Bronchial asthma is a chronic nonspecific recurrent polyetiological lung disease, which is formed with the participation of immunological and non-immunological mechanisms, characterized by pronounced airway hyperresponsiveness to specific and nonspecific stimuli and the presence of the main clinical sign – expiratory asthma attacks with reversible bronchial obstruction due to smooth muscle spasm, swelling of the mucous membrane, mucosal edema, hypersecretion of the bronchial glands.
Classification of bronchial asthma
In the former USSR, the classification of A. D. Ado and P. KBulatov (1969) was adopted, according to which there are two forms of bronchial asthma – atonic bronchial asthma (i.e., non-infectious allergic) and infectious allergic bronchial asthma. As an independent form, pre-asthma is identified that precedes the development of bronchial asthma. Based on this classification, the diagnosis must indicate the form of asthma, its stage, phase and severity of the course, complications, the presence of foci of infection, their nature, localization and degree of activity of the inflammatory process.
The classification of Rakeman (1918) is most widespread abroad, according to which bronchial asthma has two forms: exogenous (occurring from the outside) and endogenous (due to internal factors, cryptogenic). The first group includes bronchial asthma caused by non-infectious allergens (exoallergens), and the second group includes bronchial asthma due to a chronic infectious process in the airways. Allergic pathogenesis of endogenous bronchial asthma is not recognized by foreign researchers . Occupational bronchial asthma is classified separately. Classification issues continue to be developed. Currently, bronchial asthma is considered as a heterogeneous disease, represented by various clinical and pathogenetic options. Based on the classification of A.D. Ado and P.K. Bulatov, domestic clinicians (G. B. Fedoseev) identified seven variants of bronchial asthma: primary – infectious-allergic, atopic, primary altered reactivity of the bronchi and asthma of bronchial clinical pathogenetic variants secondary: autoimmune (immunopathological), neuropsychic, dishormonal, adrenergic. In the process of the disease, mixed (infectious and non-infectious) allergies can develop, autoimmune processes, changes in the nervous and endocrine systems, which can play a leading role at the beginning of the examination and treatment of the patient, can join. In foreign literature, there is also a tendency to detail immune and non-immunological forms of bronchial asthma. Immunological forms include: atopic asthma with previous allergic rhinitis and eczema caused by cytophilic antibodies related to immunoglobulin E and immunolobulin G; cytotoxic, or autoimmune, bronchial asthma caused by antibodies against adrenergic B receptors; bronchial asthma due to immune complexes and delayed hypersensitivity with previous repeated infections. Non-immunological forms include psychogenic bronchial asthma (pure and combined with immunological); bronchial asthma due to physical stress; bronchial asthma caused by acetylsalicylic acid and anti-inflammatory drugs (pure and combined with immunological forms), some medications with f-blockers), viral infection of the respiratory tract, exogenous irritating factors; bronchial asthma with a pre-asthmatic aura (dysrhythmia on an electroencephalogram); premenstrual bronchial asthma. Of these variants of bronchial asthma, the following are most recognized and studied: atopic – Extrinsik; non-atopic – Intrinsik (endogenous); “Aspirin” – an asthmatic triad; asthma induced by physical voltage. Foreign researchers, along with exogenous atopic bronchial asthma, identify exogenous non-atopic bronchial asthma associated with certain substances with which the patient often comes into contact at work (prolonged contact with a large amount of antigen). Samples for standard antigens are negative; for specific antigens, a late or double reaction develops. Antibodies related to immunoglobulin E and immunoglobulin G are detected. The release mechanism of mediators may be non-immunological due to various stimuli: infection, physical. tension, emotions, factors of circadian rhythms.
Etiology of bronchial asthma
Atopic bronchial asthma is caused by non-infectious allergens. The most common cause is house dust, the main allergenic component of which is ticks Dermatophagoides pteronyssinus, their breeding place is bedding, optimal growth is at high humidity and a temperature of about 25 ° C, the maximum reproduction is October – November. Cross reactivity with other types of ticks is supposed: Dermatophagoides farinae, Otodectes, Sunotis. Of a large number of non-pathogenic fungi, Alternaria, Aspergillus, Candida, Cladosporium, and Penicillium are most closely associated with respiratory allergies. Highly allergenic animal dander, dried daphnia and other allergens of animal origin. Of the drugs in the induction of the disease, the role of acetylsalicylic acid, penicillin, ACTH, iodine-containing radiopaque agents has been proven. Food allergy as a primary etiological factor is more important for bronchial asthma in young children than in adults. Infectious-allergic bronchial asthma is closely associated with inflammatory respiratory diseases: chronic bronchitis, chronic pneumonia, foci of infection in the nasopharynx, sinuses, as well as acute respiratory diseases, flu. Allergization of the body is caused by the microflora of the respiratory tract (about 15 species), mainly related to opportunistic microbes and saprophytes: neisseries, staphylococci, dipteroids, streptococci, etc. Non-pathogenic types of neisseria predominate. Pigment species of the neisseria, in particular Neisseria perflava, are particularly sensitive.