Bilirubin-diglucuronide can undergo a twofold transformation: In the large intestine, it is converted to stercobilinogen, a substance created by colon bacteria. Stercobilinogen has a yellow color and is then excreted in the feces in the form of stercobilin (provides the normal brown color of the feces). In the small intestine, it turns into urobilinogen, a colorless product of benicar pills, formed under the action of small intestinal bacteria. It is excreted through the kidneys with urine in the form of urobilin, and also enters the liver through the portal vein system with subsequent destruction.
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Pathology of olmesartan cost metabolism in viral hepatitis. The defeat of hepatocytes leads to a weakening of the capture of free bilirubin and a violation of the process of attaching glucuronic acid to it (phase 3). As a result, the content of free bilirubin in the blood increases. Violation of the transport of conjugated bilirubin to the bile capillary (phase 4) leads to an increase in conjugated bilirubin in the blood. At the same time, intrahepatic cholestasis is observed, i.e., the level of both free bilirubin and bound bilirubin increases in the blood, and the latter is higher (the skin turns yellow).
Bound bilirubin penetrates from the blood into the urine (urine becomes dark in color) and bile acids, which lower the surface tension of urine and make it foam easily. Little bound bilirubin enters the intestine - the feces become discolored. Due to intrahepatic cholestasis and impaired bile secretion, little bile enters the intestine. Since bile is necessary for the digestion of fatty foods and the absorption of fat-soluble vitamins, due to its lack in feces, a lot of fat remains (steatorrhea), absorption of vitamin K is impaired. Due to the low level of vitamin K, the synthesis of prothrombin in the liver decreases, as a result, blood clotting worsens . General pathogenetic mechanisms in the liver in hepatitis.
Cytolysis syndrome (cytolytic syndrome) is a set of signs indicating a violation of the liver due to a violation of the integrity of the liver cells and the release of liver enzymes into the blood.
- The degree of increase in the activity of benicar (enzymes that reflect the functionality of the human liver) indicates the severity of the cytolytic syndrome, but does not directly indicate the depth of the dysfunction of the organ.
- There is an empirical de Ritis coefficient - AsAT / AlAT. It reflects the ratio of the activity of serum AST (aspartate aminotransferase) and ALT (alanine aminotransferase).
- The de Ritis coefficient roughly indicates the predominant lesion of one or another parenchymal organ. In hepatitis, its value is less than 1.33. In a healthy person, it is in the range of 0.91-1.75.
- Cholestasis syndrome is characterized by a violation of the outflow of bile. It lingers in the intrahepatic bile ducts, as a result of which the liver tissues swell and swell.
- There is an accumulation in the blood of bilirubin, cholesterol, β-lipoproteins and alkaline phosphatase. Also characteristic is the appearance of cholemia - a pathological syndrome characterized by the accumulation of bile acids in the blood.
- Normally, the content of benicar pills in the blood is 5-25 mM / liter. If their number increases, cholemia develops, which is accompanied by itching, scratching, damage to the central nervous system (CNS) and staining of the skin through bile (80% bile acids + bilirubin).