Pneumosclerosis

Pathogenesis
The transition of pneumonia in chronic course and development of pneumosclerosis promoted by the following factors: 1) violation of bronchial drainage in the inflammatory swelling of the walls of the bronchi, nerverending impacts and lesions of nervous-muscular apparatus of the bronchi in violation of the normal motor skills and prevalence of spastic or atonic phenomena, and increase the secretion of bronchial tubes. Violation of drainage leads to the accumulation of secret favouring the development of infection, atelectasis, followed by new inflammatory outbreaks; 2) violation of blood circulation: stasis, fibrinoid necrosis, hyalinosis vessels, endo - and periarteriit, perindoprilata followed venous stasis and expansion of veins, increased capillary permeability, exit protein exudation and the development of subsequent direct (acellular) sclerosis; 3) violation of lymphatic drainage due to compression of the lymphatic vessels, lymphangitis and bronchogenic; 4) violations of the trophic; 5) the destructive processes with the development of indirect sclerosis granulation tissue.
The success of chemotherapy for tuberculosis led to the termination of the tuberculosis process and extend the life of patients. However, the hardening of this became even more pronounced due to sclerosing effect of streptomycin. Prolonged use of pneumothorax (especially if there pneumopillow) also leads to pneumosclerosis changes in collaborando lung. All this increases the share metatorbernite of pneumosclerosis.
A significant role in the pathogenesis of pneumosclerosis belongs to atelectasis due to bronchial stenosis. This mechanism is Central to the so-called syndrome average share (see below).
The leading role in the pathogenesis of diffuse P. belongs to bronchitis. Currently, it is impossible for the categorization, as it was done by A. N. Rubel, to identify chronic bronchitis and P. However, chronic bronchitis can and often leads to the development of P. when switching endobronchitis in unbranched, occurs peribronchial of lymphangitis and peribronchial, i.e., interstitial inflammation. "The weak point" of the bronchial tree [on the Brauer (L. Brauer)] are bronchioles, where only a thin basal membrane separates the interstitial tissue of the bronchi clearance.
Of great importance in the creation and maintenance of chronic bronchitis is air pollution. Chemical impurities, especially sulfur compounds, even in small concentrations destroy the ciliated epithelium of the bronchi, which is essential in the dissemination of inflammatory process in the depth of the bronchial tree. This fact probably explains the peculiarities of the course of certain toxic-chemical pneumosclerosis when, following a pronounced pattern of acute or subacute defeat comes a long period of complete well-being as a result of termination of contact with harm and only after some years we get a picture of multiple segmental or diffuse P.
In the pathogenesis of P. attention is focusing allergic reactions and the formation of autoantibodies, obvious rheumatism and other collagenoses, likely in the pathogenesis of some special forms of P.: berillios, syndrome of Hamina - rich, pulmonary sarcoidosis and the so-called idiopathic gemosideroze (essential brown induration of the lungs). Autoimmune processes play a role, apparently, and in the pathogenesis of chronic pneumonia with subsequent development of pneumosclerosis (A. I. Mounds).
In the pathogenesis of radiation pneumosclerosis there is no direct dependence severity of the value of irradiation dose [A. I., Ruderman, Pierre-Bourgeois (Pierre-Bourgeois)]. He is determined: 1) defeat of the bronchi and subsequent atelectasis and connective tissue organization; 2) sero-fibrinous the alveolitis with desquamation of the epithelium; 3) damage of blood vessels, especially the small, with the proliferation of endothelial and their partial blockage; 4) increased capillary permeability with vihodnie plasma proteins (N. N. Mogilnitsky); 5) the accession of infection.
Plevralny P. (corticolimbic) occurs: 1) due to the organization of the inflammatory process on the periphery of the lung, caused in its time the emergence of fluid in the pleura; 2) due to the release of peripheral parts of the lungs through the lymph system rich in protein exudate by arranging it in the pleural cavity (Smarty), and in the cortical layer of the lung.
Thus, pneumosclerosis is a disease not only polietiologic, but with considerable variations of pathogenesis. In most cases P. develops with the leading participation of inflammation in the bronchi, but in some cases - as an outcome of segmental lesions in lungs (metapneumoviruses segmental P.), in others it is a consequence of peribronchial and is mainly diffuse character. On the background of diffuse P. occurrence of pneumonia with the outcome in the focal P., bronhoektatical disease (see). Segmental pneumosclerosis, capturing consistently more and more segments of the lung, acquires a new quality in the form of violations of the functions of breathing, is not peculiar usually segmental P. Sclerosis in some cases is reparative character, developing on the place of death lung parenchyma (cirrhosis easy - A. I. Strukov), in others the basic structure of a light remains stored and leading value is direct sclerosis. Localization sclerosis can be mainly bronchial, while in the alveoli are observed atrophic processes. However, when possible P. and hyperplastic alveolitis.
P. may develop angiogene. For example, if the stagnation in the lungs after suffering heart attacks the lungs, when angiotech (for example, when nodosum the nodosa, pulmonary Takayasu described by the rich as a manifestation of Allergy to sulfa drugs; in so-called essential sclerosis pulmonary artery). With the defeat of vessels develops perivascular sclerosis with hypertension pulmonary, lung heart, without significant changes ventilation, but with impaired oxygen diffusion (syndrome Ayers - Arriaga).
Usually a combination of different types of inflammation (see), mostly due to secondary joined infection, and at the same time the combination of different types of localization of pneumosclerosis. A particular combination, protruding to the fore, causes clinical entity" P. Thus, if mostly peribronchiolar location P. there are violations of bronchial passability with the development of emphysema (see). When intersticialna - perivascular sclerosis in the foreground there is the rigidity of the lung. When alveolitis arise violations of diffusion of gases with the development of hypoxemia with a relatively small violation of ventilation. While focal lesions little impact on respiratory function and give the main symptoms of intoxication, diffuse forms, as a rule, lead to the development of lung-heart failure (see).
As inflammation in pneumosclerosis cannot be completed within the majority P. may be periods clinically approaching the diagnosis of chronic pneumonia, sometimes to a diagnosis of lung abscess, sometimes to an exacerbation of chronic bronchitis, including asthmatic is most often caused by sensitization to bacterial flora and sputum (see Bronchial asthma).