Morphological changes in chronic inflammation of the lungs

May 26, 2018 06:30 | Disease Treatment
The main feature of morphological changes in bronchitis is the tendency of them to penetrate into the depths and affect not only the bronchial mucosa, but also the muscular wall and peribronchial cellulose( meso- and peribronchitis).Changes are mainly small bronchi;their walls are swollen, infiltrated, the capillaries are stretched and are full of blood. In the inflammatory process, interstitial tissue takes a significant part, which was established by Rokitansky.

The inflammatory process in the interstitial lung tissue progresses with every recurrence of pneumonia in early childhood. The presence of wide lymphatic vessels is very important. In the future, the development of granulation tissue followed by the formation of fibrosis and sclerosis, resulting in narrowing of the bronchi. Along with this, atelectatic foci easily develop due to occlusion of the bronchial lumen of the exudate and reduction of their elastic properties associated with the death of( full or partial) elastic fibers. According to MA Skvortsov, any lingering catarrh of the upper respiratory tract is accompanied by the accumulation of a proteinaceous liquid under the respiratory epithelium, followed by its detachment and decay. In the future, with repeated diseases, the inflammatory process can go either in a sequential way - from bronchioles mucosa to alveolar courses and alveoli with the formation of foci of bronchopneumonia, or centrifugal pathway( in relation to the lumen of the bronchi) through interstitial tissue( peribronchial pneumonia).With the destruction of the muscular and elastic framework of the airways with peribronchitis, their evacuation, that is, self-cleaning ability, decreases. Exudate is organized and can give a carnification in more or less significant areas of the lungs.

In the future, in the bronchi often formed necrotic process in connection with the loss of their walls of elasticity with exhaled exhalation;in connection with the cough, diffuse bronchiectasis is easily developed. With measles peribronchial pneumonia such bronchiectasis develop sometimes within 1-2 days.

If necrosis of the bronchial wall occurs in the airways that are still passable for air, then the bronchiectatic enlargement develops more rapidly. In more restricted areas of pneumonia, separate bronchoectatic cavities are formed.

AI Abrikosov considers the delay of exudate in the alveoli with the subsequent fatty degeneration of its cells characteristic for chronic pneumonia. In the future, there is a proliferation of interstitial tissue with sclerosis of the lung tissue and obliteration of the bronchi and vessels.
AN Rubel at the heart of chronic nontuberculous processes in the lungs considers a diffuse or focal proliferation of connective tissue( cicatricial, fibrous, sclerotic).

A number of authors attribute bronchoectases to only one phase of chronic pneumonia, identifying a number of concepts - chronic nonspecific pneumonia, nonspecific pulmonary consumption, pneumonitis, pulmonitis, cirrhosis of the lung, and inducible pneumonia. A. Ya. Tsigelnik considers the term "pneumonitis" to be the most correct, taking into account the diffuse lesion of lung tissue in chronic pneumonia and the tendency of the latter to relapse.

With the so-called chronic bronchitis, the bronchial mucosa is not highly modified. It is hyperemic and swollen, but in the thickness of the bronchial wall and the surrounding interstitial tissue there is always a proliferation of connective tissue, its cicatricial degeneration( fibrous peribronchitis).

These changes, according to AN Rubel, are secondary, because they are caused by the transferred pneumonia, protracted influenza, measles, whooping cough, ie, processes involving intralobular connective tissue in the form of peribronchitis. From this point of view, the origins of the chronic non-tuberculous process are quite understandable. It is in early childhood, when primary interstitial pneumonia often occurs, with the process of tissue shrinking develops nested or solid pneumosclerosis. In some cases, there is a decrease in alveoli, the formation of atelectasis and carnification. It can be assumed that with each exacerbation of the chronic process in the lungs, perivasculitis develops with the formation of atrophic processes in the thickness of the bronchi( in cartilage, muscle) and with the consequent expansion of the bronchi themselves.

This condition creates favorable soil for the reproduction of microbes. The atrophic process promotes the formation of cylindrical or sachet expansions followed by the appearance of necrosis.

Panbronchitis occurs especially easily in young children in small bronchi deprived of cartilage. Such changes are described by Leszek under the name bronchiectasis of the terminal bronchial system, and even earlier - by Utinelem. In the walls of the bronchi along with the development of granulation and scar tissue there are also significant expansions as a result of increased intrabronchial pressure. According to the data of SI Volchok and A. Ya. Tsygelnik, the atherogenesis of the bronchiectasis often involves atelectasis, in which deep necrotic processes develop. Lately, much has been said about the effect of chronic sinusitis and tonsillitis on the formation of bronchiectasis. According to Yu. F. Dombrovskaya, chronic nasopharyngeal processes almost always accompany chronic pneumonia and especially bronchiectasis( sinusobronchitis, sinusopneumopathy) even in early childhood.

The necrosis of ruptured walls of bronchioles and alveolar septa with the spread of air along the lymphatic vessels lead to interstitial emphysema. According to MA Skvortsov, such ruptures are most often observed near the anterior edge of the lungs, where at the dissection can be seen under the pleura air bubbles - subpleural emphysema. With the further spread of emphysema under the influence of incoming air along the large vessels and bronchi through the lung root, mediastinal emphysema forms. More rarely, subcutaneous emphysema is observed in connection with the passage of air through the jugular fossa.

Given this variety of morphological changes, it becomes clear why in chronic pneumonia, various forms of changes are found in the lung tissue: pneumonic foci, sclerosis, emphysema, atelectasis, bronchiectasis. This is explained by the simultaneous involvement of all lungs, bronchi, interstitial tissue, alveoli, and vessels in the process. But the leading process in the lungs is the destruction of interstitial tissue with the development of granulations and foci of pneumosclerosis.

Most bronchiectasis is a consequence of chronic pneumonia. They can arise due to deformation of the bronchus located in the area of ​​cirrhotic lung compaction.

Atelectatic bronchiectasis develops most often in the lower lobes of the lungs, usually after measles, pertussis and influenza pneumonia, as well as in severe rickets. Atelectasis is formed due to the weakness of the respiratory excursion, the occlusion of the bronchi secret.

Blood and lymphatic pathways also undergo changes - productive exo-meso-periarteritis, sclerosis and thickening of the walls develop, resulting in compression of the lymphatic vessels.

Changes in bronchi can be both atrophic and hypertrophic. In children's pathology, atrophic processes with thinning of the walls of small bronchi are more common. In large bronchi hypertrophic processes predominate with hyperplasia of the mucous membrane and glands. It is difficult to say which of the two processes - hypertrophic or atrophic - leads to the development of bronchiectasis. Most of all, both processes occur simultaneously, since in the section usually along with the described changes in the walls of the bronchi, atrophy of interalveolar septa and emphysema is found. Especially brightly these changes are manifested in the presence of rickets of a blossoming form. In severe chronic interstitial pneumonia, ulceration of bronchial mucosa with metaplasia of their epithelium is observed.

We can distinguish: a) drainage, b) diffuse forms of chronic pneumonia. Both those and others are accompanied by emphysema and lung sclerosis.

Thus, the morphological changes in chronic pneumonia in children are characterized by a predominant lesion of the interstitial tissue, which is why they are often called the chronic interstitial pneumonia.

Changes in interstitial tissue can also be explained by asymptomatic microabscesses accompanied by periodic temperature flares and increased leukocytosis without certain clinical symptoms. The development of the process in the connective tissue around the bronchi and bronchioles creates a picture of the so-called cellular, or honeycomb, lung, during fluoroscopy, and a predominant bronchial lesion is characterized by a number of morphologists like panbronchitis, deforming bronchitis, etc.

There are some authors' observations on the ratio of the shape of the thorax andthe nature of the process. Thus, with the nested character of the process, a barrel-like shape of the thorax is more often observed, while in the continuous one it is narrowed. The barrel-like shape of the thorax in the nest of pneumosclerosis is due to the presence of compensatory emphysema.

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