Etiology and pathogenesis of COPD. Chronic obstructive pulmonary disease

The following processes play the most important role in the pathogenesis of COPD:

inflammatory process,

imbalance of proteinases and antiproteinases in the lungs,

oxidative stress.

Chronic inflammation affects all departments respiratory tract, parenchyma and vessels of the lungs. Over time, the inflammatory process destroys the lungs and leads to irreversible pathological changes. Enzyme imbalances and oxidative stress may result from inflammation, action environment or genetic factors.

In the pathogenesis of COPD importance has impaired functioning of the local protective system of the lungs. This system is represented by non-specific and specific mechanisms. The action of non-specific defense mechanisms, in particular phagocytosis, is directed against any foreign agent, while specific mechanisms are implemented through local immune response factors. There are several links of the local protective system of the lungs:

mucociliary apparatus - ciliated cells and rheological properties of mucus;

humoral link - immunoglobulins, lysozyme, lactoferrin, antiproteases, complement, interferon;

cellular link - alveolar macrophages (AM), neutrophils and lymphocytes, as well as broncho-associated lymphoid tissue (BALT).

The leading link in the development of the disease is a violation of the escalatory function of the mucociliary apparatus, which is the main protective mechanism of the respiratory tract. It is known that the effectiveness of bronchial cleansing depends on the rheological properties of the bronchial secretion, the coordinated work of the ciliary apparatus, and the contraction of the smooth muscles of the bronchial walls.

Long-term smoking disrupts the escalator function of the mucociliary apparatus. Mucus hypersecretion (one of the earliest signs of COPD) occurs under the influence of tobacco smoke and various kinds of pollutants. At the same time, hypersecretion is combined with a change in the rheological properties of the bronchial secretion, which becomes more viscous and dense due to an increase in sialo-, sulfo- and fucomucins. Viscous sputum, tobacco smoke, pollutants, viral and bacterial toxins suppress the function of cilia and at the same time lead to impaired function of ciliated cells due to the reabsorption of excess mucins from the bronchial lumen.

The change in the viscoelastic properties of the bronchial secretion is accompanied by significant qualitative changes in the composition of the latter: the content of nonspecific components of local immunity in the secretion, which have antiviral and antimicrobial activity - interferon, lactoferrin and lysozyme - decreases. Along with this, the content of secretory IgA decreases. All this leads to a violation of mucociliary transport, the development of mucociliary insufficiency, the accumulation of mucus in the lumen of the bronchi and its subsequent infection with microbial flora.

Violations of mucociliary clearance and the presence of local immunodeficiency create optimal conditions for the colonization of microorganisms. Thick and viscous bronchial mucus with reduced bactericidal potential is a good breeding ground for various microorganisms (viruses, bacteria, fungi). Under certain conditions, these patients have an activation of a respiratory infection. This may be due to reactivation of the autoflora or the result of superinfection with pneumotropic microorganisms, to which COPD patients are highly sensitive.

In parallel with the violation of mucociliary transport in the bronchi, the so-called "oxidative stress" is formed (a combination of increased activity of oxidants and reduced activity of antioxidants), which contributes to the activation of neutrophils during inflammation. Activated neutrophils are the main source of oxygen free radicals (superoxide, hydrogen peroxide, hypochloric acid) in the respiratory tract; in addition, they have increased activity of myeloperoxidase, a circulating neutrophil elastase, in in large numbers concentrated in the lungs under the influence of trigger factors (tobacco smoke causes the migration of neutrophils to the terminal respiratory tract). In COPD, there is an increase in the number of neutrophils, macrophages and T-lymphocytes, mainly CD8+.

Neutrophils. In sputum, bronchoalveolar lavage revealed an increased number of activated neutrophils. Their role in COPD is not yet clear. Smokers without COPD also have sputum neutrophilia. In the study of induced sputum, an increased concentration of myeloperoxidase and human neutrophilic lipocaine is determined, which indicates the activation of neutrophils. During exacerbation, the number of neutrophils in bronchoalveolar lavage also increases. Neutrophils secrete proteinases: neutrophil elastase, neutrophil cathepsin G, and neutrophil proteinase-3.

Macrophages are found in large and small bronchi, lung parenchyma, as well as in places of destruction of the alveolar wall during the development of emphysema, which is detected when histological examination sputum and lavage, bronchial biopsy and induced sputum examination. Macrophages secrete tumor necrosis factor (TNF), interleukin 8 (IL-8), leukotriene-B4 (LTV4), which contributes to the chemotaxis of neutrophils. lymphocytes. CD8+ cells found on bronchial biopsy secrete perforin, granzyme-B and TNF, these agents induce cytolysis and apoptosis of alveolar epitheliocytes.

Eosinophils. The levels of eosinophilic cationic peptide and eosinophilic peroxidase in patients with COPD in induced sputum are increased. This indicates the possibility of their presence. This may not be associated with eosinophilia - an increase in the activity of neutrophilic elastase may cause degranulation of eosinophils in their normal amount.

epithelial cells. Exposure of air pollutants such as nitrogen dioxide (NO2), ozone (O3), diesel exhaust gases to nasal and bronchial epitheliocytes leads to the synthesis and release of inflammatory mediators (eicosanoids, cytokines, [adhesion molecules], etc.). There is a violation of the regulation by epitheliocytes of the functioning of the adhesion molecules of E-selectin, which are responsible for the involvement of neutrophils in the process. At the same time, secretion by a culture of bronchial epithelium cells obtained from COPD patients in the experiment produces lower amounts of inflammatory mediators (TNF-α or IL-8) than similar cultures from non-smokers or smokers, but without COPD.

mediators of inflammation.

Tumor necrosis factor plays a major role in COPD? (TNF-?), interleukin 8 (IL-8), leukotriene-B4 (LTV4). They are able to destroy the structure of the lungs and maintain neutrophilic inflammation. The damage they cause further stimulates inflammation by releasing chemotactic peptides from the extracellular matrix.

LTV4 is a powerful neutrophil chemotaxis factor. Its content in the sputum of patients with COPD is increased. The production of LTV4 is attributed to alveolar macrophages.

IL-8 is involved in the selective involvement of neutrophils and is possibly synthesized by macrophages, neutrophils, and epithelial cells. It is present in high concentrations in induced sputum and lavage in patients with COPD.

TNF activates the nuclear transcription factor-kB (NF-kB), which in turn activates the IL-8 gene in epitheliocytes and macrophages. TNF is determined in high concentrations in sputum, as well as in bronchial biopsies in patients with COPD. In patients with severe weight loss, the level of serum TNF is increased, which indicates the possibility of participation of the factor in the development of cachexia.

Pathophysiological changes in COPD include the following pathological changes:

• - hypersecretion of mucus
• - eyelash dysfunction
• - bronchial obstruction,
• -hyperinflation of the lungs
• - destruction of the parenchyma and emphysema of the lungs,
• -disorders of gas exchange,
• - pulmonary hypertension
• - cor pulmonale.

Bronchial obstruction in COPD patients is formed due to reversible and irreversible components. The reversible component is formed as a result of spasm of smooth muscles, edema of the bronchial mucosa and mucus hypersecretion, arising under the influence of the release of a wide range of anti-inflammatory mediators (IL-8, tumor necrosis factor, neutrophil proteases and free radicals). The irreversible component of bronchial obstruction is determined by developing emphysema, epithelial hyperplasia, hypertrophy of smooth muscle cells and peribronchial fibrosis. Due to the violation of the elastic properties of the lungs, the mechanics of breathing changes and an expiratory collapse is formed, which is the most important cause of irreversible bronchial obstruction. Peribronchial fibrosis - a consequence chronic inflammation; affects the formation of an irreversible component less than emphysema. The development of emphysema leads to a reduction in the vasculature in areas of the lung tissue that are not capable of gas exchange. As a result, the blood flow is redistributed in the preserved areas of the lung tissue, and pronounced ventilation-perfusion disorders occur. The uneven ventilation-perfusion relationship is one of the important elements of COPD pathogenesis. Perfusion of poorly ventilated areas leads to a decrease in arterial oxygenation, excessive ventilation of underperfused areas leads to an increase in dead space ventilation and a delay in CO2 release. Chronic hypoxia leads to compensatory erythrocytosis - secondary polycythemia with a corresponding increase in blood viscosity and impaired microcirculation, which exacerbate ventilation-perfusion mismatches. An important component of the pathogenesis of COPD is the fatigue of the respiratory muscles, which in turn reduces the work of breathing and exacerbates ventilation disorders. Thus, arterial hypoxia develops due to uneven ventilation and violation of ventilation-perfusion relations. The outcome of COPD is the development of precapillary pulmonary hypertension due to vasoconstriction of small pulmonary arterioles and alveolar vessels as a result of alveolar hypoxia. Gradually develops hypertrophy of the right ventricle of the heart. The syndrome of chronic cor pulmonale is formed; with decompensation, it manifests itself first as transient, and then as persistent right ventricular failure.

Chronic obstructive pulmonary disease (COPD), as defined by the European Respiratory Society, is a disorder characterized by a decrease in maximum expiratory airflow and slow forced emptying of the lungs, despite the fact that these signs persist for at least several months, in most cases are slowly progressive and minimally responsive to bonchidilators.

International classification diseases X revision proposes the term COPD instead of COB (chronic obstructive bronchitis). Currently, the concept of COPD often receives a broad interpretation, constituting a group concept that, along with COPD and emphysema, also includes bronchial asthma, bronchiolitis obliterans, cystic fibrosis, and often bronchiectasis (A.G. Chuchalin, 1997; Jeffery P.K., 1997).

Prevalence. COPD is now the fourth leading cause of death in the world and is predicted to increase in its prevalence and mortality in the coming decades. In the United States, according to statistics, the prevalence of COPD is 11,900 per 100,000, and in Russia, 1863.1 per 100,000 population. Low rate incidence in our country is associated with the lack of unified methods of epidemiological research. With age, the incidence of COPD increases. Men get sick more often by 27.4% than women.

Risk factors. The main risk factors for COPD are smoking, hereditary deficiency of α 1 -antitrypsin, occupational dust and chemicals, as well as pollutants, both atmospheric and indoors, respiratory viruses, bacteria, fungi. Other risk factors may be bronchial hyperreactivity, immunological imbalance, socio-economic status.

Pathogenesis. COPD is caused by chronic inflammation of the airways. At the first stage, pathogenic factors affect the cellular elements involved in inflammation (neutrophils, macrophages and T-lymphocytes). Cellular elements secrete a number of substances that have a powerful destructive potential, which, against the background of a decrease in local antiprotease potential, leads to the destruction of the structural elements of the alveoli and the formation of emphysema. In this case, first of all, the sections of the alveolar walls that attach to the terminal bronchioles are destroyed.

In addition to inflammation, two other processes play an important role in the pathogenesis of COPD - an imbalance in the lung proteinase-antiproteinases and oxidative stress. The most pronounced sources of oxidants are smoking (oxidants in cigarette smoke) and endogenous factors (neutrophils and alveolar macrophages). Oxidative stress has a damaging effect on almost all lung structures. Recently, attention has been drawn to the role of nitric oxide in the pathogenesis of lung diseases.

As a result of chronic inflammation, bronchial remodeling occurs, manifested in an increase in the submucosal and adventitious layer, an increase in the size and number of mucous and goblet cells, an increase in the bronchial microvascular network and hypertrophy and hyperplasia of the muscles of the airways.

The most striking pathophysiological manifestation in COPD is the limitation of the flow of exhaled air. This limitation is mostly irreversible due to obstruction at the level of the small and smallest bronchi.

On the later COPD stages pulmonary hypertension develops, leading to the development of cor pulmonale.

pathological anatomy. On a section of the lungs, the walls of the bronchi are thickened due to edema and sclerosis. The lumen of the bronchi is obturated with a mucous or purulent secret. Around the bronchi and blood vessels, pneumosclerosis of varying severity is observed, in places emphysema of the lungs. Changes in the vessels of the lungs occur early, intimal thickening occurs first, followed by smooth muscle hypertrophy and infiltration. vascular wall inflammatory cells.

Microscopic examination of thick sections and ultrastructural examination of lung tissue revealed a reduction in the capillary network of the interalveolar septa. At the same time, there are different stages of this process from the narrowing of part of the capillaries to the complete obliteration of the lumen of most of the capillary network of the alveoli with pericapillary sclerosis. The consequence of pulmonary hypertension is hypertrophy of the walls of the right ventricle and atrium.

clinical picture. First symptom of COPD is cough, which is often underestimated by patients due to its association with smoking. At first, the cough disturbs periodically, sometimes it happens only at night, then it is present every day. Usually cough is accompanied by the release of a small amount of viscous sputum after a series of cough shocks.

An important symptom is shortness of breath. Initially, shortness of breath is noted only when physical activity or respiratory infections. Subsequently, she worries constantly with little physical activity and at rest. Patients sometimes note wheezing when breathing (wheezing) and tightness in the chest.

In severe cases, there are general symptoms diseases - general weakness, loss of appetite, weight loss, depression, or agitation, during an exacerbation of the disease there may be an increase in temperature to subfebrile.

An objective examination can be noted cyanosis, swelling of the jugular veins. Patients take a forced sitting position, trying to ease breathing. Patients may notice exhalation through closed lips, which serves to slow down the flow of exhaled air and allows more efficient emptying of the lungs. With the progression of the disease, the fingers take the form of "drumsticks", and the nails - "watch glasses", swelling of the ankle joints, which is a sign of the development of cor pulmonale.

At the onset of the disease in the study respiratory system one can note rapid breathing (at rest it is 20 respiratory movements per minute) and the participation of auxiliary muscles in the act of breathing. With concomitant emphysema rib cage acquires a barrel-shaped form, the percussion tone has a box shade. In areas of the perifocal inflammatory infiltration dullness is determined. Breathing is weakened, vesicular or hard, dry whistling rales are heard, sometimes moist, muffled rales.

From the side of cardio-vascular system one can note percussion an expansion of the relative dullness of the heart to the right and an increase in the area of ​​the absolute dullness of the heart. The first tone at the second point of the auscultation point is weakened, the accent of the second tone is heard at the fourth point. Sometimes symptomatic arterial hypertension is determined.

Blood tests are rejected only with exacerbations of concomitant inflammatory diseases respiratory system - leukocytosis, neutrophilic shift to the left, increased ESR. With thickening of the blood (erythrocytosis), a slowdown in ESR is observed.

Sputum examination reveals its great variability and depends on concomitant pathology (bronchitis, bronchial asthma, bronchiolitis).

The leading role in the diagnosis and determination of the severity of COPD is the study of the function external respiration using spirometry (determined by FEV 1, VC and FEV 1 / VC); sometimes tests with bronchodilators (β 2 -agonists and anticholinergics) are used. The degree of spirometric abnormalities usually correlates with the severity of the disease. At FEV 1<40% рекомендуется измерять напряжение газов артериальной крови (SaO 2 и CO 2).

X-ray examination makes it possible to make a differential diagnosis with other lung diseases similar in clinical and laboratory data, to monitor changes in the lungs throughout the patient's life. In the study of subtle signs of changes in the lung parenchyma, computed tomography is used. Bronchoscopy is not mandatory for patients with COPD. It is carried out to assess the condition of the bronchial mucosa and for differential diagnosis with other lung diseases.

In determining cor pulmonale, radiography, ECG, echocardiography and magnetic resonance imaging are used.

Flow. COPD is usually a progressive disease. Most often, infections of the upper respiratory tract, pneumonia, exacerbations of chronic bronchitis and other diseases of the broncho-pulmonary system lead to a deterioration in the condition and an increase in shortness of breath. Lung function deteriorates over time, even with adequate medical care.

During COPD, the following stages are distinguished: stage 0 (risk of developing the disease); stage I (mild stage) - chronic cough and sputum production are characteristic, FEV 1 is equal to or greater than 70% of due; stage II (moderate) - the appearance of shortness of breath and usually a visit to the doctor, FEV 1 is equal to 50-69% of the due; stage III (severe) - continued cough and sputum production, shortness of breath at rest, FEV 1 is equal to 35-49% of due; stage IV (extremely severe), FEV 1 equal to or less than 35% predicted.

Complications. Acute respiratory failure, development of bullous emphysema, pulmonary embolism, development of cor pulmonale.

Treatment. With exacerbations of the disease, treatment of patients is carried out in a hospital. Indications for hospitalization are an increase in dyspnea, the inability to stop the exacerbation with the initially used drugs, serious concomitant diseases, first manifested cardiac arrhythmias, and old age.

In acute respiratory failure, artificial lung ventilation is performed. One of the most important non-pharmacological methods of treatment, especially at an extremely severe stage, is oxygen therapy.

Bronchodilators are widely used as symptomatic therapy:

a) anticholinergics - atrovent, troventol; b) β 2 -adrenergic stimulants - drugs, the dose and frequency of their use are given in table 10a.

Treatment with β-adrenergic agonists for exacerbations of COPD begins inhalation in the form of metered-dose aerosols with a spacer or solutions sprayed through a nebulizer. Recently, combinations of β 2 -agonists and atrovent (berodual, combivent, etc.) have been used to improve bronchial patency; c) methylxanthines - theophylline.

Glucocorticosteroids (prednisolone, hydrocortisone) are used to stop severe exacerbations and outside the exacerbation of the disease as maintenance treatment with a positive response to therapy. It should be remembered that not all patients are sensitive to hormone therapy. Therefore, trial treatment is carried out to identify patients responding to steroid therapy. Glucocorticoids are prescribed in short courses parenterally and orally to relieve acute severe exacerbation of the disease and inhaled (benacort, glucocort, icosteroid, budesonide) for maintenance treatment.

Table 10a

Date added: 2014-12-12 | Views: 1148 | Copyright infringement

The pathogenic basis of COPD is:

¾ chronic inflammatory process of the respiratory tract, lung parenchyma and blood vessels, including phases of exudative, productive and sclerotic processes;

¾ oxidative stress;

¾ imbalance in the proteolysis system.

The concept of a systemic inflammatory response in COPD is relatively new. In the early stages of the disease, the inflammatory process in the airways, provoked by tobacco smoke and industrial pollutants, can be reversible. However, over time, airway inflammation takes on a chronic, persistent course. The main localization of inflammation in COPD is the small airways, but active inflammation is also present in the large bronchi, and in the lung parenchyma, and in the pulmonary vessels. In COPD, a frequent finding is an increase in the level of inflammatory markers in the peripheral blood: C-reactive protein, fibrinogen, leukocytes, pro-inflammatory cytokines IL-1β, IL-6, IL-8, tumor necrosis factor - TNFα (1,2). The relationship between local and systemic inflammation is carried out by:

1. release of stress-induced cytokines and free radicals from the bronchopulmonary system into the systemic circulation;

2. activation of peripheral blood leukocytes;

3. stimulation of the bone marrow and liver with pro-inflammatory mediators released by inflammatory cells.

Stimulation of these organs leads to even greater production of leukocytes, platelets, CRP and fibrinogen. However, the exact mechanisms of systemic inflammation in COPD are not well understood.

The severity of the inflammatory response in patients with COPD increases as the disease progresses and FEV1 decreases.

Oxidative stress develops with a powerful release of neutrophils, followed by the release of an unreasonably large amount of oxygen free radicals into the airways, which have a damaging effect on all structural components of the lungs. Subsequently, this leads to irreversible changes in the lung parenchyma, respiratory tract and pulmonary vessels. Changes in the structure of tissues and protein components caused by oxidants lead to impaired immune response, contractile properties of bronchial smooth muscles, function of β-adrenergic receptors, stimulation of bronchial secretions, activation of mast cells, increased pulmonary vascular permeability, inactivation of α 1 -proteinase inhibitor and secretory leukoprotease inhibitor. inhibitor.

An imbalance of proteases and antiproteases also contributes to irreversible changes in the lung tissue in patients with COPD. Imbalance of proteases and antiproteases in COPD may occur due to overproduction of proteases and suppression of antiprotease activity. Sources of proteases in the lungs are direct participants in inflammation - macrophages and neutrophils, and to some extent - bronchial epithelium. The most studied protease is neutrophil elastase (NE), which is involved in the natural degradation of proteins of the extracellular matrix of the lung parenchyma - elastin, collagen, fibronectin, laminin, proteoglycans. NE is a powerful inducer of mucus secretion and hyperplasia of the mucous glands. It is also an active component of infectious defense, participating in the breakdown of the protein structures of the bacterial wall. The release of NE from neutrophils into the extracellular space occurs under the influence of various substances: cytokines (TNFα, IL8), lipopolysaccharides, fragments of the bacterial wall.

The group of antiproteases that oppose the destructive action of proteases includes alpha-one antitrypsin (AAT), α 2 - macroglobulin, cystatins, secretory leukoproteinase inhibitors and tissue inhibitors. Loss of the ability of AAT to neutralize excessive amounts of NE leads to damage to the elastic framework of the lungs and the development of emphysema. There are two main types of emphysema that can form within the acinus:

1. centriacinar, accompanied by expansion and destruction of respiratory bronchioles;

2. panacinar, leads to the destruction of the entire acinus.

Centriacinar emphysema is most characteristic of COPD, often forming in the upper lungs. Panacinar emphysema is more common in patients with alpha-1 antitrypsin deficiency and is localized in the lower lung. In the early stages of the disease, these changes are microscopic and can be detected by random histological studies. In the future, with the progression of the disease, they can develop into macroscopic lesions with the formation of bullae (from 1 to 5 cm in diameter).

Thus, inflammation, oxidative stress and imbalance in the proteolysis system are important in the development of COPD (Fig. 1)

Fig.1. COPD pathogenesis

There is a certain phasing in the manifestation of clinical and morphological symptoms: the disease begins with mucus hypersecretion followed by dysfunction of the ciliated epithelium, bronchial obstruction develops, which leads to the formation of pulmonary emphysema, impaired gas exchange, respiratory failure, pulmonary hypertension and the development of cor pulmonale.

These data show that, according to etiopathogenesis and morphology, COPD is the result of chronic bronchitis and pulmonary emphysema with progressive irreversible broncho-obstructive syndrome.

12. Clinical picture. The clinical picture of COPD is characterized by the same type of clinical manifestations - cough and shortness of breath, despite the heterogeneity of the diseases that make it up. The degree of their severity depends on the stage of the disease, the rate of progression of the disease and the predominant level of damage to the bronchial tree. The rate of progression and severity of symptoms of COPD depends on the intensity of exposure to etiological factors and their summation. Thus, the standards of the American Thoracic Society emphasize that the appearance of the first clinical symptoms in patients with COPD is usually preceded by smoking at least 20 cigarettes a day for 20 years or more. The first symptoms that patients usually seek medical attention for are cough and shortness of breath, sometimes accompanied by wheezing with sputum production. These symptoms are more pronounced in the morning. The earliest symptom, appearing by the age of 40-50, is a cough. By the same time, in the cold seasons, episodes of a respiratory infection begin to occur, which are not initially associated with one disease. Dyspnea felt on exertion occurs on average 10 years after the onset of cough. However, in some cases, the onset of the disease with shortness of breath is possible. Sputum is secreted in a small amount (rarely more than 60 ml / day) in the morning, has a mucous character. Exacerbations of an infectious nature are manifested by the aggravation of all signs of the disease, the appearance of purulent sputum and an increase in its amount. It should be emphasized that bronchopulmonary infection, although frequent, is not the only cause of exacerbation. Along with this, exacerbations of the disease are possible, associated with an increased effect of exogenous damaging factors or with inadequate physical activity. In these cases, signs of infection of the respiratory system are minimal. As COPD progresses, the intervals between exacerbations become shorter. Shortness of breath can vary over a very wide range: from feeling short of breath during normal physical exertion to severe respiratory failure.

13. Objective examination. The results of an objective study of COPD patients depend on the severity of bronchial obstruction and emphysema. As the disease progresses, wheezing is added to the cough, most noticeable with accelerated exhalation. Often, auscultation reveals dry rales of different timbres. As bronchial obstruction and pulmonary emphysema progress, the anterior-posterior size of the chest increases. With severe emphysema, the appearance of the patient changes, a barrel-shaped chest appears (an increase in the anteroposterior direction). In connection with the expansion of the chest and the upward displacement of the clavicles, the neck seems short and thickened, the supraclavicular fossae protrude (filled with expanded tops of the lungs). On percussion of the chest, a boxed percussion sound is noted. In cases of severe emphysema, absolute dullness of the heart may not be completely determined. The edges of the lungs are displaced downward, their mobility during breathing is limited. As a result, a soft, painless edge of the liver may protrude from under the edge of the costal arch with its normal size. The mobility of the diaphragm is limited, the auscultatory picture changes: weakened breathing appears, the severity of wheezing decreases, exhalation lengthens.

The sensitivity of objective methods to determine the severity of COPD is low. Among the classic signs are wheezing and prolonged expiratory time (more than 5 seconds), which indicate bronchial obstruction. However, the results of an objective examination do not fully reflect the severity of the disease, and the absence of clinical symptoms does not exclude the presence of COPD in a patient. Other signs, such as incoordination of respiratory movements, central cyanosis, also do not characterize the degree of airway obstruction. In mild COPD, respiratory pathology is usually not detected. Patients with moderate disease may have dry rales or slightly decreased breathing (a sign of emphysema) on examination of the respiratory organs, but it may not be possible to determine the severity of airway obstruction from these symptoms. With the loss of the reversible component of obstruction, persistent signs of respiratory failure dominate, pulmonary hypertension increases, and chronic cor pulmonale is formed. It is difficult to identify signs of compensated cor pulmonale during physical examination. As the disease progresses, first transient, and then permanent hypoxia and hypercapnia are observed, blood viscosity often increases, which is due to secondary polycythemia. A decompensated cor pulmonale develops. For patients with severe COPD, aggravation of dyspnea, diffuse cyanosis, and weight loss are characteristic.

There are two clinical forms of the disease - emphysematous and bronchitis.

emphysematous form(type) COPD is associated predominantly with panacinar emphysema. Such patients are figuratively called "pink puffers", because in order to overcome the prematurely occurring expiratory collapse of the bronchi, exhalation is made through lips folded into a tube and is accompanied by a kind of panting. The clinical picture is dominated by dyspnea at rest due to a decrease in the diffusion surface of the lungs. Such patients are usually thin, their cough is often dry or with a small amount of thick and viscous sputum. The complexion is pink, because. sufficient oxygenation of the blood is maintained by increasing ventilation as much as possible. The limit of ventilation is reached at rest, and patients tolerate physical activity very poorly. Pulmonary hypertension is moderately pronounced, because. the reduction of the arterial bed, caused by atrophy of the interalveolar septa, does not reach significant values. Cor pulmonale is compensated for a long time. Thus, the emphysematous type of COPD is characterized by the predominant development of respiratory failure.

Bronchitis form(type) observed in centriacinar emphysema. Constant hypersecretion causes an increase in inspiratory and expiratory resistance, which contributes to a significant violation of ventilation. In turn, a sharp decrease in ventilation leads to a significant decrease in the content of O 2 in the alveoli, followed by a violation of the perfusion-diffusion ratios and blood shunting. This determines the characteristic blue tint of diffuse cyanosis in patients of this category. Such patients are obese, the clinical picture is dominated by cough with copious sputum. Diffuse pneumosclerosis and obliteration of blood vessels lead to the rapid development of cor pulmonale and its decompensation. This is facilitated by persistent pulmonary hypertension, significant hypoxemia, erythrocytosis and constant intoxication due to a pronounced inflammatory process in the bronchi.

The selection of two forms has prognostic value. Thus, in the later stages of the emphysematous type, decompensation of the cor pulmonale occurs in comparison with the bronchitis variant of COPD. In clinical conditions, patients with a mixed type of disease are more common.

Thus, COPD is characterized by a slow, gradual onset, the development and progression of the disease occurs under the influence of risk factors. The first signs of COPD are cough and shortness of breath, other signs join later as the disease progresses.

Chronic obstructive pulmonary disease (COPD) is a disease that causes a reduction in airflow in the airways.

Initially, pathology occurs in the bronchial mucosa, where there is a violation of bronchial secretions.

To this process infection is added which, in the end, leads to destructive processes in the respiratory system. Smoking is considered the main reason.

COPD pathogenesis

The pathogenesis of COPD is characterized inflammatory reactions, proteinase imbalance and antiproteinase, oxidative stress.

Inflammatory process of chronic type covers most areas of the respiratory system. The course of the disease over time leads to the destruction of lung tissue and irreversible consequences. Inflammation of other factors is also due to external and internal causes.

Due to the inflammatory process, the number of cells that affect the respiratory organs increases. They call pathogen imbalance.

plays an important role in the development of the disease tumor necrosis factor and interleukin, which destroy the pulmonary system and increase neutrophilic inflammation.

In the process of defeat, the disease produces oxidants that destroy proteins, fats, nucleic acids, as well as lead to cell death.

Etiology and clinic of the disease

The mechanisms of development of COPD are associated with exposure to risk factors. As a result the mucous membrane of the bronchi becomes inflamed, hypersection of sputum increases. This leads to edema and further spread of inflammation, and, finally, to narrowing and obstruction of the bronchi.

Reference. The order of pathogenic events is from primary and secondary mechanisms.

If the disease is not treated in time, it will lead to to inflammation of the respiratory tract, immunodeficiency, and then to destruction of the pulmonary system.

A patient with COPD has excessive bronchial secretion, hypersection of sputum and an increase in macrophages, neutrophils and CD + 8-lymphocytes.

Risk factors, causes

The etiology and pathogenesis of COPD is based on the device bilateral influence of genetic factors and factors associated with the influence of the external environment.

Important! The question of etiology is under development - scientists are still arguing about this.

The causes of COPD, which no one doubts, include deficiency in the body of alpha-antitrypsin, experts classify smoking as external factors, as well as inhalation of harmful substances, which is associated with work (cadmium, silicon, etc.).

Scientists agree that the disease can also be caused by: birth pathologies, in particular, prematurity, bronchial hyperactivity, heredity.

The external causes of COPD include an unhealthy lifestyle and poor ecology.

The main factor that causes COPD is smoking, and among smokers, the percentage of people with COPD is the highest and is about 80%. Shortness of breath in smokers on average appears 15 years earlier than people who do not lead a similar lifestyle.

The second most common cause of COPD is professional factor, which is caused by the inhalation of harmful impurities in the air - cadmium and silicon.

In this case, the most dangerous are the mining professions.- miners, builders, railway workers, metallurgists; workers who are engaged in the processing of grain, cotton and pulp.

COPD in pathological anatomy

Pathological changes in COPD occur in large and small bronchi, in lung tissue and blood vessels. The source of the development of COPD is the constantly developing inflammation under the influence of smoking and poisonous gases.

In case of damage, the lungs use a fairly strong defensive reaction. They are able to restore the affected areas. These reactions depend on genetic characteristics or on the position of external factors (infections, aerosol pollution of the external environment), which makes the disease chronic and leads to inflammation with periods of partial recovery of damage to the pulmonary organs.

Photo 1. This is how the change in the bronchi in pathological anatomy looks like in the course of the development of COPD disease.

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Pathological processes in pathology

COPD affects central and peripheral airways.

The central airways are trachea, cartilaginous bronchi, small bronchi.

In these organs, inflamed areas are located among the epithelium and in the walls of the glands. Inflammation eventually leads to impaired mucocyl-par clearance. Areas with atrophy and dysplasia of varying degrees are found.

Various pathologies continue to develop in the body ( hypertrophy and hyperplasia of the glands), which leads to an increase in the amount of sputum. The proliferation of fibroblasts increases, which leads to the appearance of lymphoid accumulations.

Often occurs degeneration and calcification of the cartilaginous plates of the bronchi. Changes that occur in the central airways are externally manifested as a cough or large sputum.

Attention! Pathological changes in COPD affect only large bronchi. In small bronchi, changes occur in combination with damage to the peripheral airways.

The peripheral airways include bronchioles with a diameter less than 2 mm. Early changes in respiratory function in COPD are similar to changes in the central airways.

When bronchitis escalates in the body occurs edema of the wall and hypersecretion of mucus. The most important sign of COPD is the progressive narrowing of the bronchioles.

Chronic exposure to cigarette smoke causes repeated cycles of destruction and restoration of elements of the bronchial wall.

Damage occurs due to the effect of toxic damaging substances on the epithelium of the bronchioles. Although the modes of repair in the walls of bronchioles are not well understood, it is believed that errors in the course of repair lead to a change in the structure of the peripheral airways.

This is mainly due to cigarette smoke, which damages the regeneration system and affects the structure of the entire lung tissue.

Peripheral airways affect the dysfunction of external respiration, which leads to an increase in bronchial resistance. As a result emphysema develops. Fibrosis in the walls of bronchioles is regulated by mediators of inflammatory effector cells.

Reference. These include TNF-a, ET-1, insulin-like growth factor-1, fibronectin, platelet-releasing growth factor-1.

COPD Prevention Methods

COPD prevention is primary and secondary.

For primary prevention, the patient needs:

• Give up cigarettes. He may see a doctor or use various nicotine replacement substances.
• Stop interacting with occupational polluters. If possible, change the place of work and place of residence.
• Avoid passive smoking from childhood.
• Treat SARS early. Go to the hospital if you have symptoms of bronchitis or pneumonia. Do not self-medicate.
• Harden the body.
• Maintain order and cleanliness at home and at work.
• do physical exercises, helping to improve breathing.

Primary prevention will help prevent the disease, but if a person is already exposed to COPD, then It is recommended to follow the instructions for secondary prevention:

• Strengthen immunity.
• Find out the nature of the pathology, risk factors, arm yourself with a memo.
• Undergo bronchodilator therapy.
• Vaccinate and revaccinate pneumococcal and influenza infections. This is especially recommended for patients after 65 years.
• Attend vitamin therapy courses, medical therapy and respiratory gymnastics.
• Get treated in special sanatoriums.

Secondary prevention also provides for the provision of normal working conditions to the patient. it reduces the frequency and intensity of relapses.

Treatment of the disease, relief of symptoms

Since the disease is constantly evolving, complete recovery cannot be achieved. Because of this, COPD treatment permanent, complex and continuous.

General recommendations play an important role in therapeutic therapy:

• To give up smoking.
• Change of work to less harmful to health.
• Swimming.
• Walks in the open air.
• Attending special events.

Drug treatment is prescribed by selecting therapy, which is characterized by the use of inhaled medications that expand the airways. In the treatment of COPD, drugs based on:

• Tiotropium bromide ( Spiriva, Tiotropium native). Important: contraindicated in children.
• Formoterol ( Foradil, Oxys, Turbuhaler, Atimos).
• Salmeterol (C erevet, salmeterol).

These drugs are available in the form of inhalers, nebulizer solutions, and powders. Indicated for moderate to severe COPD. From tablets, doctors prescribe medications based on theophylline - Theopec, Theotard.

Important! The use of hormonal drugs is indicated with little effectiveness of basic therapy.

In addition to systemic glucocorticosteroids, inhaled ones are also prescribed:

• Beclazon-ECO.

Photo 2. The drug Beclazon-ECO in the form of an aerosol for inhalation, dosage 250 mcg / 1 dose. Manufacturer Teva.

• Pulmicort.
• Flixotide.

Hormonal bronchodilators:

• Seretide.
• Symbicort.

If COPD worsens, then the following are used:

• Broad spectrum antibiotics ( Amoxiclav, Fromilid UNO, Ceftriaxone, Zoflox).
• Expectorants (Lazolvan, Ambrokegsal, Fluditec).
• Antioxidants ( Fluimucill, ACC).

Treatment for exacerbation takes place on an outpatient basis. Severe exacerbation requires hospital treatment.

Sudden attacks of COPD, which are characterized by pronounced shortness of breath, require the use of inhaled drugs for the treatment of short-acting COPD. For such cases, it is important to have Berodual N and Atrovent.

Photo 3. The drug Atrovent N in the form of an aerosol for inhalation, one dose of 20 mcg. Manufactured by Boehringer Ingelheim.

Surgery is the last resort. It is carried out with the ineffectiveness of conventional treatment. In this case, two types of operations are carried out:

• Bullectomy.
• Lung transplant.

Useful video

Watch a video that explains what COPD is and its main symptoms.

Conclusion

So, the main causes of COPD are smoking, heredity and polluted environment. To avoid pathology and prevent it, it is important to lead a healthy lifestyle, carefully monitor your health. If the disease has already begun, you should not treat it negligently, this will help to avoid complications and weaken the pathology.

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General information

The GOLD program (Global strategy: diagnosis, treatment and prevention of chronic obstructive pulmonary disease, 2003), based on the report of the working group of the National Heart, Lung and Blood Institute (USA) and the World Health Organization, gives the following definition chronic obstructive pulmonary disease (COPD): “COPD is characterized by airflow limitation that is not completely reversible.

Airflow limitation is usually progressive and is caused by an abnormal reaction of the lungs to exposure to various noxious particles and gases.

In our opinion, this definition reflects only some pathophysiological and etiological aspects of the disease and cannot satisfy the clinician. It does not contain the essence of the disease.

The most appropriate definition of the disease is the definition of COPD, which is given by the All-Russian Scientific Society of Pulmonologists:

Chronic obstructive pulmonary disease - a primary chronic inflammatory disease with a predominant lesion of the distal respiratory tract, lung parenchyma and the formation of emphysema; it is characterized by airflow limitation with the development of irreversible (or not completely reversible) bronchial obstruction caused by a productive non-specific persistent inflammatory reaction.

The disease develops in predisposed persons and is manifested by cough, sputum and increasing shortness of breath, has a steadily progressive character with an outcome in chronic respiratory failure and cor pulmonale. This formulation includes the inflammatory nature of the disease, damage to the lung parenchyma along with the airways, and the steady progression of partially reversible obstruction.

As is known, the defeat of the distal respiratory tract is the most typical for chronic obstructive bronchitis (COB). In COPD, lesions of the distal bronchi are associated with COPD. Therefore, COB, along with secondary pulmonary emphysema, is included in the concept of chronic obstructive pulmonary disease. In this regard, the American Thoracic Society gives the following definition: “COPD is a disease state characterized by the presence of bronchial obstruction due to chronic bronchitis and emphysema; the obstruction is progressive, may be accompanied by bronchial hyperreactivity, and may be partially reversible.”

Thus, "chronic obstructive bronchitis" and "emphysema" are included in the formulation of chronic obstructive pulmonary disease, so they should not be attributed to the diagnosis of COPD, because without chronic obstructive bronchitis and emphysema lung COPD does not exist. Another thing is that the degree of development of emphysema may be different depending on the stage of development of the disease.

As will be seen from the following presentation, chronic obstructive pulmonary disease is a widespread disease, but at the same time, such a diagnosis began to be made only in the most recent years. In this regard, the question arises: is COPD a new disease or a new name for an “old” disease? Oddly enough, this question cannot be answered unambiguously. COPD is a new disease, the doctrine of which has developed as a result of the revision and change in ideas about the "old" disease - chronic obstructive bronchitis.

Previously, this disease was diagnosed as COB, which is known to be complicated very early by secondary (obstructive) pulmonary emphysema. So, in 1995, when the diagnosis of COPD in the United States had just begun to be made by doctors, 14 million patients with COPD were identified, and 12.5 million of them were diagnosed with COPD.

Another question arises: has there been a substitution of one term (COB) for another (COPD) and is it possible to leave the former term to refer to the disease? We can safely say that the term COB does not fully reflect the essence of the disease, in which there is a lesion not only of the airways, but also of the lung parenchyma.

It is incorrect to call this disease chronic obstructive bronchitis even in the early stages, when pulmonary emphysema is not yet clearly defined: firstly, chronic obstructive pulmonary disease as an independent nosological unit begins with the simultaneous inclusion in the process of all pathogenetic mechanisms, both bronchial and parenchymal, and , secondly, it is incorrect to name the same disease differently at different stages of development.

The cumulative concept of "Chronic obstructive bronchitis. Pulmonary emphysema and COPD are also not equivalent, because bronchitis and pulmonary emphysema do not reflect the entire volume of pathological conditions in the airways and lung parenchyma in COPD. The key element of COPD is a chronic inflammatory process, which involves all the morphological structures of the bronchi of different sizes, interstitial (peribronchial) tissue, alveoli and blood vessels.

Chronic obstructive pulmonary disease is an independent nosological form. She belongs to the so-called obstructive pulmonary disease (OBD), occupying the first place in its frequency. Therefore, when establishing the diagnosis of COPD, other OPDs should be excluded: bronchial asthma, cystic fibrosis, bronchiolitis, bronchiectasis (with secondary bronchitis).

Based on the foregoing, the diagnosis of "chronic obstructive bronchitis" as a primary disease has no right to exist and should not be made by doctors.

social significance

COPD is a disease of the second half of life and more often develops after 45, especially after 55 years. Among people over 55 years of age, the prevalence of COPD in the United States reaches 10%. The disease is more common in men, but in countries where the prevalence of smoking among men and women is approximately the same, this difference is blurred.

It should be noted that data on the prevalence of COPD in various countries are inaccurate (underestimated), since the disease is usually diagnosed at a late stage, with a detailed clinical picture, forcing the patient to seek medical help.

According to official medical statistics, there are about half a million patients with COPD in the Russian Federation, while according to the results of selective epidemiological studies, the number of these patients should be from 5 to 10 million.

COPD as a cause of death in the age group over 45 in developed countries ranks 4-5th and is among the main causes in the structure of mortality. In Russia, the mortality rate for men is 142 per 100,000 (data from 1995).

In many countries, including the Russian Federation, both the prevalence of the disease and mortality from COPD have a steady upward trend. For every hundred patients, 12-15 new cases of COPD are diagnosed annually.

Due to the fact that COPD inevitably leads to the development of pulmonary insufficiency, chronic cor pulmonale with its subsequent decompensation, the disease is one of the most common causes of temporary and especially permanent disability. The economic cost per patient is 3 times higher than for asthma, and in the United States exceeds $1,500 per patient per year.

In accordance with international studies within the framework of the Global Damage from Diseases project, COPD among the causes of death and disability by 2020 will take 5th place among all diseases in the world - after ischemic heart disease (CHD), depression, traffic accidents and cerebrovascular disease.

In the ICD 10th revision, COPD is designated as follows:

J 44.0 - COPD in the stage of exacerbation of viral etiology (except for the influenza virus).

J 44.1 - COPD in the acute stage without specifying the cause of the exacerbation.

J 44.8 - COPD, severe course (mainly bronchitis or emphysematous type), respiratory failure (RD) III with or without congestive heart failure (CHF).

J 44.9 - unspecified COPD, severe. Chronic cor pulmonale. DN III, CHF II or III degree.

Etiology and pathogenesis. Pathomorphology

Tobacco smoke pollutants should be put in the first place. In 80-90% of patients, the development of COPD is associated with smoking. Tobacco smoke contains about 4,000 toxic substances in solid, dissolved and gaseous states. The development of the disease is mainly due to the influence of the gas component of tobacco smoke, which includes carbon monoxide, hydrogen cyanide, nitric oxide, etc., however, other components of tobacco smoke also have a pathogenic effect. Passive smoking can also lead to the development of COPD. Along with this, both active and passive smoking causes an increase in the sensitivity of the bronchi and a more rapid development of COPD when exposed to other etiological factors.

The second place is occupied by pollants of an industrial-production nature. These include organic (cotton, linen, flour, peat) and inorganic dust (cement, lime, coal, quartz, etc.), as well as toxic vapors and gases (various acids, chlorine, sulfur dioxide, carbon monoxide, ozone, harmful substances formed during gas and electric welding). Currently, among professional etiological factors, cadmium and silicon are considered the most pathogenic.

Let's name the main professions associated with an increased risk of developing COPD: miners; construction workers associated with cement; workers in the metallurgical industry (hot metal working); workers engaged in the processing of grain, cotton and paper production; railroad workers. Chronic bronchitis and COPD, which develop in workers in hazardous professions, are occupational diseases. For their development, smoking has a potentiating effect.

The cause of the disease may be pollution of the ambient air by pollutants, among which, according to WHO, sulfur dioxide, nitrogen oxides and ozone are of primary importance. Determining the concentration of these substances is used to assess air pollution. Pollution can be caused by the release into the atmosphere of products of incomplete combustion of various types of fuel, vehicle exhaust gases and chemical production products.

With long-term (usually 10-20 years) exposure to the above etiological factors, COPD develops in about 20% of people, while the duration of exposure required for the development of the disease in individual patients can vary significantly. In this regard, the importance of internal risk factors is indicated, in the presence of which the inhalation of pollutants leads to a more rapid development of the disease. The duration of inhalation of pollutants necessary for the development of the disease depends on the degree of their severity. In particularly unfavorable cases, COPD can develop as early as a few years after the start of smoking.

Internal risk factors include insufficiency of protective, in particular immune mechanisms, an imbalance in the protease-inhibitor system, mainly due to a genetically determined deficiency. alpha 1 -antitrypsin (AAT). However, in the United States, congenital AAT deficiency has been identified in only 1% of patients with COPD. According to some authors, congenital (more often) or acquired increased sensitivity and hyperreactivity of the bronchi to the action of external stimuli is much more important for the development of the disease.

One of the reasons for the development of COPD is chronic inflammatory diseases of the bronchopulmonary system that occur in childhood and continue in the future. In these cases, it is more often not COPD that develops, but an obstructive syndrome (obstructive pulmonary disease) associated with bronchiolitis, as well as secondary bronchitis in bronchiectasis and cystic fibrosis. But in rare cases, especially with congenital deficiency in 1-antitrypsin and ciliary dyskinesia syndrome, COPD can also develop.

The pathogenesis of COPD is associated with the impact of etiological factors on the bronchi, including distal bronchi with a diameter of less than 2 mm, including respiratory bronchioles, on the lung parenchyma (alveoli) and pulmonary vessels (arterioles, capillaries, venules).

The first stage of such an impact is the formation in these structures of a chronic inflammatory process associated with activation under the influence of etiological factors of cells involved in inflammation. The key role belongs to neutrophils, the protective role of which is distorted under the influence of smoking and other pollutants.

Under these conditions, neutrophils, the number of which sharply increases when exposed to pollutants, begin to secrete pro-inflammatory mediators that have a chemotactic effect on other neutrophils, vasoactive prostaglandins, and a number of substances that have a powerful destructive effect, mainly proteases (elastase) and oxygen radicals.

Along with neutrophils, macrophages, T-lymphocytes, eosinophils and epithelial cells are involved in the formation of inflammation. They secrete mediators that enhance neutrophilic inflammation: tumor necrosis factor, interleukin-8 and leukotriene B4.

A chronic inflammatory process develops primarily in the respiratory tract, especially in the distal sections. Catarrhal, catarrhal-purulent (with the addition of a secondary infection) inflammation of the bronchial epithelium in the trachea, lobar, segmental, subsegmental bronchi and bronchioles develops.

Along with inflammation, in the pathogenesis of COPD, a large role is played by an increase in lipid peroxidation, the so-called oxidative stress, that is, the release of a large amount of free radicals that exceed physiological needs, which have a powerful damaging effect. Tobacco smoke (and other etiological factors) is the most studied exogenous source of oxidants due to the content of O 2 , O 3 , OH, H 2 O 2 , NO, HOCl. A large number of oxidants are also secreted by the main "inflammatory cells" (with their function perverted!) - neutrophils and macrophages.

Inflammation of the bronchi leads to hypertrophy of the tracheobronchial glands, hyperplasia and metaplasia of goblet cells, an increase in submucosal glands, which is accompanied by hyperproduction of bronchial mucus with an increase in its viscosity and deterioration of rheological properties, and damage and a decrease in the number of cells of the ciliated epithelium as a result of inflammation makes it difficult to evacuate this mucus, as a result which part of the mucus is constantly retained in the respiratory tract.

Mucociliary insufficiency develops, that is, the insufficiency of the function of the ciliated epithelium to secrete mucus (from lat. mucus - mucus + lat. cilium - eyelash). Mucociliary insufficiency is an early pathogenetic mechanism of COPD, it is associated with the appearance of the first clinical symptoms of the disease - cough and sputum.

Due to inflammation and the damaging effect of oxidants, the local antiprotease potential is depleted, and protease inhibitors are inactivated. Under these conditions, elastase destroys the structural elements of the alveolar walls, and emphysema is formed. Thus, pulmonary emphysema develops from the early stages of COPD, in parallel with the inflammatory process in the bronchi. In this regard, pulmonary emphysema should not be considered a complication, but an obligatory manifestation of the disease.

More often, a centrilobular form of emphysema develops, initially in the upper parts of the lungs with further spread to other parts of the lungs. Subsequently, emphysema may acquire a panacinar and panlobular character.

Violation of the elastic properties of the lungs due to emphysema is associated with a violation of the mechanics of breathing, an increase in intrathoracic pressure with the formation of an expiratory collapse of small bronchi and bronchioles, which is the most important cause of irreversible bronchial obstruction.

The most important factor in the progression of COPD is the inevitable addition of infection. The adhesion of microbes to bronchial mucus mucin and bronchial epithelium with their subsequent colonization and development of infection is facilitated by damage to the integrity of the bronchial epithelium, mucociliary insufficiency, disorders of local and systemic immunity.

The most characteristic signs of local immunodeficiency in COPD, the development of which is associated with the immunosuppressive effect of etiological factors, are a decrease in the production of secretory IgA, lactoferrin, lysozyme and inhibition of the response of T-lymphocytes to standard mitogens. At the same time, at the initial stage of infection, some strengthening of protective mechanisms is observed, and then their depletion develops.

Colonization of bacteria in the respiratory tract already indicates a lack of protective factors, including local immunodeficiency. This provision is the basis for the use of vaccine therapy: in GOLD, vaccination is included in the mandatory list of therapeutic measures at all stages of COPD.

A microbiological study of the distal respiratory tract using a special bronchological technique that protects the obtained material from contamination revealed pneumotropic viruses (respiratory syncytial virus, adenoviruses, influenza viruses) in 30% and bacteria, more often pneumococcus, Haemophilus influenzae and moraxella, in 50%. Accession and activation of a bacterial infection usually follows a viral infection of the respiratory tract.

The persistence of infection is an important factor in the maintenance and progression of the chronic inflammatory process, both directly and to a greater extent due to the activation of the main effector cells: neutrophils, macrophages, lymphocytes, epithelial and endothelial cells. Along with this, it is the most common cause of exacerbation of the disease, which can be regarded as a qualitative leap in its progression. Thus, infection of the respiratory tract can be attributed to the most important factors in the pathogenesis of COPD.

Summarizing the above, we emphasize once again that COPD is based on a non-infectious chronic, steadily progressive inflammatory process. It is observed in both central and peripheral airways, lung parenchyma, and pulmonary vessels. The most important is the defeat of the peripheral airways (bronchioles and small bronchi with an internal diameter of less than 2 mm).

It is with the narrowing (obstruction) of these sections of the respiratory tract that the violation of the function of external respiration according to the obstructive type is associated, and mainly with this - the development of respiratory (pulmonary) insufficiency. The development of respiratory failure, that is, a violation of gas exchange, is associated with a decrease not only in ventilation, but also in diffusion of gases and perfusion. In this regard, damage to the parenchyma (emphysema) and vessels of the pulmonary circulation contribute to the genesis of DN.

Bronchial obstruction in COPD consists of 2 components: reversible and irreversible. The reversible component is associated with those manifestations or consequences of inflammation that can be eliminated as a result of treatment - this is inflammatory edema, mucus hypersecretion, bronchospasm.

The irreversible component of obstruction is due to such manifestations or consequences of inflammation that are not eliminated by treatment. These include fibrotic changes in the wall of the bronchi, bronchioles, and peribronchial tissues, and expiratory collapse of the small bronchi and bronchioles associated with pulmonary emphysema.

As long as the reversible component of the obstruction persists, one can expect to achieve an effect from basic drugs (bronchodilators), mucolytics, and in case of exacerbation of COPD associated with infection, from the appointment of antimicrobial agents. In the absence of a reversible component of obstruction, the emphasis in treatment is on oxygen therapy, improving the function of the respiratory muscles, and preventing and treating infectious exacerbations.

Changes in the pulmonary vessels in COPD in the form of a thickening of the vascular wall due to endothelial proliferation and hypertrophy of the muscle membrane due to inflammation are observed already at an early stage of the disease, even before the onset of disorders functions of external respiration (FVD). Changes in the vascular wall lead to a decrease in the production of nitric oxide (NO) by endothelial cells, which leads to spasm of small arteries and arterioles, an increase in vascular resistance, activates platelet aggregation and favors intravascular thrombosis.

Violation of the endothelial function of inflammatory-modified vessels of the small circle is now of great importance in the genesis of pulmonary hypertension. Apparently, endothelial dysfunction is the first link in the chain of pathogenetic factors of pulmonary hypertension.

In the future, they are joined by the anatomical reduction of the vessels of the pulmonary circulation due to emphysema, in which there is an increase in intra-alveolar pressure, atrophy of the alveolar septa, their rupture, obliteration of a significant part of the pulmonary arterioles and capillaries.

Pulmonary hypertension leads to an increase in vascular resistance in a small circle, an increase in the load on the right ventricle and its hypertrophy (cor pulmonale) with its subsequent decompensation. Here we only emphasize that the development of pulmonary hypertension and cor pulmonale is a natural outcome of COPD.

Saperov V.N., Andreeva I.I., Musalimova G.G.