Jaundice

Introduction Astragalus refers to the yellow stain caused by bilirubin deposition in the skin, sclera and diuretic membrane. The normal serum total bilirubin concentration is 1.7~1.71. When one minute of bilirubin (both direct bilirubin) is lower than 3.4 umol/L, when the total bilirubin concentration is 34umol/L, jaundice appears in clinical practice. When the concentration of bilirubin in the serum exceeds the normal range and the jaundice is not visible to the naked eye, it is called recessive jaundice. Observation of jaundice should be carried out under natural light, and it must be distinguished from the yellowing of skin caused by taking a large amount of arsenic, carotene, etc., and it must be distinguished from the accumulation of fat under the bulbar conjunctiva. A flat yellow dye is more involved in the skin exposed by the body. It has been reported in the literature that this yellow stain is distributed centripetally, and the deeper the cornea, the deeper the serum bilirubin does not increase. The yellow pigmentation caused by carotene is because carotene is yellow, and many fresh fruits and vegetables such as carrots, citrus, papaya, etc. are abundant. When eating too much, especially when hypothyroidism or liver dysfunction, The process of converting the absorbed carotene into vitamin A in the liver is a disorder, which is easy to cause retention and causes caroteneemia, yellowing, yellow staining, and the skin of the forehead and nose rich in palm, plantar and sebaceous glands. . The identification method is very easy. Take 2ml of the serum of the examinee, add 8 ml of 95% or anhydrous alcohol and 10 minutes of petroleum ether, and let stand to separate the alcohol from petroleum ether. If it is carotene, the petroleum ether layer is Yellow; if bilirubin, yellow remains in the alcohol layer. The conjunctival fat accumulation in the bulb is usually seen in the elderly. The yellow stain is more obvious. The meticulous observation shows that the bulbar conjunctiva is uneven, the skin is not yellow, and the serum bilirubin is not high.

Cause

Classification of causes:

First, hemolytic jaundice.

Second, hepatic jaundice.

(1) Yellow-brown viral hepatitis.

1. Acute jaundice-type viral hepatitis.

2. Severe viral hepatitis

1 acute severe hepatitis (typhoid hepatitis)

2 subacute severe hepatitis (subacute liver necrosis)

3 chronic severe hepatitis.

3. Chronic jaundice-type viral hepatitis.

(B) yellow straight infectious mononucleosis.

(C) systemic giant cell inclusion disease.

(4) Leptospira disease (Weil disease).

(5) Huang Li caused by other acute systemic infections.

(6) Acute fatty liver in primary pregnancy.

(7) Toxic liver damage.

(8) Acute alcoholic hepatitis.

(9) Cardiac yellow increase.

(10) Cirrhosis of the liver.

(11) Hyperthyroidism complicated by yellow increase.

Third, obstructive jaundice.

(A) intrahepatic obstructive jaundice 1. intrahepatic cholestatic; 1 capillary cholangitis inflammatory viral hepatitis. 2 drug jaundice. 3 idiopathic jaundice during pregnancy. 4 alcoholic liver syndrome. 5 jaundice after benign surgery. 6 idiopathic benign recurrent intrahepatic cholestatic.

2. Intrahepatic mechanical obstruction 1 primary sclerosing cholangitis. 2 intrahepatic bile duct stones. 3 Huazhi haemorrhagic disease. 4 Blue Giardia protozoa cholangitis. 5 obstructive jaundice type liver cancer.

(B) extrahepatic obstructive gonococcal 1. Acute obstructive suppurative cholangitis. 2. Common bile duct stones. 3. Congenital choledochal cyst. 4. Pancreatic cancer. 5. There is no cancer around the ampulla. 6. Acute and chronic pancreatitis. 7. Common bile duct and hepatobiliary carcinoma, common bile duct adenomyosis. 8. Primary gallbladder cancer. 9. Ten M refers to post-intestinal ulcer.

Fourth, bilirubin metabolism deficiency disease.

(A) congenital bilirubin metabolic deficit

1. Githert syndrome

2.Dubin-Jolmson syndrome

3.Rtr syndrome

4.Crigl6r-Najjar syndrome

(B) acquired bilirubin metabolic defects

Indirect bilirubin hyperemia after hepatitis

Mechanism: It has been mentioned that jaundice is associated with increased serum bilirubin. The main source of serum bilirubin is hemoglobin. Under normal circumstances, red blood cells in the human blood are constantly produced from the bone marrow. The red blood cell life span is about 120d, and the aging red blood cells are destroyed and decomposed in the mononuclear-macrophage (reticular endothelium) system, and become the three components of bilirubin, iron and globin. This bilirubin is freely bound, insoluble in water, but fat soluble. It is tightly bound to serum albumin and can not be filtered from the glomerulus. The serum bilirubin qualitative test is an indirect reaction, so it is called indirect bilirubin or unconjugated bilirubin. When indirect bilirubin is transported to the side of the liver cell membrane, bilirubin and albumin are dissociated, and the former is taken up by the liver. There are two kinds of carrier protein* protein and z protein in hepatocyte cytoplasm combined with bilirubin and transported into microsomes. Most of them bind to bisglucuronide bilirubin by glucuronyltransferase. This combined bilirubin is directly reacted by the qualitative test of serum bilirubin, so it is called direct bilirubin, which is water-soluble and can be excreted through the glomerulus. Combined with bilirubin excreted into the intestines by the bile, it is broken down by the intestinal bacteria into a colorless urobilinogen, most of which is oxidized to urinary biliary hormone, which is called fecal bilirubin. A part of urinary biliary is absorbed in the intestine and enters the liver through the portal vein. Most of the urinary biliary tract back to the liver becomes conjugated bilirubin, which is discharged into the intestine with bile to form the so-called "enteric circulatory circulation of bile pigment". A small portion of the urinary tract that is absorbed back into the liver is excreted by the kidneys through the systemic circulation.

Under normal conditions, the rate at which bilirubin enters and leaves the blood circulation remains dynamically balanced. Therefore, the bilirubin in normal human body is constant at 17.1umol/L (1mg%, of which direct bilirubin is about 0-0.2mg, indirect bilirubin is about 0.7-0.8mg, urinary biliary is a small amount, and feces remain normal yellow. The formation process is directly related to the destruction of red blood cells in the human blood, the normal function of the liver and the smooth flow of the biliary tract. When any of the three diseases or lesions occur, the bilirubin will flow back in the blood or remain in the blood. The amount of erythromycin can be increased, and when it is >34.2 umol/L (2 mg%), jaundice can occur.

Hemolytic jaundice is due to:

1 A large number of red blood cells are destroyed, and the reticuloendothelial system forms a large amount of unbound bilirubin, which exceeds the ability of normal liver treatment to form jaundice in the blood;

2 The toxic effects of anemia, hypoxia and red blood cell destruction products caused by the destruction of a large number of red blood cells can attenuate the biliary pigment metabolism function of normal liver cells, resulting in increased jaundice. It also leads to an increase in the amount of urobilinogen and urinary urinary bilirubin in the feces. Therefore, in the case of hemolytic jaundice, serum bilirubin is an indirect reaction, and there is no bilirubin in the urine, and the original urinary bilirubin is increased.

an examination

Related inspection

Serum transferrin-releasing antibody test Hepatitis E antibody (anti-HEIgM) Hepatitis B surface antigen fecal gallbladder

First, laboratory inspection

1. Determination of serum enzyme activity

(1) Serum aminotransferase (SGPT, SGOT): In acute jaundice-type viral hepatitis, the activity of alanine aminotransferase and aspartate aminotransferase was significantly increased, and the cholestasis of jaundice was slightly elevated. In patients with severe hepatitis, sometimes the activity of aminotransferase is decreased, serum bilirubin is significantly increased, and the phenomenon of "biliary enzyme" is separated, suggesting that the prognosis is sinister.

(2) Alkaline phosphatase (AP) people have a significant increase in alkaline phosphatase in the liver, extrahepatic obstructive jaundice and intrahepatic cholestasis. Often greater than 3 times the normal value. In primary liver cancer, alkaline phosphatase can also be increased, mainly alkaline phosphatase-11 isoenzyme, and alkaline phosphatase is normal or slightly elevated in hepatic jaundice.

(3) R-glutamate transpeptidase (R-GT) In acute hepatitis, R-GT was only mildly or moderately elevated, and primary liver cancer and cholestatic jaundice, R-GT were significantly increased. The LDH is increased in most patients with acute hepatitis. In patients with benign cholestasis jaundice, LDH is generally increased. If I-DH is significantly increased, cancer obstruction or liver parenchymal damage should be considered. Is an isoenzyme of alkaline phosphatase, for the diagnosis of primary liver cancer, cancerous hepatic duct obstruction, differential diagnosis of neonatal hepatitis or congenital biliary atresia, better than alkaline phosphatase, hepatocyte yellow value 5- The nuclease activity is normal or slightly elevated.

2, serum total cholesterol, cholesterol lipid determination in cholestasis of jaundice, total cholesterol content increased, hepatic jaundice, especially extensive liver necrosis, cholesterol lipids decreased.

3. Serum lipoprotein X (LpX) Serum lipoprotein X is an abnormal low-density lipoprotein. Serum lipoprotein X may be present in the serum of cases of cholestatic jaundice, with extrahepatic obstructive jaundice and intrahepatic cholestasis. Most or even all of them are positive, and there is very little positive in hepatic jaundice without intrahepatic cholestasis.

4. Determination of serum iron and copper The normal serum iron concentration was 14.3-23.3 umol/L, the serum steel was 15.1-22 umol/L, and the copper ratio was 0.8-1.0. Serum copper increased in cholestatic jaundice, serum iron increased in iron/copper ratio, and iron/copper ratio >1.

5, sodium sulfonate gate SP) gambling test intravenous injection of 5% sulphate after 45 minutes of blood sampling, the amount of BSP in normal serum is less than 5% of the total amount of injection, such as more than suggesting liver parenchymal damage.

6. The indo cyanine green (ICG) retention test is similar to the SBP test, which is safer and has fewer side effects. According to its blood retention, the degree of hepatocyte excretion function is impaired, and the normal retention is 0-10%.

7, prothrombin time measurement and its response to vitamin K in the liver parenchymal damage or lack of bile in the intestine to make vitamin absorption disorders, that is, hepatocyte and cholestatic jaundice, prothrombin is produced less, and because of thrombin The original time was prolonged. The prothrombin time was reviewed 24 h after the injection of vitamin K 2-4 mg. If it was shortened before the injection, it means that the liver function is normal. The jaundice can be cholestatic. If there is no change, the jaundice may be hepatocellular. .

8. Therapeutic test

1 Prednisone treatment test: patients with prednisone 10-15 mg, 3 times a day for 5-7 days, check serum bilirubin before and after taking the drug. In cholestasis-type hepatitis, serum bilirubin can be reduced to 40%-50% of the original level after taking the drug, while in the extrahepatic obstructive jaundice, or serum bilirubin is slightly reduced.

2 phenobarbital treatment test: phenobarbital induces hepatocyte microsomal enzymes, promotes bile transport and excretion, and can reduce intrahepatic cholestasis of jaundice. Usage: phenobarbital 30-60mg, 3-4 times a day orally, for 7d, clinical significance and evaluation with prednisone treatment test.

Second, hematology examination is mainly used to assist in the diagnosis of hemolytic jaundice. Such as congenital hemolytic jaundice, anemia, red blood cells and reticular cells appear in the surrounding blood significantly increased, the bone marrow red system cells are obviously active and active. In hereditary spherocytosis, there is an increase in erythrocyte fragility; in thalassemia, erythrocyte fragility is reduced. Anti-human globulin (Coombs test) is positive in body immune hemolytic anemia and neonatal hemolytic anemia.

Third, the device inspection

(A), B-mode ultrasound examination

The accuracy of identifying cholestatic jaundice and hepatic jaundice is very high, especially for the identification of jaundice caused by extrahepatic bile duct obstruction and intrahepatic cholestasis. The former can be seen in the common bile duct and intrahepatic bile duct expansion, while the latter does not. In addition, the cause of the extrahepatic bile duct obstruction, the location of the lesion can make a valuable judgment.

(B), X-ray inspection

1, esophagus, gastrointestinal barium meal imaging, such as the discovery of esophageal and gastric varices, can help diagnose liver cirrhosis. Duodenal ring widening suggests pancreatic head cancer. In Vater ampullary carcinoma, duodenal hypotension was used to observe the filling defect of the duodenal intestine, which was anti-"3" type.

2, cholecystography can understand the development of gallbladder, with or without stone shadow and gallbladder contraction function, venous cholangiography can understand the biliary tract smooth or not, the bile duct with or without thickening.

3. Retrograde cholangiopancreatography (ERCP) through duodenoscopy is important for the diagnosis of chronic pancreatitis, pancreatic cancer and understanding of the biliary system. It can distinguish the site of extrahepatic or intrahepatic biliary obstruction through the duodenum. The mirror can directly see whether there is any lesion in the ampulla region and the nipple, and can be used for biopsy.

4, percutaneous transhepatic cholangiography (PTC) can clearly show the entire biliary system in the liver, can distinguish between extrahepatic bile duct obstruction and intrahepatic cholestasis of jaundice, such as contrast agent shows intrahepatic bile duct branch expansion, indicating extrahepatic obstruction If the puncture is not easy to enter the bile duct or the bile duct is normal, it is intrahepatic cholestasis. In addition, the location, extent, and extent of lesions of the bile duct can be accurately understood.

5, computed tomography (CT) upper abdominal CT examination can display images of liver, biliary tract and pancreas at the same time, providing important information for the identification of jaundice caused by hepatobiliary and pancreatic diseases. It can accurately determine the presence or absence of obstruction and obstruction of extrahepatic biliary tract, and has high diagnostic accuracy for pancreatic and hepatic space-occupying lesions.

(C), there are many kinds of preparations used for radionuclide scanning, such as '''Iodine rose red, 'Iodine, sodium, sodium, HIDA, etc.). The drug is taken up by the liver cells and discharged to the intestine via the gallbladder. The liver and gallbladder abnormalities are known by displaying the liver and gallbladder images. When hepatocytes are jaundic, the liver absorbs nuclide slowly, and the high peak is low. When obstructive jaundice, the radionuclides are slowly discharged, which is helpful for the identification of obstructive and hepatic jaundice. In addition, scanning with nuclides facilitates the diagnosis of hepatic space-occupying lesions.

(D), liver biopsy liver biopsy can help diagnose hepatocellular jaundice. Intrahepatic cholestasis and Dubin-johnson syndrome. In cases of extrahepatic obstructive jaundice, hepatic juice peritonitis and hemorrhage may occur during liver puncture and should be used with caution.

(5) Laparoscopy. Can see a large range of liver, gallbladder, peritoneum, cards, etc., and even see part of the pancreas, at the same time can take tissue biopsy or cholangiography to help identify the jaundice.

(6), laparotomy through the existing examination, there are still a few cases can not be sure whether there is extrahepatic obstructive jaundice, laparotomy should be taken, and tissue biopsy can be taken at the same time. However, laparotomy can cause a 10% mortality rate of viral hepatitis and should be noted.

(7) Selective celiac angiography can show vascular changes and learn the location and extent of liver and pancreatic lesions. Especially for the diagnosis of space-occupying lesions. Splenic portal vein and umbilical vein angiography, through the portal vascular system, can be found in portal vein obstruction and liver occupying lesions.

Differential diagnosis

First, the hemolytic jaundice hemolytic jaundice skin and porcine yellow staining is often mild to light lemon yellow, and often accompanied by anemia accompanied by pale skin. The causes of hemolytic jaundice are: 1 The inherent defects of red blood cells themselves. 2 red blood cells are damaged by external factors. Damaged red blood cells can be destroyed prematurely in the reticuloendothelial system or destroyed directly in the blood vessels. The diagnosis of hemolytic jaundice mainly depends on the following laboratory tests: 1 The content of jejunal and urobilinogen is increased. 2 serum bilirubin increased, Vanden's test showed an indirect response. 3 The number of reticulocytes in the blood increased. 4 serum iron content increased. 5 bone marrow red system hyperplasia.

Second, the diagnosis and identification of hepatocellular jaundice hepatic jaundice, in addition to medical history and clinical examination, often rely on experimental examination. Liver biopsy has important help in the differential diagnosis of some difficult cases, but it should be strictly controlled and carefully implemented.

(1) Huang Zeng type viral hepatitis

Since the turn of the century, viral hepatitis has been considered to be only type A and type B. Since the nature of hepatitis B virus was clarified after 1965, non-A, non-B hepatitis was also proposed in 1974 after transfusion and intestinal transmission. In 1977, hepatitis D virus (factor) was discovered in 1979 for hepatitis A virus. In vitro culture was successful. At the international conference held in Tokyo in 1989, according to current research findings, the pathogen of non-A, non-B hepatitis after transfusion was named hepatitis C virus, and the pathogen of non-A, non-B hepatitis transmitted in the intestine was named . Hepatitis virus. At present, viral hepatitis should include at least A, B, C, D, E type A, B, C, D, E).

1. Acute yellow-type viral hepatitis whose jaundice is from several days to one week. The most prominent symptoms are fatigue and loss of appetite. Nausea, liver pain or discomfort, with or without fever. Some cases are mainly misdiagnosed as gastrointestinal dyspepsia due to dyspepsia and diarrhea; some mainly show upper respiratory symptoms, often misdiagnosed as acute upper respiratory tract infection, and a few cases can be misdiagnosed as fever and multiple joint pain. Rheumatic fever. The clinical diagnosis of jaundice in the early stage is difficult, but at this time, the serum aminotransferase activity is often significantly increased. The positive rate of 100% is the most early diagnostic value. After the appearance of jaundice, the symptoms are relieved. At this time, the main signs are jaundice, hepatomegaly or hepatosplenomegaly, and the quality of the spleen is painful. The liver area often has sputum pain, and there is no obvious hepatomegaly. Liver function test brain blisters, turbidity, zinc turbidity are mostly positive, urinary urinary biliary discharge increased with bilirubin positive, helpful for diagnosis. Astragalus is usually 2-4 weeks, sometimes longer.

2, severe viral hepatitis

(1) Acute severe hepatitis (burst hepatitis) This type is rare. In the course of acute hepatitis, jaundice is rapidly progressive, or (and) the body temperature continues to rise, the disease should be considered first. Other signs of aura are persistent vomiting, psychotic symptoms, and liver odor. Psychiatric symptoms mainly manifest irritability or ambiguity or change of mind, personality changes, wing tremors during dynamism, catching clothes, lethargy, or lethargy. In some cases, diagnosis can occur, and deep coma (hepatic faint EEG often) Displaying abnormal waveforms is helpful for early diagnosis. Physical examination often finds deep yellow staining, liver turbidity and shrinkage, skin and membrane bleeding. Significantly reduced urine volume, proteinuria and casts. Liver function tests indicate severe liver Damage. If not treated early, the patient often dies within a short period of time. The pathological manifestation is acute hepatic necrosis.

(2) Subacute severe hepatitis (subacute hepatic necrosis is slower than fulminant hepatitis. Astragalus is progressively deepened, serum bilirubin is often >17umol/L, prothrombin time is prolonged, cholinesterase activity is prolonged Significantly reduced. And lack of energy. Digestive disorders, nausea and vomiting, physical decline, fever, hepatomegaly (or shrinkage) and tenderness. Gradually refractory tympanic and ascites, severe liver and kidney syndrome, or even Some people are comatose. Some patients can recover after active treatment, or develop into cirrhosis. If the infection is complicated or the liver function is severe, the prognosis is more dangerous.

(3) Chronic severe hepatitis: This type is subacute hepatic necrosis of chronic hepatitis. The clinical manifestations are as subacute severe hepatitis, but there are abnormalities in history, signs and tests of chronic hepatitis or post-hepatitis cirrhosis.

3, chronic jaundice virus hepatitis chronic jaundice hepatitis mainly based on: 1 duration of more than half a year; 2 main symptoms are fatigue, loss of appetite, postprandial fullness, tired of greasy, nausea and vomiting, jaundice is optional, and Often mild and fluent, the liver continues to enlarge and increase in hardness, accompanied by tenderness and sputum pain, the diagnosis of splenomegaly is of great significance. In patients with acute hepatitis, the splenomegaly does not retract during the recovery period, which means that the course of disease is prolonged, or to chronic development; 3 abnormal liver function test, the more sensitive test is the urine urinary bilirubin test. Determination of serum aminotransferase activity and serum floc and turbidity reaction. The increase in serum electrophoresis of gamma globulin is a sign of chronic hepatitis. Acute hepatitis A does not develop chronic, while acute hepatitis B and non-A, non-B hepatitis have a chronic tendency. If it develops into cirrhosis, the liver shrinks and the hardness increases, the spleen enlarges, the serum albumin continues to decrease, and the gamma globulin continues to increase.

(B) Huang Heng type of infectious mononucleosis This disease is associated with jaundice about 5% -7%. Astragalus is generally mild. l% bed showed fever, hepatosplenomegaly, and lack of appetite. Abnormal liver function tests, atypical lymphocytes in flesh and blood, quite similar to acute jaundice-type viral hepatitis. Infectious mononucleosis is often epidemic, pharyngitis is more obvious, often there are obvious lymph nodes (especially cervical lymph nodes, gastrointestinal symptoms are mild, and there are typical blood cell morphology changes and heterophilic agglutination effect The price increases. In acute viral hepatitis, the absolute value of blood-type heterotypic lymphocytes is generally less than 900 per cubic millimeter, which lasts for only a few days (slowly after the fever period L; in the case of infectious mononucleosis, atypical lymphocytes The absolute value is usually more than 1000 per cubic millimeter and often lasts for more than two weeks.

(C) systemic giant cell inclusion disease. The disease mainly affects infants and young children, and there are also adult cases reported in the domestic literature. The pathogen is Cytomegalov-irus, which can infect the fetus through the placenta through asymptomatic pregnant women with viral infection. The newborn is born with a lack of energy, pertussis-like cough, hepatosplenomegaly, digestive disorder, growth within one month of birth. Stagnant, jaundice can also occur. Infants and young children mostly exhibit interstitial pneumonia or giant cell hepatitis. Brain damage can also occur. Adults can exhibit symptoms similar to infectious mononucleosis and blood, but negative heterophilic agglutination. Liver function test serum aminotransferase activity increased, some cases of turbidity reaction abnormal. Often occurs after losing a lot of fresh blood. Diagnosis should be based on a special serum complement binding test, cytomegalovirus is isolated from urine (or saliva), which is particularly diagnostic.

(4) Leptospirosis. The diagnosis of this disease needs to be based on: 1 epidemiological history, the disease is mainly infected by contact with infected water, more common in the rice harvest season in rural areas; 2 sudden fever, conjunctival hyperemia, intestinal muscle pain, bleeding tendency, jaundice, lymphadenopathy And clinical manifestations such as liver and kidney dysfunction; 3 early onset culture and animal vaccination can obtain positive results, serum agglutination dissolution test and complement fixation test can be positive 1 week after onset. The onset of severe hepatitis is not as fast as leptospirosis, often with symptoms such as toxic jejunum and ascites, and no ball conjunctival hyperemia and intestinal irritations, no abnormal X-ray signs in the lungs, and early renal damage is not obvious. The differential diagnosis of special pathogens and serological tests is more significant.

(5) Yellow values caused by other acute systemic infections. Some acute systemic infections such as lobar pneumonia, return to heat. Malaria, typhus, typhoid fever, wavy fever, acute miliary tuberculosis, etc., can be complicated by jaundice. Astragalus is generally mild, due to liver parenchymal damage or hemolysis, or both. Acutely transmitted diseases complicated by jaundice, most of the lesions are located on the right side, especially in the lower right lobe.

(6) Primary acute pregnancy fatty liver. The disease is rare in clinical practice. The cause is unknown. Whether it is secondary to endocrine or nutritional disorders remains undetermined. It is a serious complication of obstetrics and is often misdiagnosed as fulminant hepatitis. Clinically, the following characteristics are distinguished from fulminant hepatitis: 1 more common in the first trimester of pregnancy 36 to 40 weeks; 2 different degrees of pregnancy edema, proteinuria or hypertension; 3 no cause of nausea, vomiting, and then serious Bleeding tendency, such as gums, skin, vaginal bleeding, morphine-like vomit or vomiting blood; 4 serum direct bilirubin quantification 171 umol / L%), and urinary bilirubin negative; 5 serum brain flocculent reaction Negative; 3 coma, jaundice depth, liver progressive reduction is generally less severe than fulminant hepatitis, acute renal insufficiency compared with early appearance; ultrasound or CT examination found typical fatty liver signs. It is not difficult to identify the two in histopathological examination. The literature reports that a large number of intravenous tetracyclines (about 1.5 g / d) in pregnant women can also show the performance of acute fatty liver like pregnancy, which can be distinguished from the history of drug treatment and the above characteristics.

(7) Toxic liver damage. Some drugs or poisons have hepatotoxic effects, which can cause hepatic steatosis and central necrosis of hepatic lobules. The clinical manifestations are hepatomegaly, yellow colonization and liver damage.

1. The following drugs have been reported to cause similar viral hepatitis, such as Xin Kefen, isoniazid, and Fushun, PAS. Halothane. Methyldopa and bisphenol are called to protect the pine. Alkali amines, sulfonamides. The general therapeutic dose of chlortetracycline, novobiocin, phenobarbital, thioxime, etc. / but antibiotics has few side effects unless the patient has allergies.

2, cotton seeds, Xanthium, some virulence rate contain cell virgin toxic, after taking it can cause severe liver damage and jaundice, and even hepatic coma.

3. The main chemical substances that can cause chemically toxic hepatitis are as follows: 1 metal, metalloid and its compounds such as lead. Mercury, manganese, arsenic, yellow phosphorus, chromium, antimony, key, hesitation, etc. 2 organic compounds: amino and nitro compounds of benzene, phenols, gasoline, carbon disulfide, methane, methyl chloride, formaldehyde, ethanol, tea, carbon tetrachloride. Tetrachloroethylene, etc. 3 pesticides: organic phosphorus, organic chlorine, organic mercury, etc. Acute chemical toxicity hepatitis has the following clinical features: 1 short incubation period, the fastest 2-3d, such as yellow phosphorus, the longer one is about 1 week, such as DDT, M carbon sulfide, p-chloronitroaniline poisoning; 2 often There are jaundice and hepatomegaly, but often no obvious fever, spleen is not enlarged; 3 serum aminotransferase and bilirubin increased; 4 has obvious history of toxic contact.

(8) Acute alcoholic hepatitis. There are many reports on foreign literature in this disease. People who have been drinking hard alcohol for many years have recently had alcoholism, and this disease must be considered when the following conditions occur: 1 new appetite loss, weakness, weight loss, nausea and vomiting, jaundice and abdominal pain; 2 hepatomegaly and tenderness, Sometimes splenomegaly, accompanied by unexplained fever; 3 serum bilirubin increased, serum albumin decreased and globulin increased, serum flocculosis reaction, serum aminotransferase increased, many cases have serum alkaline phosphate Enzymes and elevated blood sugar, anemia, leukocytosis and mononuclear cells; 4 liver biopsy found special inflammatory lesions.

(9) Cardiac yellow increase. The causes of cardiogenic jaundice are complicated, and the most important one is caused by hepatic cell congestion and hepatocyte hypoxia, resulting in poor function of hepatocytes to treat bilirubin. Mild jaundice can be seen in right heart failure caused by various causes, especially when accompanied by relative or organic tricuspid regurgitation. In cases of recurrent right heart failure, the incidence of cardiogenic jaundice is increased, but serum total bilirubin usually does not exceed 51 umol / L (3mg / L), occasionally a deep yellow value can occur, at this time the patient It can present green jaundice similar to biliary obstruction. Urinary urinary bilirubin excretion often increases in patients, and occasionally mild bilirubinuria can occur. The retention of sodium sulfonate is often increased, and the serum flocculation and turbidity tests are mostly normal, with a few positive. There was no significant increase in serum transaminase activity in simple hepatic congestion.

(10) Cirrhosis of the liver. All types of cirrhosis can be complicated by jaundice.

(11) Hyperthyroidism is a common cause of yellow disease. Hyperthyroidism can be complicated by fatty liver and hepatocyte necrosis, and jaundice, but this is rare and occurs in heavier cases. This type of jaundice is not easily distinguished from concurrent acute viral hepatitis. If the patient has no history of hepatitis exposure, no pre-yellowing symptoms, no obvious loss of appetite, nausea, bloating and other symptoms of digestive disorders. The jaundice is likely to originate from hyperthyroidism. If there is no high serum aminotransferase activity, it is more supportive for the diagnosis of this type of jaundice.

Third, obstructive jaundice. Obstructive jaundice is due to intrahepatic capillary bile ducts. Caused by mechanical obstruction of the hepatic bile duct or common bile duct. Skin cancer itching and bradycardia are common symptoms. Hepatomegaly is a common sign. Mechanical obstruction without concomitant infection does not cause splenomegaly. The early yellow scutellaria is golden yellow, later yellow-green, late green-brown, and even near black (black jaundice, such as the gallbladder that touches the swell, suggesting that the obstruction is in the common bile duct, the origin of the tumor is more, and the origin of the stone Very few. The diagnosis of obstructive yellowness and the identification of obstructive jaundice inside and outside the liver are shown in the laboratory and device examination.

(1) Obstructive yellow disease in the liver. The intrahepatic obstructive yellow value is mostly manifested in intrahepatic cholestatic syndrome. Clinical and pathological has a unique content, the course of the disease can be divided into acute and chronic, the clinical is more common in acute type, a few acute cases can develop chronic, and even evolve into primary biliary cirrhosis. Intrahepatic cholestatic syndrome has the following clinical and pathological features: 1 has a history of close contact with hepatitis patients or some history of drug treatment, jaundice is more acute, skin itching, dark urine. Light color stool, hepatomegaly and other signs; 2 blood biochemical examination in line with the characteristics of obstructive jaundice, suggesting signs of liver parenchymal damage or no liver parenchymal damage; 3 the main changes in liver biopsy are capillary bile duct and small bile duct cholestasis Formed with a gallbladder, and the liver parenchyma is mild.

(1) Capillary inflammatory viral hepatitis: This type of hepatitis is a rare type of viral hepatitis, also known as cholestasis-type viral hepatitis. The main clinical features: 1 onset more urgent, jaundice gradually deepened, skin cancer itching, jaundice depth and symptom severity is not commensurate; 2 examination showed jaundice and hepatomegaly, or both splenomegaly; 3 blood biochemical examination completely Consistent with obstructive jaundice, most of the serum flocculating reactions did not change significantly, but often moderate serum iron and serum aminotransferase activity increased, suggesting that liver parenchymal damage is mild. Liver biopsy showed intrahepatic cholestatic, capillary bile duct thrombosis, often accompanied by mild liver parenchymal inflammation; 4 after the diagnosis of adrenal cortical hormone diagnosis, most cases of jaundice significantly reduced in the short term, contributing to the diagnosis of this disease However, bacterial infections must be excluded before this test can be performed. Some people think that it is not appropriate to give this test before the third week of the disease. Because it can interfere with the body's defense function, the jaundice is easy to re-appear after stopping the drug, or it can become chronic. If the jaundice is not obvious, it can not exclude viral hepatitis. 5 must be excluded from other causes of intrahepatic extrahepatic obstructive jaundice, especially drug. Capillary inflammatory inflammatory hepatitis, the prognosis is generally good, the course of disease is no more than 3-6 months, a few can be extended more than years, and a few cases can evolve into secondary biliary cirrhosis.

(2) drug-induced jaundice: Many drugs can cause acute intrahepatic cholestatic syndrome, which can be divided into two categories:

a, acute intrahepatic cholestatic syndrome with inflammatory response: this type of jaundice is most common with chlorpromazine. There are also new ones. Chlorosulfonium porpoise, thioxine chewing compound, tamoxifen, sulfonamides, chloranil waste, amino-salicylic acid, yaw erythromycin propionate, etc., but the incidence is very low, generally for the drug users 1% or less. The pathogenesis is considered to be the body's allergic reaction to the drug. It has the following clinical features: 1 The occurrence of jaundice has nothing to do with the dose size, usually occurs within 1 to 4 weeks of the drug; 2 clinical often accompanied by fever, rash and eosinophils Asthenia; 3 jaundice lasts for several weeks to several days, but jaundice reappears after re-medication; 4 pathological biopsy shows intrahepatic cholestatic, capillary bile duct thrombosis, eosinophil infiltration around the portal area, liver Substantial changes have been made, mainly due to ballooning of hepatocytes, disappearance of glycogen, and accumulation of bile pigments. Foreign literature reports that this type can be chronically developed and developed into primary biliary cirrhosis.

b, acute intrahepatic cholestatic syndrome without inflammatory reaction: this type of jaundice can be found in the application of methyltestosterone and oral contraceptives and other drugs, the structure of which contains 17a-hydroxyl, currently believed that the pathogenesis is due to this class The drug interferes with the excretion of hepatocytes on bilirubin and sodium sulphate, especially in the capillary bile duct and lysosomes. Clinically, it has the following characteristics: 1 After taking a certain dose of this kind of medicine, almost every case can be caused by sulphate and sodium sputum retention, and some cases have jaundice; 2 no clinical fever, rash and eosinophilia; After the drug, Huang is good at regressing within days to weeks, and re-use of the drug often causes recurrence; 4 liver biopsy only shows intrahepatic cholestatic, but no inflammatory reaction.

(3) Idiopathic jaundice during pregnancy: The cause of this type of jaundice is unknown, very rare, and only a few cases have been reported in China. Astragalus often occurs in the late third trimester of pregnancy. The first symptom is usually skin itching, which can occur several weeks before the onset of jaundice. There may be dark urine and white clay-like stools, which peaked around the first week after the occurrence of Astragalus. Other symptoms are mild and mild hepatomegaly. Astragalus is consistent with intrahepatic obstruction, serum flocculent reaction is often negative, aminotransferase is normal or slightly increased, and jaundice rapidly resolves within 1 to 2 weeks after delivery. Astragalus often reappears when it is re-pregnancy. The mother and child have a good prognosis.

(4) Alcohol-Liver-Syndrome This syndrome is a unique type of clinical pathology, the pathogenesis is unknown, but related to heavy drinking, can be the end stage of alcoholic cirrhosis. The main clinical manifestation is obstructive jaundice in the liver. Patients with loss of appetite, nausea, vomiting, upper abdominal pain and hepatomegaly can be misdiagnosed as gallstone colic. Fatty liver can also cause this syndrome. At this time, liver biopsy has no inflammatory lesions in the liver parenchyma except for liver steatosis and intrahepatic cholestatic. Clinical diagnosis is determined only by the history of drinking and other factors that cause obstructive jaundice in the liver. If necessary, liver biopsy is used. Because of the clinical manifestations of biliary obstruction, the original fatty liver is often ignored. This syndrome has not been reported in China. Such as alcoholic toxic fatty liver with jaundice, hemolytic anemia and hyperlipidemia, it is called Zieve syndrome. In recent years, there have been case reports in China.

(5) After jaundice after benign surgery: Astragalus appeared in cases with more difficult operation and long operation time, mostly for abdominal or chest and abdomen surgery. In recent years, many foreign literature reports have been reported. Most of the patients developed jaundice after l-2 days (individually at 11 days) and resolved after 2-3 weeks. The patient had no fever, itchy skin, no obvious hepatosplenomegaly, and bilirubinuria. Serum aminotransferase activity is normal or slightly increased. Liver biopsy proved to be central cholecystosis in the liver without substantial inflammation, similar to drug-induced jaundice caused by methyltestosterone. This type of jaundice has a good prognosis. The pathogenesis is unknown. In the determination of jaundice after benign surgery, other reasons must be caused to cause postoperative jaundice, such as cholangitis caused by surgery, obstructive jaundice caused by cholelithiasis, occasional viral hepatitis after surgery, postoperative infection and drug Huang Wei and so on.

(6) Idiopathic benign recurrent intrahepatic cholestatic: This disease is rare and has not been reported in China. The onset age is 1-37 years old. There are familial case reports. The clinical manifestations are recurrent obstructive jaundice, no abdominal pain, chills and fever, often without hepatomegaly. Serum alkaline phosphatase activity increased during the jaundice stage, aminotransferase activity increased slightly, serum cholic acid, aggrecan and p-globulin increased, and liver biopsy showed central cholecystosis without any inflammation and necrosis. Retrograde angiography of the duodenal biliary tract shows normal biliary system. The above blood biochemical changes returned to normal during the remission period of Astragalus. The recovery period of Astragalus has been reported for up to nine years. The recurrence can be seasonal.

(7) Primary biliary cirrhosis: This disease is caused by long-term obstruction of intrahepatic bile ducts and biliary cirrhosis caused by cholestatic. Clinically rare, the cause is not yet clear. Clinical features: 1 The incidence is more than 20-4O years old, the onset of attack is slow, the course of disease is slow, and the systemic condition is better for a long time; 2 The main clinical manifestations are chronic obstructive jaundice, hepatosplenomegaly, Gastrointestinal symptoms, skin cancer itching and intermittent right upper abdominal pain with cold and heat attacks, similar to acute cholangitis episodes; 3 hepatomas are mostly moderate, but also high, hard, smooth surface, late nodular; 4 jaundice For volatility, deepen in the onset of upper abdominal pain and cold fever. At this time, the total number of white blood cells also increased, after the inflammation control, jaundice also reduced or subsided; 5 laboratory tests consistent with obstructive jaundice, serum anti-mitochondrial antibody (AMA) positive rate of 84% -96%, or with increased serum, liver Biopsy is consistent with histological changes in primary biliary cirrhosis. Ascites and upper gastrointestinal bleeding can occur in the late stage of the disease.

2. Intrahepatic mechanical obstruction (1) Primary sclerosing cholangitis: This disease involves intrahepatic or (and) extrahepatic bile ducts. In recent years, there have been dozens of reports in China. Take 1 intraductal factors: such as stones, mites, Chinese worms, blood clots, etc.; 2 bile duct wall factors: such as bile duct stricture, cholangiocarcinoma, periampullary carcinoma, cholangitis, congenital biliary atresia, etc.; Extrabiliary factors: such as pancreatic cancer, pancreatitis, lymph node metastasis of the hilar region. The disease often has a history of cholelithiasis, biliary tract mites or a history of biliary tract surgery, can touch the gallbladder swell, barium meal examination shows duodenal curvature or duodenal descending inner wall membrane damage, suggesting extrahepatic obstruction The possibility. Endoscopic retrograde cholangiopancreatography can be performed under conditions, and the diagnosis often requires surgical exploration.

1, acute obstructive suppurative cholangitis due to stones. Aphids or stenosis caused by obstruction of the common bile duct and/or intrahepatic bile duct. Patients often have paroxysmal cramps in the right upper quadrant, chills and high fever are relaxation heat, vomiting during nausea, with varying degrees of obstructive jaundice, and can be complicated by toxic shock. The liver is mildly and moderately enlarged, and white blood cells are significantly increased with neutrophils predominating. If there is acute right upper abdominal pain, high fever, jaundice, it is called CoK triad, showing acute suppurative biliary tract infection. Such as accompanied by symptoms of central nervous system poisoning, shock is called Regnold five-link, showing acute obstructive suppurative cholangitis.

2, the clinical features of common bile duct stones are paroxysmal upper right abdominal cramps after jaundice, in the past may have the same history of seizures. If the infection is combined, there will be chills and fever. Astragalus was moderate (the total amount of bilirubin was less than 120 umol/L). The test showed obstructive jaundice without liver damage. The occurrence of yellow value is not only due to stone obstruction, but also due to edema of the common bile duct smooth muscle spasm or membrane inflammation; in some cases, the gallbladder can be reached in some cases. After inflammatory edema and sputum subsidence, although the common bile duct stones are not ruled out, bile can still flow out, and jaundice can be alleviated. The X-ray film can show the shadow of the X-ray. Intravenous cholecystography can show the common bile duct dilatation and X-ray calculus, but it is not appropriate to have this examination when there is jaundice. B-mode ultrasound T examination, combined with clinical often can determine the diagnosis.

3, congenital choledochal cyst typical manifestations of triad: jaundice, abdominal pain and abdominal mass. 80% are women, mostly children and adolescents. B-mode ultrasound is important for the diagnosis of this disease.

4, men with pancreatic head cancer are more common, the incidence is mostly 40-60 years old. Cancer occurs most in the head of the pancreas, showing progressive obstructive 1 intrabiliary factors: such as stones, mites, worms, clogging of blood clots, etc.; 2 bile duct wall factors: such as bile duct stricture, cholangiocarcinoma, ampulla around Cancer, cholangitis, congenital biliary atresia, etc.; 3 extrabiliary factors: such as pancreatic cancer, pancreatitis, lymph node metastasis of the hilar area. The disease often has a history of cholelithiasis, biliary tract mites or a history of biliary tract surgery, can touch the gallbladder swell, barium meal examination shows duodenal curvature or duodenal descending inner wall membrane damage, suggesting extrahepatic obstruction The possibility. Endoscopic retrograde cholangiopancreatography can be performed under conditions, and the diagnosis often requires surgical exploration.

1, acute obstructive suppurative cholangitis due to stones. Aphids or stenosis caused by obstruction of the common bile duct and/or intrahepatic bile duct. Patients often have paroxysmal cramps in the right upper quadrant, chills and high fever are relaxation heat, vomiting during nausea, with varying degrees of obstructive jaundice, and can be complicated by toxic shock. The liver is mildly and moderately enlarged, and white blood cells are significantly increased with neutrophils predominating. If there is acute right upper abdominal pain, high fever, jaundice, it is called CoK triad, showing acute suppurative biliary tract infection. Such as accompanied by symptoms of central nervous system poisoning, shock is called Regnold five-link, showing acute obstructive suppurative cholangitis.

2, the clinical features of common bile duct stones are paroxysmal upper right abdominal cramps after jaundice, in the past may have the same history of seizures. If the infection is combined, there will be chills and fever. Astragalus was moderate (the total amount of bilirubin was less than 120 eL) and the test showed obstructive jaundice without liver damage. The occurrence of yellow value is not only due to stone obstruction, but also due to edema of the common bile duct smooth muscle spasm or membrane inflammation, in which case some cases can reach the enlarged gallbladder. After inflammatory edema and sputum subsidence, although the common bile duct stones are not ruled out, bile can still flow out, and jaundice can be alleviated. The X-ray film can show the shadow of the X-ray. Intravenous cholecystography can show the common bile duct dilatation and X-ray calculus, but it is not appropriate to have this examination when there is jaundice. B-mode ultrasound T examination, combined with clinical often can determine the diagnosis.

3, congenital choledochal cyst typical manifestations of triad: jaundice, abdominal pain and abdominal mass. 80% are women, mostly children and adolescents. B-mode ultrasound is important for the diagnosis of this disease.

4, men with pancreatic head cancer are more common, the incidence is mostly 40-60 years old. Cancer occurs most in the head of the pancreas and exhibits progressive obstructive jaundice. Pancreatic body and tail cancer generally do not cause jaundice, the main symptom is jumping upper abdominal pain. The main features of pancreatic head cancer are: 1 anorexia, rapid weight loss, fatigue, general condition worsening in a short period of time; 2 chronic progressive jaundice, from incomplete obstruction to complete obstruction; 3 often persistent upper abdominal pain, Often to the left back radioactivity; 4 hepatomegaly and gallbladder enlargement; 5 late can touch the abdominal mass; 3 laboratory tests: serum pancreatic amylase and pancreatic lipase increased (early due to pancreatic duct obstruction increased, late cause Pancreatic atrophy reduces the increase of human blood glucose and mild diabetes-like glucose tolerance curve. When the pancreatic duct is completely obstructed, steatorrhea and fleshy diarrhea appear. X-ray examination shows that the duodenal curvature increases, and the duodenal inner wall is compressed and eroded. Signs of narrowing of the lumen of the intestine and infiltration or compression of the antrum.

5, the surrounding cancer of the ampulla of the ampulla can also cause progressive weight loss, deep jaundice (the total amount of bilirubin often reaches 255 ~ 510 umol / L (15 ~ 30mg / dl)], hepatomegaly and gallbladder swelling, etc. symptom. Astragalus can be relieved during the course of the disease, and serum bilirubin does not fall to normal. This point has a differential diagnosis significance with stone blockage. In the latter, when the stones are displaced, the jaundice can quickly subside after the blockage is lifted, and the serum bilirubin also drops to normal. Upper gastrointestinal bleeding can be a serious symptom of ampullary cancer. If the duodenal drainage fluid is blood, it is likely to be cancerous, especially ampullary cancer. The most reliable one is cancer cells found in the eleven finger drainage. X-ray diagnosis is mainly based on indirect changes of adjacent organs, and venous cholecystography may have diagnostic value for early lesions. In recent years, duodenoscopy has been used to directly observe the lesions around the ampulla, and can be used for biopsy, which is helpful for early diagnosis. Timely radical surgery, the prognosis is better. The ampullary carcinoma has fewer signs than the pancreatic head cancer. Fiber duodenoscopy is more diagnostic.

6, acute and chronic pancreatitis domestic report 18.2% of acute pancreatitis with jaundice. Deep jaundice often indicates a serious condition. In chronic pancreatitis, granulation tissue hyperplasia can sometimes cause chronic obstructive jaundice, which can be touched and differentiated from pancreatic cancer. This situation is very rare. Occasionally, the history of acute pancreatitis is not obvious, especially confusing. The jaundice of this disease is intermittent and fluctuating; the jaundice of pancreatic head cancer is progressive and has no tendency to relieve. CT scan, fiber duodenoscopy, and laparotomy for frozen biopsy help to identify the two.

7, common bile duct or hepatobiliary carcinoma in the common bile duct or hepatobiliary duct, occasionally can occur cancer, usually adenocarcinoma, clinical manifestations of painless extrahepatic obstructive jaundice. The size of the cancer is usually small, but early symptoms of obstructive jaundice, such as white clay. Bilirubinuria, hepatomegaly, etc. Gallbladder often swells when the common bile duct cancer occurs. The biliary tract infection often occurs in the late stage of the two, which may be temporarily relieved due to the collapse of the cancer tissue and the biliary drainage. This condition is difficult to see in the head cancer. Middle-aged patients, especially males, have the above-mentioned situation. The degree of jaundice is significantly greater than that of liver function. Repeated examination of duodenal angiography is necessary, and the possibility of common bile duct or hepatobiliary carcinoma should be considered. If the gallbladder is touched, the former is supported.()

840%-50%BCT

92/3

()

1Gilbert(85.5 dL(85.5 ML)

2DubinJohnsonGILBERT45min45min(lipoforo-in).

3Rotor11Dubin-johnson(50 g3 h15%)

4Grigler-Najjar256.5~84 umol/LL3-5GilbertABORh

()* 50mg3h30%-100%()

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