Page 554 - Small Animal Internal Medicine, 6th Edition
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526    PART IV   Hepatobiliary and Exocrine Pancreatic Disorders





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                     A                                         B

                          FIG 33.6
                          Jaundiced mucous membranes in a dog (A, gum; B, sclera). Note that this dog had
                          jaundice because of immune-mediated hemolytic anemia and not liver disease—hence, the
                          mucous membranes are pale and yellow, which makes them more easily photographed.
                          (Courtesy Sara Gould.)


            canaliculi. Conjugated bilirubin is  then incorporated  into   Portal triad
            micelles and stored with other bile constituents in the gall-
            bladder until it is discharged into the duodenum. However,
            in dogs, only 29% to 53% of bile produced is stored in the
            gallbladder; the rest is secreted directly into the duodenum.
            After arrival in the intestine, conjugated bilirubin undergoes
                                                                                            Zone
            bacterial deconjugation and then reduction to urobilinogen,   Central      Zone 1 2
            with most urobilinogen being resorbed into the enterohe-      vein
            patic circulation. A small fraction of urobilinogen is then                        Zone
                                                                                                 3
            excreted in the urine, and a small portion remains in the
            intestinal tract to be converted to stercobilin, which imparts
            normal fecal color.
              Inherited abnormalities of bilirubin metabolism have not
            been identified in cats and dogs, so in the absence of massive
            increases in bile pigment production by hemolysis, jaundice
            is attributable to impaired excretion of bilirubin, and usually   FIG 33.7
                                                                 Rappaport scheme of the hepatic functional lobule (acinus),
            other constituents of bile, by diffuse intrahepatic hepatocel-  organized according to biochemical considerations (1958).
            lular or biliary disease or by interrupted delivery of bile to   This is centered on a line connecting two portal triads and
            the  duodenum.  The  inability  to take up,  process  intracel-  describes functional zones radiating from the triad to the
            lularly, or excrete bilirubin into the bile canaliculi (the rate-  central vein. For example, zone 1 cells are responsible for
            limiting step) is the mechanism of cholestasis believed to be   protein synthesis, urea and cholesterol production,
            operational in many primary hepatocellular diseases. Jaun-  gluconeogenesis, bile formation, and β oxidation of fatty
                                                                 acids; zone 2 cells also produce albumin and are actively
            dice is more likely to be a clinical feature if the liver disorder   involved in glycolysis and pigment formation; and zone 3
            primarily involves the periportal (zone 1) hepatocytes (Fig.   cells are the major site of liponeogenesis, ketogenesis, and
            33.7) than if the lesion involves centrilobular (zone 3) hepa-  drug metabolism. Zone 3 hepatocytes, being farther from
            tocytes. Inflammation and swelling of larger intrahepatic   the hepatic artery and hepatic portal veins, also have the
            biliary structures could similarly delay bile excretion.  lowest oxygen supply and are therefore most susceptible to
              Extrahepatic biliary duct obstruction (EBDO) occurs as   hypoxic damage. Arrows show direction of blood flow. The
            a result of intraluminal or extraluminal obstruction of the   portal triad comprises one or more branches of bile duct
                                                                 (green), hepatic artery (red), and hepatic portal vein (violet).
            bile duct at any point along its length. This may be obstruc-
            tion of the cystic duct by a gallbladder mucocele in dogs or
            obstruction of the common bile duct in dogs and cats by   tocellular regurgitation of bile constituents into the circu-
            choleliths, neoplasia of occasionally foreign bodies. Jaundice   lation, and jaundice. If only one of the hepatic bile ducts
            can develop in both cats and dogs as a result of acute flare-up   exiting the liver is blocked, or if only the cystic duct exiting
            of a chronic pancreatitis causing transient extrahepatic   the gallbladder is obstructed for some reason, there may
            biliary obstruction. Indeed, an acute flare-up of chronic pan-  be biochemical clues for localized cholestasis, such as high
            creatitis is the commonest cause of EBDO in dogs.    serum alkaline phosphatase activity; however, the liver’s
              Obstruction of the bile duct near the duodenum results   overall ability to excrete is preserved, and jaundice may
            in increased intraluminal biliary tract pressure, interhepa-  not ensue.
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