The main endogenous etiological factors of bronchial asthma are as follows. 1. Hereditary predisposition (allergic heredity according to a family history) is a factor in the development of AD. So, if one of the parents is ill with AD, then the child has a 25% chance of getting sick, if both are ill, then – 70% (moreover, AD is prevalent in children in the first generation). Transmission of atopy – rhinitis, severe eczema (in 20% and 80% of children later develop AD), conjunctivitis or AD by inheritance occurs along an autosomal dominant pathway, possibly through many genes. Conversely, half of asthma patients later develop rhinitis. Bronchial asthma and nasal pathology (allergic rhinitis) coexist due to the pathophysiological connection of the upper and lower respiratory tract. A certain role in the formation of AD is played by the age of the parents (over 40 years), prematurity and artificial feeding of the child. Hypersensitivity of the skin is also a factor in the development of airway hyperresponsiveness, even in the absence of symptoms of bronchial asthma. However, a third of healthy individuals (without signs of allergies) have positive skin tests and elevated levels of IgE. 2. Genetic factors – the system of HLA antigens, damage to the sympathetic nervous system (decreased mucociliary clearance and tone of beta2-adrenergic receptors against the background of increased tone of the parasympathetic system). In general, bronchial asthma is a multi-genetic disease. 3. Congenital biological defects (may be genetic or may form during pregnancy and childbirth): bronchopulmonary dysplasia, nasal and sinus pathology, lack of IgA, M- and T-suppressors or the inferiority of their function; congenital hypersensitivity of smooth muscles to biologically active substances; changes in enzyme systems involved in the formation of cyclic nucleotides; hypersensitivity of the bronchi and membrane permeability. Airway hyperreactivity is the main biological defect that determines the formation of bronchial asthma. Biological defects, compensated before the onset of clinical manifestations of the disease, after their occurrence become mechanisms of AD pathogenesis. The mechanism of development of bronchial asthma. The main aspects of the pathogenesis of bronchial asthma are chronic inflammation of the airways, reversibility of obstruction, hyperresponsiveness of the bronchi, vagal reflex and immune reactions (mechanisms of allergy, inflammation and T-cell immunity). Although many agents can cause an attack, the nature of an individual attack is not very dependent on the incentive. Triggers can be different, and the resulting bronchial response can be standard. An attack of bronchial asthma cannot be considered only as a bronchospasm (spasm of smooth muscles). The primary, fundamental link in pathogenesis is a special form of chronic, serous-desquamative persistent inflammation in the bronchi (eosinophilic CB, not directly associated with the infectious process). Inflammation of the bronchi arises as a natural defense against environmental antigens (foreign proteins, dust, bacteria) or an endogenous environment. The response to them causes clinical symptoms. Chronic inflammation leads to permanent damage to normal epithelial tissue, leading to chronic bronchial obstruction over the years. Damaged tissue secrets mediators, which attract even more inflammatory cells, causing swelling of the walls of the respiratory tract, increased secretion of sputum and blockage of small bronchi, bronchioles and erosion of epithelial membranes (stimulating irritation of nerve receptors in the submucosa). All this makes bronchial tissue more sensitive to agents that provoke bronchospasm due to bronchial hyperreactivity. The immune system also becomes more sensitive to mediators. The interaction of inflammatory cells, mediators of cells and tissues of the bronchi in a complex way leads to bronchial hyperreactivity and the formation of 4 typesobstruction (acute, subacute, chronic and irreversible). So, the acute type of obstruction is caused by spasm of smooth muscles, subacute – by swelling of the bronchial mucosa; obstructive (chronic) – blockage of small bronchi by viscous sputum Irreversible obstruction occurs due to the development of sclerotic processes in the bronchial wall (remodeling) against the background of a long and severe course of AD and inadequate treatment.