Endogenous bronchial asthma (idiopathic) usually develops in adulthood and includes all other types of the disease (triggers – non-immune and non-obvious). With this form, there is no family history of atopic diseases (there is no rhinitis, conjunctivitis), the level of eosinophils in the blood and sputum is increased, seizures occur under the influence of internal stimuli (more often – tolerated pneumonia, CB or SARS); not known allergen; there is hypersensitivity to bacteria or their products; no other allergic symptoms; IgE level is normal. Usually, this AD occurs after 30–40 years (more often in individuals already having chronic inflammatory changes in the respiratory tract and prolonged contact with irritants), beta-2-AH is poorly treated, therefore, administration of GCS is required. Hyposensitization is ineffective (since the allergen is not determined), there is no tendency to “mitigate” the course of the disease, but, on the contrary, its steady progression is characteristic due to the development of mixed airway obstruction (asthmatic form of COPD) and the frequent development of AS. Aspirin bronchial asthma occurs in 7% of cases. Aspirin can sometimes cause a fatal attack of bronchial asthma within a few minutes after taking it. The basis of this AD is a violation of the metabolism of arachidonic acid: aspirin blocks the production of cyclooxygenase and the metabolism follows the lipoxygenase pathway (the production of bronchodilator prostaglandin E decreases and the production of bronchoconstrictors (prostaglandin F2a, leukotrienes, a slow-reacting substance of anaphylaxis is slow): intolerance to aspirin (NSAIDs, or vegetable saliylates) – recurrent polypous rhinosinusopathy – asthma attacks. and FN (8%) is more often observed in young people with asthma, which is based on excess moisture loss from the respiratory tract during fast breathing, which causes them to cool, release mediators and bronchospasm with the following symptoms – chest pain, sighting with coughing or without it, shortness of breath.The asthma attack usually occurs 15-20 minutes after the FN (more often running, cycling) on ​​the background of inhaling cold air. Sometimes the attack appears or intensifies after the cessation of FN. Warming of inhaled air can reduce clinical manifestations. This phenomenon is well known to asthmatics who wrap a scarf around their faces while moving in cold air. Common complications of bronchial asthma: • respiratory: AS, EL, ODN (CDI is very rare in bronchial asthma), pneumonia, spontaneous pneumothorax (with the appearance of emphysema under the skin or in the mediastinum) at the height of the attack (often due to medical procedures – using intermittent positive pressure and bronchial lavage), atelectasis or collapse of the lungs (due to mucous plugs), which are often difficult to detect radiologically; • cardiac (often due to the use of large, toxic doses of theophylline and beta2-AG): a drop in blood pressure, cardiac arrest, MI, arrhythmias, myocardial dystrophy, acute pulmonary heart (rarely chronic); • gastrointestinal (often caused by oral corticosteroids): peptic ulcer, bleeding, ulcer perforation; • metabolic: hypokalemia (due to taking GCS and beta-2-AH) and metabolic acidosis; • hypoxic brain damage (“respiratory encephalopathy”). Bronchial asthma is usually not a fatal disease, but its lethality is more likely due to non-stopping AS (the development of asphyxia due to severe obstruction of the small bronchi by viscous sputum) or sudden death (due to fatal cardiac arrhythmia – ventricular fibrillation) caused by the paradoxical interaction of excess beta-2 AH with its own adrenal asthmatic system under stress, which is accompanied by a large release of endogenous catecholamines. Phases of bronchial asthma: exacerbation, remission (stable, unstable). BA exacerbation criteria(based on the clinical picture and peak flow metrics): obvious insufficiency of the previous basic therapy (decreased sensitivity to I (32-AH and increased need for them by more than 4 inhalations in the previous 24 hours compared with the usual dosage), the appearance and increase of bronchial obstruction – decrease in FEV, or peak expiratory flow rate (PSV), according to the peak flow meter, more than 25% of the individual norm, measured in the morning, for more than 3 days and out of asthma attacks; impaired bronchial drainage function (worse failure sputum can be exacerbated) An exacerbation can occur in the form of: • an acute attack (expiratory dyspnea, wheezing, spastic cough or a combination of these symptoms against a background of a marked decrease in FEV); • protracted state of bronchial obstruction – prolonged (days, weeks) difficult breathing with clinically pronounced obstruction of the bronchi (the severity of dyspnea of ​​FN and difficulty in breathing depends on it in many respects), against the background of which regular asthma attacks of varying severity may appear.