LECTURE No. 6. Diseases of the respiratory system. Bronchial asthma

An exhaustive definition of asthma does not exist to date, however, the most complete definition of this disease was given by G. B. Fedoseev in 1982. Bronchial asthma (BA) is an independent, chronic, recurrent disease with a predominant lesion of the respiratory tract, the main and obligatory pathogenetic mechanism of which is an altered bronchial reactivity due to specific (immunological) and (or) non-specific, congenital or acquired mechanisms, and the main (mandatory) clinical sign is an asthma attack and (or) an asthmatic condition (asthmatic status) due to spasm of bronchial smooth muscles, hypersecretion, dyscrinia and edema of the bronchial mucosa.

Etiology. A combination of several factors plays an important role in the occurrence of asthma. In this regard, there are 2 forms of asthma - atopic (from the Latin athopia - “hereditary predisposition”) and infectious-allergic. Hereditary predisposition is due to the association of certain histocompatibility antigens (HLA) with the severity of asthma, and an increase in the severity of the disease is especially often observed in carriers of B antigens₃₅ and B₄₀.

Internal factors in the development of the disease are biological defects in the immune, endocrine systems, autonomic nervous system, bronchial sensitivity and reactivity, mucociliary clearance, pulmonary vascular endothelium, rapid response system (mast cells, etc.), metabolism of arachidonic acid, etc.

External factors include:

1) infectious allergens (viruses, bacteria, fungi, yeast, etc.);

2) non-infectious allergens (pollen, dust, industrial, medicinal, food; allergens of ticks, insects and animals);

3) mechanical and chemical irritants (metal, wood, silicate, cotton dust; vapors of acids, alkalis; fumes, etc.);

4) meteorological and physico-chemical factors (changes in air temperature and humidity, fluctuations in barometric pressure, the Earth's magnetic field, physical effort, etc.);

5) stressful, neuropsychic effects and physical activity.

Infectious agents can have not only an allergenic effect, but also reduce the body's sensitivity threshold to non-infectious (atopic) allergens, increase the permeability of the respiratory mucosa for them; to form a change in the reactivity of target cells (mast cells, basophils, monocytes, etc.) and effector systems.

Pathogenesis. Altered bronchial reactivity is a central link in the pathogenesis of the disease and can be primary or secondary. In the first case, changes in reactivity can be congenital or acquired due to direct exposure to chemical, mechanical, physical factors and infection. Secondary changes in bronchial reactivity are a manifestation of changes in the reactivity of the body's immune, endocrine, and nervous systems. Thus, speaking about the pathogenesis of AD, we can distinguish 2 groups of mechanisms: immunological and non-immunological.

Immunological mechanisms in the vast majority of cases are dominant in the course of the disease. Violations of the immunocompetent system in the mucous membrane of the respiratory tract, occurring according to types I, III and IV of hypersensitivity reactions, i.e. with a change in humoral and cellular immunities, lead to a change in bronchial reactivity. At the same time, there is a decrease in secretory IgA, the phagocytosis system is disturbed, the T-suppressor function of lymphocytes decreases, the production of interferon decreases, which ultimately leads to a decrease in the body's antiviral defense.

Type I (atopic, reaginic, or anaphylactic). In response to the ingestion of exoallergen antigens (pollen, animal and plant proteins, bacteria and drugs) into the body, there is an increased production of IgE (reagins), which are fixed and accumulate on mast cells (primary effector cells). This is the immunological stage of AD. Following this, the pathochemical stage of the process develops - degranulation of mast cells with the release of vasoactive, bronchospastic and chemotactic substances (histamine, serotonin, various chemotactic factors, etc.). These are primary mediators acting on vessels and target cells (secondary effector cells) - eosinophils, neutrophils, platelets, macrophage monocytes. The latter, when exposed to primary mediators, secrete secondary mediators (leukotrienes, prostaglandins, thromboxanes, platelet-activating factor and other substances belonging to the group of eicosanoids).

Under the influence of biologically active substances, the pathophysiological stage of pathogenesis begins: the permeability of the microcirculatory bed increases, which leads to the development of edema, serous inflammation, and bronchospasm. Clinically, this is manifested by an acute violation of bronchial patency and the development of an asthma attack.

Type III reaction (immunocomplex type, or Arthus phenomenon) develops under the influence of exoallergens and endoallergens (autoallergens, which are formed by the denaturation of proteins of bronchioles and alveoli as a result of infectious or allergic inflammation and the action of various irritants).

The reaction occurs in the zone of excess antigen with the participation of precipitating antibodies belonging to the immunoglobulins of classes O and M. The damaging effect of the formed antigen-antibody complex is realized through complement activation, the release of lysosomal enzymes.

There is damage to the basal membranes, spasm of smooth muscles of the bronchi, vasodilation, and the permeability of the microvasculature increases.

Type IV (cellular, delayed-type hypersensitivity) is characterized by the fact that sensitized lymphocytes have a damaging effect. In this case, the mediators of the allergic reaction are lymphokines (act on macrophages, epithelial cells), lysosomal enzymes, and an activated kinin system. Under the influence of these substances, the development of edema, swelling of the mucous membrane, bronchospasm, hyperproduction of viscous bronchial secretions occur. The consequence is an acute violation of the patency of the bronchi, manifested by an attack of suffocation.

Non-immunological mechanisms are the primary change in bronchial reactivity as a result of congenital and acquired biological defects. Non-immunological mechanisms act on primary or secondary effector cells or on the receptors of the smooth muscles of the bronchi, blood vessels, cells of the bronchial glands. This changes the reactivity of target cells and, above all, mast cells, which is accompanied by excessive production of biologically active substances (histamine, leukotrienes, etc.). In response to their release, bronchospasm, swelling of the mucous membrane, hyper- and discrinia of the bronchial glands develop. All this dramatically changes the patency of the bronchi and causes an asthma attack.

Bronchial resistance can change conditionally and unconditionally as a reflex. For example, obstruction arising from exposure to cold air, inhalation of irritating gases and dust, and physical activity is caused by bronchospasm through the vagal reflex. The causes of bronchospasm can also be damage to the effector zones of the vagal bronchoconstrictive reflex or blockade of β-adrenergic receptors.

Recently, they talk about a special role in the pathogenesis of violations of bronchial patency of glucocorticoid insufficiency and disovarian disorders. Insufficiency of glucocorticosteroids leads to the development of hyperreactivity of mast cells, a decrease in the synthesis of catecholamines, and activation of prostaglandins F_2a, as well as a violation of the immunocompetent system (here we talk about the complex participation in the pathogenesis of AD and immunological and non-immunological mechanisms).

Hyperestrogenemia and hypoprogesteronemia act on α- and β-adrenergic receptors, increasing the activity of the former and reducing the activity of the latter.

Classification. The predominance of one or another mechanism in the pathogenesis of asthma allows us to identify its various pathogenetic features. Currently, the classification proposed by G. B. Fedoseev (1982) is used.

Stages of AD development.

I - pre-asthma (conditions that threaten development: acute and chronic bronchitis, acute and chronic pneumonia with elements of bronchospasm in combination with vasomotor rhinitis, urticaria).

II - clinically formed BA (considered as such after the first attack or immediately onset of status asthmaticus).

BA forms:

1) immunological;

2) non-immunological.

Pathogenetic mechanisms (clinical and pathogenetic variants) of AD:

1) atopic;

2) infection-dependent;

3) autoimmune;

4) dishormonal;

5) neuropsychic imbalance;

6) adrenergic imbalance;

7) cholinergic imbalance;

8) primary altered bronchial reactivity.

In one patient, a combination of several clinical and pathogenetic variants is possible. In such a situation, it is necessary at the time of the examination to highlight the main variant for this patient, which is important for adequate therapy. In the course of a long course of BA, a change in the pathogenetic mechanism is possible.

Severity of BA:

1) mild course (exacerbations are rare, 2-3 times a year, short-term asthma attacks are stopped by taking various bronchodilator drugs inside);

2) moderate (more frequent exacerbations 3-4 times a year, asthma attacks are more severe and stopped by injections of drugs);

3) severe course (characterized by frequent and prolonged exacerbations, severe attacks, often turning into an asthmatic state).

The division of BA according to the severity of the course is conditional. So, with a mild course of BA, the patient may die from a suddenly developed status asthmaticus.

Phases of the course of BA:

1) exacerbation (the presence of recurrent attacks of asthma or asthmatic condition);

2) subsiding exacerbation (attacks become more rare and mild, physical and functional signs of the disease are less pronounced than in the exacerbation phase);

3) remission (typical manifestations of BA disappear: asthma attacks do not occur; bronchial patency is fully or partially restored).

Complications:

1) pulmonary: emphysema, pulmonary insufficiency, atelectasis, pneumothorax, status asthmaticus, etc.;

2) extrapulmonary: cor pulmonale (compensated and decompensated with the development of right heart failure), myocardial dystrophy, etc.

clinical picture. The most characteristic sign of asthma is complaints of attacks of suffocation (difficulty breathing mainly during exhalation), shortness of breath and cough of various types (from dry, paroxysmal or with the release of viscous sputum). The development of bronchopulmonary infection causes an increase in body temperature. The resulting difficulty in nasal breathing is a manifestation of allergic rhinosinusopathy (vasomotor rhinitis, polyposis), which usually occurs during the pre-asthma phase.

History data helps to establish a connection between the development of seizures and exposure to certain allergens and other factors. Most often it is a respiratory tract infection, especially in an exacerbation of the disease.

From the anamnesis, they learn about the influence of physical effort (such as brisk walking, laughter, etc.), changes in meteorological factors (such as cold, high humidity, etc.), disovarial disorders, professional factors on the occurrence of asthma attacks.

The study of an allergic history contributes to the diagnosis of an atopic variant of BA. In such cases, exacerbations of the disease are seasonal (more often in spring and summer), accompanied by rhinitis, conjunctivitis. Such patients have urticaria, Quincke's edema; food intolerance, a number of medicinal substances are detected; there is a hereditary predisposition to allergic diseases.

History data often allow to establish the presence of the so-called aspirin asthma. In this case, there is no hereditary form of allergic diseases. Such patients are concerned about impaired nasal breathing (polypous growths), and the most characteristic symptom is intolerance to non-steroidal anti-inflammatory drugs (acetylsalicylic acid, indomethacin, etc.), which cause asthmatic attacks. In this case, it is already possible to assume a prostaglandin mechanism of AD.

Data on the development of asthmatic status in the past indicate the severity of the course of the disease and indicate the need for corticosteroid therapy.

Diagnostics. Of great importance is the identification of extrapulmonary manifestations of allergies, signs of broncho-obstruction, complications of asthma, and other diseases accompanied by bronchospasm attacks.

When examining the skin, allergic manifestations can be detected: urticaria, papular erythematous rashes, which indicates an immunological variant of BA. The combination of asthma with eczema, neurodermatitis, psoriasis predisposes to severe asthma.

It is often possible to identify a violation of nasal breathing. Rhinitis and polyps are considered pre-asthma. Sinusitis and other sinusitis can cause choking.

Physical examination of the lungs, often due to underlying chronic bronchitis, may reveal signs of emphysema leading to the development of chronic respiratory failure and cor pulmonale.

Auscultatory signs of bronchial obstruction are detected: a change in breathing (long expiration, dry, mostly wheezing, wheezing), forced expiration, which reveals latent bronchospasm (appearance or increase of dry wheezing).

Auscultation of the lungs must be carried out in the position of the patient lying down: the number of dry rales increases with their "vagal" mechanism. Constantly listened to in a certain area, moist voiced ("crackling") fine bubbling rales may indicate a developed pneumosclerosis.

An objective examination of the patient reveals symptoms of other diseases ("butterfly" on the skin of the face, lymphadenopathy in combination with an increase in the liver and spleen, a persistent increase in blood pressure, persistent fever, etc.), in which attacks of bronchospasm occur, manifested by suffocation (systemic lupus erythematosus, nodular periarteritis). Then the alleged diagnosis of AD becomes unlikely.

Spirography reveals the characteristic signs of obstructive bronchial obstruction: a decrease in forced expiratory volume in the first second (FEV1), a decrease in the Tiffno coefficient (FEV₁ to VC as a percentage) and the percentage of FEV₁ to FZhEL. During exacerbation of BA, the residual lung volume (RLV) and functional residual capacity (FOC) exceed the initial level by 100% or more. When analyzing the spirogram, signs of tracheobronchial dyskinesia are found, contributing to the violation of bronchial patency, by the presence of a notch in the upper part of the descending color of the spirogram (Kolbet-Wyss symptom). Pneumotachometry shows the predominance of inspiratory power over expiratory power, which is characteristic of bronchial obstruction. According to pneumotachography with the construction of the "flow - volume" curve, a violation of bronchial patency is diagnosed separately at the level of large, medium and small bronchi.

The appearance of increased bronchial resistance, recorded using spirography, pneumotachometry and pneumotachography, in response to physical activity, inhalation of cold air, irritating gases and acetylcholine indicates an altered bronchial reactivity.

Allergological testing is carried out using a set of various non-infectious and infectious allergens, it is carried out only outside the exacerbation of the disease. To assess the provoking effect of the allergen, skin allergic tests are performed (application, scarification and intradermal methods of applying the allergen), the allergen can be applied to the conjunctiva of the eye, the nasal mucosa. The most reliable is the specific diagnosis of asthma - the identification of specific bronchial hyperreactivity with the help of inhalation provocative tests. However, one should not lose sight of the fact that this route of administration can provoke a severe attack of asthma or the development of status asthmaticus.

For the specific diagnosis of AD, for example, when it is impossible to conduct an allergological test, a radioimmunosorbent test is also used, which makes it possible to quantify IgE antibodies. Laboratory studies help confirm the proposed diagnosis, evaluate the evolution of the disease and the effectiveness of the treatment.

The main diagnostic criterion for AD is the appearance of eosinophils in the sputum, but this is a non-specific sign, it can serve as a manifestation of a general allergic reaction of the body. Also of diagnostic importance is the detection of Kurshman spirals and Charcot-Leiden crystals in sputum.

Laboratory studies prove the presence of an active inflammatory process and the degree of its severity in terms of an increase in acute phase indicators. With an increase in respiratory failure in case of exacerbation of asthma and status asthmaticus, it is important to study the acid-base state and blood gas composition. X-ray examination diagnoses foci of infection (in the paranasal sinuses, teeth, gallbladder) and the presence of acute (pneumonia) or exacerbation of a chronic inflammatory process in the lungs, emphysema and pneumosclerosis. ECG data prove signs of the development of compensated cor pulmonale - hypertrophy of the right heart.

Differential diagnostics. BA is differentiated from cardiac asthma (see Table 8).

Table 8

Differential diagnosis of AD

It is also necessary to differentiate infectious-allergic and atopic asthma (see Table 9).

Table 9

Infectious-allergic and atopic asthma

Treatment. In the treatment of asthma, a stepwise approach is recommended, which is explained by the variable severity of its course in different people and in the same patient. Stage 1 is the least severe asthma, stage 4 is the greatest.

Step 1: A mild intermittent course in which asthma symptoms appear on exposure to a trigger (eg, pollen or animal hair) or due to exercise. Long-term use of anti-inflammatory drugs in the treatment of such patients is not indicated. Treatment consists of prophylactic medication if necessary (inhaled β₂agonists, cromoglycate, nedocromil, or anticholinergics). Occasionally, more severe and prolonged exacerbations require a short course of oral corticosteroids. If asthma manifests itself with more frequent symptoms, an increase in the need for bronchodilators, then it becomes necessary to move to the next stage.

Stage 2. Slight persistent course. Primary therapy includes anti-inflammatory drugs, inhaled corticosteroids, sodium cromoglycate, or nedocromil sodium. The dosage of corticosteroids is 200-500 micrograms of beclomethasone dipropionate or budesonide per day. For symptomatic treatment, inhaled β₂-agonists, but not more than 3-4 times a day. For more severe and prolonged exacerbations, a short course of oral corticosteroids is given. If symptoms persist despite an initial dose of inhaled corticosteroids, the dose of beclomethasone dipropionate should be increased to 750-800 micrograms per day. However, an alternative to increasing the dose of inhaled hormones, especially to control nocturnal attacks of asthma, is the addition of long-acting bronchodilators taken at night (at a dose of inhaled corticosteroids of at least 500 mcg).

Stage 3 is characterized by moderate severity of BA. Such patients require daily intake of prophylactic anti-inflammatory drugs. The dose of inhaled corticosteroids is 800-2000 mcg in combination with long-acting bronchodilators. You can use long-acting theophyllines (with constant monitoring of their concentration no more than 5-15 µg / ml), oral and inhaled β₂long-acting agonists. Symptomatically appoint β₂-short-acting agonists or alternative drugs (stage 2).

Stage 4. Severe asthma, when it is not completely controlled. In this case, the goal of treatment is to achieve the best possible results. Primary treatment involves high-dose inhaled corticosteroids (between 800 and 2000 micrograms per day of beclomethasone dipropionate) in combination with long-acting bronchodilators. If necessary, inhaled β is indicated to relieve symptoms.₂-short-acting agonists (not more than 3-4 times a day). A more severe exacerbation may require a course of treatment with oral corticosteroids, which are prescribed in minimal doses or every other day. To prevent the development of side effects, high doses of inhaled corticosteroids are administered through a spacer.

Step 5 involves reducing supportive medication. This is possible if the asthma remains under control for at least 3 months, which helps to reduce the risk of side effects and increases the patient's susceptibility to the planned treatment. "Reduction" of treatment is carried out under the constant control of symptoms, clinical manifestations and indicators of respiratory functions by gradually reducing (cancelling) the last dose or additional drugs.

Stopping attacks. A mild attack can be treated at home with short-acting bronchodilators. Treatment is carried out until the symptoms disappear completely. Moderate and severe attacks require not only adequate doses of short-acting bronchodilators (inhaled β₂-short-acting agonists), but also the appointment of systemic corticosteroids. If the patient has hypoxemia, oxygen should be administered.

For the treatment of asthma attacks in a medical center or hospital, high doses of inhaled β₂agonists through a nebulizer. The use of a metered-dose aerosol inhaler through a spacer is very effective. Preferably, corticosteroids are administered orally, not intravenously. When using theophylline or aminophylline in combination with high doses of β₂-agonists additional bronchodilating effect is not provided, but the risk of side effects increases.

Theophyllines can only be used in the absence of β₂-agonists, however, they can be administered intravenously at the rate of 6 mg/kg aminophylline (or 5 mg/kg theophylline) with a constant dose of 0,5-1,0 mg/kg per hour for 24 hours. Alternatively, β₂Short-acting agonists can also use epinephrine, but significant side effects are possible with its use. Inhaled mucolytic drugs, sedatives and antihistamines, magnesium sulfate, chest physiotherapy, hydration with large volumes of fluids for adults and older children are not recommended for the treatment of asthma attacks to avoid increased coughing.

Prevention. Primary prevention of asthma includes treatment of patients in a state of pre-asthma, identification of biological defects in practically healthy individuals with a family history that pose a threat to the occurrence of asthma, elimination of potentially dangerous allergens, irritants and other factors from the environment of patients that can lead to the development of the disease.

In the treatment of patients in a state of preasthma, it is necessary to sanitize the foci of infection, treat allergic rhinosinusopathy, apply various methods of non-drug treatment, including acupuncture and psychotherapy, exercise therapy, barotherapy, and spa treatment. Carrying out specific and nonspecific hyposensitization is shown.

Author: Mostovaya O.S.

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