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Necrosis– necrosis, death of cells and tissues in a living organism, while their vital activity completely ceases.

The necrotic process goes through a series of stages :

1. paranecrosis - reversible changes similar to necrotic
2. necrobiosis – irreversible dystrophic changes (in this case, catabolic reactions predominate over anabolic ones)
3. cell death
4. autolysis - decomposition of a dead substrate under the action of hydrolytic enzymes and macrophages

Microscopic signs of necrosis:

1) Kernel changes

1. Karyopyknosis– core shrinkage. At this stage, it becomes intensely basophilic—it turns dark blue with hematoxylin.
2. Karyorrhexis– disintegration of the nucleus into basophilic fragments.
3. Karyolysis– core dissolution

Pyknosis, rhexis and nuclear lysis occur sequentially one after another and reflect the dynamics of activation of proteases - ribonuclease and deoxyribonuclease. With rapidly developing necrosis, the nucleus undergoes lysis without the stage of karyopyknosis.

2) Changes in the cytoplasm

• plasmacoagulation. First, the cytoplasm becomes homogeneous and acidophilic, then protein coagulation occurs.
• plasmorrhexis
• plasmolysis

Melting in some cases involves the entire cell (cytolysis), and in others only a part (focal liquefaction necrosis or balloon dystrophy)

3) Changes in the intercellular substance

A) collagen, elastic and reticulin fibers swell, saturated with plasma proteins, transform into dense homogeneous masses, which either undergo fragmentation, or clumpy decay, or are lysed.

The breakdown of fibrous structures is associated with the activation of collagenase and elastase.

Reticulin fibers do not undergo necrotic changes for a very long time, and therefore are found in many necrotic tissues.

b) the interstitial substance swells and melts due to depolymerization of its glycosaminoglycans and impregnation with blood plasma proteins

With tissue necrosis, their consistency, color and smell change. The tissue may become dense and dry (mummification), or it may become flabby and melted.

The fabric is often white and has a white-yellow color. And sometimes it is dark red when it is soaked in blood. Necrosis of the skin, uterus, and skin often becomes gray-green or black.

Causes of necrosis.

Depending on the cause of necrosis, the following types are distinguished:

1) traumatic necrosis

It is the result of direct action on the tissue of physical and chemical factors (radiation, temperature, electricity, etc.)

Example: when exposed to high temperatures, tissue burns occur, and when exposed to low temperatures, frostbite occurs.

2) toxic necrosis

It is the result of the direct action of toxins of bacterial and non-bacterial origin on tissue.

Example: necrosis of cardiomyocytes when exposed to diphtheria exotoxin.

3) trophoneurotic necrosis

Occurs when there is a violation of the nervous trophism of tissues. The result is a circulatory disorder, dystrophic and necrobiotic changes that lead to necrosis.

Example: bedsores.

4) allergic necrosis

It is an expression of an immediate hypersensitivity reaction in a sensitized organism.

Example: Arthus phenomenon.

5) vascular necrosis– heart attack

Occurs when blood flow in the arteries is disrupted or stopped due to thromboembolism or prolonged spasm. Insufficient blood flow causes ischemia, hypoxia and tissue death due to the cessation of redox processes.

TO direct Necrosis includes traumatic and toxic necrosis. Direct necrosis is caused by the direct influence of a pathogenic factor.

Indirect necrosis occurs indirectly through the vascular and neuroendocrine systems. This mechanism of necrosis development is typical for species 3-5.

Clinical and morphological forms of necrosis.

They are distinguished, taking into account the structural and functional characteristics of the organs and tissues in which necrosis occurs, the reasons for its occurrence and the conditions of development.

1) coagulation (dry) necrosis

Dry necrosis is based on the processes of protein denaturation with the formation of sparingly soluble compounds that may not undergo hydrolytic degradation for a long time.

The dead areas that appear are dry, dense, gray-yellow in color.

Coagulative necrosis occurs in organs rich in proteins and poor in fluids (kidneys, myocardium, adrenal glands, etc.).

Typically, a clear boundary between dead tissue and living tissue can be clearly marked. There is strong demarcation inflammation at the border.

Examples:

Waxy (Zenker's) necrosis (in the rectus abdominis muscles in acute infectious diseases)

Heart attack

Caseous (cheesy necrosis) with syphilis, tuberculosis

Dry gangrene

Fibrinoid - necrosis of connective tissues, which is observed in allergic and autoimmune diseases. Collagen fibers and smooth muscles of the middle lining of blood vessels are severely damaged. It is characterized by the loss of the normal structure of collagen fibers and the accumulation of homogeneous necrotic material of a bright pink color, which is similar (!) to fibrin.

2) liquefaction (wet) necrosis

Characterized by the melting of dead tissue, the formation of cysts. It develops in tissues that are relatively poor in proteins and rich in fluid. Cell lysis occurs as a result of the action of its own enzymes (autolysis).

There is no clear zone between dead and living tissue.

Examples:

Ischemic cerebral infarction

When masses of dry necrosis melt, they speak of secondary colliquation.

3) Gangrene

Gangrene– necrosis of tissues in contact with the external environment (skin, intestines, lungs). In this case, the tissues become gray-brown or black, which is associated with the transformation of blood pigments into iron sulfide.

a) dry gangrene

Necrosis of tissues in contact with the external environment without the participation of microorganisms. Most often occurs in the extremities as a result of ischemic coagulation necrosis.

Necrotic tissues dry out, shrink and harden when exposed to air, and are clearly demarcated from viable tissue. At the border with healthy tissues, demarcation inflammation occurs.

Demarcation inflammation– reactive inflammation around dead tissue, which delimits dead tissue. The restriction zone, accordingly, is a demarcation zone.

Example: - gangrene of the limb with atherosclerosis and thrombosis

For frostbite or burns

b) wet gangrene

Develops as a result of bacterial infection layering on necrotic changes in tissue. Under the action of enzymes, secondary colliquation occurs.

The tissue swells, becomes swollen, and smelly.

The occurrence of wet gangrene is facilitated by circulatory and lymph circulation disorders.

With wet gangrene, there is no clear distinction between living and dead tissue, which complicates treatment. For treatment, it is necessary to transform wet gangrene into dry gangrene, only then carry out amputation.

Examples:

Intestinal gangrene. Develops with obstruction of the mesenteric arteries (thrombi, embolism), ischemic colitis, acute peritonitis. The serous membrane is dull and covered with fibrin.

Bedsores. Bedsore is the death of superficial areas of the body that are subject to pressure.

Noma is a watery cancer.

c) gas gangrene

Occurs when a wound becomes infected with anaerobic flora. It is characterized by extensive tissue necrosis and the formation of gases as a result of the enzymatic activity of bacteria. A common clinical symptom is crepitus.

4) sequester

An area of ​​dead tissue that does not undergo autolysis is not replaced by connective tissue and is freely located among living tissues.

Example: - sequester in osteomyelitis. Around such a sequester a capsule and a cavity filled with pus will form.

Soft fabrics

5) heart attack

Vascular necrosis, a consequence and extreme expression of ischemia. The reasons for the development of a heart attack are prolonged spasm, thrombosis, arterial embolism, as well as functional stress of the organ in conditions of insufficient blood supply.

a) forms of heart attack

Most often, infarctions are wedge-shaped (the base of the wedge faces the capsule, and the tip faces the hilum of the organ). Such infarctions form in the spleen, kidneys, and lungs, which is determined by the nature of the architectonics of these organs - the main type of branching of their arteries.

Less often, necrosis has an irregular shape. Such necrosis occurs in the heart, intestines, i.e. in those organs where non-main, scattered or mixed types of branching of arteries predominate.

b) magnitude

An infarction may involve most or all of an organ (subtotal or total infarction) or may be detected only under a microscope (microinfarction).

c) appearance

- white

It is a white-yellow area, well demarcated from the surrounding tissue. Usually occurs in tissues with insufficient collateral circulation (spleen, kidneys).

- white with hemorrhagic rim

It is represented by a white-yellow area, but this area is surrounded by a zone of hemorrhages. It is formed as a result of the fact that vascular spasm along the periphery of the infarction is replaced by their expansion and the development of hemorrhages. Such an infarction is found in the myocardium.

- red (hemorrhagic)

The area of ​​necrosis is saturated with blood, it is dark red and well demarcated. It is found in those organs where venous congestion is characteristic, where there is no main type of blood supply. It is found in the lungs (since there are anastomoses between the bronchial and pulmonary arteries), and the intestines.

Clinical manifestations of necrosis.

1) systemic manifestations: fever, neutrophilic leukocytosis. Intracellular enzymes are determined in the blood: the MB isoenzyme of kratin kinase increases with myocardial necrosis.

2) Local manifestations

3) Dysfunction

Outcomes of necrosis:

1) demarcation

With a relatively favorable outcome, reactive inflammation occurs around the dead tissue, which separates the dead tissue from healthy tissue. In this zone, blood vessels dilate, congestion and swelling occur, and a large number of leukocytes appear.

2) organization

Replacement of dead masses with connective tissue. In such cases, a scar forms at the site of necrosis.

3) encapsulation

Overgrowth of the area of ​​necrosis with connective tissue.

4) petrification

Calcification. Accumulation of calcium salts in the capsule.

5) ossification

Extreme degree of petrification. Bone formation in the area of ​​necrosis.

6) purulent melting

This is the purulent melting of infarcts during sepsis.

Disorders of metabolism and tissue nutrition are expressed by both functional and morphological changes.

Basically, quantitative and qualitative changes manifest themselves in two main forms: hypobiosis (weakened function and decreased tissue volume) and hyperbiosis (increased function and increased number of tissue elements).

Disruption of tissue nutrition in any part of the body or organ leads to their necrosis.

Necrosis, necrosis- rapid death of cells or cellular elements of a living organism. The death of cells and tissues can occur a short time after a harmful effect, or it may be preceded by their degeneration. In this case, the extinction of metabolic processes and irreversible changes in proteins develop slowly and gradually, therefore such slow cell death is called necrobiosis. The process is considered irreversible, as it turns into tissue necrosis. The gradual transition from a living state to death with dystrophic processes is called parabiosis, the process is considered reversible.

Physiologically, necrosis is not so dangerous, because in the process of life, tissue destruction and reproduction continuously occurs due to the production of substances (necrohormones) by dead tissues that stimulate the formation of new cells and tissues in place of the dead. Necrosis is preceded by periods of dying, weakening and cessation of cell and tissue functions, often due to circulatory disorders.

The sensitivity to necrosis of different tissues varies. Dense tissues (bones, cartilage, tendons, ligaments, fascia) can remain viable even after five hours of complete exsanguination, while the cells of the central nervous system undergo irreversible changes as a result of anemia lasting only a few minutes. Parenchymal organs (kidneys, liver, spleen, testes) are very sensitive. The development of necrosis is facilitated by many pathological conditions of the body: weakness of the cardiovascular system, cachexia, cooling, anemia. Necrosis occurs especially rapidly when an anaerobic infection is added to vascular disorders.

There are several forms of necrosis. Depending on whether tissue proteins are compacted or liquefied, coagulation (dry) and liquefaction (wet) necrosis are distinguished.

Dry necrosis occurs when the process is associated with compaction and drying of tissue as a result of rapid coagulation of the protein of dead tissue. This necrosis most often develops in tissues poor in moisture (bones, fascia, ligaments, tendons). Complete drying of dead tissue is called mummification. A type of dry necrosis is casein (curdled) tissue necrosis, which is characterized by the appearance of crumbling masses. Observed in tuberculosis, syphilis, ischemic infarction of the myocardium, spleen and kidneys, waxy muscle necrosis (typhoid fever).

Wet necrosis is the phenomenon when dead tissue does not dry out, but, on the contrary, becomes saturated with liquid. Under the influence of enzymes, dead tissue softens, swells, disintegrates and turns into a fine-grained emulsion or cloudy liquid mass, which contains a lot of water and does not evaporate.

The process of softening and liquefying tissue under the action of enzymes, but without the access of microorganisms, is called maceration.

Wet necrosis develops in tissues rich in moisture (the brain, where, as a result of liquefaction of necrotic masses, a cavity is formed - a cyst).

There are direct and indirect causes of necrosis.

Direct causes include: mechanical damage to tissue (compression, bruises, impacts, ruptures, wounds, pinching, crushing of cells and tissues);

Indirect reasons include:

• circulatory disorders with impaired tissue nutrition (thromboembolism);
• trophoneurotic disorders leading to the cessation of metabolic processes in the cell.

Necrosis is observed in many pathological processes (inflammation, tumors, wounds, ulcers, fistulas). The development of necrosis is facilitated by weakened cardiovascular activity, cachexia, hypothermia, blood loss, and penetration of pathogenic microorganisms into tissues.

Necrosis of traumatic origin occurs due to tissue destruction under the influence of mechanical force or as a result of severe disturbances in the circulatory system as a whole.

Necrotic tissue undergoes a number of changes: protoplasm loosens and vacuolates, the cell decreases in volume; the core dissolves, shrinks and ruptures; Changes are also noted in the interstitial tissue.

The outcome of necrosis occurs in several stages:

1. stage of organization, connective tissue grows at the site of necrosis, replacing dead tissue, forming a scar;
2. encapsulation stage - the dried necrotic mass is overgrown with connective tissue (encapsulated);
3. petrification stage - petrification (calcification) of the necrotic focus;
4. sequestration - rejection of a dead area from living tissue. Sequesters can remain at the site of inflammation for a long time, being a source of prolonged suppuration.

A special form of manifestation of necrosis is gangrene. Gangrene is a progressive type of necrosis of tissues and organs with their subsequent change under the influence of the external environment. The skin, subcutaneous tissue, mucous membranes, limbs, respiratory, digestive and genitourinary systems are most often affected. Unlike necrosis, with gangrene the tissues acquire the brown-gray, gray-green or black color of burnt tissue. This is due to the breakdown of hemoglobin with the formation of blood pigments (sulfmethemoglobin) and their conversion into iron sulfide. Gangrenous areas of the body do not have defined boundaries.

According to the clinical course, dry, wet and gas gangrene are distinguished.

Dry gangrene is a coagulation (dry) necrosis followed by tissue drying due to the release of moisture into the environment. It develops slowly and usually occurs without symptoms of intoxication, since microorganisms develop poorly in dry tissues, there is almost no decay of dead tissue, so absorption of toxic products does not occur. Dry gangrene is observed in the area of ​​the ears, withers, limbs, tail, comb and earrings in birds. The general condition of sick animals with dry gangrene changes little.

Wet gangrene- this is liquefaction (wet) necrosis, complicated by putrefactive decomposition of tissues under the influence of microorganisms, often anaerobic, causing rotting of necrotic masses and accompanied by a fetid odor. This type of necrosis is typical for internal organs (lungs, intestines) containing large amounts of fluid. The general condition of the animals is severe, depressed, and is accompanied by a sharp increase in body temperature.

Gas (anaerobic) gangrene occurs during injuries and other wounds with great destruction of muscles and even crushing of bones under the influence of certain anaerobic microorganisms that form gases in the process of vital activity. Gas gangrene develops very quickly and is complicated by sepsis, leading to death.

In all cases of necrosis, surgical intervention (removal of dead tissue) is necessary. General and local treatment is used.

General treatment is aimed at maintaining the body as a whole and combating intoxication. The treatment is complex. Antibiotics, cardiac drugs, blood transfusions, and the administration of large amounts of fluid in various ways are prescribed.

Local treatment is aimed at removing dead tissue. With dry necrosis, it is better to wait for the appearance of a clearly defined border in areas of spontaneous rejection. It is recommended to use drying antiseptic agents (3-5% alcohol solutions of pyoctanin, iodine, zinc ointment, etc.) followed by the use of a protective bandage.

In case of wet necrosis, surgical intervention is necessary without delay. The remaining defects after tissue excision are treated as wounds that heal by secondary intention.

Prevention comes down to eliminating injuries, timely detection and treatment of mechanical damage, feeding good-quality feed, increasing the body’s resistance to pathogenic factors through proper feeding, compliance with the rules of animal hygiene, operation and care of animals.

Ulcer- a process that occurs in a chronic form in the skin or mucous membranes and leads them to a defect, accompanied by the breakdown of cellular elements and the development of pathological regulations that do not have a tendency to heal. Ulcers are also called wound surfaces on which developing granulations undergo disintegration, but scarring and epidermization do not occur, which leads to prolonged healing. Sometimes healing does not occur at all, that is, in the wound, degenerative processes prevail over regenerative ones, and the frame turns into an ulcer.

Ulcers can be caused by prolonged mechanical damage (pressure, stretching, friction); chemical or temperature irritations; the presence of foreign bodies (glass, pieces of wood, brick, gunshot fragments) and dead tissue in the wound; disorders of blood and lymph circulation of tissues in the wound area (compression of blood vessels by tumors, edema, growing tissues, thromboembolism); development of purulent or specific (actinomycosis, botryomycosis) infection; trophic disorders due to dysfunction of the nervous system; disorders of the endocrine system and metabolism; decreased reactivity of the body due to cachexia, poor feeding, maintenance and exploitation of animals; excessive blood loss; vitamin deficiencies.

In the pathogenesis of peptic ulcer disease, the leading role belongs to the cerebral cortex, which regulates tissue trophism.

The ulcer can be round, oval and various irregular shapes; may have small and large defects (with burns); secretes serous, purulent or putrefactive exudate. All five local signs of inflammation may be present around the ulcer (swelling, edema, tenderness, impaired skin function - skin sclerosis, or multiple scars).

According to the nature of the growth of granulations, several types of ulcers are distinguished: simple, edematous, inflamed, callous, fungal, gangrenous, decubital, neurotrophic.

Simple ulcer characterized by gradual and very slow healing, the predominance of regenerative processes over processes of tissue decay. Granulation in this type of ulcer has a pink-red color, a small amount of purulent exudate is released, which dries out and forms crusts; swelling and tenderness of the tissues are practically absent. Healing occurs with the formation of a scar.

Edema ulcer develops from blood stagnation due to compression of the veins and weakening of cardiac activity in animals. The ulcers are swollen and cannot heal. The granulation tissue is pale, flabby, and easily destroyed when touched.

Inflamed ulcer is a consequence of the development of infection. The tissue around the ulcer is swollen, painful, with burgundy-red granulations and the presence of a purulent infiltrate.

Callous (callous) ulcer cannot be healed; granulation tissue is pale pink, with thickened edges (made of dense calloused connective tissue); there is no growth of granulations; sensitivity is slightly expressed.

Fungal ulcer occurs on the extremities, its appearance is promoted by frequent irritations of granulation tissue (bruises, movements of muscles, tendons, bandages and microbial contamination of tissue defects). The formation of granulations occurs faster than their disintegration. It is filled with uneven, lumpy granulations that protrude beyond the edges of the skin and resemble a mushroom or cauliflower in appearance. The surface is covered with mucopurulent exudate. The skin and subcutaneous tissue around the circumference are swollen and painful. There is no regeneration of the skin epithelium.

Gangrenous ulcer occurs with wet gangrene, severe frostbite, sepsis, anaerobic infection. The surface of the ulcer is covered with grayish-white disintegrating tissue, has a foul odor, and there is no granulation tissue. The ulcer forms very quickly and is accompanied by progressive tissue necrosis.

Decubital ulcer (bedsore)- this is gangrene of the skin in places of bone tubercles and protrusions. It is caused by impaired blood circulation in these areas due to pressure on them. A bedsore can clinically occur in the form of dry and wet gangrene (extensive ulcerative surfaces with streaks of pus are formed).

Neurotrophic ulcer develops with diseases of the central nervous system (tumors, myelitis), tissue nutritional disorders, inflammation, mechanical damage to peripheral nerves. The skin is dry, thinned, and painless. The ulcer does not heal for a long time and often spreads over the surface and deep into the tissue.

Treatment depends on the causes of the ulcer, so it is necessary to eliminate the root cause that resulted in the underlying disease. Treatment can be general and local.

General treatment includes the use of novocaine blockades, antibiotics, tissue therapy according to Filatov, and blood transfusions.

Various antiseptics are used locally in the form of ointments (Vishnevsky, ichthyol, zinc, penicillin, xeroform) and powders (xeroform, iodoform). In case of sluggish granulation, irritants (iodine solution, turpentine, camphor and ichthyol ointments), ultraviolet light, fortified preparations (fish oil, rose hip extract), and autohemotherapy are used. Fungal granulations are cauterized with perhydrol or a strong solution of potassium permanganate, and then a pressure bandage is applied. For neurotrophic ulcers, pathogenetic and stimulating therapy is used (tissue therapy, autohemotherapy, novocaine blockade).

Prevention is aimed at increasing the general protective properties of the body, eliminating injuries (especially wounds), burns, frostbite, timely treatment of wounds and removing dead tissue, foreign bodies, and pus from them.

Fistula is a narrow pathological canal with a small outlet through which exudate is released, connecting the natural anatomical cavity (thoracic, abdominal, articular) or pathological (dead tissue, foreign bodies, purulent cavities) with the surface of the animal’s body (external environment).

Fistulas can be the result of an inflammatory process when pus or a foreign body is retained in the tissue that supports inflammation (purulent fistula), accidental injury (secretory fistula) or surgical intervention when fistulas are applied deliberately (urinary, excretory fistula).

Secretory and excretory fistulas classified as acquired, arising from penetrating wounds of the ducts and the secretory organ itself (fistulas of the salivary gland and its duct, ducts and cistern of the mammary gland). These fistulas are first covered with granulation tissue and then epithelialized.

Purulent fistula- this is a tubular channel that opens at one end on the skin (mucous membrane), and the other goes deep into the tissue, into the cavity where the foreign body is located (pieces of glass, brick, pieces of wood, fragments of firearms, tampons; dead tissue lingering in the depths wounds - fragments of ligaments, tendons, bone fragments, pus, necrotic tissue or pathogen). With purulent fistulas, there is a small hole in the skin or mucous membrane from which pus is released if there is a free drainage for it. In old fistulas, the opening is usually retracted inward. The channel can be of various lengths (set by probing) and widths, straight and tortuous along the way.

Congenital fistulas is a malformation of the embryonic development of the body (fistula of the bladder, navel). The drip of such a fistula is lined with a mucous membrane, from which secretions are released (saliva, milk - for secretory ones; urine and excrement - for excretory ones; for purulent ones - purulent exudate).

The main method of treating fistulas is surgery. It comes down mainly to eliminating the foreign body, necrotic tissue, pus and ensuring good drainage in the future. Animals with fistulas located in hard-to-reach places (thoracic, abdominal, pelvic cavities) are culled and killed for meat.

Prevention comes down to systematic monitoring of the condition of wounds, burns, frostbite, and open bone fractures. If foreign bodies are present, it is necessary to remove them and ensure the outflow of wound fluid.

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Fever. Causes of febrile reactions: infectious and non-infectious fevers. Stages of fevers. Forms of fevers depending on the degree of temperature rise and types of temperature curves

Hypothermia: types, stages and mechanisms of development. Adaptive reactions during hypothermia

Typical forms of thermoregulation disorders. Hyperthermia: types, stages and mechanisms of development. Heatstroke. Sunstroke. Adaptive reactions of the body during hyperthermia

Coma: general characteristics. Concepts, types of comatose states, main pathological factors in the development of comatose states

Coma: general mechanisms of development and clinical and morphological manifestations of comatose states, significance for the body

Collapse as a form of acute vascular insufficiency. Causes, development mechanisms and main manifestations. Possible outcomes

Shock: general characteristics, types of shock. Pathogenesis and stages of shock. Clinical and morphological manifestations in shock conditions of various origins

Stress: a general description of stress as a nonspecific reaction of the body to the actions of various extreme factors. Adaptive and damaging meaning of stress

Autoimmunization and autoimmune diseases. Definition of form. Reasons. Outcomes

Characteristics of individual types of allergies. Anaphylactic shock

Immune deficiency: concepts and etiology. Acquired immunodeficiency syndrome. General characteristics, significance for the body

Allergic reactions. Definition of concepts: allergy, allergen, sensitization. Types, stages of development of allergic reactions

Adaptation, compensation. Mechanisms, stages of development of protective-adaptive reactions of the body

Productive inflammation. Basic forms. Reasons. Outcomes

Granulomatous inflammation (acute and chronic): etiology, development mechanisms, clinical and morphological characteristics. Types of granulomas

21. Main signs of inflammation

Exudation. Changes in local blood circulation and their structures. Clinical and morphological manifestations of exudation. Types and composition of exudate

Alteration. Changes in metabolism, physicochemical properties of tissues and their structure in areas of inflammation

The role of inflammation in pathology

Embolism: definition, causes, types, clinical and morphological characteristics

Infarction: definition, clinical and morphological characteristics, complications, outcome

Thrombosis: definition, local and general factors of thrombosis. The meaning and outcomes of thrombosis. Thrombus and its types

Ischemia: definition, causes, clinical and morphological manifestations. Acute and chronic ischemia

Microcirculation disorders: main forms, causes and mechanisms of violation

Venous hyperemia (venous stagnation). Local and general causative factors. Mechanisms of development, clinical and morphological manifestations

Arterial hyperemia: mechanism of development and clinical and morphological manifestations

Circulatory disorders. Types, general characteristics, developmental mechanisms and clinical manifestations, implications for the body

Necrosis as a pathological form of cell death. Causes, pathogenesis and morphogenesis, clinical and morphological characteristics, outcomes

Violation of water metabolism. Hypo- and hyperhydration. Edema. Main pathological factors of edema

Bilirubin metabolism disorder. Jaundice: types, mechanisms of occurrence and clinical and morphological manifestations (Mixed dystrophies)

Mesenchymal dystrophies (protein, fat, carbohydrates)

Parenchymal dystrophies (protein, fat, carbohydrates)

Dystrophy - definition, essence, development mechanisms. Classification

General etiology of the disease. The concept of risk factors. Heredity and pathology

Pathogenesis and morphogenesis of diseases. The concept of “symptoms” and “syndromes”, their clinical significance

The subject and objectives of pathology, its connection with biomedical and clinical disciplines

Necrosis as a pathological form of cell death. Causes, pathogenesis and morphogenesis, clinical and morphological characteristics, outcomes

Necrosis is an irreversible process that is characterized by the death of individual cells, parts of organs and tissues in a living organism.

Causes of necrosis. Factors causing necrosis:

physical(gunshot wound, radiation, electricity, low and high temperatures - frostbite and burns);

toxic(acids, alkalis, salts of heavy metals, enzymes, medications, ethyl alcohol, etc.);

biological(bacteria, viruses, protozoa, etc.);

allergic(endo- and exoantigens, for example, fibrinoid necrosis in infectious-allergic and autoimmune diseases, Arthus phenomenon);

vascular(infarction - vascular necrosis);

trophoneurotic(bedsores, non-healing ulcers).

Depending on mechanism of action pathogenic factors are distinguished:

direct necrosis caused by the direct action of a factor (traumatic, toxic and biological necrosis);

indirect necrosis, arising indirectly through the vascular and neuroendocrine systems (allergic, vascular and trophoneurotic necrosis).

Etiological types of necrosis:

traumatic- occurs under the influence of physical and chemical factors;

toxic- occurs under the influence of toxins of bacterial and other nature;

trophoneurotic- associated with impaired microcirculation and tissue innervation;

allergic- develops during immunopathological reactions;

vascular- associated with impaired blood supply to an organ or tissue.

Pathogenesis of necrosis.

Of the variety of pathogenetic pathways of necrosis, five most significant can probably be identified:

binding of cellular proteins to ubiquitin(a small conserved protein that attaches to proteins in eukaryotes);

ATP deficiency;

generation of reactive oxygen species;

disturbance of calcium homeostasis;

loss of selective permeability of cell membranes.

Morphogenesis of necrosis.

The necrotic process goes through a number of morphogenetic stages: paranecrosis, necrobiosis, cell death, autolysis.

Paranecrosis- similar to necrotic, but reversible changes.

Necrobiosis- irreversible dystrophic changes, characterized by a predominance of catabolic reactions over anabolic ones. [ Anabolism(from the Greek anabolē - rise), a set of chemical processes that make up one of the aspects of metabolism in the body, aimed at the formation of the constituent parts of cells and tissues. Catabolism(from the Greek καταβολη, “base, base”) or energy metabolism is the process of metabolic breakdown, decomposition into simpler substances (differentiation) or oxidation of any substance, usually occurring with the release of energy in the form of heat and in the form of ATP.].

Autolysis- decomposition of dead substrate under the action of hydrolytic enzymes of dead cells and cells of the inflammatory infiltrate

Morphological signs of necrosis.

Necrosis is preceded by a period of necrobiosis, the morphological substrate of which is dystrophic changes. (dystrophy → necrosis).

Clinical and morphological forms of necrosis

Necrosis is manifested by various clinical and morphological changes. The differences depend on the structural and functional characteristics of organs and tissues, the rate and type of necrosis, as well as the causes of its occurrence and development conditions. Among the clinical and morphological forms of necrosis there are coagulation(dry) necrosis and colliquation(wet) necrosis.

Coagulative necrosis usually occurs in organs rich in proteins and poor in fluids, for example, in the kidneys, myocardium, adrenal glands, spleen, usually as a result of insufficient blood circulation and anoxia (lack of oxygen), the action of physical, chemical and other damaging factors, for example, coagulative necrosis of liver cells during viral damage or under the influence of toxic agents of bacterial and non-bacterial origin.

(The mechanism of coagulative necrosis is not clear enough. Coagulation of cytoplasmic proteins makes them resistant to the action of lysosomal enzymes and, therefore, their liquefaction slows down.)

TO coagulative necrosis include:

1) Heart attack- a type of vascular (ischemic) necrosis of internal organs (except the brain - stroke). This is the most common type of necrosis.

2) Cheesy(curdled) necrosis also develops with tuberculosis, syphilis, leprosy, as well as with lymphogranulomatosis. It is also called specific, since it most often occurs with specific infectious granulomas. In the internal organs, a limited area of ​​dry, crumbly, whitish-yellow tissue is revealed. In syphilitic granulomas, very often such areas are not crumbly, but pasty, reminiscent of Arabian glue. This is a mixed (that is, extra- and intracellular) type of necrosis, in which both parenchyma and stroma (both cells and fibers) die simultaneously. Microscopically, such a section of tissue is structureless, homogeneous, stained pink with hematoxylin and eosin, and clumps of nuclear chromatin (karyorrhexis) are clearly visible.

3) Waxy, or Zenker necrosis (muscle necrosis, most often of the anterior abdominal wall and thigh, in severe infections - typhoid and typhus, cholera);

4) Fibrinoid necrosis is a type of connective tissue necrosis that has already been studied as an outcome of fibrinoid swelling, most often it is observed in allergic and autoimmune diseases (for example, rheumatism, rheumatoid arthritis and systemic lupus erythematosus). Collagen fibers and smooth muscles of the middle lining of blood vessels are most severely damaged. Fibrinoid necrosis of arterioles is observed in malignant hypertension. Fibrinoid necrosis is characterized by loss of normal structure and accumulation of homogeneous, bright pink necrotic material that resembles fibrin microscopically. Note that the term fibrinoid is different from fibrinous, as the latter refers to the accumulation of fibrin, such as during blood clotting or inflammation. Areas of fibrinoid necrosis contain varying amounts of immunoglobulins and complement, albumin, collagen and fibrin breakdown products.

5) Fatty necrosis:

enzymatic fat necrosis (most often occurs in acute pancreatitis and damage to the pancreas);

non-enzymatic fat necrosis (observed in the mammary gland, subcutaneous adipose tissue and in the abdominal cavity).

6) Gangrene(from the Greek gangraina - fire): this is the necrosis of tissues communicating with the external environment and changing under its influence. The term "gangrene" is widely used to designate a clinical and morphological condition in which tissue necrosis is often complicated by a secondary bacterial infection of varying severity or, being in contact with the external environment, undergoes secondary changes. There are dry, wet, gas gangrene and bedsores.

Dry gangrene- This is necrosis of tissues in contact with the external environment, occurring without the participation of microorganisms. Dry gangrene most often occurs on the extremities as a result of ischemic coagulative tissue necrosis.

• atherosclerotic gangrene - gangrene of the limb due to atherosclerosis and thrombosis of its arteries, obliterating endarteritis;

  with frostbite or burns;

  fingers with Raynaud's disease or vibration disease;

  skin for typhus and other infections.

Wet gangrene: develops as a result of a severe bacterial infection superimposed on necrotic tissue changes. Wet gangrene usually develops in tissues rich in moisture. It can occur on the extremities, but more often in internal organs, for example, in the intestines with obstruction of the mesenteric arteries (thrombosis, embolism), in the lungs as a complication of pneumonia (influenza, measles). Children weakened by an infectious disease (usually measles) may develop wet gangrene of the soft tissues of the cheeks and perineum, which is called noma (from the Greek nome - water cancer). As a result of the activity of bacteria, a specific odor arises. The mortality rate is very high.

Gas gangrene: Gas gangrene occurs when a wound becomes infected with anaerobic flora, for example, Clostridium perfringens and other microorganisms of this group. It is characterized by extensive tissue necrosis and the formation of gases as a result of the enzymatic activity of bacteria. The main manifestations are similar to wet gangrene, but with the additional presence of gas in the tissues. Crepitus (crackling phenomenon upon palpation) is a common clinical symptom of gas gangrene. The fatality rate is also very high.

Bedsore(decubitus): as a type of gangrene, bedsores are distinguished - necrosis of superficial areas of the body (skin, soft tissues) subject to compression between the bed and the bone. Therefore, bedsores often appear in the area of ​​the sacrum, spinous processes of the vertebrae, and the greater trochanter of the femur. By its genesis, this is trophoneurotic necrosis, since blood vessels and nerves are compressed, which aggravates tissue trophic disorders in seriously ill patients suffering from cardiovascular, oncological, infectious or nervous diseases.

Liquation (wet) necrosis: Characterized by the melting of dead tissue. It develops in tissues that are relatively poor in proteins and rich in fluid, where there are favorable conditions for hydrolytic processes. Cell lysis occurs as a result of the action of its own enzymes (autolysis). A typical example of wet liquefaction necrosis is a focus of gray softening (ischemic infarction) of the brain.

Outcomes of necrosis are mainly associated with the processes of delimitation and reparation spreading from the zone of demarcation inflammation.

necrotic cells are fragmented and removed with the help of phagocytes (macrophages and leukocytes) and proteolysis by lysosomal enzymes of leukocytes;

organization (scarring) - replacement of necrotic masses with connective tissue;

encapsulation - delimitation of the area of ​​necrosis by a connective tissue capsule;

petrification (calcification) - impregnation of the necrosis area with calcium salts (dystrophic calcification) (if the cells or their remains are not completely destroyed and reabsorbed);

ossification - the appearance of bone tissue necrosis in the area (very rarely, in particular, in Gon's lesions - healed foci of primary tuberculosis);

cyst formation (as a result of liquefaction necrosis);

purulent melting of necrotic masses with the possible development of sepsis.

Unfavorable outcome of necrosis- purulent (septic) melting of the necrosis focus. Sequestration is the formation of a section of dead tissue that does not undergo autolysis, is not replaced by connective tissue, and is freely located among living tissues.

The meaning of necrosis is determined by its essence - “local death” and the exclusion of such zones from function, therefore necrosis of vital organs, especially large sections of them, often leads to death. These are myocardial infarction, ischemic necrosis of the brain, necrosis of the renal cortex, progressive liver necrosis, acute pancreatitis complicated by pancreatic necrosis. Often, tissue necrosis is the cause of severe complications of many diseases (heart rupture with myomalacia, paralysis with hemorrhagic and ischemic strokes, infections with massive bedsores, intoxication due to the impact of tissue decay products on the body, for example, with gangrene of the limb, etc.). Clinical manifestations of necrosis can be very diverse. Abnormal electrical activity occurring in areas of necrosis in the brain or myocardium can lead to epileptic seizures or cardiac arrhythmias. Impaired peristalsis in a necrotic intestine can cause functional (dynamic) intestinal obstruction. Hemorrhages into necrotic tissue are often observed, for example, hemoptysis with necrosis of the lung.

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Necrosis I Necrosis (necrōsis, Greek nekrōsis necrosis)

death of cells and tissues in a living organism, accompanied by irreversible cessation of their functions. N. not only, but also a necessary component of the normal functioning of cells and tissues in the process of physiological regeneration. N. is characterized by certain changes in the cell and intercellular substance. As a result of the activation of hydrolytic enzymes of lysosomes, the cell shrinks, concentrates in it (), then the nucleus breaks up into clumps () and dissolves (). In the cytoplasm of the cell, coagulation of proteins occurs, which is replaced by the disintegration of the cytoplasm (), and then its melting (). N. can capture part of a cell (N.), or the entire cell ().

In the intercellular substance during N. depolymerization of glycosaminoglycans occurs, it is saturated with blood plasma proteins, swells and undergoes lysis. The fibrous structures also swell and become saturated with plasma proteins. Fibrinoid N. develops in collagen fibers, they disintegrate and dissolve. The swollen elastic fibers disintegrate and melt (). Reticular fibers disintegrate later than other fibrous structures, and the remains of cells and intercellular substance undergo phagocytosis.

Some necrotic tissues become flabby and melt (), others thicken and dry out (). With the putrefactive melting of such tissues, an unpleasant appearance appears and their tissue also changes. N.'s areas of internal organs become white-yellow or become saturated with blood, acquiring a dark red color. Dead tissue of organs associated with the external environment, as a result of the interaction of blood pigments impregnating them with air, acquire a dirty brown, black or gray-green color.

Among the complex mechanisms of N., the factors that cause N. and the duration of their action on the tissue, the structural and functional characteristics of the organs that have undergone N., the level of metabolism in them, and the level of metabolism in them are of leading importance. The rate of development of N. depends on the combination of these factors. A distinction is made between direct N., caused by the direct action of a pathogenic factor on cells and tissues, and indirect N., which occurs indirectly through the vascular system. nervous and endocrine systems.

The causes of N. can be exogenous and endogenous influences. Among the exogenous causes are mechanical, high or low temperature, the action of various chemicals, microorganisms, ionizing radiation, etc. Endogenous causes of N. can be disorders of a vascular, trophic, metabolic and allergic nature. Depending on the cause and conditions of development of N., as well as on the structural and functional characteristics of the organ in which it develops, several clinical and morphological forms of N. are distinguished: coagulation (dry), colliquation (wet), gangrene, infarction.

Coagulative N. is based on the processes of protein denaturation with the formation of sparingly soluble compounds. At the same time, the tissues are dehydrated and compacted. This form of N. occurs in tissues rich in proteins and poor in fluid, for example, in the kidneys, spleen, and muscles. Coagulation is curdled (caseous) N. in tuberculosis ( rice. 1 ), leprosy, fibrinoid N. in allergic diseases, etc.

Colliquation N. develops in tissues rich in fluid, for example in the brain. The melting of dead masses in the focus of dry N. is called secondary colliquation.

Gangrene is necrosis of tissues that come into contact with the external environment and thereby acquire a gray-brown or black color.

Sequestrum is an area of ​​necrotic, usually bone, tissue that has not undergone autolysis. Purulent fluid develops around the sequestrum.

A heart attack is one of the types of N., which develops as a result of a sudden circulatory disorder in a part of an organ ( rice. 2 ).

With a favorable outcome of N., necrotic masses occur, or the N. area becomes overgrown with connective tissue and becomes encapsulated. With dry N., calcium salts may be deposited in the dead masses (). Sometimes N. is formed at the site of the outbreak (). Around the foci of colliquation N. is formed, dead masses resolve and appear. Necrotic parts of organs can be rejected ().

N.'s outcome is determined by the functional significance of the dying part of the organ. In some cases, tissue damage does not leave significant consequences, in others it leads to severe complications.

Bibliography: Davydovsky I.V. General human, p. 156, M., 1969; General human pathology, ed. A.I. Strukova et al., p. 116, M., 1982.

Hematoxylin and eosin staining; ×250">

Rice. 1. Microscopic specimen of a tuberculous granuloma with caseous necrosis in the center. Hematoxylin and eosin staining; ×250.

II Necrosis (necrosis; Greek nekrosis necrosis,)

irreversible cessation of vital activity of tissues of a certain part of a living organism.

Allergic necrosis(n. allergica) - N. sensitized tissues when exposed to a specific allergen, for example the Arthus phenomenon.

Wet necrosis(n. humida; N. colliquation) - N., accompanied by softening (lysis) of the affected tissues: observed in tissues rich in fluid.

Waxy necrosis(n. ceroidea; synonym: waxy, vitreous dystrophy, Zenker's necrosis) - dry N. of muscles, in which the lesions have a gray-yellow color with a greasy sheen, i.e. resemble wax; observed in some infectious diseases (abdominal and), injuries, convulsive conditions.

Hemorrhagic necrosis(n. haemorrhagica) - N., accompanied by soaking of the affected tissues with blood.

Fat necrosis(n. adiposa; synonym adiponcrosis) - N. adipose tissue; occurs under the influence of lipolytic enzymes.

Ischemic necrosis(n. ischaemica: sp. N.) - N. caused by insufficiency of local circulation.

Caseous necrosis(n. caseosa) - see Cheesy necrosis .

Coagulation necrosis- see Dry necrosis .

Colliquation necrosis(n. colliquativa: lat. colliquesco to liquefy) - see Wet necrosis .

Necrosis of the renal cortex, bilateral(n. corticis renurn bilateralis) - see Cortical kidney necrosis .

Necrosis of the renal cortex, symmetrical(n. corticis renum symmetrica) - see Cortical kidney necrosis .

Aseptic bone necrosis(osteonecrosis aseptica; synonym: avascular, osteonecrosis) - ischemic N. of the bone area: develops more often in the epiphyses of tubular bones.

Acute radiation necrosis(n. radialis acuta) - N. l., occurring several weeks after irradiation.

Late radiation necrosis- N. l., arising many years after irradiation.

Early radiation necrosis- N. l., occurring several months after irradiation.

Marantic necrosis(n. marantica; Greek marantikos fading, weak) - N. tissues subject to pressure; in debilitated patients leads to the development of bedsores.

Neurogenic necrosis(n. neurogena) - see Neurotic necrosis .

Neurotic necrosis(n. neurotica: synonym N. neurogenic) - N. caused by a violation of nervous trophism; observed in some diseases of the nervous system.

Necrosis indirect(n. indirecta) - N., not associated with the direct effect of a damaging factor on.

Necrosis of the kidneys, cortical(n. renum corticalis; synonym: N. renal cortex, N. renal cortex symmetrical) - bilateral N. renal cortex with preservation of the intermediary zone and pyramids; manifests itself as acute renal failure; observed, for example, in severe shock.

Medullary necrosis of the kidney(n. renis medullaris; syn.) - N. renal pyramid; develops as one of the complications of purulent pyelonephritis.

Direct necrosis(n. directa) - N., caused by the direct effect of a damaging factor on the tissue.

Dry necrosis(n. sicca; synonym: coagulation, N. coagulation) - N., characterized by dehydration of tissue with denaturation and coagulation of tissue proteins.

Cheesy necrosis(n. caseosa; synonym: N. caseous) - dry N. with the formation of protein denaturation products that are not subject to hydrolysis for a long time and look like cottage cheese.

Traumatic necrosis secondary(n. traumatica secundaria) - N, damaged tissues, caused by the development of inflammatory, vascular and other secondary changes in them.

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Necrosis is a pathological condition characterized by the cessation of cell activity in soft tissues under the influence of pathogens. This pathology is often considered critical, requiring full treatment in a hospital setting. But before starting treatment for soft tissue necrosis, doctors examine the patient and identify the specific type of disease and the cause of its development.

Classification of necrosis

There are two forms of necrosis:

1. Dry, or coagulative. It will be characterized by protein coagulation and its transformation into a mass identical to cottage cheese. The skin at the site of dry necrosis will have a gray-yellow tint and a clear boundary of the pathological process. With coagulation necrosis, in the place where the dead tissue is rejected, an ulcer forms, turning into an abscess. After opening the purulent abscess, a fistula is formed. The initial stage of the pathology is characterized by high body temperature and disruption of the affected organ. For example, signs of acute kidney necrosis include a violation of the outflow of urine, and in some cases a complete cessation of this process.
2. Wet, or colliquation. Its main symptoms are active “swelling” of soft tissues, their liquefaction in places of complete necrosis, and the formation of a putrefactive substrate. All this is accompanied by a pronounced smell of rotten meat, and it is impossible to get rid of it, even if all medical measures are taken. Most often, this form of pathology develops in tissues rich in fluids (skin, brain, and so on). The rapid development of pathology can lead to complications - the consequences of brain necrosis often include loss of memory and basic skills.

Separately, doctors consider sequestration - this is a form of necrosis inherent in bone tissue. This can happen with progressive osteomyelitis (inflammation of bone tissue). In this case, any symptoms of cell death will be absent until a purulent abscess appears. After its breakthrough, a fistula with purulent discharge is formed.

When diagnosing, in addition to the forms, types of necrosis are also distinguished:

1. A heart attack is diagnosed when the blood supply to a specific area of ​​an internal organ suddenly stops. For example, myocardial necrosis during cardiac infarction or similar damage to the soft tissue of the brain may be detected.
2. Gangrene is a condition that develops after rapid necrosis and is characterized by necrosis of the skin, muscle tissue and mucous membranes. The causes of necrosis of the skin area around the wound can be very different (from improper treatment of the wound surface to its infection), but gangrene of a specific area begins precisely as a consequence of the condition in question.
3. Bedsores - occur only in bedridden patients who are not properly cared for.
4. Avascular or aseptic. This classification applies only to necrosis of the femoral head. Most often it is diagnosed due to injury to this part of the musculoskeletal system or against the background of blockage of small arteries by a blood clot. Aseptic necrosis of the femoral head is characterized by rapid development - its first signs (severe pain in the problem area, inability to move independently) are intensely expressed already on the third day of the pathology.
5. Fibrinoid. Necrotic changes will be characterized by impregnation of pathologically altered tissues with fibrin. Often this type of disease is diagnosed in the walls of blood vessels, and its predecessor can be long-term atherosclerosis.

Treatment of necrosis

The disease in question can be successfully treated, but only if it is carried out in a medical institution and under constant monitoring by doctors. General principles of therapy:

1. Necrosis of the teeth, jaw or gums is diagnosed quickly enough, because it is accompanied by severe pain and an extremely unpleasant odor from the oral cavity. Patients, as a rule, immediately seek medical help and therefore treatment consists of prescribing medications - antibacterial drugs, disinfectants. In some cases, dentists have to surgically remove already necrotic areas of soft tissue.
2. Necrosis of tissues of internal organs is often diagnosed already in the extreme stages. For example, the symptoms of pancreatic necrosis are often blurred. Even when visiting a doctor, the patient is often given an incorrect diagnosis, which can lead to the death of a large number of cells in the internal organ. Typically, pancreatic necrosis is treated surgically, but the prognosis in this case can be very different - from favorable (full recovery) to imminent death.
3. Bone death almost always requires surgery. Surgery for necrosis of the hip joint, for example, involves removing the problem area and using an endoprosthesis. With timely diagnosis, such treatment always has a favorable prognosis.
4. The stages of liver necrosis are the main factor in choosing the method of its treatment. If at the initial stage drug therapy is quite acceptable, then at the moderate and severe stages only surgery is considered.

Consultation on how intestinal necrosis is treated and what the first symptoms of the pathology are can only be obtained from a qualified doctor. You can make an appointment on our website Dobrobut.com.