The main etiological factor is cigarette smoking compared to pipe and cigar smoking. It should be noted that smoking cessation to a lesser extent than with lung cancer, affects the reduction in mortality from COPD. Using spirography, the presence of small bronchial obstruction in young smokers can be demonstrated even in the absence of any clinical symptoms. Recently, much attention has been paid to the effects of passive inhalation of tobacco smoke. It was shown that wives and children of smokers are much more likely to experience symptoms of lung damage, in particular cough and dry rales, than in non-smoking families.
Smoking leads to the development of chronic inflammation of the respiratory tract and hypertrophy of the glands of the mucous membrane, characteristic of chronic bronchitis. Smokers have an increased number of neutrophils in the bronchoalveolar washout, possibly due to the allocation of chemotactic factors by alveolar macrophages and epithelial cells. Neutrophils and, to a lesser extent, alveolar macrophages secrete elastase and other proteolytic enzymes, myeloperoxidase and oxidants. Proteinases destroy the elastic tissue of the lungs, while myeloperoxidase and oxidants damage the lung parenchyma cells and inactivate proteinase inhibitors. Proteins formed during the destruction of collagen, elastin and other components of the interstitium of the lungs, in turn, attract new neutrophils and support the course of chronic inflammation. In addition, inhalation of tobacco smoke inhibits elastin biosynthesis. Thus, smoking causes an imbalance between proteolytic enzymes and their inhibitors, which, apparently, is the main reason for the development of emphysema in smokers. An important role in the etiology of COPD is played by environmental pollution and various occupational factors. The degree of air pollution is especially high in industrial densely populated cities, especially with the formation of sedentary air masses. In this case, a significant increase in the number of exacerbations of COPD can be observed. Air mainly pollutes SO2 and ozone, resulting from incomplete combustion of combustible substances and exposure to UV radiation with the release of oxidants. Some harmful substances (nitric oxide, carbon monoxide), irritating to the respiratory tract, are formed in apartments when using gas stoves. Irritation of the bronchial mucosa and hypersecretion of mucus is caused by many organic (cotton, grain, etc.) and inorganic (cement, coal, cadmium, etc.) dusts that a person comes into contact with during production activities. Occupational dust bronchitis can occur alone or in combination with other occupational diseases, in particular pneumoconiosis. Especially severe consequences are observed when toxic substances (toxic bronchitis) are exposed to the bronchi – phthalic anhydrite, ozone, phosgene, etc. In patients with chronic bronchitis, bronchopulmonary infections are much more common than in healthy individuals, in which the phenomena of airway obstruction increase due to accumulation viscous sputum, swelling and infiltration of the bronchial mucosa. In patients with pulmonary emphysema, any bronchopulmonary infection can be the cause of death as a result of acute respiratory failure. During bacteriological examination of sputum in patients with chronic bronchitis, various types of bacteria and viruses can be detected. Hereditary factors have a greater effect on the development of emphysema than chronic bronchitis. However, in recent years, the possibility of a genetic predisposition to chronic bronchitis in twins has been shown, regardless of bad habits and the degree of air pollution. The specific genetic transmission of such a predisposition is still unknown. In contrast to chronic bronchitis, acute bronchitis (tracheobronchitis, bronchiolitis) most often develops due to viral (influenza, parainfluenza, respiratory syncytial viruses), bacterial (pneumococcus, Pfeiffer’s stick), mycoplasma infection, but also under the influence of chemical (chlorine vapor , nitrogen oxides) and physical (hot air) factors. The main symptoms of acute bronchitis is characterized by enough – paroxysmal dry unproductive cough, is replaced by the painful emergence of a small amount of sputum mucous or muco-purulent character. Body temperature rarely reaches febrile numbers. Symptoms of bronchitis disappear on the 4th-7th day, although a slight cough may persist for 2 weeks. A prolonged course of bronchitis is observed with bacterial superinfection, when antibiotics (ampicillin, erythromycin) are required, as well as in smokers. Smoking, impaired immunological reactivity, adverse environmental factors contribute to the transition of the disease into a chronic form.
Chronic bronchitis is characterized by cough with sputum for at least 3 months a year for more than 2 years. Hypersecretion of mucus is considered to be the cause of the cough, the earliest sign of the disease. The secretion of mucus in the bronchial tree occurs in healthy people, however, its quantity is not enough for sputum formation. In addition, the composition of the mucous secretion is different from normal. Hypersecretion of mucus begins in the large bronchi and may not be accompanied by bronchial obstruction. In the presence of bronchopulmonary infection, sputum becomes mucopurulent or purulent. Depending on the nature of sputum, catarrhal and purulent bronchitis is secreted. Sometimes when sowing sputum, bacteria growth may be observed, despite the absence of pus in secret. Morphologically, in large bronchi, hypertrophy of the glands in the submucosa is detected. As chronic bronchitis persists and progresses, the process extends to smaller bronchi, in which goblet cell hyperplasia, formation of mucous plugs, edema and inflammatory infiltration of the mucous and submucous layers, an increase in smooth muscle cells, and peribronchial fibrosis are observed. The listed structural changes are accompanied by a narrowing of the lumen of the bronchioles and the development of bronchial obstruction. Chronic bronchitis, proceeding with a violation of bronchial obstruction, is often called obstructive. In the early stages of chronic bronchitis, obstruction is partially reversible due to a possible reduction in edema and inflammatory infiltration of the bronchial wall and improved sputum discharge. However, over time, its degree of reversibility decreases as a result of increased fibrosis and other irreversible changes. In some patients with chronic bronchitis, bronchospasm plays a role in the development of transient airway obstruction, which is usually observed against irritation of the respiratory tract and bronchopulmonary infections, chronic bronchitis with a bronchospastic component or chronic asthmatic bronchitis, which is difficult to differentiate from bronchial asthma. In contrast to bronchial asthma, the main symptom of chronic asthmatic bronchitis is a long-term productive cough, asthma attacks join much later. In bronchial asthma, reverse kartinia is observed
Emphysema is characterized by stretching of air spaces distal to the terminal bronchiole. There are two main types of emphysema – centroacinar, in which respiratory bronchioles and alveolar passages in the center of the acinus are affected, and panacinar with the defeat of the entire acinus. Centroacinar emphysema, which is not accompanied by impaired respiratory function, is often detected by autopsy of patients older than 40-50 years, who during life had no clinical and radiological signs of lung damage. Sites of centroacinar emphysema are more often found in men in the upper lobes of the lungs. Signs of limited panacinar emphysema are found in half of people over the age of 70 years. Emphysema (predominantly panacinar) is of clinical importance, accompanied by obstruction of the airways as a result of a decrease in the elastic properties of the acinus and the decline of respiratory bronchioles on exhalation. With common emphysema, the respiratory surface is significantly reduced and ventilation-perfusion disorders develop.
Over a long period of time, the development of pulmonary emphysema was explained by mechanical factors, for example, pulmonary emphysema in musicians playing wind instruments. In 1963, COPD was found to be associated with a deficiency of si-antitrypsin and a model of emphysema was introduced in an animal experiment by introducing proteolytic enzymes from plants into the lungs. These observations have shown that the cause of emphysema can be an imbalance between proteinases and their inhibitors. An increase in the activity of proteolytic enzymes as a result of their enhanced isolation or deficiency of inhibitors is accompanied by the destruction of the structural proteins of the acinus and the violation of the elastic properties of the lung tissue. It is known that in a healthy person, neutrophils and alveolar macrophages in the lungs secrete proteolytic enzymes (primarily elastase) in sufficient quantities for the development of emphysema, but this is prevented by their inhibitors circulating in the blood. The highest level of si-proteinase inhibitor, or ai-antitrypsin (AT), which can be found in bronchoalveolar washout and other tissue fluids is highest in the blood. Glycoprotein AT is synthesized in the liver. It is more correct to call it an ai-proteinase inhibitor, since it has an effect not only on trypsin, but also on other enzymes. There are more than 80 phenotypes of AT, the synthesis of which is encoded by genes located on the 14th chromosome. In 90% of people, the M-phenotype AT (genotype MM) is detected. In individuals with the AT Z-phenotype (ZZ genotype), as a result of the replacement of glutamic acid in the amino acid chain with lysine, AT accumulates in the endoplasmic reticulum of hepatocytes and is not secreted into the blood. Changes in AT metabolism increase the risk of developing not only pulmonary emphysema, but also liver diseases. In particular, cirrhosis of the liver is observed in 10-20% of patients with Z-phenotype AT over the age of 50 years. Various complex and inaccessible methods are used to determine the level of AT in the blood and its phenotype, however, AT deficiency can also be suspected during electrophoresis of blood serum proteins (the absence of a curve peak in the region of si-globulin).
Chronic bronchitis and pulmonary emphysema develop in parallel and almost always to one degree or another accompany each other, especially since COPD patients often consult a doctor during the advanced stage of the disease, when it is extremely difficult to distinguish between chronic bronchitis and pulmonary emphysema. In this regard, it is more correct to talk about the predominance of emphysema or chronic bronchitis. Accordingly, two clinical types of COPD are distinguished: emphysema and bronchitis.
Patients suffering mainly from pulmonary emphysema have complained of shortness of breath for many years. The cough is slight and is accompanied by the release of only a small amount of sputum. Bronchopulmonary infection rarely joins, but can lead to death as a result of the development of ONE. The appearance of patients is characteristic – thin asthenics with a barrel-shaped chest, which are often called “pink puffs”, given the presence of severe shortness of breath with difficulty wheezing, and the absence of cyanosis. Auxiliary muscles are actively involved in breathing. Such patients usually breathe through closed lips, which prevents the bronchioles from falling down at the end of exhalation due to increased intrabronchial pressure. On examination, signs of severe emphysema are seen: a barrel-shaped chest, weakened voice trembling, boxed percussion sound, lowering of the lower borders of the lungs and decrease in excursion of their lower edge, weakening of vesicular respiration. At the end of the exhalation, dry wheezing can be heard. The boundaries of the relative dullness of the heart are determined with difficulty or not at all. Heart sounds are muffled. Patients are characterized by tympanic fingers, nails of Hippocrates. When examining the function of external respiration, an increase in OEL due to the residual volume is observed, while the VC decreases. FEV1 and diffusion capacity of the lungs are also sharply reduced. Due to rapid breathing, the values of PaCO2 and PaCO2 are not significantly changed. Patients with pulmonary emphysema sometimes have no objective symptoms and radiological changes. Thus, changes in radiographs appear only with panacinar emphysema, involving at least 2/3 of the lung. In severe disseminated pulmonary emphysema, radiographs show an increase in the airiness of the lung tissue, bullous changes, diaphragm prolapse, vertical position of the heart.