Chronic obstructive pulmonary disease presentation. Pulmonary syndromes. Chronic obstructive pulmonary disease. Bronchial asthma. Etiology of exacerbations of COPD

Description of the presentation Chronic obstructive pulmonary disease on slides

Chronic obstructive pulmonary disease (COPD) Morbus pulmonum obstructivus chronicus Chronic obstructive pulmonary disease (COPD)

COPD is an independent nosological form with corresponding stages; each stage has its own functional, clinical and morphological characteristics. COPD more accurately reflects the essence of the pathology, in which the respiratory part of the lung changes to a greater extent than the bronchi. COPD is induced by an inflammatory response (different from asthma), which exists regardless of the severity of the disease. Pathogenetic processes in COPD: airway obstruction - CB (damage to large-medium bronchi); bronchiolitis (progressive inflammation and fibrosis of small, cartilaginous bronchi with their obstruction and limitation of air flow) pulmonary emphysema (EL) - destruction of the walls of the alveoli and their attachments to the walls terminal bronchioles. extrapulmonary changes (osteoporosis, anemia, myopathy, etc.) COPD is complicated by gradual and steady: decreased bronchial patency, increased airiness of the lungs; increasing chronic respiratory failure(CDN) and the formation of chronic pulmonary heart disease (CPC).

COPD BA scheme – completely reversible bronchial obstruction! Patients with CB and EL without obstruction are not included in COPD! 1. CB + EL with obstruction, usually occur together. 2. patients with asthma + symptoms of chronic disease (asthmatic form of COPD). 3. 4. patients with CB + EL + BA and with incomplete reversibility of obstruction.

Etiology of COPD (risk factors) Exogenous (leading): 1. Long-term and intense smoking (specific weight > 90%). 2. Air pollution with aggressive, harmful industrial pollutants. 3. Infectious agents. Endogenous: 4. severe deficiency of α 1 -antitrypsin: bronchial hyperreactivity; age > 45 years; frequent or chronic diseases ENT organs; frequent acute respiratory infections, acute bronchitis, pneumonia; genetically determined defects of cilia, alveolar macrophages, qualitative changes in bronchial mucus; family tendency to chronic bronchopulmonary diseases(COPD is not inherited!); low level life, poor nutrition; long-term alcohol abuse. Factors 1, 2, 3, 4 are unconditional in the development of COPD, while others are probable. Factors predisposing to the development of COPD are usually combined (they are rare in their pure form).

The main components of the pathophysiology of COPD: inflammation of the airways (deposition of neutrophils in them - the “master cell”), with the release of a large number of pro-inflammatory cytokines; disturbances of mucociliary transport, obstruction of the respiratory tract, structural changes in them (remodeling) with damage to the lung parenchyma, systemic effects (endocrine and skeletal muscle dysfunction, anemia, osteoporosis, weight loss). 2 main processes of the complex mechanism of inflammation in COPD: impaired bronchial obstruction; development of centrilobular EL.

During the evolution of COPD, respiratory infection is not the main reason for its formation. We can conditionally distinguish two periods of development of the disease: initial - non-infectious (the pathogenesis is dominated by exogenous risk factors - under the influence of pollutants, predisposed individuals develop changes in the structure of the respiratory tract, lung tissue, sputum rheology and local bronchial protection) and late infectious: due to deterioration in bronchial clearance ( decrease in the natural resistance of the bronchi) the inflammatory process spreads to the distal bronchi (infection is constantly “smoldering” in them, especially in the areas of formation of secondary bronchiectasis).

Mechanisms of obstruction in COPD: Reversible: inflammatory edema (infiltration) of the bronchial mucosa and submucosa; obstruction by excess mucus; bronchospasm. Later (during the evolution of the disease), the reversible component is lost and irreversible obstruction is formed due to: expiratory collapse of small, cartilaginous bronchi during exhalation due to concomitant EL; stenosis, deformation and obliteration of the bronchial lumen; fibroplastic changes in the bronchial wall.

4 stages of COPD evolution: stage 1. Disease threat situation: exposure to exo- and/or endogenous AH on a healthy person, which can cause “gaps” in the local protection of the respiratory tract. Stage 2. Pre-illness state - symptoms appear pathological process in different variants: habitual smoker's cough; cough from exposure to irritating aerosols; cough due to impaired drainage and calorific function of the nose; respiratory discomfort (bronchospasm) upon contact with irritating aerosols and when the ambient temperature changes; protracted or recurrent course of acute bronchitis. Stage 3 (by 40-50 years). An extensive COPD clinic with a triad of symptoms: cough and sputum (excessive production of bronchial secretions), shortness of breath (due to progressive obstruction of the small bronchi and overinflation of the lungs during an exacerbation). It is likely that COPD can begin already in childhood (against the background of periodic infections, passive exposure to tobacco smoke). The gradual evolution of COPD and the greater compensatory capabilities of the young body contribute to the fact that clinical symptoms appear after 40 years. Stage 4. The development of complications of COPD caused by infection (secondary pneumonia, lung abscess, tracheobronchial dyskinesia) and the evolution of the disease - bronchitis pneumosclerosis, PH and chronic pulmonary hypertension with arrhythmias, pneumothorax, pathological night apnea, severe DN (according to the speed of development it is divided into - ARF, which appears over several h during exacerbation and CHF, which develops over many years), hemoptysis, CHF, PE (detected on section in a third of COPD patients), pneumothorax or atelectasis of the lobe.

Classification of CB (ICD-10) J. 41. Simple, mucopurulent (damage to large bronchi and absence of shortness of breath). J. 42. Not designated as CB (bronchitis, tracheitis, tracheobronchitis) excluded: CB, COPD, emphysema-bronchitis, simple and mucopurulent CB). J. 43. Primary pulmonary emphysema excluded: due to inhalation chemical substances, gases, smoke; compensatory, interstitial against the background of COB: traumatic, emphysema, bronchitis. J. 44. COPD (damage to small bronchi and dominance of shortness of breath) - COPD + EL, asthma with constant obstruction of the bronchi. Excluded: BA with reversible bronchial obstruction, bronchiectasis, CB (J. 41), EL (J. 43).

Clinical manifestations of COPD vary. The first symptoms are persistent shortness of breath with FN (the “stigma” of the disease) and cough, and other manifestations (for example, wheezing or chest pain) appear later, as the disease progresses. In COPD, there are quite pronounced clinical symptoms - shortness of breath and wheezing (which worsens as it progresses), cough (often unproductive), prolonged exhalation, pain in the chest(caused by ischemia of the intercostal muscles; sometimes associated with ischemic heart disease or bronchogenic cancer), weight loss, swelling of the ankles, often “winter bronchitis”, disability with a decrease in quality of life. Symptoms of COPD are episodic and worsen during an exacerbation (productive cough, shortness of breath and wheezing increase).

Exacerbation of COPD is an acute, episodic significant deterioration in condition (≥ 3 days), superimposed on a stable course of the disease and accompanied by: increased inflammation of the airways, obstruction (FEV 1 decreases >20% of the usual level) and symptoms - shortness of breath (sometimes appears in rest), an increase in the volume and purulence of discharged sputum (according to Antonisen, the presence of 3 of these signs indicates a severe exacerbation, and 2 indicate a moderate exacerbation), as well as increased cough, decreased daytime performance, increased body temperature (for no apparent reason), an increase in RR or heart rate >20% of the initial level and the need to change the usual treatment regimen. Fever, manifestations of acute respiratory viral infections and the appearance of swelling of the ankles are often noted. The rate of decline in FEV 1 correlates with the frequency of exacerbations per year—patients with a greater number of exacerbations had a greater rate of decline in FEV 1 (and worse quality of life). Types of exacerbations of COPD: simple (patient age 4 times a year and FEV 1>50%) and complicated (patient age >60 years, concomitant diseases, exacerbation frequency >4 r/g, FEV 1<50%, применялись ГКС и АБ в последние 3 мес); легкое, средней степени тяжести (лечится в стационаре), тяжелое (признаки ОДН р. О 2 25/мин) и рецидивирующее (утяжеление симптоматики в течение 14 дней, несмотря на проводимое лечение); инфекционно-зависимое (до 80% случаев) и неинфекционное. В трети случаев обострение вызвано респираторными вирусами.

Classification of COPD (“GOLD”, 2003) according to severity Stage Characteristics I – mild FEV 1 /FVC<70%; O ФВ 1 ≥ 80%; хронический кашель и продукция мокроты обычно, но не всегда; м. б. одышка при ФН; больной может не замечать, что функция легких у него нарушена II — средне-тя желая ОФВ 1 /ФЖЕЛ<70%; 50%≤ O ФВ 1 <80%; хронический кашель и продукция мокроты — обычно (они многие годы предшествуют обструкции бронхов); симптомы прогрессируют; больные обращаются за медицинской помощью из-за типичной одышки при ФН и обострений III – тяжелая ОФВ 1 /ФЖЕЛ<70%; 30%≥ O ФВ 1 <50%; хронический кашель и продукция мокроты обычно; нарастают одышка (ограничивающая дневную активность), цианоз и число обострений; снижается качество жизни IV — крайне тяжелая ОФВ 1 /ФЖЕЛ<70%; O ФВ 1 <30% или <50% в сочетании с хронической ДН (одышка и цианоз в покое) и/или ХСН по ПЖ типу. Качество жизни резко ухудшено. Обострения могут быть опасными для жизни.

Diagnosis of CB 1. History (+ careful consideration of risk factors). 2. Clinic (verification of bronchial obstruction, presence of EL and vising during exhalation). The diagnosis of COPD is made clinically and anamnestiically. An important component of diagnosis is an indication of the progression of the disease and a decrease in physical function). Dyspnea progresses (worsens over time), persists (noted every day), worsens during exercise or respiratory infection 3. Laboratory data: spirometry (↓FEV 1 + tests with bronchodilators) to verify bronchial obstruction; blood test (leukocytosis, increase in ESR and HB to exclude frequent anemia); level a 1 -antiprotease; arterial blood gases (detection of hypoxemia - pa. O 2< 60 мм рт. ст.) иногда пульсоксиметрия; анализ мокроты; рентгенологическое обследование грудной клетки (рентгенологический диагноз ХОБЛ не ставят!); ЭКГ и Эхо. КГ; Бронхоскопия (характер и степень выраженности эндобронхита)

The differential diagnosis of COPD is with a group of diseases accompanied by cough with sputum and shortness of breath: asthma (COPD and asthma can be combined! More often than not, COPD is associated with asthma); bronchial cancer; pneumoconiosis; bronchiectasis; diffuse obliterating bronchiolitis; cystic fibrosis; pulmonary tuberculosis; gastroesophageal reflux disease; CHF with severe LV dysfunction.

The goals of COPD treatment are to prevent further deterioration of bronchopulmonary function and symptoms; reducing the rate of progression of diffuse bronchial damage; increase in TfN; reducing the frequency of exacerbations of COPD and prolonging remissions; Prevention and treatment of complications if they occur; improving quality of life and reducing mortality. 2 stages of therapy: tactical - active treatment of exacerbation; strategic - subsequent long-term basic, maintenance therapy with physical rehabilitation, until stable remission is achieved. Treatment of COPD is complex: elimination (or reduction of the effect) of RFs (substances that irritate the bronchi); the use of bronchodilators, ABs and GCS (to reduce inflammation); immunomodulators and vaccination; correction of CDN (long-term oxygen therapy); rehabilitation (including respiratory muscle training).

3 groups of bronchodilators - basic therapy for COPD: anticholinergics (1st line drugs); Iβ 2 -AG short- and long-acting; theophyllines. The goal of treatment is to prevent exacerbations, return the bronchial lumen to its original level and increase FEV 1. Treatment of COPD is similar to asthma, but there is no stepwise reduction in treatment as well-being improves, as with asthma. In COPD, there is a greater effect from anticholinergics (predominantly acting on large bronchi) and a smaller effect from the use of Iβ 2 -AG (predominantly acting on small bronchi) than in BA.

Prescribed: aerosol tiotropium bromide (TB) (long-acting - 1 r / day through a handhaler in the morning, the bronchodilator effect depends on the dose and lasts for 24 hours) or ipratropium bromide (IB) with a spacer (short-acting; 1-2 puffs of 3 -4 r/day;< 12 вдохов/сут). Лучше назначать бронхолитик в небулайзере, повышающем на 40% доставку аэрозоля в дыхательные пути (особенно при тяжелом ХОБЛ с утомлением дыхательных мышц). (+) ТБ и ИБ (по сравнению с Иβ 2 -АГ): больше терапевтический коридор и период действия ~ 5 -6 ч (хотя начинают действовать медленнее, через 30 мин), сохранение активности при многолетнем приеме, нет кардиотоксического действия. ТБ и ИБ — высокоэффективны у пожилых больных (особенно тех, кто плохо переносит Иβ 2 -АГ) для длительной и многолетней терапии ХОБЛ (к ним не развивается тахифилаксия). При средней тяжести ХОБЛ назначают постоянно бронходилататоры длительного действия (ТБ). Более сильный аэрозольный бронходилятатор — беродуал (комбинация фенотерола с ИБ), 1 -2 ингаляции, 3 -4 р/сут.

Selective Iβ 2 -AGs (phenaterol, salbutamol, terbutaline) stimulate β-adrenergic receptors (their maximum density is determined at the level of small and medium bronchi) and relax the smooth muscles of the bronchi; reduce hyperreactivity of the respiratory tract, secretion of mediators from mast cells, secretion production in the bronchi and swelling of their mucosa; accelerate MCT and alleviate the patient’s symptoms (reduce shortness of breath due to bronchospasm). In contrast to asthma, in COPD, episodic shortness of breath is associated with physical function. Most patients with COPD require constant therapy with bronchodilators, so the use of short-acting Iβ 2 -AGs is unsatisfactory - they must be inhaled frequently and addiction to them quickly develops (tachyphylaxis). Iβ 2 -AGs do not have true anti-inflammatory activity and do not affect mucus production. They are prescribed “on demand”, also with a spacer, in small doses (3-4 r/day), in which cardiotoxic effects (a sharp increase in myocardial oxygen demand, tachycardia, arrhythmias), hypokalemia and hand tremors are very rare. The effect of Iβ 2 -AG is rapid (after 4-8 minutes), and the duration is 3-6 hours. Larger doses have a greater effect. The selection of a bronchodilator is carried out after assessing its effect on FEV 1 - there should be an increase of >20% from the initial level after 15 minutes (in this case the test is considered positive). If the reversibility of obstruction is proven (usually it is detected in a third of patients with COPD), then the prescription of Iβ 2 -AG is justified. Bronchodilators are prescribed to patients with COPD for at least 7 days. For regular treatment of COPD, more effective long-acting Iβ 2 -AGs (salmeterol, formoterol, 1 puff, 2 times a day) are usually used, which provide bronchoconstriction throughout the day and in the long term reduce the frequency of exacerbations of the disease.

Indications for taking GCS are persistent bronchial obstruction (FEV 13 times over the last 3 g), poorly controlled by taking maximum doses of bronchodilators, a positive response to GCS (increase in FEV 1>15% of the initial level), episodes of severe bronchial obstruction in history. Initially, ICS with a spacer is prescribed (they are less effective than oral forms): Ingacort, becotide, budesonide, fluticasone - 1 puff 3-4 times / day (maximum dose 800 mcg). Duration of treatment from 2 weeks to 10 months. When the (+) effect occurs, the dose is gradually reduced. ICS has almost no side effects in such small doses. In the hospital, GCS (30-40 mg of prednisolone) is prescribed to all patients (iv or orally) with severe exacerbation, in the absence of contraindications, for 10 days. An integrated approach to the treatment of COPD is ensured by long-term administration of combined aerosol therapy with salmeterol (long-acting Iβ 2 -AG, 2 times / day, 50 mcg) with fluticasone (ICS 500 mcg, 2 times / day) or seretide (salmeterol + beclamethasone) or Symbicort (formoterol + budesonide). After the entire arsenal of drugs has been used, oral corticosteroids are used for a short trial course: prednisolone for the first 7–14 days at 20–40 mg/day, then the dose is quickly reduced to 10 mg and after 2 weeks the corticosteroids are “gone.” This makes it possible to identify patients with a significant asthmatic component, accelerate recovery from an exacerbation, and maintain a low level of symptoms in a significant proportion of patients.

Drug therapy of patients depending on the severity of COPD (GOLD) Stage Treatment I. Mild Elimination of the effects of unfavorable risk factors; annual vaccination (against influenza and pneumococcus); M-anticholinergics, short-acting Iβ 2 -AG as needed (“no symptoms - no drugs”, if there are any, control them) II. Moderate + regular use of one or more long-acting bronchodilators (M-anticholinergic, Iβ 2 -AG short or long-acting, long-acting theophyllines); pulmonary rehabilitation III. Severe + ICS for repeated exacerbations; treatment of exacerbations IV. Very severe + long-term oxygen therapy for symptoms of chronic renal failure; deciding on lung resection or lung transplantation

AB therapy for exacerbation of COPD Simple exacerbation: ≤ 4 exacerbations per year, no concomitant diseases, FEV 1 >50% Complicated exacerbation Age >65 years, >4 exacerbations/g, presence of serious chronic concomitant diseases (CHF, diabetes, liver pathology or kidneys), FEV 1 4 r/g, or recent (last 3 months) prescription of an AB; chronic “bronchial sepsis”, long-term use of corticosteroids, severe course with FEV 1<30%; выделение сине-гнойной палочки во время предшествующих обострений или ее носительство АБ при пока-заниях: орально амоксициллин, доксициклин. Альтернатива – амоксиклав, кла-ритромицин, рес-пираторные ФХ, К АБ часто отмечается резистентность. АБ выбора: орально амоксиклав или респираторные ФХ. Парентерально – амоксиклав, Цеф2 -3 п, респираторные ФХ АБ: ФХ с антисинегнойной активностью (ципрофло-ксацин, левофлоксацин) или β-лактамы с антисинегнойной активностью ±Ам. Г

Chronic obstructive pulmonary disease (COPD) is a collective concept that includes chronic diseases of the respiratory system with primary involvement distal sections respiratory tract with partially reversible bronchial obstruction, characterized by progression and increasing chronic respiratory failure. This definition includes chronic obstructive bronchitis, emphysema, and severe forms of bronchial asthma. DEFINITION OF COPD

Stage 0: chronic cough and sputum production, spirometry readings are normal, shortness of breath only with very intense exertion. Stage I: Mild COPD FEV 1/FVC 80%. Obstructive disorders - FEV 1 / FVC 80%. Shortness of breath when walking quickly or climbing slightly Stage II: COPD of moderate severity (50%

Complaints: Cough is the earliest symptom of the disease. In the first stages of the disease it appears sporadically, later it occurs daily; Sputum; Shortness of breath varies from a feeling of lack of air during normal physical activity to severe respiratory failure, and becomes more pronounced over time. “Cyanotic edema” “Cyanotic edema” cyanotic have peripheral edema as a manifestation of heart failure. When examining them, signs of chronic bronchitis and “pulmonary heart” are revealed. Shortness of breath is insignificant, the main manifestations of exacerbation of the disease are cough with purulent sputum, cyanosis and signs of hypercapnia (headache, anxiety, tremor, confusion of speech, etc.) “Pink puffers” “Pink puffers” do not look cyanotic, they have low nutrition. When examined, signs of pulmonary emphysema predominate. The cough is minor, and the main complaint is shortness of breath on exertion. The work of the respiratory muscles is significantly increased. Changes in the gas composition of arterial blood are minimal. The patient usually breathes shallowly. Exhalation is carried out through half-closed lips (“puffing” breathing). Patients with COPD often sit with their torso bent forward, resting their hands on their knees, on the skin of which trophic changes form. COPD CLINIC

According to clinical signs, there are two main phases of COPD: stable and exacerbation of the disease. A condition is considered stable when the progression of the disease can be detected only with long-term follow-up of the patient, and the severity of symptoms does not change significantly over the course of weeks or even months. Exacerbation is a deterioration in the patient’s condition, manifested by an increase in symptoms and functional disorders and lasting at least 5 days. Exacerbations can begin gradually, gradually, or can be characterized by a rapid deterioration of the patient’s condition with the development of acute respiratory and right ventricular failure. PHASES OF COPD

In the basic treatment of COPD, the main role is given to inhaled pharmacotherapy using mainly three groups modern drugs anticholinergics (anticholinergic bronchodilators), (long-acting beta2-agonists and inhaled glucocorticosteroids (GCS). Treatment should begin with monotherapy with an anticholinergic or long-acting beta2-agonist. anticholinergics beta2-agonists inhaled glucocorticosteroids with an anticholinergic beta2 agonist BASIC TREATMENT

Ph.D. Associate Professor Bulieva N.B. Department of Therapy, IKBFU

Slide 2: Chronic obstructive pulmonary disease (COPD)

is a preventable and treatable disease characterized by persistent airflow limitation that is usually progressive and associated with an increased chronic inflammatory response of the lungs to pathogenic particles or gases.

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Chronic obstructive pulmonary disease (COPD) remains one of the most important health problems. According to data published by the World Bank and the World Health Organization (WHO), it is expected to become the 5th largest disease cause globally in 2020.

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In order to draw more attention to the problem of COPD, its treatment and prevention, in 1998, an initiative group of scientists created the Global Initiative for Chronic Obstructive Lung Disease (GOLD). GOLD's most important goals include increasing knowledge about COPD and helping the millions of people who suffer from the disease and die prematurely from COPD or its complications.

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Mechanisms underlying airflow limitation in COPD Disease of small bronchi Destruction of parenchyma Inflammation of the bronchi Loss of alveolar Remodeling of bronchial attachments Blockage of the bronchial lumen Decrease in elasticity Increased resistance to airway draft Airflow limitation

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Slide 9: Risk factors

Smoking Occupational hazards such as organic and inorganic dusts, as well as chemical agents and fumes, Indoor air pollution due to the combustion of bio-organic fuels for cooking and heating in poorly ventilated residential areas

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A severe respiratory infection in childhood can lead to decreased lung function and more frequent respiratory symptoms in adulthood

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Key features to suggest a diagnosis of COPD COPD should be suspected and spirometry performed if any of the following features are present in an individual over 40 years of age. These signs are not diagnostic in themselves, but the presence of several signs increases the likelihood of a COPD diagnosis. Dyspnea is progressive (worsens over time). Usually worsens with physical activity. Persistent. Chronic cough. May appear sporadically and may be counterproductive. Chronic discharge Any case of chronic discharge of sputum may cause sputum. indicate COPD. History of exposure to risk factors. Tobacco smoking (including popular local blends), Kitchen and home heating smoke Professional dust pollutants and chemicals. Family history of COPD

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Slide 15: Symptoms

Dyspnea is the most important symptom of COPD and is the main cause of disability and complaints associated with the disease. In typical cases, patients with COPD describe shortness of breath as a feeling of increasing effort to breathe, heaviness, lack of air, and suffocation.

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Cough: chronic cough is often the first symptom of COPD and is often underestimated by patients, as it is considered an expected consequence of smoking and/or exposure to factors environment. At first the cough may be intermittent, but later it is present every day, often throughout the day. In COPD, a chronic cough may be nonproductive.

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Causes of chronic cough Intrathoracic COPD BA Lung cancer Tuberculosis Bronchiectasis Left ventricular failure Interstitial lung diseases Cystic fibrosis Idiopathic cough Extrathoracic Chronic allergic rhinitis Cough as a result of upper respiratory tract pathology Gastroesophageal reflux Drug therapy (for example, ACE inhibitors)

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Sputum production: Patients with COPD typically produce small amounts of viscous sputum after a series of coughs. Regular sputum production for 3 months. or more for two consecutive years (in the absence of any other reasons that could explain this phenomenon) serves as the epidemiological definition of chronic bronchitis. The production of large amounts of sputum may indicate the presence of bronchiectasis. The purulent nature of sputum reflects an increase in the level of inflammatory mediators; the appearance of purulent sputum may indicate the development of an exacerbation.

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Wheezing and chest tightness: These symptoms are relatively uncommon in COPD and can vary from day to day, as well as within a day. Distant rales can occur in the laryngeal region and are usually not accompanied by pathological auscultatory phenomena. On the other hand, in some cases, widespread dry inspiratory or expiratory wheezing may be heard.

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Slide 20: Additional symptoms for severe disease

Fatigue, weight loss and anorexia are common problems in patients with severe to extremely severe COPD. Cough fainting (syncope) occurs as a result of a rapid increase in intrathoracic pressure during coughing attacks. Swelling of the ankle joints may be the only sign of cor pulmonale. Symptoms of depression and/or anxiety merit specific questions during the history, as such symptoms are common in COPD and are associated with an increased risk of exacerbations and worsened patient outcomes.

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Slide 21: Diagnostics

Physical examination is an important part of patient monitoring. Physical signs of airflow limitation are usually absent until significant impairment of pulmonary function has developed.

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Slide 22: Spirometry

The most repeatable and accessible method for measuring airflow limitation. With spirometry, it is necessary to measure the volume of air exhaled during forced expiration from the point of maximum inspiration (forced vital capacity, FVC), and the volume of air exhaled in 1 second during forced expiration (forced expiratory volume in 1 second, FEV1), and you should also calculate the ratio of these two indicators (FEV1/FVC (threshold value is a ratio of 0.7).

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Spirometry normal FEV1=4L FVC=5L FEV1/FVC=0.8 Spirometry – obstructive disease FEV1=1.8L FVC=3.2L FEV1/FVC=0.56

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Slide 24: Classification of severity of airflow limitation in COPD

In patients with FEV1/FVC<0,70: GOLD 1: Легкая ОФВ1 ≥80% от должного GOLD 2: Средней тяжести 50% ≤ ОФВ1 < 80% от должного GOLD 3: Тяжелая 30% ≤ ОФВ1 < 50% от должного GOLD 4: Крайне тяжелая ОФВ1 <30% от должного

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Slide 25: Additional research

Radiation diagnostics. Chest X-ray is not helpful in diagnosing COPD but is important in ruling out alternative diagnoses and identifying significant comorbidities. Radiological changes associated with COPD include signs of hyperinflation, increased transparency of the lungs, and rapid disappearance of the vascular pattern. Computed tomography (CT) of the chest is not recommended in routine practice.

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Lung volumes and diffusion capacity (plethysmography or measurement of lung volume by helium dilution method): the severity of COPD is assessed, but is not decisive for the choice of treatment tactics. Measurement of lung diffusing capacity for carbon monoxide (DLCO) provides information about the functional contribution of emphysema to COPD and is often useful in the evaluation of patients with dyspnea disproportionate to the severity of airflow limitation.

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Oximetry and arterial blood gas studies. Pulse oximetry can be used to assess the degree of oxygen saturation of hemoglobin in arterial blood (saturation) and the need for additional oxygen therapy. Pulse oximetry should be performed in all stable patients with FEV1<35% от должного или с клиническими признаками развития дыхательной или правожелудочковой сердечной недостаточности. Если периферийная сатурация по данным пульсоксиметрии составляет <92%, надо провести исследование газов артериальной крови.

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Screening for α1-antitrypsin deficiency. WHO recommends that patients with COPD living in areas with a high incidence of α1-antitrypsin deficiency should be screened for the presence of this genetic disorder.

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Load tests. An objectively measured decrease in exercise tolerance by the magnitude of the decrease in the maximum distance covered by the patient at his usual pace or during laboratory testing with increasing load is an informative indicator of the deterioration of the patient’s health and a prognostic factor.

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Complex scales. The BODE method (Body mass index, Obstruction, Dyspnea, Exercise) provides a combined score that predicts subsequent survival better than any of the above indicators taken separately.

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Slide 31: Differential diagnosis of COPD

Diagnosis Presumptive signs of COPD Begins in middle age. Symptoms progress slowly. History of tobacco smoking or exposure to other types of smoke. Bronchial asthma Begins at a young age (often in childhood). Symptoms vary widely from day to day. Symptoms are worse at night and early in the morning. There are also allergies, rhinitis and/or eczema. Family history of asthma.

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Congestive heart failure Chest x-ray shows cardiac enlargement and pulmonary edema. Pulmonary function tests reveal volumetric restriction rather than bronchial obstruction. Bronchiectasis Copious discharge of purulent sputum. Usually combined with a bacterial infection. Chest X-ray/CT scan reveals dilatation of the bronchi and thickening of the bronchial wall. Tuberculosis Begins at any age. Pulmonary infiltrate is observed on chest x-ray. Microbiological confirmation. High local prevalence of tuberculosis. Bronchiolitis obliterans Onset at a young age, in non-smokers. There may be a history of rheumatoid arthritis or acute exposure to noxious gases. Observed after lung or bone marrow transplantation. An expiratory CT scan reveals areas of decreased density.

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Diffuse panbronchiolitis Occurs predominantly in patients of Asian origin. Most patients are non-smoking men. Almost everyone suffers from chronic sinusitis. Chest x-ray and high-resolution CT scan reveal diffuse small centrilobular nodular opacities and hyperinflation.

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Slide 35: CHOICE OF TREATMENT

KEY POINTS Quitting smoking is very important for patients who smoke. Pharmacotherapy and nicotine replacement therapy significantly increase the success of smoking cessation. Appropriate pharmacotherapy can reduce the severity COPD symptoms, reduce the frequency and severity of exacerbations and improve overall health and exercise tolerance.

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3. Currently, none of the drugs for the treatment of COPD has a significant effect on the decline in lung function. 4. The pharmacotherapy regimen should be selected individually in each specific case, depending on the severity of symptoms, the risk of complications, the availability of medications and the patient’s response to treatment.

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Slide 37

5. Every patient with COPD should be offered vaccination against influenza and pneumococcal disease; they are most effective in elderly patients and patients with severe forms of the disease or with concomitant cardiac pathology. 6. All patients who experience shortness of breath when walking on level ground at their usual pace should be offered rehabilitation to improve symptoms, quality of life, daily physical and emotional functioning in daily life.

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Slide 40

The Five-Step Treatment Program provides a strategic plan useful for health care providers who are interested in helping their patients quit smoking.

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Slide 41: A quick guide to helping patients who want to quit smoking

1. ASK: Systematically identify all tobacco smokers during each visit. Implement a health care practice that ensures that EVERY patient at EVERY health care visit is interviewed about their tobacco smoking status and documented. 2. RECOMMEND: Strongly encourage all tobacco smokers to quit smoking. Persuade every tobacco smoker to quit smoking in a clear, persistent, and personal manner.

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Slide 42

3. EVALUATE: Determine your desire to try to quit smoking. Ask each tobacco smoker whether he or she would like to make a quit attempt at this time (for example, in the next 30 days). 4. PROVIDE HELP: Help the patient quit smoking. Help the patient create a smoking cessation plan; provide practical advice; provide social support as part of the treatment process, help the patient obtain social support after treatment; Recommend the use of proven pharmacotherapy except in special circumstances; Provide the patient with additional materials. 5. ORGANIZE: Create a post-treatment contact schedule. Schedule visits or telephone contacts to monitor the patient's progress after treatment.

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Slide 43: Treatment goals for stable COPD

Reduce symptoms Increase tolerance to physical activity symptoms Improve health status

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Slide 45: Dosage forms and doses of drugs used for COPD

Drug Duration of action, h β 2 - agonists Short-acting Fenoterol 4–6 Levalbuterol 6–8 Salbutamol (albuterol) 4–6 Terbutaline 4–6

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Slide 46

Long-acting Formoterol 12 Arformoterol 12 Indacaterol 24 Anticholinergic drugs Short-acting Ipratropium bromide 6-8 Oxitropium bromide 7-9 Long-acting Tiotropium 24

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Combination of short-acting β2Kagonists and anticholinergic drugs in one inhaler Fenoterol / ipratropium 6-8 Salbutamol / ipratropium 6-8 Methylxanthines Aminophylline Up to 24 hours Theophylline (slow release) Up to 24 hours Inhaled corticosteroids Beclomethasone Budesonide

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Slide 48

Combination of long-acting β2-agonists and corticosteroids in one inhaler Formoterol / budesonide Salmeterol / fluticasone Systemic corticosteroids Prednisone Methylprednisolone Phosphodiesterase 4 inhibitors Roflumilast 24h

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Slide 49

Patients in group A have mild symptoms of the disease and a low risk of exacerbations. There are no specific data regarding the effectiveness of pharmacotherapy for patients with FEV1 >80% predicted (GOLD 1). Patients in group B have a more developed clinical picture of the disease, but the risk of exacerbations remains low.

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Slide 50

Patients in group C have sparse symptoms of the disease, but a high risk of exacerbations. Patients in group D have a developed clinical picture of the disease and a high risk of exacerbations.

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Slide 51: Initial tactics of drug treatment for COPD

Patient group First-line therapy Second-line therapy Alternative A Short-acting anticholinergic on demand or short-acting β2 agonist on demand Long-acting anticholinergic or long-acting β2 agonist or short-acting anticholinergic or short-acting β2 agonist Theophylline B Long-acting anticholinergic or long-acting β2 agonist Long-acting cozy anticholinergic drug and long-acting β2-agonist Short-acting β2-agonist and/or short-acting anticholinergic drug Theophylline

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Slide 52

C Inhaled GCS + long-acting β2 agonist or long-acting anticholinergic drug Long-acting anticholinergic drug and long-acting β2 agonist Phosphodiesterase-4 inhibitor Short-acting β2 agonist and/or short-acting anticholinergic drug Theophylline D Inhaled GCS + long-acting β2 agonist or long-acting active anticholinergic drug Inhaled GCS and long-acting anticholinergic drug or inhaled corticosteroids + long-acting β2-agonist and Carbocysteine ​​Short-acting β2-agonist and/or short-acting anticholinergic drug Theophylline

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Slide 53

long-acting anticholinergic drug and long-acting anticholinergic drug or inhaled corticosteroids + long-acting β2-agonist and phosphodiesterase-4 inhibitor or long-acting anticholinergic drug and long-acting β2-agonist or long-acting anticholinergic drug and phosphodiesterase-4 inhibitor

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Slide 54: TREATMENT OF EXacERBATIONS

Exacerbation of COPD is an acute condition characterized by a worsening of a patient's respiratory symptoms beyond normal daily fluctuations and leading to a change in current therapy. Exacerbations of COPD can be triggered by several factors. The most common causes of exacerbation are viral infections of the upper respiratory tract and infection of the tracheobronchial tree.

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Slide 55

The diagnosis of exacerbation is made solely on the clinical basis of the patient's complaints of acute worsening of symptoms (shortness of breath at rest, cough and/or sputum production) beyond normal daily fluctuations. The goal of treating exacerbations of COPD is to minimize the impact of the current exacerbation and prevent the development of future exacerbations.

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Slide 56

For the treatment of exacerbations of COPD, the bronchodilators of choice are usually short-acting inhaled β2-agonists, with or without short-acting anticholinergics. The use of systemic corticosteroids and antibiotics can speed up recovery, improve pulmonary function (FEV1), reduce arterial hypoxemia (PaO2), reduce the risk of early relapses and adverse treatment outcomes, and shorten the length of hospital stay.

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Slide 57

Exacerbations of COPD can often be prevented. Therapeutic interventions that reduce the number of exacerbations and hospitalizations are: smoking cessation, vaccination against influenza and pneumococcal disease, awareness of the therapy, including inhalation technique, treatment with long-acting inhaled bronchodilators with or without inhaled corticosteroids, and also treatment with a phosphodiesterase inhibitor - 4.

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Slide 58: Potential indications for hospitalization for evaluation or treatment of exacerbations of COPD

Significant increase in the intensity of symptoms, such as the sudden development of shortness of breath at rest Severe forms of COPD The emergence of new clinical manifestations (for example, cyanosis, peripheral edema) Inability to control the exacerbation with the initially used drugs

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Slide 59

Serious comorbidities (eg, heart failure or recent arrhythmias) Frequent exacerbations Older age Inadequate care at home

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Slide 60: Research methods for assessing the severity of exacerbation

Pulse oximetry (to regulate supplemental oxygen therapy). Chest X-ray (to rule out alternative diagnoses). ECG (for diagnosing concomitant heart pathologies). Complete blood count (may reveal polycythemia (hematocrit >55%), anemia, or leukocytosis).

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Slide 61

The presence of purulent sputum during an exacerbation is sufficient grounds for initiating empirical antibacterial therapy. The most common pathogens during exacerbations of COPD are Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis. Spirometry is not recommended during an exacerbation because it may be difficult to perform and the measurements are not accurate enough.

Slide 65: Criteria for discharge from hospital

The patient is able to take long-acting bronchodilators (β2 agonists and/or anticholinergic drugs) in combination with or without inhaled corticosteroids; Short-acting inhaled β2-agonists should be taken no more frequently than every 4 hours; The patient’s ability to move around the room independently;

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The patient is able to eat and can sleep without frequent awakenings due to shortness of breath; Clinical stability of the condition during the day; Stable arterial blood gas values ​​for 12–24 hours; The patient (or home care provider) fully understands the correct medication regimen; Issues of further monitoring of the patient have been resolved (for example, visits to the patient by a nurse, supply of oxygen and food); The patient, family and physician are confident that the patient can successfully manage everyday life.

Slide 2

Appeared November 20, 2006 First full revision of the GOLD document General structure 2001-05 saved Includes data from new Evidence-based studies New chapter on primary care 02/27/2017 2 SSMU, Department of Polyclinic Therapy

Slide 3

Global strategy for the diagnosis, treatment and prevention of COPD

Definition, classification Damage from COPD Risk factors Pathogenesis, pathophysiology Treatment Recommendations for primary care 02/27/2017 3 SSMU, Department of Polyclinic Therapy

Slide 4

Epidemiology of COPD

The prevalence of COPD in the world among men is 9.3 per 1000, women - 7.3 per 1000 population. Only 25% of cases of the disease are detected in the early stages. Official data from the Ministry of Health of the Russian Federation - about 2.4 million patients with COPD in Russia (according to epidemiological studies - exceeds 16 million people) COPD is the only most common disease for which mortality continues to increase Mortality from COPD is one of the main causes in the structure of mortality in older age groups - from 2.3 to 41.4 per 100,000 population (depending on smoking ) 02/27/2017 4 SSMU, Department of Polyclinic Therapy

Slide 5

COPD is a disease characterized by airflow limitation that is not completely reversible. Airflow limitation is progressive and is associated with a pathological inflammatory response of the lungs to the action of inhaled pathogenic particles or gases GOLD (Global strategy: diagnosis, treatment and prevention of chronic obstructive pulmonary disease, 2003) 02/27/2017 5 SSMU, Department of Polyclinic Therapy

Slide 6

COPD

Chronic inflammatory disease Occurring in people over 35 years of age under the influence of various factors of environmental aggression (risk factors), the main one of which is smoking Occurs with predominant damage to the distal parts of the respiratory tract and lung parenchyma, the formation of emphysema Characterized by partially reversible and irreversible airflow limitation Induced by inflammatory a reaction that differs from inflammation in asthma and exists regardless of the severity of the disease 02/27/2017 6 SSMU, Department of Polyclinic Therapy

Slide 7

Develops in predisposed individuals, manifests itself as cough, sputum production and increasing shortness of breath, has a steadily progressive nature with the outcome in chronic respiratory failure and cor pulmonale. Partially reversible airflow limitation associated with the presence of bronchiectasis, cystic fibrosis, post-tuberculous fibrosis, and asthma is excluded from the concept of COPD. 02/27/2017 7 SSMU, Department of Polyclinic Therapy

Slide 8

Definition of COPD (2006)

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease that is accompanied by extrapulmonary manifestations that increase the severity of the disease. Characterized by airflow limitation that is not completely reversible. Airflow limitation is usually progressive and is associated with an inflammatory response of the lungs to pathogenic particles or gases. 02/27/2017 8 SSMU, Department of Polyclinic Therapy

Slide 9

ICD-10

J 44.0 Chronic obstructive pulmonary disease with acute respiratory infection of the lower respiratory tract J 44.1 Chronic obstructive pulmonary disease with exacerbation, unspecified J 44.8 Other specified chronic obstructive pulmonary disease J 44.9 Chronic obstructive pulmonary disease, unspecified 02/27/2017 9 SSMU, Department of Polyclinic Therapy

Slide 10

Example of a diagnosis statement (Primary Health Care Manual)

Nosology – COPD Severity (stage of disease): mild (stage I), moderate (stage II), severe (stage III), extremely severe (stage IV) Clinical form (for severe disease): bronchitis, emphysematous , mixed (emphysematous-bronchitis) Phase of the course: exacerbation, subsiding exacerbation, stable course. Identify 2 types of course: with frequent exacerbations (3 or more exacerbations per year), with rare exacerbations Complications: CDN, ARF against the background of chronic, pneumothorax, pneumonia, thromboembolism, in the presence of bronchiectasis, indicate their location, cor pulmonale, degree of circulatory failure If possible combination with asthma (in 10%) give its detailed diagnosis Indicate the index of the smoking person (in units of “pack/years”) EXAMPLE: severe COPD, bronchitis form, exacerbation phase, 3rd degree DN. CHL, HF 2nd degree. 02/27/2017 10 SSMU, Department of Polyclinic Therapy

Slide 11

Mechanisms underlying bronchial obstruction in COPD

Inflammation Disease of small bronchi Destruction of parenchyma Limitation of air flow speed 02/27/2017 11 SSMU, Department of Polyclinic Therapy

Slide 12

Pathomorphological changes

Chronic inflammation and structural changes develop in the proximal and distal parts of the bronchi, parenchyma and vessels of the lungs. Inflammation in COPD is characterized by an increase in the number of neutrophils (airway lumen), macrophages (bronchial lumen and wall, parenchyma), and CD8+ lymphocytes (bronchial wall and parenchyma). The inflammation is different from that of asthma. 02/27/2017 12 SSMU, Department of Polyclinic Therapy

Slide 13

Bronchial asthma and COPD

Bronchial asthma Sensitizing agent Inflammation of the airways, characteristic of BA CD4+ T-lymphocytes Eosinophils COPD Pathogenic agent Inflammation of the airways, characteristic of COPD CD8+ T-lymphocytes Macrophages, neutrophils Limitation Fully air velocity Fully Reversible flow irreversible 02/27/2017 13 SSMU, Department of Polyclinic Therapy

Slide 14

COPD and Bronchial Asthma

Inflammation in COPD and asthma is different, which leads to different pathomorphological changes, clinical symptoms, and approaches to treatment. In severe forms of asthma and COPD, inflammation may acquire similar features. Long-term asthma may have signs of irreversible obstruction. COPD and asthma can be combined in one patient. Especially in a smoking asthmatic patient. 02/27/2017 14 SSMU, Department of Polyclinic Therapy

Slide 15

Significant systemic effects Weight loss, nutritional disorders Skeletal muscle dysfunction Increased risk of developing: Myocardial infarction, angina pectoris osteoporosis Respiratory tract infections depression diabetes Lung cancer COPD and related diseases 02/27/2017 15 SSMU, Department of Polyclinic Therapy

Slide 16

Risk factors for COPD

02/27/2017 16 SSMU, Department of Polyclinic Therapy

Slide 17

Smoking history assessment

ICI - index of a smoking person - potential for developing COPD = number of cigarettes smoked per day X number of months per year when a person smokes ICI > 120 - “heavy smoker” Total number of pack/years = number of packs of cigarettes smoked per day X number of years smoking 10 pack/years - risk of developing COPD more than 25 packs/years - heavy smoker COPD develops in approximately 15% of smokers and about 7% of former smokers 02/27/2017 17 SSMU, Department of Polyclinic Therapy

Slide 18

Changes in lung function depending on age and smoking experience

02/27/2017 18 SSMU, Department of Polyclinic Therapy

Slide 19

Peak initiation into smoking: for boys - up to 10 years old, for girls - 13 - 14 years old. The prevalence of smoking among urban adolescents aged 15–17 years: for boys – 39.1%, for girls – 27.5%. According to a survey of SSMU students (18 – 23 years old), about 30% of respondents smoke. 02/27/2017 19 SSMU, Department of Polyclinic Therapy

Slide 20

Fagerstrom test for determining nicotine addiction

1. How long after waking up do you light your first cigarette? More than 60 minutes (0 points) 31-60 minutes (1 point) 6-30 minutes (2 points) Less than 5 minutes (3 points) 2. You find it difficult to resist smoking in places where smoking is prohibited, for example, at a meeting, on an airplane, in a movie, etc.? No (0 points) Yes (1 point) 3. Which cigarette is most difficult for you to give up? From the first one in the morning (1 point) From any other (0 points) 02/27/2017 20 SSMU, Department of Polyclinic Therapy

Slide 21

4. How many cigarettes do you smoke per day? 10 or less (0 points) 11-20 (1 point) 21-30 (2 points) 31 or more (3 points) 5. Do you smoke more often in the early morning hours than at other times of the day? No (0 points) Yes (1 point) 6. Do you smoke even if you are sick and have to lie in bed most of the day? No (0 points) Yes (1 point) Fagerstrom test to determine nicotine addiction 02/27/2017 21 SSMU, Department of Polyclinic Therapy

Slide 22

0-3 points - You will probably be able to quit smoking without resorting to medication. Don't put off this step until tomorrow! 4-6 points – Your dependence on nicotine can be assessed as average. Having gathered all your willpower, you are quite capable of quitting smoking. 7-10 points – You have a high degree of dependence on nicotine. You and your doctor should consider using medications to help you quit smoking. In any case, remember: anyone can quit smoking! Fagerstrom test for determining nicotine addiction 02/27/2017 22 SSMU, Department of Polyclinic Therapy

Slide 23

COPD and everyday life

Pulmonary dysfunction Disability 02/27/2017 23 SSMU, Department of Polyclinic Therapy

Slide 24

Perspective on COPD

"I'm running out of air." “I used to walk to the store for 5-7 minutes, now it takes 10-20: I stop to catch my breath.” “Now I have to rest after every flight of stairs when I get to my floor.” “I can’t even walk with my dog ​​- I’m out of breath when I walk.” “I can’t breathe normally, leaving the house is a big problem.” etc. 02/27/2017 24 SSMU, Department of Polyclinic Therapy

Slide 25

Spiral progression of dyspnea

Typically, patients consciously or unconsciously change their lives in ways that reduce the symptoms of shortness of breath. 02/27/2017 25 SSMU, Department of Polyclinic Therapy

Slide 26

Obstruction in COPD

Chronic bronchial obstruction – registered at least 3 times within one year, despite the therapy. The unifying feature of COPD is a post-bronchodilator decrease in FEV1/FVC

Slide 27

Spirometry for COPD diagnosis and severity classification

02/27/2017 27 SSMU, Department of Polyclinic Therapy

Slide 28

stage I: mild stage II: moderate stage III: severe stage IV: very severe chronic DN FEV1/FVC 80% of predicted FEV1/FVC

Slide 29

New version of the global initiative on chronic obstructive pulmonary disease (Revision December 2006)

Changes in COPD classification: COPD stage 0, risk of developing COPD, which was present in the 2001 version, has been removed. Stage 0 according to the 2001 version corresponded to chronic cough with sputum production with normal spirometry. In the latest version, stage 0 is excluded, since there is no evidence that chronically coughing patients will necessarily develop stage 1 COPD. 02/27/2017 29 SSMU, Department of Polyclinic Therapy

Slide 30

For the first time, a definition of exacerbation of COPD has been formulated: Exacerbation of COPD is part of the natural course of the disease, characterized by a change in the severity of shortness of breath, cough, and sputum production compared to the baseline and exceeding the usual variability of symptoms. An exacerbation has an acute onset and leads to the need to change the patient's daily therapy for COPD. Indications for the use of ICS in COPD are limited. Indications for the use of ICS are formulated as follows: FEV1

Slide 33

The main signs to suspect the diagnosis of COPD

COPD should be suspected and spirometry performed if any of the following signs are present. These signs are not diagnostic in themselves, but the presence of multiple signs increases the likelihood of a diagnosis of COPD. Spirometry is necessary to establish the diagnosis of COPD. 02/27/2017 33 SSMU, Department of Polyclinic Therapy

Slide 34

Diagnosis of COPD

Symptoms: cough sputum shortness of breath Risk factors smoking occupational hazards environmental pollution environmental pollution Spirometry 02/27/2017 34 SSMU, Department of Polyclinic Therapy

Slide 35

GOLD questionnaire for screening patients with COPD

1. Do you cough several times a day most days? 2. Do you cough up mucus most days? 3. Do you experience shortness of breath more quickly than people your age? 4. Are you over 40 years old? 5. Do you currently smoke or have you smoked before? If you answered “Yes” 3 times or more, consult a doctor! 02/27/2017 35 SSMU, Department of Polyclinic Therapy

Slide 36

Clinical forms of COPD (moderate and severe)

02/27/2017 36 SSMU, Department of Polyclinic Therapy

Slide 37

Clinical forms of COPD (with moderate and severe cases) 02/27/2017 37 SSMU, Department of Polyclinic Therapy

Slide 38

Respiratory failure is the inability of the respiratory system to provide a normal gas composition of arterial blood; pathological syndrome in which the partial oxygen tension of arterial blood (PaO2) is less than 60 mm Hg. Art. or oxygen saturation less than 88% in combination (or without) PaCO2 more than 45 mm Hg. Art. 02/27/2017 38 SSMU, Department of Polyclinic Therapy

Slide 39

Obstructive apnea-hypopnea syndrome (OSAHS)

Sleep apnea is a potentially life-threatening respiratory disorder, defined as a period of asphyxia during sleep, leading to the development of excessive daytime sleepiness, hemodynamic disorders and cardiac instability. The combination of COPD and OSAHS contributes to the rapid progression of the disease and airway obstruction, leading to early disability and reduced life expectancy. The presence of OSAHS is typical for patients with the bronchitis type of severe COPD. Non-invasive mask ventilation prevents the development of nocturnal breathing devices and reduces mortality. 02/27/2017 39 SSMU, Department of Polyclinic Therapy

Slide 40

Diagnostic criteria for OSAHS

Symptoms: Excessive daytime sleepiness, weakness, reducing performance and quality of life. Loud night snoring or periods of shortness of breath, “breathing damper” during sleep. Accidents at work and at home (road accidents), the cause of which was daytime sleepiness. Markers: Increased body weight (BMI > 29 kg/m2). Increased neck size (collar size) - men >43 cm, women >40 cm. Hypertension (BP > 140/90 mHg) or pulmonary hypertension or cor pulmonale. The combination of 2 symptoms + 2 markers allows us to suspect the presence of a respiratory disorder. Objective verification – polysomnography. 02/27/2017 40 SSMU, Department of Polyclinic Therapy

Slide 41

6-minute walk test

Walk along the measured corridor at your own pace, trying to cover the maximum distance in 6 minutes. Before the start and at the end of the test, shortness of breath is assessed on the Borg scale (from 0 to 10), heart rate, respiratory rate and SaO2. Walking stops if very severe shortness of breath, chest pain, dizziness, pain in the legs, and a decrease in SaO2 to 80-86% occur. The distance covered in 6 minutes in meters (6MWD) is measured and compared with the proper indicator 6MWD (i) The proper indicator for men: 6MWD (i) = 7.57 x height - 5.02 x age - 1.76 x weight - 309 or = 1140 – 5.61 x BMI – 6.94 x age Lower limit of normal = proper 6MWD (i) – 153 m Proper indicator for women: 6MWD (i)=2.11 x height – 2.29 X weight – 5.78 x age + 667 or =1017 – 6.24 x BMI – 5.83 x age Lower limit of normal = proper 6MWD (i) – 139 m 02/27/2017 41 SSMU, Department of Polyclinic Therapy

Slide 42

SCORE scale for assessing the severity of a COPD patient's condition (Symptoms Chronic Obstruction Resting Nutrition Endurance - B. Celli, 2000) Calculating the sum of points for 4 indicators (maximum sum 10 points)

02/27/2017 42 SSMU, Department of Polyclinic Therapy

Slide 43

Mandatory examination plan for COPD:

1. CBC + platelets (erythrocytosis - secondary, anemia - exclude tumor; thrombocytosis - tumor, paraneoplastic syndrome, high leukocytosis does not occur, p.i. shift - rarely: pneumonia, purulent bronchitis, ESR -1-2, with exacerbation 12-13mm /hour); increase in fibrinogen – tumor. Anemia may cause shortness of breath or increase it. Polycythemic syndrome – increased number of red blood cells, high level of HB (>160 g/l for women and 180 for men), low ESR, hematocrit>47% for women and >52% for men. Low albumin - reduced nutritional status (poor prognosis) 2. General urine analysis (amyloidosis - purulent obstructive bronchitis or PEB) 3. General sputum analysis - not very informative, cytology is needed (allows, among other things, to identify atypical cells) 4. Peak flowmetry 5. Spirometry + bronchodilator test (annually): degree of severity, differential. diagnosis with asthma, annual dynamics: decrease in FEV1 by 50 ml per year - rapid progression 02/27/2017 43 SSMU, Department of Polyclinic Therapy

Slide 44

Mandatory examination plan for COPD

6. X-ray or fluorography - once a year (exclude other causes of cough with sputum). HRCT - diagnosis of emphysema 7. ECG (signs of cor pulmonale, differential diagnosis) 8. EchoCG (cor pulmonale), rheography of the pulmonary artery - uninformative 9. FBS - not necessary (bronchitis - heterogeneous), suspected of cancer 10. ACG - in severe exacerbation. Blood gases - at FEV1

Slide 45

Scheme of outpatient observation of a patient with COPD with a local therapist

Stage I: clinical examination, spirometry with a test once a year, consultation with a pulmonologist (to confirm the diagnosis) if there is no effect of treatment within 7-14 days. For exacerbation of COPD - CBC, chest x-ray. Stage II: the same Stage III: clinical examination 2 times a year, spirometry test 1 time a year; CBC and chest X-ray, ECG – once a year. Consultation with a pulmonologist - in case of exacerbation, progression of DN, to confirm DD, to determine persistent disability stage IV: the same 02/27/2017 45 SSMU, Department of Polyclinic Therapy

Slide 46

Who is he, a COPD patient?

Middle-aged or elderly smoker Suffering from shortness of breath Having a chronic cough with sputum, especially in the morning Complaining of regular exacerbations of bronchitis Having partially reversible obstruction 02/27/2017 46 SSMU, Department of Polyclinic Therapy

Slide 47

Differential diagnosis of COPD

BA (in 10% of patients with COPD - a combination of BA and COPD) Heart failure (EchoCG - decreased LVEF, dilatation of the heart) Bronchiectasis (CT - dilatation of the bronchi, thickening of their walls) Tuberculosis Obliterative bronchiolitis (development in young people, no connection with smoking, contact with vapors and smoke. CT scan - foci of reduced density during exhalation. M. rheumatoid arthritis) 02/27/2017 47 SSMU, Department of Polyclinic Therapy

Slide 48

02/27/2017 48 SSMU, Department of Polyclinic Therapy

Slide 49

Goals of modern therapy for COPD

Improved pulmonary function; Symptomatic control; Increasing tolerance to physical activity; Improving quality of life; Prevention and treatment of exacerbations; Prevention and treatment of complications; Preventing the progression of COPD; Decrease in mortality; Minimizing adverse effects of therapy. 02/27/2017 49 SSMU, Department of Polyclinic Therapy

Slide 50

Smoking cessation is the only method that allows you to slow down the progression of bronchial obstruction 3 tobacco addiction treatment programs: short (1-3 months), long-term (6-12 months) and reducing smoking intensity; Medications not indicated for patients who smoke less than 10 cigarettes per day. 02/27/2017 50 SSMU, Department of Polyclinic Therapy

Slide 51

There is a strong relationship between the frequency of conversations health workers have about tobacco addiction and their effectiveness. There are 3 types of work with patients - practical advice, social support as often as treatment and social support outside the treatment program. There are 5 types of effective medicines first line: bupropion SR, chewing gum, inhaler, nasal spray, and nicotine patch. They should be prescribed to patients in the absence of contraindications. Treatment of tobacco addiction is more significant than the use of other methods of therapy. Does not exist drug therapy that can slow down the deterioration lung functions if the patient continues to smoke. 02/27/2017 51 SSMU, Department of Polyclinic Therapy

Slide 52

First-line medications for people who smoke 10 or more cigarettes per day

Chewing gum with nicotine Patch with nicotine Intranasal aerosol with nicotine Nicotine inhaler 02/27/2017 52 SSMU, Department of Polyclinic Therapy

Slide 53

Chewing gum with nicotine

2 or 4 mg, 4-15 gummies per day from 7-12 weeks to 6 months. Gradual reduction to 2-4 mg/day of nicotine per day. Chew slowly for 20-30 minutes. After 15 chewing movements, it is placed behind the cheek, and after the tingling disappears, chewing is resumed. Absorption in the main environment - do not drink tea, coffee, or orange juice before using chewing gum. 02/27/2017 53 SSMU, Department of Polyclinic Therapy

Slide 54

Nicotine inhaler

6-16 cartridges per day Duration - up to 6 months You should not eat or drink before or while using the inhaler Side effects: local irritation of the oral cavity 02/27/2017 54 SSMU, Department of Polyclinic Therapy

Slide 55

Nicotine patch (7,14,21 mg)

A new patch is applied to a dry, hairless area of ​​skin every morning. Changing the attachment sites reduces skin irritation. The course of treatment is 8 weeks. The effectiveness of the patch increases when combined with bupropion. 02/27/2017 55 SSMU, Department of Polyclinic Therapy

Slide 56

Contraindications for nicotine replacement therapy

Unstable angina Myocardial infarction (less than 2 weeks) Episodic smoking Severe arrhythmias Recent cerebrovascular accident Erosive disorders of the gastrointestinal tract Pregnancy Age under 18 years and over 65 years 02/27/2017 56 SSMU, Department of Polyclinic Therapy

Slide 57

Monitoring a patient with COPD

Spirometry Weight Nutritional support for a patient with COPD (protein, AA mixtures - in between meals or complete replacement in combination with anabolic steroids: increasing weight by 3-4 kg reduces shortness of breath) 02/27/2017 57 SSMU, Department of Polyclinic Therapy

Slide 58

Therapeutic measures

1. Training 2. Smoking cessation 3. Bronchodilator therapy - basis 02/27/2017 58 SSMU, Department of Polyclinic Therapy

Slide 59

Treatment of COPD depending on severity (GOLD-2003)

02/27/2017 59 SSMU, Department of Polyclinic Therapy

Slide 61

Inhaled corticosteroids/long-acting beta 2-agonists 02/27/2017 61 SSMU, Department of Polyclinic Therapy

Slide 62

Vaccination

In order to prevent exacerbation of COPD during epidemic outbreaks of influenza, vaccines containing killed or inactivated viruses are recommended for use, administered once in October - the first half of November annually (reduces the severity and mortality in patients with COPD by 50%). Pneumococcal vaccine (23 virulent serotypes) - data on its effectiveness in COPD are insufficient, but patients with COPD are among those at high risk of developing pneumococcal infection and are included in the target group for vaccination 02/27/2017 62 SSMU, Department of Polyclinic Therapy

Slide 63

1. The volume of treatment increases as the severity of the disease increases. Its reduction in COPD, unlike asthma, is usually impossible. 2. Drug therapy is used to prevent and reduce the severity of symptoms, complications, frequency and severity of exacerbations, increase exercise tolerance and improve the patient’s quality of life. 3. None of the available drugs affects the rate of decrease in bronchial obstruction, which is a hallmark of COPD 02/27/2017 63 SSMU, Department of Polyclinic Therapy

Slide 64

4. Bronchodilators are central to the treatment of COPD. They reduce the severity of the reversible component of bronchial obstruction. These funds are used on an on-demand or regular basis. 5. ICS are indicated for severe and extremely severe COPD (with FEV1 less than 50% of predicted and frequent (usually more than 3 in the last 3 years or 1-2 exacerbations in 1 year) exacerbations, for the treatment of which oral steroids and antibiotics are used These drugs are prescribed if there is no effect from properly selected bronchodilator therapy. 02/27/2017 64 SSMU, Department of Polyclinic Therapy

Slide 65

Principles of treatment of stable COPD

6. Combined treatment with ICS and long-acting β2-adrenergic agonists has a significant additional effect on pulmonary function and clinical symptoms of COPD compared to monotherapy with each drug. The greatest effect on the frequency of exacerbations and quality of life was obtained in patients with COPD with FEV1 less than 50% of predicted. These drugs are preferably prescribed as an inhaler containing their fixed combinations (formoterol/budesonide=symbicort, salmeterol/fluticasone propionate=seretide). 02/27/2017 65 SSMU, Department of Polyclinic Therapy

Slide 66

Principles of treatment for stable COPD

7. Long-term use of tableted GCS is not recommended due to the risk of systemic side effects. 8. At all stages of COPD, physical training programs are highly effective, increasing exercise tolerance and reducing the severity of shortness of breath and fatigue. 9. Long-term administration of oxygen (more than 15 hours per day) to patients with DN increases their survival. 02/27/2017 66 SSMU, Department of Polyclinic Therapy

Slide 67

Principles of bronchodilator therapy for COPD

1. The preferred route of administration of bronchodilators is inhalation. 2. The choice between b2-adrenergic agonists, anticholinergics, theophylline depends on their availability, the individual sensitivity of patients to their action and the absence of side effects. In stage II-IV COPD and in elderly patients with concomitant cardiovascular diseases (coronary artery disease, heart rate, hypertension, etc.), anticholinergics are preferred as first-line drugs. Short-acting beta2-agonists are not recommended as monotherapy for regular use. 3. Methylxanthines are effective for COPD, but due to the possibility of developing side effects, they are classified as second-line drugs. Only long-acting theophyllines have a positive effect on the course of COPD. 02/27/2017 67 SSMU, Department of Polyclinic Therapy

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4. Regular treatment with long-acting bronchodilators (tiopropium bromide = Spiriva, salmeterol = Serevent, formoterol = Oxis, Foradil) is indicated for moderate, severe and extremely severe COPD 5. A combination of several bronchodilators (for example, anticholinergics and short-acting β2-adrenergic agonists or long-acting, anticholinergics and theophyllines, b2-adrenergic agonists and theophyllines) may increase effectiveness and reduce the likelihood of side effects compared to single-drug monotherapy. 6. Nebulizer therapy with bronchodilators is carried out for COPD stages III and IV. 02/27/2017 68 SSMU, Department of Polyclinic Therapy

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Ascoril

Quickly, on the very first day, it relieves wet cough due to the simultaneous dilution of sputum, reducing its adhesion to the wall of the bronchi, and dilation of the bronchi - Bromhexine dilutes sputum; – Guaifenesin reduces mucus adhesion; – Salbutamol dilates the bronchi. 02/27/2017 69 SSMU, Department of Polyclinic Therapy

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Treatment regimen depending on the stage of COPD (GOLD, 2003, with additions)

All stages: Elimination of risk factors Annual vaccination with influenza vaccine Inhalation, if necessary, of one of: Atrovent 40 mcg, Berodual - 2 doses, Berotec - 200-400 mcg, salbutamol 200-400 mcg Stages II, III and IV (but not at stage I) Regular inhalations (Atrovent 40 mcg 4 times a day or Spiriva 18 mcg once a day ± Serevent 50 mcg twice a day or formoterol 12 mcg twice a day) ± oral theophylline 0.2-0.3 g twice a day or Berodual 2 doses 4 times a day or Serevent 50 mcg 2 times a day or formoterol 12 mcg 2 times a day ± theophylline 0.2-0.3 g 2 times a day Rehabilitation measures 02/27/2017 70 SSMU, Department of Polyclinic Therapy

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Stages III and IV (but not stages I and II) Regular inhalations (beclomethasone 1000-1500 mcg/day or budesonide 800-1600 mcg/day or fluticasone 500-1000 mcg/day or seretide 50/250 mcg (1-2 doses 2 times a day) (or Symbicort 4.5/160 mcg (2-4 doses 2 times a day) with annual or more frequent exacerbations over the past 3 years and a positive functional response (efficacy is assessed after 6-12 weeks using a bronchodilation test) Rehabilitation measures 02/27/2017 71 SSMU, Department of Polyclinic Therapy

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Inhalation therapy for COPD

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Features of inhaled anticholinergics

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Features of inhaled anticholinergic drugs 02/27/2017 74 SSMU, Department of Polyclinic Therapy

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Characteristics of the main inhaled bronchodilators for the treatment of stable COPD

02/27/2017 75 SSMU, Department of Polyclinic Therapy

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Characteristics of the main inhaled bronchodilators for the treatment of stable COPD 02/27/2017 76 SSMU, Department of Polyclinic Therapy

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Glucocorticoids

Short courses (10-14 days) 30-40 mg courses of systemic steroids - for the treatment of exacerbation of COPD (with a history of ulcers, erosions, NK - IV 2 times a day) ICS - do not have an effect on the progressive decrease in bronchial patency in patients COPD Prescribed when FEV1 is less than 50% and there are frequent exacerbations. Doses are medium and high. Flixotide 1000 mcg/day can improve the quality of life of patients and reduce the frequency of exacerbations of severe and extremely severe COPD. Combination therapy with ICS and long-acting β2-adrenergic agonists (fluticasone propionate/salmeterol = seretide 500/50 mcg, 1 ing twice daily and budesonide/formoterol = symbicort 160/4.5 mg, 2 ing twice daily) is effective in patients COPD of severe and extremely severe course. Long-term administration for 12 months improves bronchial patency, reduces the severity of symptoms, the need for bronchodilators, the frequency of moderate and severe exacerbations, and improves the quality of life of patients compared to monotherapy with ICS and long-acting β2-adrenergic agonists. 02/27/2017 77 SSMU, Department of Polyclinic Therapy

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Mucolytics (mucokinetics, mucoregulators)

Recommended for patients with COPD who have a cough and viscous sputum Ambroxol - 150 mg/day for 12 months - reduces the frequency of exacerbations in some patients with COPD of moderate severity who have severe clinical symptoms, increases the penetration of a/b into the tracheobronchial secretion Fluimucil - 600-1200 mg/day 3-6 months – reduces lung hyperinflation and the frequency of exacerbations of COPD in patients not receiving ICS. Antioxidant activity 02/27/2017 78 SSMU, Department of Polyclinic Therapy

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Oxygen therapy

DN is the leading cause of death in patients with COPD. Oxygen therapy is a pathogenetically based method of treatment. The only treatment that reduces mortality. Indications for long-term oxygen therapy in patients with extremely severe COPD (with FEV1 less than 30% of predicted or less than 1.5 l) 1. PaO2 less than 55% of predicted, SaO2 below 88% with or without hypercapnia 2. PaO2 55-60% from normal, SaO2 89% in the presence of pulmonary hypertension, peripheral edema associated with decompensation of the cor pulmonale or polycythemia (hematocrit more than 55%) 02/27/2017 79 SSMU, Department of Polyclinic Therapy

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Long-term oxygen therapy - at least 15 hours a day, gas flow rate - 1-2 l/min (up to 4 l/min). Oxygen sources are compressed gas cylinders, oxygen concentrators and liquid oxygen cylinders. Oxygen delivery - using masks, nasal cannulas (oxygen-air mixture with 30-40% O2). Oxygen therapy should never be prescribed to patients who continue to smoke or suffer from alcoholism. Before prescribing, make sure that the possibilities of drug therapy have been exhausted. 02/27/2017 80 SSMU, Department of Polyclinic Therapy

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Rehabilitation

Rehabilitation is a multidisciplinary program of individual care for patients with COPD, which is designed to improve their physical, social adaptation and autonomy. Rehabilitation components: 1. Physical training (walking, increasing endurance and strength, bicycle ergometer, lifting dumbbells 0.2-1.4 kg) – 6-minute step test. 8 weeks, 10-45 min, 1-5 times a week. 2. Education of patients (energy-saving technologies - how to breathe, cough, wash properly). 3. Psychotherapy. 4. Rational nutrition (a decrease in body weight of more than 10% within 6 months or more than 5% during the last month and especially loss of muscle mass in patients with COPD are associated with high mortality): a high-calorie diet with a high protein content and dosed physical activity, which has an anabolic effect action. Groups of patients of 6-8 people with the participation of specialists of various profiles for 6-8 weeks, 3 times/week 02/27/2017 81 SSMU, Department of Polyclinic Therapy

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Surgery

1. Bullectomy (bullous pulmonary emphysema with large bullae causing shortness of breath, hemoptysis, pulmonary infections and chest pain) - reducing shortness of breath and improving lung function. 2. Surgeries to reduce lung volume - experimental palliative, not recommended for widespread use 3. Lung transplantation (FEV1 less than 25% of predicted, PaCO2 more than 55% and progressive pulmonary hypertension). Problems: selection of a donor lung, postoperative complications(mortality rate in the USA is 10-15%), high cost (110-200 thousand dollars). 02/27/2017 82 SSMU, Department of Polyclinic Therapy

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Treatment of pulmonary hypertension and cor pulmonale

CHL – changes in the right ventricle (hypertrophy, dilatation and dysfunction) resulting from pulmonary hypertension, which developed as a result of a series of pulmonary diseases, not associated with the primary lesion or congenital heart disease. These are complications of severe and extremely severe COPD 1. Optimal therapy for COPD 2. Long-term oxygen therapy (more than 15 hours) 3. Diuretics (in the presence of edema) 4. Digoxin (only for atrial fibrillation and concomitant left ventricular failure, since cardiac glycosides do not influence contractility and ejection fraction of the right ventricle) Controversial: vasodilators (nitrates, Ca antagonists, ACE inhibitors) - deterioration of blood oxygenation and arterial hypotension. But Ca antagonists (nifedipine SR 30-240 mg/day and diltiazem SR 120-720 mg/day) can be used in patients with severe pulmonary hypertension when bronchodilators and oxygen therapy are insufficiently effective. 02/27/2017 83 SSMU, Department of Polyclinic Therapy

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Causes of exacerbation of COPD

Primary: Infections of the tracheobronchial tree (often viral) Atmospheric pollutants Secondary Pneumonia Heart failure, arrhythmias PE Spontaneous pneumothorax Uncontrolled oxygen therapy Drugs (hypnotics, tranquilizers, diuretics, etc.) Metabolic disorders (DM, electrolyte imbalance, etc.) 02/27/2017 84 SSMU, Department of Polyclinic Therapy

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Low nutritional status Other diseases (gastrointestinal bleeding, etc.) End-stage disease (respiratory muscle fatigue, etc.) Risk factors for recurrent exacerbations of COPD: low FEV1, increased need for bronchodilators and corticosteroids, previous exacerbations of COPD (more 3 over the last 2 years), previous antibacterial therapy (predominantly with ampicillin), concomitant diseases (HF, chronic renal failure and liver failure) Causes of exacerbation of COPD 02/27/2017 85 SSMU, Department of Polyclinic Therapy

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Etiology of exacerbations of COPD

Haemophilu Haemophilus influenzae – 13-46% Moraxellaсatarrhalis – 9-20% Streptococcus pneumoniae – 7-26% Complicated exacerbation of COPD: Gr (-) enterobacteria P. aeroginosa penicillin-resistant S. pneumoniae β-lactamase-producing strains H. influenzae In general: aerobic bacteria – 45% viruses – 30% “atypical” bacteria – 5% non-infectious causes – 20% 02/27/2017 86 SSMU, Department of Polyclinic Therapy

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Types of exacerbation of COPD

Exacerbation is a deterioration in the patient’s condition for 2 or more consecutive days, occurring acutely and accompanied by increased coughing, an increase in the volume of sputum discharge and/or a change in its color, and the appearance/increase of shortness of breath. Classic criteria N.R.Anthonisena: Appearance or intensification of shortness of breath Increased volume of sputum Increased purulence of sputum Type I: the presence of all 3 signs Type II: the presence of 2 signs Type III: the presence of 1 sign 02/27/2017 87 SSMU, Department of Polyclinic Therapy

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Simple (uncomplicated) exacerbation of COPD: Infrequent exacerbations (less than 4 per year) Occurring in patients under 65 years of age No serious concomitant diseases FEV1>50% of predicted values ​​Complicated exacerbation of COPD: Age ≥65 years and/or FEV1

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Exacerbation severity:

Mild – relieved by intensifying bronchodilator therapy, does not require hospitalization of the patient Moderate – the need for treatment in a hospital Severe – accompanied by symptoms of ARF (PaO2 45 mm Hg, RR>25, dysfunction of the respiratory muscles) Relapse of exacerbation of COPD – persistence or worsening of symptoms of exacerbation COPD within the next 14 days after its onset, despite the therapy 02/27/2017 89 SSMU, Department of Polyclinic Therapy

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Tactics for managing patients with exacerbation of COPD in an outpatient setting

Standard of laboratory control and instrumental monitoring: 1. CBC 2. Chest X-ray 3. General sputum analysis 4. Bacterioscopic examination of sputum 5. Bacteriological research sputum (according to indications) 6. ECG 7. Spirometry 8. Peak flowmetry 02/27/2017 90 SSMU, Department of Polyclinic Therapy

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Treatment of exacerbations

Inhaled Inhaled bronchodilators (especially short-acting β2-agonists with or without AChE) (Evidence A). Systemic corticosteroids (Evidence A). Antibiotics according to indications (Evidence B). Non-invasive mechanical ventilation (Evidence A). 02/27/2017 91 SSMU, Department of Polyclinic Therapy

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Therapy algorithm

1. Bronchodilators – increasing the frequency and/or dose of the bronchodilator used. If not used previously, add anticholinergic drugs. Preference is combined bronchodilators - Berodual. If it is impossible to use inhalation forms or if there is insufficient effective application bronchodilators and glucocorticoids - it is possible to prescribe theophylline preparations 2. GCS - for FEV1

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Indications for hospitalization of patients with exacerbation of COPD in hospital

Significantly Significant increase in the intensity of symptoms (for example, sudden development of shortness of breath at rest) Exacerbation in a patient with severe COPD Appearance of new symptoms (cyanosis, peripheral edema) No improvement in symptoms in response to initial treatment for exacerbation New arrhythmias Diagnostic difficulties Older age Insufficient treatment resources at home 02/27/2017 93 SSMU, Department of Polyclinic Therapy

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Drug therapy for exacerbation of COPD

Oxygen Bronchodilators via nebulizer: Atrovent 0.5 mg (40 drops) at intervals from 2 to 4-6 hours, salbutamol 2.5 mg (Berotec 1 mg = 20 drops) at intervals from 30 minutes to 4-6 hours, Berodual 2 .0 ml (40 drops) at intervals from 2 to 4-6 hours GCS: IV during the first 48 hours or orally: methylprednisolone 40-80 mg or hydrocortisone 100-200 mg every 6 hours, prednisolone 30-40 mg/ days orally, budesonide 2 mg every 6-12 hours via nebulizer (no more than 2 weeks) Eufillin IV: loading dose 5 mg/kg for 30 minutes, then maintenance dose - 0.4-0.5 mg/kg/ h Antibacterial therapy Heparin subcutaneously (5,000 thousand units 2-3 times a day, enoxaparin 40 mg 1 time a day) Treatment of concomitant diseases Non-invasive ventilation Invasive ventilation 02/27/2017 94 SSMU, Department of Polyclinic Therapy

Criteria for discharge of patients with exacerbation of COPD from hospital

The need for inhaled bronchodilators no more than every 4 hours The patient's ability to move around the room independently The patient is able to eat and sleep without frequent awakenings due to shortness of breath Clinical stability for 24 hours Stable arterial blood gas values ​​for 24 hours The patient fully understands the correct regimen taking medications Issues of further monitoring of the patient were resolved 02/27/2017 100 SSMU, Department of Polyclinic Therapy

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Chronic obstructive pulmonary disease (COPD) is an independent disease characterized by partially irreversible restriction of air flow in the respiratory tract. Airflow limitation is typically progressive and is caused by an abnormal inflammatory response of lung tissue to irritation from various pathogenic particles and gases. The pathological process begins in the bronchial mucosa: in response to the influence of external pathogenic factors a change in the function of the secretory apparatus occurs (hypersecretion of mucus, changes in bronchial secretions), an infection occurs, and a cascade of reactions develops, leading to damage to the bronchi, bronchioles and adjacent alveoli. Violation of the ratio of proteolytic enzymes and antiproteases, defects in the antioxidant defense of the lungs aggravate the damage.

COPD üChronic inflammatory disease üArises in people over 35 years of age under the influence of various factors of environmental aggression (risk factors), the main of which is tobacco smoking üProceeds with primary damage to the distal parts of the respiratory tract and lung parenchyma, the formation of emphysema üCharacterized by partially reversible and irreversible limitation of air flow rate ü Develops in predisposed individuals, manifests itself as cough, sputum production and increasing shortness of breath, has a steadily progressive nature with the outcome in chronic respiratory failure and cor pulmonale. 3

Etiology The European Respiratory Society provides the following classification of risk factors depending on their significance: Risk factors for COPD Probability of the significance of the factors External factors Internal factors Established Smoking α 1 -antitrypsin deficiency Occupational hazards (cadmium, silicon) High Ambient air pollution (SO 2, NO 2, O 3) Occupational hazards Low socio-economic status Passive smoking in childhood Prematurity High level Ig. E Bronchial hyperreactivity Familial nature of the disease Possible Adenoviral infection Vitamin C deficiency Genetic predisposition(blood type A(II), absence of Ig. A)

Occupational factors Smoking The main risk factor (80-90% of cases) is smoking. Mortality rates from COPD are highest among smokers, who develop airway obstruction and shortness of breath more quickly. However, cases of the onset and progression of COPD are also observed in non-smokers. Shortness of breath appears at approximately 40 years of age in smokers, and 13-15 years later in non-smokers. The most harmful occupational factors are dusts containing cadmium and silicon. The mining industry ranks first in the development of COPD. High-risk professions: miners, builders in contact with cement, workers in the metallurgical (due to fumes of molten metals) and pulp and paper industries, railway workers, workers involved in grain and cotton processing. Hereditary predisposition The role of heredity is supported by the fact that not all long-term smokers become sick with COPD. The most studied genetic risk factor is a rare hereditary deficiency of α 1 -antitrypsin (A 1 AT), which inhibits serine proteinases in the systemic circulation. In the USA, among patients with COPD, congenital deficiency of A 1 AT was detected in less than 1% of cases

Pathogenesis In the pathogenesis of COPD, the following processes play the greatest role: inflammatory process, imbalance of proteinases and antiproteinases in the lungs, oxidative stress. Chronic inflammation affects all parts of the respiratory tract, parenchyma and blood 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

Inflammatory cells In COPD, there is an increase in the number of neutrophils, macrophages and T-lymphocytes, mainly CD 8+. Neutrophils. An increased number of activated neutrophils is detected in sputum and bronchoalveolar lavage. Smokers without COPD also have sputum neutrophilia. When examining induced sputum, an increased concentration of myeloperoxidase and human neutrophil lipocaine is determined, which indicates activation of neutrophils. During an 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 with histological examination sputum and lavage, bronchial biopsy and study of induced sputum. Macrophages secrete tumor necrosis factor α (TNF-α), interleukin 8 (IL-8), leukotriene B 4 (LTB 4), which promotes neutrophil chemotaxis. T-lymphocytes. CD 8+ cells found in bronchial biopsy secrete perforin and granzyme. B and TNF-α, these agents cause cytolysis and apoptosis of alveolar epithelial cells.

Eosinophils. Levels of eosinophil cationic peptide and eosinophil peroxidase in induced sputum of COPD patients are increased. This indicates the possibility of their presence. This may not be associated with eosinophilia - an increase in the activity of neutrophil elastase may cause degranulation of eosinophils when their number is normal. Epithelial cells. The impact of air pollutants, such as nitrogen dioxide (NO 2), ozone (O 3), diesel exhaust gases on nasal and bronchial epithelial cells, leads to the synthesis and release of inflammatory mediators (eicosanoids, cytokines, adhesion molecules, etc.). There is a disruption in the regulation of the functioning of E-selectin adhesion molecules by epithelial cells, which are responsible for the involvement of neutrophils in the process. At the same time, the secretion of a culture of bronchial epithelial cells obtained from patients with COPD in an experiment produces lower amounts of inflammatory mediators (TNF-α or IL-8) than similar cultures from non-smokers or smokers, but without COPD

Inflammatory mediators The most important role in COPD is played by tumor necrosis factor α (TNF-α), interleukin 8 (IL-8), leukotriene B 4 (LTB 4). They are capable of destroying the structure of the lungs and maintaining neutrophilic inflammation. The damage they cause further stimulates inflammation by releasing chemotactic peptides from the extracellular matrix. LTV 4 is a powerful neutrophil chemotaxis factor. Its content in the sputum of patients with COPD is increased. The production of LTV 4 is attributed to alveolar macrophages. IL-8 is involved in the selective recruitment of neutrophils and is possibly synthesized by macrophages, neutrophils and epithelial cells. Present in high concentrations in induced sputum and lavage from COPD patients. TNF-α activates nuclear factor-k. B transcription factor (NF-k. B), which, in turn, activates the IL-8 gene of epithelial cells and macrophages. TNF-α is detected in high concentrations in sputum, as well as in bronchial biopsies of COPD patients. In patients with severe weight loss, the level of serum TNF-α is increased, which suggests the possible participation of the factor in the development of cachexia].

Other agents are also involved in inflammation in COPD. Below are some of them: Mediator Abbreviation Function Test material Macrophage chemotactic protein-1 MCP-1 Attraction of monocytes, recruitment of macrophages Broncho alveolar lavage Patient smokers COPD, Non-smokers, smokers Macrophage inflammatory protein-1β MIP-1β Attraction of lymphocytes monocytes, T-Broncho alveolar lavage Patients smokers COPD, Non-smokers, smokers, former smokers Macrophage inflammatory protein-1α MIP-1α Attraction of lymphocytes monocytes, T- Patients smokers COPD, Granulocyte-macrophage colony-stimulating factor GMCSF Stimulates the activity of neutrophils, eosinophils, monocytes and macrophages Broncho alveolar lavage Patients X OBL , content increases during exacerbation Transforming growth factor-β TGF-β Suppresses the activity of natural killer cells, reduces the proliferation of B- and T-lymphocytes Expression in epithelial cells, eosinophils, fibroblasts Patients smokers COPD, Endothelin-1 ET-1 Constricts blood vessels Induced Patients with COPD, Expression in epithelial cells B which group has increased content in the studied material in Control group former smokers Non-smokers, former smokers

Course of the pathological process Pathophysiological changes in COPD include the following pathological changes: systemic manifestations of gas exchange disorders, pulmonary hypertension, ciliary dysfunction, bronchial obstruction, parenchymal destruction and pulmonary emphysema, mucus hypersecretion

Bronchial obstruction Hypersecretion of mucus is caused by stimulation of secreting glands and goblet cells by leukotrienes, proteinases and neuropeptides. Dysfunction of cilia The ciliated epithelium undergoes squamous metaplasia, which leads to impaired mucociliary clearance (impaired evacuation of sputum from the lungs). These initial manifestations of COPD may persist for many years without progressing. Bronchial obstruction corresponding to stages of COPD from 1 to 4 is irreversible in nature with the presence of a small reversible component. The following causes of bronchial obstruction are distinguished: Irreversible: Remodeling and fibrosis of the airways, Loss of elastic traction of the lung as a result of destruction of the alveoli, Destruction of the alveolar support of the lumen of the small airways; Reversible: Accumulation of inflammatory cells, mucus and plasma exudate in the bronchi, Contraction of bronchial smooth muscle, Dynamic hyperinflation during exercise. Obstruction in COPD is mainly formed at the level of small and minute bronchi. Due to the large number of small bronchi, when they narrow, the total resistance of the lower parts of the respiratory tract approximately doubles. Spasm of bronchial smooth muscles, inflammation and hypersecretion of mucus can form a small part obstruction, reversible with treatment. Inflammation and exudation are especially important during exacerbation

Pulmonary hyperinflation (PHI) is an increase in the airiness of the lung tissue, the formation and increase of an “air cushion” in the lungs. Depending on the cause of its occurrence, it is divided into two types: static LGI: due to incomplete emptying of the alveoli on exhalation due to a decrease in the elastic traction of the lungs dynamic LGI: due to a decrease in expiratory time under conditions of pronounced limitation of expiratory air flow From the point of view of pathophysiology, LGI is an adaptation mechanism, since leads to a decrease in airway resistance, improved air distribution and an increase in minute ventilation at rest. However, LGI leads to the following adverse consequences: Weakness of the respiratory muscles. The diaphragm shortens and flattens, making its contractions ineffective. Limiting the increase in tidal volume during physical activity. U healthy people During exercise, the minute volume of breathing increases due to an increase in the frequency and depth of breathing. In patients with COPD, pulmonary hyperinflation increases during exercise, since an increase in respiratory rate in COPD leads to a shortening of exhalation, and also most of air is retained in the alveoli. An increase in the “air cushion” does not allow for a significant increase in the depth of breathing. Hypercapnia during exercise. Due to a decrease in the ratio of TLC to VC due to a decrease in VC due to LHI, an increase in Pa occurs. CO 2 in arterial blood.

Emphysema Destruction of the parenchyma leads to a decrease in the elastic traction of the lungs, and therefore is directly related to limiting the speed of air flow and increasing air resistance in the lungs. Small bronchi, losing connection with the alveoli, which were previously in a straightened state, collapse and cease to be passable. Gas exchange disorders Airway obstruction, parenchymal destruction, and pulmonary blood flow disorders reduce the pulmonary capacity for gas exchange, leading first to hypoxemia and then to hypercapnia. The correlation between pulmonary function values ​​and arterial blood gas levels is weak, but significant changes in blood gas composition rarely occur at FEV 1 greater than 1 L. In the initial stages, hypoxemia occurs only during physical activity, and as the disease progresses, it also occurs at rest. Pulmonary hypertension Pulmonary hypertension develops at stage IV - an extremely severe course of COPD, with hypoxemia (Pa. O 2 less than 8 kPa or 60 mm Hg) and often also hypercapnia. This is the main thing cardiovascular complication COPD is associated with a poor prognosis. Typically, in patients with severe COPD, resting pulmonary artery pressure is moderately elevated, although it may increase with exercise. The complication progresses slowly, even without treatment. Narrowing of pulmonary vessels and thickening of the vascular wall due to remodeling are related to the development of pulmonary hypertension pulmonary arteries, destruction of pulmonary capillaries in emphysema, which further increases the pressure required for blood to pass through the lungs. Vasoconstriction can occur due to hypoxia, which causes contraction of the smooth muscles of the pulmonary arteries, disruption of the mechanisms of endothelium-dependent vasodilation (decreased NO production), and pathological secretion of vasoconstrictor peptides (such as ET-1, a product of inflammatory cells). Vascular remodeling is one of the main causes of the development of pulmonary hypertension, which in turn occurs due to the release of growth factors or due to mechanical stress during hypoxic vasoconstriction.

Cor pulmonale Pulmonary hypertension is defined as “hypertrophy of the right ventricle resulting from diseases affecting the function and/or structure of the lungs, excluding those lung disorders resulting from diseases primarily affecting the left side of the heart, as in congenital diseases hearts." The prevalence and course of cor pulmonale in COPD are still unclear. Pulmonary hypertension and reduction of the vascular bed due to emphysema lead to hypertrophy of the right ventricle and its failure only in some patients. Systemic manifestations In COPD, there is systemic inflammation and skeletal muscle dysfunction. Systemic inflammation is manifested by the presence of systemic oxidative stress, increased concentrations of circulating cytokines, and activation of inflammatory cells. The manifestation of skeletal muscle dysfunction is loss of muscle mass and various bioenergetic disorders. These manifestations lead to limitation physical capabilities patient, reduce the level of health, worsen the prognosis of the disease

Pathomorphology It is based on an inflammatory process that affects all structures of the lung tissue: bronchi, bronchioles, alveoli, pulmonary vessels. Morphological changes are characterized by epithelial metaplasia, death of epithelial cilia, hypertrophy of submucosal glands that secrete mucus, and proliferation of smooth muscle in the wall of the respiratory tract. All this leads to hypersecretion of mucus, the appearance of sputum, and disruption of the drainage function of the bronchi. Narrowing of the bronchi occurs as a result of fibrosis. Damage to the lung parenchyma is characterized by the development of centrilobular emphysema, changes in the alveolar-capillary membrane and impaired diffusion capacity, leading to the development of hypoxemia. Dysfunction of the respiratory muscles and alveolar hypoventilation lead to chronic hypercapnia, vasospasm, remodeling of the pulmonary arteries with thickening of the vascular wall and a decrease in the lumen of blood vessels. Pulmonary hypertension and vascular damage lead to the formation of cor pulmonale. Progressive morphological changes in the lungs and related violations respiratory functions lead to the development of cough, sputum hypersecretion, respiratory failure

Clinical picture Cough is the earliest symptom of the disease. It is often underestimated by patients, being expected with smoking and exposure to pollutants. In the first stages of the disease, it appears sporadically, but later it occurs daily, occasionally - it appears only at night. Outside of an exacerbation, the cough, as a rule, is not accompanied by sputum production. Sometimes there is no cough in the presence of spirometric evidence of bronchial obstruction. Dyspnea occurs approximately 10 years later than cough and is noted initially only with significant and intense physical activity, intensifying with respiratory infections. Dyspnea is often of a mixed type; expiratory dyspnea is less common. In later stages, shortness of breath ranges from a feeling of shortness of breath during normal physical activity to severe respiratory failure, and becomes more severe over time. It is a common reason for visiting a doctor. Sputum is a relatively early symptom of the disease. In the initial stages, it is released in small quantities, usually in the morning, and is mucous in nature. Purulent, profuse sputum is a sign of exacerbation of the disease.

Clinical forms (in moderate and severe cases) COPD Signs Type A (emphysematous) “pink puffers” Panacinar emphysema Type B (bronchitis) “blue puffers” Centroacinar emphysema Appearance Asthenics, pink-gray complexion, cold limbs Picnics, diffuse cyanosis, warm limbs First symptoms Shortness of breath Cough Wheezing in the lungs Absent Characteristic Sputum Scanty mucous Copious, purulent Bronchial infections Uncommon Often Exercise tolerance Sharply reduced Reduced to a lesser extent Cor pulmonale In the elderly age, at terminal stages, death in old age In middle and old age, often, earlier decompensation 21

The goals of COPD therapy are to prevent the progression of the disease, to reduce the severity clinical symptoms, - achieving better tolerance to physical activity, - improving the quality of life of patients, - preventing complications and exacerbations, - reducing mortality. The main directions of treatment for COPD are 1) reducing the impact of adverse environmental factors (including smoking cessation), 2) patient education, 3) drug therapy, 4) non-drug therapy(oxygen therapy, rehabilitation, etc.). Various combinations of these methods are used in patients with COPD in remission and exacerbation.

Basic therapy for COPD The main role is given to inhaled pharmacotherapy using mainly three groups of modern drugs - anticholinergics (anticholinergic bronchodilators), - long-acting β 2-agonists, - inhaled glucocorticosteroids (ICS). Treatment should begin with monotherapy with an anticholinergic or long-acting β 2 agonist. 1) Anticholinergic drug - ipratropium bromide (Atrovent), released in the form of an aerosol metered dose inhaler (1 single dose - 20 mcg) or dry powder inhaler (1 single dose - 40 mcg). The drug is prescribed 40 mcg 4 times a day. The drug does not cause tachycardia or other heart rhythm disturbances. When used, mucus formation is reduced and the rheological properties of bronchial secretions are normalized. Duration of use: - for stage I COPD - at least 3-4 weeks, - for stages II-III - several months, sometimes - constantly. The dose is selected individually, and the effect is assessed after 3-4 weeks from the start of use based on the results of spirography over time. Currently, a new long-acting drug is being used - tiotropium bromide

2) β 2 -agonists of prolonged action - salmeterol and formoterol. Used from the second stage of COPD as monotherapy or in combination with an anticholinergic. The consequence of its action is a decrease in the degree of neutrophilic inflammation, a decrease in swelling of the bronchial mucosa, a decrease in capillary permeability, a decrease in the release of inflammatory mediators, and an improvement in mucociliary clearance. Salmeterol combines well with methylxanthines, as well as ICS. A new drug for the treatment of COPD is roflumilast (Daxas), which, according to GINA recommendations, is recommended to be taken in combination with long-acting anticholinergics at stage III COPD.

Stepwise scheme for symptomatic treatment of COPD Stage I b 2 -agonists if necessary Stage II Stage IV Ipratropium bromide + + + b 2 -agonists if necessary Theophylline Corticosteroids + + b 2 -agonists if necessary Theophylline + b 2 -agonists

Medication COPD treatment Bronchodilators: β 2 -adrenergic agonists, anticholinergics, and theophylline. Principles of bronchodilator therapy for COPD: - The preferred route of administration is inhalation. - Changes in pulmonary function after short-term administration of drugs are not an indicator of their effectiveness. - The choice between bronchodilators depends on their availability, the individual sensitivity of patients to their action and the absence of side effects. In elderly patients with concomitant cardiovascular diseases, anticholinergics are preferable. - Xanthines are effective for COPD, but due to the possibility of developing side effects, they are classified as “second-line” drugs. When prescribing them, it is recommended to measure the concentration of theophylline in the blood. - A combination of several bronchodilators (for example, anticholinergics and β 2 adrenergic agonists, anticholinergics and theophyllines) may increase effectiveness and reduce the likelihood of side effects

Glucocorticoids. Short (10–14 days) courses of systemic steroids are used to treat exacerbations of COPD. Long-term use of these drugs is not recommended due to the risk of side effects (myopathy, osteoporosis, etc.). High doses (for example, fluticasone propionate 1000 mcg/day) improve the quality of life of patients and reduce the frequency of exacerbations of severe and extremely severe COPD. IN Lately new data on effectiveness have been obtained combination drugs(fluticasone propionate/salmeterol 500/50 mcg, 1 inhalation 2 times a day and budesonide/formoterol 160/4, 5 mcg, 2 inhalations 2 times a day, budesonide/salbutamol 100/200 mcg 2 inhalations 2 times a day) in patients COPD of severe and extremely severe course. Long-term (12 months) administration of combination drugs: - improves bronchial patency, - reduces the severity of symptoms, - reduces the need for bronchodilators, - reduces the frequency of moderate and severe exacerbations

Antibiotics. Indicated for the treatment of infectious exacerbations of the disease, they directly affect the duration of elimination of COPD symptoms, and some help to lengthen the interval between relapses. Mucolytics (mucokinetics, mucoregulators) (ambroxol, carbocysteine, iodine preparations, etc.) can be used in a small proportion of patients with viscous sputum. Widespread use of these agents in patients with COPD is not recommended. Antioxidants. N-acetylcysteine, which has antioxidant and mucolytic activity, can reduce the duration and frequency of exacerbations of COPD. This drug can be used in patients for a long time (3–6 months) at a dose of 600 mg/day. Immunoregulators (immunostimulants, immunomodulators). Regular use of these drugs is not recommended. Patients with genetically determined α 1 -antitrypsin deficiency who develop COPD at a young age (up to 40 years) are possible candidates for replacement therapy.

Non-drug treatment COPD Oxygen therapy The goal is to increase the partial oxygen tension (Pa. O 2) in arterial blood to at least 60 mm Hg. Art. or saturation (Sa. O 2) to at least 90% at rest, during physical activity and during sleep. In stable COPD, continuous long-term oxygen therapy is preferable. It has been proven that it increases the survival rate of patients with COPD, reduces the severity of shortness of breath, reduces the frequency of episodes of hypoxemia during sleep, increases exercise tolerance, quality of life and neuropsychological status of patients. Indications for long-term oxygen therapy in patients with extremely severe COPD (with FEV 1

Rehabilitation is a program of individualized care for COPD patients designed to improve their physical, social adaptation and autonomy. Its components are physical training, patient education, psychotherapy and balanced nutrition. In recent years, much attention has been paid to rational nutrition, since loss of body weight (> 10% within 6 months or > 5% within the last month) and especially loss of muscle mass in patients with COPD is associated with high mortality. Such patients should be recommended a high-calorie diet with a high protein content and dosed physical activity that has an anabolic effect. Surgical Treatment Role surgical treatment in patients with COPD is currently the subject of research. The possibilities of using bullectomy, lung volume reduction surgery, and lung transplantation are currently being discussed.