When the red blood cells in the blood die, the hemoglobin in the red blood cells will be converted into bilirubin in the Kuffer cells of the liver and the spleen, and the bilirubin will be processed by the liver, secreted with the bile to the duodenum, and finally excreted through the digestive system, together with the feces. Liver cells have certain congenital defects, can not complete the normal metabolism of bilirubin and the occurrence of congenital non-hemolytic jaundice, then, the following specific for everyone to introduce the causes of jaundice: a, hemolytic jaundice etiology: where a large number of red blood cells can cause destruction and hemolysis of disease, can cause hemolytic jaundice, the following two common diseases: 1, congenital hemolytic anemia: such as thalassemia ( Hemoglobinopathies), hereditary spherocytosis, 2, acquired acquired hemolytic anemia: such as autoimmune hemolytic anemia, hereditary glucose-6-phosphate dehydrogenase deficiency (sericulture), hemolysis after allogeneic transfusion, neonatal hemolysis, falciparum malaria, drugs such as primaquine, snake venom, mushroom poisoning, paroxysmal sleep hemoglobinuria, etc., II, hepatocellular jaundice etiology: various liver Diseases, such as viral hepatitis, toxic drug liver, hepatitis, drug liver disease, various types of cirrhosis, primary and secondary liver cancer, sepsis and leptospirosis, etc., can cause jaundice due to diffuse damage to hepatocytes. The common diseases causing extrahepatic bile duct obstruction include common bile duct stones, stenosis, inflammatory edema, roundworms, tumors and congenital biliary atresia; common diseases or causes of bile duct obstruction due to extra-biliary compression include cancer of the head of the pancreas, chronic pancreatitis with an enlarged head of the pancreas, carcinoma of the jugular, common bile duct, hepatocellular carcinoma, and cancer of the portal or hepatic duct. 2, intrahepatic bile duct obstruction can be divided into intrahepatic obstructive bile depression and intrahepatic bile depression, the former is common in intrahepatic bile duct sediment-like stones, cancerous emboli (mostly hepatocellular carcinoma), bilharziasis, etc.; the latter is common in capillary bile duct viral hepatitis, drug biliary depression (such as chlorpromazine, methyltestosterone, oral contraceptives, etc.), bacterial sepsis, recurrent jaundice during pregnancy, primary biliary cirrhosis and Fourth, congenital non-hemolytic jaundice etiology: refers to a congenital defect in the metabolism of bilirubin, the onset of the disease is mostly seen in infants, young children and young adults, often with a family history, such as in infancy and childhood did not die and can survive, the jaundice can recur, often induced after a cold or exercise, infection, fatigue. However, the patient is generally in good health. This type of jaundice is clinically rare, sometimes easily misdiagnosed as hepatobiliary disease, the following common diseases belong to this type of jaundice, 1, Gilbert’s syndrome: the mechanism of jaundice is the uptake of non-conjugated bilirubin by hepatocytes is impaired (light, is the most common clinically familial jaundice) and hepatocyte microsomes in glucuronosyltransferase deficiency (heavy, poor prognosis) caused by this disease is characterized by, in addition to jaundice The disease is characterized by jaundice, normal liver function tests, increased serum concentration of unconjugated bilirubin, and increased erythrocyte fragility; after oral cholangiography, the gallbladder is well visualized, and liver biopsy is not abnormal. 2, Dabin-Johnson syndrome: the cause of jaundice is the conversion of unconjugated bilirubin into conjugated bilirubin in the hepatocytes, and the dysfunction of conjugated bilirubin transport and secretion to the capillary bile ducts. The disease is characterized by increased serum conjugated bilirubin; the gallbladder is not visualized after oral cholangiocontrast; the liver has a greenish-black appearance (observed under laparoscopy), and liver biopsy reveals diffuse brown pigment granules in the hepatocytes, which has a good prognosis. Rotor syndrome: jaundice occurs because of partial impairment of hepatocyte uptake of unconjugated bilirubin and excretion of conjugated bilirubin into the capillary bile ducts, characterized by increased serum unconjugated and conjugated bilirubin; impaired (reduced) indocyanine green (ICG) excretion test; cholangiogram is mostly well developed, only a few do not develop; no pigment granules in the liver, normal liver biopsy. 4, Crigler-Najjar syndrome: jaundice occurs because of the lack of glucuronosyltransferase in the hepatocyte particles, so that non-conjugated bilirubin can not be converted into conjugated bilirubin, the syndrome can be divided into heavy or light, the former because of the high concentration of non-conjugated bilirubin in the blood, and brain tissue has a strong affinity for adipose tissue, so prone to bilirubin encephalopathy (nuclear jaundice). The latter is a partial lack of glucuronosyltransferase in the body of hepatocyte particles, so its symptoms are milder and the prognosis is slightly better than that of heavy jaundice. The diagnosis of jaundice is mainly based on the patient’s clinical manifestations and auxiliary examinations to confirm the diagnosis, observation of the patient’s sclera, mucous membrane and skin jaundice should be carried out in good natural light, and should be distinguished from pseudo-jaundice caused by eating too much pumpkin, carrots, tomatoes and citrus (pseudo-jaundice with normal serum bilirubin), the sclera of the elderly may have a little fatty deposits and appear slightly yellow, should not be regarded as the occurrence of Jaundice, the diagnosis and differential diagnosis of jaundice should be detailed history, and careful physical examination, combined with the necessary laboratory and special tests for comprehensive analysis and judgment, in order to correctly make the etiological diagnosis of jaundice.