Within the lobule, hepatocytes are organized into anastomosing sheets or “plates” extending from portal tracts to the terminal hepatic veins. Between the trabecular plates of hepatocytes are vascular sinusoids. Blood traverses the sinusoids and exits into the terminal hepatic veins through numerous orifices in the vein wall. Hepatocytes are thus bathed by well-mixed portal venous blood on one side and hepatic arterial blood on the other. The sinusoids are lined by a fenestrated endothelium that overlies a perisinusoidal space (the space of Disse) into which abundant hepatocyte microvilli protrude. Attached to the luminal face of the sinusoids are scattered Kupffer cells, specialized long-lived tissue macrophages that arise early in embryogenesis. Another specialized cell type, the hepatic stellate cell, is found in the space of Disse and has a role in the storage of vitamin A. Between abutting hepatocytes are bile canaliculi, channels 1 to 2 µm in diameter that are formed by grooves in the plasma membranes of adjacent hepatocytes and are separated from the vascular space by tight junctions. These channels drain successively into the intralobular canals of Hering, periportal bile ductules, and finally into the terminal bile ducts within the portal tracts.
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Fig. 16.1 Modelsofliveranatomy.Inthelobularmodel,theterminalhepaticveinisatthecenterofa“lobule,”whiletheportaltractsareattheperiphery.Pathologistsoftenrefertotheregionsoftheparenchymaas“periportalandcentrilobular.”Intheacinarmodel,onthebasisofbloodflow,threezonescanbedefined,zone1beingtheclosesttothebloodsupplyandzone3beingthefarthest.BD, Bileduct;CV, centralhepaticvein;HA, hepaticartery;PV, portaltracts.
The major primary diseases of the liver are viral hepatitis, alcoholic liver disease, nonalcoholic fatty liver disease (NAFLD), and hepatocellular carcinoma (HCC). The liver also is frequently damaged secondarily in a variety of common disorders, such as cardiac disease, disseminated cancer, and extrahepatic infections. The functional reserve of the liver masks the clinical impact of mild liver damage, but severe diffuse liver disease often has life-threatening consequences.
With the rare exception of fulminant hepatic failure, liver disease is an insidious process in which the signs and symptoms of hepatic decompensation appear weeks, months, or even years after the onset of injury. The hepatic injury may be imperceptible to the patient and be manifest only by laboratory test abnormalities (
Table 16.1 ), and liver injury and healing also may be subclinical. Hence, individuals with hepatic abnormalities who are referred to hepatologists most frequently have chronic liver disease.
Injured hepatocytes may show several potentially reversible changes, such as accumulation of fat and bilirubin (cholestasis); when injury is not reversible, hepatocytes die by necrosis or apoptosis. Necrosis (
Fig. 16.2 ) is commonly seen following hepatic injury caused by hypoxia and ischemia. Apoptotic cell death (
Fig. 16.3 ) predominates in viral, autoimmune, and drug-and toxin-induced hepatitides.
Table 16.1 Laboratory Evaluation of Liver Disease
Total: unconjugatedplusconjugated
Direct: conjugatedonly *Mostcommonlyusedtestsareinitalics;†anelevationsuggestsliverdisease;‡adecreasesuggestsliverdisease.