1. Physical and chemical stage. At this stage there are no characteristic clinical symptoms. It is diagnosed on bile research (a portion In), in it cholesteric "flakes", crystals of cholesterol and their precipitated calcium superphosphates are found. Bile is oversaturated by cholesterol, the content of phospholipids and bile acids (litogenny bile) is reduced. Duration of this stage considerable. At ultrasonography "zamazkoobrazny" bile can come to light.
2. Latent asymptomatic kamnenositelstvo. There are no clinical symptoms. Gallstones often are an accidental diagnostic find. Stones by means of ultrasonography, a X-ray analysis, KT come to light. At duodenal sounding bile rich with cholesterol and poor in phospholipids is defined. At this stage the mucous membrane of a gall bladder is injured, its inflammation is possible, permeability for bile acids increases. The majority of stones are located at the bottom of a gall bladder.
3. Stage of clinical manifestations. Acute calculous cholecystitis, chronic cholecystitis. The stone can obturirovat a neck of a gall bladder, causing bilious (hepatic) colic. Perhaps spontaneous return of a stone to a bubble or — with a diameter less than 0,5 cm, it can move ahead and obturirovat the general bilious channel, causing mechanical jaundice and quite often a cholangitis. In most cases existence of stones in bilious channels is result of migration them from a gall bladder and is usually observed against chronic cholecystitis. Symptoms of mechanical jaundice of a "stone" origin are: yellowing of mucous membranes (scleras, a soft and hard palate), and then and skin, coming soon after an attack of bilious colic. Often precedes jaundice and accompanies her skin itch. It develops owing to transition to blood of bile acids — irritants of nervous receptors of skin. At partial obstruction of bilious channels of jaundice can not be, but the skin itch usually happens (it is the so-called "dissociated" jaundice). At a full obturaniya of the general bilious channel, along with the expressed jaundice of skin and scleras (in blood the content of kopjyugirovanpy bilirubin increases), decolorization a calla (an akholichny chair) and lack of urobilin in urine in the presence in it bilirubin is observed. These characteristic disturbances of a pigmental exchange are connected with the fact that urobilin is formed in intestines of bilirubin (urobilin always has an intestinal origin). Therefore at the termination of intake of bilirubin in intestines education and urobilin stops. It is not formed as well an end product of an exchange of bilirubin in intestines — sterkobiliya. In urine at the same time a large amount of the bilirubin getting there from blood is defined. If mechanical jaundice is followed by long temperature increase to 38 — 40 °C, a fever, vomiting, the accruing leukocytosis in blood and the increased SOE, it is necessary to think of development of purulent inflammatory process in a gall bladder or hepatic channels (cholangitis).