Liver dystrophy

Description:

Dystrophy of a liver is a coma which is connected with deep oppression of functionality of a liver. The hepatic coma arises because of acute or chronic diseases of a liver.

Liver Dystrophy symptoms:

There are several kinds of a syndrome of dystrophy.

- Parenchymatous proteinaceous dystrophy.
Allocate granular, gidropichesky and hyaline proteinaceous dystrophy.

At granular dystrophy in cytoplasm of hepatocytes rough proteinaceous granularity appears. Cells of a liver increase in volume, look bulked up, muddy (muddy swelling); in their cytoplasm protein content and waters which is in a type of grains, coagulates increases. At a histochemical research decrease in intensity of reaction to the crude and main protein, ribonukleoproteina is observed. Disintegration of the proteinaceous and lipidic complex which is a part of membranes of organellas is the cornerstone of dystrophy. At granular dystrophy the water salt metabolism, intensity of oxidation-reduction processes, oxidizing phosphorylation is broken, there is an accumulation of acid products of exchange. Granular dystrophy has compensatory and adaptive character, as a rule, does not involve a functional hepatic unsufficiency and is reversible process It is the most widespread type of damage of hepatocytes at various pathogenic (virus, bacterial, toxic) influences (an easy form of chronic hepatitis, inactive forms of cirrhosis, etc.)

Gidropichesky dystrophy is characterized by light swelling of cells (unlike muddy swelling at granular dystrophy). Hepatocytes are increased in volume, their cytoplasm seems optically empty, are reduced protein content, a glycogen, activity оксидорелуктаз, hyperactivity of hydrolases. The most expressed form of gidropichesky dystrophy is balloon dystrophy which at height of development is irreversible that demonstrates transition of process to a kollikvatsionny necrosis. At the same time cytoplasm optically is empty, does not give histochemical reactions. Gidropichesky dystrophy occurs at patients with a viral hepatitis (especially at severe and medium-weight forms), at a dystrophic form of cirrhosis, at long inside - and an extrahepatic cholestasia and so forth.

Hyaline and drop dystrophy is characterized by reduction of hepatocytes in sizes, the homogeneous cytoplasm which is intensively painted by acid dyes (like eosine) that formed the basis to call this type of dystrophy acidophilic. Increase in number of CHIC-positive structures is observed. This type of dystrophy is connected with disturbance of permeability of cellular membranes, loss of liquid and physical and chemical changes of protein. As a result proteinaceous substances become more dense and homogeneous. Hyaline dystrophy is observed at various pathogenic influences, especially virus etiology.

- Parenchymatous fatty dystrophy.
It is characterized by accumulation in cytoplasm of hepatocytes of the small drops of fat merging then in larger or in one fatty vacuole which occupies all cytoplasm and displaces a kernel on the periphery of a cell.

At a gross obesity liver tissue on a section dim, yellow color. If more than 50% of a parenchyma of a liver underwent obesity, speak about a fatty hepatosis. When coloring by hematoxylin and eosine in cells of a liver light, uncolored vacuoles (drops) of a round or oval form are visible Fatty drops can merge and fill all cytoplasm of a hepatocyte. At a gross obesity the hepatocytes overflowed with fat are broken off, and fatty drops, merging with each other, form fatty "cysts".

Allocate the following polymorphological forms of obesity of a liver.

the disseminated obesity at which fatty drops contain in separate hepatocytes (observe preferential in physiological conditions)
zone obesity when the central, ntramuralny or peripheral areas of a hepatic segment are exposed to obesity;
diffusion obesity, i.e. obesity of all (or almost all) hepatic segment. Obesity of a liver is reversible. It can be krupnokapelny and small-drop:
Krupnokapelny (macroscopic) obesity is characterized by existence in hepatocytes of "empty" vacuoles with the shift of kernels to the periphery.
At small-drop obesity of a drop of fat small, at the same time kernels with clear kernels are located in the center, the necrosis of hepatic cells is expressed in different degree.
- Parenchymatous carbohydrate dystrophy.
In clinical practice the leading value has the disturbance of exchange of a glycogen meeting at a diabetes mellitus and glycogenoses more often. At a diabetes mellitus the glycogen stock in hepatic cells which maintenance decreases at 30-50 times considerably decreases. At the same time note accumulation of a glycogen in kernels of hepatocytes that creates a picture of their peculiar vacuolation ("empty" kernels). The most expressed disturbances of carbohydrate metabolism in a liver come at glycogenoses - the fermentopatiya caused by deficit of the enzymes participating in processes of splitting of a glycogen Now there are more than 10 types of glycogenoses. At glycogenoses the maintenance of a glycogen sharply increases in liver tissues, hepatocytes increase in sizes, are very poorly painted by eosine, thanks to it their cytoplasm looks "optically empty", light, badly perceiving coloring, giperplazirovanny smooth EPS, not numerous large lysosomes, cellular membranes konturirutsya accurately.

When coloring by hematoxylin and eosine in kernels of hepatocytes empty vacuoles of roundish or incorrectly oval form, with a diameter of 4-8 microns which are limited to the accurate membrane which is well perceiving the main dyes are visible optically. Most often the hyalinosis of kernels meets at a diabetes mellitus, diseases of a gall bladder and pancreas. Sometimes excess adjournment of a glycogen is observed in a kernel - a glycogenosis of kernels of hepatocytes. Due to increase in the sizes of cells of a sinusoid considerably decrease. In the drugs painted by hematoxylin and eosine or by a method Van Gizona, the "empty" cells reminding a picture at balloon dystrophy, however the sizes of hepatocytes at a glycogenosis much more also come to light than at balloon dystrophy. At a glycogenosis in cytoplasm of cells CHIC reaction, disappearing after processing of control cuts a diastase or amylase is noted sharply positive. III and IV types cirrhosis can be an outcome of glycogenoses.

At chronic damages of a liver disturbance of maintenance of glycoproteins is noted. At a fukoidoza in tissue of a liver adjournment of the glycolipids supporting Ministry of Railways and a fukoza is observed.

Often leads deficit of antitrypsin to dystrophy of hepatocytes, antitrypsin is synthesized in a liver. At its deficit develop emphysema of lungs, and at 10% of patients - cirrhosis. Adjournment of antitrypsin is connected with lack of sialic acids and defect сиалотрансфераз, participating in functioning of a complex Golgi Naibolei a characteristic sign of deficit of antitrypsin adjournment of round slaboatsidofilny CHIC-positive granules, resistant to a diastase, in cytoplasm of hepatocytes is. The sizes of granules fluctuate from 1 to 40 microns. In the absence of cirrhosis of a granule are located preferential in periportal hepatocytes, in a cirrhotic liver - in the hepatocytes adjacent to fibrous septa. The final diagnosis is possible only after immunomorphological identification of antitrypsin.

Mesenchymal dystrophy
These damages of a liver meet at primary and secondary amyloidosis. Clinical manifestations of an amyloidosis of a liver are insignificant therefore morphological methods of a research gain great value. Microscopically at an amyloidosis find deposits of unstructured homogeneous zozinofilny mass of amyloid between star-shaped retikuloz-ndoteliotsita on the course of a reticular stroma, in walls of vessels and bilious channels and in portal paths. Preferential intermedialny department of an acinus is surprised. At the expressed process substance is laid on all segment, squeezes hepatic beams, hepatocytes are exposed to an atrophy. Amyloid is painted by Congo red and in the polarized light gives a dichroism picture (brown-red coloring becomes green). Deposits of amyloid are similar at primary and secondary amyloidosis, however at primary amyloidosis liver vessels whereas in Disse's space amyloid is absent separately are surprised.

Liver Dystrophy reasons:

The hepatocellular coma, in most cases, is caused by an acute viral hepatitis. Sometimes it arises because of poisoning with genototropny poisons (poisonous mushrooms, nitrates of a toul and so forth), sometimes - from use of quinophan, a halothane, etc. The porto-caval coma is a consequence of cirrhosis, arises after the bleeding connected with an infection. Sometimes, that the porto-caval coma arises because of irrational treatment by diuretics, and also from the wrong use of sedative and somnolent drugs.

Treatment of Dystrophy of a liver:

At emergence of signs of a prekoma it is necessary to limit sharply amount of protein in a daily diet to 50 g, and at further progressing of a disease to stop administration of proteins through a mouth.

Intestines are daily cleared an enema and laxatives, orally or via the probe enter the antibiotics suppressing intestinal microflora (Kanamycinum on 2 - 4 g a day, ampicillin of 3-6 g a day, tetracycline of 1 g a day). Apply vitamins, cocarboxylase, potassium drugs, glucose, plentiful parenteral administration of liquid.

For neutralization of ammonia of blood enter 1 arginine (25-75 g a day into 5% glucose solution), glyutaminovy acid (30-50 g in the form of 10% of solution). At psychomotor excitement appoint a haloperidol, GOMK, Chlorali hydras (1 g in an enema). In case of development of a metabolic acidosis 4% sodium bicarbonate solution on 200-600 ml a day are entered, at the expressed metabolic alkalosis large amounts of potassium are entered (to 10 g a day and more).

Glucocorticosteroid hormones are appointed in high doses; Prednisolonum in a prekoma - 120 mg a day, from them 60 mg intravenously kapelno, in a coma stage - 200 mg a day intravenously kapelno; a hydrocortisone to 1000 mg a day intravenously kapelno. Purpose of diuretic drugs is categorically contraindicated.

At a hepatocellular coma exchange hemotransfusions (5-6 l daily), extracorporal perfusion of blood through a heteroliver or a cadaveric liver, or cross circulation are applied in recent years. Efficiency of heterotopic liver transplantation is doubtful.

At development in patients with a hepatic coma of a renal failure carry out a peritoneal or extracorporal hemodialysis which it is very important to appoint timely.

Forecast. In most cases the lethal outcome comes in several days. At subacute dystrophy of a liver the outcome in quickly forming cirrhosis is possible.