Degeneration of the liver - a coma, which is associated with a profound inhibition of liver function lasix use. Hepatic coma occurs because of an acute or chronic liver disease.

Hepatocellular coma, in most cases, caused by acute viral hepatitis. Sometimes it occurs due to poisoning genototropnymi toxins (poisonous mushrooms, nitrates Towle, etc..), Sometimes - on the application atofana, halothane, etc. Portocaval coma is the result of cirrhosis, occurs when bleeding associated with the infection. Sometimes portocaval coma occurs because of an irrational treatment with diuretics, as well as the improper use of sedatives and opiates.

When granular dystrophy in the cytoplasm of hepatocytes appears crude protein grain. Liver cells increase in volume, look swollen, turbid (cloudy swelling); the cytoplasm increases in protein and water, which is in the form of grains, coagulates. When histochemical study observed a decrease of the reaction rate and the overall basic protein, ribonucleoprotein. The basis of dystrophy is the disintegration of protein-lipid complex, part of the organelle membranes. When granular dystrophy impaired water-salt metabolism, the intensity of redox processes, oxidative phosphorylation, accumulation of acidic metabolites. Granular dystrophy is compensatory-adaptive character usually does not entail a functional impairment of the liver and is a reversible process is the most common type of injury of hepatocytes under various pathogens (viruses, bacteria, toxic) effects (mild form of chronic hepatitis B, the inactive form of cirrhosis, etc. ).

Hydropic degeneration is characterized by swelling of light cells (as opposed to cloudy swelling upon granular dystrophy). Hepatocytes are increased to the extent of their cytoplasm seems optically empty, reduced protein content, glycogen, oksidoreluktaz activity, increased activity of hydrolases. The most severe form of hydropic dystrophy dystrophy is a balloon which is at the height of the development is irreversible, indicating that the transition process in liquefactive necrosis. Thus cytoplasm optically empty, it gives histochemical reactions. Hydropic dystrophy occurs in patients with viral hepatitis (especially in severe and moderate forms), with dystrophic form of cirrhosis, long-term intra- and extrahepatic cholestasis, etc.

Hyaline-drop dystrophy is characterized by a decrease in the size of hepatocytes, homogeneous cytoplasm intensely painted acid dyes (eosin-type), which served as a basis to call this type of dystrophy acidophilus. There has been an increase in the number of PAS-positive structures. This type of dystrophy is associated with impaired cell membrane permeability, fluid loss, and physical and chemical changes in the protein. As a result, proteinaceous substances become more dense and homogeneous. Hyaline degeneration observed in various pathogenic influences, especially viral.

Parenchymal fatty degeneration. Characterized by the accumulation in the cytoplasm of hepatocytes of small fat droplets coalescing into larger then one or fatty vacuole, which occupies the entire cytoplasm and nucleus of cells displaces periphery.

In marked obesity on liver tissue section dim, yellow. If obesity has undergone more than 50% of liver parenchyma, talk about fat gepatoze. When stained with hematoxylin and eosin staining in the cells of the liver visible light, unstained vacuoles (drops) round or oval fat droplets may coalesce and fill all the cytoplasm of hepatocytes. In marked obesity hepatocytes crowded fat are broken, and the fat droplets merge together to form fat "cysts".

In clinical practice, the leading role is a violation of glycogen metabolism, are more common in diabetes and glycogen storage disease. In diabetes significantly reduced supply of glycogen in liver cells, the content of which is reduced to 30-50 times. At the same time celebrate the accumulation of glycogen in the nucleus of hepatocytes, which creates a picture of a kind of vacuolization ( "empty" core). The most pronounced disorders of carbohydrate metabolism in the liver with glycogen storage disease occur - enzymopathies caused by deficiency of enzymes involved in the degradation of glycogen, Currently, there are more than 10 types of glycogen storage disease. When glycogen storage disease glycogen content in the liver tissue increases dramatically, hepatocytes increase in size, very weakly stained with eosin, thanks to their cytoplasm looks "optically empty" light, do not take the color, hyperplastic smooth EPS few large lysosomes, cell membranes clearly konturiruyutsya.

When stained with hematoxylin and eosin staining in the nuclei of hepatocytes can be seen optically empty vacuoles round or the wrong oval, 4-8 mm in diameter, which are restricted to a clear membrane, receiving good basic dyes. Most often hyalinosis nuclei occurs in diabetes, diseases of the gallbladder and pancreas. Sometimes excessive deposition of glycogen observed in the nucleus - glycogen nuclei hepatocytes. By increasing the size of the sinusoid cells significantly reduced. The preparations stained with hematoxylin and eosin or van Gieson method for, and identifies an "empty" cells resembling picture when balloon dystrophy, but while hepatocytes glycogenosis dimensions much larger than the balloon dystrophy. When glycogen in the cytoplasm of cells observed sharply positive Schick reaction, which disappears after treatment with control slices diastase or amylase. The outcome of glycogen storage disease type III and IV may be cirrhosis.

In chronic liver lesions observed violation of the content of glycoproteins. When fukoidoze in liver tissue observed deposition of glycolipids containing IPU and fucose.