Asthmatics undergo deep morphological changes in the bronchi – remodeling (increase in smooth muscle mass and secretion of viscous sputum, thickening of BM, bronchospasm), which largely determines the severity of bronchial asthma. So, in the case of death of a patient from asthmatic status (AS), five characteristic structural changes are found that are unevenly distributed across the bronchial tree. 1. Pathology of mucociliary clearance: in preterminal and terminal bronchioles, there are primarily plugs of viscous sputum (a mixture of mucus, serum protein, inflammatory cells and fragments containing eosinophils, lymphocytes, many desquamated epithelial cells, Kurshman spirals and Charcot – Leiden crystals), which significantly reduce or clogging the lumen of the bronchi with the possible subsequent development of the “silent lung” syndrome (up to asphyxiation) and atelectasis. 2. An increase in the size and number of mucous glands (goblet cells) with subsequent excessive secretion of mucus (the development of hyper-, dyskrinia). The restructuring of the epithelium of the respiratory tract is formed. 3. Thickening and irregularity, “coarsening” of BM, subendothelial fibrosis (due to the deposition of collagen), which thickens the wall of the bronchi. In addition, a fibrotic process in the wall of the bronchi is noted. Subepithelial fibrosis is not associated with the severity of bronchial asthma and the duration of treatment. These changes arise due to the action of eosinophil proteins and increased metaplasia of epithelial cells along the entire bronchial tree (they persist even after treatment). “Passages” are visible in the basal membrane, which increases the access of mediators to the intraepithelial nerves with the mediated development of edema, increased secretion of mucus and bronchospasm (all that characterizes an asthma attack). In patients with asthma, thickening of the reticular layer of the basement membrane and loss of superficial epithelium are key signs (in COPD there is no such thickening of the basement membrane). Unlike COPD, with bronchial asthma (if the patient does not smoke), there is no loss of alveolar attachment to the small airways. The morphological criterion for the severity of bronchial asthma is the thickness of the basement membrane: the thicker it is, the greater the severity and duration of the disease. It is believed that severe corticosteroids-dependent AD can be resistant to therapy due to the fact that the airways become more fibrous or remodeled to a greater extent than with mild AD. 4. Variable inflammatory infiltrate (intense inflammation, vasodilation of the microvasculature and mucosal edema, formed as a result of increased permeability, the number of vessels in the bronchial wall and their infiltration by different inflammatory cells) from activated mononuclear cells, eosinophils and T-lymphocytes (DM + 4) tissue in patients with atopic and endogenous form of bronchial asthma. This internal edema of the wall of the respiratory tract significantly narrows their lumen. The integrity of the epithelial lining is violated, followed by sweating of the plasma proteins, which makes it difficult to remove secretions from the small airways. Tissue eosinophilia (unevenly distributed along the large and small bronchi) can determine the functional consequences and decrease after treatment with corticosteroids. 5. Hypertrophy of the smooth muscles of bronchioles (their area increases longer than a 2 times) due to the influence of inflammatory mediators, which most correlates with the severity of bronchial asthma. Large muscle mass exerts pressure on the lumen of the small bronchi – the same degree of shortening of the muscles with their larger mass can cause a more pronounced narrowing of the bronchi than normal. Anti-asthmatic drugs beta-2-AG, theophyllines, corticosteroids) do not affect the process of hypertrophy of the smooth muscles of the bronchi. Often, patients with severe bronchial asthma develop fatigue of the respiratory muscles due to the appearance of degenerative processes in them – myopathic syndrome.