The theoretical part.

Prolongation of dystrophic process in the course of time can cause irreversible changes of the local (necrosis) or general character (death of organism).

Necrosis is the mortification of the body part or organ in life of the whole organism. The character of necrosis is determined by its localization, spreading of process, by the degree of blood circulation and lymphokinesis in the damaged area, by the immunologic organism’s responsiveness. In necrotic process development there is a number of stages which are accompanied by hydrolase activation: RNA- and DNA- hydrolase, as a result of what nucleic acids are released from compound with albumens and become depolymerized.

The mortification process can have a physiological character. Death is constantly present in any organism (of those or other cells in different organs and systems) as a result of normal vital processes (renovation of blood cells, flat stratified epithelium, mucous membrane epithelium and others).

The causes of the pathological mortification (necrosis) can be physical, chemical, biological, mechanical and others factors. Depending on the features of their correlation with tissues, necrosis can be direct or indirect (ischemic necrosis, infarction). The necrotic changes begin with paranecrosis - the state of cells, which has reversible character and emerges with albumen denaturation in cytoplasm; then necrobiosis develops (it is a complex of changes in a cell, that begins from the moment of pathogenic factor action and ends with its death). Cessation of vital functions in the cell is the eventual stage of necrotic process. Death of cell is followed by removal of dead parts due to self-digestion as a result of lysosome enzymes hyperactivity (necrosis).

In this stage changes of nucleus and cytoplasm origin take their place in the cell. A nucleus exfoliates (karyopyknosis), disintegrates into lumps (karyorrhexis) or dissolves (karyolysis). In the cytoplasm denaturation and coagulation of albumen first of all occurs only in separate areas (focal coagulation necrosis), and later it involves the whole cell (total coagulation necrosis).

The early changes are observed in chondriosomes and endoplasmic reticulum. Destruction processes in these organellas are characterized by swelling of chondriosomes, diffuse edema of matrix with clearing of it, local or total disorganization of cristas and dissociation of their membranes. The damage of external membrane of organellas as it breaks is considered to be the absolute sign of irreversible character (necrosis of organella). Canaliculi fragmentations, their uneven amplification and membrane focal lysis take their place in the endoplasmic reticulum.

Activity of lysosome enzymes grows with the development of the noted changes, it is followed by albumen coagulation in the cytoplasm with their subsequent disintegration (plasmorrhexis). Alongside with that, cytoplasm hydratation grows, that causes irreversible changes, first in separate its areas (focal colliquative necrosis), and then the whole cell is involved (total colliquative necrosis). The noted changes in cytoplasm (coagulation, plasmorrhexis, plasmolysis), and the changes of nucleus (pyknosis, rhexis, lysis) are the morphologic representation of enzymatic process; activation of lysosome enzymes lies in the basis of it.

In other words, the change of coagulation and colliquation processes take place in the dynamics of necrotic process. Thus predomination of each of them is possible, that and lies in the development basis of dry (coagulation) and humid (colliquative) necrosises.

In coagulation necrosis dead tissues are dry, they are macroscopically indurated, of clay-yellow or gray-yellow color (ischemic infarction of the spleen, kidneys, Zenker's degeneration of somatic muscles in some infectious diseases, caseous necrosis of definite internal organs in tuberculosis, fibrinoid necrosis of intermediate tissue in rheumatic diseases).

In colliquative necrosis softening of tissue takes place. Frequently it is observed in tissues enriched with fluid: cerebrum in hemorrhagic or ischemic infarction, tissues of fetus in case of fetal death.

Thus, in necrosis development it is possible to define some stages: paranecrosis, necrobiosis, death of cell and autolysis. The morphologic signs of necrosis appear only in the autolysis stage, that is a few hours after the moment of cell death.

Apoptosis is one of the forms of death; it is genetically programmed death of cell in a living organism. Basic role of apoptosis in norma is establishment of necessary equilibrium between the processes of proliferation and death of cell, that on the one hand provides the stable state of the organism, on the other – growth or atrophy of tissues and organs. Apoptosis is present in the process of embryogenesis (in implantation, organogenesis, involution), due to changes of hormonal dependent organs after cesation of proper hormone action (abruption of endometrium in menstruation, atrophy of ovaries in menopause), in atrophy of parenchymatous organs in the conditions of ducts obstruction (pancreas, kidneys) and others.

In morphogenesis of apoptosis the following stages are distinguished (Serov V.V., Palcev M.A., Ganzen T.N., 1998):

1. Condensation and margination of chromatin (the most characteristic sign of apoptosis) with formation of lumps under the nuclear membrane; a nucleus forms deep invaginations, with rugged contours, can be fragmented.

2. Contraction of the cell as a result of condensation of intracellular organellas.

3. Formation of apoptosis bodies which consist of cytoplasm fragments with very tightly packed organellas and fragments of nucleus (sometimes even without it).

4. Phagocytosis of apoptosis bodies of adjacenet cells (parenchymatous) or macrophages.

Microscopically apoptosis bodies have the appearance of round or oval particles with intensively eosinophilic cytoplasm and with the dark fragments of nuclear chromatin.

In contrast to actual necrosis apoptosis refers only to separate cells or groups of cells. Destruction of the cells here takes place due to non-activated hydrolases, and with participation of special calcium-magnesium dependent endonucleases, which “cut” nucleus into separate fragments. These fragments of cells (apoptosis bodies) are phagocytized adjacent cells – parenchymatous and stromal. In addition, apoptosis is never accompanied by inflammation development, which is observed in case of beginning actual necrosis.

Gangrene is a type of necrosis (the “coloured necrosis”). Dry gangrene, or mummification, occures in those cases, when dead tissues are found on the surface of the body, that is why fluid is given to the environment, and that tissues dry out and become inspissated. On the border with healthy tissue in these cases there is a reactive inflammatory process as a line of demarcation. Humid (moist) gangrene arises up as a result of anaerobic infection penetration in dead tissues, as a result there is ichorization of them, with a characteristic unpleasant smell. It is observed on lower extremities at cold injury, at bedsores, in soft tissues of cheek at noma. Humid gangrene can occur also in internal organs that have the contact with the environment (lungs, intestine, uterus).

Among the favorable consequences of necrosis there are organization - forming of the scar, encapsulation, petrification, ossification and formation of a cyst. Festering melting of the cell in focus of mortification is unfavorable complication.

General death is cessation of organism vital functions. The direct causes of it are different. There are natural death, physiological death, or death from “senile decrepitude”, and precocious pathological death that can come in any age. Precocious death can be violent (it is subject of medicolegal examination) and result from the diseases (it is the subject for pathological anatomy study). Depending on development duration death can be lingering or sudden. The causes of a sudden death are cesation of the brain function (ischemic, hemorrhagic infarctions) or heart disorders (arrhythmia, acute myocardial infarction, acute coronary insufficiency).

Depending on the inversive or irreversible character of changes in the organism there are clinical (possible restore to life) and biological death (restore to life is impossible). The original state of hypoxia of the central nervous system, duration of which is determined by the period of survival of nervous cells, lies in the basis of clinical death (5-7 min.). The terminal states of the organism precede the nascency of clinical death (agony, arrhythmia, paralysis of sphincters, pulmonary oedema, shock, bleeding and oth.). In biological death changes are of irreversible character.

Cesation of breathing and blood circulation are the basic and absolute implications of general death. The absolute signs of death are: exposure to cold of body (algor mortis), cadaveric rigidity (rigor mortis), mummification, blood redistribution, postmortem lividity and disintegration of body tissues.

Exposure to cold of body arises up as a result of temperature smoothing of it with the temperature of environment. Cadaveric rigidity comes through 6-10 h. post mortem and is characterized by contraction of somatic muscles as a result of colloids swelling of retractive substance due to action of postmortal lactic acid.

Postmortem lividity results from blood redistribution in the cardiovascular system and its output outside the vessels. As a result of arteries constriction blood passes to the vein system, flows down in the below located areas of body, and then goes outside the vessels (cadaveric imbibition). Disintegration of body tissues occurs as a result of enzymatic processes in tissues, and also action of microorganisms.

Practical part.

Ischemic infarction of the spleen. Gross specimen.

The spleen is enlarged, indurated, its surface is smooth. On the section there is the area of yellow-white color as a triangle, basis of which turned to the capsule, and apex - to the gates of the organ.

Gangrene of the foot. Gross specimen.

Mortified tissues are indurated, black, clearly marked off from healthy shin part in the region of its lower third.

Ischemic infarction of the spleen.Microscopic specimen.

The border between necrotic and healthy areas is enough clear. In the necrosis area nuclei are painted pale, erythrocytes are absent in sinuses. With prolongation of infarction term the necrosis area is other: all tissue, except for trabecules, grows into fine-grained, pale painted mass, the structure of the organ in these places is absent. Polymorphonuclear leucocytes (neutrophiles) appear in the periphery of the infarction area, some of them have the signs of karyorrhexis. Leucocytes are absent in the central sections of necrosis.

Coagulation necrosis of the lymphoglandula. Microscopic specimen.

The necrosis area is represented by the homogeneous, anhistic area of pink color while stain with hematoxylin and eosin. In the necrosis area karyorrhexis and karyopyknosis take place, there are the separate fragments of fibre structures (in impregnation connective tissue by Gomori).

Karyolysis. Microscopic specimen.

Epithelial cells of uriniferous tubules are homogeneous, of rose color, nuclei in them do not turn out, cytoplasm is sometimes fine-grained, lumen of the tubules is not narrowed. A process has a focal-disseminated character. Thus adjacent tubules save their structure.

Pancreatonecrosis. Microscopic specimen.

The area of necrosis is anhistic, homogeneous, of pink color, cellular elements with the signs of karyorrhexis and karyopyknosis. In the necrosis periphery the structures of the pancreas turns out markedly.

Plasmolysis.Electronogram.

Сharacteristic melting of sarcostyles and destruction of chondriosomes in cardiac cells are seen in acute myocardial infarction.

Karyolysis.Electronogram.

There is lysis of the membrane of the nucleus, diffusion in cytoplasm of chromatin granules, that are freely disposed in it as grainy material of high electronic magnification.

Date: 2016-03-03; view: 732