Chronic obstructive pulmonary disease pathology. Chronic obstructive pulmonary disease - general information, etiology, pathogenesis. Indications for expert advice

The pathogenesis of COPD determines the development of a rather dangerous lung disease, fraught with serious complications. The disease is an urgent problem because of its prevalence and the risk of human disability. Many scientific centers around the world are engaged in the study of the disease and methods of dealing with it.

WHO has developed a number of criteria to help assess the severity of the disease. The established pathogenesis of COPD helps to correctly use these criteria and develop a scheme for the treatment, prevention and rehabilitation of patients.

The essence of the disease

Chronic obstructive pulmonary disease (COPD) is a disease that causes an irreversible reduction in airflow in the respiratory tract. The change in the flow is constantly shifting towards its limitation, and is caused by an inflammatory reaction of the lung tissues to the impact of various particles and gases. Pathology first occurs in the bronchial mucosa, where, in response to pathogenic effects, the secretion of enzymes changes: the production of mucus increases, the separation of bronchial secretions is disturbed. Infection is added to this process, which leads to a series of reflexive reactions that ultimately lead to destructive phenomena in the bronchi, bronchioles and alveoli.

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Etiology of the disease

The etiology and pathogenesis of COPD are based on the mechanism of mutual influence of genetic factors and environmental factors.

The question of the etiology of the disease is still at the stage of controversy and discussion by scientists.

The reasons that do not raise doubts about the reliability include internal parameters - lack of alpha-antitrypsin; external influences - smoking and harmful substances used in professional activities (cadmium, silicon, etc.).

With a high degree of probability, the etiology of COPD is due to the following reasons: internal - birth pathology, in particular prematurity, bronchial hyperreactivity, heredity, elevated levels of lgE; external - harmful impurities in the air, lifestyle and diet, passive smoking, especially in childhood.

Smoking is recognized as the main provoking factor in the development of the disease, and the proportion of COPD patients who smoke reaches 80% of all registered cases of the disease. Shortness of breath caused by this disease appears in smokers by about 40 years, which is almost 15 years earlier than in non-smokers.

The second most common cause of COPD is occupational exposure to dust containing silicon and cadmium.

In this regard, the mining industry is considered the most harmful industry, and the professions included in the maximum risk group are miners, concrete builders, metallurgists, railway workers; workers engaged in the processing of cellulose, grain and cotton.

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Disease pathogenesis

The pathogenesis of COPD is based on the following characteristic processes, such as inflammatory response, proteinase and antiproteinase imbalance, and oxidative stress.

The inflammatory process of a chronic nature extends to most areas of the respiratory system, parenchyma and pulmonary vessels. The chronic course of inflammation leads to the gradual destruction of lung tissues and irreversible pathologies. The remaining two processes of pathogenesis are also due to the development of an inflammatory reaction in combination with the influence of external and internal factors.

As a result of inflammatory reactions, there is a significant increase in the concentration of so-called inflammatory cells: neutrophils, macrophages and T-lymphocytes, causing a pathogenic imbalance. So, neutrophils increase the secretion of different types of proteinase. Macrophages secrete tumor necrosis factor, leukotriene, and T-lymphocytes contribute to the cytolysis of alveolar epithelial cells.

The most significant role in the development of COPD is played by tumor necrosis factor and interleukin, which actively destroy the lung structure and increase neutrophilic inflammation.

In the process of inflammation, oxidants are actively formed that can destroy proteins, fats, nucleic acids that cause cell death.

As a result of oxidative stress, proteinase imbalance increases. Under its influence, bronchial obstruction of a reversible nature is detected.

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pathological physiology

The pathogenesis of COPD develops in the direction of the appearance of such pathological disorders as excessive production of mucus, dysfunction of the cilia, bronchial obstruction, destruction of the parenchyma and emphysema, impaired gas metabolism, pulmonary hypertension, the occurrence of "cor pulmonale", systemic pathologies.

In the process of disease progression, the following main elements of pathological physiology should be noted:

1. Restriction of the movement of air flow, obstruction to the flow. The processes of pathogenesis lead to obstruction of the bronchi, which creates obstacles for the exit of the flow during exhalation; the resulting hyperinflation leads to a decrease in the volume of inhaled air, shortness of breath and premature fatigue, which, in turn, disrupts the contractile functions of the respiratory muscles.
2. Anomaly of gas exchange: hypoxemia and hypercapnia develop, carbon dioxide accumulates and oxygen transport deteriorates.
3. Excessive mucus production: leads to a characteristic cough with phlegm.
4. Pulmonary hypertension: due to spasm of small pulmonary arteries and develops in the later stages of COPD; the progression of pulmonary hypertension leads to atrophy of the right heart ventricle and the appearance of "cor pulmonale".
5. Exacerbation of respiratory manifestations: provoked by the addition of a viral or bacterial infection, exposure to external factors (harmful air components); the inflammatory reaction intensifies, the air flow decreases even more due to increased hyperinflation and the emergence of new sources of resistance to the movement of the flow; ventilation imbalance can lead to complicated hypoxia; exacerbation of respiratory manifestations of COPD may also be due to heart failure, pneumonia.
6. Systemic disorders: violation of the respiratory rhythm and hyperinflation affect the functioning of the cardiovascular system and metabolism in the body, which leads to the onset of other diseases (ischemia, diabetes, depression, etc.), a significant decrease in muscle tone and cachexia.

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 parts of the 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, environmental or genetic factors.

In the pathogenesis of COPD, dysfunction of the local defense system of the lungs is important. 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, circulating blood neutrophil elastase, which are concentrated in large quantities in the lungs under the influence of trigger factors (tobacco smoke causes 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 by histological examination of sputum and lavage, bronchial biopsy and the study of induced sputum. 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 number.

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 is a consequence of 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.

COPD (chronic obstructive pulmonary disease) is a disease that develops as a result of an inflammatory response to the action of certain environmental stimuli, with damage to the distal bronchi and the development of emphysema, and which is manifested by a progressive decrease in the air flow rate in the lungs, an increase, as well as damage to other organs.

COPD ranks second among chronic non-communicable diseases and fourth among causes of death, and this figure is steadily increasing. Due to the fact that this disease is inevitably progressive, it occupies one of the first places among the causes of disability, as it leads to a violation of the main function of our body - the respiratory function.

COPD is a truly global problem. In 1998, an initiative group of scientists created the Global Initiative for Chronic Obstructive Lung Disease (GOLD). The main tasks of GOLD are the wide dissemination of information about this disease, the systematization of experience, the explanation of the causes and the corresponding preventive measures. The main idea that doctors want to convey to humanity: COPD can be prevented and treated this postulate is even included in the modern working definition of COPD.

Causes of COPD

COPD develops with a combination of predisposing factors and provoking environmental agents.

Predisposing factors

1. hereditary predisposition. It has already been proven that congenital deficiency of certain enzymes predisposes to the development of COPD. This explains the family history of the disease, as well as the fact that not all smokers, even long-term smokers, get sick.
2. Gender and age. Men over the age of 40 suffer more from COPD, but this can be explained both by the aging of the body and the duration of smoking. Data are given that now the incidence rate among men and women is almost equal. The reason for this may be the spread of smoking among women, as well as the increased sensitivity of the female body to passive smoking.
3. Any negative impact which affect the development of the child's respiratory organs in the prenatal period and early childhood, increase the risk of COPD in the future. In itself, physical underdevelopment is also accompanied by a decrease in lung volume.
4. Infections. Frequent respiratory infections in childhood, as well as increased susceptibility to them at an older age.
5. Bronchial hyperreactivity. Although bronchial hyperreactivity is the main mechanism of development, this factor is also considered a risk factor for COPD.

Provoking factors

COPD pathogenesis

Exposure to tobacco smoke and other irritants in susceptible individuals leads to chronic inflammation in the walls of the bronchi. The key is the defeat of their distal departments (that is, those located closer to the lung parenchyma and alveoli).

As a result of inflammation, there is a violation of the normal secretion and discharge of mucus, blockage of small bronchi, infection easily joins, inflammation spreads to the submucosal and muscle layers, muscle cells die and are replaced by connective tissue (bronchial remodeling process). At the same time, the destruction of the parenchyma of the lung tissue, the bridges between the alveoli occurs - emphysema develops, that is, hyperairiness of the lung tissue. The lungs seem to swell with air, their elasticity decreases.

Small bronchi on exhalation do not expand well - the air hardly comes out of the emphysematous tissue. Normal gas exchange is disturbed, as the volume of inhalation also decreases. As a result, the main symptom of all patients with COPD occurs - shortness of breath, especially aggravated by movement, walking.

Respiratory failure results in chronic hypoxia. The whole body suffers from this. Prolonged hypoxia leads to a narrowing of the lumen of the pulmonary vessels - occurs, which leads to the expansion of the right heart (cor pulmonale) and the addition of heart failure.

Why is COPD singled out as a separate nosology?

The awareness of this term is so low that most of the patients who already suffer from this disease do not know that they have COPD. Even if such a diagnosis is made in the medical documentation, in the everyday life of both patients and doctors, the previously familiar “emphysema” still prevails.

The main components in the development of COPD are indeed chronic inflammation and emphysema. So why, then, is COPD singled out as a separate diagnosis?

In the name of this nosology, we see the main pathological process - chronic obstruction, that is, narrowing of the airway lumen. But the process of obstruction is also present in other diseases.

The difference between COPD and bronchial asthma is that in COPD, the obstruction is almost or completely irreversible. This is confirmed by spirometric measurements using bronchodilators. In bronchial asthma, after the use of bronchodilators, there is an improvement in FEV1 and PSV by more than 15%. This obstruction is treated as reversible. With COPD, these numbers change slightly.

Chronic bronchitis may precede or accompany COPD, but it is an independent disease with well-defined criteria (prolonged cough and), and the term itself implies damage only to the bronchi. With COPD, all structural elements of the lungs are affected - bronchi, alveoli, blood vessels, pleura. Not always chronic bronchitis is accompanied by obstructive disorders. On the other hand, increased sputum production is not always observed in COPD. So, in other words, there can be chronic bronchitis without COPD, and COPD doesn't quite fit the definition of bronchitis.

Chronic obstructive pulmonary disease

Thus, COPD is now a separate diagnosis, has its own criteria, and in no way replaces other diagnoses.

Diagnostic Criteria for COPD

You can suspect COPD in the presence of a combination of all or several signs, if they occur in people over 40 years of age:

A reliable confirmation of COPD is a spirometric indicator of the ratio of forced expiratory volume in 1 s to forced vital capacity (FEV1 / FVC), carried out 10-15 minutes after the use of bronchodilators (beta-sympathomimetics, salbutamol, berotek or 35-40 minutes after short-acting anticholinergics -ipratropium bromide). The value of this indicator<0,7 подтверждает ограничение скорости воздушного потока и в сочетании с подтвержденными факторами риска является достоверным критерием диагноза ХОБЛ.

Other spirometry measures, such as peak expiratory flow, and FEV1 measurement without a bronchodilator test, can be used as a screening test, but do not confirm the diagnosis of COPD.

Of the other methods prescribed for COPD, in addition to the usual clinical minimum, one can note x-ray of the lungs, pulse oximetry (determination of blood oxygen saturation), blood gas examination (hypoxemia, hypercapnia), bronchoscopy, chest CT, sputum examination.

COPD classification

There are several classifications of COPD according to stages, severity, clinical options.

Classification by stages takes into account the severity of symptoms and spirometry data:

• Stage 0. Risk group. Impact of adverse factors (smoking). No complaints, lung function is not impaired.
• Stage 1. Mild COPD.
• Stage 2. Moderate course of COPD.
• Stage 3. Severe course.
• Stage 4. Extremely severe course.

The latest GOLD report (2011) proposed to exclude the classification by stages, it remains severity classification based on FEV1:

In patients with FEV1/FVC<0,70:

• GOLD 1: Mild FEV1 ≥80% predicted
• GOLD 2: Moderate 50% ≤ FEV1< 80%.
• GOLD 3: Severe 30% ≤ FEV1< 50%.
• GOLD 4: Extremely severe FEV1<30%.

It should be noted that the severity of symptoms does not always correlate with the degree of bronchial obstruction. Patients with mild obstruction may be bothered by fairly severe dyspnea, and, conversely, patients with GOLD 3 and GOLD 4 may feel quite satisfactory for a long time. To assess the severity of dyspnea in patients, special questionnaires are used, the severity of symptoms is determined in points. It is also necessary to focus on the frequency of exacerbations and the risk of complications in assessing the course of the disease.

Therefore, this report proposes, based on the analysis of subjective symptoms, spirometry data and the risk of exacerbations, to divide patients into clinical groups - A, B, C, D.

Practitioners also distinguish clinical forms of COPD:

1. Emphysematous variant of COPD. Of the complaints in such patients, shortness of breath predominates. Cough is observed less often, sputum may not be. Hypoxemia, pulmonary hypertension come late. Such patients, as a rule, have a low body weight, the color of the skin is pink-gray. They are called "pink puffers".
2. bronchitis variant. Such patients complain mainly of cough with sputum, shortness of breath is less disturbing, they develop cor pulmonale quite quickly with a corresponding picture of heart failure - cyanosis, edema. Such patients are called "blue puffers".

The division into emphysematous and bronchitis variants is rather conditional, mixed forms are more often observed.

During the course of the disease, a phase of a stable course and an exacerbation phase are distinguished.

Exacerbation of COPD

An exacerbation of COPD is an acutely developing condition when the symptoms of the disease go beyond its usual course. There is an increase in shortness of breath, cough and deterioration of the general condition of the patient. Conventional therapy, which he used previously, does not stop these symptoms to the usual state, a change in dose or treatment regimen is required. Usually, hospitalization is required for an exacerbation of COPD.

Diagnosis of exacerbations is based solely on complaints, anamnesis, clinical manifestations, and can also be confirmed by additional studies (spirometry, complete blood count, microscopy and bacteriological examination of sputum, pulse oximetry).

The causes of exacerbation are most often respiratory viral and bacterial infections, less often - other factors (exposure to harmful factors in the surrounding air). A common event in a patient with COPD is an event that significantly reduces lung function, and return to baseline may take a long time, or stabilization will occur at a more severe stage of the disease.

The more frequent exacerbations occur, the worse the prognosis of the disease and the higher the risk of complications.

Complications of COPD

Due to the fact that patients with COPD exist in a state of constant hypoxia, they often develop the following complications:

COPD treatment

Basic principles of therapeutic and preventive measures for COPD:

1. To give up smoking. At first glance, a simple, but the most difficult to implement moment.
2. Pharmacotherapy. Early initiation of basic drug treatment can significantly improve the patient's quality of life, reduce the risk of exacerbations and increase life expectancy.
3. The drug therapy regimen should be selected individually, taking into account the severity of the course, the patient's adherence to long-term treatment, the availability and cost of drugs for each individual patient.
4. Influenza and pneumococcal vaccinations should be offered to patients with COPD.
5. The positive effect of physical rehabilitation (training) has been proven. This method is under development, while there are no effective therapeutic programs. The easiest way that can be offered to the patient is daily walking for 20 minutes.
6. In the case of a severe course of the disease with severe respiratory failure, long-term oxygen inhalation as a means of palliative care improves the patient's condition and prolongs life.

To give up smoking

Tobacco cessation has been proven to have a significant impact on the course and prognosis of COPD. Despite the fact that the chronic inflammatory process is considered irreversible, smoking cessation slows down its progression, especially in the early stages of the disease.

Tobacco addiction is a serious problem that requires a lot of time and effort not only for the patient himself, but also for doctors and relatives. A special long-term study was conducted with a group of smokers, which offered various activities aimed at combating this addiction (conversations, persuasion, practical advice, psychological support, visual agitation). With such an investment of attention and time, it was possible to achieve smoking cessation in 25% of patients. Moreover, the longer and more often the conversations are held, the more likely they are to be effective.

Anti-tobacco programs are becoming national targets. There is a need not only to promote a healthy lifestyle, but also to legislate punishment for smoking in public places. This will help limit the harm from at least passive smoking. Tobacco smoke is especially harmful for pregnant women (both active and passive smoking) and children.

For some patients, tobacco addiction is akin to drug addiction, and in this case, interviews will not be enough.

In addition to agitation, there are also medical ways to combat smoking. These are nicotine replacement tablets, sprays, chewing gums, skin patches. The effectiveness of some antidepressants (bupropion, nortriptyline) in the formation of long-term smoking cessation has also been proven.

Pharmacotherapy for COPD

Drug therapy for COPD is aimed at managing symptoms, preventing exacerbations, and slowing the progression of chronic inflammation. It is impossible to completely stop or cure the destructive processes in the lungs with currently existing drugs.

The main drugs used to treat COPD are:

Bronchodilators

Bronchodilators, used to treat COPD, relax the smooth muscles of the bronchi, thereby expanding their lumen and facilitating the passage of air on exhalation. All bronchodilators have been shown to increase exercise tolerance.

Bronchodilators include:

1. Short-acting beta stimulants ( salbutamol, fenoterol).
2. Long acting beta stimulants ( salmoterol, formoterol).
3. Short acting anticholinergics ipratropium bromide - atrovent).
4. Long acting anticholinergics ( tiotropium bromide - spiriva).
5. Xanthines ( eufillin, theophylline).

Almost all existing bronchodilators are used in inhaled form, which is more preferable than oral administration. There are different types of inhalers (metered dose aerosol, powder inhalers, breath-activated inhalers, liquid forms for nebulizer inhalation). In severely ill patients, as well as in patients with intellectual disabilities, it is better to carry out inhalation through a nebulizer.

This group of drugs is the main one in the treatment of COPD; it is used at all stages of the disease as monotherapy or (more often) in combination with other drugs. For permanent therapy, the use of long-acting bronchodilators is preferable. If it is necessary to prescribe short-acting bronchodilators, combinations are preferred fenoterol and ipratropium bromide (berodual).

Xanthines (eufillin, theophylline) are used in the form of tablets and injections, have many side effects, and are not recommended for long-term treatment.

Glucocorticosteroid hormones (GCS)

GCS are a powerful anti-inflammatory agent. They are used in patients with a severe and extremely severe degree, and are also prescribed in short courses for exacerbations in the moderate stage.

The best form of application is inhaled corticosteroids ( beclomethasone, fluticasone, budesonide). The use of such forms of corticosteroids minimizes the risk of systemic side effects of this group of drugs, which inevitably occur when taken orally.

GCS monotherapy is not recommended for patients with COPD, more often they are prescribed in combination with long-acting beta-agonists. The main combination drugs: formoterol + budesonide (symbicort), salmoterol + fluticasone (seretide).

In severe cases, as well as during an exacerbation, systemic corticosteroids can be prescribed - prednisolone, dexamethasone, kenalog. Long-term therapy with these drugs is fraught with the development of severe side effects (erosive and ulcerative lesions of the gastrointestinal tract, Itsenko-Cushing's syndrome, steroid diabetes, osteoporosis, and others).

Bronchodilators and corticosteroids (and more often a combination of them) are the main most affordable drugs that are prescribed for COPD. The doctor selects the treatment regimen, doses and combinations individually for each patient. When choosing a treatment, not only the recommended GOLD schemes for different clinical groups are important, but also the social status of the patient, the cost of drugs and its availability for a particular patient, the ability to learn, and motivation.

Other drugs used in COPD

Mucolytics(sputum thinning agents) are prescribed in the presence of viscous, difficult to expectorate sputum.

Phosphodiesterase-4 inhibitor roflumilast (Daxas) is a relatively new drug. It has a prolonged anti-inflammatory effect, is a kind of alternative to GCS. It is used in tablets of 500 mg 1 time per day in patients with severe and extremely severe COPD. Its high efficiency has been proven, but its use is limited due to the high cost of the drug, as well as a rather high percentage of side effects (nausea, vomiting, diarrhea, headache).

There are studies that the drug fenspiride (Erespal) has an anti-inflammatory effect similar to corticosteroids, and can also be recommended for such patients.

Of the physiotherapeutic methods of treatment, the method of intrapulmonary percussion ventilation of the lungs is gaining popularity: a special device generates small volumes of air that are supplied to the lungs with quick shocks. From such a pneumomassage, the collapsed bronchi are straightened and the ventilation of the lungs is improved.

Treatment of exacerbation of COPD

The goal of exacerbation treatment is to manage the current exacerbation as much as possible and prevent future exacerbations. Depending on the severity, exacerbations can be treated on an outpatient basis or in a hospital.

Basic principles of treatment of exacerbations:

• It is necessary to correctly assess the severity of the patient's condition, exclude complications that can be disguised as exacerbations of COPD, and promptly send for hospitalization in life-threatening situations.
• With an exacerbation of the disease, the use of short-acting bronchodilators is preferable to long-acting ones. Doses and frequency of administration, as a rule, increase compared to usual. It is advisable to use spacers or nebulizers, especially in critically ill patients.
• With insufficient effect of bronchodilators, intravenous administration of aminophylline is added.
• If monotherapy was previously used, a combination of beta-stimulants with anticholinergics (also short-acting) is used.
• In the presence of symptoms of bacterial inflammation (the first sign of which is the appearance of purulent sputum), broad-spectrum antibiotics are prescribed.
• Connection of intravenous or oral administration of glucocorticosteroids. An alternative to the systemic use of corticosteroids is the inhalation of pulmicort through a nebulizer 2 mg twice a day after berodual inhalations.
• Dosed oxygen therapy in the treatment of patients in a hospital through nasal catheters or a Venturi mask. The oxygen content in the inhaled mixture is 24-28%.
• Other activities - maintaining water balance, anticoagulants, treatment of concomitant diseases.

Caring for patients with severe COPD

As already mentioned, COPD is a disease that is steadily progressing and inevitably leads to the development of respiratory failure. The speed of this process depends on many things: the patient's refusal to smoke, adherence to treatment, the patient's financial capabilities, his memory abilities, and the availability of medical care. Starting with a moderate degree of COPD, patients are referred to MSEC to receive a disability group.

With an extremely severe degree of respiratory failure, the patient cannot even perform normal household activities, sometimes he cannot even take a few steps. These patients require constant care. Inhalations for seriously ill patients are carried out only with the help of a nebulizer. Significantly facilitates the condition of many hours of low-flow oxygen therapy (more than 15 hours a day).

For these purposes, special portable oxygen concentrators have been developed. They do not require filling with pure oxygen, but concentrate oxygen directly from the air. Oxygen therapy increases the life expectancy of such patients.

COPD prevention

COPD is a preventable disease. It is important that the level of COPD prevention depends very little on physicians. The main measures should be taken either by the person himself (quitting smoking) or by the state (anti-smoking laws, improving the environment, promoting and stimulating a healthy lifestyle). It has been proven that COPD prevention is economically beneficial by reducing the incidence and reducing the disability of the working population.

Video: COPD in the program “Live healthy”

Video: what is COPD and how to detect it in time

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General information

To date, there has been controversy over the definition of the disease.

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 "pulmonary emphysema" are included in the formulation of chronic obstructive pulmonary disease, so they should not be attributed to the diagnosis of COPD, because COPD does not exist without chronic obstructive bronchitis and emphysema. 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

Chronic obstructive pulmonary disease is one of the leading causes of morbidity and mortality worldwide. The number of patients with COPD is directly related to the prevalence among the population of one of the main risk factors for the disease - smoking. So, according to WHO, with an average COPD morbidity of about 1%, in countries with a high prevalence of smoking, this percentage rises to 6-10.

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

The main etiological factors (in modern literature they are often called risk factors) are pollutants, which are various impurities contained in the inhaled air, which mechanically and chemically have a pathogenic irritating effect on the mucous membrane of the bronchi and alveoli.

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.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) -

primary chronic inflammatory disease of the lungs with a predominant lesion of the distal respiratory tract and parenchyma, the formation of emphysema, impaired bronchial patency with the development of incompletely reversible or irreversible bronchial obstruction caused by a pathological 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.

COPD is one of the most common diseases.

According to WHO, the prevalence of COPD among men is 9.34:1000, among women - 7.33:1000. Persons over 40 years of age predominate.

In Russia, there are about 1 million patients with COPD (official data of the Ministry of Health of the Russian Federation), but in reality their number may exceed 11 million people (data from epidemiological studies).

Classification COPD is classified according to the severity (stages) of the disease. There are 4 stages of COPD.

According to international recommendations [Global Initiative for Chronic Obstructive Lung Disease (GOLD), 2003], the defining and unifying feature of all stages of COPD is a decrease in the ratio of FEV^FVC< 70 %, характеризующее ограничение экспираторного воз­душного потока. Разделяющим признаком, позволяющим оценить степень тяжести (стадию) ХОБЛ - легкое (I стадия), среднетяжелое (II стадия), тя­желое (III stage) and extremely severe (stage IV) course, - is the value of the FEV indicator (determined after the appointment of bronchodilators).

Stage I: mild COPD. FEV /FVC< 70 %. На этой стадии больной может не замечать, что функция легких у него нарушена. Обструктивные нарушения выражены незначительно - FEV value, > 80% of the expected values. Usually, but not always, COPD presents with chronic cough and sputum production. Therefore, only in 25% of cases the disease is diagnosed in a timely manner (data of the European Respiratory Society), i.e. at this stage in the development of COPD.

Stage II: moderate course of COPD. FEV/FVC< 70 %. This is the stage at which patients seek medical attention due to shortness of breath or an exacerbation of the disease, characterized by an increase in obstructive disorders (50%< ОФВ 1 < 80 % от должных величин). Отмечается усиление симптомов заболевания и одышки, появляющейся при физической нагрузке.

Stage III: severe course of COPD. FEV/FVC< 70 %. Characterized by a further increase in airflow limitation (30 % < ОФВ, < 50 % от должных величин), нарастанием одышки, частыми обострениями.

Stage IV: extremely severe COPD. FEV /FVC< 70%. At this stage, the quality of life deteriorates markedly, and exacerbations can be life-threatening. The disease acquires a disabling course. It is characterized by extremely severe bronchial obstruction (FEV,< 30 % от должных величин или ОФВ, < 50 % от должных величин при наличии дыхательной недостаточности). На этой стадии возможно раз­витие легочного сердца.

Etiology. The main risk factors for developing COPD are:

1) smoking (both active and passive);

2) exposure to occupational hazards (dust, chemical pollutants, vapors of acids and alkalis) and industrial pollutants (S0 2 , K0 2 , black smoke, etc.);

3) atmospheric and domestic (smoke from cooking and fossil fuels) air pollution;

4) hereditary predisposition (most often, a deficiency of a g anti-

trypsin);

5) respiratory diseases in early childhood, low weight

body at birth.

Epidemiological studies confirm that active cigarette smoking is the most important risk factor for COPD. Only 10% of COPD cases are associated solely with other risk factors.

Each of these factors can act alone or in combination with each other.

Pathogenesis. Exposure to tobacco smoke and toxic gases has an irritating effect on the irritative vagus nerve receptors located in the bronchial epithelium, which leads to the activation of cholinergic mechanisms of the autonomic nervous system, which are realized by bronchospastic reactions.

Under the influence of risk factors at the first stage of the development of the disease, the movement of the cilia of the ciliated epithelium of the bronchi is disrupted up to their complete stop. Metaplasia of the epithelium develops with the loss of ciliated epithelial cells and an increase in the number of goblet cells. The composition of the bronchial secretion changes (its viscosity and adhesion increase), which disrupts the movement of significantly thinned cilia. There is a violation of mucociliary transport in the bronchi, which contributes to the occurrence of mucostasis, causing blockade of small airways and further creates optimal conditions for the colonization of microorganisms.

The main consequence of the impact of etiological factors (risk factors) is the development of a specific chronic inflammation, the biomarker of which is the neutrophil. Along with neutrophils, macrophages and T-lymphocytes take part in the formation and implementation of inflammation. Under the influence of trigger factors, neutrophils circulating in the blood are concentrated in large numbers in the lungs and are the main source of free radicals, biologically active substances and enzymes. Neutrophils secrete a large amount of myeloperoxidase, neutrophil elastase, metalloproteases, which, along with interleukins and tumor necrosis factor, are the main mediators of inflammation in COPD. Under conditions of high concentration of neutrophils in the respiratory tract, the balance of the “proteolysis-antiproteolysis” and “oxidants-antioxidants” systems is disturbed. “Oxidative stress” develops, which in turn contributes to the release of a large amount of free radicals in the airways. Due to “oxidative stress”, local protease inhibitors are depleted, which, along with the release of a large number of proteases by neutrophils, leads to a violation of the elastic stroma of the alveoli, involvement of the lung parenchyma in the pathological process and the development of emphysema.

The whole complex of inflammation mechanisms leads to the formation of two main processes characteristic of COPD: impaired bronchial

patency and development of centrilobular, panlobular emphysema. Impaired bronchial patency in COPD patients is formed due to reversible (spasm of smooth muscles, mucosal edema and mucus hypersecretion) and irreversible (formation of expiratory collapse of small bronchi and bronchioles, peribronchial fibrosis and emphysema with changes in respiratory mechanics) components. At the first stages of COPD development, bronchial obstruction is formed mainly due to the reversible component. As the disease progresses, an irreversible component becomes the leading one in violation of bronchial patency.

The main difference between the development of COPD and CB is that emphysema is not a complication, but a manifestation of the disease, which develops in parallel with changes occurring in the airways.

The development of emphysema leads to a reduction in the vascular network in areas of the lung tissue that are not capable of gas exchange, resulting in pronounced ventilation-perfusion disorders. Conditions are created for increasing pressure in the pulmonary artery basin. At this stage, pulmonary hypertension is formed with the further development of cor pulmonale.

Pathological changes characteristic of COPD are found in the cartilaginous (more than 2 mm in diameter) and distal bronchi (less than 2 mm) of the 9th-17th generation and acini, including respiratory bronchioles, alveolar ducts, sacs, alveolar wall, as well as in the lungs. arterioles, venules and capillaries. Thus, COPD is characterized by the development of a chronic inflammatory process of the respiratory tract, lung parenchyma and blood vessels, in which an increased number of neutrophils, macrophages and T-lymphocytes is detected in various anatomical formations of the respiratory organs.

clinical picture. On the I the diagnostic search stage reveals the main symptoms of COPD: chronic cough, sputum production and / or shortness of breath. When studying the anamnesis, much attention is paid to identifying risk factors for the development of COPD (smoking and tobacco smoke, industrial dust and chemicals, smoke from household heating appliances and burning from cooking) due to the fact that the disease begins to develop long before the onset of severe symptoms and lasts for a long time. without clear clinical symptoms. As the disease progresses, COPD is characterized by the severity of clinical manifestations and a steadily progressive course.

The severity of the main symptoms depends on the severity of the disease and the phase of the course - stable or exacerbation. A state is considered stable when the progression of the disease can be detected during long-term dynamic monitoring of the patient (6-12 months), and the severity of symptoms does not change significantly for weeks or even months. An exacerbation is characterized by a deterioration in the patient's condition, manifested by an increase in symptoms and functional disorders that occur suddenly or gradually and last at least 5 days.

At the first stage of the diagnostic search, a thorough analysis of the complaints presented by the patient is carried out. In cases where the patient underestimates his condition and does not complain on his own, the doctor, when talking with the patient, should actively detect the presence of cough and sputum production.

Cough(it is necessary to establish the frequency of its occurrence and intensity) is the earliest symptom that manifests itself by the age of 40-50

ladies of life. It is noted daily or is intermittent in nature (more often observed during the day, rarely at night).

Sputum(it is necessary to find out the nature and its amount), as a rule, it is excreted in a small amount in the morning (rarely> 50 ml per day), has a mucous character. The appearance of purulent sputum and an increase in its amount are signs of an exacerbation of the disease. The appearance of blood in the sputum suggests another cause of cough (lung cancer, tuberculosis, or bronchiectasis), although streaks of blood in the sputum may appear in a COPD patient as a result of persistent coughing.

Chronic cough and excessive sputum production in most cases long precede ventilation disorders leading to dyspnoea.

Dyspnea(it is necessary to assess its severity, its relationship with physical activity) is a cardinal sign of COPD and serves as the reason for which the majority of patients go to the doctor, since it is the main factor limiting their physical activity. Quite often, the diagnosis of COPD is established at this stage of the disease. Dyspnea felt on exertion occurs on average 10 years after coughing. Very rarely, the debut of the disease can begin with shortness of breath. This happens in the presence of emphysema, which develops in situations where a person comes into contact with finely dispersed (less than 5 microns) pollutants at work, as well as in hereditary deficiency of wasp-antitrypsin, leading to the early development of panlobular emphysema.

As lung function decreases, dyspnea becomes more pronounced and can vary over a very wide range: from a feeling of lack of air during habitual physical exertion to severe respiratory failure. Patients describe shortness of breath in different ways: “increase in effort during breathing”, “heaviness”, “air starvation”, “difficulty breathing”. Shortness of breath in COPD is characterized by progression (constant increase), persistence (every day), exacerbation with exertion and with respiratory infections.

In addition, the patient may be disturbed by morning headache, drowsiness during the day and insomnia at night due to hypoxia and hypercapnia developing in the later stages of the disease.

When collecting an anamnesis, attention is paid to the study of factors provoking an exacerbation of the disease (bronchopulmonary infection, increased exposure to exogenous damaging factors, inadequate physical activity, etc.), the frequency of exacerbations and hospitalizations for COPD. As the disease progresses, the intervals between exacerbations become shorter, and with increasing severity, they become almost persistent.

The presence of concomitant diseases (pathology of the cardiovascular system, gastrointestinal tract) that occur in more than 90% of COPD patients and affect the severity of COPD and the nature of complex drug therapy is specified. The effectiveness and tolerability of previously prescribed therapy, the regularity of its implementation by the patient are being clarified.

At stage II of the diagnostic search, the most information can be obtained at the stage of advanced clinical manifestations of the disease and the development of complications. In the early stages of the disease, clinical symptoms may be absent. Pathological symptoms that can be detected as the disease progresses depend on the severity of bronchial obstruction, emphysema and the severity of pulmonary hyperinflation.

inflation (overstretching of the lungs), the presence of complications such as respiratory failure and chronic cor pulmonale.

Examining the patient, evaluate his appearance, behavior, reaction of the respiratory system to the conversation, movement around the office. The lips are collected in a “tube”, the forced position of the body indicates severe COPD. The color of the skin is assessed: central gray cyanosis usually serves as a manifestation of hypoxemia; the acrocyanosis detected at the same time is usually a consequence of heart failure. Examining the chest, pay attention to its shape - deformed, "barrel-shaped", inactive during breathing, paradoxical retraction (retraction) of the lower intercostal spaces on inspiration (Hoover's sign) and participation in the act of breathing of the auxiliary muscles of the chest, abdominal press, significant expansion of the chest cells in the lower sections are all signs of severe COPD. With percussion of the chest, a boxed percussion sound and lowered lower borders of the lungs (signs of emphysema) are determined. The auscultatory picture of the lungs depends on the prevalence of emphysema or bronchial obstruction. So, with emphysema, breathing is weakened vesicular, and in patients with severe bronchial obstruction, as a rule, it is hard, and the main auscultatory symptom is dry, predominantly wheezing, aggravated by forced expiration, imitation of cough, in the supine position.

With irreversible bronchial obstruction, signs of respiratory failure predominate, pulmonary hypertension increases, and chronic cor pulmonale is formed. It is difficult to identify signs of compensated cor pulmonale during physical examination, heart sounds are difficult to listen to, but it is possible to identify an accent of II tone over the pulmonary artery. It is possible to detect a pulsation in the epigastric region due to the right ventricle. As the disease progresses, diffuse cyanosis is determined. In the future, a decompensated cor pulmonale is formed: the liver enlarges, pastosity appears, and then swelling of the legs and feet.

In patients with moderate and severe course of the disease, two clinical forms of COPD are distinguished - emphysematous (panacinar emphysema, "pink puffers") and bronchitis (centroacinar emphysema, "blue puffiness"). Their main differences are given in table. 5. However, in practice, a mixed form of the disease is most common.

The sensitivity of physical (objective) methods of examination of patients in diagnosing COPD and determining its severity is low. They provide guidelines for the further direction of diagnostic research using instrumental and laboratory methods.

Stage III of the diagnostic search is a defining stage in the diagnosis of COPD.

FVD study serves as the most important method in the diagnosis of COPD and differentiation from CB. It should be performed in all patients with chronic cough and sputum production, a history of risk factors even in the absence of dyspnoea, in order to detect COPD in the early stages of the disease. This study is carried out not only to make a diagnosis, but also to determine the severity of the disease, select individual therapy, evaluate its effectiveness, clarify the prognosis of the course of the disease and in the examination of working capacity.