157. Bronchial asthma: definition, etiology, mechanism of development, pathological anatomy, outcomes, complications.

Bronchial asthma is a disease with attacks of expiratory dyspnea caused by an allergic reaction in the bronchial tree, with impaired bronchial patency.

Etiology. The main factors causing bronchial asthma are exogenous allergens with an undoubted role of heredity. The causes that determine repeated attacks of bronchial asthma: infectious disease, especially in the upper respiratory tract, allergic rhinosinusitopathy, environmental exposure, the action of substances suspended in the air.

Pathogenesis. Binding of the allergen to antibodies fixed on cells (labrocytes, basophils, etc.). " The antigen—antibody complex leads to the release of biologically active substances from effector cells (histamine, serotonin, kinins, slow-reacting substance of anaphylaxis, etc.), causing a vascular exudative reaction in the bronchi, muscle spasm, increased secretion.

Pathological anatomy. Changes in the bronchi and lungs in bronchial asthma can be acute, occurring at the time of the attack, and chronic due to repeated attacks and prolonged course of the disease. In the acute period (during an attack) of bronchial asthma, pronounced fullness of the vessels of the microcirculatory bed and an increase in their permeability are observed in the bronchial wall. Edema of the mucous membrane and submucosal layer develops, their infiltration by labrocytes, basophils, eosinophils, lymphoid, plasma cells. The basal membrane of the bronchi thickens and swells. Hypersecretion of mucus by goblet cells and mucous glands is noted. As a result of allergic inflammation, functional and mechanical obstruction of the respiratory tract is created with a violation of the drainage function of the bronchi and their patency. Acute obstructive emphysema develops in the lung, areas of atelectasis appear, respiratory failure occurs, which can lead to death of the patient during an attack of bronchial asthma.

With repeated attacks of bronchial asthma, diffuse chronic inflammation, thickening and hyalinosis of the basement membrane, sclerosis of the interalveolar septa, and chronic obstructive pulmonary emphysema develop over time in the bronchial wall. There is a desolation of the capillary bed, secondary hypertension appears in the small circle of blood circulation, leading to hypertrophy of the right heart and eventually to cardiopulmonary insufficiency.

Complications:

- pulmonary heart disease, up to acute heart failure

- emphysema and pneumosclerosis of the lungs, respiratory failure

- atelectasis of the lungs

- interstitial, subcutaneous emphysema

- spontaneous pneumothorax

Outcomes: remission, death

158. Interstitial lung diseases: definition, etiology, pathogenesis, morphogenesis, classification, pathological anatomy, complications, clinical significance.

Interstitial lung diseases (IBD) is a group of diseases united by the radiological syndrome of bilateral dissemination, represented by approximately 200 nosological units, which accounts for about 20% of all lung diseases.

Among them, fibrosing (fibrous) alveolitis is of primary importance — a heterogeneous group of lung diseases characterized by primary inflammation in the interalveolar pulmonary interstitium (pneumonitis) with the development of bilateral diffuse pneumofibrosis. There are three nosological forms of fibrosing alveolitis.

Classification

Idiopathic fibrosing alveolitis is a manifestation of other diseases, primarily systemic connective tissue diseases.

• Exogenous allergic alveolitis

• Toxic fibrosing alveolitis

The etiology of idiopathic fibrosing alveolitis has not been established, its viral nature is assumed. Among the etiological factors of exogenous allergic alveolitis, a number of bacteria and fungi, dust containing antigens of animal and plant origin, and medications are of great importance. Toxic fibrosing alveolitis is associated with the pneumotropic effect of drugs.

The main role in the pathogenesis of fibrosing alveolitis is played by immunocomplex damage to the capillaries of the interalveolar septa and the stroma of the lungs, which is joined by cellular immune cytolysis. The role of autoimmunization and hereditary failure of collagen in the lung stroma is not excluded.

Pathological anatomy. Based on the study of lung biopsies, three stages of morphological changes in the lungs have been established:

• In the stage of alveolitis, which has existed for a long time, there is an increasing diffuse infiltration of the interstitium of the alveoli, alveolar passages. Cellular infiltration leads to thickening of the alveolar interstitium, compression of capillaries, hypoxia.

• The stage of disorganization of alveolar structures and pneumofibrosis is characterized by deep damage — destruction of endothelial and epithelial membranes, elastic fibers, increased cellular infiltration of the alveolar interstitium, which spreads beyond its limits and affects blood vessels and perivascular tissue. In the interstitial of the alveoli, the formation of collagen fibers is enhanced, diffuse pneumofibrosis develops.

• At the stage of formation of the cellular lung, alveolar capillary block and panacinar emphysema, bronchiolectasis develop, cysts with fibrously altered walls appear in place of the alveoli. As a rule, hypertension occurs in the small circle of blood circulation. Hypertrophy of the right heart, which appears in the second stage, progresses, and cardiopulmonary insufficiency develops in the final.

Pneumofibrosis is an overgrowth of connective tissue in the lung, which completes many processes in the lungs. It develops in the areas of carnification of unresolved pneumonia, along the outflow of lymph from the foci of inflammation, around the lymphatic vessels of the interlobular septa, in the peribronchial and perivascular tissues, in the outcome of pneumonitis. With pneumofibrosis, due to vascular sclerosis and reduction of the capillary bed, hypoxia of the lung tissue occurs, which activates the collagen-forming function of fibroblasts, further promotes pneumofibrosis and complicates blood circulation in a small circle. Hypertrophy of the right ventricle of the heart (pulmonary heart) develops, which ends with cardiac decompensation.