Bronchial asthma and pathogenesis

Bronchial asthma is characterized by the occurrence of chronic allergic inflammation. The development of the disease is based on spasm of smooth muscles of the bronchi, edema and increased secretion of mucus.

The inflammatory process involves eosinophils, mast cells, lymphocytes, macrophages, neutrophils, epithelial cells. Sensitization of the body by allergens promotes the activation of 1eE synthesis, which are localized on mast cells.

In case of repeated exposure of the allergen to the body, antigens (allergens) interact with antibodies, and mast cells are destroyed with the release of inflammatory mediators.

The inflammatory mediators include histamine-chemotoxic factor. T-helper cells synthesize interleukins, activating eosinophils, which, in turn, produce inflammatory mediators, leukotrienes. Eosinophils and mast cells activate the formation of cytokines that support the synthesis of 1dE, closing the circle of allergic inflammation.

Inflammatory mediators act on target cells and the following reactions develop:

1. Increases the content of cyclic guanosine monophosphate and decreases cyclic adenosine monophosphate in bronchial cells, which leads to bronchospasm.

2. The formation of mucus sharply increases, mucous plugs form.

3. There is an increase in the permeability of the vascular wall, and edema develops.

4. There is a thickening of the mucous and submucous layers of the bronchi as a result of cell infiltration.

5. Microcirculation is disturbed, blood stasis occurs with platelet aggregation.

The course of bronchial asthma is aggravated by neurogenic disorders, which are based on an increase in the synthesis of neuropeptides (substance P) and a decrease in the vasointestinal peptide.

Clinic

When studying the history, it is necessary to pay attention to the presence of allergic diseases in close relatives.

During the out-of-attack period, the presence of bronchial asthma is indicated by:

– repeated bronchitis, especially with obstruction, and acute respiratory viral infections that occur without an increase in temperature;

– the appearance of paroxysmal cough and shortness of breath during stressful situations, increased physical activity, with a decrease in temperature;

– persistent painful cough, especially at night;

– periodically appearing feeling of compression in the chest.

However, when examining a child outside of an attack, pulmonary symptoms may not be detected.

As a rule, an attack of bronchial asthma begins with a period of precursors (pre-stage period). The duration of the entrepreneurial period can be from several hours to 2-3 days. The general condition of the child is disturbed: anxiety, irritability, increased fatigue, emotional instability, and decreased appetite are noted. When examining a child during this period, pallor or redness of the face, glitter of the eyes, and increased sweating are revealed. Children may complain of headache, nausea, and abdominal pain. There is nasal congestion, profuse watery discharge from the nose, itching, sneezing, watery eyes, sore throat. Many children have sleep disturbances. A painful, dry, paroxysmal cough may disturb. Gradually, shortness of breath appears with difficulty exhaling and wheezing rales heard from a distance. As a rule, there are signs of acute respiratory viral infection.

Then comes the onset period, which lasts from several minutes to several days and develops sharply. Most often, the attack begins at night or early in the morning. Patients in the attack period become very restless, rushing about. Body temperature remains normal. Respiratory discomfort increases, there is a feeling of lack of air, chest compression. The expressed expiratory shortness of breath joins. The breath is noisy, audible from a distance. There is a dry, paroxysmal cough with difficult to separate, viscous sputum. When examining a sick child, the skin is pale, perioral cyanosis is detected. The respiratory rate is higher than the age norm. The auxiliary muscles are involved in the act of breathing, there is a bloating of the wings of the nose, swelling of the cervical veins, retraction of the jugular, supraclavicular, subclavian fossae, intercostal spaces. The muscles of the chest abs, sternocleidomastoid, and pectoral muscles are tensed by inhalation. The rib cage is enlarged in anteroposterior size, rigid. A sick child takes a forced sitting position with his hands resting on his knees. With percussion of the lungs, a boxed shade of sound is noted, the lower boundaries of the lungs are omitted, mobility is limited. With percussion of the heart, a decrease in the relative cardiac dullness is revealed. During auscultation of the lungs, dry whistling, buzzing and varied wet rales are heard throughout all pulmonary fields against the background of an elongated exhalation. The heart rate is increased. There is an increase in blood pressure.

Then comes the post-attack period, which is characterized by the addition of a productive, moist cough with separation of the sputum mucosa and the disappearance of shortness of breath. The duration of the post-attack period is on average 2-5 days. Weakness, some deafness, drowsiness and lethargy are noted. There is a tendency to bradycardia (decrease in heart rate).

In the interictal period, signs of bronchospasm are not detected. However, in most children, complete normalization of bronchial conduction does not occur.

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