Pathophysiology of bronchial asthma: • decreased airway clearance due to smooth muscle spasm, edema and inflammatory cell infiltration of the bronchial mucosa, viscous secretion accumulation; • increased lung airiness (and residual volume); • ventilation and perfusion disorders (due to a prolonged increase in resistance to air flow or a decrease in the resulting pressure), leading to varying degrees of hypoxemia and an increase in PH. In a simplified form, the pathogenesis of bronchial asthma can be represented as a combination of two fundamental mechanisms: chronic inflammation of the respiratory tract and bronchial hyperreactivity. Due to the initiation by various mechanisms, chronic inflammation of the respiratory tract occurs (edema, vasodilation, cell infiltration, an increase in the mucous glands and muscle mass of the bronchi) and inflammatory mediators begin to be released. The regular nature of the development of inflammation in bronchial asthma is largely due to inflammatory mediators. They are released from primary (mast, epithelial, macrophages) and secondary (eosinophils, neutrophils, macrophages, platelets) inflammatory cells that migrate into the lumen of the respiratory tract. Inflammatory mediators are released not only from inflammatory cells, but also from structural cells of the respiratory tract (epithelium and endothelium, fibroblasts, smooth muscle cells of the bronchi) that change their phenotype (they become mediator-producing cells). The impact of mediators leads to toxic effects on surrounding tissues (with their local damage), the development of spasm of smooth muscles, increased permeability of the epithelium, edema and hyperdiscrinia. Mediators can act directly on the smooth muscles of the bronchi or indirectly, due to stimulation of afferent nerves in the airways. Thus, inflammatory cells and their mediators located in the allergen area form an inflammatory reaction in the bronchial wall. The eosinophilic type of inflammation with growth is dominant in bronchial asthma. the level of IL-4,5 (with atonic BA) and IL-2 (with endogenous BA). BA is a disease of large, medium and small bronchi, localized after the 7-8th generation of the bronchial tree, which make up about 80% of the pulmonary surface. Peripheral airways are the most important component of hyperreactivity. Morphological data show that with AD, the existing severe inflammation of small bronchi (with a diameter of less than 2 mm) to a greater extent than large ones is the main manifestation of the pathogenesis of the disease. A lesser degree of destruction and necrosis of the bronchial wall in bronchial asthma is a pathomorphological feature of “eosinophilic” inflammation, in contrast to COPD (where “neutrophilic” inflammation with the formation of a purulent focus is dominant). The latter type of inflammation can also occur in patients with asthma, but in the case of a long, long-term course of the disease, with the addition of a bacterial infection (exacerbation of COPD against the background of existing endogenous bronchial asthma). Airway inflammation is a complex process that begins with damage to the epithelium, impaired mucociliary clearance and subsequent interaction of primary, secondary effector cells and their mediators. The inflammatory process captures all layers of the bronchial wall: the epithelium, the basement membrane, blood vessels and smooth muscles. Chronic airway inflammation contributes to structural changes in the bronchial wall and contractility of smooth muscle cells (which affects the response to acute irritants). So, many non-specific stimuli (smoke, sulfur dioxide, dust, cold air) provoke reflex bronchospasm in asthmatics. In them, the response of the bronchial tree develops with a lower level of stimulation. But the intensity of this response is more pronounced compared with healthy individuals (bronchi are reduced easily and too much). Airway hyperreactivity is associated with the development of a late asthmatic response (when exposed to various exo-, endogenous stimuli causing bronchospasm: cold air, sulfurdioxide, FN, tests with acetylcholine or histamine) and reflects the increased response of the bronchial tree. The caliber of the bronchial tree changes throughout the day and on various days with the onset of symptoms. The underlying mechanisms of airway hyperreactivity are an imbalance in the autonomic (autonomous) nervous system – an increase in activity: the cholinergic nervous system and alpha-adrenergic receptors (which allows them to dominate, leading to bronchoconstriction) against the background of a decrease in the activity of adrenergic bronchodilator systems. The latter is due to a decrease in the activity of adrenergic receptors, their number or “poor” regulation of their function (after exposure to high-dose air irritants or a viral infection) against the background of unchanged cholinergic receptor activity, which leads to beta-adrenoreceptor blockade. In patients with long-term bronchial asthma, over time, an excess of sputum in the airways accumulates, which reduces the total cross-section of the bronchi and enhances their response to external stimuli (even in the absence of smooth muscle hypertrophy of the respiratory tract), leading to spasm of smooth muscles, affecting the volume and composition of sputum . Mediators released from cells of secondary inflammation entering the respiratory tract (under the influence of risk factors) lead to the same consequences, but over a longer period (delayed asthmatic reaction).