Bronchial asthma

Bronchial asthma

Bronchial asthma is a disease characterized by the development of reversible bronchial obstruction under the influence of various stimuli and caused by hyperreactivity of the bronchi. With bronchial astmenus, a triad of clinical symptoms is observed – asphyxiation, cough and shortness of breath, in a small part of patients the only manifestation of the disease may be a paroxysmal cough. More often, young people are sick: in half of patients, asthma develops in childhood, in 1/3 – under the age of 40. There is no single classification of bronchial asthma. Two main types of bronchial asthma are distinguished – exogenous (atopic, allergic) and endogenous, which is believed to be caused by non-immune mechanisms. Endogenous bronchial asthma includes asthma of physical effort, aspirin psychogenic, infectious, hypereosinophilic asthma, asthma associated with environmental pollution, as well as many cases of occupational bronchial asthma. The main differences between the two types of bronchial asthma are given below.

Etiology and pathogenesis of bronchial asthma

To date, the most fully studied mechanisms of development of atopic bronchial asthma. An allergen (pollen, house dust, fungal spores, food, medicines), when ingested, causes the production of antibodies of the IgE class, which are fixed on the membrane of mast cells. With repeated exposure to the allergen, antibodies combine with it, causing mast cells to release a number of biologically active substances – histamine, eosinophilic anaphylaxis factor, neutrophilic chemotactic factor. Following degranulation, mast cells synthesize a slow-reacting anaphylaxis substance (which includes leukotrienes), a platelet activating factor and, possibly, prostaglandins, some mast cell mediators (histamine, most leukotrienes, prostaglandins E1 and E2, platelet activating factor) cause bronchospasm increase vascular wall permeability and mucus secretion. Others (eosinophilic, lymphocytic, neutrophilic chemotactic factors, leukotriene B4) attract neutrophils, lymphocytes, eosinophils and thrombodites.

In recent years, new data have been obtained that better understand the role of mediators in the occurrence of bronchial asthma. The metabolism of arachidonic acid 5 and the synthesis of slow-reacting anaphylaxis substances were studied. Arachidonic acid is a product of the phospholipid membrane of a mast cell activated by a phospholipase under the influence of the antigen-antibody reaction. There are two ways of converting arachidonic acid – cyclooxygenase, which results in the formation of prostaglandins E2 and E2a and thromboxanes, and lipoxygenase, leading to the synthesis of leukotrienes, some of which form slowly reactive anaphylaxis substances. Leukotrienes and thromboxanes have a stronger effect on the smooth muscles of the bronchi than histamine and prostaglandins, while their point of application is mainly small bronchi.

It is assumed that the process of bronchial obstruction passes through two phases, the first, which occurs several minutes after inhalation of the allergen and lasts from 30 to 60 minutes, due to mediators that directly act on the vessels and bronchial wall; the second (repeated wave of bronchial obstruction several hours after the end of the first phase) is caused by the action of chemotactic factors and the effector cells attracted by them. The leading role in this period is played by eosinophils, the proteins of which damage the ciliary epithelium of the respiratory tract and increase the permeability of the mucous membrane, bronchi for allergens. At the same time, eosinophils secrete substances that inhibit histamine, platelet activating leukotrienes. Factor release of bronchospasm mediators depends on the ratio of cAMP and cGMP content in mast cells. cAMP inhibits the release of histamine, slow-reacting anaphylaxis, other mediators, while cGMP has the opposite effect. B-adrenoreceptors are known to activate adenylate cyclase, which is involved in the synthesis of cAMP. Drugs that stimulate a-adrenergic receptors increase the content of intracellular cAMP, which is destroyed by phosphodiesterase. Methylxanthines, potent phosphodiesterase inhibitors, also increase cAMP levels in cells. The synthesis of cAMP is enhanced by the excitation of H2 receptors and prostaglandin receptors, which respond to increased levels of histamine and other mediators. Cholinergic receptors are responsible for the activation of guanyl cyclase, which is involved in the synthesis of cGMP, so cholinolytic agents can also prevent the release of mediators. The role of calcium ions in the occurrence of bronchospasm is not fully understood. Moving them from the outer membrane of the cell and dealing with the cytoplasm is a sign of mast cell activation. It is also known that a decrease in the content of calcium ions in the smooth muscle cells of the bronchi contributes to the expansion of the latter.

The pathogenesis of endogenous bronchial asthma is not well understood. In development, it attaches importance to violations of the parasympathetic innervation of the bronchial tree, leading to the development of bronchospasm and a change in the secretion of bronchial glands, as well as a decrease in the threshold of sensitivity of the vagus nerve receptors to irritants. However, it is not possible to explain the development of various forms of endogenous bronchial asthma using a single hypothesis.

In the pathogenesis of asthma, physical effort suggests the importance of cooling the bronchial tree as a result of hyperventilation and inhalation of cold air. In this case, the excitation of specific temperature receptors in the airways that respond to a decrease in temperature occurs. Other mechanisms for the development of this form of asthma are discussed, in particular, IgE-independent mast cell degranulation with the release of mediators, activation of cholinergic receptors.

Exacerbation of bronchial asthma can be triggered by an infection of the upper respiratory tract, and the main role in the occurrence of bronchospasm is played not by bacteria, but by viruses (influenza, parainfluenza). Possible causes of bronchospasm are virus replication in the epithelium of the respiratory tract, causing cell damage and the release of arachidonic acid metabolites, as well as a decrease in the sensitivity threshold of bronchial tree receptors to various external stimuli under the influence of a viral infection, “Aspirin” or prostaglandin, asthma is observed in patients with polyposis nasal cavity and intolerance to acetylsalicylic acid, indomethacin, phenacetin or yellow food coloring (yellow tartrazine). Its development is associated with a violation of the synthesis of prostaglandins and an increase in the synthesis of leukotrienes due to a violation of the metabolism of arachidonic acid under the action of acetylsalicylic acid and its derivatives.

Occupational bronchial asthma occurs when in contact with various substances: 1) metal salts (chromium, nickel, manganese); 2) wood (dust of pine, oak) and vegetable (cotton, linen) dust; 3) industrial chemicals (phthalic anhydride, ethylenediamine, formaldehyde); 4) drugs (antibiotics, cimetidine, piperazine); 5) enzymes; 6) animal proteins (bird droppings, fish isolations, beekeeping products). Occupational factors can induce an immune response (metal salts, animal proteins, certain types of plant dust), act on specific cellular receptors (cotton, a substance that promotes the release of histamine, organophosphorus insecticides with anticholinesterase effects) and irritate, causing inflammation mucous membrane of the bronchi (silicon dioxide, ammonia, hydrochloric acid). Psychogenic bronchial asthma was described as early as the 17th century. In its pathogenesis, an increase in vagus nerve activity plays a role.

Bronchial asthma resulting from environmental pollution has become widespread in recent years. In its pathogenesis, along with the effect on the bronchial mucosa of irritating substances that pollute the atmosphere (sulfur oxides, ozone, carbon oxides, nitrogen dioxide), bronchial hyperreactivity plays a role. Hypereosinophilic bronchial asthma is also distinguished, which may be one of the manifestations of periarteritis nodosa (asthmatic variant). Its peculiarity is the presence of a large number of eosinophils in the blood (40-60% or more) and sputum.

Clinic of bronchial asthma

In most patients, asthma attacks begin with an unproductive cough. Usually they occur upon contact with allergen 1} at night, after exercise, in the cold, when inhaling substances with irritating properties or a pungent odor. Attacks can last up to several hours and stop on their own or under the influence of treatment. The end of the attack is preceded by the discharge of sputum in the form of mucous plugs. During an attack of suffocation, exhalation is difficult, wheezing can be heard at a distance during both phases of the respiratory cycle; with a more severe attack, an increase in shortness of breath is sometimes accompanied by a decrease or disappearance of wheezing. The patient occupies a forced position – he usually hoarsens, resting his hands on his knees or the edge of the bed and thus fixing the shoulder girdle. The auxiliary muscles actively participate in the act of breathing; the chest is enlarged (“swollen”), its anteroposterior dimensions are enlarged, percussion sound with a box-like tint or box-like sound, the lower borders of the lungs are omitted; sharply elongated exhalation and a large number of dry rales are heard in the lungs, after the discharge of sputum, the exhalation is shortened, the number of dry snores decreases, but the last two symptoms can persist for some time after the attack of suffocation.

Frequent asthma attacks or in time an uncured, prolonged asthma attack can go into asthmatic status (status asthmaticus). In many patients, the development of it is preceded by uncontrolled (up to tens of times) use of inhalers of B-adrenergic agonists (drug blockade of B-adrenergic receptors). Asthmatic status is characterized by an increase in bronchial obstruction with tachypnea and shallow breathing and the lack of effect in the treatment of adrenomimetic drugs. As a result of the formation of mucous plugs, clogging the lumen of the boronchus and disrupting the conduct of sound to the surface of the chest, the sonority and the number of dry rales are reduced (until they disappear, the “dumb” lung). The progression of respiratory failure leads to the development of decompensated respiratory acidosis and hypercapnia. Death occurs with hypoxemic coma due to paralysis of the respiratory center. Bronchial asthma can be complicated by obstructive pulmonary emphysema, pulmonary heart, pneumothorax, pneumomediastinum.

Diagnosis and differential diagnosis of bronchial asthma

Eosinophilia is detected in the blood during attacks of suffocation or with their increased frequency. With atopic bronchial asthma, the level of IgE is increased in the blood. Kurshman spirals (elements of mucus), Charcot-Leiden crystals (decay products of eosinophils), a large number of eosinophils are found in sputum. An X-ray examination of the chest organs increased the transparency of the pulmonary fields. In severe cases, atelectasis may develop due to obstruction of the bronchi with mucous plugs.
Examination of the function of external respiration is an important method for determining the severity of an attack, as well as the effectiveness of the treatment used. In the acute period, there is a significant decrease in FEV1, other speed indicators, in addition, a decrease in VC and an increase in residual lung volume can be recorded. In the interictal period, especially at the beginning of the disease, only a decrease in FEV1 is detected . In patients with a severe or protracted attack of suffocation, hypoxemia is observed, usually accompanied by hypocapnia, and an increase in the pH of arterial blood. Hypocapnia and respiratory alkalosis are caused by hyperventilation. Normalizing or increasing PaCO2, indicating severe bronchial obstruction or progressive respiratory failure, is considered a poor prognostic symptom.

Bronchospastic syndrome also occurs in congestive heart failure (cardiac asthma), pulmonary thromboembolism, chronic bronchitis, and airway volume formations. Attacks of shortness of breath with cardiac asthma occur when lying down and can be stopped with nitroglycerin. Cough usually does not appear at the beginning, but at the end of the attack. During auscultation of the lungs, moist rales are heard, mainly in the lower sections. Distinctive features of recurrent thromboembolism of the pulmonary artery are pleural pain, signs of overload of the right heart chambers (ECG). Crucial for the diagnosis are the data of scanning and angiography of the lungs. Volumetric formations of large bronchi (tumors, polyps, foreign bodies) are detected using bronchoscopy and X-ray examination. For chronic asthmatic bronchitis, a long-term cough is characteristic. Eosinophilia is not observed; there are no elements of bronchial asthma in sputum.

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