Types of inflammation, types of inflammation, their signs and causes. Painful sexual intercourse

Inflammation I Inflammation (inflammatio)

protective-adaptive local organism to the action of various damaging factors, one of the most common forms of the body’s response to pathogenic stimuli.

The causes of V. are diverse. It can be caused by various factors: biological (for example, bacteria, viruses), physical (high and low temperature, mechanical, etc.), chemical (for example, exposure to acids, alkalis). Classic signs of V. are: redness, fever, swelling, and dysfunction. However, in many cases only some of these signs are expressed.

Inflammation begins with alteration (cells and tissues), which is the result direct action etiological factor. At the same time, a number of changes occur in the cell - ultrastructural, occurring in the components of the cytoplasm, the cell nucleus and its membrane, to pronounced dystrophic processes and even complete destruction of cells and tissue. Alteration phenomena are observed both in the parenchyma and in the stroma. Primary entails the release of biologically active substances (inflammatory mediators) in the affected tissues. These substances, differing in origin, chemical nature and characteristics of action, play the role of a trigger link in the chain of mechanisms for the development of the inflammatory process and are responsible for its various components. The release of inflammatory mediators may be a direct result of the damaging effects of pathogenic factors, but to a large extent it is an indirect process that occurs under the influence of lysosomal hydrolytic enzymes, which are released from lysosomes when their membrane is destroyed. Lysosomes are called the “launching pad of inflammation” because lysosomal hydrolytic break down all types of macromolecules that make up animal tissues (nucleic acids, lipids). Under the influence of lysosomal hydrolytic enzymes, the connective tissue framework of microvessels continues. inflammation, both cellular and humoral in origin, accumulating as V. develops, increasingly deepens tissue alteration. Thus, the most powerful histamine causes dilation of microvessels, increasing their permeability. found in granules of mast cells (mast cells), as well as in basophils, and is released during granulation of these cells. Another cellular mediator is Serotonin , increases vascularity. Its source is . Cellular mediators of V. include those formed in lymphocytes, prostaglandins, etc. Of the humoral mediators, the most important are (, kallidin), which dilate precapillary arterioles, increase the permeability of the capillary wall and are involved in the formation of pain. - a group of neurovasoactive polypeptides formed as a result of a cascade of chemical reactions, the trigger of which is the activation of blood coagulation factor XII. Lysosomal hydrolytic enzymes can also be classified as V.’s mediators, because they not only stimulate the formation of other mediators, but also act as mediators themselves, participating in phagocytosis and chemotaxis.

Under the influence of V. mediators, the next, main link in the inflammation mechanism is formed - a hyperemic reaction (see Hyperemia) , characterized by an increase in vascular permeability and a violation of the rheological properties of blood. The vascular reaction in V. is expressed in a sharp expansion of the microvascular bed, primarily capillaries, both active and passive (see Microcirculation) . It is precisely this vascular reaction that determines the first sign of V. - redness and its features (diffuseness, delimitation from neighboring tissues, etc.). In contrast to various types of arterial hyperemia (thermal, reactive, etc.), the expansion of capillaries in V. depends not so much on the blood flow through the arterial segments, but on local (primary) mechanisms. The latter include the expansion of precapillary microvessels under the influence of vasodilator mediators of the blood and an increase in pressure in them, which causes an increase in the lumen of active capillaries and the opening of the lumen of previously non-functioning ones. This is facilitated by a change in the mechanical properties of the loose connective tissue framework of the capillary bed. The diffuse expansion of the capillaries is joined by a reflex arterial one both at the site of inflammation and along its periphery, developing according to the mechanism of the axon reflex (i.e., a reflex carried out along the branches of the axon). During this initial period of the inflammatory process (after 2-3 h after exposure to a damaging factor), due to an increase in the total cross-sectional area of ​​the vascular bed in the affected area, the intensity of blood flow (volume velocity) increases, despite a decrease in its linear velocity. At this stage, increased blood flow in the area of ​​inflammation determines the second sign of V. - an increase in local temperature (fever).

Subsequent links in the process are characterized by the appearance of not only chain reactions, but also “vicious circles” in which pathological phenomena follow each other, accompanied by an increase in their severity. This can be seen in the example of such a rheological phenomenon inherent in V. as erythrocytes (formation of erythrocyte conglomerates) in microvessels. Slowing blood flow creates conditions for erythrocyte aggregation, and erythrocyte aggregation, in turn, further reduces the circulation rate.

With V., other changes in rheological properties occur, which ultimately lead to an increase in blood clotting and thrombus formation. Erythrocyte aggregates and blood clots (platelet clots), partially or completely closing the lumen of blood vessels, are one of the main reasons why the slow in some places turns into prestasis and. Arterial hyperemia is gradually joined by increasing phenomena of venous hyperemia and stagnation. The development of venous hyperemia is also associated with compression of the veins and lymphatic vessels (up to lymphostasis) by the inflammatory fluid accumulated in the surrounding tissues - Exudate om . The third sign of V. depends on the accumulation of exudate in the tissues - swelling. As the volume of tissue increases, nerve endings occur, which results in the fourth sign of V. - pain. manifested by the release of blood components - water, salts, proteins, as well as formed elements (emigration) from the blood vessels of the tissue. The emigration of leukocytes is due to both purely physical (hemodynamic) and biological laws. When blood flow slows down, the transition of leukocytes from the axial layer of blood cells to the wall (plasma) layer occurs in full accordance with the physical laws of particles suspended in the flowing fluid; a decrease in the difference in the speed of movement in the axial and near-wall layers causes a decrease in the pressure difference between them, and the lighter ones, compared to erythrocytes, seem to be thrown towards the inner lining of the blood vessel. In places where the blood flow is especially strongly slowed down (the transition of capillaries into venules), where the blood vessel becomes wider, forming “coves”, the marginal location of leukocytes turns into a marginal position, they begin to attach to the wall of the blood vessel, which during V. is covered with a flocculent layer. After this, leukocytes form thin protoplasmic processes - with the help of which they penetrate through the interendothelial gaps, and then through the basement membrane - outside the blood vessel. There may also be a transcellular pathway for leukocyte emigration, i.e. through the cytoplasm of endothelial cells, the emigrated leukocytes in the focus of V. continue active (migration), and mainly in the direction of chemical stimuli. They can be products of tissue proteolysis or the vital activity of microorganisms. This property of leukocytes to move towards certain substances(chemotaxis) I.I. Mechnikov attached leading importance to all stages of the movement of leukocytes from the blood to the tissues. It later became clear that it plays a minor role during the passage of leukocytes through the vascular wall. In the focus of V., the main function of leukocytes is to absorb and digest foreign particles ().

Exudation primarily depends on an increase in the permeability of microvessels and an increase in the hydrodynamic pressure of blood in them. An increase in microvascular permeability is associated with deformation of normal permeability pathways through the endothelial vascular wall and the emergence of new ones. Due to the expansion of microvessels and, possibly, contraction of contractile structures (myofibrils) of endothelial cells, the gaps between them increase, forming so-called small pores, and even channels or large pores may appear in the endothelial cell. In addition, with V., the transfer of substances is activated by microvesicular transport - the active “swallowing” of tiny bubbles and plasma droplets by endothelial cells (micropinocytosis), carrying them through the cells to the opposite side and pushing them beyond its limits. The second factor that determines the process of exudation - an increase in blood pressure in the capillary network - is primarily the result of an increase in the lumen of the precapillary and larger afferent arterial vessels, from which the resistance and energy consumption (i.e. pressure) in them decrease, and therefore remains more “unspent” energy.

An indispensable link of V. is () cells, especially pronounced in the final stages of inflammation, when recovery processes come to the fore. Proliferative processes involve local cambial cells (precursor cells), primarily mesenchymal cells, which give rise to fibroblasts that synthesize (the main part of scar tissue); adventitial and endothelial cells multiply, as well as cells of hematogenous origin - B- and T-lymphocytes and monocytes. Some of the cells that make up the cell, having fulfilled their phagocytic function, die, while others undergo a series of transformations. for example, monocytes are transformed into histiocytes (macrophages), and macrophages can be a source of epithelioid cells, from which the so-called giant mono- or multinucleated cells arise (see Mononuclear phagocyte system) .

Depending on the nature of the prevailing local changes, alterative, exudative and productive V. are distinguished. With alterative V., the phenomena of damage and necrosis are expressed. They are more often observed in parenchymal organs (liver, kidneys, etc.).

Exudative V. is characterized by a predominance of exudation processes. Depending on the nature of the exudate, serous, catarrhal, fibrinous, purulent and hemorrhagic inflammation is distinguished. In serous V. it contains from 3 to 8% serum protein and single leukocytes (serous exudate). Serous V., as a rule, is acute, localized most often in serous cavities; serous exudate is easily absorbed, V. leaves virtually no traces. Catarrhal V. develops on the mucous membranes. It occurs acutely or chronically. Serous or purulent exudate mixed with mucus is released. Fibrinous V. occurs on serous or mucous membranes; usually spicy. contains a lot of fibrin, which in the form of a film can lie freely on the surface of the mucous or serous membrane or adhere to the underlying surface. Fibrinous V. is one of the severe forms of inflammation; its outcome depends on the location and depth of tissue damage. Purulent V. can develop in any tissue and organ; the course is acute or chronic, can take the form of an abscess or phlegmon; the process is accompanied by histolysis (melting) of the tissue. The exudate contains mainly leukocytes that are in a state of decay. When the exudate contains a large number of red blood cells, the inflammation is called hemorrhagic. It is characterized by a sharp increase in the permeability of blood vessels and even a violation of the integrity of their walls. Any V. can take on a character.

Productive (proliferative) V., as a rule, occurs chronically : the phenomena of proliferation of cellular elements of the affected tissues predominate. A common outcome is scar formation.

Inflammation depends on the immunological reactivity of the body, so it can have a clinically completely different course and outcome. If the inflammatory reaction is of a normal nature, i.e. the one that is observed most often is called normergic inflammation. If the inflammatory process is sluggish and becomes protracted with mildly expressed main signs of inflammation, it is called hypoergic inflammation. In some cases, the damaging agent causes an extremely violent inflammatory reaction that is inadequate to its strength and dose. This kind of V., called hyperergic, is most typical for the state of allergy (Allergy) .

The outcome of V. is determined by the nature and intensity of the inflammatory agent, the form of the inflammatory process, its localization, the size of the affected area and the reactivity of the body (Body reactivity) . V. is accompanied by the death of cellular elements if necrosis covers large areas, especially in vital organs; the consequences for the body can be very severe. More often, the focus is demarcated from the surrounding healthy tissue, the products of tissue breakdown undergo enzymatic breakdown and phagocytic resorption, and the inflammatory focus, as a result of cell proliferation, is filled with granulation tissue. If the area of ​​damage is small, complete restoration of the previous tissue may occur (see Regeneration) , with a more extensive lesion, a lesion is formed at the site of the defect.

From the point of view of biological expediency, the inflammatory process has a dual nature. On the one side. V. is a protective-adaptive reaction developed in the process of evolution. Thanks to it, it delimits itself from harmful factors located in the source of V. and prevents the generalization of the process. This is achieved through various mechanisms. Thus, venous and lymphatic congestion and stasis, the occurrence of blood clots prevent the spread of the process beyond the affected area. The resulting exudate contains components that can bind, fix and destroy bacterial; phagocytosis is carried out by emigrated leukocytes, proliferation of lymphocytes and plasma cells contributes to the production of antibodies and an increase in local and general immunity. During the proliferation stage, a protective wall of granulation tissue is formed. At the same time, V. can have a destructive and life-threatening effect on the body. In the V. zone, the death of cellular elements always occurs. The accumulated exudate can cause enzymatic melting of the tissue, their compression with impaired blood circulation and nutrition. Exudate and tissue breakdown products cause intoxication and metabolic disorders. The inconsistency of the meaning of V. for the body dictates the need to distinguish between phenomena of a protective nature from elements of the breakdown of compensatory mechanisms.

Bibliography: Alpern D.E. Inflammation. (Questions of pathogenesis), M., 1959, bibliogr.; General human, ed. A.I. Strukova et al., M., 1982; Strukov A.I. and Chernukh A.M. Inflammation, BME, 3rd ed., vol. 4, p. 413, M, 1976; Chernukh A.M. Inflammation, M., 1979, bibliogr.

1. Small medical encyclopedia. - M.: Medical encyclopedia. 1991-96 2. First aid. - M.: Great Russian Encyclopedia. 1994 3. encyclopedic Dictionary medical terms. - M.: Soviet encyclopedia. - 1982-1984.

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Inflammatory diseases in gynecology rank first among other types of pathologies. Approximately 65% ​​of women who come for a consultation are diagnosed with inflammation. Many of them do not even go to the doctor, since the diseases occur without obvious manifestations.

Recently, the number of inflammatory diseases has been growing, this is a consequence of improper sexual behavior, environmental influences, as well as reduced immunity.

Classification of inflammation and methods of protection against infections

Depending on where the process is localized, they are divided into:

Inflammation of the appendages can be acute or chronic. In a chronic process, the clinic boils down to a decrease in the intensity of symptoms and the formation of adhesions in the pelvis. Treatment includes antibiotic therapy.

Pelvioperitonitis is the final link in the development of inflammatory pathologies of the female genital area. It can be considered a complication of running processes. Peritonitis occurs when the infection further spreads from the appendages and uterus into the pelvic cavity.

The main manifestations are:

• increased body temperature;
• significant ongoing pain in the lower abdomen;
• purulent discharge;
• the general condition of the patients deteriorates significantly;
• weakness is noted;
• severe dehydration.

The process cannot be resolved on its own; the help of a competent specialist is needed here. As for diagnosis, the key method is laparoscopy, which allows one to detect severe hyperemia and swelling of the peritoneum, as well as the presence of purulent effusion.

The only treatment option is surgery. During the intervention, the pelvic cavity is examined, the source of inflammation is identified and removed, and the pelvic cavity is sanitized. Additionally, therapy with antibacterial drugs, dressings, local antiseptics and antifungal therapy is prescribed.

The prognosis for pelvioperitonitis is quite doubtful, patients require recovery, and the treatment itself continues for a long period.

Thus, even the smallest inflammatory problems of the reproductive sphere cannot be ignored, as the consequences can be quite disastrous.

Inflammation of the ovaries (appendages)

Among all gynecological diseases, the leading positions are occupied by various inflammatory diseases. The most common inflammation of the appendages affects women of childbearing age - 20 years and older.

Symptoms of ovarian inflammation:

1. Aching, nagging pain in the lower abdomen, which occurs when the body is hypothermic and during menstruation,
2. Pain during sex

Later, when the disease develops, the following symptoms are added:

1. chills
2. a sharp increase in temperature - up to 38-39 ° C
3. intense pain that radiates to the lower back
4. frequent urge to urinate,
5. copious vaginal discharge, clear in appearance.

In particularly severe cases, nausea and vomiting may occur. Chronic inflammation appendages contributes to increased pain sensations and their range. Therefore, symptoms of adnexitis (inflammation of the ovaries) include pain in the lower abdomen, in the sacrum, in the groin, and in the vagina. Chronic inflammation may be accompanied by disorders menstrual cycle, sexual dysfunction, miscarriages and the development of ectopic pregnancy.

Causes of the disease

The infection can enter the body through sexual contact (during sexual intercourse from an infected partner). In this case, microorganisms penetrate the appendages and cause an inflammatory process. These may be gonococci, chlamydia, mycoplasma or trichomonas. Women who are promiscuous are susceptible to such inflammation, as well as women who continue sexual activity immediately after childbirth or abortion.

The disease also causes the activity of microflora located in the body or entered into it through non-sexual contact (activation of autoinfection). Staphylococci, E. coli, streptococci penetrate the appendages and cause inflammation. Usually they cause other types of inflammation, but due to some reasons, such as a general decrease in immunity or the presence of other diseases in the body (sinusitis, dysbacteriosis and even ordinary caries), this microflora can become aggressive.

What is the danger of the disease

Inflammatory processes in the appendages disrupt the integrity of the epithelium of the fallopian tubes. Because of this, adhesions occur, making the fallopian tubes obstructed, which in turn causes infertility.

Factors that can cause inflammation:

1. Messy sex life, frequent change of partners, lack of contraception
2. Hypothermia. You should not neglect a hat in severe frost, or wear nylon tights and stockings in the cold season.
3. Stress, overwork, poor, irregular nutrition.
4. Advanced diseases: gastritis, tonsillitis, dysbacteriosis, untreated caries.
5. Use a heating pad when pain occurs. This only provokes further development of inflammation.

What to do when symptoms appear

1. To avoid aggravating your condition, you should immediately consult a doctor.
2. To make a diagnosis, a smear from the vagina and cervix is ​​required, which will determine the nature of the microflora.
3. Complete the entire prescribed course of treatment

Remember that treatment should only be carried out by an obstetrician-gynecologist!

SEXUALLY TRANSMITTED INFECTIONS (STIs)

STI - This is a large group of microorganisms that are mainly conditionally dangerous. In small quantities, they create a certain “ecology” in the vagina, becoming part of its microflora. This flora also includes microorganisms that act as orderlies, preventing the proliferation of the above-mentioned conditionally pathogenic flora. But with a decrease in immunity, an imbalance occurs and vaginal dysbiosis develops.

A decrease in immunity occurs during exacerbations of chronic diseases, during acute infectious diseases (such as acute respiratory viral infections, influenza), as well as after suffering emotional stress or against the background of chronic stress that develops over a long time. Also, a decrease in immunity can occur against the background of pregnancy or a sudden change in climate.

Each sexually transmitted disease has its own distinctive features, but all of them are characterized by a chronic course and minor symptoms. Most often, a woman does not notice the disease. And only against the background of a common cold does she notice increased vaginal discharge, discomfort in the genital area, vague periodic nagging pain in the lower abdomen, and itching.

CHLAMYDIA

Infection occurs through sexual contact, not necessarily genital, but also oral or anal. Incubation period averages from 7 to 14 days.

There are no problems with the treatment of chlamydia. With the correct selection of an antibacterial drug, its dosage and calculated duration of treatment, and - what is very important - if the patient follows all the doctor’s prescriptions, the treatment will be successful. In most European countries, as well as in the USA and Russia, the cost of treatment for chlamydia and other latent infections is significantly lower than the cost of diagnosis.

Hidden infections - chlamydia, ureaplasma, mycoplasma, and trichomonas are always subject to mandatory treatment in both partners, even if only one of them is sick.

COMPLICATIONS

Chlamydia causes inflammation of the epididymis (epididymitis) in men.

In women - diseases of the cervix, inflammation of the appendages and tubal infertility. During pregnancy, chlamydia can cause serious fetal pathology.

This infection also leads to Reiter's disease - severe damage to the joints and eyes.

Monitoring the results of treatment for chlamydia and other hidden STIs should be carried out no earlier than 3 weeks after completing the medication. Symptoms may persist for several weeks or even months after successful treatment. Resumption of sexual activity is possible only after a follow-up examination of both partners.

UREAPLASMOSIS

These are the smallest microorganisms that do not have and do not need their own cell membrane. This feature allows them to penetrate host cells, so they are often invisible to protective immune cells. Thus, ureaplasma can exist in the body for more than 10 years. Ureaplasmosis occurs more often in women than in men.

Ureaplasma got its name because of its ability to break down urea - ureolysis. Therefore, ureaplasmosis is a urinary infection; ureaplasma cannot survive without urea. Ureaplasmosis is often associated with diseases of the urinary system, urethritis, chronic cystitis and pyelonephritis.

Ureaplasma is usually transmitted sexually. It is also possible for the baby to become infected during childbirth.

The incubation period lasts about 1 month. The further development of the disease depends on immunity, the presence or absence of other vaginal diseases and other reasons.

Most often there are no symptoms. Sometimes patients may complain of more abundant discharge than usual, discomfort in the external genitalia, burning sensation when urinating, intermittent nagging pain in the lower abdomen and lower back.

UREAPLASMA AND PREGNANCY

Ureaplasma can lead to a destructive process in the uterus and appendages, contributing to the development of complications that can lead to pathologies during pregnancy. Therefore, during this period it is necessary to undergo tests for this infection and treatment if it is confirmed.

Ureaplasma does not cause malformations in the fetus. Most often, a child becomes infected during childbirth when the fetus passes through infected birth canal. In addition, ureaplasmosis can cause miscarriage, threatened miscarriage, premature birth, as well as endometritis, one of the postpartum complications.

Treatment during pregnancy most often occurs at 18-20 weeks.

TREATMENT

Treatment of ureaplasmosis should be complex and long-term. First of all, antibacterial drugs are prescribed. But using antibiotics alone is not enough. Ureaplasma can easily adapt to the effects of antibiotics during treatment. The treatment also uses drugs that increase general and local immunity, and antifungal drugs, because Antibiotics can cause thrush. The drug complex also includes drugs that protect the intestines from the effects of antibiotics.

There is a controversial opinion regarding the need to treat a partner if he does not have an infection. This is decided by the attending physician and the partners themselves.

During pregnancy, the choice of drugs is limited because only those drugs that are approved for use during pregnancy can be used. Antibiotics include Rovamycin, Erythromycin, Vilprafen.

MYCOPLASMOSIS

Mycoplasmas are “relatives” of ureaplasmas. They also do not have their own cell membrane and have all the same qualities and properties as ureaplasma. Therefore, we will not dwell on mycoplasma in detail. The disease has the same symptoms, diagnostic methods and treatment principles as ureaplasmosis.

GARDNERELLOSIS

This disease is not an STD. It is caused by gardnerella vaginalis and, in fact, is a manifestation of vaginal dysbiosis. Those. This is not an inflammation of the vagina, so the disease has received another name - bacterial vaginosis.

Unlike other infections, gardnerellosis has pronounced and specific symptoms. This is a profuse liquid discharge from the vagina that is white or yellowish in color, which has a very unpleasant odor, reminiscent of the smell of rotten fish. The smell can intensify after sexual intercourse, as well as during or after menstruation. Gardnerellosis causes discomfort and burning in the genital area. During a gynecological examination experienced doctor can immediately make a diagnosis, since the discharge has a slightly foamy characteristic appearance. Although in some cases there may again be no symptoms, and gardnerella can only be detected during examination.

Gardnerella are located directly in the vagina. The infection most often does not penetrate further, so symptoms such as pain in the lower abdomen do not occur.

GARDNERELLA AND PREGNANCY

Gardnerella can cause a lot of trouble during pregnancy. It is possible, although very rare, that intrauterine infection may occur. Also, gardnerella can cause inflammation of the uterus after childbirth or abortion. Therefore, bacterial vaginosis during pregnancy should be treated immediately.

Usually, gardnerella can appear in a regular smear on the flora. Also, the PCR diagnostic method can be used to identify them.

TREATMENT

Treatment consists of 2 stages. First, the infection is destroyed, then the microflora in the vagina is restored.

At the first stage, drugs such as fasigin, flagyl, trichopolum, and clindamycin are used.

The second stage is long, it can last 1 month or more. You need to be patient. If the microflora is not restored, the disease will return. During the treatment period, sexual activity is possible, provided that the partners use a condom.

In men, gardnerella “takes root” and does not develop, so treatment of sexual partners is not required.

HUMAN PAPILLOMA VIRUS

In recent years, this infection has attracted the attention of most researchers and medical practitioners. This interest is explained by the fact that the ability of this infection to cause cancer of the genital organs in both women and men has been absolutely proven. Very often, human papillomavirus infection, like many other STDs, is asymptomatic, and thereby contributes to its even greater spread in the body. Not every case of HPV causes cancer, but almost every case of cancer is caused by HPV.

To date, more than 120 types of HPV have been identified. Of these, there are 34 types that affect the genitals and perineal area. Moreover, each virus is responsible only for its own “region”.

HOW INFECTION WITH THIS VIRUS OCCURS

HPV can be transmitted through direct contact of skin and mucous membranes with:

• traditional sexual intercourse (this is the main route of transmission of infection)
• non-traditional sexual intercourse (homosexual or anal sex). It is believed that HPV can also be transmitted through oral-genital contact.
• during childbirth when the fetus passes through the mother's infected genital tract
• It is also possible that the infection can be transmitted through household means - through bath accessories, hands, dirty clothes.

FACTORS provoking the development of HPV:

1. early sexual activity, promiscuity,
2. a large number of partners, the presence of other STDs (chlamydia, mycoplasma, ureaplasma),
3. smoking, repeated abortions,
4. chronic diseases of the genital organs (inflammation of the appendages, uterus, vagina),
5. aggravated medical history (presence of cervical cancer in close relatives).
6. anal sex

Sometimes the virus can leave the body on its own. And this happens more often among young people over 30 years old. Unfortunately, if the virus enters the body after 35 years of age, the likelihood that it will leave the body on its own, without treatment, is small.

The infection can occur in 3 forms:

1. Asymptomatic. In this case, there are no changes or abnormalities, but the infected partner can transmit the infection through sexual contact. This is a latent form.
2. Patients may complain of symptoms such as: vaginal discharge, itching, burning, a feeling of dryness and discomfort in the external genital area, which intensifies after sexual intercourse. At the same time the usual gynecological examination will not reveal any changes in the genital area. But with a detailed examination, for example, during colposcopy, changes can be detected. This is a subclinical form of the infection.
3. Finally, the most common symptom of HPV is condylomas. This is a type of wart located on the mucous membrane of the genital organs: at the entrance to the vagina, in the area of ​​the clitoris, anus, urethra, on the walls of the vagina. Occasionally, condylomas are found on the skin of the labia and perineum. These are symptoms of a clinical form of infection.

Condylomas are skin growths that look like a cock's comb. Condylomas can be pedunculated or based. In color they do not differ in any way from the color of the surrounding tissues.

HPV is detected by PCR diagnostics.

TREATMENT

Condylomas are removed chemically (using various medications), using a laser or by cryodestruction. Next, treatment is carried out aimed at increasing the body's immunity. In this case, vaginal and rectal suppositories are used for local immunity and various drugs that stimulate general immunity - in the form of tablets or administered intramuscularly.

It is necessary to examine your partner for this disease. During treatment, sexual intercourse is possible using a condom.

PREGNANCY AND HPV

If HPV is detected during pregnancy planning, a comprehensive examination is necessary: ​​smears for all STDs, a smear for oncocytology, colposcopy (examination of the genital tract under a microscope). You also need to examine your sexual partner.

If an infection is detected, it is necessary to treat it and remove existing condylomas before pregnancy. Asymptomatic carriage of HPV IS NOT a contraindication for pregnancy. If condylomas are detected after pregnancy, they are carried out. It is advisable to do this in the 1st trimester. For this purpose, chemical and physical methods are used. Drugs that enhance immunity are also prescribed (such as Genferon, Viferon, Immunofan)

The issue of caesarean section is decided individually in each case.

Prevention of STDs

1. healthy lifestyle
2. reduction in the number of sexual partners,
3. regular visits to the gynecologist.
4. use of contraceptives, in particular barrier methods (condoms).
5. taking vitamins and herbal preparations that improve immunity

Over the past year, the preventive vaccine Gardasil has been increasingly promoted. It can protect against infection with the most common types of HPV. It should be noted that the vaccine does not have a therapeutic, but a preventive effect. But, if you have been diagnosed with any of the types of HPV, for example, the 16th, it is still better to administer the vaccine, because it will protect you from other types. Presence in the body HPV virus is not a contraindication for its administration. The vaccine will not cause complications in the course of the infection.

The vaccine has age restrictions; it is administered up to 26 years of age inclusive. But research is currently being conducted to study the effect of the vaccine on the body of older women.

INFLAMMATION- complex, complex local vascular-tissue (mesenchymal) protective-adaptive reaction of the whole organism to the action of a pathogenic stimulus. This reaction is manifested by the development of changes in blood circulation at the site of tissue or organ damage, mainly in the microvasculature, an increase in vascular permeability in combination with tissue degeneration and cell proliferation.

General pathology

Brief historical information and theories

The question of the meaning and essence of V. has always been given a large place in medicine. Hippocrates also believed that V. has a neutralizing value for the body, that harmful principles are destroyed in a purulent focus, and therefore the formation of pus is useful and healing, unless a certain limit of the intensity of the inflammatory process is exceeded. Hippocrates' views on the nature of inflammation prevailed until the 18th century, supplemented by a description of the “cardinal signs” of inflammation.

A. Celsus described four main wedges, signs of V.: redness ( rubor), swelling ( tumor), pain ( dolor), temperature increase ( calor). The fifth sign is dysfunction ( functio laesa) described by K. Galen; he spoke of inflammation as a local fever and pointed to the variety of etiol and factors that can cause it.

The first concept of V. close to the modern one was formulated in English. surgeon J. Gunter, who defined V. as the body’s reaction to any damage. Gunter considered V. a protective process that always occurs at the site of damage, with the help of which the normal function of the damaged tissue or organ is restored.

The study of V. began to develop after the improvement of the light microscope (mid-19th century), as well as in the first half of the 20th century. in connection with the development of biochemical, biophysical, and histochemical. methods and methods of electron microscopic study of tissues. R. Virchow (1859) drew attention to damage to the parenchyma of organs (dystrophic changes in cells) with V. and created the so-called. nutritional (“nutritional”) theory B. This theory lost its significance in connection with the studies of Samuel (S. Samuel, 1873) and Y. Konheim (1887), which gave the main importance in the pathogenesis of V. to the reactions of small vessels (vascular theory B .).

A. S. Shklyarevsky (1869) applied an experimental method to study blood flow during V. and gave physical. explanation of the phenomenon of “marginal standing of leukocytes”. A. G. Mamurovsky (1886) noted thrombosis and blockade of lymphatic vessels in the focus of V.

A particularly great contribution to the development of the problem of V. was made by I. I. Mechnikov, who in 1892 formulated the biological theory of V., developed the doctrine of phagocytosis (see), laid the foundation for the comparative pathology of V. and the theory of cellular and humoral immunity ( cm.). The process of absorption of foreign particles by phagocytes, including bacteria, was recognized by I. I. Mechnikov as the main, central process characterizing V. In his lectures on the comparative pathology of inflammation, I. I. Mechnikov wrote about the process of intracellular digestion carried out in the cytoplasm of phagocytes .

The idea of ​​I. I. Mechnikov on the importance of phagocytosis for protecting the body from pathogenic factors and the formation of immunity was developed in the works of N. N. Anichkov, A. D. Ado, Cohn (E. J. Cohn, 1892 - 1953) and many other scientists . With the discovery in 1955 of cytoplasmic organelles - lysosomes (see) - the doctrine of I. I. Mechnikov about cytases as carriers of the digestive function of the cell received further confirmation.

V.V. Voronin in 1897 established the importance of the state of the interstitial tissue and vascular tone during V. Assigning a secondary role to the process of phagocytosis, he considered the processes occurring in the interstitial substance of connective tissue to be the main mechanisms underlying V., and gave a different Mechnikovsky's interpretation of the phenomenon of emigration, cell wandering and phagocytosis. Voronin's theory did not reveal the biol, the essence of inflammation. V. V. Podvysotsky in “Fundamentals of General and experimental pathology"(1899) wrote that with V. there is a divergence of endothelial cells, as a result of which holes are formed between them, through which leukocytes penetrate from the vessel into the perivascular space.

In 1923, H. Schade put forward a physical-chemical V.'s theory: in his opinion, the basis of V. is tissue acidosis, the Crimea is determined by the entire set of changes. Ricker (G. Ricker, 1924) considered the phenomena of V. as a manifestation of neurovascular disorders (neurovascular theory of V.).

Of great importance for elucidating the histogenesis of V. and the role of cellular forms involved in the inflammatory reaction were the works of A. A. Maksimov (1916, 1927), A. A. Zavarzin (1950) and other scientists who created experimental models of V. and studied transformation cellular forms in the focus of B.

Comparative pathology

The classic description of the comparative pathology of V. was given by I. I. Mechnikov, showing that V. always represents an active reaction of the body, no matter what stage of evolutionary development it is at. I. I. Mechnikov traced at different stages of phylogenesis the development of all phases of the inflammatory reaction - alteration, exudation and proliferation, and described in detail phagocytosis; in highly organized animals, a large role in phagocytosis was assigned to neuroregulatory mechanisms. The body, I. I. Mechnikov points out, defends itself with the means at its disposal. Even the simplest single-celled organisms do not react passively to harmful stimuli, but fight them through phagocytosis and the digestive action of the cytoplasm. However, even in the simplest unicellular organisms, when exposed to a pathogenic factor, alteration phenomena occur, similar to certain dystrophic processes in multicellular organisms. In multicellular organisms, the response to damage becomes more complex due to cell proliferation and the established vascular system; the body can already “send” a significant number of phagocytes to the site of damage. At later stages of phylogenesis, cell emigration occurs in organisms. With the formation of endocrine and nervous systems in organisms, neurohumoral factors for regulating the inflammatory response appear.

In highly organized animals, other protective and adaptive processes are added to phagocytosis: blockade of venous and lymphatic vessels draining from the source of V., exudation of serous fluid that dilutes toxic products, the formation of antibodies by proliferating plasma cells that neutralize the pathogenic factor.

Data on the phases of inflammation obtained from the study of the inflammatory reaction in phylogenesis show its complication as organisms evolve; phases of V. are repeated to a certain extent in the prenatal period of a person. Yu. V. Gulkevich (1973) showed that the embryo has significantly less reactivity compared to an adult organism and at the earliest stages of development the embryo reacts to harmful effects only with death, however, cell proliferation can also be observed already at the early stages of development. Exudation with the presence of leukocytes was detected in the fetal part of the placenta and the fetal membrane already by 10-12 weeks. and is the most recent ontogenetic component of the inflammatory response. Phagocytosis in the human embryo is carried out by Ch. arr. connective tissue macrophages, and later segmented granulocytes.

The development of the inflammatory reaction in human ontogenesis is closely related to the formation of immunol, reactivity, which is morphologically expressed by the appearance of a large number of plasma cells producing immunoglobulins, the number of which increases markedly when an inflammatory focus occurs in the body of the embryo. Studies show that an inflammatory reaction with the presence of all the signs of V. is established in the 4-5th month of a person’s intrauterine life. In the postnatal period, with V., the impact on the body of antigenic environmental stimuli and immunol increases, the processes further complicate the clinical morphology. profile B.

Etiology and pathogenetic mechanisms

The inflammatory reaction consists of several interconnected phases: a) alteration of tissues and their constituent cells; b) release of physiologically active substances (the so-called V. mediators), which constitute the triggering mechanisms of V. and entail a reaction of microcirculatory vessels; c) increasing the permeability of the walls of capillaries and venules; d) reactions of the blood system to damage, including changes in the rheological properties of blood (see Blood, Rheology); e) proliferation - reparative stage B.

For practical purposes, it is advisable to conditionally separate the three main interrelated components of V., which have a clear clinical morphology. expression: alteration with the release of mediators, vascular reaction with exudation and proliferation. The classification of the main morphol, forms of V. is based on the predominance of one or another of these components.

Alteration (damage to tissue and cells) can be considered as a result of the direct action of a pathogenic factor and metabolic disorders that occur in damaged tissue. This is the first phase of V.; it characterizes initial processes and morphologically manifests itself from barely noticeable structural and functional disturbances to complete destruction and death (necrobiosis, necrosis) of tissues and cells (see Alteration). Alterative changes in V. are especially pronounced in highly differentiated tissues that perform complex functions, for example, in neurons; in tissues that perform ch. arr. supporting function and components of the organ stroma, for example, in connective tissue, alterative changes are often difficult to detect. In parenchymal organs, alteration is manifested by various types of protein degeneration (see) and fatty degeneration (see), in their stroma mucoid and fibrinoid swelling can occur, up to fibrinoid necrosis (see Fibrinoid transformation).

In c. n. With. alteration is expressed by a change in ganglion cells (neurocytes) in the form of lysis of basophilic (tigroid) substance, displacement of nuclei to the periphery and pyknosis (see), swelling or shrinkage of cells. In mucous membranes, alteration is expressed by damage to the epithelium, desquamation (see) with exposure of the basement membrane; mucous glands intensively secrete mucus, to which desquamated epithelium is mixed, the lumens of the glands expand (see Mucous dystrophy).

Ultrastructural changes in V. occur both in the components of the cytoplasm and in the cell nucleus and its membrane. Mitochondria increase in size and swell; some mitochondria, on the contrary, shrink, cristae are destroyed; the shape and size of the cisterns of the endoplasmic reticulum change (see), vesicles, concentric structures, etc. appear. Ribosomes also change (see). In the cell nucleus, damage is manifested by the marginal arrangement of chromatin and ruptures of the nuclear membrane.

In many cases, alteration develops through the so-called. lysosomal effect: when the membranes of lysosomes (see) are destroyed, various, especially hydrolytic, enzymes are released, which play a significant role in damage to cell structures.

Inflammatory mediators- a number of physiologically active substances considered as triggers of V., under the influence of which the main link of V. arises - the reaction of the microcirculatory vessels and flowing blood with a violation of the rheological properties of the blood, which constitutes the initial phase of the inflammatory reaction. V.'s mediators help increase the permeability of the vessels of the microcirculatory system, especially its venular section, with subsequent exudation of plasma proteins, emigration of all types of leukocytes, as well as erythrocytes through the walls of these vessels. These physiologically active substances play an important role in the manifestations of V., and some researchers call them “internal engines” of V.

Spector and Willoughby (W. G. Spector, D. A. Willoughby, 1968) give 25 names of physiologically active substances (chemical mediators) different spectrum actions that appear after tissue damage. Especially many works on V.’s mediators appeared after the discovery of histamine and leukotaxin. Although leukotaxin in subsequent testing works turned out to be a substance of a heterogeneous nature, its study served as an incentive for further research into endogenous chemicals. V. mediators, the most important of which are considered to be histamine, serotonin, plasma kinins, RNA and DNA breakdown products, hyaluronidase, prostaglandins, etc.

One of the main sources of chemicals. V.'s mediators are mast cells (see), in the granules of which histamine, serotonin, heparin, etc. are found; Cytochrome oxidase, acid and alkaline phosphatases, enzymes for the synthesis of nucleotides, proteases, exterases, leucine aminopeptidases, and plasmin were found in the cytoplasm of mast cells.

Spector and Willoughby most convincingly demonstrated the particularly important role of histamine (see) in the triggering mechanisms of B. Histamine is the first vasoactive substance that appears immediately after tissue damage; it is with this that the triggering stages of vasodilation, increased vascular permeability and exudation are associated; histamine has a predominant effect on venules. Serotonin is also of great importance (see).

Among the mediators of V., it is necessary to note the globulin permeability factor (PF/dil.), discovered in the blood plasma of a guinea pig by A. A. Miles et al. (1953, 1955) and T. S. Pashina (1953, 1955) in aseptic inflammatory exudate, blood serum of rabbits, dogs and humans; this factor promotes the release of bradykinin with the help of kallikrein. Spector believes that the globulin permeability factor has a close relationship with the blood coagulation mechanism, and in particular with the Hageman factor (see Blood coagulation system). According to Miles, the Hageman factor activates the globulin precursor PF/dil., active PF/dil. is formed, and then a chain of sequential reactions is activated: prekininogenase - kininogenase - kallikrein - kininogen - kinin.

Certain nucleosides take part in the inflammatory reaction; adenosine can cause increased permeability of microvascular walls and local accumulation of leukocytes; Some nucleosides are liberators (releasing) of histamine.

Vascular reaction with exudation plays a very important role in the mechanisms of inflammation. A number of authors argue that the entire “shape of inflammation,” all its features, the entire range of tissue changes are determined by the vascular reaction, the permeability of the microvasculature, and the severity of its damage.

In the earliest phases of V., activation of the functions of the capillary endothelium is noted. In the cytoplasm of the endothelium, the number of microvesicles increases, accumulations of cytogranules appear, polyribosomes are formed, mitochondria swell, cavities expand endoplasmic reticulum. Endothelial cells slightly change their configuration, swell, and their membranes become loose (see Permeability).

The mechanisms of passage of substances of different molecular weights and blood cells through the endothelial lining and basement membrane of capillaries and venules have long remained unclear. Using electron microscopy methods, it was established that endothelial cells in capillaries with continuous endothelium, closely adjacent to each other, are only in certain places linked to each other using desmosomes (tight junctions). The cell is anchored on the basement membrane and bonded to neighboring cells by a colloidal mass such as calcium proteinate in combination with mucopolysaccharides. In pathol conditions, the cell body can contract, change its shape and move. Complex of endothelial cells lining inner surface Microcirculation vessels are a mobile system; when the cut is functioning, gaps can appear in the spaces between endothelial cells, and even channels can appear in the cell body. Interendothelial gaps should be classified as so-called. small pores, and the channels in the body of the endothelial cell (microvesicular transport) are the so-called. large pores, through which transcapillary transport occurs. Dynamic electron microscopic observations

A. M. Chernukha et al. showed that, for example, in pneumonia, microvesiculation of the capillary endothelium and the formation of larger endothelial microbubbles is significantly enhanced, which indicates an increase in tissue metabolism.

In the focus of V., severe disorders of blood flow and lymph circulation occur. After tissue damage, the earliest change in an acute inflammatory reaction is a rapid (from 10-20 seconds to several minutes) contraction of arterioles. Most researchers do not attach much importance to this phenomenon, but Spector and Willoughby consider it a protective reaction caused by catecholamines. Soon two phases of vasodilation develop. The first phase (immediate vasodilation), accompanied by an increase in permeability to blood proteins, reaches a maximum after an average of 10 minutes; the second phase, much longer, lasts several hours. Due to the second phase of vasodilation, tissue infiltration with leukocytes, inflammatory hyperemia (see), the rheological properties of blood change, stasis, local hemorrhages, and thrombosis of small vessels occur; in the focus of V., metabolism increases, which is expressed by an increase in the concentration of hydrogen ions, acidosis, and hyperosmia. Lymphostasis and lymphothrombosis develop in lymph and microvessels.

Shifts in the rheological properties of blood begin with a change in the speed of blood flow, disruption of the axial flow, the release of white blood cells from it and their location along the walls of post-capillary venules (the so-called marginal position of leukocytes); aggregates of platelets and erythrocytes, stasis and thrombosis of venules and capillaries are formed. Thrombosis occurs due to the activation of Hageman factor, important component blood coagulation system. Then exudation occurs (see), i.e., the release of blood components from the vessels into the tissue - water, proteins, salts and blood cells. Metabolic products and toxins released from the bloodstream are found in the V. focus, i.e., the V. focus performs a kind of drainage elimination function. Substances (eg, paints) that have been exuded or injected directly into the lesion are poorly excreted due to thrombosis of the venous and lymph vessels in the inflamed tissues.

Exudation of proteins occurs in a sequence, the edges of which are explained by the size of the molecules (the smallest molecule is albumin, the largest is fibrinogen): with a small degree of increase in permeability, albumins are released, and as permeability increases, globulins and fibrinogen are released. Exudation of protein molecules occurs. arr. through channels in the endothelial cell body (large pores) and, to a lesser extent, through gaps between endothelial cells (small pores).

The release of blood cellular elements from the blood flow through the wall of venules and capillaries, Ch. arr. leukocytes (segmented granulocytes and monocytes), preceded by the marginal position of leukocytes, gluing them to the wall of the vessel. A. S. Shklyarevsky (1869) showed that the release of leukocytes from the axial current is in full accordance with physical. the law of behavior of particles suspended in a flowing liquid when its speed of movement slows down. After adhering to endothelial cells, segmented granulocytes form pseudopodia that penetrate the vessel wall, the cell contents flow towards the leg extended beyond the vessel, and the leukocyte ends up outside the vessel. In the perivascular tissue, segmented granulocytes continue to move and mix with the exudate.

The process of emigration of leukocytes is called leukodiapedesis. It has been established that the emigration of segmented granulocytes and mononuclear cells is somewhat different. Thus, segmented granulocytes (neutrophils, eosinophils and basophils) emigrate between endothelial cells (interendothelial), and agranulocytes (large and small lymphocytes and monocytes) - through the cytoplasm of the endothelial cell (transendothelial).

Rice. 1. Interendothelial emigration of leukocytes through the vessel wall during inflammation: a - segmented granulocytes (1) penetrated into the space under the endothelial cell and are located between the endothelium (2) and the basement membrane (3). The junctions of endothelial cells (4), collagen fibers (5), and granulocyte nuclei (6) are visible; x 20,000; b - two segmented granulocytes (1) are located in the perivascular connective tissue (the basement membrane has been restored to a dense gel). The endothelium (2) is not changed, the junctions (4) of its cells and collagen fibers of the perivascular connective tissue (5) are visible; lumen of the vessel (7); x 12,000.

Interendothelial emigration occurs as follows. In the very initial phase of B., the segmented granulocyte adheres to the endothelial cell and threads seem to stretch between it and the leukocyte. Then contraction of the endothelial cell occurs and pseudopodia rush into the gap formed between the two cells; with their help, the segmented granulocyte quite quickly penetrates into the space under the endothelial cell, the edges seem to peel off, and the hole above it is closed by the endothelial cells connecting again - the segmented granulocyte finds itself between the endothelium and the basement membrane (Fig. 1, a). The segmented granulocyte overcomes the next obstacle - the basement membrane - apparently by the mechanism of thixotropy (an isothermal reversible decrease in the viscosity of a colloidal solution), i.e., the transition of the membrane gel into a sol with slight contact of the granulocyte to the membrane. The granulocyte easily overcomes the sol, ends up in the tissue outside the vessel (Fig. 1, b), and the basement membrane is again restored to a dense gel.

During transendothelial emigration, agranulocytes initially adhere to the endothelial cell, and the activity of the cut increases sharply; The finger-like processes that appear at the membrane of the endothelial cell seem to capture the mononuclear cell from all sides, absorb it by forming a large vacuole and throw it onto the basement membrane. Then, using the thixotropy mechanism, mononuclear cells penetrate the basement membrane into the perivascular space and mix with the exudate.

With V., red blood cells also exit from the vessels into the tissue (see Diapedesis). They pass the vessel wall passively with a sharp increase in vascular permeability, which is observed with highly toxic infections (plague, anthrax), damage to the vessel walls by a tumor, radiation sickness and etc.

I. I. Mechnikov explained the exit of segmented granulocytes from the vessel and movement towards the focus of damage by chemotaxis, that is, the effect on leukocytes of substances that caused V. or formed in the focus of V. (see Taxis). Menkin (V. Menkin, 1937) isolated the so-called from inflammatory tissue. leukotaxin, which causes positive chemotaxis of segmented granulocytes; positive chemotaxis is more pronounced in segmented granulocytes, less pronounced in agranulocytes.

The most important phenomenon of V. is phagocytosis (see), carried out by cells - phagocytes; these include segmented granulocytes - microphages and agranulocytes - macrophages (see), in the cytoplasm of which the process of intracellular digestion occurs. A positive role in the processes of phagocytosis of aluminum, chromium, iron and calcium ions, opsonins has been revealed (see).

It has been established that various particles and bacteria invaginate the phagocyte membrane; in the cytoplasm of the phagocyte, the invaginated part of the membrane with the material enclosed in it is split off, forming a vacuole, or phagosome. When a phagosome merges with a lysosome, a phagolysosome (secondary lysosome) is formed, which carries out intracellular digestion with the help of acid hydrolases. At the moment of phagocytosis, the activity of lysosomal proteolytic enzymes sharply increases, especially acid phosphatase, collagenase, cathepsins, arylsulfatase A and B, etc. Thanks to these same enzymes, dead tissues are broken down; removal of decay products from the V. focus occurs by phagocytosis.

With the help of the phenomena of pinocytosis, droplets of liquid and macromolecules are absorbed, for example, ferritin, protein, antigen (see Pinocytosis). Nossal (G. Nossal, 1966) showed that Salmonella antigen, labeled with radioactive iodine and introduced into the body of a rabbit, is absorbed by macrophages in the order of micropinocytosis. Antigen molecules in the macrophage cytoplasm are exposed to lysosomal hydrolases, which leads to the release of antigenic determinants. The latter are complexed with the RNA of macrophages, and then information about the antigen is transmitted to lymphocytes, which are transformed into plasma cells that form antibodies. Thus, intracellular digestion of the antigen is completed by an immunogenic process (see Immunomorphology), and the protective and immunogenic function of the inflammatory reaction is carried out, in the process of which cellular and humoral immunity arises.

However, along with completed phagocytosis in macrophages, for example, in certain infections, incomplete phagocytosis, or endocytobiosis, is observed, when phagocytosed bacteria or viruses are not completely digested, and sometimes even begin to multiply in the cytoplasm of the cell. Endocytobiosis is explained by the lack or even absence of antibacterial cationic proteins in the lysosomes of macrophages, which reduces the digestive ability of lysosomal enzymes.

As a result of changes in microcirculation, increased vascular permeability and subsequent exudation of plasma proteins, water, salts and emigration of blood cells in the tissues, a cloudy, protein-rich (from 3 to 8%) liquid is formed - exudate (see). Exudate can accumulate in the serous cavities, between the fibrous structures of the organ stroma, in the subcutaneous tissue, which leads to an increase in the volume of inflamed tissue. Exudate consists of a liquid part and cellular mass and contains tissue decay products. The nature of the exudate is not uniform: with a small degree of vascular permeability, albumin and a few cells predominate in the exudate; with significant permeability, globulin, fibrin, and many cells predominate.

The dynamics of cellular changes in the exudate show that, under the influence of treatment, the number of neutrophils initially decreases, and the number of monocytes increases, and a large number of macrophages appear. The change from segmented granulocytes to agranulocytes in the exudate is considered a favorable prognostic sign.

Proliferation (reproduction) of cells is the final, reparative phase B. Cell reproduction occurs ch. arr. due to the mesenchymal elements of the stroma, as well as elements of the parenchyma of organs. Connective tissue stem cells multiply - polyblasts, or lymphoid cells, adventitial and endothelial cells of small vessels, reticular cells of lymph nodes, small and large lymphoblasts (see Granulation tissue, Connective tissue). When they differentiate, mature and specialized cells appear in the V.'s focus: fibroblasts, fibrocytes, mast and plasma cells, which differentiate from their predecessors - plasmablasts and large and small lymphocytes; new capillaries appear. With proliferation (see), exudation of neutrophilic, eosinophilic, basophilic leukocytes and lymphocytes, etc. is also observed; in this regard, lymphoid, plasma cell, eosinophilic and other infiltrates are distinguished.

Cellular elements in the inflammatory focus undergo transformation processes. Segmented granulocytes, having fulfilled their phagocytic function, die quite quickly. Lymphocytes partly die, partly transform into plasma cells, which gradually die, leaving the product of their secretion - hyaline balls. Mast cells die, blood monocytes that have entered the tissues become macrophages, clearing the V. focus from cellular detritus, and are carried away by the lymph current to regional lymph nodes, where they also die. The most persistent cellular forms in the inflammatory focus remain polyblasts and their differentiation products - epithelioid cells, fibroblasts and fibrocytes. Occasionally, multinucleated giant cells appear, arising from epithelioid and proliferating endothelial cells. Active collagen synthesis occurs with the participation of fibroblasts. The cytoplasm of fibroblasts becomes pyroninophilic, that is, it is enriched with ribonucleoproteins that form a matrix for collagen. V. ends with the formation of mature fibrous connective tissue.

Metabolic disorders that occur in the focus of V., according to Lindner (J. Lindner, 1966), can be divided into catabolic and anabolic processes.

Catabolic processes are manifested by disturbances in physiology, the balance of the basic substance of connective tissue: processes of depolymerization of protein-mucopolysaccharide complexes, the formation of breakdown products, the appearance of free amino acids, uronic acids (which leads to acidosis), amino sugars, polypeptides, low molecular weight polysaccharides are observed. This disorganization of the interstitial substance increases vascular-tissue permeability and exudation; this is accompanied by the deposition of blood proteins, including fibrinogen, between collagen fibrils and protofibrils, which, in turn, contributes to a change in the properties of collagens.

Defensive reactions the body is largely determined by anabolic processes and the degree of their intensity. These processes in V. are expressed by an increase in the synthesis of RNA and DNA, the synthesis of the main interstitial substance and cellular enzymes, including hydrolytic ones. Histochem. studies conducted by Lindner to study enzymes in cells in the outbreak of V. showed that monocytes, macrophages, giant cells, and segmented granulocytes exhibit especially great enzymatic activity from the moment of appearance in the outbreak of V.. The activity of hydrolase enzymes, which are markers of lysosomes, increases, which suggests an increase in the activity of lysosomes in lesion B. In fibroblasts and granulocytes, the activity of redox enzymes increases, due to which the coupled process of tissue respiration and oxidative phosphorylation is enhanced.

The early appearance of cells rich in hydrolases (lysosomes), and primarily segmented granulocytes, can be considered as one of the manifestations of catabolic processes due to the need for increased processing of breakdown products; at the same time, it promotes anabolic processes.

Regulatory factors and course

V. is considered as a local tissue reaction, however, its occurrence and course are largely determined by the general condition of the body. The general principle of self-regulation with information feedback is already presented at the cellular level. However, adaptive reactions within the cell have independent significance as long as the functional systems of the entire organism, reflecting the complex complex of self-regulation of cells and organs, maintain their relatively stable state. When this state is violated, adaptive and compensatory mechanisms are activated, representing complex neurohumoral reactions. This should be kept in mind when analyzing local features of the development of the outbreak of B.

V.'s character can be influenced by both hormonal and nervous factors. Certain hormones are very important for the inflammatory reaction, Ch. arr. hormones of the adrenal cortex and pituitary gland, which was convincingly shown in experiment and in the clinic by the Canadian pathologist G. Selye. It has been established that the somatotropic hormone of the pituitary gland deoxycorticosterone acetate and aldosterone are able to increase the inflammatory “potential” of the body, that is, increase V., although they themselves cannot cause it. Mineralocorticoids, influencing the electrolyte composition of tissues, have a pro-inflammatory effect (activate V.). Along with this, glucocorticoids (hydrocortisone and others), adrenocorticotropic hormone, without having bactericidal properties, have an anti-inflammatory effect, reducing the inflammatory response. Cortisone, delaying the development of the earliest signs of V. (hyperemia, exudation, emigration of cells), prevents the occurrence of edema; This property of cortisone is widely used in practical medicine. Cortisone deprives the connective tissue of mast cell precursors (large lymphocytes and polyblasts), resulting in a depletion of connective tissue in mast cells. This may be the basis for the anti-inflammatory effect of cortisone, since in the absence of mast cells, the activity of V. triggering factors, for example, histamine, formed from mast cell granules, is significantly reduced.

The influence of nervous factors on V. has not been studied enough. However, it is known that when peripheral innervation, especially sensitive, is disrupted, V. becomes sluggish and protracted. For example, trophic ulcers of the extremities that occur as a result of injuries to the spinal cord or sciatic nerve take a very long time to heal. This is explained by the fact that in tissues deprived of sensitive innervation, metabolic processes are disrupted, alterative changes intensify, vascular permeability increases and edema increases.

Wedge, the course of V. depends on many factors. The state of the body's reactive readiness and the degree of its sensitization are especially important for the course of V. In some cases, especially with increased sensitivity, V. occurs acutely, in others it takes a protracted course, acquiring the character of subacute or chronic. A wave-like course of V. is also observed, when periods of subsidence of the process alternate with exacerbations; outbreaks of the inflammatory process are possible over a number of years, for example, with brucellosis, tuberculosis, collagen diseases. In these cases, during the course of the disease, the period (phase) of immediate-type hypersensitivity is replaced by a period of delayed-type hypersensitivity. In the phases of hypersensitivity, exudative and even necrotic changes predominate with a pronounced reaction of the microcirculatory system. As V. subsides or the process transitions to a subacute form, vascular phenomena subside and proliferation phenomena, dominant during chronic, come to the fore. B. With hron, abscess, for example, along with the formation of pus, there are pronounced proliferative phenomena up to the development of mature connective tissue. At the same time, proliferative nodules with a very weakly expressed vascular-exudative reaction occur primarily in certain infectious diseases with an acute course (typhoid and typhus, malaria, tularemia).

When hron, inflammation with a wave-like course wedge, the picture can be very motley depending on the predominance of one or another phase of V., and both old and fresh morphol changes are possible in the tissues.

Main clinical signs

Five classic wedges, signs characteristic of acute V. of the external integument, retain their significance, having passed the test of time and received modern pathophysiol. and morphol, characteristics: redness, swelling, pain, fever, dysfunction. With chronic V. and V. of internal organs, some of these signs may be absent.

Redness- a very bright wedge, a sign of V., caused by inflammatory hyperemia, dilation of arterioles, venules, capillaries, slowing of blood flow; As the blood flow slows down, the scarlet-red color of the inflamed tissue becomes bluish. Inflammatory hyperemia is combined with tissue alteration, increased vascular-tissue permeability, exudation and proliferation of cells, i.e. with the whole complex of tissue changes characteristic of V.

Swelling with V. it is caused in the initial period by the consequences of a vascular reaction and the formation of infiltrate and perifocal edema, which develops especially easily around the V. focus, surrounded by loose tissue; in later periods of V. proliferation is also important.

Pain- constant companion of V., arising as a result of irritation by exudate of the endings of sensory nerves or certain physiological active substances, for example, kinins.

Temperature increase develops with an increased influx of arterial blood, as well as as a result of increased metabolism in the focus of B.

Dysfunction As a rule, it always arises on the basis of V.; sometimes this may be limited to a disorder of the functions of the affected tissue, but more often the entire body suffers, especially when V. occurs in vital organs.

Main forms of inflammation

According to morphological characteristics, three forms of V. are distinguished: alterative, exudative, productive (proliferative).

Alterative inflammation

Alterative inflammation is characterized by predominant tissue damage, although exudation and proliferation also occur. This type of V. is also called parenchymal, because it is observed most often in parenchymal organs (myocardium, liver, kidneys, skeletal muscles).

Alteration is expressed by various types of degeneration of the parenchyma cells of the organ and stroma, ranging from cloudy swelling of the cytoplasm to necrobiotic and necrotic changes, which can occur in the parenchyma of the organ and in the interstitial tissue in the form of fibrinoid swelling and fibrinoid necrosis.

Alternative V. with a predominance of necrobiotic changes is called necrotic V. This type of V. is observed during an immediate allergic reaction (see Allergy), as well as when exposed to highly toxic substances. When the body is exposed to bacterial toxins, for example, diphtheria, alterative myocardial inflammation occurs, which is expressed by the appearance in various layers of the myocardium, especially in the subendocardial zone, of foci of fatty degeneration, clumpy disintegration of myofibrils, up to the appearance in severe cases of foci of necrosis; the same is observed in allergic myocarditis (tsvetn. Fig. 1). Vascular-mesenchymal and proliferative reactions are weakly expressed.

In the liver, alterative V. is observed with infectious hepatitis, when exposed to, for example, chloroform, carbon tetrachloride and is expressed by cloudy swelling and fatty degeneration of hepatocytes, an increase in their size and the size of the liver as a whole.

In the kidney, alterative V. is expressed by granular degeneration of the epithelium of the proximal and distal parts of the nephron, up to necrosis of the epithelium with a weakly expressed vascular-mesenchymal reaction.

The outcomes of alternative V. are determined by the intensity and depth of tissue damage. With a mild degree of dystrophy, after eliminating the cause that caused V., complete tissue restoration occurs; areas of irreversible damage to the parenchyma are replaced by connective tissue (for example, after diphtheria myocarditis, cardiosclerosis develops).

Exudative inflammation

Exudative inflammation is characterized by a predominance of the reaction of the microcirculatory system, Ch. arr. its venular section, over the processes of alteration and proliferation. The exudation of liquid parts of the plasma, the emigration of blood cells, i.e., the formation of exudate, comes to the fore. For exudative V., a variety of morphol, and wedge, manifestations is typical, since depending on the degree of disturbance of vascular permeability, the nature of the exudate may be different. In this regard, exudative V. can be serous, catarrhal, fibrinous (croupous and diphtheritic), purulent, putrefactive, hemorrhagic, mixed.

Serous inflammation characterized by the accumulation in tissues, often in serous cavities, of slightly turbid, almost transparent exudate containing from 3 to 8% serum protein, and in the sediment - single segmented granulocytes and desquamated cells of the serous membranes.

Serous V. can be caused by thermal (burns), chemical, infectious (especially viruses), endocrine, or allergic agents. This form of V. often develops in serous cavities (serous pleurisy, peritonitis, pericarditis, arthritis, etc.), less often in parenchymal organs - the myocardium, liver, kidneys.

Serous V. of the myocardium is expressed by the accumulation of exudate between bundles of muscle fibers, around the capillaries; in the liver - in the surrounding sinusoidal spaces (Disse spaces); in the kidneys (with serous glomerulitis) - in the lumen of the glomerular capsule (Shumlyansky-Bowman capsule). In the lung, serous effusion accumulates in the lumen of the alveoli (color fig. 2). When the skin is burned, serous effusion accumulates under the epidermis, which leads to the formation of large blisters. Hyperemia is noted in the serous membranes, they become dull and lose their characteristic shine.

Serous effusion can occur around foci of purulent V. (for example, with periostitis of the jaw) or around a tuberculous focus, increasing the area of ​​​​the lesion - the so-called. perifocal B.

Serous V. usually occurs acutely. With a large amount of effusion, cardiac activity becomes difficult, respiratory failure occurs, joint mobility is limited, etc.

The outcome of serous V., if it has not turned purulent or hemorrhagic, is generally favorable. Serous exudate is easily absorbed and does not leave any traces or a slight thickening of the serous membranes is formed. Small areas of sclerosis may occur in the myocardium and liver due to the proliferation of fibroblasts and the formation of collagen fibers.

Catarrhal inflammation (catarrh) develops on the mucous membranes and is characterized by the formation of a liquid, often transparent exudate mixed with a large amount of mucus, which is secreted in increased quantities by the mucous glands. The exudate contains leukocytes, lymphocytes and desquamated epithelial cells and usually flows down the mucous membrane. These are catarrhal rhinitis, rhinosinusitis, gastritis, enterocolitis. According to the nature of the exudate, i.e., according to the predominance of certain elements in the exudate, they speak of serous, mucous or purulent catarrh. V. of the mucous membrane often begins with serous catarrh, which turns into mucous, then purulent.

The reasons are very varied. Microbes, thermal and chemical, are of great importance. irritants, etc. Catarrh can occur when the body's defenses are weakened, when saprophytic bacteria growing on the mucous membranes become pathogenic.

Catarrhal V. can occur acutely and chronically. In acute cases, the mucous membrane looks full-blooded, swollen, and covered with liquid exudate. Acute serous and mucous catarrh lasts two to three weeks and usually goes away without leaving any consequences. With purulent catarrh, erosions and ulcers may occur on the mucous membrane. With hron, catarrh, in some cases the mucous membrane can remain swollen for a long time and become thickened, polyps of different sizes may appear on it (hypertrophic catarrh), in other cases the mucous membrane becomes very thin (atrophic catarrh).

Fibrinous inflammation It is characterized by liquid exudate, in which fibrinogen accumulates in a short time, turning into fibrin upon contact with damaged tissues, as a result of which the exudate thickens. The etiology of fibrous V. is diverse: it can be caused by microbes (diphtheria bacillus, dysentery microbes, mycobacterium tuberculosis, etc.), viruses, poisons of endogenous (eg, uremia) and exogenous (eg, mercuric chloride) origin. Fibrinous V. is localized on the serous and mucous membranes, less often - in the depths of the organ. Fibrinous V. is usually acute, but in some cases it can take a chronic course or proceed in waves.

Rice. 12. Croupous inflammation of the lung in the stage of gray hepatization.

Fibrin deposits on the surface of the serous membranes in the form of villous masses, and on the surface of the mucous membranes - in the form of a continuous film (color. Fig. 3). In the lumen of the pulmonary alveoli, fibrin precipitates in the form of fibrinous plugs, for example, when lobar pneumonia(tsvetn. fig. 7), as a result of which the lung tissue becomes dense and its consistency resembles the liver (tsvetn. fig. 12).

The serous membranes take on a dull appearance, and villous deposits of fibrin are formed on them, fused with the serous membrane (eg, fibrinous pericarditis - Fig. 2). On the mucous membranes, fibrinous deposits in some cases are located loosely, superficially, and are easily separated, in others they are tightly fused to the underlying tissue, which depends on the depth of the damage and the nature of the epithelium of the mucous membrane. Thus, the connection between the prismatic epithelium and the underlying tissue is weak and fibrin, even precipitated in the depths of the submucosal layer, forms a loose film (for example, on the mucous membrane of the stomach, intestines, trachea, bronchi).

Rice. 10. Diphtheritic tonsillitis and lobar tracheitis. The surface of the tonsils and the mucous membrane are covered with filmy deposits.

The squamous epithelium is tightly connected to the underlying connective tissue, and the fibrin film is therefore tightly fused with the mucous membrane, although fibrin falls out in the superficial layer of the squamous epithelium (between the cells preserved during damage), which is observed, for example, on the mucous membrane of the tonsils, oral cavity, esophagus. In connection with these features, fibrinous V. (tsvetn. Fig. 10) is divided into diphtheritic (tightly seated films) and croupous (loosely seated films).

Diphtheritic V. proceeds more severely: microbes multiply under tightly fitting films, releasing large amounts of toxin; films can close the airways, for example, with diphtheria of the pharynx, which can cause asphyxia. With lobar V., the films are easily separated, intoxication is less pronounced, but the danger of blockage of the respiratory tract is also possible.

Fibrinous V. is one of the severe forms of V.; its prognosis is largely determined by the localization of the process and the depth of tissue damage, and the outcome of fibrinous V. of serous and mucous membranes is different. On the serous membranes, masses of fibrin are partially subjected to enzymatic melting, most of them undergo organizational processes, i.e., germination by young connective tissue from the cambial layers of the visceral and parietal serous membranes, and therefore connective tissue adhesions (adhesions) are formed, which can disrupt organ function.

On mucous membranes, fibrinous films are usually rejected due to autolysis (see), unfolding around the lesion, and demarcation V. At the site of the rejected film, a defect of the mucous membrane is formed, an ulcer, the depth of the cut is determined by the depth of fibrin loss. Healing of ulcers sometimes occurs quickly, but in some cases (especially in the large intestine with dysentery) it is delayed for a long time. In the pulmonary alveoli, fibrinous exudate, with a favorable course of lobar pneumonia, undergoes lytic decay and resolves; in rare cases, the exudate grows with cells of young connective tissue, the edges gradually mature, and fields of sclerosis appear, which is referred to as carnification of the lung.

Purulent inflammation characterized by liquid exudate containing albumin and globulins, and sometimes fibrin strands; in the sediment - neutrophils, mostly disintegrated (purulent bodies). Such a product V. - a cloudy liquid with a greenish tint - is called pus (see). The etiology of purulent V. is varied: it can be caused by bacteria (staphylococci, streptococci, gonococci, meningococci, less commonly salmonella typhus, tuberculous mycobacteria, etc.), pathogenic fungi, or be aseptic, caused by chemicals. substances. Purulent V. can occur in any tissue and organ, serous cavities, or skin (Fig. 3). Its course can be acute and chronic, in some cases very severe.

Morphologically, purulent V. can have two forms - abscess (see) and phlegmon (see) and is accompanied by histolysis (melting of tissue). An abscess can occur primarily (its cavity is formed as a result of tissue melting), and also by embolism during septicopyemia, for example, focal purulent V. of the myocardium with the formation of an abscess (print. Fig. 8).

Acute diffuse purulent V. (phlegmon) tends to spread along the interfascial layers and intertissue cracks (tsvetn. Fig. 4); with phlegmon of organs went.-intestinal. tract in the infiltrate there are many eosinophils (tsvetn. Fig. 5).

With hron, form B. purulent focus surrounded by a dense fibrous capsule; in the exudate, along with purulent bodies, there are small numbers of lymphocytes, macrophages and plasma cells. There may be periods of exacerbation of V., formation of a fistula with the discharge of pus. The accumulation of purulent exudate in certain cavities of the body is designated as empyema (see).

In the outcome of acute purulent V., in favorable cases, the process is limited, even large ulcers can heal by replacing their cavity with granulation tissue, which gradually matures into a scar, which remains at the site of the abscess. Chron, purulent V. can proceed for a very long time and lead to amyloidosis (see). In unfavorable cases, the purulent focus is not delimited, the purulent process spreads to the lymph, vessels and veins, which leads to generalization of the process, sometimes even to sepsis (see).

Putrid inflammation(gangrenous, ichorous) develops due to the participation of putrefactive bacteria (pathogenic anaerobes) in one or another type of exudative V. Putrefactive V. poses a great danger to the body and can occur in those organs that come into contact with the environment (see Gangrene, Ludwig's tonsillitis). Inflamed tissues undergo putrefactive decomposition, acquire a dirty green color, become flabby, and seem to creep apart with the formation of foul-smelling gases (see Anaerobic infection).

Hemorrhagic inflammation characterized by the presence of different numbers of red blood cells in the exudate. Any type of V. can take on a hemorrhagic character (serous, fibrinous, purulent), which depends on a high degree of increased permeability, up to the destruction of microcirculation vessels. This type of V. occurs when exposed to highly virulent microbes; with plague, anthrax, and toxic flu, the hemorrhagic focus of V. resembles a hemorrhage. Hemorrhagic exudate is observed in serous cavities in malignant tumors. This type of V. is a sign of a very serious illness; its outcome depends on the underlying disease.

Mixed forms of inflammation are observed when the body’s defenses are weakened, or a secondary infection occurs, for example. staphylococci. In these cases, purulent or fibrinous may join the serous exudate, then V. is called serous-purulent, serous-fibrinous, etc. Catarrhal V. can also have a mixed character. A particularly unfavorable prognostic sign is the transformation of serous exudate into hemorrhagic, which always indicates to the addition of a severe infection or progression of a malignant tumor.

Productive inflammation

This form is also called proliferative inflammation, since it is characterized by the predominance of reproduction (proliferation) of cellular elements of the affected tissue. Alteration and exudation are weakly expressed and difficult to recognize; segmented granulocytes are rare.

Productive V. can be caused primarily by biological, physical. and chem. factors or is observed during the transition of acute V. to chronic.

Productive V. occurs, as a rule, chronically, but can be acute, for example, granulomatous V. with typhoid and typhus, with vasculitis of various etiologies, etc.

Productive V. is based on the reproduction of young cells of local connective tissue, as well as cambial cells of blood capillaries, which, upon differentiation, form new capillaries. All cells that multiply during productive V. have both local, histiogenic, and hematogenous origin. For example, in the focus of V. you can see large and small lymphocytes, monocytes, as well as a small amount of eosinophils and basophils that came from the bloodstream. As the cells mature, macrophages, fibroblasts, fibrocytes, lymphoid cells, single plasma cells, and mast cells remain in the V. lesion. Productive V. is completed, as it were, by fibroblasts; they secrete tropocollagen - a precursor of collagen in fibrous connective tissue, the edges remain at the site of the focus of productive B.

The outcomes of productive inflammation vary. Complete resorption of the cellular infiltrate may occur; however, more often, at the site of the infiltrate, as a result of the maturation of the mesenchymal cells included in the infiltrate, connective tissue fibers are formed and scars appear.

There are two types of productive V.: nonspecific and specific. In nonspecific productive V., proliferating cells are located diffusely in the inflamed tissue; morphol, there is no specific picture characteristic of the pathogen that caused V. With specific productive V. cellular composition exudate, cell grouping and process cycle are characteristic of the pathogen B. Specific B. for the most part has the character of a so-called infectious granulomas - nodules consisting of elements of granulation tissue.

Intermediate inflammation, or interstitial, usually has a chronic course and is characterized by the fact that the inflammatory infiltrate is formed in the stroma of the organ surrounding the vessels (myocardium, liver, kidneys, lungs, striated muscles, uterus, endocrine glands). The infiltrate, consisting of various cells, is located diffusely, covering the entire organ, or in separate foci, mainly around the vessels (tsvetn. Fig. 9). In some cases, one type of cell predominates; sometimes the infiltrate consists of lymphocytes and macrophages and resembles V. on an immune basis. With certain types of interstitial V., a large number of plasma cells secreting gamma globulins accumulate. When plasma cells die, their metabolic products remain in the tissues in the form of free-lying fuchsinophilic spherical formations - the so-called. hyaline balls, or Roussel's bodies. As a result of interstitial productive V., sclerosis (see) or cirrhosis (see) develops.

Formation of granulomas(nodules) occurs as a result of cell proliferation in the interstitial tissue of an organ under the influence of a pathogenic factor. These nodules may be composed of a variety of mesenchymal cells or a single cell type; sometimes they are located in close connection with small vessels and even form in the artery wall. The diameter of the granuloma usually does not exceed 1-2 mm, but can reach 2 cm. In the center of the granuloma, cellular or tissue detritus is sometimes found, in which the causative agent of the disease can sometimes be identified, and along the periphery of the detritus, lymphoid, epithelioid, and plasma macrophages are located in different proportions and mast cells, among which multinucleated giant cells can be found. Granulomas are usually poor in capillaries.

The formation of granulomas in tissues reflects protective and immune processes, which develop during infectious diseases, and to a certain extent determines the dynamics of immunol, the process from the beginning of tissue damage to the final stage of the disease, expressed by scarring of granulomas.

The formation of granulomas is observed in a number of acute infectious diseases (typhoid and typhus, tularemia, viral encephalitis, rabies) and certain chronic diseases (rheumatism, brucellosis, mycoses, sarcoidosis, tuberculosis, syphilis, etc.).

In certain hron, infectious diseases, granulomas acquire to a certain extent the morphol, structure and dynamics of development characteristic of the disease. In this regard, they are designated as follows: tubercle - for tuberculosis, gumma - for syphilis, leproma - for leprosy, nodules - for glanders and rhinoscleroma. In the listed diseases, V. occurs specifically, that is, it is characteristic only of this disease; in granulomas of specific V., the cellular composition is quite similar, the most characteristic are epithelioid and multinucleated giant cells: Pirogov-Langhans cells - in tuberculous granuloma; cells, or balls, of Virchow - in leprosy; Mikulicz cells - for scleroma, etc.

Rice. 11. Miliary tuberculous granulomas of the lung.

The specificity of granulomas is determined not only by their morphol, structure (color fig. 6), but also by the characteristics of the wedge. course and pathological manifestations of V. (color. Fig. 11). In some cases, granulomas in tuberculosis, syphilis and leprosy have so much in common in structure that without special staining of the pathogen, diagnosis can be difficult; therefore, in morphological diagnosis of specific V., clinical and anatomical analysis of the disease as a whole is very important.

In typhoid fever, granulomas form in group lymphs, follicles (Peyer's patches), in ileocecal lymph nodes, liver, spleen, and bone marrow. They arise from proliferating reticular cells capable of phagocytosing typhoid Salmonella; these nodular collections then undergo necrosis. The process of granuloma formation, including scar formation, takes 4-5 weeks. (see Typhoid fever).

Granulomas in typhus occur in the c. n. pp., especially in the medulla oblongata at the level of the olives, in close connection with small vessels, in which productive-destructive endothrombovasculitis, characteristic of typhus, is observed (see Epidemic typhus). Granulomas similar in structure, but with less pronounced vascular damage, appear in the c. n. With. for viral encephalitis and rabies.

In rheumatism, granulomas appear in the connective tissue of the myocardium, heart valves, periarticular tissue, and in the capsule of the tonsils; they are constructed from large cells with basophilic cytoplasm of the macrophage type, the accumulation of which is considered as a reaction to the processes of disorganization of connective tissue (see Rheumatism).

With tularemia, granuloma develops in lymph nodes regional to the skin lesion. In the center of the granuloma there is a focus of necrosis, along the periphery there is a shaft of epithelioid and lymphoid cells and a large number of segmented granulocytes; sometimes multinucleated giant cells are found (see Tularemia).

In brucellosis, granulomas have a different structure. In some cases, in the center of the granuloma and around the circumference there is an accumulation of epithelioid and giant multinucleated cells, in others - in the center of the granuloma there is necrosis and along the periphery there are epithelioid and giant cells (see Brucellosis); morphol, the picture is very similar to tuberculous granuloma.

Sarcoidosis is characterized by the formation of granulomas in the lymph nodes, built from epithelioid and giant cells without signs of necrosis in the center (see Sarcoidosis).

When granulomas heal, small, barely noticeable scars form (see Granuloma).

Formation of polyps and genital warts- productive V. of mucous membranes. At the same time, cells of the stroma and prismatic epithelium grow, polyps of inflammatory origin are formed (hypertrophic catarrh); such as, for example, polypous rhinitis, colitis, etc. On the mucous membranes, at the border of the prismatic and squamous epithelium, for example, in the anus, on the genitals, genital warts are formed from growths of the squamous epithelium (see Warts). Discharge from the mucous membranes irritates and macerates the squamous epithelium, causing chronic conditions in the stroma. V., the cut stimulates the stroma and epithelium to further grow (see Papilloma, Polyp, polyposis).

The favorable course of V. is determined by the perfection of the processes of phagocytosis, the formation of antibodies, the proliferation of connective tissue cells, and the delimitation of the inflammatory focus. Such an adequate reaction is characteristic of a healthy body and is called normergic. However, the development of all components of V., the course and outcome also depend on the state of the body: on previous diseases, age, metabolic rate, etc.

Wedge, observations show that often the same pathogen does not cause any reaction in one person, but in another it causes a very violent local and general reaction, sometimes even leading to death.

For example, cases of diphtheria have been described, when one person in a family died from a severe toxic manifestation of the disease, and other family members either did not get sick at all, or their infection manifested itself in an erased form of the disease, although everyone had the same source of infection.

It has been established that, depending on the reactivity of the body, V. can be hyperergic, which occurs in a sensitized organism (see Allergy), or hypoergic, which is observed in the presence of immunity to agent V.

There are many observations when V.’s picture does not correspond to the usual, normergic type and depends not so much on the toxicity of the pathogen as on the inappropriately violent reaction of the affected organism, which can be caused by preliminary sensitization (see). This type of V. is called allergic inflammation.

In the experiment, in animals infected with diphtheria bacilli after sensitization with horse serum, the disease proceeds very violently and uniquely compared to non-sensitized animals. The fact that such a different course of the disease from the normergic one is associated with sensitization of the body was noted in the works on anaphylaxis by G. P. Sakharov (1905), according to tuberculin reaction K. Pirke (1907), in studies on the morphology of allergic reactions by A. I. Abrikosov (1938) and R. Ressle (1935), in works on the development of V. in ontogenesis by H. N. Sirotinin (1940).

Immune-based inflammation

Research by F. Burnet (1962) and R.V. Petrov (1968) established that the rate of growth can increase or slow down depending on the state of cellular and humoral immunity, i.e., with an altered reactivity of the body, V. acquires features that distinguish it from normergic V. Thus, the introduction of a protein substance into the body as an antigen leads to the development of hypersensitivity and with repeated administration of even an insignificant dose of the same substance, inadequate general or local development develops a reaction with a clearly defined difference from a normergic reaction - a discrepancy between a small dose of antigen and a very violent reaction of the body (see Anaphylaxis, Arthus phenomenon).

This reaction is called hyperergic, V.-hyperergic, or an immediate-type hypersensitivity reaction: it develops in the tissue 1-2 hours after repeated administration of the antigen. The cause of V. in immediate-type hypersensitivity is immune complexes, which consist of an antibody circulating in the blood to a previously introduced antigen, a newly introduced antigen into the tissue, and activated complement. Cochrane (Ch. Cochrane, 1963) showed that immune complexes have a cytopathic and leukotactic effect: they are fixed in the vessel wall, especially post-capillary venules, damaging it, increasing permeability and leukodiapedesis.

In allergic V., which occurs as an immediate hypersensitivity reaction, the so-called. inflammatory protease (rich in sulfhydryl groups), sharply increasing vascular permeability and stimulating the emigration of segmented granulocytes. With this type of V., both experimentally and in pathology, significant tissue damage occurs in humans, a very pronounced reaction of the microcirculatory bed, abundant emigration of segmented granulocytes, plasma impregnation and fibrinoid necrosis of the walls of small vessels and tissues surrounding the vessels, edema, hemorrhages, etc. That is, a characteristic picture of necrotic V. develops. The immune nature of this V. is confirmed by the detection of immune complexes in the lesion, determined by the Koons method (see Immunofluorescence).

Electron microscopy and immunochemical. Shirasawa's studies (H. Schirasawa, 1965) show the following sequence of tissue changes in the focus of immediate-type isherergic V.: 1) the formation of immune precipitates (antigen-antibody complexes) in the lumen of the venules; 2) binding to complement; 3) chemotactic effect of precipitates on segmented granulocytes and their accumulation near veins and capillaries; 4) phagocytosis and digestion of immune complexes by segmented granulocytes using lysosome enzymes; 5) release of lysosomal enzymes and formation of vasoactive substances; 6) damage to the vascular wall with subsequent hemorrhage, edema and necrosis.

Hyperergic inflammation, i.e., inflammation occurring on an immune basis, is observed in patients prone to allergic reactions, nair, with drug intolerance, in the acute phase of collagen diseases, with hay fever, etc.

There is another type of increased sensitivity of the body - delayed-type hypersensitivity; It is based on manifestations not of humoral, but of cellular immunity. In this case, a local reaction in the tissues of the sensitized organism occurs 12 or more hours after repeated administration of the corresponding antigen. This reaction is usually observed in children infected with Mycobacterium tuberculosis after intradermal administration of tuberculin, therefore a delayed-type hypersensitivity reaction is also called a tuberculin-type reaction. The main role in the focus of such V. belongs to T-lymphocytes and macrophages. Lymphocytes are representatives of the population of thymic lymphocytes; they migrate from lymphoid organs to the blood and back (recirculating lymphocytes), as if they find antigen in tissues and carry out a pathogenic effect on the tissue. Lymphocytes come into contact with macrophages rich in acid phosphatase and, as it were, mutually inform each other about the nature of the antigen. Changes in the microcirculatory bed in the focus of V. with this type of reaction are very weakly expressed, segmented granulocytes are absent, and the signs of V. are not clearly expressed. Meanwhile, V., which occurs as a delayed hypersensitivity, is observed in a number of severe autoimmune diseases (in the skin, liver, kidneys, etc.). having a weakly expressed wedge, and morphol, dynamics, and ends with sclerosis.

Often gistol, the picture with hron, interstitial V. in humans resembles a delayed-type reaction (predominance of lymphocytes and macrophages in the infiltrate); V. takes a protracted course, reflecting autoimmune processes occurring in the body. The same type of V. is observed during the formation of granulomas. In some cases, granulomas perform the function of macrophages in relation to antigen, in others, the granuloma is intended to resorption of tissue breakdown products at the site of immune damage (for example, rheumatic granuloma).

V., which develops on an immune basis, can manifest itself in a mixed form, when the boundaries between two types of hyperergic V. are difficult to establish.

Differentiation of inflammation and morphologically similar processes

In its developed form, V. does not present great difficulties for wedge, and morphol, diagnosis. However, only morphol, the criterion cannot be limited when recognizing V., especially its individual forms; it is necessary to take into account the entire complex of manifestations, including the wedge, data. In the body, such tissue and vascular-cellular reactions are observed, as, for example, with delayed-type hypersensitivity, when it is difficult to detect all the signs of V. in the tissues: for example, there is no pronounced reaction of microcirculation vessels, there are no segmented granulocytes or, as is observed in the wall stomach in the midst of digestion, a lot of segmented granulocytes as a manifestation of distributive leukocytosis. It is known that during postpartum involution of the uterus, infiltrates from lymphoid cells can be detected in the glandular organs as an expression of metabolic changes. A pronounced proliferation of plasmablasts and plasmacytes in the organs of immunogenesis (bone marrow, lymph nodes, spleen, thymus gland) as an expression of a protective reaction manifested by the production of antibodies. In the peripelvic tissue, foci of extramarrow hematopoiesis have been described, resembling an inflammatory infiltrate.

Great difficulties arise when distinguishing between inflammatory and dystrophic processes, inflammatory cell proliferation and proliferation of non-inflammatory cells, in particular tumor ones.

Outcomes and significance of inflammation for the body

The outcomes of V. are different and depend on the cause, the state of the body and the structure of the organ. The death of vital tissues is possible with the most severe consequences for the body. However, usually the inflamed tissue is gradually delimited from the surrounding healthy tissue, the products of tissue breakdown undergo enzymatic breakdown and are resorbed by phagocytosis, absorbed by the capillaries of the newly formed lymph. networks. Thanks to cellular proliferation, V.'s focus is gradually replaced by granulation tissue (see). If there has been no significant tissue damage, complete recovery may occur. With a significant defect at the site of the V. focus, a scar is formed as a result of the maturation of granulation tissue (see). In organs and tissues, certain patols and changes may remain (thickening and adhesions of serous membranes, overgrowing of serous cavities, scars in organs), which in severe cases disrupt the function of a regional organ, sometimes the whole organism. So, for example, fibrinous effusion on the surface of the serous membranes, in the lumen of the alveoli, can resolve or, with significant accumulation, undergoes organization and connective tissue transformation. Diffuse interstitial productive V. usually ends in diffuse sclerosis of the organ (for example, cardiosclerosis). When a large number of granulomas heal, for example, in the myocardium during rheumatism, significant fields of cardiosclerosis are formed, which negatively affect the activity of the heart. In cases where the resulting connective tissue wrinkles and compresses the parenchyma, the organ is deformed, which is usually accompanied by a restructuring of its structure and regeneration phenomena (see). This process is referred to as cirrhosis of the organ, for example, cirrhosis of the liver, nephrocirrhosis, pneumocirrhosis.

Inflammation is an important protective-adaptive and, in general biological terms, quite expedient reaction developed in the process of phylogenesis; this reaction gradually became more complex during the evolution of living organisms (see Defense reactions of the body, Adaptive reactions). V. carries protection from the effects of pathogenic factors in the form of a kind of biol barrier, which is expressed by the phenomenon of phagocytosis and the development of cellular and humoral immunity. However, this reaction is automatic; it is carried out through self-regulation mechanisms with the help of reflex and humoral influences. Occurring as an adaptive reaction, V. under certain conditions can sometimes acquire harmful significance for the body: with V. tissue damage occurs, in some forms up to necrosis.

Thanks to the inflammatory reaction, the focus of damage is demarcated from the entire body, white blood cells emigrate to the source of inflammation and phagocytosis, and harmful elements are eliminated. The proliferation of lymphocytes and plasma cells contributes to the production of antibodies and increased local and general immunity. At the same time, it is well known that the accumulation of exudate during V. can be very dangerous. So, for example, exudate in the alveoli during pneumonia, from the very beginning of its occurrence, has a harmful effect on the body, because gas exchange is disrupted, the formation of fibrinous effusion on the mucous membrane of the larynx causes a narrowing of the lumen, irritates the receptors of the larynx, which is accompanied by spasm of the muscles of the larynx and can lead to asphyxia (see). Phagocytosis may be incomplete: a phagocyte that has absorbed a bacterium but is unable to digest it becomes a carrier of infection throughout the body.

Violations with V. are not only local; usually occurs and general reaction organism, expressed by fever, leukocytosis, accelerated ROE, changes in protein and carbohydrate metabolism, phenomena of general intoxication of the body, which in turn changes the reactivity of the body.

I. I. Mechnikov wrote in 1892: “... the healing power of nature, the main element of which is inflammatory reactions, is not at all an adaptation that has reached perfection. Private illnesses and cases of premature death sufficiently prove this.” And further: “This imperfection made necessary the active intervention of a person dissatisfied with the function of his natural healing power" The imperfection of the “healing power” of nature makes it necessary surgical intervention and the use of therapeutic agents aimed at strengthening the body’s protective and compensatory reactions and eliminating V.

V. underlies many diseases, therefore it is one of the most important problems of experimental and wedge medicine. It is studied at all levels of biol, structures, starting from molecular, subcellular, cellular and ending with the whole organism. Etiol, factors, biochemical, changes, morphophysiol are studied. characteristics, reactivity of tissues and the body as a whole, wedge, picture of V. A special section arose in the development of the problem of V. - pharmacology of V. - study of the mechanisms of action of V. mediators, with the participation of which various stages of the inflammatory reaction are realized; Active anti-inflammatory drugs are being sought that inhibit the release of these mediators, therefore contributing to the subsidence of V.

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A. I. Strukov, A. M. Chernukh.