Liver necrosis

Description:

Necrosis - necrosis of fabric under the influence of disturbance of blood circulation, chemical or thermal influence, an injury, etc. The zone of a necrosis has a clear boundary, afterwards is torn away or exposed to purulent fusion; on site defect of fabric the hem is formed.

This concept includes a necrobiosis (far come irreversible dystrophic changes of fabrics - dying off process) and actually a necrosis (necrosis of fabrics) in a live organism. The necrosis always testifies to the heavy, progressing course of pathological process.

Liver Necrosis symptoms:

Acute emergence of painful and dispepsichesky syndromes is characteristic, however at some patients the disease can gradually develop.

The most frequent icteric option: sharp weakness, lack of appetite, nausea, vomiting, jaundice, diarrhea, sharp loss in body weight increases. Pains are localized in right hypochondrium and an anticardium. There can be fever.

At inspection jaundice, a hepatomegalia and fever comes to light. The liver is painful at a palpation, smooth. A fate of patients the spleen increases, there is a palmar roofing material (erythema), skin vascular asterisks, a tremor of hands (астериксис) that is a symptom of hepatic encephalopathy, disturbance of mentality (block, excitement, hallucinations), the ascites steady against diuretics.

Cholestatic option meet a skin itch, a light stake and dark urine seldom. In blood - the expressed hyperbilirubinemia, a hypercholesterolemia, increase in activity of an alkaline phosphatase, gammaglyutamiltranspeptidaza and slight increase of AST, ALT.

Liver Necrosis reasons:

On the volume of the affected liver tissue necroses can be:

    * focal (partial);
    * monocellular, focal or scattered;
    * zone;
    * acinar;
    * submassive or massive.

Microscopically the necrosis is characterized by change of a cellular kernel (a karyopyknosis, a karyorrhexis, a karyolysis) and cytoplasms (coagulation and lysis of cytoplasmatic proteins, their disintegration with formation of a detritis) a hepatocyte. At a karyopyknosis intensive coloring of a kernel is observed by the main dyes. At a karyorrhexis nucleic acids gather in glybk. Further there is their splitting on phosphoric acid, pentoses, the purine and pirimidinovy bases, not perceiving dyes (karyolysis). In cytoplasm the maintenance of a glycogen, ribonukleoprotein, activity of oxidoreductases goes down, activity of acid phosphatase increases.

The coagulative, kollikvatsionny (cytolysis) necrosis and heart attacks are characteristic of hepatocytes.

    * Coagulative necrosis

It is observed in the hepatic cells rich with protein. It is connected with penetration into fabric of calcium ions, activation of enzymes. This necrosis can be partial (partial) and total (with capture of all cytoplasm). At a partial necrosis homogeneous little bodies of Mallory of rounded shape come to light. The total necrosis is characterized by consolidation and wrinkling of all hepatocyte that leads to emergence of homogeneous educations - acidophilic little bodies of Kaunsilmen.

    * Kollikvatsionny necrosis (cytolysis)

Meets in the hepatocytes rather poor in protein and rich with proteases more often. At the same time cells increase in sizes, do not perceive dyes, do not contain a kernel and seem optically empty.

On degree of manifestation and localization in a segment of a liver distinguish the following types of a necrosis:

    * focal (a necrosis of one or several a number of the located hepatocytes - an acute and chronic viral hepatitis, the CPU);
    * zone and centrolobular (chronic hepatitises, hepatogenous hepatotoxic influences, piecemeal (a "step" necrosis) at peroral poisoning with hepatotoxins);
    * submassive and massive (necrosis of almost all parenchyma of a hepatic segment; is the cornerstone of a hepatic coma).

In the centers of a necrosis the collapse of a reticulin stroma of a liver is observed. On the periphery of the center of a necrosis reactive and reparative processes develop: migration of leukocytes from vessels, proliferation of mesenchymal and cellular elements, accumulation of few macrophages.

    * Focal necroses

Strike parts of a hepatic cell, a certain group of organellas with emergence autofagosy and a protein denaturation. At a coagulative necrosis Mzllori's little bodies form, at kollikvatsionny - balloon dystrophy. A special type of a necrosis is apoptosis at which there is "self-destruction" of hepatocytes, their wrinkling and separation to formation of the condensed fragments of the cells filled with organellas. These torn-away fragments are taken by macrophages or hepatocytes.

    * Monocellular necroses (can be scattered and focal)

Meet at acute more often (virus and medicamentous) hepatitis and are coagulative. Development of a coagulative necrosis is preceded by a stage of acidophilic dystrophy. At the same time hepatocytes decrease in volume, as if shrivel, they have dense homogeneous cytoplasm with pyknotic kernels. The shape of a hepatocyte is got out of, their contours take a form of the broken line. Hepatocytes are exposed to "mummification" and are pushed out in sinusoids. Thin ekrotizirovanny hepatocytes are called Kaunsilmen's little bodies. have various sizes, the toplazma which is intensively painted by eosine and the wrinkled kernel which is pushed aside to the periphery with the uneven borders which are often getting a semilunum form. Little bodies of Calminum meet in all departments of a segment. Quite often we surround them ezdchaty retikuloendoteliotsita. The similar picture, is designated by the term "sattelioz", observed at hepatitis B.

    * Monocellular kollikvatsionny necrosis

Is the final of balloon dystrophy. At the same time hepatocytes are not pushed out in sinusoids, and perish, being in a hepatic plate. Similar process is more often observed in the third zone of an acinus of the Cell, undergone a kollikvatsionny necrosis, it is possible to see seldom - nekrotizirovanny hepatocytes quickly collapse macrophages. Their existence allows to speak about a necrosis when in drugs there are no nekrotizirovanny cells. Accumulations of macrophages can have an appearance of granulomas. An indirect sign of a necrosis is the focal collapse of a stroma revealed on the drugs, impregnirovanny by silver painted by a method Van Gizona and orcein.

The origin of zone and acinar necroses is connected with features of an acinar structure of a liver. Most often the necrosis under the influence of the most various reasons arises in the third zone of an acinus that is caused by features of microcirculation of this zone, the most remote from blood supply sources. The necrosis of hepatocytes of this zone is caused not by direct toxic effect of various poisons and medicines, and Hepatocytes of the first zone of an acinus are injured by the low content of glutathione much less often.

    * Step necroses

These are necroses of small groups of hepatocytes near portal paths. They represent destruction of hepatic cells on border of a parenchyma and connecting fabric with lymphocytic (sometimes with limfoplazmotsitarny) infiltration, meet at chronic hepatitis the expressed activity, an acute viral hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, Wilson-Konovalov's disease, cirrhosis. Not only the periportal, but also periseptalny necroses located at connective tissue sept (usually active) belong to step necroses. In tissue specimens at a step necrosis (as well as at bridge-like) nekrotizirovanny hepatocytes are, as a rule, not visible.

Not lack in general of hepatocytes in the zones adjacent to portal paths or to septa, and substitution by lymphoid and cellular infiltrate of sites where were available earlier is important for recognition of step necroses, but hepatocytes were not exposed to a necrosis. In this site it is possible to see the low-changed hepatocytes or their small groups "immured" separate. The activity of process is higher, the more mononuclear phagocytes contact to hepatic cells. Mononuclear cells can directly damage hepatic cells the Mechanism of such action is not clear. Do not exclude direct action on hepatocytes of proteolytic enzymes, the lymphokines produced by T lymphocytes.

Development of necroses at chronic hepatitis with the expressed activity is explained with the cell-mediated cytotoxic mechanism by penetration of lymphocytes into structure of a hepatocyte (эмпириополез). Lymphocytes can be both on the periphery of a cell, and near a kernel. At chronic hepatitis with the expressed activity in bioptata of a liver there are more than 10 cells with signs of an aggressive empiriopolez in a circle of six portal paths, at hepatitis with the minimum activity their less than ten. Detection of aggression of an empiriopolez at chronic hepatitis has diagnostic value, demonstrates progressing of a disease.

    * Bridge-like necroses

Progressing of necrotic changes leads to connection of various zones of an acinus necrotic bridges. The great value in forecasting of a course of both acute, and chronic hepatitis is attached to bridge-like necroses. The bridge-like necrosis is characteristic of all forms of a necrosis at which there is a connection of vascular structures of a liver. This definition includes also a necrosis of the whole segments which is designated by multi-lobulyarnym. Depending on topography distinguish the following types of bridge-like necroses: tsentrotsentralny, tsentroportalny, portoportalny. The combination of step and portotsentralny necroses is considered adverse. The bridge-like necrosis cuts a segment, and it promotes further formation of cirrhosis. The necrosis comes to the end with education септ, containing vessels which shunt portal blood directly in a hepatic vein, passing system of sinusoid. It leads to partial ischemia of a parenchyma that exerts impact on the course of its regeneration, and also leads to the fact that portal blood, passing the hepatic filter, comes to the general blood stream.

Treatment of the Necrosis of a liver:

Elimination of the reason which caused it is the cornerstone of treatment of different types of a necrosis: prevent further action of the injuring agent, carry out the antibacterial, disintoxication, desensibilizing therapy, normalize cordial activity, liquidate vascular impassability or recover integrity of a vessel, eliminate a prelum and injury of nerves, a spinal cord, etc.

Elements of complex treatment are improvement of the general condition of the patient, stimulation of immunobiological forces and regenerative properties, symptomatic therapy.

The necretomy (excision of devitalized fabrics) is carried out within viable fabrics after emergence of a line of demarcation or after delimitation of a necrosis by means of mechanical irritation (a prick by a needle from the syringe, a contact with a surgical instrument, a ball, etc.). The defect of fabric formed after a necretomy is closed suture or a dermatoplasty.