The liver is an essential organ for metobolische metabolic processes. Hepatocytes (liver parenchyma cells) are responsible in the liver for the metabolic functions: formation and excretion of bile in the context of the bilirubin metabolism (overview of the Bilirubinmetabolismus) control of carbohydrate homeostasis lipid synthesis and secretion of plasma lipoproteins control of cholesterol metabolism formation of urea, serum albumin, clotting factors, enzymes, and numerous other proteins absorb and process or detoxification of drugs and other foreign substances overview of the Bilirubinmetabolismus the degradation of heme produced bilirubin (an insoluble waste product) and other bile pigments. Bilirubin must be made water soluble to be eliminated to. This transformation takes place in five stages instead: education, transport in plasma, uptake by the liver, conjugation and biliary excretion. Education: about 250-350 mg are formed by unconjugated bilirubin Daily. 70-80% comes from the breakdown of red blood cells degenerate and 20-30% primarily from other heme proteins in the bone marrow and liver. Hemoglobin is degraded to iron and biliverdin is converted to bilirubin. Plasma Transport: Unconjugated (indirect) bilirubin is not water soluble and is transported coupled to albumin in the plasma. It can not pass the glomerular membrane and will not appear in the urine. The albumin binding under certain conditions (eg. B. acidosis) weaker, and some substances (eg. B. salicylates, certain antibiotics) compete for the binding sites. Liver uptake: The liver takes the bilirubin fast on, but not bound to serum albumin. Conjugation: Unconjugated bilirubin is conjugated in the liver, primarily to bilirubin diglucuronide (conjugated [direct] bilirubin). This reaction, which is catalyzed by the microsomal enzyme glucuronyl, makes the bilirubin water soluble. Biliary tract: Tiny Gallekanalikuli which are formed by adjacent hepatocytes grown into ductules, interlobular bile ducts and larger hepatic passages together. Outside the hepatic portal of the common hepatic duct runs together with the cystic duct of the gall bladder, to form the common bile duct that drains of the ampulla of Vater into the duodenum. Conjugated bilirubin is excreted along with other bile components in the Gallekanalikulus. In the intestinal bacteria metabolize bilirubin to urobilinogen, of which a majority is further metabolized to stercobilin that stains the chair brown. For complete closure of the bile chair loses its normal color and light gray (such as bran). Part of the urobilinogen is reabsorbed, taken up by hepatocytes and in turn excreted in the bile (enterohepatic circulation). A smaller proportion is excreted in urine. Because only conjugated bilirubin and not unconjugated bilirubin is excreted in the urine, a conjugated hyperbilirubinemia (z. B. due to a hepatocellular, cholestatic jaundice) may generate a bilirubinuria. At the cellular level, the portal fields consist of adjacent and parallel terminal branches of bile ducts, portal vein and branches of the hepatic artery (structure of the liver.). The terminal branches of the hepatic veins are located in the center of the lobules (central vein). Because the blood flows past of the portal fields to the hepatocytes in the central vein of the lobule, the Läppchenzentrum is most sensitive to ischemia. Structure of the liver. The liver is composed of cloth around the terminal branches of the hepatic vein. Between the lobules are portal triads. Each triad consists of the branches of the bile duct, the portal vein and the hepatic artery. Pathophysiology liver disease are the result of various injuries, such as by infection, drugs, toxins, ischemia or autoimmune diseases. Occasionally, liver disease postoperatively. Most liver diseases give rise to some degree of liver cell damage and necrosis and lead to abnormal liver function and symptoms. The symptoms may be caused directly by the liver disease (eg. B. jaundice in acute hepatitis), or be due to complications of liver disease (eg. As acute gastrointestinal bleeding), as a result of cirrhosis and portal hypertension. The liver can regenerate outstanding. Even larger Nekrosefelder form completely disappear (eg. As acute viral hepatitis). Incomplete regeneration and the occurrence of fibrosis occur on the floor of Brückennekrosen and those that affect the entire lobules, or as a result of, although less pronounced, but chronic liver damage. Specific diseases focus preferably on certain hepatobiliary structures and functions such. B. the acute viral hepatitis preferably is characterized by damage to hepatocytes, primary biliary cirrhosis caused by impairment of bile secretion, and cryptogenic cirrhosis through liver fibrosis and portal hypertension resulting. The affected part of the hepatobiliary system determines symptoms, signs and laboratory abnormalities (tests for liver and biliary disorders). Some diseases (eg. As severe alcoholic liver disease) affect multiple liver structures, resulting in a combination of patterns of symptoms, signs and laboratory abnormalities. The prognosis of severe complications is worse in older adults who are less able to recover from severe physiological stress and to tolerate cumulative toxicities.