The term refers to a syndrome associated with the violation of the separation of bile into the duodenum.
Bile is produced and excreted by hepatocytes. Violation of current bile can occur within hepatocytes, on his biliary surface or anywhere from gall of the capillary to papilla of Vater. There are extrahepatic and intrahepatic holestaza. The first is called a violation of current bile in extrahepatic biliary tract and covers all the biliary tree. Intrahepatic cholestasis as an independent disease process is rare, more often it is developing as a non-specific syndrome in many diseases of the liver (X. X. Mansurov, A. S. Shelepin, 1969; Iber, 1968). When hepatocellular form violation of transport bilirubin occurs somewhere between the microsomes and gall capillaries in congenital diseases or at the level of the capillary membranes with cholestasis caused by steroids, pregnancy. When doctolero form, developing hypersensitivity reactions to chlorpromazine, promotin and the so-called benign return cholestasis, besides the usual signs of cholestasis, there is a cellular reaction around cholangio. In primary biliary cirrhosis in the process involved magdalsophia bile ducts; sclerosing cholangitis comes obliteration septal large and intrahepatic bile ducts (Sherlock, 1968).
Morphological signs of cholestasis are deposits of bile pigment in hepatocytes and coppersky cells, red-clots in the gall tubules, the presence of extravasation bile, proliferation gall tubules. Often there pericolanti with subsequent development of fibrosis in the portal fields. Gall dilated capillaries, edematous (with the exception of cases of congenital hyperbilirubinemia); microbikini shortened, overblown, their number reduced, sometimes they are just not there. The Golgi apparatus vacuolation. Complementary mechanism numerous and include bile pigment. In elastoplasticity zone bubbles containing bile. In mitochondria is marked irregularity and tortuosity Krist, appear intramitochondrial structures resembling the myelin figures. These changes are not specific and meet with extrahepatic and intrahepatic cholestatic (Popper, 1960; Sherlock, 1968, Sasaki, Schaffner, Popper, 1967). Only after three weeks there are some features that distinguish extrahepatic cholestasis from intrahepatic; greatly multiplied and expanded bile canals in the portal areas. They winding, lined with high cubic epithelium sometimes last atrophies. Appear focal necrosis of the liver cells, first in the middle zones, later on the periphery of the segments. Formed red-lake - significant expansion mitakovich Protocol containing clots bile, sometimes they are empty (the A. F. of Bluger, 1964; Sherlock, 1968; Phillips, 1968).
Jaundice when beletaza arises as a consequence of the regurgitation of bile through direct messages gall capillaries with spaces the Diss (Kitani, 1960; Miva, f963) or, if you raise secretory pressure bile above 35 cm of water. century, through the gap cholangio.