Jaundice - is not a disease but a symptom of liver disease, biliary tract or human blood, which is characterized by staining of the skin, sclera eyes and mucous membranes yellow.How to treat people's means jaundice see here.
There are three types of jaundice: manual (with blockage of the bile ducts), hemolytic (red blood cells in the amplification of the collapse in the blood) or liver (hepatitis appears or chronic alcoholism).
sclera and skin turn yellow.Urine becomes dark brown in color and can resemble tea or beer.White, pale, colorless, like a chair dogs.Fever, chills.Pain in the right upper abdomen.Loss of appetite and / or weight.For more information about hepatitis symptoms, see here.
most commonly observed with an increase in blood levels of bilirubin pigment.
study is typically conducted for differential diagnosis of jaundice.In hepatocellular jaundice, destruction of liver cells, impaired excretion of direct bilirubin in the bile capillaries, and it goes directly into the blood, where i
When obstructive jaundice disrupted bile excretion, which leads to a sharp increase in the content of direct bilirubin in the blood.Several increases in the blood and the concentration of indirect bilirubin.
blood levels of direct bilirubin is not changed Hemolytic jaundice.
The content of indirect bilirubin is increased in hemolytic anemia, pernicious anemia, jaundice newborns, Gilbert's syndrome, Crigler-Najjar, Rotor.Increasing the concentration of indirect bilirubin in hemolytic anemia is caused due to an intense form of his hemolysis of red blood cells, and the liver is unable to form such a large amount of bilirubin glucuronide.When these syndromes impaired conjugation of indirect bilirubin with glucuronic acid.
Reference values of serum concentrations of total bilirubin less than 0.2-1.0 mg / dL (less than 3,4-17,1 mmol / l).
increase in serum bilirubin concentrations above 17.1 mmol / L is called hyperbilirubinemia.This condition may be due to the formation of bilirubin in quantities exceeding the normal ability of the liver to excrete it;liver damage in the excretion of bilirubin in normal amounts, as well as due to blockage of the bile ducts, which prevents excretion of bilirubin.In all these cases, bilirubin accumulates in the blood and diffuse into the tissues, turning them into yellow after reaching certain concentrations.This condition is called jaundice.There are an easy form of jaundice ( concentration of bilirubin in the blood to 86 mmol / l), srednetyazhёluyu (87-159 mmol / L) and heavy (more than 160 mmol / l).
Depending on what type of bilirubin present in the serum - unconjugated (indirect) or conjugated (direct) - classified as postgepatitnuyu hyperbilirubinemia (unconjugated) and regurgitant (conjugated) respectively.In clinical practice, the most widespread in the division of jaundice hemolytic, parenchymatous and obstructive.Hemolytic and parenchymal jaundice - unconjugated and obstructive - conjugated hyperbilirubinemia.In some cases, it can be mixed with jaundice Pathogenesis.Thus, long-term violation of the outflow of bile (jaundice) as a result of secondary lesions of the liver parenchyma may be disturbed excretion of direct bilirubin in the bile capillaries, and it goes directly into the blood;in addition, it reduces the ability of liver cells to synthesize gluon kuronidy bilirubin, therefore the amount of indirect bilirubin increases as well.
Increasing the intensity of hemolysis is observed in hemolytic anemia.Hemolysis can also be enhanced with vitamin B12-deficient anemia, malaria, massive hemorrhage in the tissue, pulmonary infarction, crush syndrome when (unconjugated hyperbilirubinemia).As a result of enhanced haemolysis is an intensive education in the reticuloendothelial cells from free bilirubin Hb.At the same time, the liver is unable to form such a large amount of bilirubin glucuronides, which leads to the accumulation of free bilirubin (indirect) in blood and tissues.However, even with significant hemolysis unconjugated hyperbilirubinemia usually negligible (less than 68.4 mmol / l) due to the large liver power for conjugation of bilirubin.In addition to increasing the concentration of total bilirubin in hemolytic jaundice reveal elevated urobilinogen excretion in the urine and feces, as it is produced in the gut in large numbers.
most common form of unconjugated hyperbilirubinemia - physiological jaundice in newborns.The reasons for this include jaundice accelerated hemolysis and immaturity of hepatic uptake systems, conjugation (reduced activity uridindifosfatglyukuroniltransferazy) and secretion of bilirubin.Due to the fact that bilirubin, accumulates in the blood is in unconjugated (free) state when its concentration in blood exceeds the saturation level of albumin (34,2-42,75 mol / l), it is able to overcome the blood-brain barrier.This can lead to giperbilirubinemicheskoy encephalopathy.On the first day after birth often bilirubin concentration is increased to 135 mmol / l, preterm it can reach values of 262 mmol / l.For the treatment of jaundice such effective stimulation of conjugation of bilirubin phenobarbital.
By unconjugated hyperbilirubinemia include jaundice, caused by the action of drugs that enhance the disintegration (hemolysis) of red blood cells, for example, acetylsalicylic acid, tetracycline, etc., As well as metabolized involving uridindifosfatglyukuroniltransferazy.
In hepatocellular jaundice, hepatocytes destruction, broken excretion of direct (conjugated) bilirubin in the bile capillaries and it goes directly into the blood, where its content is greatly increased.Furthermore, a reduced ability to synthesize liver cells glucuronide bilirubin, whereby an indirect bilirubin amount also increases.Increased blood concentration of direct bilirubin leads to its appearance in urine due to membrane filtration of renal glomeruli.Indirect bilirubin, despite an increase in the blood concentration in the urine does not flow.The defeat of hepatocytes accompanied by a breach of their ability to destroy the di- and tripirrolov sucked from the small intestine mezobilinogen (urobilinogen).
Improving content of urobilinogen can be observed even in dozheltushny period.In the midst of viral hepatitis may be reduced and even the disappearance of urobilinogen.This is because the increasing stagnation of bile in the hepatic cells leads to a decrease in allocation of bilirubin and therefore to a decrease in the formation of urobilinogen in the biliary tract.Later on, when the function of liver cells starts to recover, bile is released in large quantities, and urobilinogen svnova appears in large quantities, that in this situation are regarded as a favorable prognostic sign.Sterkobilinogena enters the systemic circulation and excreted by the kidneys in the urine as urobilin.
main causes of parenchymal jaundice include acute and chronic hepatitis, liver cirrhosis, toxic substances (chloroform, carbon tetrachloride, paracetamol), a massive spread of liver cancer, alveolar echinococcus and multiple liver abscesses.
When viral hepatitis degree bilirubinemia to some extent correlate with disease severity.Thus, in hepatitis B under mild form of the disease bilirubin content does not exceed 90 mmol / l (5 mg%), with srednetyazhёloy is within 90-170 mmol / l (510 mg%), with severe exceeds 170 mmol / l (above 10mg%).With the development of hepatic coma bilirubin may be increased to 300 mmol / l or more.It will be appreciated that the amount of increase of bilirubin in the blood does not always depend on the severity of the pathological process, and may be due to rates of viral hepatitis and hepatic failure.
By unconjugated hyperbilirubinemia type include a number of rare syndromes.
When obstructive jaundice (conjugated hyperbilirubinemia) does excretion of bile due to blockage of the common bile duct stone or tumor, as a complication of hepatitis, primary cirrhosis, when taking drugs which cause cholestasis.Increasing pressure in the bile capillary permeability increases or impairing their integrity and ingress of bilirubin in the blood.Due to the fact that the concentration of bilirubin in bile is 100 times higher than in blood, and conjugated bilirubin in blood sharply increases the concentration of direct (conjugated) bilirubin.Several increases the concentration and indirect bilirubin.Jaundice usually leads to the highest concentration of bilirubin in the blood (up to 800-1000 mmol / l).The stool is sharply reduced content sterkobilinogena full of bile duct obstruction is accompanied by a complete absence of bile pigments in the feces.If the concentration of conjugated (direct) bilirubin greater than the renal threshold (13-30 mol / L), it is excreted in the urine.
In clinical practice, the serum bilirubin concentration is used for the following tasks.
content in the blood of bilirubin can be reduced at low hemolysis that observed with hemorrhagic anemia and malnutrition.The decrease bilirubin diagnostic irrelevant.
Below pathogenetic classification of jaundice, which makes it easy to establish the etiology of hyperbilirubinemia.
Mostly indirect hyperbilirubinemia
I. The excess production of bilirubin.
A. Hemolysis (intra- and extravascular).
B. Ineffective erythropoiesis.
II.Reduced capture of bilirubin in the liver.
A. Prolonged fasting.
III.Violation of conjugation of bilirubin.
A. Hereditary deficiency glyukuroniltransferazy
- Gilbert's syndrome (Light failure glyukuroniltrans-ferazy).
- Crigler-Najjar syndrome type II (moderate insufficiency of glucuronyl).
- Crigler-Najjar syndrome type I (lack of activity Gluck-roniltransferazy)
B. neonatal jaundice (transient failure glyukuroniltransferazy; increased formation of indirect bilirubin).
B. Acquired deficiency glyukuroniltransferazy.
- Admission of some drugs (eg, chloramphenicol).
- jaundice from breast milk (oppression Gluck-roniltransferazy pregnandiol activity and fatty acids contained in breast milk).
- parenchymal liver (hepatitis, cirrhosis).
Mostly direct hyperbilirubinemia
I. Violation of excretion of bilirubin in the bile.A. Hereditary disorders.
- Dubin-Johnson syndrome.
- Rotor syndrome.
- Benign recurrent intrahepatic cholesteric
- cholestasis of pregnancy.
B. Acquired disorders.
- The defeat of the liver parenchyma (for example, viral or drug-induced hepatitis, cirrhosis).
- Admission of some drugs (oral contraceptives, Andes-rogeny, chlorpromazine).
- alcoholic liver disease.
- Postoperative period.
- Parenteral nutrition.
- biliary cirrhosis (primary or secondary).
II.Obstruction of extrahepatic bile ducts.A. obturation.
- Malformations of the biliary tract (stricture, atresia, bile duct cysts).
- Helminthiases (clonorchiasis and other hepatic Trematodozy, ascariasis).
- Malignant neoplasms (cholangiocarcinoma, cancer of the nipple F Noetherian).
- hemobilia (trauma, tumor).
- Primary sclerosing cholangitis.B. Compression.
- Malignant tumors (pancreatic cancer, lymphoma, Hodgkin's disease, metastases in the lymph nodes of the liver gate).