22. Hepatic jaundice: definition, causes, bilirubin metabolism, macro- and microscopic changes in the liver, clinical signs, complications, outcomes.

Hepatic (parenchymal) jaundice occurs when hepatocytes are affected.

Reasons: As a result, their capture of bilirubin, its conjugation with glucurononic acid and excretion are disrupted. Such jaundice is observed in acute and chronic hepatitis, cirrhosis of the liver, drug-induced damage and auto-intoxication, during pregnancy, leading to intrahepatic cholestasis.

A special group is enzymopathic hepatic jaundice, which occurs in hereditary pigmented hepatoses, in which one of the phases of intrahepatic bilirubin metabolism is disrupted.

In the pathogenesis of parenchymal jaundice, the main role is played by a violation of bilirubin secretion by the liver and damage to the barrier between bile and blood, which develop as a result of necrosis of hepatocytes. As a result, all the components of bile enter the bloodstream — direct bilirubin and bile acids.

In parenchymal jaundice, the blood levels of both bound and unbound bilirubin are usually increased. Bound, water-soluble bilirubin usually appears in urine. The level of urobilin in urine is usually elevated because liver dysfunction prevents the normal uptake and re-secretion of urobilinogen absorbed from the intestine.

Outcome and complications:At the same time, dystrophic changes occur in both the kidneys and other parenchymal organs, which is accompanied by a decrease in their function.

23. Subhepatic jaundice: definition, causes, bilirubin metabolism, macro- and microscopic changes in the liver, clinical signs, complications, outcomes.

Subhepatic (mechanical) jaundice. It is also called obstructive jaundice.

Pathogenesis:With subhepatic jaundice, the biliary tract is obstructed, which leads to the accumulation of bound bilirubin proximal to the barrier in the biliary tract and liver (cholestasis). Bound bilirubin enters the bloodstream, causing jaundice. A certain amount of bound bilirubin is excreted in the urine. Bilirubin does not enter the intestine, while the amount of urobilinogen in feces and urine decreases. With complete obstruction of the biliary tract, the absence of bilirubin changes the normal color of feces.

Reasons:

• cholelithiasis;

• cancer of the biliary tract of the pancreatic needle, the Fater papilla of the duodenum; metastases of cancer of another localization to the periportal lymph nodes and to the liver in the area of its gates,

• parasitic liver diseases (echinococcus, helminths, etc.),

• atresia (hypoplasia) of the biliary tract, post-inflammatory and postoperative strictures.

Macro-: With subhepatic (mechanical) jaundice, the bile ducts expand and the bile capillaries rupture, cholemia develops, which causes not only intense skin coloring, but also the phenomena of general intoxication, mainly from the effects of bile acids circulating in the blood on the body.

Outcome and complications: Due to intoxication, the ability of blood to coagulate decreases, multiple hemorrhages appear (hemorrhagic syndrome). The accumulation of bilirubin in liver cells with obturation jaundice leads to toxic damage — dystrophy, and, with severe damage, necrosis. Then fibrosis develops in the necrosis sites, which can lead to biliary cirrhosis and chronic liver failure. Kidney damage and the development of hepatic-renal insufficiency are associated with autointoxication.