Allergy. Treat urgent. What is allergic reactions of the immediate type of allergic reaction of a slow-type type

Chapter 5. Slow-type allergic reactions

Allergic reactions of slow (cellular) type are called reactions that occur only after a few hours or even a day after the resolution of the specific allergen. In modern literature, this type of reaction is called "slow-type hypersensitivity".

§ 95. General characteristics of slow allergies

Slow-type allergic reactions differ from immediate allergies with the following features:

1. The response of the sensitized organism on the action of the resolution dose of allergen occurs after 6-48 hours.
2. The passive transfer of slow allergies using a sensitized animal serum cannot be unable. Consequently, the antibodies are circulating in the blood - immunoglobulins - do not matter in the pathogenesis of slow allergies.
3. Passive transfer of slow allergies is possible by a suspension of lymphocytes taken from a sensitized organism. At the surface of these lymphocytes, chemically active determinants appear (receptors), with the help of which the lymphocyte is connected to a specific allergen, that is, these receptors are functioning like circulating antibodies in allergic reactions of instant type.
4. The possibility of passive transmission of slow allergies in humans is due to the presence in sensitized lymphocytes of the so-called "transfer factor", for the first time revealed Lawrence (1955). This factor is a peptide nature substance having a molecular weight of 700-4000, sustainable tripsin, DNA-Ase, RNA. It is neither an antigen (small molecular weight) nor an antibody, since it is not neutralized by an antigen.

§ 96. Types of delayed allergies

Slow allergies include bacterial (tuberculin) allergies, contact dermatitis, transplant reaction, auto allergic reactions and diseases, etc.

Bacterial allergies. For the first time, this type of response was described in 1890 by Robert Koh in patients with tuberculosis with subcutaneous introduction to them Tuborkulin. Tuberculin is a filtrate of a tuberculosis sticks of a bouillon culture. Persons who do not suffer from tuberculosis give a negative reaction to tuberculin. In patients with tuberculosis in 6-12 hours at the site of the introduction of tuberculin, it appears red, it increases, swelling appears, seal. After 24-48 hours, the reaction reaches the maximum. With a particularly strong reaction, even skin necrosis is possible. When injecting small doses of allergen necrosis is missing.

The reaction to tuberculin was the first detailed allergic reaction, so sometimes all types of delayed allergic reactions are called "tuberculin allergies". Slow allergic reactions may occur under other infections - diphtheria, scarletin, brucellosis, cock, viral, fungal diseases, during preventive and therapeutic vaccinations, etc.

In the clinic, skin allergic reactions of slow-type are used to determine the degree of sensitization of the body in infectious diseases - the reaction of the pyrque and manta during tuberculosis, the reaction of the Burne - during Brucelese, etc.

Slow allergic reactions in the sensitized organism may occur not only in the skin, but also in other organs and tissues, for example, in the cornea, bronchi, parenchymal organs.

In the experiment, tuberculin allergies easily turns out to have guinea pigs, sensitized BCG vaccine.

When such pigs are injected with such pigs, they develop, as in humans, the skin allergic delayed type reaction. Histologically reaction is characterized as inflammation with lymphocyte infiltration. Giant multi-core cells, light cells, histiocyte derivatives - epithelioid cells are also formed.

When the tuberculin is introduced with a sensitized pig in blood, it develops tuberculin shock.

Contact allergies The skin reaction is called (contact dermatitis), which occurs as a result of a long contact of various chemicals with leather.

Contact allergies more often occurs to low molecular weight substances of organic and inorganic origin, which has the ability to connect with skin proteins: various chemicals (phenols, picrylic acid, dinitrochlorobenzene, etc.). Paints (Ursol and its derivatives), metals (platinum, cobalt, nickel compounds), detergents, cosmetics, etc. In the skin they are connected to proteins (punctured) and acquire allergenic properties. The ability to connect with proteins is directly proportional to the allergenic activity of these substances. In case of contact dermatitis, the inflammatory reaction is developing mainly in surface layers of the skin - the skin infiltration of mononuclear leukocytes, degeneration and delaying of the epidermis occurs.

Transplant rejection reactions. As is known, the true adhesion of the transplanted tissue or the organ is possible only with autotransplantation or singen transplantation (isotransplantation) in single-person twins and inbred animals. In cases of transplanting genetically alien fabric, the transplanted fabric or organ rejected. The transplant rejection is the result of a slow-type allergic reaction (see § 98-100).

§ 97. Autoallergia

Allergic reactions of a slow-type type include a large group of reactions and diseases resulting from damage to cells and tissues by auto allergens, i.e. allergens arising in the very organism. This condition is called autoallergia and characterizes the body's ability to respond to their own proteins.

Usually in the body there is a device, with which the immunological mechanisms are distinguished by their own proteins from alien. Normally in the body to its own proteins and components of the body there is tolerance (stability), i.e., antibodies and sensitized lymphocytes are not formed against their own proteins, therefore own tissues are not damaged. It is assumed that the inhibition of an immune response to their own autoantigines is implemented by T-lymphocytes suppressors. The hereditary defect in the work of T-suppressors and leads to the fact that sensitized lymphocytes damage the tissues of their own owner, i.e., an auto-allergic reaction occurs. If these processes become rather pronounced, then the auto allergic reaction passes into an auto allergic disease.

Due to the fact that the tissues are damaged by their own immune mechanisms, auto-allergies are also called autoagression, and auto-allergic diseases are autoimmune diseases. Sometimes, both are called immunopathology. However, the last term is unsuccessful and to use it as a synonym for autoamellergia should not, for immunopathology is a very broad concept and in it, except for auto-allergies, are also included:

• immunodeficiency diseases, i.e., diseases associated or with the loss of the ability to form any immunoglobulins and associated with these immunoglobulins of the antibody, or with the loss of the ability to form sensitized lymphocytes;
• immuno-proliferative diseases, i.e., diseases associated with the overhaul of any class of immunoglobulins.

Autoamellergic diseases include: systemic red lupus, some types of hemolytic anemia, severe myasthenia (pseudo-paralytic form of muscular weakness), rheumatoid arthritis, glomerulonephritis, thyroiditis Hasimoto and a number of other diseases.

Autoallergic syndromes should be distinguished from autoallergic diseases that join diseases with a non-allergic development mechanism and complicate them. Such syndromes include: post-infarction syndrome (the formation of an autoantibodel to the death of myocardials, and damage to them of healthy hearts of the heart attack), an acute liver dystrophy with infectious hepatitis - Botkin's disease (the formation of autoantibodies to hepatic cells), autoameric syndromes for burns, beam Diseases and some other diseases.

The mechanisms for the formation of autoallergens. The main issue in the study of the mechanisms of auto-allergic reactions is the question of the ways of the formation of autoallergens. At least 3 ways of forming autoallergens are possible:

1. Autoallergmen are contained in the body as its normal component. They are called natural (primary) autoallergens (A. D. ADO). They include some proteins of normal tissues of the nervous system (main protein), lens, tester, thyroid colloid, retina eye. Some proteins of these organs by virtue of embryogenesis features are perceived by immunocompetent cells (lymphocytes) as foreign. However, under normal conditions, these proteins are located so that they do not come into contact with lymphoid cells. Therefore, the autoallergic process does not develop. Disruption of the insulation of these autoallergens may result in contact with lymphoid cells, as a result of which autoantibodes and sensitized lymphocytes will begin to form, which will cause damage to the relevant authority. It also matters the hereditary defect of T-lymphocyte-suppressors.

   This process can be schematically represented on the example of the development of thyroiditis. In the thyroid gland there are three autoallergens - in epithelial cells, in the microsomal fraction and in the colloid of the gland. Normally, in the cell of the follicular epithelium of the thyroid gland, thyroxine is cleaned from thyreoglobulin, after which the thyroxine enters the blood capillary. Thyroglobulin itself remains in the follicle and does not fall into the blood circuit. In case of damage to the thyroid gland (infection, inflammation, injury) thyroglobulin comes out of the follicle of the thyroid gland and enters the blood. This leads to stimulation of immune mechanisms and the formation of autoantoantibodies and sensitized lymphocytes, which cause thyroid damage and the new flow of thyroglobulin into the blood. So the process of damage to the thyroid gland becomes wave-like and continuous.

   It is believed that the same mechanism underlies the development of sympathetic ophthalmia, when after an injury of one eye, an inflammatory process is developing in the tissues of another eye. On this mechanism, orchites may develop - inflammation of one egg after the damage to the other.

2. Autoallergens are not preserved in the body, but are formed as a result of infectious or non-infectious damage to tissues. They are called acquired or secondary autoallergens (A. D. ADO).

   Such auto allergenam includes, for example, protein denaturation products. It has been established that blood and tissue proteins with different pathological conditions are acquired by allergenic, alien for the body of their carrier properties and become auto allergens. They are found in the burn and radial illness, during dystrophy and necrosis. In all these cases, changes occur with proteins that make them alien for the body.

   Autoallergens can be formed as a result of the combination of drugs that fell into the body, chemicals with tissue proteins. At the same time, the alien substance entered into a complex usually plays the role of Hapten.

   Complex autoallergens are formed in the body as a result of the combination of bacterial toxins and other products of infectious origin with tissue proteins. Such complex auto allergens may, for example, to form when connecting certain components of streptococcus with proteins of the alignment tissue of myocardium, with the interaction of viruses with tissue cells.

   In all these cases, the essence of the autoallergic restructuring is that unusual proteins appear in the body, which are perceived by immunocompetent cells as "not their own", alien and therefore stimulate them to develop antibodies and the formation of sensitized T-lymphocytes.

   Hypothesis Bernet Explains the formation of an autoantor of the tweems in the genome of some immunocompetent cells that can produce antibodies to their own tissues. As a result, the "Forbidden clone" of cells carrying antibodies, complementary to the antigens of their own intact cells appear.

3. Some tissue proteins may be autoallergens due to the presence of common antigens with certain bacteria. In the process of adapting to existence in macroorganism, many microbes have antigens common with host antigens. It slowed down the inclusion of immunological mechanisms for protection against such microflora, since in relation to its antigens in the body there is immunological tolerance and such microbial antigens were taken as "their". However, due to some differences in the structure of common antigens, the immunological mechanisms of protection against microflora took place, which simultaneously led to damage to their own tissues. Such a mechanism is expected to participate in the development of rheumatism due to the presence of common antigens in some strains of streptococcus groups A and tissue of the heart; Ulcerative colitis due to common antigens in the intestinal mucosa and some sishemnel strains.

   In the serum of patients with infectious-allergic form of bronchial asthma, antibodies were found, reacting both with antigens of microflora of bronchi (neasery, klebseyella) and with lung tissues.

According to modern ideas, all allergic reactions, all manifestations of allergies depending on the rate of occurrence and intensity of the manifestation of clinical signs After the allergen re-meeting, the organism is divided into two groups:

* Allergic reactions of instant type;

* Allergic delayed type reactions.

Allergic reactions of immediate type (hypersensitivity of immediate type, anaphylactic type reaction, chimergic type reaction, in - dependent reactions). These reactions are characteristic of the fact that antibodies are in most cases circulated in liquid media of the body, and they develop within a few minutes after the allergen re-entering.

Allergic reactions of the immediate type proceed with the participation of antibodies in response to the antigenic load in circulating humoral media. The re-entering the antigen leads to its rapid interaction with circulating antibodies, the formation of antigen antibody complexes. According to the nature of the interaction of antibodies and allergens, three types of reactions of immediate hypersensitivity are distinguished: first type - R e a g and n about in y, including anaphylactic reactions. The reinvitable antigen is found with an antibody (IG E) fixed on tissue basophilas. As a result of degranulation, histamine, heparin, hyaluronic acid, Callermine, other biologically active compounds are released and entered into blood. Complement in the reactions of this type of participation does not accept. The overall anaphylactic reaction is manifested by an anaphylactic shock, local - bronchial asthma, hay fever, urticaria, swelling of Queenka.

Second Type - C and T about T about to C and Ch E C and th, characteristic of the fact that the antigen is sorbed on the cell surface or is some kind of its structure, and the antibody circulates in the blood. The resulting antigen-antibody complex in the presence of complement has a direct cytotoxic effect. In addition, activated killer immunocytes, phagocytes involved in cytolysis. Cytolysis occurs when the introduction of large doses of anti-etcular cytotoxic serum. Cytotoxic reactions can be obtained relative to any animal recipient tissues, if it is inserted by a donor blood serum pre-immunized to them.

Third type - The reactions of the type f e n o n and a r t u s a. Described by the author in 1903 in pre-sensitized horsepower serum rabbits after subcutaneous introduction to them the same antigen. At the injection site develops acute necrotic inflammation of the skin. The main pathogenetic mechanism is the formation of a complex of antigen + antibody (Ig G) with a system complement. The formed complex should be large, otherwise it does not fall into the sediment. At the same time, thrombochetarian serotonin is important, which increases the permeability of the vascular wall, promoting microprecipitation of immune complexes, depositing them in the walls of vessels and other structures. In this case, there is always a small amount (IG E) fixed on basophils and fat cells. Immune complexes attract neutrophils to themselves, phagocying them, they distinguish the lysosomal enzymes, which, in turn, determine the chemotaxis of macrophages. Under the influence of hydrolytic enzymes released by phagotizing cells, damage (pathophysiological stage) of the vascular wall, breaking endothelium, thrombosis, hemorrhage, sharp disorders of microcirculation with foci of necrotization. Inflammation develops.

In addition to the phenomenon of Artus, the manifestation of allergic reactions of this type can serve serum disease.

Serum disease - symptom complex arising after parenteral administration to the organism of animals and man of serums with a prophylactic or therapeutic goal (anti-library, anti-beadable, anticipated, etc.); immunoglobulins; transfused blood plasma; hormones (ACTH, insulin, estrogen, etc.) of some antibiotics, sulfonamides; With insect bites that allocate poisonous compounds. The basis of the formation of serum diseases are immune complexes, arising in response to the primary, one-time attachment of the antigen in the body.

The properties of the antigen and the features of the reactivity of the body affect the severity of the manifestation of serum disease. If an alien antigen invested in an animal, there are three types of response: 1) antibodies are not at all formed and the disease does not develop; 2) there is a pronounced formation of antibodies and immune complexes. Clinical signs arise quickly, as the antibody titer is increasing - disappear; 3) weak anti-befenesis, insufficient elimination of the antigen. Favorable conditions are created for long-term persistence of immune complexes and their cytotoxic effect.

Symbolism is characteristic of a pronounced polymorphism. The long period is characterized by hyperemia, an increase in skin sensitivity, an increase in lymph nodes, an acute lung emphysema, lesion and swelling of joints, edema mucous membranes, albuminuria, leukopenia, thrombocytopenia, an increase in ESO, hypoglycemia. In more severe cases, the acute glomerulonephritis is observed, violation of the function of myocardium, arrhythmia, vomiting, diarrhea. In most cases, after 1-3 weeks, clinical signs disappear and recovery.

Bronchial asthma - It is characterized by a suddenly the upcoming attack of choking with a sharp difficulty of the exhalation phase as a result of a diffuse breakdown in the system of small bronchi. It is manifested by bronchospasm, swelling of the mucous membrane of the bronchi, hypersection of the mucous gland gland. With an atopic form, the attack begins with cough, then a picture of expiratory suffocation is developing, a large number of dry wheezing wheezing is listened to the lungs.

Polynomy (hay fever, allergic rhinitis) -periodically arising from the disease associated with entering the respiratory tract and the conjunctiva of pollen plants from the air during the period of their flowering. It is characterized by hereditary predisposition, seasonality (usually spring-summer, due to the flowering period of plants). It is manifested by rhinitis, conjunctivitis, irritation and itching age arises, sometimes general weakness, an increase in body temperature. In the blood, an increased amount of histamine, reacts (Ig E), eosinophilic granulocytes, the globulin fraction of blood serum, an increase in the activity of transaminase) is detected. The attacks of the disease pass after the cessation of contact with vegetable allergens in a few hours, sometimes in a few days. The rino-conjunctival form of half aulinosis can be completed by visceral syndrome, in which the defeat of a number of internal organs (pneumonia, pleurisy, myocarditis, etc.) is observed.

Urticaria and swelling - arise when exposed to plant, pollen, chemical, epidermal, serum, medicinal allergens, domestic dust, with insect bite, etc. This disease is usually beginning suddenly, with a manifestation of very often unbearable itch. At the place of combing, hyperemia instantly occurs, then there is a rash on the skin of itchy blisters, which are swelling of a limited area, mainly a papilla skin layer. There is an increase in body temperature, joints swell. The disease lasts from several hours to several days.

One of the types of urticissal is the swelling of Quincke (Giganskaya Urtiamnitsa, angioedema swelling). Under the swelling of the quinque, the skin it usually does not happen, since the process is localized in the subcutaneous layer without extending to sensitive ending of the skin nerves. Sometimes the urticaria and swelling of quinics proceed very violently, preceding the development of anaphylactic shock. In most cases, sharp phenomena of urticaria and swelling are completely cured. Chronic forms are difficult to treat, characterized by the wave-like flow with the change of exacerbation and remission periods. The generalized form of urticaria is very difficult, in which the swelling captures the mucous membrane of the mouth, the soft sky, the language, and the language is hardly placed in the oral cavity, the swallowing is greatly difficult. In the blood, the increase in the content of eosinophilic granulocytes, globulins and fibrinogen, decrease in albumin levels.

General pathogenesis of allergic reactions of immediate type .

Allergic reactions of instant type, various on external manifestations, have general development mechanisms. In the genesis of hypersensitivity, three stages are distinguished: immunological, biochemical (Patochimic) and pathophysiological. Immunological stage It begins with the first contact of allergen with the body. Antigen's hit stimulates macrophages, they begin to release interleukins, activating T-lymphocytes. The latter, in turn, launch the processes of synthesis and secretion in B-lymphocytes that turn into plasmocytes. Plasmocytes in the development of the allergic reaction of the first type produced mainly Ig E, the second type - Ig G 1,2,3, Ig M, the third type is predominantly Ig G, Ig M.

Immunoglobulins are fixed by cells, on the surface of which there are appropriate receptors - on circulating basophils, fat cells of connective tissue, platelets, smooth muscle cells, skin epithelium, etc. occurs period of sensitization, increases sensitivity to re-entering the same allergen. The maximum severity of sensitization occurs after 15-21 days, although the reaction can manifest itself much earlier. In the case of an antigen reinputation with a sensitized animal, the interaction of allergen with antibodies will occur on the surface of basophils, platelets, fat and other cells. When the allergen binds to more than two adjacent immunoglobulin molecules, the membrane structure is disturbed, the cell is activated, previously synthesized or newly formed allergy mediators begin to emit. Moreover, only about 30% of biologically active substances contained there are allocated from the cells, since they are emitted only through the deformed area of \u200b\u200bthe membrane of target cells.

IN patochemical stagechanges occurring on the cell membrane into the immunological phase due to the formation of immune complexes, the reaction cascade is launched, the initial step of which is apparently the activation of cell eserase. As a result, a number of allergy mediators are exempted and again. Mediators have vasoactive and precision activity, chemotoxic properties, the ability to damage tissue and stimulate reparation processes. The role of individual mediators in the general response of the organism to repeated allergen is as follows.

Histamine - One of the most important allergy mediators. Its liberation from fat cells and basophils is carried out by secretion, which is an energy-dependent process. The source of energy is ATP, disintegrating under the influence of activated adenylate cyclase. Histamine expands capillaries, increases the permeability of the vessels by expanding the terminal arterioles and the narrowing of the postcase veul. It inhibits the cytotoxic and helper activity of T-lymphocytes, their proliferation, differentiation of B cells and antibody synthesis plasmocytes; Activates T-suppressors, it has a chemokinetic and chemotaxic effect on neutrophils and eosinophils, inhibits the secretion of neutrophils of lysosomal enzymes.

Serotonin -creates a reduction in smooth muscles, an increase in permeability and spasm of blood vessels, brain, kidneys, lungs. Released in animals from fat cells. Unlike histamine, it does not have an anti-inflammatory effect. Activates the suppressor population of Timus T-lymphocytes and spleen. Under his influence, T-suppressors of the spleen migrate into the bone marrow and lymph nodes. Along with the immunosuppressing influence, serotonin can have an immunostimulating effect implemented through thymus. Enhances the sensitivity of mononuclear to various hemotaxis factors.

Bradykin -the most active component of Kinin Sospecia. It changes the tone and permeability of blood vessels; reduces blood pressure, stimulates the secretion of leukocytes mediators; to one degree or another affects the mobility of leukocytes; Causes a reduction in smooth muscles. In patients with asthma, Brudikinin leads to bronchospasm. Many Bradikinin effects are due to the secondary increase in the secretion of foregnostin.

Heparin -proteoglycan forming complexes with antithrombin, which prevent the coagulating effect of thrombin (blood coagulation). It is released in allergic reactions from fat cells, where it is contained in large quantities. In addition to the anticoagulant, it has other functions: participates in the cell proliferation reaction, stimulates the migration of endothelial cells in the capillary, suppresses the effect of the complement, activates the pinot and phagocytosis.

Complement fragments - have an anaphylastoxic (histaminospeant) activity against obese cells, basophils, other leukocytes, increase the tone of smooth muscles. The permeability of vessels increases under their influence.

Slowly reacting anaphylaxis substance (MRSA) - as opposed to histamine, a slow reducing the smooth muscles of the trachea and the ileum of the guinea pig, the bronchiole of man and the monument, increases the permeability of the skin vessels, has a more pronounced than histamine, bronchospast effect. MRSA is not removed by antihistamine drugs. It is highlighted by basophilic, peritoneal alveolar monocytes and blood monocytes, fat cells, various sensitized lung structures.

Property -in the tissues of the body, forebanding E, F, D. Exogenous foregnostine have the ability to stimulate or inject the inflammatory process, cause fever, expand the vessels, increase their permeability, cause erythema. Fast stamp F cause strongly pronounced bronchospasm. Easternandines have the opposite effect, possessing high bridal activity.

Pathophysiological stage.It is a clinical manifestation of allergic reactions. Biologically active substances secreted by target cells have a synergistic effect on the structure and function of organs and tissues of an animal body. The resulting vasomotor reactions are accompanied by blood flow disorders in the microcirculatory line, reflected on the systemic blood circulation. The expansion of the capillaries and an increase in the permeability of the histohematic barrier lead to the exit of the fluid beyond the walls of the vessels, the development of serous inflammation. The damage to the mucous membranes is accompanied by an edema, hypersecretion of mucus. Many allergy mediators stimulate the contractile function of myofibrils of the bronchi walls, intestines, other hollow organs. The results of spastic abbreviations of muscle elements can manifest itself in asphyxia, disorders of the motor function of the gastrointestinal tract, such as vomiting, diarrhea, acute pain from excessive contraction of the stomach and intestines.

The nerve component of the genesis of an instant type allergy is obliged to influence the kinines (bradykinin), histamine, serotonin on neurons and their sensitive education. Disorders of nervous activity during allergies can manifest themselves with trimmed states, feeling pain, burning, unbearable itch. The reactions of the hypersensitivity of the immediate type either are being completed, or by recovery, or fatal, the cause of which may be asphyxia or acute hypotension.

Slow-type allergic reactions (increased sensitivity of slow-type, hypersensitivity of slow-type, T - dependent reactions). This form of allergies are characteristic of the fact that the antibodies are fixed on the diaphragm of lymphocytes and are the latter receptors. Clinically revealed 24-48 hours after contact of the sensitized organism with an allergen. This type of reaction proceeds with the predominant participation of sensitized lymphocytes, so it is considered as a pathology of cellular immunity. The slowing down of the reaction to the antigen is explained by the need for a longer time for the accumulation of lymphocytic cells (T- and B - lymphocytes of different populations, macrophages, basophils, fat cells) in the zone of the alien substance compared with a humoral reaction an antigen + antibody with an immediate type of hypersensitivity. The delayed type reactions are developing in infectious diseases, vaccinations, contact allergies, autoimmune diseases, with the introduction of animals of various antigenic substances, gapten appliques. They are widely used in veterinary medicine for the allergic diagnosis of hidden forms of such chronically occurring infectious diseases as tuberculosis, SAP, some wicked invasions (echinococcosis). The reactions of slow-type are tuberculin and maleoin allergic reactions, reacting reaction of transplanted tissue, auto allergic reactions, bacterial allergies.

General pathogenesis of delayed allergic reactions

Slow-type hypersensitivity flows into three stages:

IN Patochemical stagestimulated T - lymphocytes synthesize a large number of lymphokins - MEDIATORS PCST. They, in turn, involve into a response to a foreign antigen of other types of cells, such as monocytes / macrophages, neutrophils. The following mediators are the most important in the development of the Patozyme stage:

the factor inhibiting migration is responsible for the presence in the inflammatory infiltrate of monocytes / macrophages, it is distinguished by the most important role in the formation of a response phagocytic reaction;

factors affecting chemotaxis macrophages, their adhesion, resistance;

mediators affecting the activity of lymphocytes, such as the transfer factor that promotes the ripening of T cells in the recipient body after administered by sensitized cells; a factor causing blastransformation and proliferation; Suppression factor, inhibiting immune response to the antigen, etc.;

chemotaxis factor for granulocytes, which stimulates their emigration, and the inhibition factor acting in the opposite way;

interferon, protecting the cell from the introduction of viruses;

the skin-jet factor, under the influence of which the permeability of the vessels of the skin is increased, swelling, redness, tissue seal appear in the reinformization of the antigen.

The effect of allergy mediators is limited to opposing systems protecting target cells.

IN pathophysiological stagingbiologically active substances isolated by damaged or stimulated cells determine the further development of delayed allergic reactions.

Local fabric changes in slow-type reactions can be detected after 2-3 hours after the impact of the resolution of the antigen. They are manifested by the initial development of the granulocytic reaction to irritation, then lymphocytes, monocytes and macrophages, accumulating around the vessels, migrate here. Along with migration, cell proliferation in the allergic reaction focus is also. However, the most pronounced changes are observed after 24-48 hours. These changes are characterized by hyperergic inflammation with pronounced signs.

Slow allergic reactions are induced mainly by thymus-dependent antigens - purified and crude proteins, microbial cell components and exotoxins, virus antigens, low molecular weight haptins conjugated with proteins. The reaction to the antigen at the same time the type of allergies can be formed in any organ, tissue. It is not related to the participation of the system's complement. The main role in pathogenesis belongs to T-lymphocytes. Genetic control of the reaction is carried out either at the level of individual subpopulations of T- and B-lymphocytes, or at the level of intercellular relationships.

Maller's allergic reaction -used to detect a spa in horses. Application of the disease received from the pathogens of the purified drug Mullein on the mucous membrane of the infected animals after 24 hours is accompanied by the development of acute hypergic conjunctivitis. At the same time, there is an abundant outflow from the angle of the eye of the grayish-purulent exudate, arterial hyperemia, eyelids.

Reaction of rehabilitation of transplanted fabric -as a result of the transplantation of someone else's fabric, the recipient lymphocytes are sensitizing (become carriers of the transfer factor or cell antibodies). These immune lymphocytes are then migrated into the transplant, they are destroyed and exempt the antibody, which causes the destruction of transplanted tissue. Transplanted fabric or organ rejected. Transplant rejection is the result of a slow-type allergic reaction.

Autoallergic reactions - reactions resulting from damage to cells and tissues by auto allergenami, i.e. Allergens arising in the very organism.

Bacterial allergies - appears in preventive vaccinations and in some infectious diseases (with tuberculosis, brucellosis, cock, virus and fungal infections). If the sensitized animal to enter an allergen intraodelly, or apply to the scarified skin, the response reaction begins not earlier than after 6 hours. At the point of contact with the allergen, hyperemia occurs, seal and sometimes skin necrosis. When injecting small doses of allergen necrosis is missing. In clinical practice, skin delayed reactions by the pirgin, manta are used to determine the densitability of the body with a particular infection.

Second classification. Depending on the type of allergenall allergies are divided into:

Serum

Infectious

1. Plant

   Animal origin

   Dosage Allergy

   Idiosyncrasy

   Household allergies

   Autoallergia

Serum allergy. This is such an allergy that occurs after the introduction of any healing serum. An important condition for the development of this allergy is the presence of an allergic constitution. This is due to the peculiarity of the vegetative nervous system, the activity of blood histaminate and other indicators characterizing the organism setting to an allergic reaction.

This type of allergy has a particular importance in veterinary practice. Film serum, with an imperative treatment causes an allergy phenomenon, an allergen can be anti-strong serum, with a repeated introduction of allergen can be anti-informy serum.

The mechanism for the development of serum disease is that the alien protein introduced into the body causes the formation of precipitin antibodies. The antibodies are partially fixed on the cells, part of them circulates in the blood. After about a week, the antibody titer reaches a level sufficient to react with the allergen-specific allergen - alien serum still survived in the body. As a result of the allergen compound with an antibody, an immune complex arises, which settles the skin capillaries, kidney and other organs on endothelium, it causes damage to the endothelium of capillaries, an increase in permeability. Allergic swelling, urticaria, inflammation of lymph nodes, kidney glomes and other disorders characteristic of this disease are developing.

Infectious allergy – such an allergy when an allergen is any pathogen. Such a property can possess tuberculosis wand, sap, brucellosis, helminths.

Infectious allergies are used with a diagnostic purpose. This means that microorganisms increase the sensitivity of the body to preparations prepared from these microorganisms, extracts, extracts.

Food allergy – various clinical manifestations of allergies associated with food intake. The etiological factor is food proteins, polysaccharides, low molecular weight substances, acting as haptins (food allergens). The most commonly found is allergic food to milk, eggs, fish, meat and products from these products (cheeses, butter, creams), strawberries, strawberries, honey, nuts, citrus. Allergenic properties have additives and impurities contained in food products, preservatives (benzoic and acetylsalicylic acids), food dyes, etc.

The early and late reactions of food allergies are distinguished. Early develops within one hour from the moment of food intake, heavy anaphylactic shock is possible, right up to death, acute gastroenteritis, hemorrhagic diarrhea, vomiting, collapse, bronchospasm, tongue edema and larynx. Late manifestations of allergies are associated with lesions of the skin, dermatitis, urticaria, angioedema edema. Symptoms of food allergies are observed in different departments of the gastrointestinal tract. The development of stomatitis of allergic, gingivitis, the defeat of the esophagus with edema phenomena, hyperemia, rashes on the mucous membrane, the sensation of difficulty swallowing, burning and soreness in the course of the esophagus are possible. Often amazed stomach. Such a defeat on the clinic is similar to acute gastritis: nausea, vomiting, soreness in the epigastric region, the tension of the abdominal wall, the eosinophilic of gastric content. With gastroscopy, the swelling of the stomach mucosa is observed, hemorrhagic rashes are possible. Under the intestinal damage, there is a grapple-shaped or constant pain, bloating, stress stress, tachycardia, a drop in blood pressure.

Vegetable allergy – such an allergy when an allergen is pollen plants. Pollen meadow meadow, hedgehogs of the national team, wormwood, Timofeevka, meadow oatmeal, ambrosia and other herbs. Pollen of various plants differs from each other with antigenic composition, however, there are general antigens. This is the cause of the development of polyvalent sensitization caused by pollen of many herbs, as well as the emergence of cross-reactions to different allergens in patients with pollinozes.

Allergenic properties of pollen depend on the conditions in which it is. Fresh pollen, i.e. When it stands out in the air from the dust shoes of herbs and trees, very active. Finding into a wet medium, for example, on the mucous membranes, the pollen grain swells, its sheath is bursting, and the internal contents of the plasma, which has allergenic properties, is absorbed into blood and lymph, sensitizing the body. It has been established that the pollen of herbs has more pronounced allergenic properties than the pollen of trees. In addition to pollen, and other parts of plants may have allergenic properties. The most studied from them are fruits (cotton).

When re-hit, pollen plants may arise, bronchial asthma, inflammation of the upper respiratory tract, etc.

Allergy of animal origin - pronounced allergenic properties have cells of various tissues, components of various structures of the living organism. The most significant are the epidermal allergens, the poisons of refigulates and ticks. Epidermal allergens consist of coating fabrics: dandruff, epidermis and wool of various animals and humans, pieces of claws, beaks, nails, feathers, animal hoofs, fish scales and snakes. Allergic reactions are frequent in the form of anaphylactic shock from insect bite. The presence of cross-allergic reactions caused by insect bites is shown within the class or species. Poison insects is a product of special glands. It consists of substances with pronounced biological activity: biogenic amines (histamine, dopamine, acetylcholine, norepinerenaline), proteins and peptides. Allergens of ticks (bedding, barn, dermatophagi, etc.) are often the cause of bronchial asthma. When they are inhaled with inhaled air, the sensitivity of the body is perverted.

Dosage Allergy - when an allergen is any medicinal substance. Allergic reactions caused by drugs are currently given the most serious complications in drug therapy. The most often allergens are antibiotics, especially injected inward (penicillin, streptomycin, etc.). Most of the drugs are not full-fledged antigens, but have the properties of Gapten. In the body they form complexes with serum proteins (albumin, globulin) or tissues (punctured, histone, etc.). This indicates the ability of almost every drug or chemical to cause allergic reactions. In some cases, antibiotics or chemotherapy are not antibiotics as haptennes, but the products of their metabolism. Thus, sulfonamide drugs do not have allergenic properties, but they acquire them after oxidation in the body. A characteristic feature of medicinal allergens is their pronounced ability to cause parapecific or cross reactions, which causes the polyvalence of drug allergies. The manifestations of drug allergies vary from light reactions in the form of skin rashes and fever, to the development of anaphylactic shock.

Idiosyncrasy - (from Grech . iDIOS is an independent, syncrasis - mixing) is a congenital increased sensitivity to food or drug substances. When taking some foods (strawberries, milk, chicken protein, etc.) or medicinal substances (iodine, iodoform, bromine, chinin), disorders arise in certain individuals. The pathogenesis of idiosyncrasia has not yet been established. Some researchers indicate that in idiosyncraysia, in contrast to anaphylaxis, it is not possible to detect specific antibodies in the blood. It is assumed that the food idiosyncrasy is associated with the presence of a congenital or acquired increased permeability of the intestinal wall. As a result, protein and other allergens can be bored in the blood in an unreserved form and thereby sensitizing the organism to them. At the meeting of the body with these allergens, an attack of idiosyncrasy arises. In some people, characteristic allergic phenomena arise mainly by the skin and vascular system: hyperemia of mucous membranes, swelling, urticaria, temperature increase, vomiting.

Household allergies - In this case, the allergen can be mold, sometimes fish feed - dried by Daphnia, plankton (lower races), home dust, household dust, ticks. Household dust is dust of residential premises, the composition of which varies on the content of various mushrooms, bacteria and particles of organic and inorganic origin in it. Large dust in large quantities contains remnants of paper, cardboard, etc. According to most of the modern data, the allergen of home dust is a mucoprotein and glycoprotein. Household allergens are capable of sensitizing the body.

Autoallergia- It occurs when the allergens are formed from their own fabrics. With the normal function of the immune system, the body removes, neutralizes its own, reborn cells, and if the body's immune system does not cope, then the reborn cells and tissues become allergens, i.e. autoallergens. In response to the effect of autoallergens, autoantibodes are formed (react). The autoantibodies are connected to autoallergenices (autoantignes) and at the same time a complex is formed, which damages cells of healthy tissue. The complex (antigen + antibody) is able to settle on the surface of the muscles, other tissues (cerebral), on the surface of the joints and causes allergic diseases.

According to the mechanism of autoamellergia, there are diseases such as rheumatism, rheumokart, encephalitis, collagenoses - (the non-tank parts of the connective tissue are damaged), the kidneys are affected.

Third classification of allergies.

Depending on the sensitizing agent distinguish two types of allergies:

* Specific

* Nonspecific

Allergy is called specific If the sensitivity of the body is perverted only to the allergen, which the body is sensitized i.e. There is a strict specificity here.

A representative of specific allergies is anaphylaxia. Anaphylaxis consists of two words (Ana - without, Phylaxis - protection) and literally translates - defenselessness.

Anaphylaxis- This is an increased and qualitatively perverted response of the body, to that allergen, to which the body is sensitized.

The first introduction of allergen in the body is called sensitizing administration,or otherwise increases sensitivity. The magnitude of the sensitizing dose can be very small sometimes succeeded sensitizing such a dose as 0.0001 g allergen. Allergen should enter the body parenterally, i.e., bypassing the gastrointestinal tract.

The state of the increased sensitivity of the body or the state of sensitization occurs in 8-21 days (this is the time required for the production of antibodies KL.E), depending on the type of animal or individual characteristics.

The sensitized organism externally does not differ from the body not sensitized.

Repeated administration of antigen is called introduction of a resolution or reinware.

The value of the resolution dose is 5-10 times higher than the sensitizing dose and the resolution dose should also be introduced parliantly.

The clinical picture that occurs after the administration of the resolution dose (by perfectly) is called anaphylactic shock.

Anaphylactic shock is a severe clinical manifestation of allergies. Anaphylactic shock can develop lightning, within a few minutes after the administration of allergen, less often in a few hours. Shock's harbingers can be a feeling of heat, redness of the skin, itching, a feeling of fear, nausea. The development of shock is characterized by a rapidly increasing collapse (there is a pallor, cyanosis, tachycardia, a threaded pulse, a cold sweat, a sharp decrease in blood pressure), suffocating, weakness, loss of consciousness, swelling mucous membranes, the appearance of convulsion. In severe cases, there is an acute insufficiency of the heart, the swelling of the lungs, the acute insufficiency of the kidneys, is possible allergic lesions of the intestine until obstruction.

In severe cases, dystrophic and necrotic changes in the brain and internal organs can develop, interstitial pneumonia, glomerulonephritis. At the height of the shock in the blood, eritrea, leukocytosis, eosinophilia, an increase in ESO, are noted; In the urine - proteinuria, hematuria, leukocyturia.

In the rate of occurrence, anaphylactic shock may be (acute, subacute, chronic). Acute form - changes occur in a few minutes; Prostula occurs in a few hours; chronic - changes occur in 2-3 days.

Different types of animals exhibit not the same sensitivity to anaphylactic shock. The most sensitive anaphylaxis are guinea pigs, and then according to the degree of sensitivity animals are located in the following order - rabbits, sheep, goats, cattle, horses, dogs, pigs, birds, monkeys.

So, the guinea pigs appear anxiety, itching, scratching, sneezing, pigs rubbing pockets, tremble, observed involuntary defecation, takes a lateral position, breathing becomes difficult, intermittent, respiratory movements slow down, convulsions appear and may be a deadly outcome. This clinical picture is combined with a drop in blood pressure, a decrease in body temperature, acidosis, an increase in the permeability of blood vessels. At the opening of the guinea pig that died from anaphylactic shock, the elbows of emphysema and atelectasis in the lungs, multiple hemorrhages on the mucous membranes, which inveluded blood is found.

Rabbits - 1-2 minutes after the administration of the serum dose, the animal begins to worry, shakes his head, falls on the stomach, appears shortness of breath. Then there is a relaxation of the sphincters and the water and feces are involuntarily separated, the rabbit falls, bends his head back, convulsions appear, after that breathing stops, death comes.

The sheep anaphylactic shock takes place very acute. After administering the resolution of the serum after a few minutes, shortness of breath occurs, reinforced salivation, tearing, pupils are expanding. Observation of the scar is observed, blood pressure decreases, an involuntary separation of urine and feces appear. Then there are paresis, paralysis, convulsions and often occurs the death of an animal.

In goats, cattle, horses symptoms of anaphylactic shock, to some extent similar to the symptoms arising from the rabbit. However, they most clearly show signs of paresis, paralysis, and there is also a decrease in blood pressure.

Dogs. An essential value in the dynamics of anaphylactic shock have portal blood circulation and blood stagnation in the liver and intestinal vessels. Therefore, the anaphylactic shock in dogs proceeds by the type of acute vascular failure, initially there is an excitement, shortness of breath, vomiting occurs, blood pressure falls sharply, the involuntary separation of urine and feces appear, preferably red (admixture of erythrocytes). Then the animal flows into a stuporial state, while there is a bloody expiration from the rectum. Anaphylactic shock in dogs in rare cases is fatal.

Cats and fur animals (sands, foxes, mink) there is a similar dynamics of shock. However, the sands are more sensitive to anaphylaxis than dogs.

Monkey. Anaphylactic shock by monkeys can not always reproduce. With a shock, monkeys observed difficulty breathing, collapse. The number of platelets drops, blood clotting decreases.

In the occurrence of anaphylactic shock, the functional state of the nervous system is important. It is impossible to cause an anaphylactic shock in narcotic animals (narcotic blocking of the central nervous system turns off the pulses going to the place of deployment of allergen), during the winter hook, in newborns, with sharp cooling, as well as fish, amphibians and reptiles.

Antianafilaxia- This is a state of the body, which is observed after transferring anaphylactic shock (if the animal does not died). This condition is characterized by the fact that the body becomes not sensitive to this antigen (Allergen for 8-40 days). The state of anti-aquilaxia occurs after 10 or 20 minutes after anaphylactic shock.

The development of anaphylactic shock can be warned by the introduction of a sensitized animal of small doses of the antigen 1-2 hours before the injection of the required volume of the drug. Small amounts of antigen bind antibodies, and the resolution dose is not accompanied by the development of the immunological and other stages of the hypersensitivity of the immediate type.

Nonspecific allergy - This is a phenomenon when the organism is sensitized by one allergen, and the sensitivity response to another allergen is perverted.

There are two kinds of non-specific allergies (parallergia and heteroallergia).

Parallergia - call such an allergies when the body is sensitized by one antigen, and sensitivity increases to another antigen, i.e. One allergen increases the sensitivity of the body to another allergen.

Heteroallergia is such a phenomenon when the body is sensitized by a factor of non-antigenic origin, and sensitivity increases, is perverted to any factor of antigenic origin or vice versa. Factors of non-antigenic origin can be cold, exhaustion, overheating.

The cold can increase the sensitivity of the body to alien proteins, antigens. That is why in a cold state can not be administered; The influenza virus manifests its action very quickly if the body is percooled.

Fourth classification - By character of manifestationallergies distinguish:

General- This is such an allergy when the general condition of the body is disturbed with the introduction of a resolution dose, the functions of various organs and systems are disturbed. To obtain incredible allergies, one-time single sensitization.

Local allergy - this is such an allergy when the change in the administration of the allergen is arising when the allergen is introduced, and in this place can develop:

hyperergic inflammation

ulceration

thickening of the skin fold

swelling

To obtain local allergies, multiple sensitization is required with an interval of 4-6 days. If you enter the same body in the same body several times the same antigen with an interval of 4-6 days, then after the first administration, the antigen is completely absorbed, and after the sixth, seventh introduction at the injection site there is swelling, redness, and sometimes inflammatory Reaction with extensive swelling, extensive hemorrhage, i.e. Local morphological changes are observed.

A few hours later, and sometimes weeks after contact with an allergen, a slow-type response occurs. The occurrence of the disease is one of the main disease factors that distinguish it from immediate allergies. Another name is a tuberculin reaction.

Late hypersensibilization characterizes the lack of participation of antibodies of the human body in the reaction. Immunity does not respond to the invasion of antigens. Instead, an attack is attacked by the pathogens of a negative reaction of specific clones, in the science of the sensitized lymphocytes. They are formed due to repeated penetration of allergy provocateurs in the body.

As in the case of an immediate nature, the late reaction is the awakening of inflammatory processes in tissues and organs, lymph nodes. The patient has a step intensification of the phagocytic reaction, when the tissues, individual organs and their integer systems are gradually begin to react.

Stages

The disease is characterized by the fact that shortly after the implementation of the provocateur in the body begins the stage of sensabilization, when it gradually spreads blood, tissues and damages them. T-killer recognizes the target cell and is attached to it to apply a toxic death blow and make damage to the membrane.

Slow-type allergic reactions include the following phases - immunological, Patochimic and pathophysiological. The first includes sensitization up to recognition and interaction of antigen with cells.

In the Patochimic phase, the liberation of GZT mediators is released when repeated contact with the antigen. And on the last, pathophysiological, stage, the biological effects of GZT mediators and cytoxic T-lymphocytes are manifested. This stage is characterized by the destruction of tissues.

The reasons

With allergens, anyone may face at home at work, in a public place. Typically, the patient does not suspect that the inflammatory process catalyzed in its cells. His condition worsens far away.

In a painful response of the body, the following factors are guilty:

• disputes of mushrooms;
• bacteria;
• chronic inflammation;
• microorganisms;
• substances of a simple chemical composition;
• pets;
• funds for vaccination.

For a long time, scientists have discussed whether the delayed type reaction is a contagious disease. Modern science adheres to the opinion that tuberculin allergies are not transmitted from a sick person to healthy through blood serum, but they can transmit with cells of lymphoid organs and leukocytes.

Diagnostics

Diagnosis of the disease is possible if there are immunoglobulins in the blood of immunoglobulins M and G. Allergologist collects anamnesis, polishing the patient and his relatives. The doctor is important to find out if the patient has a predisposition to allergies, as a poor manifested itself, to find out his cause. The specialist appoints skin tests and blood tests, so as not to be mistaken in the identification of allergen and promptly begin treatment.

Examples and species

The classification of the types of disease directly depends on the antigens that caused it. Allergologists make a bacterial, contact, auto-allergic reaction, transplant rejection and others.

Each patient should know that all these types of allergies are certain damage in its body. The task of the patient is to help the doctor find and eliminate the cause of the ailment.

Bacterial

Quite often, this allergy is called tuberculin. Its development occurs after hitting bacterial allergens. These are usually provocateurs of infections of diphtheria, tuberculosis, fungal diseases, scarletins.

Recently, cases of enclosure of allergen through therapeutic and preventive vaccines increased. Medical practice uses skin delayed reactions of Mantu, Pirka, Burne to determine the excitability of the body under various types of infections.

The painting of the disease is characterized by a slow skin reaction with swelling and redness at a place of direct contact with the antigen. The reactions at the cornea of \u200b\u200bthe eyes are less common, in the organs of the respiratory system, in other fabrics and organs. The formation of the disease can sometimes last for several years. Therefore, it is more common in children over 3 years and adults.

Symptoms of the disease depends on the type of bacteria-provocateurs. Skin manifestations include redness and rash, accompanied by itching. The factors of the disorder of the digestive system organs during slow bacterial allergies include pain in the area of \u200b\u200bthe stomach, diarrhea and vomiting.

When defeating the eyes, itching, redness of mucosa and tearing. The respiratory symptoms allergologists include a feeling of coma in the area of \u200b\u200bthe throat, the difficulty of breathing, cough, bouts of sneezing, disruption of the sense of smell due to the prelation of the nose, transparent discharge and itching in the nose.

Features of the treatment of a bacterial allergic reaction to destroy pathogens. For example, if it started due to a viral infection, the therapy begins with antiviral drugs, and if due to bacterial disease, then with antibacterial treatment.

In order to facilitate the flow of allergy, the doctor may record antihistamine drugs - zetrin, suprastine, diazoline, etc. Possible rinsing of the oral cavity, nasal chamomile booze and calendula, reception of the egg shell powder.

Important! The funds of traditional medicine must be combined with drugs, since the habitat infections can exacerbate and go through, for example, in the heap of bronchial asthma.

Contact

This type of disease is due to a long-term contact with a chemical. It is divided into acute, subacute and chronic. Typically, the last type is a professional disease. Most of all people subject to such fellowship live in industrialized cities.

Synthetic and semi-synthetic fabrics, industrial paints and chemicals, pets, metals, household chemicals, cosmetics, contact lenses, etc. can be caused by contact allergies, and so on. It is possible to encounter a disease. For example, when pets in touch with pets, or when diaper is sewn from non-trial materials.

The first signs of allergies can be seen only after 2 weeks, sometimes - after a week. Dermatitis is always accompanied by an edema, skin itching, peeling, papural appearance. Heavy cases are accompanied by necrosis of the skin and the spread of the disease throughout the body.

Allergologists note that if the penetration of allergen in the skin layers happened for the first time, then you can cure a person in a few days. At the same time, the affected areas are covered with a crust, which soon disappears, giving a place to regenerate healthy cells.

It is possible to detect an allergizing factor by injection and applications and by putting blood to immunoglobulins. Only after establishing a provocateur allergies, the doctor may assign treatment.

Its basis is to exclude a catalyst of the disease from a person's life, information of contacts with him to a minimum. For example, if the malaria has been detected to the paint, he will have to change the profession.

Contact dermatitis is treated with cool approachs or overlapping compresses with drow liquid. With acute manifestations, the allergist prescribes topical glucocorticosteroids. Patients with such allergies need to be taken antihistamines - Erius, phenyatil, zirtek and others. They help reduce swelling and itching.

From the folk remedies, the decoction of Celery was well established (take 100 ml after meals), treatment of leather bravery turns, cleanliness, calendula or hunter. The juices of cucumbers and apples, sour cream and kefir helps from inflammation.

Autoimune

During this disease, immunity responds to its own cells. If a healthy person is physiologically tolerant of its proteins, then the patient uses antibodies to fight with its proteins.

Most often to this disease include: Glominonephritis, hemolytic anemia, myasthenia, red lupus, rheumatoid arthritis. The danger is that the disease can hit any person.

Pathogenesis can be launched in dystrophy, tissue necrosis, radiation disease. Almost all autoimnoy allergies occur very hard, so the patient is necessarily treated in the hospital.

The pattern of therapy depends on the type and stage of the disease. Symptomatic treatment is to reduce the signs of illness, the relief of pain attacks, improving the functioning of the affected organ.

In the pathogenetic treatment of the doctor's auto allergies, immunosuppressants use. Almost always treatment requires connecting corticosteroids. They are able to suppress the products of antibodies, remove inflammation and replace missing corticosteroids.

A prerequisite for therapy is the rehabilitation of chronic foci of infection and enhancing human immunity. Folk remedies in treatment are almost no applied, only for the removal of symptoms.

Transplant rejection

This type of disease appears to be about 7-10 days after tissue transplantation due to genetic differences. The slow motion reaction of donor cells is accompanied by lymphocytosis and destruction of transplanted tissue, temperature, arrhythmia.

To extend the life of the transplantation, the doctors take measures to suppress the function of lymphocyte with chemical or physical impacts.

It is possible to treat the reaction by reducing the activity of the immune response. The treatment diagram is made up by a physician immunologist and a transplantologist. Usually nonspecific immunosuppressive therapy are prescribed.

It consists of the use of several groups of preparations - steroid, analogues of nitrogen bases, alkylating agents, folic acid antagonists, antibiotics.

Output

If you encountered one of the above types of slow motion allergies listed above, follow the instructions of the doctor. Only integrated therapy at a timely reduced diagnosis is able to effectively eliminate the problem. The effects of self-treatment are sometimes crying.

In contact with

Allergies - the state of the increased sensitivity of the body to the effects of some environmental factors.

Allergic reaction - a response of a sensitized organism on the re-administration of allergen, flowing with damage to its own tissues. Under allergic reactions in clinical practice, the manifestations are understood, the emergence of which is immunological conflict.

Sensitization - (Lat Sensibilis - sensitive) - improving the sensitivity of the organism to the effects of some kind of environmental factor or inner medium.

Etiology

The cause of allergic reactions are protein or non-protein (hapten) of nature, called allergens in this case.

The conditions for the development of allergic reactions are:

Allergy Properties

Body condition (hereditary predisposition, state of barrier fabrics)

Three stages of allergic reactions are distinguished:

Immunological stage. (Sensitization)

Patochemical stage (stage of education, release or activation of mediators).

Pathophysiological stage (stage of clinical manifestations).

According to the classification of R.A. Cook adopted in 1947 distinguish 2 types of allergic reactions:

Allergic reactions of immediate type (reaction of the hypersensitivity of the immediate type). For 20 minutes - 1 hour.

Allergic reactions of slow-type (reaction of slow-type hypersensitivity). A few hours after contact with the allergen.

At the heart of the first type of reaction is the reactive fabric damage mechanism, which flows with participation usually IgE, less rarely class IgG, on the surface of the membranes of basophils and puffed cells. A number of biologically active substances are released into blood: histamine, serotonin, bradykinins, heparin, leukotrienes, etc., which lead to violation of the permeability of the cell membranes, an interstitial edema, a smooth muscles spasm, to increase secretion. Typical clinical examples of the first type allergic reaction are anaphylactic shock, bronchial asthma, urticaria, false croup, vasomotor rhinitis.

The second type of allergic reaction is a cytotoxic, occurring with the participation of immunoglobulins of classes G and M, as well as when activating the complement system, which leads to damage to the cell membrane. This type of allergic reaction is observed in drug allergies with the development of leukopenia, thrombocytopenia, hemolytic anemia, as well as hemolysis during hemotransphus, the hemolytic disease of the newborn during the resukeconflict.

The third type of allergic reaction (according to Artus type) is associated with damage to the tissues by immune complexes circulating in the bloodstream, proceed with the participation of immunoglobulins of classes G and M. The damaging effect of immune complexes on tissue occurs through the activation of complement and lysosomal enzymes. This type of reaction is developing with exogenous allergic allergic allergic, glomerulonephritis, allergic dermatitis, serum diseases, individual types of medicinal and food allergies, rheumatoid arthritis, systemic red lchanque, etc.

The fourth type of allergic reaction is tuberculin, slow - occurs after 2448 hours, proceeds with the participation of sensitized lymphocytes. It is characteristic of infectious-allergic bronchial asthma, tuberculosis, brucellosis, etc.

Clinical manifestations of allergic reactions are distinguished by severe polymorphism. Any fabrics and organs can be involved in the process. Skin coverings, a gastrointestinal tract, the respiratory path is more likely to suffer from the development of allergic reactions.

The following clinical variants of allergic reactions are distinguished:

local allergic reaction

allergic toxicodermia

polleoz

bronchial asthma

angioedema swelling Qincke

hives

serum disease

hemolytic crisis

allergic thrombocytopenia

anaphylactic shock

Clinical symptoms of allergic reactions may be:

General symptoms:

general malaise

bad state of health

headache

dizziness

skin itch

Local symptoms:

Nose: Nose mucosa (allergic rhinitis)

Eyes: redness and pain in the area of \u200b\u200bconjunctiva (allergic conjunctivitis)

Upper respiratory tract: bronchospasm, whistling breath, and shortness of breath, sometimes there are true asthma attacks.

Ears: the feeling of completeness, possibly pain and decline in hearing is the reduction of the drainage of the Eustachius pipe.

Leather: various rash. Perhaps: eczema, urticaria and contact dermatitis. Typical location places in the food path of allergen penetration: elbow bends (symmetrically), belly, groin.

Head: sometimes a headache, which occurs in some types of allergies.

Atopic bronchial asthma, atopic dermatitis, allergic rhinitis, polynosis belong to the group of so-called atopic diseases. In their development, hereditary predisposition plays a major role - an increased ability to respond to the formation of IgE and an allergic reaction to the actions of allergens.

Diagnosis of allergic reactions:

Collecting anamnesis Patient

Skin tests - entering into the skin (forearm or back) of small amounts of purified allergens in known concentrations. There are three methods of such samples: a scarification test, intradermal sample, needle test (touch).

Blood test

Provocative tests

Allergen contact exception

Immunotherapy. Hyposensitization and desensitization.

Medications:

• - Antihistamines are used only in order to prevent the development of allergy symptoms and to facilitate the symptoms already have the place.
• - Cromons (Krodoglikat, unoccolved) found the wider use in allergology as preventive anti-inflammatory funds.
• - Local (inhalation) corticosteroid hormones.
• - Anti-tech drugs. New antiallergic preparations for intake. To hormones, these funds do not belong.
• - Broncholitics or broutine.
• - glucocorticoid hormones, cromons and anti-sticker drugs are prescribed for long-term prevention of asthma exacerbations.
• - system steroid hormones. In severe cases, and with pronounced exacerbations, the doctor may prescribe steroid hormones in tablets or injections.
• - Combined medicinal treatment. Practice shows that in most cases one drug does not happen enough, especially when the disease is expressed. Therefore, in order to enhance the therapeutic effect of drugs are combined.

Anaphylactic shock or anaphylaxamm (from other protection "Protection") - an allergic reaction of an immediate type, the condition of a sharply increased sensitivity of the body, developing with the re-administration of allergen.

One of the most dangerous complications of medicinal allergies, ending in about 10--20% of cases.

The prevalence of cases of anaphylactic shock: 5 cases per 100,000 people per year. The increase in the number of anaphylaxis cases increased from 20: 100,000 in 1980 and up to 50: 100,000 in 1990. Such growth is explained by an increase in the number of cases of food allergies. Anaphylaxis are more susceptible to young people and women.

The rate of occurrence of anaphylactic shock - from a few seconds or minutes to 5 hours from the start of contact with the allergen. In the development of an anaphylactic reaction in patients with a high degree of sensitization, neither dose nor the method of administering allergen do not play a decisive role. However, a large dose of the drug increases the severity and duration of the course of shock.

Causes of anaphylactic shock

The root cause of anaphylactic shock was the penetration of poison to the human body, for example, when the snake bite. In recent years, anaphylactic shock has become often observed in therapeutic and diagnostic interventions - the use of drugs (penicillin and its analogs, streptomycin, vitamin B1, diclofenac, amidopyrin, analgin, novocaine), immune sera, iodine-containing radiocontrase substances, with cable testing and hyposensitizing Therapies with allergens, in errors of blood transfusion, blood substitutes, etc.

Pan of stinging or biting insects, for example, from a flint-free (wasps or bee) or triatomic bedbugs, can cause anaphylactic shock in susceptible people. The symptoms described in this article showing anywhere except the place of bite can be attributed to risk factors. However, in about half of death, people did not have seen described symptoms.

Medications

In the event of the first signs of anaphylactic shock, the immediate injections of adrenaline and prednisolone are needed. These drugs should be in the first-aid kit of each person with a tendency to allergies. Prednisolone is a hormone, an overwhelming allergic reaction. Adrenaline is a substance that causes vessels spasms and prevents eatery.

Many food can cause anaphylactic shock. This can happen immediately after the first admission of allergen in food. Depending on the geographical position in the list of allergens, certain foods may prevail. In Western cultures, it may be peanuts, wheat, nuts, some seafood (for example, mollusks), milk or eggs. In the Middle East, this may be seed seeds, and in Asia, an example can serve as an example. Heavy cases are caused by the use of allergen inside, however, the reaction occurs when contact with the allergen. In children, allergies can pass with age. By age, 16 years, 80% of children with intolerance to milk and eggs can use these products without consequences. For peanut, this indicator is 20%.

Risk factors

People with diseases such as asthma, eczema, allergic rhinitis have an increased risk of developing anaphylactic shock caused by food, latex, contrast substances, but not medicines or insect bite. One study showed that 60% of those who in the history of the disease had atopic diseases and those who died from anaphylactic shock had also asthma. Those who have mastocytosis or high socioeconomic status are in the zone of increased risk. The more time passed since the last contact with the allergen, the less the risk of anaphylactic shock.

Pathogenesis

The basis of pathogenesis is the reaction of the hypersensitivity of the immediate type. The overall and most significant sign of shock is acute the upcoming reduction in blood flow with a disturbance of peripheral, and then the central blood circulation under the influence of histamine and other mediators, abundantly secreted cells. Skin covers become cold, wet and cyanotic. In connection with the decrease in blood flow in the brain and other organs, anxiety appears, darkening of consciousness, shortness of breath, violated urination.

Symptoms of anaphylactic shock

Anaphylactic shock is usually manifested by various symptoms within a few minutes or hours. The first symptom or even harbing the development of anaphylactic shock is a sharply pronounced local response at the place of allergen hitting the body - unusually sharp pain, strong swelling, swelling and redness at the site of the bite of an insect or injection of a medicinal product, a heavy skin, quickly spreading throughout the skin ( Generalized itching), a sharp drop in blood pressure. When admitting allergen inside the first symptom there may be a sharp pain in the abdomen, nausea and vomiting, diarrhea, oral east of the mouth and larynx. With the introduction of the drug intramuscularly observed the appearance of a stubborn pain (strong compression under the edges) 10--60 minutes after entering the drug.

Breast rash and hyperemia

Following the pronounced edema of larynx, bronchospasm and laryngospasm, leading to a sharp imperious difficulty breathing. The difficulty of breathing leads to the development of a rapid, noisy, hoarse ("asthmatic") respiratory. Hypoxia is developing. The patient is very pale; Lips and visible mucous membranes, as well as the distal ends of the limbs (fingers) can become cyanotic (blue). In the patient with an anaphylactic shock, blood pressure drops sharply and collapse develops. The patient can lose consciousness or faint.

Anaphylactic shock develops very quickly and can lead to death for a few minutes or hours after entering allergen to the body.

Treatment of anaphylactic shock

Autoinjector with adrenaline

The first event under anaphylactic shock should be the imposition of a harness above the injection or bite and urgent administration of adrenaline - 0.2-0.5 ml of 0.1% of the solution subcutaneously or, better, intravenously. In the appearance of signs of edema of the larynx, it is recommended to introduce 0.3 ml 0.1% of the pra of adrenaline (epinephrine) in 1020 ml of 0.9% PRA sodium chloride intravenously; Prednisolone 15 mg / kg intravenously or intramuscularly. In the event of an increase in acute respiratory failure, the patient should immediately intubate. If the tracheal intubation is not possible - to perform a coneer, tracheostomy or punctuate the trachea with 6 needles with a wide lumen; The administration of adrenaline can be repeated to the total total dose of 1-2 ml of 0.1% solution in a short period of time (a few minutes), but in any case, enter adrenaline should be introduced by fractional portions. In the future, adrenaline is introduced by the need, taking into account its short half-life, focusing on blood pressure, heart rate, symptoms of overdose (tremor, tachycardia, muscular twist). It is impossible to allow adrenaline overdose, since its metabolites may worsen the flow of anaphylactic shock and block the adrenoreceptors.

Following the adrenaline, glucocorticoids should be introduced. It should be known that the doses of glucocorticoids needed to relieve an anaphylactic shock are ten times higher than "physiological" dosages and many times - doses used to treat chronic inflammatory diseases such as arthritis. Typical doses of glucocorticoids necessary for an anaphylactic shock are 1 "large" ampoule of methylprednisolone (as for pulseratrapia) of 500 mg (i.e. 500 mg of methylprednisolone), or 5 ampoules of dexamethasone in 4 mg (20 mg), or 5 ampoules prednisolone 30 mg (150 mg). Smaller doses are ineffective. Sometimes the doses are required more than the above - the necessary dose is determined by the severity of the patient's condition with anaphylactic shock. The effect of glucocorticoids, unlike adrenaline, it does not occur immediately, but after dozens of minutes or a few hours, but lasts longer. For the relief of bronchospasm, resistant to the action of adrenaline (epinephrine), - Eufillin (aminofillin) 20 ml of 2.4% V / WE Slowly, prednisone 1.5 - 3 mg / kg.

Also shows the introduction of antihistamine drugs from among those who do not reduce blood pressure and not possessing high-own allergenic potential: 1-2 ml of 1% of the diploma or suprastin, Tuese. It is impossible to introduce diprazine - it, as well as other derivatives of phenothiazine, has significant own allergenic potential and, in addition, reduces the already low blood pressure in the patient with anaphilaxia. According to modern ideas, the administration of chloride or calcium gluconate, which is widely practiced earlier, not only not shown, but also can adversely affect the patient's state.

The slow intravenous administration of 10-20 ml of 2.4% of the solution of euphillin is shown to remove bronchospasm, reducing edema of lungs and relieve respiration.

The patient with an anaphylactic shock should be put in a horizontal position with lowered or horizontal (not raised!) The upper part of the body and head for the best blood supply to the brain (given the low blood pressure and low blood supply to the brain). It is recommended to adjust the inhalation of oxygen, intravenous drip administration of saline or other aqueous solution to restore hemodynamic and blood pressure.

Prevention of anaphylactic shock

Prevention of the development of anaphylactic shock is primarily in avoiding contacts with potential allergens. Patients with known allergies on chiropo (drugs, food, insect bites) Any preparations with high allergenic potential should either be avoided or assigned to caution and only after confirming the skin of the fact of the absence of allergies to a particular drug.

4. Antoslude blood system. Hemorrhagic syndrome. Classification of hemorrhagic diathesis. Ethiopathogenesis, symptoms of hemophilia, thrombocytopenic purpura and hemorrhagic vasculitis. Principles of treatment

gastritis flu diathesis hemophilia

All anticoagulants formed in the body are divided into two groups:

Anticoagulants of direct action - independently synthesized (heparin, antithrombin III - ATIII, protein C, protein S, A2Makroglobulin) :;

Non-smaller anticoagulants - formed during blood coagulation, fibrinolysis and activation of other proteolytic systems (fibrinantitrombin I, antithrombin IV, factors inhibitors VIII, IX, etc.) Prostacyclin, which is allocated by the endothelium of vessels, inhibits adhesion and aggregation of erythrocytes and thrombocytes.

The main inhibitor of the coagulation system is ATIII, which inactivates thrombin (factor on) and other coagulation factors (1ha, ha, 1h).

The most important anticoagulant - heparin; It activates ATIII, and also holds back the formation of blood thromboplastin, inhibits the fibrinogen conversion to fibrin, blocks the effects of serotonin on histamine and others.

Protein C limits the activation of factors V and VIII.

A complex consisting of a lipoprotein-associated inhibitor and factor HA, inactivates the Vila factor, that is, the outer path of the plasma hemostasis.

For states accompanied by hypercoagulation and hemostasis disorder, the following groups of drugs can be applied, differing in the mechanism of influence on individual links of the homeostasis system.

Antitrombotic drugs acting on an antoslude blood system

Anticoagulants: Direct Action; Indirect action.

Fibrinolysis facilities: direct action; Indirect action.

Tools affecting platelet aggregation.

Hemorrhagic diathesis The state of increased bleeding combines a group of diseases by their leading symptom.

The main causes of high bleeding are: disorders in the blood coagulation system, decrease in the amount or violation of platelet functions, damage to the vascular wall and the combination of listed factors.

Classification.

• 1. Hemorrhagic diathesis caused by a violation of the plasma hemostasis (congenital and acquired coagulopathy).
• 2. Hemorrhagic diathesis caused by a violation of the megacariocytic platelet system (autoimmune thrombocytopenia, thrombaste).
• 3. Hemorrhagic diathesis caused by violation of the vascular system (hemorrhagic vasculitis, randyosler disease).
• 4. Hemorrhagic diathesis caused by combined disorders (Willebrand disease).

Types of bleeding:

The type and severity of the bleeding, established during the survey, significantly facilitate the diagnostic search.

I. Hematomic with painful intense hemorrhages both in soft tissues and in joints - typical for hemophilia A and B;

II. Patechial (bruise) - characterized for thrombocytopenia, thrombocytopathops and some violations of blood coagulation (exceptionally rare) - hypo and distibrinegenemia, hereditary deficit of factors X and II, sometimes VII;

III. The mixed bruise is characterized by a combination of petechial spotted bleeding with the advent of individual large hematomas (retroperitoneal, in the intestinal wall, etc.) in the absence of damage to the joints and bones (the difference from hematomic type) or with single hemorrhages in the joints: bruises can be extensive and painful. Such a type of bleeding is observed in the severe deficit of the factors of the prothrombin complex and factor XIII, Willebrand disease, twist.

Thrombocytopenia.

Causes of thrombocytopenia:

• 1. Autoimmune thrombocytopenia.
• 2. For diseases of the liver, systemic diseases, AIDS, sepsis.
• 3. Blood diseases (aplastic anemia, megaloblastic, hemoblastosis).
• 4. Medical (myelotoxic or immune).
• 5. Hereditary.

Idiopathic autoimmune thrombocytopenia (Verlgood's disease)

Clinical picture. Clinical flow distinguish:

• - Skin or simple form Purpura Simplex
• - articular form of Purpura Reumatica
• - Abdominal form Purpura abdominalis
• - Renal form Purpura Renalis
• - Figuecent Form Purpura Fulminans

There may be a combination of various forms

The skin lesion is characterized by small-point symmetrically located petechias, mainly on the lower limbs, buttocks. The rashes of the monomorphic, first with a distinct inflammatory framework, are complicated by central necrosis in severe cases, which, in consequence covered with crusts, leaving pigmentation for a long time. Not accompanied by itching. In severe cases, petechia are complicated by necrosis. More often intensive rash is held 45 days, then gradually subsides and disappears at all after which there can be a small pigmentation. As a rule, the skin shape ends with complete recovery. The lesion of the joints is manifested by a sharp pain, swelling, violation of their function. The location of the joints is a synovial shell. The lesion of the joints is completely reversible. Abdominal vasculitis form is manifested by hemorrhages in the mucous membrane of the stomach, intestine, mesenter. With this form, severe abdominal pain arise, sometimes simulating the picture of an acute abdomen. May increase body temperature, sometimes vomiting appears. Blood is determined in feces. In most cases, abdominal manifestations are short-lived and within 23 days pass. Recurrents are possible. When they combine with skin patech rashes, the diagnosis is not of great difficulty. In the absence of skin manifestations of disease, diagnosis is difficult. The transferred viral infection should be taken into account, the presence of rashes on the skin preceding the appearance of abdominal pain. Tests are used for the resistance of capillaries (samples of Nesterov and Konchalovsky). The renal form, which flows along the type of acute or chronic nephritis, which occurs sometimes a protracted course with development in the subsequent CPN, deserves the greatest attention. Possible nephrotic syndrome. Kidney lesions, as a rule, does not occur immediately, but after 1 4 weeks after the start of the disease, the kidney defeat the dangerous manifestation of hemorrhagic vasculitis. In the presence of hemorrhagic vasculitis, it is advisable to pay attention to the indicators of the composition of the urine and the functions of the kidney throughout the entire period of the disease. A fast-flowing or cerebral form develops with hemorrhage into a cerebral shell or vital areas. The diagnosis of hemorrhagic vasculitis is based in addition to clinical manifestations to increase the level of Willebrand factor (antigenic component of the factor), hyperfybrinogenemia, increasing the content of IR, cryoglobulins, and b2 and g of globulin, B1 acid glycoprotein, determining antitrombin III and plasma heparinoresistance. Treatment. Cancel drugs with the use of which the occurrence of the disease may be associated. The main method of treating hemorrhagic vasculitis is the introduction of heparin subcutaneously or intravenously. The daily dose can be from 7500 to 15,000 units. The introduction of heparin is carried out under the control of blood coagulation. Among the new drugs used in vasculitis therapy are heparinoids.1 to this group of drugs belongs to Sulodekside (Vessel Due F), providing a comprehensive effect on the walls of blood vessels, viscosity, vascular permeability, as well as on various levels of hemostasis system - blood coagulation, Adhesion and platelet aggregation, fibrinolysis, which qualitatively and quantitatively different from the usual and low molecular weight heparin. An important feature of Vessel Due F is that it does not cause heparinic thrombocytopenia, which allows it to include in the therapy of patients who have this formidable complication of heparinotherapy. The best effect in the therapy of these states was obtained with the combined use of this drug with stage plasmapherester. With the ineffectiveness of therapy, steroid hormones are shown in small doses in the detection of cryoglobulinemia, a cryopherresis is shown. In the acute period, treatment should be carried out in the hospital in compliance with the beddown.

Twossindris (disseminated intravascular blood coagulation, thrombohemorrhagic syndrome) is observed in many diseases and all terminal (suicide) states. This syndrome is characterized by scattered intravascular coagulation and aggregation of blood cells, activation and depletion of components of coagulation and fibrinolytic systems (including physiological anticoagulants), a disorder of microcirculation in organs with their dystrophy and dysfunction, expressed inclination to thrombosis and bleeding. The process can be sharp (often lightning), subacute, chronic and recurrent aggravation and subsorative periods. Etiology and pathogenesis: acute pastry accompanies heavy infectious diseases (including abortions during childbirth, more than 50% of all cases), all types of shock, destructive processes in organs, severe injury and traumatic surgical interventions, acute intravascular hemolysis ( Including with incompatible hemotransphuses), obstetric pathology (prelation and early celaiming placenta, embolism of milk-free waters, especially infected, manual separation of placenta, hypotonic bleeding, uterine massage in its atony), massive gemotransphuses (danger increases when using blood more than 5 days of storage ), acute poisoning (acid, alkali, snake poisons, etc.), sometimes acute allergic reactions and all terminal states. The pathogenesis of the syndrome in most cases is associated with the massive flow from the tissues into the blood of blood coagulation stimulants (tissue thromboplasty, etc.) and platelet aggregation activators, damage to the large area of \u200b\u200bthe endothelium of vessels (bacterial endotoxins, immune complexes, complement components, cellular and protein decay components) . Schematically, the pathogenesis of the twistrome can be represented by the following sequence of pathological disorders: the activation of the hemostasis system with the shift of the phases of hyper and hypocoagulation intravascular blood coagulation, platelet aggregation and erythrocytes microtrombation of vessels and microcirculation blocks in organs with their dysfunction and dystrophy (Antrombin III, proteins C and S), reduced blood platelets (thrombocytopenia of consumption). It significantly affects the toxic effect of protein decay products, accumulating in large quantities, both in blood and in organs as a result of a sharp activation of proteolytic systems (coagulation, kallicreinic, fibrinolytic, complement, etc. ), infringement of blood supply, hypoxia and necrotic changes in tissues, frequent weakening of the disinfectant and excretory function of the liver and kidneys. The clinical picture is consisted of the signs of the main (background) disease, which caused the development of intravascular blood coagulation, and the twisunder itself. Stages: I hypercoagulation and thrombosis. II transition from hyper to hypochagupation with multidirectional shifts of different blood coagulation parameters. III deep hypocoagulation (up to complete non-pilotability of blood and severe thrombocytopenia). IV reverse development of twist. The acute body of the body, which places it on the line between life and death, characterized by severe phase disorders in the hemostasis system, thrombosis and hemorrhages, microcirculation disorders and severe metabolic disorders in organs with their dysfunction, proteolysis, intoxication, development, or recess of shock phenomena ( Hemokoagulanti-QOLEMIC Nature). Pharmacotherapy: The treatment of acute twist should be directed primarily on the rapid elimination of its cause. Without early started successful etiotropic therapy, it is impossible to count on the salvation of the life of the patient. The main pathogenetic methods of treatment are anti-depository, intravenous drip administration of heparin, inkjet transfusions of fresh native or freshly frozen plasma, if necessary with plasma value, the fight against blood loss and deep anemic (blood substitutes, freshcattrate blood, eryprising), acute respiratory impairment (early connection of artificial lung ventilation) and acid equilibrium, acute renal or hepatorenal failure. Heparin should be administered intravenously (in an isotonic solution of sodium chloride, with plasma, etc.), in some cases, in combination with subcutaneous injections in the fiber of the front abdominal wall below the umbilical line. The dose of heparin varies depending on the shape and phase of the twisting: in the hypercoagulation stage and at the beginning of the starting period with sufficiently stored blood coagulation of the daily dose of it in the absence of abundant initial bleeding can reach up to 40,000 60,000 units (500800 units / kg). If the beginning of the twist is accompanied by profuse bleeding (uterine, from ulcers or disintegrating tumor, etc.) or there is a high risk of its occurrence (for example, in the early postoperative period), the daily dose of heparin should be reduced by 23 times.

In these situations, as in the deep hypocoaguation phase (23, the administration of heparin is used mainly to cover plasma and blood transfusions (for example, at the beginning of each transfusion, 25005000 Ugarin droplet is introduced together with the hemopreciation). In some cases (especially with infectious-oxidic forms of twisted) transfusion of fresh frozen or fresh native plasma, they are carried out after plasmaisis sessions of 6001000 ml of the patient's plasma (only after hemodynamic stabilization!). In the twisunder of the infectiousness of nature and the development of the pulmonary distress, plasmazitheresis is shown, since leukocytes play a substantial role in the pathogenesis, the leukocytes are played, one of which begin to produce tomblalastin tomblastin (mononuclears), while other eserases that cause interstitial pulmonary edema (neutrophils). These methods of plasmotherapy and plasmament substantially increase the effectiveness of the treatment of twist and causes its diseases, reduce mortality several times, which makes it possible to consider them the main method of therapy of patients with this violation of hemostasis. With a significant anemization, transfusions of fresh canned blood (daily or up to 3 days of storage), the erythrocytic mass and erythrocyte suspension (hematrocrit, should be maintained above 25%, the hemoglobin level is higher than 80 g / l. Do not strive for fast and complete normalization. Red blood indicators, as moderate hemodilution is necessary to restore normal microcirculation in the organs. It should be remembered that the acute twist is easily complicated by swelling of the lungs, therefore significant overloading of the circulatory system during syndrome is dangerous. In the stage of the twist, and with pronounced proteolysis in the tissues (lung gangrene, Non-necrotic pancreatitis, acute liver dystrophy, etc.) Plasmapheresis and inkjet transfusions of fresh frozen plasma (under the cover of small doses of heparin 2500 units) combined with re-intravenous administration of large doses of conflict (up to 300,000 500,000 units) or other antiproteas.

In the late stages of the development of the twist and during its varieties occurring against the background of hypoplasia and bone marrow dysplasia (radiation, cytotoxic diseases, leukemia, aplastic anemia) to relieve bleeding, and transfusion of platelet concentrates. An important link of complex therapy is the use of decagnegantes and drugs that improve microcirculation in organs (KARANTIT, DIPIirDamol in combination with a trental; dopamine in renal failure, alphaadrenoblastors (sermion), tickopidine, defibroid, etc.). An important component of therapy is an early connection of artificial ventilation of the lungs. The removal of the patient from shock is facilitated by the use of Naloxan antiopoids and others. Subighteous twist. Symptoms, flow. It is characterized by a longer than in acute twist, the initial period of hypercoagulation is asymptomatic or manifested by thrombosis and disorders of microcirculation in organs (workload, anxiety, a sense of valuable fear, a decrease in diuresis, swelling, protein and cylinders in the urine). Treatment Accession to therapy of the main disease of drip intravenous and subcutaneous administrations of heparin (daily dose of 20,000 to 60,000 units), disaggregants (Dipyridamol, Trental, etc.). Rapid relief or weakening of the process is often achieved only during plasmapheresis (removal of 6001200 ml of plasma daily) with a substitute for a partially fresh, native or freshly frozen plasma, partially by coarse solutions and albumin. The procedure is carried out under the cover of small doses of heparin. Chronic twist. Symptoms, flow. Against the background of the signs of the main disease, there is a pronounced blood hypercoagulation (rapid coagulation in the veins spontaneous and when they are proof; needle, test tubes), hyperfibrinogenemia, inclination to thrombosis, positive paracoagurative tests (ethanol, protamin sulfate, etc.). Bleeding time on Duka and Burkhegrechinka is often shortened, blood platelet content is normal or elevated. It is often revealed by their spontaneous hyperagregation of small flakes in plasma. With a number of forms, an increase in hematocrit, a high level of hemoglobin (160 g / l and more) and erythrocytes, a slowdown in ESO (less than 45 mm / h) is noted. Hemorrhage, petechia, bruises, bleeding from the nose and gums, etc. (in combination with thrombosis and without them) appear easily. Treatment is the same as in the subacute form. With polyglobulia and blood thickening hemodilution (reopolyglyukin intravenously to 500 ml daily or every other day); Citafaresis (removal of red blood cells, platelets and their aggregates).

With hypertroscitosis, disaggregants (acetylsalicylic acid of 0.30.5 g daily 1 time per day, Trental, Dipyridamol, Plavix, etc.). For the treatment of subacute and chronic forms of DVS syndrome, if there are no contraindications, leeches are used. The biologically active compounds contained in the fluid injected fluid to the fluid have a stabilizing effect on the rheological properties of blood, especially with such pathology, such as disseminated intravascular blood coagulation (DVS - syndrome).

All means affecting blood coagulation affecting blood coagulation system are divided into three main groups:

• 1) funds contributing to blood coagulation - hemostatic, or coagulants;
• 2) funds depressing blood coagulation - antithrombotic (anticoagulants, anti-aggregants);
• 3) means affecting fibrinolysis.

Tools that increase blood coagulation (hemostatic)

• 1. Coagulants:
  • a) direct action - thrombin, fibrinogen;
  • b) indirect action - Vikasol (vitamin K).
• 2. Fibrinolysis inhibitors.
• 3. Adhesion and aggregation agents that reduce vessel permeability.

Coagulant

Direct-acting coagulants are drugs from donor blood plasma, which are divided into drugs for local applications (thrombin, hemostatic sponge) and drugs for systemic effects (fibrinogen).

Thrombin - the natural component of the hemochaguing system, is formed in the body from Prothrombin during enzymatic activation of it with thromboplastin. The unit of activity of thrombin takes such a quantity that is capable at a temperature of 37 ° C to cause coagulation of 1 ml of fresh plasma for 30 ° C or 1 ml of 0.1% of the purified fibrinogen solution for 1 s. The thrombin solution is used only to stop bleeding from small vessels, parenchymal organs (for example, during the operations on the liver, brain, kidneys). The thrombin solution is impregnated with gauze tampons and apply them to a bleeding surface. You can enter in inhalations, in the form of an aerosol. The introduction of thrombin solutions is parenterally not allowed, because they cause the formation of blood clots in the vessels.

The hemostatic sponge has a hemostatic and antiseptic effect, stimulates tissue regeneration. It is contraindicated in bleeding of large vessels, increased sensitivity to Furacilin and other nitrofurans.

Fibrinogen sterile human blood fraction. In the body, the transformation of fibrinogen in fibrin is carried out under the influence of thrombin than the process of thrombosis is completed. The drug is effective in hypoofibrixion, large blood loss, radial lesions, liver diseases.

Freshly prepared solution is administered intravenously drip. Contraindicated patients with myocardial infarction.

The indirect action coagulants are vitamin K and its synthetic analogue of Vikasol (WIT. K3), its international name "Menadion". Natural antigenorrhagic factors are vitamins K, (Philohyinone) and K ,. This is a group of 2 methyl derivatives1.4Naptoquinone. Philohinone (WIT. K,) comes with vegetable food (spinach leaves, cauliflower, rosehip fruits, needles, green tomatoes), and vitamin K is contained in animal products and is synthesized with intestinal flora. Life-soluble vitamins K, and K, more active than synthetic water-soluble vitamin K, (Vikasol - 2,3digidro2Methyl1.4NaptoHinone 2 sulfonate sodium), synthesized in 1942 by the Ukrainian biochemist A. V. Palladin. (For the introduction of Vikasol's medical practice, A. V. Palladia received the USSR State Prize.)

Pharmacokinetics. The fat-soluble vitamins (K, and K,) are absorbed in the small intestine in the presence of bile acids and enter blood with plasma proteins. Natural philochinone and synthetic vitamin in organs and tissues turn into vitamin K,. Its metabolites (about 70% of the dose introduced) are derived by the kidneys.

Pharmacodynamics. Vitamin K is necessary for synthesis in the liver Prombrin and other blood coagulation factors (VI, VII, IX, X). Influences fibrinogen synthesis, takes part in oxidative phosphorylation.

Indications for use: Vicasol is used for all diseases accompanied by a decrease in the content of prothrombin in the blood (hypoprothrombinemia) and bleeding. This is, first of all, jaundice and sharp hepatitis, peptic ulcer of the stomach and duodenum, radiation disease, septic diseases with hemorrhagic manifestations. Wikasol is also effective in parenchymal bleeding, bleeding after injury or surgical intervention, hemorrhoidal, long nosebleed bleeding, etc. It is also used prophylactically to a surgical operation, with long-term treatment with sulfanilaminamide drugs and antibiotics, inhibiting the intestinal flora, which synthesizes vitamin K,. It is also used in bleeding caused by overdose of neodykumarin, pheniline and other indirect anticoagulants. The effect develops slowly - after 12-78 hours after administration.

Vikasol can be cumulated, so the daily dose should not exceed 1--2 tablets or 1 - 1.5 ml of 1% solution intramuscularly not more than 3--4 days. If necessary, repeated administration of the drug is possible after a 4 days of interruption and conducting a sample for blood coagulation rate. Vikasol is contraindicated with increased hemocoagulation and thromboembolism.

As a source of vitamin K, plant preparations are used, they contain other vitamins, bioflavonoids, various substances that can contribute to blood coagulation, reduce the permeability of the vascular wall. This is, first of all, the nettle is bipher, a lagocilus, a viburnum, a water pepper, Arnica Mountain. Of the listed plants prepare infusions, tincture, extracts that are used inside. Some of these drugs are used locally, in particular, the freshly prepared innocence of the flowers and the leaves of the lagochelus wet the gauze wipes and are applied to 2--5 min to a bleeding surface.

Preparations that increase blood coagulation I. Fibrinolysis inhibitors: CTA aminocaprona; amben; Transcamic acid. II. Hemostatic tools: 1) for the system action of fibrinogen;

2) for local applications: thrombin; sponge hemostatic collagen; 3) Vitamin K: phytomenadion, vikasol; III. Funds that enhance platelet aggregation: calcium salts, adroxon, ethalate, serotonin. IY. LANs of vegetable origin: intoxicating, the leaves of nettle, yarrow grass, grass of the pepper and kidney.

Specific hemostatic HS Hematate (Benring Germany) with hemophilia type A. Factor Ixbering (Benring, Germany) with hemophilia type V. Hemophilia type A and in inherited genetically diseases are relatively rare

Heparin antagonists: Apply in the case of an overdose of heparin Protamot Sulfate (1 mg neutralizes 85 heparin units), toluidine blue (once 12 mg / kg), agess, desmopressin, stylamine. Thromboous LS: thrombovar (decilat). Pharmacodynamics: Thrombovar Winged-based drug, which forms a thrombus and is designed to close the pathologically advanced surface veins of the lower extremities (varicose veins), provided that there are deep veins.

LS, lowering the permeability of the vessel ADROCON, Ethalizila, Rutin, ascorbic acid, Askorutin, Trokevazin, Vegetable preparations (rosehip, citrus, currant, nettle, yarrow, Pepper kidney, etc.).

Allergy (Greek Allos - another and Ergon - action) - increased sensitivity of the body to various substances associated with changes in its reactivity. The term was proposed by the Austrian Pediatricians of the Pirka and Shikom (S. Pirquet, V. Schick, 1906) to explain the phenomena of serum disease observed in children in infectious diseases.

The increased sensitivity of the body during allergies is specific, that is, it rises to that antigen (or another factor), with which it was previously a contact and which caused a sensitization state. Clinical manifestations of this heightened sensitivity are usually as allergic reactions. Allergic reactions arising from people or animals during primary contact with allergens are called nonspecific. One of the variants of nonspecific allergies is parallergia. Parallergia is called an allergic reaction caused by any allergen in the body sensitized by another allergen (for example, a positive skin reaction to tuberculin in a child after vaccinating its sipop). A valuable contribution to the doctrine of infectious parallergip was made by the work of P. F. Zdodovsky. An example of such parallergia is the phenomenon of a generalized allergic reaction to cholera vibrio endotoxin (see Sanareli-Zododovsky phenomenon). The resumption of a specific allergic reaction after the introduction of nonspecific stimulus is called metalrooms (for example, the resumption of tuberculin reaction in a patient with tuberculosis after the abdominal vaccine is introduced).

Classification of allergic reactions

Allergic reactions are divided into two large groups: the reactions of immediate and reaction of slow-type types. The concept of allergic reactions of immediate and slow-type tests has emerged as a result of clinical observations: the pirk (1906) differed immediate (accelerated) and slow (stretched) forms of serum disease, cingsser (N. Zinsser, 1921) - fast anaphylactic and slow (tuberculin) forms Skin allergic reactions.

Immediate type reactions Cook (R. A. Cook, 1947) called skin and systemic allergic reactions (respiratory, digestive and other systems) arising 15-20 minutes after exposure to a patient specific allergen. Such reactions are skin blisters, bronchospasm, disorder function of the gastrointestinal tract and the other. The reactions of immediate type include: anaphylactic shock (see), Olevier phenomenon (see skin anaphylaxis), allergic urticaria (see), serum disease (see), non-infectious-allergic forms of bronchial asthma (see), hay fever ( See Polynomus), angioedema edema (see sqinke swelling), acute glomerulonephritis (see) and more.

Slow-type reactionsUnlike immediate-type reactions, develop for many hours and sometimes days. They occur with tuberculosis, diphtheria, brucellosis; They are caused by hemolytic streptococcus, pneumococcal, vaccine virus and more. The allergic reaction of the delayed type in the form of damage to the cornea is described in streptococcal, pneumococcal, tuberculous and other infections. With allergic encephalomyelitis, the reaction also proceeds by the type of slow allergies. The reactions of a slow-type type include and reactions to vegetable (primula, ivy and other), industrial (ursol), drugs (penicillin, etc.) of allergens with so-called contact dermatitis (see).

Allergic reactions of instant type differ from slow allergic reactions in a number of features.

1. Immediate allergic reactions are developing 15-20 minutes after the contact of the allergen with a sensitized cloth, slowed down - after 24-48 hours.

2. Immediate allergic reactions are characterized by the presence of circulating antibodies in the blood. In slower reactions of the antibody in the blood, are usually absent.

3. With the reactions of an immediate type, passive transfer of increased sensitivity to a healthy organism with serum serum patient is possible. In slow-down allergic reactions, such a transfer is possible, but not with serum, but with leukocytes, cells of lymphoid organs, exudate cells.

4. The reaction of the delayed type is characterized by a cytotoxic or lithical action of allergen to sensitized leukocytes. For immediate allergic reactions, this phenomenon is not characteristic.

5. For delayed type reactions, the toxic effect of allergen on the tissue culture is characterized, which is not typical for immediate reactions.

In part, the intermediate position between the reactions of immediate and slow-type is occupied by the phenomenon of Artus (see Artus Phenomenon), which in the initial stages of development stands closer to the reactions of instant type.

The evolution of allergic reactions and their manifestations in ontogenesis and phylogenesis were studied in detail by N. N. Sirotinin and his students. It is established that in the embryonic period anaphylaxius (see) can not be called in an animal. In the period of the newborn, the anaphylaxis develops only in spectrive animals, such as guinea pigs, goats, and yet in a weaker form than adult animals. The emergence of allergic reactions in the process of evolution is associated with the appearance of the ability to produce antibodies in the body. Invertebrates, the ability to produce specific antibodies is almost absent. To the greatest extent, this property is developed at the highest warm-blooded animals and especially in humans, therefore, it is precisely in person allergic reactions are observed particularly often and their manifestations are diverse.

Recently, the term "Immunopathology" arose (see). Immunopathological processes include demyelinizing lesions of nervous tissue (post-declaid encephalomyelitis, multiple sclerosis and other), various nephropathy, some forms of thyroid inflammation, testicles; An extensive blood disease group (hemolytic thrombocytopenic purple, anemia, leukopenia) is adjacent to the same processes (hemolytic thrombocytopenic purpura, anemiamatology (see).

Analysis of the actual material on the study of pathogenesis of various allergic diseases by morphological, immunological and pathophysiological methods shows that the basis of all diseases united into the group of immunopathological, allergic reactions lie and that immunopathological processes do not have fundamental differences from allergic reactions caused by various allergens.

Mechanisms for the development of allergic reactions

Allergic reactions of immediate type

The mechanism for the development of allergic reactions of an immediate type can be divided into three closely connected with each other (according to A. D. ADO): immunological, Patochimic and pathophysiological.

Immunological stage It is an interaction of allergens with allergic antibodies, that is, the allergen reaction is an antibody. Allergic reactions with allergic reactions with allergen compound with an allergen are compiled, that is, they are able to precipitate with an allergen reaction, for example. In anaphylaxis, serum disease, the phenomenon of Artus. Anaphylactic reaction can be caused in an animal not only by active or passive sensitization, but also by the introduction of an allergen-antibody cooked in the tube into the blood. In the pathogen action of the resulting complex, the complement plays a major role, which is fixed by the immune complex and is activated.

With a different group of diseases (hay fever, an atonic bronchial asthma and the other) antibodies do not have the property to be deposited during the reaction with the allergen (incomplete antibodies).

Allergic antibodies (react) in atonic diseases in humans (see Atopia) are not formed with the appropriate allergen of insoluble immune complexes. Obviously, they do not fix the complement, and the pathogenic action is carried out without its participation. The condition for the occurrence of an allergic reaction in these cases is the fixation of allergic antibodies on cells. The presence of allergic antibodies in the blood of patients with atronic allergic diseases can be determined by the Prausnitz-Cussetter reaction (see Prausnitz-Custener reaction), which proves the possibility of passive transfer of increased sensitivity with serum from a patient on the skin of a healthy person.

Patochemical stage. The consequence of the reaction of the antigen - antibody with an allergic reaction of instant type is deep changes in cell biochemism and tissues. The activity of a number of enzyme systems necessary for normal cellularity of cells is dramatically violated. As a result, a number of biologically active substances are exempt. The most important source of biologically active substances are the fat cells of the connective tissue, separating histamine (see), serotonin (see) and heparin (see). The process of release of these substances from the granules of obese cells proceeds into several stages. Initially, "active degranulation" occurs with the cost of energy and activation of enzymes, then the liberation of histamine and other substances and the exchange of ions between the cell and the environment. The liberation of the histamine is also occurs from the leukocytes (basophiles) of the blood, which can be used in the laboratory for the diagnosis of allergies. Histamine is formed by decarboxylation of histidine amino acid and may be contained in the body in two types: a fragustable tissue protein (for example, in fat cells and basophosplises, in the form of fraudums with heparin) and free, physiologically active. Serotonin (5-hydroxytriptamine) in large quantities is contained in platelets, in the tissues of the digestive tract H nervous system, in a number of animals in fat cells. A biologically active substance playing an important role in allergic reactions is also a slowly acting substance, the chemical nature of which is not completely disclosed. There is evidence that it is a mixture of nuraminic acid glucoside. During anaphylactic shock, Bradykinin is also exempt. It belongs to the group of plasma kinins and is formed from the bradykinogen plasma, destroyed by enzymes (kininos), forming inactive peptides (see allergic reaction mediators). In addition to histamine, serotonin, bradykinin, a slowly active substance, such substances such as acetylcholine (see), choline (see), norepinephrine (see), and other fat cells are discharged mainly histamine and heparin; Heparin, histamine is formed in the liver; in adrenal glands - adrenaline, norepinephrine; in thrombocytes - serotonin; in nervous tissue - serotonin, acetplecholine; In the lungs - slowly valid substance, histamine; Plasma - Bradykin and so on.

Pathophysiological stage It is characterized by functional disorders in the body developing due to the reaction of the allergen - antibody (or allergen - react) and the release of biologically active substances. The cause of these changes is both the immediate impact of the immunological response to the cells of the body and numerous biochemical intermediaries. For example, histamine at intracutaneous injection is capable of calling so called. "Lewis's triple answer" (itching at the place of administration, erythema, blister), which is characteristic of the skin allergic reaction immediately; Histamine causes a reduction in smooth muscles, serotonin - changing blood pressure (lifting or drop, depending on the initial state), reducing the smooth muscles of the bronchiole and the digestive tract, the narrowing of larger blood vessels and the expansion of small vessels and capillaries; Bradykin is able to cause a reduction in smooth muscles, vasodilation, positive chemotaxis leukocytes; The muscles of bronchiol (in humans) is particularly sensitive to the influence of a slowly acting substance.

Functional changes in the body, their combination and constitute a clinical picture of an allergic disease.

At the heart of the pathogenesis of allergic diseases, one or another forms of allergic inflammation with various localization (leather, mucous membrane, respiratory, digestive tract, nervous fabric, lymphatic glands, joints, and so on, hemodynamic disruption (with anaphylactic shock), spasm of smooth muscles (bronchospasm with bronchial asthma).

Slow-type allergic reactions

Slow allergies develops at vaccinations and various infections: bacterial, viral and fungal. A classic example of such an allergy is tuberculin hypersensitivity (see tuberculin allergies). The role of slow allergies in the pathogenesis of infectious diseases is most demonstrative for tuberculosis. Under the local administration of tuberculous bacteria with sensitized animals, a strong cellular response with caseaseous decay and cavities is arising - the koch phenomenon. Many forms of tuberculosis can be considered as a phenomenon of koche at the site of superinfection of aerogenic or hematogenic origin.

One species of slow allergies is contact dermatitis. It is caused by a variety of low molecular weight substances of plant origin, industrial chemicals, varnishes, paints, epoxy resins, detergents, metals and metalloids, cosmetics, medicines and more. To obtain contact dermatitis in the experiment, the sensitization of animals with applications on the skin of 2,4-dinitrophlorobenzene and 2,4-dinitrophlorobenzene is most commonly used.

A common feature that unites all types of contact allergens is their ability to connect to the protein. Such a compound occurs, probably through a covalent bond with free amino and sulfhydryl groups of proteins.

In the development of delayed type allergic reactions, three stages can also be distinguished.

Immunological stage. Non-immune lymphocytes after contact with an allergen (for example, in the skin) in the blood and lymph, vessels are transferred to lymphatic nodes, where the cell is transformed into a rich RNA - blast. Blasts, multiplying, turn again into lymphocytes that can "recognize" their allergen during re-contact. Some of the specifically "trained" lymphocytes are transported into the fork gland. The contact of this specifically sensitized lymphocyte with the corresponding allergen activates the lymphocyte and causes the release of a number of biologically active substances.

Modern data on two clones of blood lymphocytes (V- and T-lymphocytes) make it possible to prevent their role in the mechanisms of allergic reactions. For the reaction of the slow-type type, in particular with contact dermatitis, T-lymphocytes are needed (thymus-dependent lymphocytes). All impacts that reduce the content of T-lymphocytes in animals, sharply suppress the hypersensitivity of the slow-type type. For the reaction of the immediate type, in lymphocytes are needed as cells that can turn into immunocompetent cells producing antibodies.

There are information about the role of hormonal influences of the fork gland participating in the process of "learning" lymphocytes.

Patochemical stage It is characterized by exemption by sensitized lymphocytes of a number of biologically active substances of a protein and polypeptide. These include: transfer factor, a factor inhibiting migration of macrophages, lymphocytotoxin, a blastogenic factor, a factor that enhances phagocytosis; Chemotaxis factor and, finally, a factor that protects macrophages from the damaging action of microorganisms.

Slow-type reactions are not braked with antihistamine. They are depressed by cortisol and adrenocorticotropic hormone, passed passively only by mononuclear cells (lymphocytes). Immunological reactivity is implemented in a significant part of these cells. In the light of these data, a well-known fact is becoming a certain fact of increasing the content of blood lymphocytes with various types of bacterial allergies.

Pathophysiological stage It is characterized by changes in tissues that are developing under the action of the above mediators, as well as in connection with the direct cytotoxic and cytolytic effect of sensitized lymphocytes. The most important manifestation of this stage is the development of various types of inflammation.

Physical allergy

Allergic reaction can develop in response to the impact of not only chemical, but also physical stimulus (heat, cold, light, mechanical or radiation factors). Since physical irritation in itself does not cause the formation of antibodies, various working hypotheses are nominated.

1. We can talk about the influence of physical irritation in the body under the influence of physical irritation, that is, the secondary, endogenous autoallergens, which take on the role of sensitizing allergen.

2. The formation of antibodies begins under the influence of physical irritation. High molecular weight substances and polysaccharides can induce enzymatic processes in the body. It is possible that they stimulate the formation of antibodies (the onset of sensitization), primarily sensitizing skin (reacts), which, under the influence of specific physical irriters, are activated, with these activated antibodies like an enzyme or catalyst (as strong liberators of histamine and other biologically active agents) cause the release of tissues .

Close to this concept is a Cook hypothesis, according to which spontaneous sensitizing skin factor is an enzyme-like factor, a prosthetic group forms a continuing complex with whey protein.

3. According to the clonal-breeding theory of Berenet, it is assumed that physical irritations are just as chemical, can cause the proliferation of the "forbidden" clone of cells or mutation of immuno-lotologically competent cells.

Fabric changes with immediate and slow-type allergies

The morphology of allergies of immediate and slow-type reflects various humoral and cellular immunological mechanisms.

For allergic reactions of the immediate type, arising from the effects on the fabric complexes of the antigen - antibody, the morphology of hypeergic inflammation is characterized, which is characterized by the speed of development, the predominance of alteractive and vascularly exudative changes, the slow flow of proliferative reparative processes.

It has been established that allertative changes in the allergy of an immediate type are associated with the histopathogenic effect of the complement of immune complexes, and vascularly exudatives - with the release of vasoactive amines (inflammation mediators), primarily histamine and kinines, as well as with chemotactic (leukotaxic) and degrading (against obese cells) complement action. Alteractive changes predominantly relate to the walls of the vessels, paragliding substance and fibrous connective tissue structures. They are represented by plasma impregnation, mucoid swelling and fibrinoid transform; The extreme expression of alteration is characteristic of allergic reactions of an immediate type of fibrinoid necrosis. With pronounced plasmorgic and vascular-exudative reactions, the appearance in the immune inflammation zone of coarse proteins, fibrinogen (fibrin), polymorphic leukocytes, "digesting" immune complexes, and red blood cells is connected. Therefore, fibrinic or fibrinic-hemorrhagic exudate is most characteristic of such reactions. Proliferative reparative reactions with an immediate type allergy are delayed and weakly expressed. They are represented by the proliferation of endothelium cells and perhethery (adventitization) of vessels and in time coincide with the advent of mononucleary-histiocytic macrophage elements, reflecting the elimination of immune complexes and the beginning of immunode preparation processes. The most typically dynamics of morphological changes in an immediate type allergy is presented in the phenomenon of Artus (see artus phenomenon) and the Ouvier reaction (see skin anaphylaxis).

At the heart of many allergic diseases of a person, there are allergic reactions of immediate-type, which proceed with the predominance of allertitive or vascularly exudative changes. For example, vascular changes (fibrinoid necrosis) with a systemic red lolly (Fig. 1), glomerulonephritis, a nodule periateritis and other, vascular-exudative manifestations for serum disease, urbivnice, swelling of quinque, hay fever, bruboral pneumonia, and polyporosites, arthritis Rheumatism, tuberculosis, brucellosis and other.

The mechanism and morphology of hypersensitivity are largely determined by the nature and number of antigenic stimulus, the duration of its circulation in the blood, the position in the tissues, as well as the nature of the immune complexes (circulating or fixed complex, heterologous or autologous, formed by local due to the combination of antibodies with the fabric structural antigen) . Therefore, an assessment of morphological changes in an immediate type allergy, their belonging to the immune response require evidence using an immunogical-stochemical method (Fig. 2), which allows not only to talk about the immune nature of the process, but also identify the components of the immune complex (antigen, antibody, complement ) And establish their quality.

For slow motion allergies, the reaction of sensitized (immune) lymphocytes is of great importance. The mechanism of their action is largely hypothetical, although the fact of the histopathogenic effect caused by immune lymphocytes in the culture of tissues or in the Allotransplant is no doubt. It is believed that the lymphocyte comes into contact with the target cell (antigen) with the help of antibody-like receptors existing on its surface. The activation of the target cell leased is shown when it interacts with the immune lymphocyte and the "transmission" of them the target cell of the H3-Timidin DNA tag. However, the mergers of the membranes of these cells, even with the deep introduction of lymphocytes in the target cell, does not occur, which is convincingly proven with the help of microcinctatographic and electronically microscopic methods.

In addition to sensitized lymphocytes, macrophages (histiocytes) are involved in the allergic reactions of the slow-type, which come into a specific reaction with an antigen with cytophilic antibodies adsorbed on their surface. The relationship between the immune lymphocyte and macrophage is not clarified. Only close contacts of these two cells are established in the form of so-called cytoplasmic bridges (Fig. 3), which are detected during an electronic microscopic study. It is possible that cytoplasmic bridges are used to transmit the antigen information macrophage (in the form of RNA or RNA-antigen complexes); Perhaps the lymphocyte on its part stimulates the activity of the macrophage or exhibits a cytopogenic effect in relation to it.

It is believed that the allergic reaction of the delayed type takes place at all chronic inflammation due to the release of autoantigen from disintegrating cells and tissues. Morphologically between slow-type allergies and chronic (intermediate) inflammation a lot in common. However, the similarity of these processes is the lymphogistocitary infiltration of tissue in combination with vascular-plasmorgic and parenchymal-dystrophic processes - does not identify them. Evidence of the involvement of infiltrate cells to sensitized lymphocytes can be found in historifermetochemical and electronically microscopic studies: with the allergic reactions of the slow-type type, an increase in the activity of sour fewoatase and dehydrogenases in lymphocytes, an increase in their nuclei and nuclei, an increase in the amount of the policy, hypertrophy of the GOLGIA device.

The opposition of morphological manifestations of humoral and cellular immunity in immunopathological processes is not justified, therefore, the combinations of morphological manifestations of an immediate and slow-type allergy are quite natural.

Allergy with radiation defeat

The problem of allergies during radiation damage has two aspects: the effect of radiation on the reaction of increased sensitivity and the role of auto-allergies in the pathogenesis of radiation disease.

The effect of radiation at the reaction of the hypersensitivity of the immediate type is most detailed in the example of anaphylaxia. In the first weeks after irradiation, spent a few days before the sensitizing injection of the antigen, simultaneously with the sensitization or in the first day after it, the state of hypersensitivity is weakened or does not develop at all. If the removal injection of the antigen is carried out in a later period after the recovery of anti-air genesis, the anaphylactic shock develops. Irradiation spent in a few days or weeks after sensitization, the state of sensitization and the titers of antibodies in the blood does not affect. Radiation effect on cellular reactions of slow-type hypersensitivity (for example, allergic samples with tuberculin, tularin, brucelline, and so on) are characterized by the same patterns, but these reactions are somewhat more radioresistant.

With radiation sickness (see), the manifestation of anaphylactic shock can be reinforced, weakened or changed depending on the period of illness and clinical symptoms. In the pathogenesis of radiation sickness, the allergic reactions of the irradiated organism plays a certain role in relation to exogenous and endogenous antigens (autoantigenam). Therefore, the desensitizing therapy is useful in the treatment of both acute and chronic forms of radiation lesions.

The role of endocrine and nervous systems in the development of allergies

The study of the role of endocrine glands in the development of allergies was carried out by removing them in animals, the introduction of various hormones, studying allergenic properties of hormones.

Hypophysical adrenal glands

Data on the influence of pituitary hormones and adrenal glands to allergic contradiction. However, most facts suggests that allergic processes occur more severely against the background of adrenal insufficiency caused by hypophysome or adrenalhanectomy. Glucocorticoid hormones and ACTH, as a rule, do not inhibit the development of allergic reactions of the immediate type, and only long-term administration or the use of large doses to one degree in degree inhibit their development. Allergic delayed type reactions are well suppressed by glucocorticoids and ACTH.

The anti-allergic effect of glucocorticoids is associated with the braking of products of antibodies, phagocytosis, the development of an inflammatory reaction, a decrease in tissue permeability.

Obviously, the release of biologically active mediators is also reduced and the sensitivity to them tissues is reduced. Allergic processes are accompanied by such exchange and functional changes (hypotension, hypoglycemia, increasing sensitivity to insulin, eosinophilia, lymphocytosis, increasing concentration of potassium ions in blood plasma and decrease in sodium ions concentration), which indicate the presence of glucocorticoid failure. It is established, however, that does not always be detected by the lack of adrenal cortex. Based on these data, V.I. Pyruga (1968) put forward a hypothesis about the total adhesive mechanisms of glucocorticoid insufficiency caused by an increase in the binding of cortisol with blood plasma proteins, loss of cell sensitivity to cortisol or enhanced cortisol metabolism in tissues, which leads to a decrease in the effective concentration of hormone.

Thyroid

It is believed that the normal function of the thyroid gland is one of the main conditions for the development of sensitization. Thyreopdectomed animals can only sensitize passively. Thyroidectomy weakens sensitization and anaphylactic shock. The less time between the allowing administration of antigen and thyroidectomy, the less its effect on the intensity of the shock. Thieredoidectomy before sensitization slows down the appearance of precipitpn. If parallel with the sensitization of the thyroid hormones, the formation of antibodies increases. There is information that the thyroid hormones enhance the tuberculin reaction.

Thymus

The role of the fork gland in the mechanism of allergic reactions is studied in connection with new data on the role of this gland in immunogenesis. As you know, the pool gland has a big role in organizing the lymphatic system. It contributes to the population of lymphatic lymphocytic glands and the regeneration of the lymphatic apparatus after its various damage. Milk iron (see) plays a significant role in the formation of an immediate and slow-type allergy and primarily in newborns. In rats, tymmetomized immediately after birth, the phenomenon of artus is not developed to the subsequent injections of bovine serum albumin, although non-specific local inflammation caused by, for example, the turpentine, under the influence of timectomy does not change. In adult rats, after simultaneous removal of the fork gland and spleen, there is a braking of immediate allergic reactions. In such animals sensitized by horsepower serum, there is a distinct braking anaphylactic shock on intravenous administration of the resolution of the antigen. It is also established that the introduction of mice of the extract of the pig embryo gland is hypox and agammaglobulinemia.

Early removal of the fork gland also causes the development of all allergic reactions of slow-type. In mice and rats, after neonatal thymectomy, it is impossible to obtain local slow reactions to peeled protein antigens. A similar effect has multiple injections of anti-natural serum. Newborn rats after removal of the fork gland and sensitization killed tuberculous tuberculosis reaction to the 10-20th day of life of the animal are less pronounced than in control untextal animals. Early thymectomy in chickens significantly extends the period of rejection of the homotransplant. Timectomy has the same effect on newborn rabbits and mice. The transplanting of the fork gland or cells of lymph nodes restores the immunological competence of the recipient lymphoid cells.

Many authors bind the development of autoimmune reactions with impaired function of the fork gland. Indeed, in thymectomy mice with fork glands transplanted from donors with spontaneous hemolytic anemia, autoimmune disorders are observed.

Sex glands

There is a lot of hypotheses about the effect of sex glands on allergies. According to one data, castration causes hyperfunction of the front lobe of the pituitary. The hormones of the front proportion of the pituitary gland reduce the intensity of allergic processes. It is also known that hyperfunction of the front lobe of the pituitary gland leads to stimulation of adrenal function, which is the immediate cause of an increase in resistance to anaphylactic shock after castration. Another hypothesis suggests that castration causes a lack of genital hormones in the blood, which also reduces the intensity of allergic processes. Pregnancy, as well as estrogens, can suppress the skin reaction of a slow-type under tuberculosis. Estrogens inhibit the development of experimental autoimmune thyroiditis and polyarthritis in rats. This action cannot be obtained by applying progesterone, testosterone.

These data indicate the undoubted influence of hormones on the development and course of allergic reactions. The influence is not isolated and is implemented in the form of a comprehensive action of all glands of internal secretion, as well as various parts of the nervous system.

Nervous system

The nervous system is directly involved in each of the stages of the development of allergic reactions. In addition, the nervous tissue itself may be a source of allergens in the body after exposure to it of various damaging agents, an allergic antigen reaction with an antibody can be deployed.

Local application of the antigen on the motor area of \u200b\u200blarge hemispheres of sensitized dogs caused muscle hypotension, and sometimes an increase in tone and spontaneous muscle contractions on the side opposite to the applique. The effects of the antigen on the oblong brain caused a decrease in blood pressure, disruption of respiratory movements, leukopenia, hyperglycemia. The application of the antigen to the area of \u200b\u200bthe gray hype of the hypothalamus led to significant erythrocytosis, leukocytosis, hyperglycemia. The introduced primary heterogeneous serum has an exciting effect on the bark of large hemispheres of the brain and subcortical education. During the period of the sensitized state of the body, the power of the excitation process is weakened, the process of active braking is weakened: the mobility of nerve processes is worse, the limit of nerve cells is reduced.

The development of the anaphylactic shock reaction is accompanied by significant changes in the electrical activity of the cortex of the brain, subcortical ganglia and intermediate brain formations. Changes in electrical activity arise from the first seconds of the introduction of alien serum and in the future wearing a phase character.

Participation vegetative nervous system (see) The mechanism of anaphylactic shock and various allergic reactions assumed many researchers in experimental study of allergy phenomena. In the future, considerations on the role of the vegetative nervous system in the mechanism of allergic reactions were also expressed by many clinicians in connection with the study of the pathogenesis of bronchial asthma, allergic dermatoses and other diseases of allergic nature. Thus, the studies of the pathogenesis of serum disease showed the essential value of the violations of the autonomic nervous system in the mechanism of this disease, in particular the essential value of the Vagus phase (lowering blood pressure, sharply positive symptom of Ashner, leukopenia, eosinophilia) in the pathogenesis of serum disease in children. The development of teachings on mediators of transmission of excitation in the neurons of the vegetative nervous system and in various neuroenefector synapses was also reflected in the teaching on allergies and significantly advanced the question of the role of the autonomic nervous system in the mechanism of some allergic reactions. Along with the known histamine hypothesis of the mechanism of allergic reactions, cholinergic, dystonic and other theories of the mechanism of allergic reactions appeared.

When studying the allergic reaction of the small intestine of the rabbit, the transition of significant quantities of acetylcholine from the associated state in the free one was detected. The relationship of mediators of the vegetative nervous system (acetylcholine, sympathetic) with histamine during the development of allergic reactions is not clarified.

There are data on the role of both the sympathetic and parasympathetic department of the vegetative nervous system in the mechanism for the development of allergic reactions. According to some data, the state of allergic sensitization is expressed at the beginning in the form of the predominance of the tone of the sympathetic nervous system, which is then replaced by parasympaticotone. The influence of the sympathetic department of the autonomic nervous system on the development of allergic reactions was studied both surgical and pharmacological methods. Research A. D. ADO and T. B. Tolpegina (1952) showed that during serum, as well as with bacterial allergies in the sympathetic nervous system there is an increase in excitability to a specific antigen; The effect of antigen on the heart of respectively sensitized guinea pigs causes the release of sympathy. In the conditions of experiments with an isolated and perfisurial upper cervical sympathetic node in cats, sensitized horse serum, the introduction of a specific antigen in the perfusion current causes an excitation of a node and, accordingly, a reduction in the third century. The excitability of the node to electrical irritation and to acetylcholine after protein sensitization increases, and after the impact of the resolution dose of the antigen falls.

The change in the functional state of the sympathetic nervous system is one of the earliest expressions of the state of allergic sensitization of animals.

Many researchers have established an increase in the excitability of parasimpatic nerves during protein sensitization. It has been established that anaphylotoxin excites the end of the parasympathetic nerves of smooth muscles. The sensitivity of the parasympathetic nervous system and the innervorates it organs to choline and acetylcholine in the process of development of allergic sensitization increases. According to Dunpelopol hypothesis (D. Danielopolu, 1944), the anaphylactic (parafilactic) shock is considered as a state of increasing the tone of the entire vegetative nervous system (ampotonia in Danielopol) with an increase in the release of adrenaline (sympathy) and acetylcholine into the blood. In the state of sensitization, the production of both acetylcholine and sympathy increases. Anaphylactogen causes a nonspecific effect - exemption in acetylcholine organs (Prechvin) and a specific effect - antibody products. The accumulation of antibodies causes specific phylaxia, and the accumulation of acetylcholine (precholine) causes non-specific anaphylaxis, or parafylaxia. Anaphylactic shock is considered as "hypocholine-butter" diathesis.

Danielopol hypothesis is not accepted as a whole. However, there are numerous facts about the close relationship between the development of the state of allergic sensitization and the change in the functional state of the autonomic nervous system, for example, a sharp increase in the excitability of cholinergic innervational devices of the heart, intestines, uterus and other organs to choline and acetylcholine.

According to A. D. ADO, the allergic reactions of the cholinergic type are distinguished, under which the leading process is the reactions of cholinergic structures, the hystaminergy reaction, under which histamine plays a leading role, the reaction of the sympanthergic type (presumably), where the leading mediator is sympathy, and finally, Various mixed type reactions. The possibility of existence and such allergic reactions does not exclude, in the mechanism of which the leading place will occur other biologically active products, in particular the slowly reacting substance.

The role of heredity in the development of allergies

Allergic reactivity is largely determined by the hereditary features of the body. Against the background of hereditary predisposition to allergies in the body under the influence of the environment, the state of the allergic constitution, or allergic diatenise is formed. It is close to it exudative diathesis, eosinophilic diathesis, etc. Allergic eczema in children and exudative diathesis is often preceded by the development of bronchial asthma and other allergic diseases. Drug allergies occurs three times more often in patients with allergic reactivity (urticaria, pollinosis, eczema, bronchial asthma and other).

The study of hereditaryly burdened in patients with various allergic diseases showed that about 50% of them have in a number of generations of relatives with those or other manifestations of allergies. 50.7% of children with allergic diseases also have hereditary burdensome on allergies. In healthy persons, allergies in a hereditary history is noted no more than 3-7%.

It should be emphasized that not an allergic disease is inherited as such, but only a predisposition to the most different allergic diseases, and if the surveyed patient has, for example, the urticaria, then his relatives in various generations allergic can be expressed in the form of bronchial asthma, migraine, swelling , rhinitis and so on. Attempts to detect the patterns of inheritance of predisposition to allergic diseases showed that it is inherited as a recessive sign on Mendel.

The impact of hereditary predisposition on the occurrence of allergic reactions is clearly demonstrated by the example of studying allergies in single-engine twins. Numerous cases of completely identical manifestations of allergies have single-engine twins to the same set of allergens are described. When titrationing allergens for skin samples, single-engine twins detected completely identical titers of skin reactions, as well as the same content of allergic antibodies (reacts) to allergens causing the disease. These data show that the hereditary condition of allergic conditions represents an important factor in the formation of an allergic constitution.

In the study of the age characteristics of allergic reactivity, two lifts of the number of allergic diseases are noted. The first is in early childhood - up to 4-5 years. It is determined by the hereditary predisposition to an allergic disease and is manifested in relation to food, domestic, microbial allergens. The second lifting is observed in the period of puberty and reflects the completion of the formation of an allergic constitution under the influence of the heredity factor (genotype) and the environment.

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Fissure changes with A.

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A. For radiation defeat

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