Animal anatomy, histology, pathological anatomy

1.3. NecrosisNecrosis is the death of individual cells, tissue areas and organs. The essence of necrosis is the complete and irreversible cessation of vital activity, but not in the entire body, but only in some limited area (local death). The causes of necrosis are very diverse: the action of chemical and physical factors, viruses and microbes; damage to the nervous system; disturbance of blood supply. With slow death, dystrophic changes occur, which increase and reach a state of irreversibility. This process is called necrobiosis. Necrosis that occurs directly at the site of application of harmful agents is called direct. If they occur at a distance from the place of exposure to a harmful factor, they are called indirect. These include: 1. Angiogenic necrosis, which is formed as a result of cessation of blood flow. 2. Neurogenic necrosis, caused by damage to the central and 6 peripheral nervous systems. 3. Allergic necrosis: skin necrosis in chronic erysipelas of pigs. Morphological characteristics of necrosis. The sizes of dead areas vary: from microscopic to entire organs. The following types of necrosis are distinguished: A. Dry (coagulation) necrosis. Necrotic areas have a dense consistency, whitish-gray or grayish-yellow color. An example of dry necrosis can be anemic infarctions. Sometimes it resembles wax in appearance; This is where waxy or Zenker necrosis occurs. The cut surface is dry, the tissue pattern is erased; this includes the so-called caseous (cheesy) necrosis, in which the dead tissue is a dry crumbling mass of yellowish-gray color. B. Wet (colliquation) necrosis occurs in tissues rich in moisture (for example, the brain), and also provided that the area of ​​necrosis does not dry out. Sometimes foci of dry necrosis may undergo liquefaction (secondary colliquation). B. Gangrene is classified as necrosis, but is characterized by the fact that it may not occur throughout the entire body, but only in areas in contact with the external environment. Dry gangrene (mummification) is observed in the skin. Dead areas are dry and dense, brown or black in color. Wet gangrene (putrefactive or septic) is caused by the action of putrefactive microorganisms on dead tissue. Microscopic changes in the cell during necrosis. Changes in the nucleus have three types: karyopyknosis - wrinkling; karyorrhexis - decay or rupture; karyolysis - dissolution. With karyopyknosis, a decrease in nuclear volume occurs due to chromatin compaction; it wrinkles and therefore becomes more intensely colored. Karyorrhexis is characterized by the accumulation of chromatin clumps of varying sizes. During karyolysis, voids (vacuoles) are formed in the nucleus at the sites of chromatin dissolution. These voids merge into one large cavity, the chromatin disappears completely, the nucleus does not stain, but dies. Coagulation (folding) of proteins occurs in the cytoplasm. The cytoplasm becomes more dense. This is referred to as plasmopyknosis or hyalinization. Later, the cytoplasm breaks up into separate clumps and grains (plasmorhexis) and then the cytoplasm dissolves (plasmolysis). Collagen, elastic and reticular fibers lose their outlines, become basophilically stained and fragmented, and later liquefy. Sometimes the dead interstitial substance becomes similar to fibrin fibers (fibrinoid transformation). When the epithelium becomes necrosis, the soldering (cementing) substance liquefies - cell discomplexation and desquamation or desquamation. Outcomes of necrosis. In foci of necrosis, tissue decay products (detritus) accumulate, which irritate the surrounding living tissues and inflammation develops in them. A red stripe (demarcation line) forms at the border between living and dead tissues. At the site of necrosis, granulation tissue forms, from which a scar is formed. The replacement of necrosis by connective tissue is called organization. Calcium salts are easily deposited in dead material, which is called calcification or petrification. If dead tissue is not liquefied and replaced, a connective tissue capsule is formed around it - encapsulation occurs. When a capsule forms around the area of ​​wet necrosis, a cyst is formed - a cavity with liquid contents. If, during demarcation inflammation, increased emigration of leukocytes occurs, purulent softening occurs, leading to the delimitation of the necrotic focus from the surrounding tissues. This is called sequestration, and the isolated dead area is called sequestration. Granulation tissue develops around the sequester, from which a capsule is formed. When there is necrosis in the outer parts of the body, they can be completely rejected from the body - mutilation. The significance of necrosis is that the dead areas cease to function. Necrosis in the heart and brain often leads to death. Absorption of tissue decay products causes poisoning of the body (autointoxication). The replacement of necrosis by connective tissue is called organization. Calcium salts are easily deposited in dead material, which is called calcification or petrification. If dead tissue is not liquefied and replaced, a connective tissue capsule is formed around it - encapsulation occurs. When a capsule forms around the area of ​​wet necrosis, a cyst is formed - a cavity with liquid contents. If, during demarcation inflammation, increased emigration of leukocytes occurs, purulent softening occurs, leading to the delimitation of the necrotic focus from the surrounding tissues. This is called sequestration, and the isolated dead area is called sequestration. Granulation tissue develops around the sequester, from which a capsule is formed. When there is necrosis in the outer parts of the body, they can be completely rejected from the body - mutilation. The significance of necrosis is that the dead areas cease to function. Necrosis in the heart and brain often leads to death. Absorption of tissue decay products causes poisoning of the body (autointoxication). The replacement of necrosis by connective tissue is called organization. Calcium salts are easily deposited in dead material, which is called calcification or petrification. If dead tissue is not liquefied and replaced, a connective tissue capsule is formed around it - encapsulation occurs. When a capsule forms around the area of ​​wet necrosis, a cyst is formed - a cavity with liquid contents. If, during demarcation inflammation, increased emigration of leukocytes occurs, purulent softening occurs, leading to the delimitation of the necrotic focus from the surrounding tissues. This is called sequestration, and the isolated dead area is called sequestration. Granulation tissue develops around the sequester, from which a capsule is formed. When there is necrosis in the outer parts of the body, they can be completely rejected from the body - mutilation. The significance of necrosis is that the dead areas cease to function. Necrosis in the heart and brain often leads to death. Absorption of tissue decay products causes poisoning of the body (autointoxication).
The doctrine of death - thanatology The term "Thanatology" was derived from the Greek roots - thanatos - death and logos - doctrine and was introduced at the suggestion of I.I. Mechnikov. The origins of thanatology were the outstanding scientists M.F.L. Bisha, Claude Bernard, Virkhov, I.I. Mechnikov and others, who laid the foundation for the study of death as the natural end of life. Death is the irreversible cessation of the vital activity of an organism, the inevitable natural end of the existence of every living creature. This is exactly how modern science defines this concept. There is clinical death and biological or true death, and among doctors there is also social death and brain death. Thanatology largely studies the pathomorphological aspects of dying and postmortem changes observed in a corpse at various times after death under various external conditions, the features of the study of a corpse, as well as the diagnosis of the causes of death and pathofunctional changes occurring in terminal conditions. Many changes observed in the corpse are a consequence of terminal processes and are caused by them. Ignorance of these changes complicates expert work and does not allow one to correctly determine thanatogenesis, the duration of death, intravital or postmortem formation of injuries and other issues important for forensic veterinary examination and investigation. The onset of death is always preceded by terminal conditions, which can last for varying periods of time from several minutes to hours and even days. In general, terminal conditions include severe shock, extreme coma, collapse, preagonal state, terminal pause, agony and clinical death. Severe shock, extreme coma, collapse can turn into a state of clinical death or other terminal conditions. The term “terminal conditions” characterizes pathofunctional changes, which are based on increasing hypoxia of all tissues and, first of all, the brain, acidosis due to the accumulation of under-oxidized products, and intoxication with toxic products of impaired metabolism. During terminal conditions, the functions of the cardiovascular system, respiration, central nervous system, kidneys, liver, hormonal system, and metabolism collapse. The most significant is the decline of the functions of the central nervous system. Increasing hypoxia and subsequent anoxia in the cells of the brain and, above all, the cortex lead to the replacement of the oxidative type of metabolism with a glycolytic one. In this case, a disturbance in the synthesis of ATP and ion gradients is observed, free radicals are formed, and the permeability of cell membranes increases. These metabolic changes entail destructive changes in cells, which manifests itself in the form of cloudy swelling and hydropic degeneration. In principle, these changes are reversible and, when normal oxygen supply to tissues is restored, do not lead to life-threatening conditions. But with continued anoxia, they turn into irreversible 120 dystrophic changes, which are accompanied by protein hydrolysis followed by autolysis. The least resistant to the glycolytic type of metabolism are the tissues of the brain and spinal cord; only 4-6 minutes of anoxia are enough to develop irreversible changes in the cerebral cortex. With the glycolytic type of metabolism, the subcortical region and spinal cord can function somewhat longer. The severity of terminal conditions and their duration depend on the severity and speed of development of hypoxia and anoxia.
Questions for self-control
1. Clinical signs of death, determination of causes of death?
2. What are hypostases and the time of their occurrence?
3. What is the mechanism of the appearance of corpse green?
4. What is fibrinoid necrosis?
5. What is an organization?