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Diffuse interstitial (infiltrative and restrictive) lung diseases



In this section of the chapter, a team of non-communicable diseases is considered, characterized by predominantly diffuse and usually chronic changes that mainly affect the stroma of the lungs, i.e. interstitial tissue of the alveolar walls, consisting of the basement membrane of the endothelium and epithelial cells, collagen fibers, elastic structures, proteoglycans, fibroblasts, mast cells, as well as lymphocytes and monocytes. There is no generally accepted classification of these diseases. Many of the diffuse interstitial lung lesions have unknown causes and pathogenesis. They may differ in the nature of intra-alveolar and interstitial changes, as well as similar histological features characteristic of different forms. Observed and similar clinical manifestations, radiographic data. All this led to the unification of these diseases in one group (about 15% of all non-infectious lung diseases). Changes in the lungs and symptoms are restrictive (restrictive) and to a much lesser extent obstructive (see sections 15.5 and 15.6). Patients noted shortness of breath, rapid shallow breathing, cyanosis. Stridor and other signs of airway obstruction are absent. Oxygen diffusion rates, lung volume, and volume changes during breathing are usually reduced. With fluoroscopy, it can be seen that the lung tissue is diffusely penetrated by small nodules, strands or darkening like frosted glass (hence the name “infiltrative changes”). In the end, patients with chronic infiltrative changes of this kind develop secondary pulmonary hypertension, pulmonary heart, and right ventricular failure. Despite the possibility of recognizing many pulmonary changes in the early stages of development, advanced forms differ with difficulty due to scarring and impaired lung architectonics (“QQTQBQe”, cdts “reschetztre” l $ SCR). The most common causes of diffuse interstitial lung diseases are diseases caused by environmental factors (24% of cases), sarcoidosis (20%), idiopathic pulmonary fibrosis (15%); The remaining 51% of observations have more than 100 different causes.

Nowadays, it is considered that irrespective of one or another type of interstitial lung disease or the cause that determined it, the earliest and most common manifestation is alveolitis.
Alveolitis is represented by the accumulation of cells of the inflammatory and effector immune response in the alveoli and the thickness of the alveolar walls. In healthy individuals, these cells do not exceed 7% of the total number of cells in the lung tissue. Their population consists of 93% of macrophages, approximately 7% of lymphocytes, as well as neutrophils and eosinophils (less than 1%). When alveolitis is observed a significant increase in the total number of these cells. The accumulation of leukocytes leads to a distortion of the normal alveolar structure of the lung and leads to the release of mediators that can damage parenchymal cells and stimulate fibrosis. As a result, pneumofibrosis develops, in zones of which ordinary alveolar tissue is replaced by cystic spaces, which are separated by thick fibrous layers permeated with inflammatory cells.

The causes of alveolitis are varied. For example, free radicals - derivatives of oxygen and some other chemical compounds have a direct toxic effect on the endothelium and epithelium. In addition, the replenishment and activation of inflammatory and immune effector cells are important factors. In some diseases, neutrophil replenishment can be provided by activation of complement. However, along with this, alveolar macrophages, the number of which increases with all interstitial lung diseases, emit chemotaxis factors for neutrophils (interleukin-8, leukotriene B4). Some agents that induce chemotaxis also activate neutrophils and stimulate them to synthesize protease and oxygen free radicals. All of these products further contribute to tissue damage and, thus, are involved in the maintenance of alveolitis. In diseases such as sarcoidosis, cell-mediated immune responses lead to the accumulation of monocytes and T-lymphocytes, as well as the formation of granulomas. It is believed that the interaction of lymphocytes and macrophages, as well as the secretion of lymphocytes and monokines, ensures the development of slowly progressive pulmonary fibrosis. In particular, alveolar macrophages play a central role in the occurrence of sclerotic changes.

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Diffuse interstitial (infiltrative and restrictive) lung diseases

  1. LUNG DISEASES. CHRONIC DIFFUSE ASTHMA. INTERSTICIAL LUNG DISEASES. CANCER INFLAMMATORY DISEASES OF THE LUNGS. BRONCHIAL LUNG
    LUNG DISEASES. CHRONIC DIFFUSE ASTHMA. INTERSTICIAL LUNG DISEASES. CANCER INFLAMMATORY DISEASES OF THE LUNGS. BRONCHIAL
  2. Chronic diffuse inflammatory lung disease. Bronchial asthma. Lungs' cancer. Pneumoconiosis
    1. Main types of diffuse pulmonary lesions 1. interstitial 4. small-focal 2. obstructive 5. panacinal 3. restrictive 2. Causes of death in obstructive pulmonary emphysema 1. gas acidosis and coma 2. renal failure 3. left ventricular heart failure 4. right ventricular heart failure 5. lung collapse in spontaneous pneumothorax 3. The most important
  3. Restrictive lung diseases
    Causes of restrictive lung disease Causes of acute restrictive disease: • ????? pulmonary edema; • ???? ARDS; •????aspiration; • ???? neurogenic edema; • ????? opioid overdose; • ???? congestive myocardial insufficiency; • ???? pleural effusion; •????pneumothorax; • ???? increase mediastinum; • ???? pneumomediastinum. Chronic lung disease leading to restrictive
  4. Restrictive lung diseases
    Restrictive diseases are characterized by a decrease in lung compliance. Lung volumes are below normal, while the volumetric flow rate on the exhalation is not reduced. Thus, FEV1 and FZHEL are reduced, but the value of the OFVch / FZHEL ratio remains normal. Restrictive diseases include many acute and chronic pathological conditions of the lungs, as well as lesions of the pleura, chest wall, diaphragm and
  5. INTERSTICIAL DISEASES OF THE LUNGS
    Ronald G. Crystal (Ronald G. Cristal) Interstitial lung disease (IZL) - chronic non-malignant, non-infectious diseases characterized by inflammation and disorganization of the walls of the alveoli. The most natural and serious outcome of this pathology is a decrease in the number of functioning alveolar-capillary complexes and, as a result, a violation of blood oxygenation.
  6. Obstructive and restrictive lung diseases
    There are two types of diffuse lung lesions. These are obstructive processes, affecting mainly the airways and characterized by an increase in resistance to the passage of air due to partial or complete obstruction at any level (from the trachea to the respiratory bronchioles), and restrictive processes that are associated with a decreased expansion of the lung parenchyma during inhalation and
  7. Chronic diffuse inflammatory lung disease
    in accordance with the functional and morphological features of the defeat of their air-conducting or respiratory departments, they are divided into three groups: obstructive, restrictive, mixed - obstructive with restrictive disorders or restrictive with obstructive disorders. The combination of restriction with obstruction is observed in the late stages of almost all chronic diffuse
  8. Interstitial lung disease.
    Interstitial lung diseases (IPL) are a heterogeneous group of diseases characterized by the prevalence of diffuse and usually chronic lesions of the pulmonary interstitium of the respiratory parts of the lungs, primarily alveoli and bronchioles. The history of the study of IBL is associated with the names of American doctors Hamman and Rich, who were first described in 1935 and then in 1944 in the Hospital Johl Hopkins Special Gazette.
  9. Acute left ventricular failure - interstitial and alveolar pulmonary edema. Non-cardiogenic pulmonary edema.
    Pulmonary edema is cardiogenic and non-cardiogenic and is considered as the immediate cause of death in every fourth deceased. Pathogenesis. In a healthy person, the hydrostatic pressure in the pulmonary capillaries is 7–9 mm Hg. st., it is somewhat higher than that in the interstitium. The fluid is retained in the capillaries due to its viscous properties, rather high oncotic numbers.
  10. Head DIFFUSIVE DISEASES OF CONNECTIVE TISSUE
    Diffuse connective tissue diseases are a group of diseases that are characterized by the systemic type of inflammation of various organs and systems as a result of the combined development of autoimmune and immunocomplex processes, as well as excessive fibrosis. A feature of this group of diseases is the multifactorial type of predisposition with a certain role of immunogenetic
  11. Diffuse connective tissue diseases
    Diffuse diseases of the connective tissue (syn .: collagenosis, collagen diseases) is a group concept that combines several diseases in which there is a diffuse lesion of connective tissue and blood vessels. In 1942, Klemperer (P. Klemperer) proposed to call diffuse collagen disease diseases that are anatomically characterized by generalized alteration (damage)
  12. Idiopathic diffuse pulmonary fibrosis (Hammen-Rich syndrome, idiopathic fibrosing alveolitis - ELISA)
    Pathogenesis. The pathogenesis of ELISA is considered as an autoimmune process; in childhood is rare, more often in people 50-60 years. The clinical picture. Shortness of breath (breathing is mostly difficult), coughing (dry, unproductive), shortness of breathlessness with relatively minor physical changes in the lungs, nail plates in the form of “drumsticks”, sometimes hemoptysis, auscultation
  13. Diffuse connective tissue diseases
    DIFFUSE DISEASES OF THE CONNECTIVE TISSUE (DZST), or collagenosis (a term that has historical significance), is a group of diseases characterized by a systemic immune-inflammatory lesion of connective tissue and its derivatives. This concept is a group, but not nosological, in connection with which this term should not denote individual nosological forms. DZST unite enough
  14. DIFFUSE DISEASES OF CONNECTIVE TISSUE
    This concept implies a number of nosological forms characterized by the systemic type of damage to various organs and systems, the development of autoimmune and immune complex processes, and excessive fibrosis. In this lecture, we will focus on three large collagenoses: systemic lupus erythematosus, systemic scleroderma and dermatomyositis. A few years ago in this group
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