Abnormal liver function

Description:

Damage of a liver pathological process is followed by disturbance of protective (barrier) function of a liver that is shown in decrease in phagocytal activity of kupferovsky cells (star-shaped endotheliocytes) and other macrophagic elements and the anti-toxic (neutralizing) function.

Reasons of Abnormal liver functions:

At liver diseases (cirrhosis, hepatitis, liver cancer) the abnormal liver function can be caused not only by insufficient blood supply (hypoxia) and structural deformation of body, but also blockade of kupferovsky cells the decomposition products of cells and metabolites which are formed in the liver. At the same time ability of hepatic macrophages to eliminirovat by phagocytosis from blood the fatty drops, erythrocytes, microorganisms, their toxins which are especially arriving with a portal blood-groove from intestines that leads to emergence of a toxaemia with various manifestations decreases (a leukocytosis, fever, hemolysis of erythrocytes, a renal failure, intestines erosion, etc.). Existence of a porto-caval anastomosis aggravates a current of a toxemic syndrome which sometimes proceeds as toxic shock in connection with intake of toxic substances from intestines in a system blood stream against the background of the switched-off phagocytal function of a liver. Besides, when weakening phagocytosis as nonspecific defense reaction resistance of an organism to infectious factors decreases. At the same time the frequency of development of allergic (autoallergichesky) processes both in the liver, and in other bodies and systems increases that is caused by disturbance of capture from blood and destruction by macrophages of a liver of antigens and cell-bound immune complexes (normal in star-shaped retikuloendoteliotsita 95% of substances with antigenic properties are split).

Decrease in anti-toxic function of a liver is connected with disturbance of its metabolic function - urea synthesis (neutralization of toxic ammonia), oxidation (aromatic hydrocarbons), recovery (nitrobenzene in rodinal), acetylations (sulfanamide drugs), hydrolysis (alkaloids, cardiac glycosides), conjugation (formation of pair connections with glucuronic acid, glycine, cysteine, taurine - for binding of an indirect bilirubin, skatole, phenol, an indole, etc.). Besides, at an abnormal liver function one more way of a detoxication - transformation of water insoluble (non-polar) substances into soluble (polar) compounds which can be brought out of an organism with bile and urine is broken. Leads injury of hepatocytes to weakening of anti-toxic function of a liver as neutralization loci, reduction of activity of the enzymes catalyzing reactions of a detoxication and deficit of energy. Disturbance of anti-toxic function of a liver at its defeat can cause increase in sensitivity of an organism to various medicines - quinine, morphine, barbiturates, a foxglove, etc. It is connected with the fact that at reduction of their splitting in a liver toxicity of these substances for an organism increases, causing poisoning. Besides, in the course of metabolic transformations of toxic connections in hepatocytes even more toxic substances can be formed (synthesis of hepatotoxic substances - metabolites of a number of medicines, for example an isoniazid; formation of carcinogenic substances). Disturbance of excretory function of a liver at difficulty of biliation can also lead to accumulation of toxic substances in an organism.

Switching off of anti-toxic function of a liver leads to development of a hepatocerebral syndrome (hepatic encephalopathy) and the most severe form of clinical implication liver failureof - hepatic coma. The hepatocerebral syndrome which is characterized by disturbances of mentality, consciousness and motive frustration (trembling, an ataxy, muscle tension) can pass into a hepatic coma.

Disturbance of zhelcheobrazovatelny and zhelchevydelitelny (excretory) function of a liver.

Hepatic cells cosecrete bile which part bile acids, bilious pigments, cholesterol, phospholipids, fatty acids, mucin, water and other substances are.

The liver participates in formation, metabolism and excretion of bilious pigments. In star-shaped endotheliocytes of a liver, in macrophages of marrow, spleen from hemoglobin of the destroyed erythrocytes verdohemoglobin, is formed of it after eliminating of atom of iron and a globin - biliverdin which turns, being recovered, in bilirubin. In blood bilirubin connects preferential to albumine, and this complex is called the free, not conjugated, indirect bilirubin (indirect as gives coloring with Ehrlich's diazoreactant only after protein sedimentation). It is insoluble in water, normal makes 75% of the general bilirubin of blood (6,8 - 20,5 µmol/l by Endrashik's method and соавт.), it is non-toxical, does not get into a brain and, therefore, cannot cause bilirubinovy encephalopathy. The free bilirubin which is not included in bilirubin - an albuminous complex, easily passes through a blood-brain barrier and, interacting with phospholipids of membranes of neurons, comes to cells of the central nervous system and can damage them. However normal concentration of free bilirubin in blood is so small, and it to connect ability of albumine is so high that it has no toxic effect.

At the vascular pole hepatocytes carry out capture from blood of not conjugated bilirubin from which in a cytoplasmic membrane albumine separates. In transfer of bilirubin through a cell membrane, and then from cytoplasm in a membrane of an endoplasmic reticulum proteins Y (лигандин) and Z (glutationtransferaza) participate. In a membrane of an endoplasmic reticulum of a hepatocyte bilirubin is conjugated with uridinediphosphoglucuronic acid (UDFGK) under the influence of UDF-glyukuroniltransferaza's enzyme and the monoglucuronide of bilirubin (MGB) which at a biliary pole of a hepatocyte passes through a gepatokanalikulyarny membrane into bile on the concentration gradient created by bile acids (volatile process) is formed. In bilious tubules diglucuronide of bilirubin (DGB) is formed of two molecules MGB with participation bilirubin-glyukuronidtransferazy. Thus, bile contains the conjugated bilirubin (in the main DGB), soluble in water, so-called connected, or a straight line, bilirubin (gives forward reaction with a diazoreactant).
In the extrahepatic courses, a gall bladder and small intestine (mainly) from DGB under the influence of enzymes of intestinal microflora glucuronic acid (deconjugation) is chipped off, free bilirubin gets into blood, and the remained DGB is recovered to urobilinigen (mezobilinogen) which part is soaked up through an intestinal wall in blood and from a portal vein comes to a liver (a hepatoenteric circulation) where collapses before pyrrol connections. Because urobilinigen normal does not get to the general blood stream, it is absent also in urine. The most part of urobilinigen in a large intestine is recovered to the stercobilinogen emitted with a stake in the form of the oxidized form - stercobilin. Insignificant amount of stercobilinogen, having soaked up in blood in a lower part of a large intestine, through the lower hemorrhoidal veins comes to system of the lower vena cava and it is removed with urine which normal contains stercobilinogen traces. However in clinical practice it is accepted to call it urobilinigen or urobilinovy bodies (the general term for the bilirubin exchange products allocated with urine).

Disturbance of a bile production is shown in increase or reduction of biliary secretion, as a rule, with simultaneous change of its structure.

The following can be the reasons of increase or reduction of a bile production:
1) change of neurohumoral regulation (for example, increase in biliary secretion during the strengthening of a tone of a vagus nerve or increase in an inkretion of secretin and gastrin);
2) alimentary factors, some medicinal plants and drugs (fats, egg yolk, infusion corn rylets, sorbite, deficit of protein);
3) the exogenous and internal causes breaking energy balance in an organism including in the liver which is not affected with pathological process (a hypoxia, overheating, a hypothermia, a poisoning with cyanides);
4) the damage of a liver and biliary tract (hepatitis, a hepatosis, cholecystitis) leading to disturbance of secretory function of hepatocytes owing to their dystrophy and destruction and to change of a reabsorption of components of bile;
5) the decrease of the activity of intestinal microflora reducing a hepatoenteric circulation of components of bile and, therefore, their concentration in bile (at pathological processes in a small bowel, under the influence of antibiotics);
6) disturbance of education and exchange of bilirubin and bile acids and change of their content in bile.

Often the abnormal liver function arises at its traumatic damages, infectious diseases (an alveococcosis, an echinococcosis), liver abscesses, not parasitic cysts of a liver.

Disturbance of a zhelchevydeleniye.

Causes of infringement of passing of bile on biliary tract in a duodenum can be the following:
1) a mechanical obstacle to outflow of bile at a prelum of biliary tract from the outside (a tumor of a head of the pancreas inflamed by fabric, a hem) or their obstruction (a stone, helminths, dense bile);
2) disturbance of an innervation of biliary tract - hyper - and hypokinetic dyskinesia (for example, reduction of a zhelchevydeleniye at a spasm of a sphincter of a neck of a gall bladder);
3) change of humoral regulation of a zhelchevydeleniye (the zhelchevydeleniye amplifies at hyperproduction of secretin, cholecystokinin, a motilin).