The inability of bile and many of its components to flow into the intestines after biliary obstruction (especially in cases of complete obstruction) leads to increased intraductal pressure, altered hepatic blood flow, and a series of biochemical, immunologic, hepatic, renal, and metabolic changes in the body, the characteristics and extent of which depend on the site and duration of the biliary obstruction, the extent of the obstruction, and the presence or absence of co-infections. Hepatocyte apoptosis increases with the prolongation of biliary obstruction, and liver damage and impaired liver function also increase with the prolongation of obstruction, and apoptosis is positively correlated with it. Obstructive jaundice is caused by obstruction of bile outflow and is the main cause of hepatocellular damage, which often culminates in cirrhosis, hepatic failure, and death. Accumulation of bile acid salts in the liver induces apoptosis in hepatocytes and bile duct cells, and excessive apoptosis in turn causes abnormal anti-apoptosis, which results in the abnormal proliferation of hepatic fibrosis, which constitutes another major cause of liver damage. With the increase of pressure in the bile duct during bile duct obstruction, bile reflux occurs, which increases the pressure of hepatic sinusoids significantly and leads to the increase of portal venous pressure and hepatic arterial resistance, which reduces the blood flow into the liver, resulting in relative ischemia and hypoxia of hepatocytes, and the aggravation of hepatic pathologic changes. At the same time, bile acid salts can not be discharged into the intestines through the bile duct, and the inhibitory effect of bile salts on intestinal bacteria can not be exerted, resulting in the acceleration of intestinal endotoxin reproduction, dysfunction of the bacterial flora, a significant increase in the number of Gˉ bacteria, and an increase in the production of endotoxin; at this time, the barrier of the intestinal mucosa is impaired, and endotoxin and bacteria are translocated into the liver via the portal vein, and the function of the Kupffer cells in the liver is impaired, with a decrease in the clearance capacity for endotoxin. The combined effect of the above causes leads to changes in the ultrastructure of hepatocytes, abnormal nuclear morphology, solid shrinkage, mitochondrial swelling, cristae disappearance, fracture, homogeneous material in the bile ducts, lipid storage cells, endoplasmic reticulum decrease and Kupffer cells increase and swelling. In addition, a decrease in systemic immune function is present in obstructive jaundice, and the decrease in cellular immune function is particularly significant. The narrowing and obstruction of the bile duct caused by the tumor results in the return of bilirubin and bile acids into the bloodstream, resulting in hyperbilirubinemia and bile acidemia. Studies have shown that when bile duct obstruction is 1 or 2 weeks and endotoxemia is not obvious, myocardial, hepatic and renal cells have mitochondrial swelling, deformation, loss of cristae, etc., and there are myofilament disorders in the fashion of 2 weeks of obstruction. At this time, the blood bile acid concentration was significantly elevated, and tube feeding of sodium cholate brought the bile acid concentration to the average concentration of 2 weeks of biliary obstruction, and the myocardium had similar ultrastructural changes. This suggests that bile acid stasis in obstructive jaundice damages the ultrastructure of organs or tissues such as the myocardium.