Page 1114 - Small Animal Clinical Nutrition 5th Edition
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1160       Small Animal Clinical Nutrition



                  and cats. It is localized in the cytoplasm of hepatocytes and  equivocal, an ammonia tolerance test can be performed. Bile
        VetBooks.ir  released with even mild damage to cell membranes. Hep-  salts (primarily taurocholate in dogs and cats), also erroneous-
                                                                      ly called bile acids, are produced by the liver and excreted in
                  atocytes, however, do not need to be irreversibly damaged and
                  a number of metabolic or systemic conditions can alter mem-
                                                                      the bile. After uptake in the portal blood, the liver re-extracts
                  brane function without being a primary liver disorder.The bio-  bile salts (i.e., enterohepatic circulation). Concentration of
                  logic half-life of ALT is about two and one-half days in dogs  bile salts increases in the systemic circulation in cholestasis
                  and approximately six hours in cats (Webster and Cooper,  (either intrahepatic or extrahepatic), hepatocyte dysfunction
                  2009). ALT is fairly sensitive and specific in dogs and cats and  (failure to extract bile acids from the sinusoidal circulation)
                  thus a good parameter for use in screening for liver disease.  and when vascular portosystemic shunting is present. Thus,
                    AST is not liver specific. In dogs, it is mainly present in car-  determination of the venous concentration of total bile salts is
                  diac and skeletal muscle and other tissues and to a lesser degree  a specific and an early, sensitive indicator of liver function.
                  in the liver. In cats, AST is more limited to the liver. Although  Bile salts are stable and easy to measure (Webster and Cooper,
                  not liver specific, AST is useful because it is chiefly located in  2009). An eight-hour fasted sample should be obtained fol-
                  the mitochondria and thus only released by cell death.The half-  lowed by a postprandial sample two hours later in dogs and
                  life of serum AST in dogs is five to 12 hours and 77 minutes in  cats. After hemolysis has been ruled out, bilirubin elevations
                  cats (Webster, 2005). Increased activities of AST and ALT gen-  reflect hepatic or extrahepatic cholestasis. The ratio between
                  erally indicate more severe hepatocellular damage than does an  conjugated and unconjugated bilirubin fractions is not useful
                  increase in ALT alone. However, this reasoning has proved to  for differentiating among various hepatic disorders; other
                  have no real diagnostic meaning, hence AST is not used.  diagnostic testing is required. Also, urinary urobilinogen con-
                                                                      centrations have a very low diagnostic accuracy for supporting
                  Other Blood Examinations                            a diagnosis of extrahepatic cholestasis.
                  Laboratory tests found in most biochemistry profiles that can
                  reflect, in part, hepatic function include bilirubin, albumin,  Imaging the Liver
                  cholesterol, glucose and urea nitrogen. Other specialized tests  Radiographs are useful to determine the size and shape of the
                  of hepatic function include serum bile acid concentrations.  liver and to identify other concurrent abdominal disorders. Ad-
                  Because the liver is involved in a multitude of functions, no sin-  vanced studies of the hepatobiliary system include ultrasono-
                  gle test can reflect its functional state and interpretation of  graphic imaging (Szatmari and Rothuizen, 2006). Hepatic
                  function must be made in light of the clinical and laboratory  ultrasonography is useful for initially identifying disease and
                  testing results. Chronic hepatic dysfunction can cause hypoal-  monitoring its progression (Partington and Biller, 1995, 1996;
                  buminemia and clotting disorders. The liver exclusively pro-  Barr, 1990; Nyland et al, 1995; Lamb, 1998). Ultrasonography
                  duces albumin and coagulation factors except factor VIII. A  can detect and differentiate focal and diffuse hepatic parenchy-
                  number of non-hepatic conditions cause hypoalbuminemia;  mal disorders and changes in the hepatobiliary (gallbladder and
                  however, albumin synthesis declines with the loss of approxi-  bile ducts) system. The evaluation should also include the
                  mately 70% of hepatic function. Serum albumin concentrations  hepatic vascular system because portosystemic anomalies are
                  may fall even lower with concurrent ascites and third-spacing in  extremely common. Ultrasonography is highly operator depen-
                  the ascitic fluid. The biologic half-life of albumin is approxi-  dent and imaging expertise takes time to develop. Readers are
                  mately two weeks. Glucose and clotting factor concentrations  referred to diagnostic imaging textbooks and manuals for de-
                  decline when more than 75% of hepatic function is lost.  tailed descriptions and classifications of hepatic lesions identi-
                    Abnormal blood coagulation generally reflects significant  fied by ultrasonography (Barr, 1990; Nyland et al, 1995; Part-
                  hepatic dysfunction due to reduced protein synthesis. Rarely,  ington and Biller, 1996; Lamb, 1998).
                  chronic bile duct obstruction can deplete intestinal bile acid  Nuclear imaging procedures (e.g., hepatic scintigraphy) and
                  concentrations required for adequate vitamin K absorption and  magnetic resonance imaging are used to further assess hepatic
                  can result in depletion of hepatic production of vitamin K-  structure and vasculature or measure the degree of portosys-
                  dependent clotting factors (factors II, VII, IX and X). When  temic vascular shunting. These techniques are usually only
                  this situation occurs, clotting times are quickly corrected fol-  available at specialty referral centers.
                  lowing parenteral vitamin K administration.
                    Ammonia is an important parameter to consider when HE  Liver Biopsy
                  is suspected. Elevated ammonia concentrations generally re-  Histopathologic tissue examination is essential for definitive
                  flect the presence of portosystemic circulation abnormalities  diagnosis of hepatobiliary disease (Center, 1995; Meyer, 1996;
                  (e.g., congenital PSS or acquired shunts from portal hyper-  Kerwin, 1995). Liver biopsy is an invasive procedure that must
                  tension). Plasma ammonia concentration is less sensitive and  be carefully considered before implementation. Common op-
                  specific in reflecting hepatocellular function but is the method  tions for securing liver tissue include ultrasonographic-guided
                  of choice when HE is suspected. Most in-house dry chemical  needle biopsy,“blind” biopsy techniques, laparoscopic needle or
                  methods provide reliable results (Sterczer et al, 1999). Care  pinch biopsy and celiotomy for wedge biopsy (Center, 1995). A
                  should be taken when handling samples because a number of  minimum of three full 16-gauge needle samples should be col-
                  factors may interfere with accurate results. When results are  lected if a needle procedure is used. Small sample size decreas-
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