Dyshormonal disorders leading to the development of bronchial asthma. – Bronchial asthma due to glucocorticoid insufficiency. Relative glucocorticoid insufficiency is manifested by symptoms of hypocorticism, while the cortisol content usually corresponds to normal values. In this case, it is necessary to check the tissue sensitivity to glucocorticoids. In the presence of tissue glucocorticoid resistance of tissues, a very persistent variant of AD develops in the clinical course, leading to the need for glucocorticoid drugs in very large doses. – Dysovarial bronchial asthma is characterized by an exacerbation that occurs 2-3 days before the onset of menstruation. This is due to a defect in the synthesis of bronchodilating progesterone and an excess of estrogen. It is manifested by an increase in rectal temperature by more than 1 ° C. – Bronchial asthma with severe adrenergic imbalance is characterized by increased activity of a-adrenergic receptors. In this case, even a normal amount of adrenaline can cause a pathological bronchospastic reaction. Often such a reaction occurs with an overdose of adrenergic agonists (when more than 5 inhalations of 2 inhalations are carried out during the day). • The cholinergic variant of bronchial asthma is associated with constitutional features or diseases of the internal organs, accompanied by severe vagotonia. This option is found in 1% of AD patients who produce a lot of sputum (1 / 2-1 cup per day). A history of ulcer disease, bradycardia, arterial hypotension, and palm hyperhidrosis are usually noted. You can stop an asthma attack with atropine. • Nerve mechanisms of bronchial asthma. – The conditioned-reflex mechanism may be leading in some patients (a classic example – artificial paper rose provokes an attack of asthma with its appearance). Perhaps conditioned reflex cessation of asthma attack. It was noted that odor intolerance in AD patients by 70% is not allergic, but a conditioned reflex. Such patients can be treated by suggestion. – The dominant mechanism boils down to the fact that minor irritations can lead to the summation of excitement and the occurrence of an asthma attack. The emergence of another, stronger dominant may for some time suppress the dominant BA. It was also noted that with an increase in body temperature above 38 ° C, asthma attacks do not occur. – The vagal mechanism is manifested, as a rule, in that asthma attacks occur in the second half of the night. This is due to a shortage of mediators of the non-adrenergic system, in particular VIL (having a powerful bronchodilating effect). • The mechanism due to the inadequate adaptation of the body to the microsocial environment can also underlie the development of AD. According to this mechanism, asthma occurs in 10-20% of patients (more often in children, less often in adults). • Obstructive changes in the bronchi with asthma can also be explained by the influence of pro-inflammatory mediators (tissue hormones), which are intensely released by mast cells in the walls of the respiratory tract. A special place among them is occupied by histamine, which causes spasm of smooth muscles, the development of arterial hyperemia, increased permeability of the walls of capillaries, increased secretion of mucus. In recent years, in the pathogenesis of AD, great importance has been attached to an increase in the formation of prostaglandin PGF2a and a decrease in the synthesis of PGE2.