Hospital pediatrics. Chronic bronchitis (most important)

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Hospital pediatrics. Chronic bronchitis (most important)

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54. Chronic bronchitis. Etiology. Pathogenesis

Chronical bronchitis - this is a progressive diffuse inflammation of the bronchi, not associated with local or generalized lung damage, manifested by cough. You can talk about chronic bronchitis if the cough continues for 3 months in the 1st year - 2 years in a row.

Etiology. The disease is associated with prolonged irritation of the bronchi by various harmful factors (inhalation of air contaminated with dust, smoke, carbon monoxide, sulfur dioxide, nitrogen oxides and other compounds of a chemical nature) and recurrent respiratory infection (a major role is played by respiratory viruses, Pfeiffer's bacillus, pneumococci), less commonly occurs in cystic fibrosis. Predisposing factors are chronic inflammatory, suppurative processes in the lungs, chronic foci of infection and chronic diseases localized in the upper respiratory tract, decreased reactivity of the body, hereditary factors.

Pathogenesis. The main pathogenetic mechanism is hypertrophy and hyperfunction of the bronchial glands with increased mucus secretion, a decrease in serous secretion and a change in the composition of the secretion, as well as an increase in acidic mucopolysaccharides in it, which increases the viscosity of sputum. Under these conditions, the ciliated epithelium does not improve the emptying of the bronchial tree; normally, the entire layer of secretion is renewed (partial cleansing of the bronchi is possible only with a cough). Long-term hyperfunction is characterized by depletion of the mucociliary apparatus of the bronchi, the development of dystrophy and atrophy of the epithelium. When the drainage function of the bronchi is disrupted, a bronchogenic infection occurs, the activity and recurrence of which depend on the local immunity of the bronchi and the occurrence of secondary immunological deficiency. With the development of bronchial obstruction due to hyperplasia of the epithelium of the mucous glands, swelling and inflammatory thickening of the bronchial wall, obstruction of the bronchi, excess viscous bronchial secretion, and bronchospasm are observed. With obstruction of the small bronchi, overstretching of the alveoli during exhalation and disruption of the elastic structures of the alveolar walls and the appearance of hypoventilated or unventilated zones develop, and therefore the blood passing through them is not oxygenated and arterial hypoxemia develops. In response to alveolar hypoxia, spasm of the pulmonary arterioles and an increase in total pulmonary and pulmonary arteriolar resistance develop; pericapillary pulmonary hypertension develops. Chronic hypoxemia leads to an increase in blood viscosity, which is accompanied by metabolic acidosis, which further increases vasoconstriction in the pulmonary circulation. Inflammatory infiltration in large bronchi is superficial, and in medium and small bronchi and bronchioles it is deep with the development of erosions and the formation of meso- and panbronchitis. The remission phase is manifested by a decrease in inflammation and a large decrease in exudation, proliferation of connective tissue and epithelium, especially with ulceration of the mucous membrane.

Author: Pavlova N.V.

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