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Symptoms of jaundice
Last reviewed: 23.04.2024
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Superhepatic jaundice. The main symptom of jaundice is an increase in the content of indirect bilirubin in the blood. This makes it easy to distinguish it from the hepatic and jaundice. Superhepatic jaundice can be a consequence of:
- increase in the formation of bilirubin (hemolysis of erythrocytes);
- violations of bilirubin transport (disruption of binding with albumin);
- disturbance of metabolism (conjugation) of bilirubin in hepatocytes.
During hemolysis of erythrocytes, a large amount of direct bilirubin is formed in the liver and enter the intestine. In the intestine, under the influence of microflora, bilirubin is reduced to mesobylirubinogen, from which urobilinogen (urobilin) and sterocilinogen (stercobilin) are formed. Urobilinogen is excreted by the kidneys with urine, sterocilinogen - with feces.
Hepatic jaundice. In connection with the defeat and necrosis of a part of hepatocytes, the concentration of total bilirubin in the blood serum increases mainly due to the fraction of direct bilirubin. The resulting direct bilirubin partially falls into the large circle of the circulation, which leads to jaundice. Bile excretion is also impaired, so bilirubin enters the intestine less than normal. The amount of urobilinogen formed decreases, the stool is less colored (hypochlorous). Urine, on the contrary, has a more intense coloration due to the presence in it of not only urobilinogen, but also the excess of indirect bilirubin, which dissolves well in water and is excreted in urine. Hepatic jaundice is accompanied by hyperfermentemia and a violation of the synthetic function of the liver.
Bile duct jaundice develops if there is a violation of bile secretion into the duodenum. It can be a consequence of the disease or caused by a postoperative narrowing of the common bile duct. In this type of jaundice, hepatocytes produce conjugated bilirubin, but it does not enter the intestine in the bile. Since normal ways of excretion of bilirubin are blocked, its retrograde transport to the blood takes place. In the blood, the concentration of direct bilirubin increases. Since bilirubin does not enter the intestine, urinary and fecal products of its catabolism are absent. The feces become acholic, and urine is colored orange-brown in color. The condition of the patient is not significantly disturbed, but, in addition to the symptoms of the underlying disease, there may be symptoms of jaundice, such as itching. With the progression of jaundice in the serum, the activity of GGT, alkaline phosphatase, and also the level of total cholesterol and conjugated bile acids increases. Due to the steatorrhea, the body weight decreases and absorption of vitamins A, D, E, K and calcium is impaired.
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