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Diffuse interstitial (infiltrative and restrictive) lung diseases



In this section of the chapter, a combined group of noncommunicable diseases is described, characterized mainly by diffuse and usually chronic changes that affect mainly the stroma of the lungs, i.e. interstitial tissue of the alveolar walls, consisting of the endothelial basement membrane 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 intraalveolar and interstitial changes, as well as similar histological signs characteristic of different forms. Similar clinical manifestations, radiological data are also observed. All this led to the integration of these diseases into 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 surface respiration, cyanosis. Stridor and other signs of airway obstruction are absent. Oxygen diffusion, lung volume, and volume changes during breathing are generally reduced. When fluoroscopy shows that the lung tissue is diffusely penetrated by small nodules, cords or blackouts such as 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, far-reaching forms are difficult to distinguish because of scarring and impaired lung architectonics (QQTQBQe, CCR Reshetchtre l $ SCRE). 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 has more than 100 different reasons.

Currently, it is believed that, regardless of a particular type of interstitial lung disease or the reason that predetermined 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 in the thickness of the alveolar walls. In healthy individuals, these cells do not exceed 7% of the total number of cells in lung tissue. Their population is 93% macrophages, approximately 7% lymphocytes, as well as neutrophils and eosinophils (less than 1%). With alveolitis, a significant increase in the total number of these cells is observed. The accumulation of leukocytes causes 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 the areas of which the usual alveolar tissue is replaced by cystic spaces, which are separated by thick fibrous layers penetrated by inflammatory infiltrate cells.

The causes of alveolitis are diverse. 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 may be provided by complement activation. However, along with this, alveolar macrophages, the number of which increases with all interstitial pulmonary diseases, distinguish chemotaxis factors for neutrophils (interleukin-8, leukotriene B4). Some chemotaxis inducing agents also activate neutrophils and stimulate them to synthesize proteases and oxygen free radicals. All these products further contribute to tissue damage and, thus, are involved in maintaining the 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 release of lympho- and monokines, provide 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 DIFFUSIVE ASTHMA. INTERSTITIAL LUNG DISEASES. CANCER INFLAMMATORY LUNG DISEASES. Bronchial lung
    LUNG DISEASES. CHRONIC DIFFUSIVE ASTHMA. INTERSTITIAL LUNG DISEASES. CANCER INFLAMMATORY LUNG DISEASES. BRONCHIAL
  2. Chronic diffuse inflammatory diseases of the lungs. Bronchial asthma. Lungs' cancer. Pneumoconiosis
    1. The main types of diffuse lung lesions 1. interstitial 4. small focal 2. obstructive 5. panacinar 3. restrictive 2. Causes of death with obstructive emphysema 1. gas acidosis and coma 2. renal failure 3. left ventricular heart failure 4. right ventricular heart failure 5. collapse of the lungs with spontaneous pneumothorax 3. The most important
  3. Restrictive lung disease
    Causes of restrictive pulmonary pathology Causes of acute restrictive pulmonary pathology: • ???? pulmonary edema; • ???? ARDS; •????aspiration; • ???? neurogenic edema; • ???? overdose of opioids; • ???? congestive myocardial failure; • ???? pleural effusion; •????pneumothorax; • ???? an increase in the mediastinum; • ???? pneumomediastinum. Chronic lung disease leading to restrictive
  4. Restrictive lung disease
    Restrictive diseases are characterized by a decrease in lung distensibility. Pulmonary volumes are below normal, while the volumetric flow rate on the exhale is not reduced. Thus, FEV1 and FVC are reduced, but the ratio of FEVc / FVC 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. INTERSTITIAL LUNG DISEASES
    Ronald G. Crystal (Ronald G. Cristal) Interstitial lung disease (LLL) is a chronic, non-cancerous, non-communicable disease characterized by inflammation and disorganization of the walls of the alveoli. The most logical and serious outcome of this pathology is a decrease in the number of functioning alveolar-capillary complexes and, as a consequence, a violation of blood oxygenation.
  6. Obstructive and restrictive pulmonary diseases
    There are two types of diffuse lung lesions. These are obstructive processes that affect mainly the airways and are characterized by an increase in resistance to air passage due to partial or complete obstruction at any level (from the trachea to respiratory bronchioles), and restrictive processes, which are characterized by a decreased expansion of the lung parenchyma during inspiration and,
  7. Chronic diffuse inflammatory lung disease
    in accordance with the functional and morphological features, the lesions of their air-conducting or respiratory departments 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 pulmonary disease (IBL) is a heterogeneous group of diseases characterized by a predominance of diffuse and usually chronic damage to the pulmonary interstitium of the respiratory parts of the lungs, especially alveoli and bronchioles. The history of the study of ILL is associated with the names of the American doctors Hamman and Rich, who first described in 1935 and then in 1944 in the Bulletin of the Johns Hopkins Hospital
  9. Acute left ventricular failure - interstitial and alveolar pulmonary edema. Non-cardiogenic pulmonary edema.
    Cardiogenic and non-cardiogenic pulmonary edema are considered as the immediate cause of death in every fourth person who died. Pathogenesis. In a healthy person, the hydrostatic pressure in the pulmonary capillaries is 7–9 mm Hg. Art., it slightly exceeds that in interstitium. The liquid is retained in the capillaries due to its viscous properties, sufficiently high figures of oncotic
  10. Chapter DIFFUSIVE DISEASES OF CONNECTIVE TISSUE
    Diffuse diseases of the connective tissue is a group of diseases that are characterized by a 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 specific role of immunogenetic
  11. Diffuse connective tissue diseases
    Diffuse diseases of the connective tissue (syn: collagenoses, collagen diseases) is a group concept that combines several diseases in which diffuse damage to the connective tissue and blood vessels is noted. In 1942, Klemperer (P. Klemperer) proposed calling diffuse collagen disease diseases that are anatomically characterized by generalized alteration (damage)
  12. Idiopathic diffuse pulmonary fibrosis (Hamman-Rich syndrome, idiopathic fibrosing alveolitis - ELISA)
    Pathogenesis. The pathogenesis of ELISA is considered as an autoimmune process; it is rare in childhood, more often in people 50-60 years old. The clinical picture. Dyspnea (mostly difficult to breath), cough (dry, unproductive), mismatch of dyspnea with relatively small physical changes in the lungs, nail plates in the form of "drumsticks", sometimes hemoptysis, auscultation
  13. Diffuse connective tissue diseases
    DIFFUSIVE DISEASES OF THE CONNECTIVE TISSUE (DZST), or collagenosis (a term having historical significance), is a group of diseases characterized by a systemic immuno-inflammatory lesion of the 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 combine enough
  14. DIFFUSIVE CONNECTIVE TISSUE DISEASES
    By this concept is meant a number of nosological forms characterized by a 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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