with excreted bilirubin; (ii) Common bile duct obstruction causes extrahepatic cholestasis (EHBDO), leading to increased serum ALP because ALP is both regurgitated into the blood and its synthesis is induced. Bilirubin cannot be excreted and the patient becomes icteric. Accumulation of bile acids damages the hepatocyte membrane, leading to the release of ALT; (iii) Hepatocyte damage causes release of ALT, but swelling of the hepatocytes occludes the narrow biliary canaliculi that run between hepatocytes. This causes intrahepatic cholestasis. Jaundice sometimes occurs if there is significant hepatocyte dysfunction. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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12.4 Pattern of changes in serum liver enzymes after an acute hepatic injury and during resolution. Note that there is a parallel increase in ALT and AST but a longer persistence of ALT because of its longer serum half-life and continued synthesis and release during hepatic repair. The increase in ALP lags behind the hepatocellular marker enzymes, as hepatocyte swelling causes intrahepatic cholestasis.
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12.5 Pattern of changes in serum hepatocellular marker enzymes (ALT, AST) with chronic injury and progressive hepatic dysfunction. Note that ALT and AST fluctuate but remain persistently elevated, although there is an overall decrease as liver function (assessed by serum bile acids) declines, and terminally, serum enzyme activity may be within the reference range.
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12.6 Pattern of changes in serum liver enzymes following extrahepatic bile duct obstruction. Note the rise and plateau of ALP, which will parallel the rise in bilirubin. Lesser increases in ALT and AST follow the accumulation of toxic bile acids that increase hepatocyte cell membrane permeability.
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12.8 Logical approach to a patient with an unexplained increase in serum ALT activity
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12.10 Blood smears from: (a) a dog with a congenital portosystemic shunt, showing anisocytosis, microcytosis, mild hypochromia and a number of acanthocytes (spur cells); (b) a Cocker Spaniel with chronic hepatitis showing slight anisocytosis, hypochromia and target cells. (Wright–Giesma stain; original magnification X1000)
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12.11 Schematic representation of the normal metabolism of bilirubin and excretion of urobilinogen. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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12.12 (a) Gross appearance of massive amounts of ammonium biurate crystals in urine from a dog with chronic hepatitis. (b) Microscopic appearance of urate crystals in urine sediment from a dog with a congenital portosystemic shunt. (Original magnification X400)
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12.14 Extrahepatic bile duct obstruction. (a) Acholic faeces. Pale faeces lacking bile pigments from a dog with complete bile duct obstruction. (b) Massive bilirubinuria. Urine collected from the dog with complete bile duct obstruction that passed the acholic faeces in (a). Urinary urobilinogen is absent but the bilirubinuria obscures all dipstick test results.
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12.15 Abdominal fluid drained from a dog with bile peritonitis.
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12.16 Schematic representation of the normal enterohepatic recycling of bile salts. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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12.17 Metabolism of ammonia (NH) in (a) normal dogs, and dogs with (b) a urea cycle enzyme defect (rare), (c) congenital portosystemic shunt and (d) cirrhosis with secondary acquired shunting and GI bleeding because of coagulopathy and portal hypertension.
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12.19 Fine-needle aspirates. (a) From the liver of a cat with hepatic lipidosis, showing foamy vacuolated hepatocytes. (Original magnification X1000). (b) From the liver of a dog with intrahepatic cholestasis, showing hepatocyte vacuolation and darkly staining bile plugs. (Original magnification X500). (c) From the gallbladder of a dog with cholecystitis showing bacterbilia. (Original magnification X1000) (a, Courtesy of Marta Costa, Langford Veterinary Services; b, Courtesy of Kathleen Tennant, Langford Veterinary Services; c, Courtesy of Emma O’Neil, University College Dublin)
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12.20 Impression smear of liver from a dog that died of infectious canine hepatitis, showing characteristic intranuclear inclusions. (Haematoxylin and eosin stain; original magnification X400)

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