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Internal illnesses. Bronchial asthma (lecture notes)

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LECTURE No. 29. Bronchial asthma

Bronchial asthma is a chronic inflammatory disease of the airways in which many cells and cellular elements play a role. Chronic inflammation causes a concomitant increase in airway hyperresponsiveness, leading to recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing, especially at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible, either spontaneously or with treatment.

A similar definition of asthma is presented in the 1995 GINA Working Group report (USA), revised in 2002; GINA - Global Initiative for Asthma, a global strategy for the treatment and prevention of asthma.

Etiology. The causes that cause the development of the disease are divided into internal factors (innate characteristics of the body) and external factors (modify the likelihood of developing the disease in predisposed people).

Pathogenesis. A specific inflammatory process is formed in the bronchial wall in response to damaging risk factors (activated eosinophils, mast cells, macrophages, T-lymphocytes), bronchial obstruction develops, bronchial hyperreactivity increases. An increased predisposition of the bronchi to constriction in response to various triggers is formed, signs of the disease persist in the asymptomatic period. Persistent structural and functional changes are formed, accompanied by remodeling of the airways.

Airway obstruction has 4 forms: acute bronchoconstriction (due to spasm of smooth muscles), subacute (due to swelling of the mucous membrane of the respiratory tract), obstructive (due to the formation of mucous plugs), sclerotic (sclerosis of the bronchial wall with a long and severe course of the disease) (Table 4 ).

Classification. Asthma can be of the following types: with a predominance of an allergic component, non-allergic, mixed.

When making a diagnosis, the etiology, severity of the course, and complications are taken into account.

Clinic. Period of harbingers characterized by a runny nose, sneezing, lacrimation, a feeling of sore throat, paroxysmal cough appears.

В expanded period patients take a forced position (orthopnea), expiratory dyspnea appears, distant dry rales, deep rare breathing, diffuse cyanosis, swelling of the cervical veins, auxiliary muscles participate in the act of breathing, there is an expansion of the intercostal spaces. Percussion is determined by hard breathing, a lot of dry wheezing. Increasing tachycardia.

В permission period there is a cough with hard-to-separate vitreous viscous sputum, distant wheezing disappears. Percussion is determined by the reduction of the box sound. Auscultatory - reduction of dry wheezing.

Additional instrumental study. A general blood test is performed, where leukocytosis, eosinophilia, and an increase in ESR are detected. Allergic status (presence of IgE) is determined, skin tests with allergens are performed. Sputum is examined (macroscopically - viscous, transparent; microscopically - eosinophils, Charcot-Leiden crystals and Kurshman spirals, neutrophils). A functional study of the lungs is carried out (a study of OVF1, FZhEL, PSV), samples with bronchodilators are put (a study of airway hyperreactivity). A non-invasive measurement of airway inflammation markers is carried out (sputum examination for the presence of eosinophils or metachromatic cells after inhalation of hypertonic saline or spontaneously isolated). ECG: overload of the right ventricle.

Complications. Complications of the disease are status asthmaticus (a complication of severe bronchial asthma), pulmonary and pulmonary heart failure, chronic cor pulmonale.

Differential diagnostics. Should be carried out with chronic bronchitis, cardiac asthma, tumors of the trachea, larynx, foreign bodies, cystic fibrosis, bronchiectasis.

Flow. The course of the disease is often progressive, periods of exacerbations and remissions.

Treatment. The goals of management of patients with bronchial asthma are as follows: to achieve and maintain control over the symptoms of the disease, to prevent exacerbation of the disease, to maintain lung function as close to normal as possible, to maintain a normal level of activity, including physical activity, to eliminate the side effects of anti-asthmatic drugs, to prevent the development of irreversible bronchial obstruction, prevention of asthma-related mortality.

Basic principles of management of patients with bronchial asthma: education of patients to form partnerships in the course of their management, assessment and monitoring of the severity of bronchial asthma both by recording symptoms and, if possible, measuring lung function, eliminating exposure to risk factors, developing individual drug therapy plans for long-term management of children and adults, development of individual plans for the relief of exacerbations, ensuring regular follow-up.

Prevention of an asthma attack includes:

1) teaching the patient proper breathing and self-control when feeling worse is the most important factor in managing the patient;

2) elimination of exposure to risk factors.

Treatment is selected based on the severity of the course, the availability of anti-asthma drugs, the individual living conditions of the patient to ensure minimal severity of chronic symptoms, including nocturnal symptoms.

Inhaled glucocorticoids: Becotid, Beclocort, Pulmicort, Ingocort, Becladjet. The route of administration is inhalation.

Systemic glucocorticoids: prednisone, prednisolone, methylprednisolone. They have a minimal mineralocorticoid effect, a relatively short half-life, and a mildly pronounced effect on striated muscles. The route of administration is oral or parenteral.

Cromons: sodium cromoglycate (intal), nedocromil sodium (Tyled).

Stabilize the membrane of mast cells and suppress the mediated release of IgE from them. They are prescribed by inhalation, mainly with mild persistent bronchial asthma.

Methylxanthines: theophylline, eufillin, aminophylline, teodur, teopek, teoteolek, teotard, retophil. They inhibit the activity of phosphodiesterase, are used to control the course of bronchial asthma. The route of administration is oral.

Table 4. Sequence and volume of bronchodilator therapy

After achieving stabilization of bronchial asthma and maintaining it for 3 months, a gradual decrease in maintenance therapy is possible.

Inhaled β2long-acting agonists: formoterol, salmeterol. The duration of action is more than 12 hours. They relax the smooth muscles of the bronchi, increase mucociliary clearance, reduce vascular permeability, and may reduce the release of mediators from mast cells and basophils.

Inhaled β2 - short acting agonists: fenoterol, pirbuterol, prokaterol, salbutamol, terbutaline, berotek, asthmapent. The duration of action is from 4 to 6 hours. The route of administration is inhalation.

Oral β2 - short acting agonists: salbutamol, terbutaline, bambuterol (converts to terbutaline in the body). Relax the smooth muscles of the bronchi, increase mucociliary clearance, reduce vascular permeability, modulate the release of mediators of mast cells and basophils.

Antileukotriene drugs: montelukast, pranlukast, zafirlukast are cysteinyl-leukotriene receptor antagonists, zileuton is a 5-lipoxygenase inhibitor. The 5-lipoxygenase inhibitor inhibits the synthesis of all leukotrienes, cysteinyl leukotriene receptor antagonists block the cisLT1 receptors of the smooth muscles of the bronchi and other cells, inhibit the effects of cysteinyl leukotrienes, which are released from mast cells and eosinophils. The route of administration is oral.

Second generation antihistamines: (n1 blockers): (acrivastine, astemizole, acelastine, cetirizine, ebastine, fexofenadine, ketotifen, loratadine, mizolastine, terfenadine). Suppress the development of allergic reactions. The route of administration is oral.

Other oral antiallergic drugs: tranilastin, repyrinast, tazanolast, pemirolast, tanned, celatrodast, amlexanox, ibudilast. They suppress the activity of mast cells, influence the synthesis of mediators of inflammation and allergies, act as antagonists of mediators.

Systemic nonsteroidal therapy: troleandomycin, methotrexate, cyclosporine, gold preparations. Include immunomodulators for unwanted effects of glucocorticoids to reduce the need for oral glucocorticoids. They are prescribed only under the supervision of a pulmonologist. The route of administration is oral.

Allergen specific immunotherapy: allergen extracts. The route of administration is subcutaneous, the possibility of sublingual use is being studied.

To quickly eliminate bronchospasm and its symptoms, inhaled β2-fast-acting agonists (salbutamol, terbutaline, fenoterol, pirbuterol), systemic glucocorticoids, anticholinergics - intratropium bromide - atrovent, oxitropium bromide - troventrol (block the effect of acetylcholine, inhalation route of administration), methylxanthines (short-acting theophylline), oral β2 short-acting agonists.

With mild suffocation shows inhalation of short-acting β2-agonists (berotek or salbutamol) up to 6 times within an hour, inhalation of anticholinergics (atrovent, troventol) simultaneously or independently, taking methylxanthines (eufillin in tablets) simultaneously or independently.

Relief of moderate suffocation is carried out as a therapy for a mild asthma attack with the addition (optional): aminofillin 2,4% - 10,0 ml intravenously by stream, ephedrine 5% - 0,5 ml subcutaneously, alupent 1 ml intravenously by stream. Corticosteroids are used orally or by infusion (in the absence of effect). If there is no effect, stop the introduction of β2-agonists.

Forecast. In severe cases - disability.

Prevention. Primary prevention measures include: control of persons with a hereditary predisposition to bronchial asthma, sanitation of foci of infection, smoking cessation, reducing the impact of asthma triggers and reducing the need for drug therapy. Secondary prevention measures include dispensary observation, specific desensitization, anti-relapse treatment, systematic use of bronchodilators, and spa treatment.

Author: Myshkina A.A.

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