Necrosis I. Necrosis (Necrōsis, Greek. Nekrōsis Omnation)

omnation of cells and tissues in a living organism, accompanied by an irreversible cessation of their functions. N. Not only, but also the necessary component of the normal vital activity of cells and tissues in the process of physiological regeneration. N. is characterized by certain changes in the cell and the intercellular substance. As a result of activation of hydrolytic enzymes, the cellular is wrinkled, it is concentrated (), then the kernel disintegrates on the boulder () and dissolves (). In the cytoplasm of cells, coagulation of proteins occurs, which is replaced by the decay of the cytoplasm (), and then with its melting (). N. can capture a part of the cell (N.), or the entire cell ().

In the intercellular substance at N., the depolymerization of glycosaminoglycans occurs, it is impregnated with blood plasma proteins swelling and exposed to lysis. Fibrous structures also swell and soaked with plasma proteins. Fibrinoid N. develops in collagen fibers, they disintegrate and dissolve. Nobuch elastic fibers disintegrate and melted (). Reticular fibers decompose later than other fibrous structures, and the residues of cells and the intercellular substance are subjected to phagocytosis.

Some obstructed tissues become flabbles and melted (), others are compacted and dry (). With a rotten melting of such tissues, it appears unpleasant, changes them. Plots N. internal organs become white-yellow or soaked in blood, acquiring dark red. Deaded fabrics of organs associated with the external environment, as a result of the interaction of the impregnation of their blood pigments with air acquire a dirty-brown, black or gray-green color.

Among complex mechanisms N. The leading importance is of proving N. factors and the duration of their action on tissue, structural and functional features of organs subjected to N., the level of metabolism in them as well. From the combination of these factors, the rate of development N. is distinguished by direct N., due to the direct effect of the pathogenic factor on cells and tissues, and N. Indirect, arising indirectly through the vascular. nervous and endocrine systems.

The causes of N. can be exogenous and endogenous effects. Among exogenous reasons are a mechanical, high or low temperature, the effect of various chemicals, microorganisms, ionizing radiation, etc. endogenic causes of N. may be violations of 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 body in which it develops, several clinical and morphological forms N.: Coagulative (dry), collique (wet), gangrene, heart attack.

At the heart of Coagulant N. Lead protein denaturation processes to form labor-soluble compounds. In this case, the tissues are dehydrated and compacted. This form of N. occurs in tissues rich in proteins and poor liquid, for example in kidneys, spleen, muscles. Coagulation is a curly (caseous) N. with tuberculosis ( fig. one ), lepreing, fibrinoid N. with allergic diseases, etc.

Commissioning N. develops in tissues rich in liquid, for example in the brain. The melting of dead masses in the area of \u200b\u200bdry N. is called secondary kolinkivation.

Gangrena - tissue necrosis in contact with the external environment and acquiring gray-brown or black color.

Sequestration - a plot of necrotized, usually bone, fabric, not subject to autolysis. Around the sequestration is a purulent.

The heart attack is one of N. species, which develops as a result of a sudden circulatory disorder in part of the body ( fig. 2. ).

With a favorable outcome of N., necrotized masses either section of N. occurs with a connective tissue and encapsulated. During dry N., calcium salts () can be postponed in dead mass. Sometimes on the site of the hearth N. is formed (). Around the foci of the Kolkivational N. is formed, the dead masses are dissolved and arises. Uncrolized parts of the organs can turn back ().

The outcome of N. is determined by the functional value of the fracturing part of the organ. In some cases, N. Tissue does not leave significant consequences, in others leads to severe complications.

Bibliography: Davydovsky I.V. General man, p. 156, M., 1969; General pathology of man, ed. A.I. Storm et al., P. 116, M., 1982.

Coloring hematoxylin and eosin; × 250 "\u003e

Fig. 1. Tuberculosis granuloma micro-casic necrosis in the center. Coloring hematoxylin and eosin; × 250.

II. Necrosis (Necrosis; Greek. Nekrosis Omnation,)

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

Necrosis allergic (N. Allergica) - N. Sensitized tissues when exposed to a specific allergen, such as the phenomenon of Artus.

Necrosis wet (N. Humida;. N. Kriblevational) - N., accompanied by softening (lysis) of affected tissues: is observed in liquid rich tissues.

Nurses waxy (N. Ceroidea; Sin.: Sky-shaped, dystrophy of vitreous, core necrosis) - Dry N. muscles, in which foci have gray-yellow color with greasy gloss, i.e. have resemblance to wax; It is observed in some infectious diseases (abdominal and), injuries, convulsive states.

Hemorrhagic necrosis (N. HaemorRhagica) - N., accompanied by impregnation of infectious blood.

Necrosis fat (n. Adiposa; Sin. Adiponskosis) - N. fatty fiber; It occurs under the influence of lipolytic enzymes.

Necrosis ischemic (N. Ischaemica: Sleep. N.) - N., due to the deficiency of local blood circulation.

Casomic necrosis (n. Caseosa) - see Nursing Curly .

Necrosis coagulative - See Necrosis Dry .

Non-necrosis (N. Colliquativa: lat. Colliquesco diluted) - see Net Crims .

Necrosis kidney bilateral (n. Corticis Renurn Bilateralis) - see kidneys cortical necrosis .

Multician kidney crust symmetrical (n. Corticis Renum Symmetrica) - see kidneys cortical necrosis .

Necrosis dice aseptic (Osteonecrosis Aseptica; Sin: Avascular, OsteEnecosis) - Ischemic N. Site of Bone: develops more often in tubular bone epiphyuses.

Necrosis radial sharp (N. Radialis Acuta) - N. L., Arising in a few weeks after irradiation.

Necrosis radius Late - N. L., Arising many years after irradiation.

Nursing radius Early - N. L., Arising a few months after irradiation.

Marametic necrosis (N. Marantica; Greek. Marantikos fading, intimid) - N. Pressure tissues; In exhausted patients, it leads to the development of bedtime.

Neurogenic neurogenic (n. neurogene) - see neurotic neurotic .

Neurotic neurotic (N. NeuroTica: Sin. N. Neurogenic) - N., due to disruption of nervous trophic; observed in certain diseases nervous system.

Necrosis indirect (N. Indirecta) - N., not associated with the immediate action of the damaging factor on.

Cortical kidney necrosis (No. manifests itself acute renal failure; Observed, for example, with severe shock.

Multician kidney necrosis (n. Renis Medullaris; Sin.) - N. Renal Pyramid; Developed as one of the complications of purulent pyelonephritis.

Necrosis are direct (N. Directa) - N., due to the immediate effect of the damaging factor on the fabric.

Necrosis is dry (N. SICCA; SIN: Coagulation, N. Coagulative) - N., characterized by dehydration of tissue with denaturation and coagulation of tissue proteins.

Curly crumbs (n. Caseosa; Sin.:, N. Kazometric) - Dry N. with the formation of protein denaturation products, non-subjected to hydrolysis and externally resembling cottage cheese.

Necrosis traumatic secondary (N. Traumatica Secundaria) - H, damaged tissues caused by the development of inflammatory, vascular and other secondary changes.

The disease under consideration is a pathological process, during which living cells in the body cease their existence, their absolute death occurs. There are 4 stages of necrosis, each of which is represented by certain symptoms, is fraught with a number of consequences.

Causes and symptoms of necrosis

R the affected disease may occur under the influence of external (high / low temperatures, toxins, mechanical impact), internal (hypersensitivity of the body, defects in metabolism) factors.

Some types of necrosis (Allergic) There are quite rare, other (vascular) are very common among the population.

A common time for all types of this pathology is its danger to health, human life when Ignoring treatment.

Traumatic necrosis

The specified type of necrosis may occur due to several factors:

• Physical.

This includes injury as a result of impact, fall. Traumatic necrosis May develop during electrician. The effect of temperatures (high / low) into human skin can serve as the cause of burns / frostbite in the future.

The affected skin area is changing in color (pale yellow), elasticity (compacted) becomes insensitive to mechanical effects. After a certain time, an emergency appears in the wound zone, vessel thrombosis.

With extensive damage, the patient is strongly rising, the body weight decreases sharply (due to vomiting, the loss of appetite).

• Chemical.

Empting of the cell cells takes place on the background of radioactive radiation.

Toxic necrosis

The viewed view of necrosis can develop under the influence of toxins of various origin:

• Bacterial character.

Often, necrosis of this kind is diagnosed in patients with leprosy, syphilis, diphtheria.

• Nebaster nature.
• Impact of chemical compounds.

Alkali, medicines, acids are calculated here.
Depending on the location of the lesion focus, the symptoms of toxic necrosis will be varied. The general manifestations of the considered type of necrosis include: general weakness, temperature rise, cough, weight loss.

Trophophonewurotic necrosis

This pathology occurs as a consequence of failures in the work of the central nervous system, which affects the quality of the supply of body tissues by nerves.
The defective "cooperation" of the CNS, the peripheral nervous system with the body provokes dystrophic changes in the tissues, organs, which leads to necrosis.

An example of the specified type of necrosis is the breakdown. The frequent causes of the occurrence of the arms are served regular / excessive transmission of the skin with tight bandages, corsets, plaster.

• In the first stage of the formation of standard-headed necrosis, the skin color changes on pale yellow, pain sensations No.
• After a certain period, small bubbles filled with liquid appear on the affected place. The skin under the bubbles becomes bright red. In the absence of treatment, the surface of the skin takes place in the future.

Allergic necrosis

This kind of illness suffer from patients whose organism is hypersensitive to microparticles, which provoke an allergic reaction.
An example of such irritants are protein, polypeptide injections. From the sickness, there are complaints about the swelling of the skin in those places where injection, itching, pain, pain is perfect.
When ignoring the symptoms described, the pain increases, the body temperature is increased. The viewed view of necrosis is often often against the background of infectious-allergic, autoimmune diseases.

Vascular necrosis - heart attack

One of the most common varieties of necrosis. It appears due to a failure / termination of blood circulation in the arteries. The cause of the specified phenomenon is the blockage of vessels of blood vessels with blood closures, embols, spasm of vessel walls. The defective supply of tissue with blood leads to their death.
The location of the localization of necrosis can be kidneys, lungs, brain, heart, intestines, some other organs.
According to the parameters of damage, the total, subtotal infarction, microinfarct is distinguished. Depending on the size of vascular necrosis, location sites, the presence / absence of concomitant diseases, the overall health status of the patient symptomatology, the outcome of this ailment will differ.

Microscopic signs of necrosis

The disease under consideration within the framework of laboratory studies will manifest itself in the form of changes in the parenchyma, stroma.

Change the kernel when necrosis

The core of the pathological cells undergo several stages of change, which follows one after another:

• Caryopicosis.

The parameters of the nucleus are reduced, chromatin compresses inside it. If necrosis is developing rapidly, the specified stage of deformation of the nucleus may be absent. Changes begin immediately from the second stage.

• Kariorexis.

The kernel disintegrates into several fragments.

• Caryolysis.

Total dissolution of the kernel.

Change of cytoplasm with necrosis

Cell cytoplasm, with pathological phenomena, which occurs due to necrosis, has several stages of development:

• Coagulation protein.

All structures of the damaged cell perish. In some cases, the changes affect the cell partly. If the devastating phenomena covers the entire cage, there is a coagulation of cytoplasm.

• Plasmorexis.

The integrity of the cytoplasm is broken: it is disassembled into several boulders.

• Plasmolysis.

The cytoplasm is completely melted (cytolysis), partly (focal necrosis). With a partial melting of cells in the future it is possible to restore it

Changing the intercellular substance with necrosis

Changes in the specified cell component cover several structures:

• Intermediate substance.

Under the influence of blood plasma proteins, this substance is deformed: swells, melts.

• Collagen fibers.

On the initial stage Destruction changes their shape (swelling), disintegrate into fragments, in the future - melted.

• Nervous fibers.

The algorithm of changes is similar to what is happening in the destruction of collagen fibers.

Clinico-morphological forms of necrosis

Depending on the location of the pathology under consideration, the severity of its flow, possible consequences for the patient, several forms of necrosis are distinguished.

Coagulative or dry necrosis

With this form of the considered illness, dead tissues are gradually dried, decreasing in volume. A clear boundary is formed, which divides pathological tissues from healthy. In the specified border, inflammatory phenomena are noted.
Dry necrosis occurs under such conditions:

• Lack of normal blood circulation on a small piece of fabric. Physical properties Such a tissue is changing: it becomes more dense, dry, pale gray.
• The influence of chemical / physical factors on the specified areas.
• The development of pathological phenomena under the form of necrosis is considered. This phenomenon occurs in organs rich in proteins, with limited liquid content. Often, dry necrosis is striking myocardium, adrenal glands, kidneys.
• Lack of infection within the affected area. From the patient, there are no complaints about general malaise, an increase in temperature.

Coagulative necrosis occurs among the patients, with errors in power mode, good protective reaction organism.

Collective or wet necrosis

Endowed with the following signs:

Chickening necrosis develops against the background of the following factors:

• Failures in blood circulation on a certain area. The reason may be thrombosis, embolism, violation of the integrity of the arteries.
• The presence in the pathological site of tissues, in which a considerable percentage of liquid content. Wet necrosis struck muscle tissue, fiber.
• The presence of a patient with additional diseases ( diabetes, rheumatoid arthritis, cancer), which negatively affects the possibilities of the body's protective forces.

Gangrena as a view of necrosis

The considered species of necrosis often takes place after injury, due to the closure of the closure of the blood vessel. The location of the Localization of gangremen can be any internal organ, any tissue: intestines, bronchi, leather, subcutaneous fiber, muscle tissue.
What affects the course of the disease:

• Dry.

It has a number of characteristic features:

1. Deformation of damaged tissue (complete loss of elasticity, elasticity), change its color (dark brown).
2. A clearly pronounced border between a healthy, infected fabric.
3. The absence of any exacerbations. Special complaints from the patient is not observed.
4. Slow rejection of damaged tissue.
5. No infection. In case of pathogenic microorganisms in the infected area, dry gangrene can turn into a wet.

• Wet.

Often diagnosed in people who have a predisposition to the formation of thromboms. Wet gangrene - a consequence of instant blockage of the vessel at which blood circulation is broken / stops. All these phenomena occur against the background of the total infection of damaged tissue.
Signs of the considered type of gangrene:

• Changes in color of the deformed fabric (dirty green).
• The presence of strong unpleasant odor At the site of gangrene.
• The appearance on the modified section of bubbles filled with transparent / reddish liquid.
• Fever.
• Nausea, vomiting, stool violation.

When untimely responding to this type of gangrene, the death of the patient may come from intoxication.

Sequesther as a kind of necrosis

Often it occurs, develops against the background of osteomyelitis. It is almost impossible to get rid of this type of necrosis: antibiotic therapy is ineffective.
There are several species of sequestration:

• Cortical . Pathological phenomenon is localized on the bone surface, in soft tissues. In the presence of fistinous passes, there is an outlet of necrosis outside.
• Domestic. The cavity of the bone marrow canal is the environment where the products of sequestration rejection are coming.
• Penetrating. The location of the localization of the pathological phenomenon is the thickness of the bone. The destructive effect of penetrating sequestrate is subject to soft fabrics, bone marrow channel.
• Total . Destructive processes cover extensive areas, around the bone circumference.

Myocardial infarction or necrosis

The emergence of the considered form of necrosis is associated with a long lack of a complete supply of a certain piece of tissue.
Several forms of myocardial necrosis are isolated:

• Wedge-shaped .

Necrosis, which have the form of a wedge, are often located in the kidneys, spleen, lungs: in those organs where the main branch type is present blood vessels.

• Necrosis of the wrong shape .

These internal organs affect, where mixed / loose type of branching arteries (heart, intestines).
Given the volume of affected areas, myocardial necrosis can be 3 species:

• Subtotal . Separate influence of the internal organ zones are exposed.
• Total . The entire body is involved in the pathological process.
• Microsophartic . On the scale of damage can be judged only by means of a microscope.

The appearance of the lesion with myocardial necrosis causes the presence of the following types of infarction:

• White . The damaged zone has a white-yellow color, which is clearly visualized on a common fabric background. Most often, white heart attack occurs in the spleen, kidneys.
• White with a red wedge . The pathological site has a white-yellow color, with the presence of traces of hemorrhage. Characterized for myocardium.
• Red. The donation zone has a bardal color - the consequence of saturation by blood. The contours of the pathological site are clearly limited. It is characteristic of the lungs, intestines.

It is a pathological process at which tissue death occurs in a living organism. The reason for this is an irreversible process, as a rule, is exogenous or endogenous damage to tissues or cells.

This disease is dangerous for a person, can lead to severe consequences and requires serious medication treatment. When ignoring or late therapy may be dangerous to human life.

Forms, types and stages of necrosis

Depending on changes in the tissues, two necrosis forms:

1. 1 dry or coagulative - appears as a result of dehydration of tissues due to circulatory disorders;
2. 2 wet or collective - the defeat of the muscles and fabrics with obvious signs of swelling is developing very quickly;

Views:

• heart attack - the death of part of the internal organ;
• sequestration - bone lesion;
• gangrena - necrosis of muscles, mucous or skin;
• prolesidery - ulcers that appear in immobilized people.

Stages:

1. 1 Pararakrosis Quickly succumb to therapy. The first stage should not cause special concern, the main thing is to diagnose the disease on time and contact the doctor;
2. 2 necrobiasis - The second stage in which irreversible processes occur in the tissues and organs. The metabolism is disturbed and the formation of new cells is terminated;
3. 3 at the third stage begins cell death;
4. 4 Autolysis - In the fourth stage, the dead cells are distinguished to toxic enzymes that provoke decomposition of tissues.

Causes of necrosis development

• traumatic necrosis can provoke lesion to current, burns, frostbite, radioactive radiation and tissue injury as a result of impact;
• toxic necrosis It may be bacterial origin, it appears during diphtheria, syphilis, leprosy. This type of necrosis can cause chemical compounds: The impact of medicines, acids, alkalis and toxins for skin;
• trophophonewurotic necrosis It is formed as a result of a malfunction of the central nervous system, a vivid example of this type of necrosis is the breakdowns that may occur with the systematic transmission of the skin with plaster or tight bandages;
• allergic necrosis Provocate polypeptide protein injections;
• vascular necrosis Arises as a result of blood clogs. As a result, the tissue is deficiently supplied with cloth and die away. This type of necrosis is most common;
• coagulative necrosis Often there are people with impaired power mode. It can also provoke chemical and physical impacts on the skin;
• collective necrosis It may be a consequence of blood circulation failure on a certain area;
• gangrene can damage any fabrics and internal organs, it usually provoke injuries;
• Necrosis joints can cause injuries, bad habits and reception of some medicines;
• sequestrel Forms against the background of osteomyelitis. This type of necrosis is practically not amenable to therapy.

Symptoms of necrosis

With necrosis, fatigue appears after a short walk, convulsions, then form poorly healing ulcers, which are subsequently unkind.

If necrosis struck internal organs, the general well-being deteriorates and the work of the system whose body is amazed.

Traumatic necrosis is manifested by the pallor of the skin, the seal at the site of the defeat, then an ecudate appears in the affected area.

In the toxic necrosis, patients are concerned about weakness, fever, weight loss, cough.

Necrosis of the joints accompany sharp pains that lead to disability.

In case of standard, necrosis appear strands, while the color of the skin becomes light yellow, the patient does not experience pain. After some time, small bubbles filled with liquid are formed on the affected area.

Allergic necrosis is accompanied by a strong itching, swelling, increasing temperature.

Complication with necrosis

With the unfavorable outcome of the necrosis, purulent melting of tissues, which accompanies bleeding, sepsis develops subsequently. Vascular necrosis in the form of a heart attack and stroke often ends with a fatal outcome.

Non-critical lesions of vital internal organs can also lead to patient's death.

With the necrosis of the lower extremities, amputation is possible.

With incorrect therapy of necrosis of the joints, the patient threatens disability.

Prevention of necrosis

Necrosis of cells and tissues is most often developing against the background of bedside and peptic lesions of the skin. Therefore, you need to treat and avoid injury and abrasion, to use enough vitamins, to ensure that there are no diameters, sleep on bedding from natural materials.

If we are talking about a fixed patient, then the bed linen should be changed as often as possible, to make it a light massage, try to diversify the movements of the patient, to delicately clean the skin and process it with special anti-headquarters.

IN preventive purposes It is necessary to treat chronic diseases in time, minimizing the possibility of injury.

Treatment of necrosis in official medicine

The sooner the patient necrosis appeals to the doctor, the fact the therapy will be successful. It is advisable to be treated in a hospital. The doctor prescribes medicines that restore blood circulation on affected areas, antibiotics are also prescribed, the skin is constantly treated with disinfectants.

In some cases, the surgery is resorted to surgical interference. According to life testimony, amputation is carried out.

Useful products when necrosis

An important element complex therapy It is a properly compiled diet that will provide patient with all necessary vitamins, microelements and nutrients and should include:

1. 1 cereals;
2. 2 boiled poultry meat, since it is minimal cholesterol content;
3. 3 high-quality dairy products;
4. 4 greens;
5. 5 sufficient amounts of proteins;
6. 6 blueberries and cranberries - powerful antioxidants;
7. 7 fish - source of fatty acids and phosphorus;
8. 8 Asparagus and lentils who are rich in potassium and fiber;
9. 9 Pumpkin seeds, sesame, flax, as a source of useful cholesterol.

Funds of traditional medicine when necrosis

In necrosis therapy successfully use funds folk Medicine:

• on the affected areas of the skin, apply ointment from a smaller, hated lime and crushed oak bark taken in equal proportions;
• before applying ointments or compress for disinfection, folk healers are recommended to rinse with water with a brown household soap;
• with dry gangrene, a row with a prostrochy;
• good results gives a powder from juniper leaves, applied to the wound;
• regularly applying to ulcers, Cashitz from sorrel can be suspended by gangrene;
• take the sorveless juice;
• apply chilled sprawled millet to the affected areas;
• healing wounds contribute to the compresses of cloves;
• with a stroke, it is useful to drink with propolis and mummia mixed with juice juice;
• daily drink 1 cup of freshly peaked carrot juice;
• check out fresh rye bread, mix the resulting cleaner with salt and apply to ulcers;
• taking warm baths from chestnut fruits brave;
• drinking during the day as tea decoction from young conifer shoots;
• slightly repel the cabbage sheet, smear it with honey and apply to the affected areas;
• in the fight against pancreaticosis, good results use three times a day of blueberries.

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

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

Causes of necrosis. Non-crushing factors:

physical (firearm, radiation, electricity, low and high temperatures - frostbite and burn);

toxic (acids, lumps, salts of heavy metals, enzymes, medications, ethanol and etc.);

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

allergic (endo- and exoantigines, for example, fibrinoid necrosis with infectious-allergic and autoimmune diseases, the phenomenon of Artus);

vascular (infarction - vascular necrosis);

tROFONEEEEEEMTIC (Prolesidery, non-healing ulcers).

Depending on the mechanism of action The pathogenic factor distinguish:

direct necrosisdue to the direct action of the factor (traumatic, toxic and biological necrosis);

indirect necrosisarising indirectly through the vascular and neuro-endocrine systems (allergic, vascular and t-farmetic necrosis).

Etiological types of necrosis:

traumatic - arises under the action of physical and chemical factors;

toxic - arises with the action of toxins of bacterial and other nature;

tROFONEEEEEEMTIC - associated with a violation of microcirculation and innervation of tissues;

allergic - develops with immunopathological reactions;

vascular - associated with a violation of the blood supply to the organ or tissue.

Pathogenesis of necrosis.

Of the variety of pathogenetic paths of necrosis, it is likely possible to distinguish five most significant:

binding of cell proteins with ubiquitin (a small conservative protein, which in eukaryotes joins proteins);

aTP deficiency;

generation of active forms of oxygen;

violation of calcium homeostasis;

loss of cell membranes of electoral permeability.

Morphogenesis of necrosis.

The necrotic process passes a number of morphogenetic stages: parancosis, necrobiosis, cell death, autolysis.

Pararakrosis - similar necrotic but reversible changes.

Necrobiasis - irreversible dystrophic changes, characterized by the predominance of catabolic reactions over anabolic. [ Anabolism (from Greek. Anabolē - rise), a combination of chemical processes that make up one of the parties to the metabolism in the body aimed at the formation of component parts of cells and tissues. Catabolism (from Greek. καταβολη, "base, basis") or energy exchange - the process of metabolic decay, decomposition into simpler substances (differentiation) or oxidation of any substance, usually flowing with the release of energy in the form of heat and in the form of ATP.].

Autolysis - Decomposition of the dead substrate under the action of hydrolytic enzymes of dead cells and inflammatory infiltration cells

Morphological signs of necrosis.

Necrosis is preceded by the period of necrobiosis, the morphological substrate of which are dystrophic changes. (Dystrophy → Necrosis).

Clinico-morphological forms of necrosis

Necrosis is manifested by various clinical and morphological changes. Differences depend on the structural and functional features of organs and tissues, speed and type of necrosis, as well as the causes of its occurrence and conditions of development. Among clinical and morphological forms of necrosis is distinguished coagulative (dry) necrosis and collective (wet) necrosis.

Coagulative necrosis Usually occurs in protein and poor organs, for example, in kidneys, myocardium, adrenal glands, spleen, usually as a result of insufficient blood circulation and anoxia (lack of oxygen), the actions of physical, chemical and other damaging factors, for example, coagulation of liver cells with viral lesion or under the action of toxic agents of bacterial and non-bacterial genesis.

(The mechanism of coagulation necrosis is not clear enough. Coagulation of cytoplasmic proteins makes them resistant to the action of lysosomal enzymes and in connection with this slow down their discharge.)

TO coagulation necrosis Believe:

1) Infarction - A variety of vascular (ischemic) internal organ necrosis (except for the brain - stroke). This is the most common view of necrosis.

2) Cheesy (Curly) necrosis develops with tuberculosis, syphilis, lepreing, as well as in lymphogranulomatosis. It is also called specific, since most often occurs with specific infectious granules. In internal organs A limited piece of fabric dry, crumbling, whitish yellow color is revealed. In syphilitic granules, such sections are not crumbling, and pasty, resemble the Arabian glue. This is mixed (that is, the extra- and intracellular) type of necrosis, in which the parenchyma, and the stromter (and cells, and fibers) are at the same time. Microscopically, such a plot of fabric is unstructured, homogeneous, painted with hematoxylin and eosin in pink color, chromatin chromatin (karyorexis) is clearly visible.

3) Waxy, or core necrosis (muscle necrosis, more often than the front abdominal wall and hips, with heavy infections - abdominal and rapid sites, cholera);

4) Fibrinooid Necrosis is the type of necrosis of the connective tissue, which has already been studied as the outcome of the fibrinoid swelling, is most often observed in allergic and autoimmune diseases (for example, rheumatism, rheumatoid arthritis and systemic red lupus). Collagen fibers and smooth muscles of the middle shell of blood vessels are most strongly damaged. Fibrinoid necrosis arteriol is observed with malignant hypertension. Fibrino-shaped necrosis is characterized by loss of normal structure and accumulation of homogeneous, bright pink necrotic material, which is similar to microscopically on fibrin. Please note that the concept of "fibrinoid" differs from the concept of "fibrinous", since the latter indicates the accumulation of fibrin, for example, when coating blood or when inflammation. Plots of fibrinoid necrosis contain various amounts of immunoglobulins and complement, albumin, collagen decay products and fibrin.

5) Fatty necrosis:

enzyme fat necrosis (most often occurs during acute pancreatitis and pancreatic damage);

necriminal fat necrosis (observed in breast, subcutaneous adipose tissue and in abdominal cavity).

6) Gangrene (from Greek Gangraina - Fire): These are necrosis of tissues communicating with an external environment and changing under its impact. The term "gangrene" is widely used to designate a clinical and morphological condition, in which the tissue necrosis is often complicated by a secondary bacterial infection of varying degrees of severity or, while in contact with the external environment, relevant changes. Different dry, wet, gas gangrene and breakdown.

Dry gangrene - These are necrosis of tissues in contact with the external environment flowing without the participation of microorganisms. Dry gangrene most often occurs on the limbs as a result of ischemic coagulation tissue necrosis.

• atherosclerotic gangrene - gangrene of limbs during atherosclerosis and thrombosis of its arteries, obliterating endarteritis;

  when frostbite or burn;

  fingers with raino disease or vibration disease;

  skin with a rapid tit and other infections.

Wet gangrene: develops as a result of layering on necrotic changes in tissue of a heavy bacterial infection. Wet gangrene is usually developing in moisture tissues. It can occur on the limbs, but more often - in the internal organs, for example, in the intestine in the obstruction of the mesenteric arteries (thrombosis, embolism), in the lungs as a complication of pneumonia (influenza, cortex). At weakened infectious disease (more often measles) Children can develop a wet gangrene of soft tissues, the crotch, which is called Nome (from Greek. Nome - Water Cancer). As a result of the vital activity of bacteria, a specific smell occurs. Very high percentage of mortality.

Gas gangrene: Gas gangrene occurs when infection with the wound 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 the humid gangrene, but with the additional presence of gas in the tissues. Capitation (Perevotka Penominal at Palpation) is a frequent clinical symptom with gas gangrene. The percentage of mortality is also very high.

Proleside (Decubitus): As a type of gangrenes, it is distinguished by the samples of the surface areas of the body (skin, soft tissue), subjected to squeezing between bed and bone. Therefore, the proligests appear more often in the region of the sacrum, the awesome processes of the vertebrae, a large skewer of the femoral bone. According to its genesis, these are standard non-neurosis, as the vessels and nerves are squeezed, which aggravates the tissue trophic disorders in seriously ill, suffering from cardiovascular, oncological, infectious or nervous diseases.

Collective (wet) necrosis: Characterized by melting the dead fabric. It develops in tissues, relatively poor proteins and a rich liquid, where there are favorable conditions for hydrolytic processes. Lisace cells occurs as a result of the action of own enzymes (autolysis). A typical example of a wet conservation necrosis is a hearth softening (ischemic infarction) of the brain.

Outcomes of necrosis Basically associated with the processes of separation and repair, propagating from the zone of demarcation inflammation.

necrotized cells are fragmented and removed using phagocytes (macrophages and leukocytes) and proteolysis by lycocyte enzymes;

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

encapsulation - the accommodation of the necrosis section of the connecting and woven capsule;

petrification (Calcification) - the impregnation of the necrosis section of calcium salts (dystrophic occurrence) (if the cells or their residues are fully destroyed and not reabsorbed);

osification - the appearance in the bone necrosis area (very rarely, in particular, in the foci of Gon - healing the foci of primary tuberculosis);

the formation of cysts (in the outcome of the collicration necrosis);

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

An unfavorable outcome of necrosis - purulent (septic) melting of the lesion. Sequestration is the formation of a portion of the dead fabric, which is not subjected to autolysis, is not replaced by a junction tissue and freely located among the living fabrics.

The value of necrosis It is determined by its essence - "local death" and shutting down from the function of such zones, therefore necrosis of vital organs, especially the major sections of them, often leads to death. Such are myocardial infarction, coronary brain necrosis, kidney cortical necrosis, progressive liver necrosis, acute pancreatitis, complicated by pancreatic. Often, the leaning of the fabric is the cause of heavy complications of many diseases (the discontinuity of the heart in myomalysis, paralysis in hemorrhagic and ischemic strokes, infection during massive proligence, intoxication due to the effect on the body of the tissue decay products, for example, with limb gangrene, etc.). Clinical manifestations Necrosis can be the most diverse. Pathological electrical activity arising in areas of necrosis in the brain or myocardium can lead to epileptic sections or cardiac arrhythmia. Violation of the peristaltics in the necrotic intestine can cause functional (dynamic) intestinal obstruction. Hemorrhage in necrotic fabric, for example, hemoptysis, such as hemoptysis, are observed.

Necrosis (from Greek. nekros. - Dead) - sacrifice, death of cells and tissues in a living organism under the influence of pathogenic factors. This kind of cell death is genetically controlled.

Non-crushing factors:

ü Physical (firearms, radiation, electricity, low and high temperatures - frostbite and burn);

ü Toxic (acid, alkalis, salts of heavy metals, enzymes, drugs, ethyl alcohol, etc.);

ü biological (bacteria, viruses, simplest, etc.);

ü allergic (endo- and exoantigentes, for example, fibrino-shaped necrosis with infectious allergic and autoimmune diseases, the phenomenon of artus);

ü vascular (heart attack - vascular necrosis);

ü TROPHONEEEEEEEEMIC (SPLESSORS, NEW-SUPPLY).

Depending on the mechanism of the pathogenic factor, distinguishes:

• direct necrosis due to the direct action of the factor (traumatic, toxic and biological necrosis);
• indirect necrosis occurring indirectly through the vascular and neuro-endocrine systems (allergic, vascular and tid-componublic necrosis).

Morphological signs of necrosis

Necrosis is preceded by the period of necrobiosis, the morphological substrate of which are dystrophic changes.

Changes in nuclei.

Chromatin of a dead cage condenses into large blocks. The core decreases in volume, becomes wrinkled, dense, intensively basophilic, that is, it is painted in a dark blue color by hematoxylin. This process is called karyopicosis (wrinkling). Picnotic core can then break on numerous small basophil particles (Kariorexis) Or subjected to lysis (dissolution) as a result of the action of lysosomal deoxyribonuclease (Caryolysis). Then it increases in volume, it is weakly colored by hematoxylin, the core contours are gradually lost. With a quickly developing necrosis, the kernel is subject to lysis without a picnotic stage.

Cytoplasmic changes.

• cell cytoplasm becomes homogeneous and pronounced acidophilic as a result of coagulation of cytoplasmic proteins and destruction (disappearance) ribosomes.
• mitochondria swelling and destruction (destruction) Orgell membrane cause cytoplasm vacuolaization.
• the digestion of the cell enzymes, which are released from their own lysosomes, causes cell lysis (autolysis).

Thus, in the cytoplasm there is coagulation of proteins, and transmitted by their collections.

Changes in the intercellular substance Envelop both intermediate substance and fibrous structures. Most often, changes characteristic of fibrinoid necrosis are developing: collagen, elastic and reticuline fibers are converted into dense, homogeneous pink, sometimes basophil masses that may be subject to fragmentation, shackled decay or lysed. It is less likely to observe swelling, lysis and the ease of fibrous structures, which is characteristic of the collicration necrosis.

Clinico-morphological forms of necrosis

Distinguish coagulation (dry) necrosis and collicration (wet) necrosis.

A. Coagulative (dry) necrosis.

Coagulative necrosis usually occurs in protein and poor organs, for example, in kidneys, myocardium, adrenal glands, spleen, usually as a result of insufficient blood circulation and anoxia, actions of physical, chemical and other damaging factors, for example, coagulation of liver cells in viral lesion or under the action of toxic agents of bacterial and non-bacterial genesis. Coagulative necrosis is also called dry, since it is characterized by the fact that the dead plots of dry, dense, crumbling, white or yellow arising during it.

Coagulative necrosis include:

Infarction - A variety of vascular (ischemic) internal organ necrosis (except for the brain). This is the most common view of necrosis.

Heart attack (from lat. infarcire. - Stop, stuff) - this is a dead section of the organ or tissue, off from blood circulation as a result of a sudden cessation of blood flow (ischemia). The heart attack is a variety of vascular (ischemic) coagulative or conservation necrosis. This is the most common view of necrosis.

The necrosis is subjected both parenchymal cells and interstitial tissue. Most often, the heart attack occurs during thrombosis or embolism, spasme, squeezing arterial vessels. A very rarely cause of a heart attack may be a violation of venous outflow.

Causes of infarction development:

• acute ischemia due to long-lasting spasm, thrombosis or embolism, squeezing the artery;
• functional voltage of the organ in conditions of insufficient blood supply. The insufficiency of anastomoses and collaterals, which depends on the degree of damage to the walls of the arteries and the narrowing of their lumen (atherosclerosis, obliterating endarteritic), on the degree of circulatory disorders (for example, venous stagnation) And on the level of shutdown artery thromb or embolomes.

Therefore, heart attacks usually occur with those diseases for which severe changes of the walls of arteries and common circulatory disorders are characterized. It:

• rheumatic diseases;
• heart defects;
• atherosclerosis;
• hypertonic disease;
• bacterial (infectious) endocarditis.

Morphology of heart attacks

Macroscopic picture of heart attacks. Form, value, color and consistency of heart attack can be different.

Infarct form. Usually, heart attacks have a wedge-shaped form. At the same time, the pointed part of the wedge is facing the gate of the body, and the wide part goes to the periphery, for example, under the body capsule, under the peritoneum (spleen infarction), near the pleura (lung infarction), etc. The characteristic form of heart attacks in the kidneys, spleen, lungs is determined by the nature of the angioarchitectonics of these organs - the main (symmetric dichotomous) type of the branching of the arteries. Less often, heart attacks have an irregular form. Such infarction is found in the heart, the brain, the intestines, since it is not a trunk, but a loose or mixed type of branching arteries in these organs.

The magnitude of heart attacks. The heart attack can cover most or the entire organ (subtotal or total infarction) or detected only under a microscope (microinfarct).

Color and consistency of heart attacks. If the heart attack develops by the type of coagulation necrosis, then the leaning fabric is compacted, becomes dry, white and yellow (myocardial infarction, kidney, spleen). If the heart attack is formed by the type of conservation necrosis, then the dead fabric softens and dilutes (the brain infarction or the hearth softening center).

Depending on the mechanism of development and external view distinguish:

• white (ischemic) heart attack;
• red (hemorrhagic) infarction;
• white heart attack with a hemorrhagic wedge.

The white (ischemic) infarction arises as a result of the complete cessation of the inflow of arterial blood in organs, for example, in the heart, kidneys, spleen, the brain above the Willisian circle. Usually it occurs in areas with one blood flow system (the main type of branching arteries), in which collateral blood circulation Developed weakly. Thanks to the unscrewed venous outflow from the stylish tissue, and due to the spasm of the distal section of the arteries after the cessation of blood flow, the paleness of these heart attacks is observed. The white (ischemic) infarction is a plot that is clearly delivered from the surrounding tissues, white and yellow color, unstructured.

White heart attack with a hemorrhagic wedge is represented by a white-yellow area, but this site is surrounded by the hemorrhage zone. It is formed as a result of the fact that the spasm of the vessels along the periphery of the infarction is replaced by their parethic expansion and development of hemorrhages. Such a heart attack may occur in the kidneys, myocardium.

Red (hemorrhagic) infarction is characterized by the fact that the area of \u200b\u200bthe death is impregnated with blood, it is dark red and well deliberate. The heart attack becomes red due to the exit in the zone of blood infarction from necrotized vessels of the microcirculatory bed. For the development of a red infarction, the characteristics of the organ angioarchitectonics are the following and more system of blood flow, the development of collaterals: in the lungs - the presence of anastomoses between bronchial and pulmonary arteries, in the intestine - the abundance of the anastomoses between the branches of the mesenteric arteries, in the brain in the area of \u200b\u200bthe Willisian region of the anastomosis between internal sleepy and branches of Basilar arteries. Red heart attacks can also occur in tissue when dissolving or fragmentation (decay) of the compound thrombus, which resumes arterial blood flow in the infarct zone.

Hemorrhagic heart attack is rarely found in the kidneys and heart. A prerequisite for such hemorrhagic impregnation is venous stagnation.

Venous infarction occurs when occlusion of all venous drainage system fabrics (for example, thrombosis of the upper sagittal sinus, renal vein thrombosis, the thrombosis of the upper mesenteric vein). At the same time, severe swelling, stagnation, hemorrhage and progressive increase in hydrostatic pressure in tissues occur. With a strong increase in hydrostatic pressure, arterial blood influx is difficult in fabric, which leads to ischemia and infarction. Venous heart attacks are always hemorrhagic.

Microscopically, a dead plot is distinguished by loss of structure, cell contours and nuclear disappearance.

Heart (myocardium), brain, intestines, lungs, kidneys, spleen have the greatest clinical significance.

In the heartthe heart attack is usually white with a hemorrhagic wedge, has the wrong shape, it is more common in the left ventricle and the interventricular partition, it is extremely rare - in the right ventricle and atria. The sketch can be localized under the endocardium (sub-endocardial infarction), epicardial (subepicardial infarction), in the thickness of myocardium (intramural) or cover the whole strata of myocardium ( transmural infarction). In the field of infarction on endocardium, thrombotic, and on pericardia - fibrinous overlays, which is associated with the development of reactive inflammation around necrosis areas. Most often, myocardial infarction is found against the background of atherosclerosis and hypertension with the attachment of spasm or arteries thrombosis, being acute form ischemic Disease Hearts.

In the brainabove the Willisye of the circle there is a white heart attack, which quickly softens (the hearth of the gray softening of the brain). If the heart attack is formed against the background of significant circulatory disorders, venous stagnation, the heart of the brain is impregnated with blood and becomes red (the focus of the red softening of the brain). In the region of the brain, the red infarction is also developing below the Willisyev Circle. The heart attack is usually localized in subcortical nodes, destroying the conducting brain paths, which is manifested by paralymps. The brain infarction, as well as myocardial infarction, is most often found against the background of atherosclerosis and hypertension and is one of the manifestations of cerebrovascular diseases.

In the lungsin the overwhelming majority of cases, a hemorrhagic heart attack is formed. The cause is more often a thromboembolism, less frequently, thrombosis when vasculite. The infarct site is well degraded, has a cone form, the base of which is drawn to Plevra. In the pleura in the field of infarction appear fibrin (reactive pleurisy). The island of the cone facing the root of the lung is often detected by thrombus or embol in the lung artery branch. Demacious tissue tight, grain, dark red. Hemorrhagic infarction of the lungs usually arises against the background of venous stagnation, and its development is largely determined by the peculiarities of the lung angioarchitectonics, the presence of anastomoses between the systems of pulmonary and bronchial arteries. In conditions of stagnant full-blood and closure of the lumen of the pulmonary artery branch in the leaf of the lung fabric from the bronchial artery, blood is entered, which breaks the capillaries and is poured into the lumen Alveol. The infarction of pulmonary tissue is often developing around the heart attack (peripartic pneumonia). Massive hemorrhagic lung infarction can be the cause of the admirement jaundice. White infarction in the lungs is an exceptional rarity. It occurs during sclerosis and obliteration of the lumen of bronchial arteries.

In kidneysinfarction, as a rule, white with a hemorrhagic wedge, a cone-shaped section of necrosis covers either a cortical substance, or the whole crowd of parenchyma. When closing the main arterial barrel, a total or subtotal kidney infarction is developing. A kind of kind of heart attacks are symmetric necrosis of the kidney cortical substance, leading to the development of acute renal failure. The development of coronary chemical kidney hearters is usually associated with thromboembolism, less often with thrombosis of the branches of the renal artery in rheumatism, bacterial endocarditis, hypertension, ischemic heart disease. Rarely, trombosis of renal veins arises venous kidney heart attack.

In Selezenkawhite heart attacks are found, often with reactive fibrinous inflammation of the capsule and the subsequent formation of adhesions with a diaphragm, a parietal leaflet of peritoneum, intestinal loops. Ischemic spleen infarctions are associated with thrombosis and embolism. When thrombosis of the spleen vein sometimes, very rarely, venous heart attacks are formed.

In the intestines Hemorrhagic heart attacks and are always subjected to septic decay, which leads to caming of the intestine and the development of peritonitis. The reason, most often, serves a break, invagination of the intestine, strangulated hernialess often - atherosclerosis with the addition of thrombosis.

Casomic (Curly) necrosis It also develops with tuberculosis, syphilis, lepreing, as well as during lymphoganoomatosis. It is also called specific, since most often occurs with specific infectious granulomas. In the internal organs, a dry, crumbling limited area of \u200b\u200bwhite-yellow fabric fabric is revealed. In syphilitic granulomas, very often such sites are not crumbling, and pasty, resemble Arabic glue. This is mixed (that is, the extra- and intracellular) type of necrosis, in which the parenchyma, and the stromter (and cells, and fibers) are at the same time. Microscopically, such a piece of fabric looks like unstructured, homogeneous, painted with hematoxylin and eosin in pink color, the chromatin chromatin (karyorexis) is clearly visible.

Waxy, or core necrosis (muscle necrosis, more often the front abdominal wall and hips, heavy infections - abdominal and rapid sites, cholera);

Fibrinoid necrosis - Type of necrosis of connective tissue. It is observed in allergic and autoimmune diseases (for example, rheumatism, rheumatoid arthritis and systemic red lolly). Collagen fibers and smooth muscles of the middle shell of blood vessels are damaged. Fibrinoid necrosis arteriol is observed with malignant hypertension. This necrosis is characterized by the loss of the normal structure of collagen fibers and the accumulation of homogeneous, bright pink necrotic material, which is similar to microscopically on fibrin.

Fat necrosis.

Enzyme fat necrosis:fat necrosis is most often happening in acute pancreatitis and pancreatic damage, when pancreatic enzymes come out of the ducts to the surrounding tissues. At the same time, opaque, white (like chalk) plaques and nodules (steatonenecosis) appear in adapter fabric surrounding the pancreas.

Need enzyme fat necrosis: Need enzyme fat necrosis is observed in the mammary gland, subcutaneous adipose tissue and in the abdominal cavity. Most patients have an element of injury. Need enzyme fat necrosis causes an inflammatory response characterized by the presence of numerous macrophages with foamy cytoplasm, neutrophils and lymphocytes. Then it follows fibrosis, while this process is difficult to distinguish from the tumor.

Gangrene (from Greek. gangraina. - Fire): These are necrosis of tissues communicating with an external environment and changing under its impact. Different dry, wet, gas gangrene and breakdown.

Dry gangrene - These are necrosis of tissues in contact with the external environment flowing without the participation of microorganisms. Dry gangrene most often occurs on the limbs as a result of ischemic coagulation tissue necrosis. Uncrolized fabrics seem black, dry, they are clearly excluded from adjacent viable tissue. On the border with healthy fabrics there is a demarcation inflammation. Color change is due to the transformation of hemoglobine pigments in the presence of hydrogen sulfide into iron sulphide. Examples can serve dry gangrene:

• limbs during atherosclerosis and thrombosis of its arteries (atherosclerotic gangrene), which obliterates endarteritis;
• when frostbite or burn;
• fingers with raino disease or vibration disease;
• skin with a rapid typhoid and other infections.

Wet gangren: Developed as a result of layering on necrotic changes in the tissue of severe bacterial infection. Under the action of microorganisms enzymes there is a secondary kolinkivation. Wet gangrene is usually developing in moisture tissues. It can occur on the limbs, but more often - in the internal organs, for example, in the intestine in the obstruction of the mesenteric arteries (thrombosis, embolism), in the lungs as a complication of pneumonia (influenza, cortex). In a weakened infectious disease (more often measles), children can develop wet gangrenes of soft tissues of cheeks, crotch, which is called Nome (from Greek. Nome - water cancer).

Sweeper (Decubitus): As a type of gangrenes, it is distinguished by the samples of tissues (leather, soft tissue) exposed to long pressure. The proligeses are more often appearing in the region of the sacrum, the awesome processes of the vertebrae, the large skewer of the femoral bone (in lying patients). According to its genesis, these are standard non-neurosis, as the vessels and nerves are squeezed, which aggravates the tissue trophic disorders in seriously ill, suffering from cardiovascular, oncological, infectious or nervous diseases.

B. Collective (wet) necrosis

It is characterized by melting dead fabric. It develops in tissues, relatively poor proteins and a rich liquid, where there are favorable conditions for hydrolytic processes. Lisace cells occurs as a result of the action of own enzymes (autolysis). A typical example of a wet conservation necrosis is a hearth softening (ischemic infarction) of the brain.

Outcome of necrosis.

Favorable necrosis outcomes:

• lysis;
• the organization, on the site of necrosis in such cases, the scar (scar at the scene of the infarction) is formed.
• encapsulation;
• petrification;
• ossification;
• the formation of cysts.

Adverse outcomes of necrosis:

• purulent (septic) melting of the midst of death;
• sequestration is the formation of a plot of dead fabric that is not subject to autolysis and organization. Sequestrs usually occur in the bones when inflammation bone marrow - osteomyelitis. A sequestral capsule and cavity filled with pus are formed around such a sequestration;
• mutilation - rejection of necrotic tissues.

Apoptosis , or the programmed cell death, is a process by which internal or external factors activating the genetic program leads to the death of the cell and its effective removal from fabric. Morphologically apoptosis is manifested by the death of single, randomly located cells, which is accompanied by the formation of rounded, surrounded by the membrane of the Taurus ("Apoptotic Taurus"), which are immediately phased by surrounding cells.

This is an energy-dependent process by which unwanted and defective cell cells are removed. It plays a large role in morphogenesis and is a mechanism for permanent control of organ sizes. When the apoptosis is reduced, cell accumulation occurs, an example is tumor growth. With an increase in apoptosis, a progressive decrease in the number of cells in the tissue is observed, an example is atrophy.

Morphological manifestations of apoptosis

Apoptotic cells look like rounded or oval clusters of intensively eosinophilic cytoplasm with dense fragments of nuclear chromatin. Since the cell compression and the formation of apoptotic taurus occurs quickly and also quickly, they are phagocycable, disintegrate or discarded into the enumeration of the organ, then on histological preparations it is found in cases of its significant severity. In addition, apoptosis - unlike necrosis - is never accompanied by an inflammatory response, which also makes it difficult to histological identification.

Comparative characteristic of necrosis and apoptosis

Fig. 1. Sequence of ultrastructural changes in apoptosis (right) and necrosis (left)

1 - normal cell; 2 - the beginning of apoptosis; 3 - fragmentation of apoptotic cell; 4 - phagocytosis of apoptotic taurus surrounding cells; 5 - the death of intracellular structures with necrosis; 6 - the destruction of the cell membrane.

Apoptosis takes part in the following physiological and pathological processes:

ü programmed cell destruction during embryogenesis (including implantation, organogenesis);

ü hormone-dependent involution of organs in adults, such as endometrial rejection during menstrual cycle, the atresia of follicles in the ovaries in menopause and the regression of the breast after the cessation of lactation;

ü removing some cells during cell population proliferation;

ü the death of individual cells in tumors, mainly during its regression, but also in an active growing tumor;

ü Cell death immune system, both in and T-lymphocytes, after the exhaustion of the stocks of cytokines, as well as the death of autoreactive T cells during development in the thymus;

ü pathological atrophy of parenchymal organs after the obturation of output ducts, which is observed in the pancreas and salivary glands, kidneys;

ü cell death caused by the action of cytotoxic T cells, for example, when the graft is rejected and the "transplant against host" disease;

ü cell damage under certain viral diseases, for example, viral hepatitisWhen fragments of apoptotic cells are found in the liver, like the Caedsillman Taurus.

Regulation of apoptosis

Apoptosis is a genetically controlled cell death. Currently identified a large number of genes that encode substances necessary for the regulation of apoptosis.

Apoptosis can be adjusted:

• external factors
• autonomous mechanisms.