Chronic obstructive pulmonary disease (COPD). chronic obstructive pulmonary disease (COPD) is a collective concept that includes chronic diseases

“Acute respiratory failure” - Absolute indications. Moderate condition. Aspiration pneumonitis. Tension pneumothorax. Signs of tracheobronchitis with copious mucopurulent discharge. Accumulation of fluid in the interstitial space. Clinic. Violation of ventilation-perfusion relationships. Restrictive bronchopulmonary ARF.

“Occupational bronchitis” - Additional medical contraindications. Inflammation of the bronchi. Carrying out examination of insurance cases. Classification of occupational bronchitis by severity. List occupational diseases. Criteria for determining occupational status of chronic bronchitis. Morphological changes.

“Bronchial asthma” - Glucocorticosteroids. Drugs for the treatment of bronchial asthma. Difficulties in diagnosing asthma. Fluticanose propionate. Inhaled glucocorticosteroids. Identification of the clinical variant of the course. Sympathomimetics. Severe exacerbation. Peak flowmetry. Prepare the nebulizer. Fast-acting inhaled bronchodilators.

“Diseases of the respiratory system” - Diagnosis of pneumonia. Angina. The impact of smoking on the health of adolescents. The effect of smoking on the lung parenchyma. Flu prevention. Symptoms of sore throat. Pneumonia. Infectious disease. Flu symptoms. Prevention of tuberculosis. Prevention of organ diseases respiratory system. Main symptoms of tuberculosis.

“Chronic obstructive pulmonary disease” - Changes in lung function. Regular treatment. Oxygen therapy. Lung disease. Signs. Fagerstrom test. COPD and everyday life. Etiology of exacerbations. Monitoring the patient. Glucocorticoids. Step-by-step treatment. Goals of modern therapy. Spiriva. Accompanying illnesses. Causes of exacerbation. Treatment of pulmonary hypertension.

“Purulent lung diseases” - Bronchiectasis. Bronchography for bronchiectasis. Empyema of the pleura. Stages of a lung abscess. Puncture image. Phases of development of a lung abscess. X-ray diagnosis of pleural empyema. Morphological changes in the pleura. Options for the development of pleural empyema. Schematic representation of pleurectomy with lung decortication.

There are 15 presentations in total

Chronic obstructive disease lungs (COPD) is a collective concept that includes chronic diseases respiratory system with predominant 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, severe forms 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 shortness of breath during normal physical activity to severe respiratory failure, and over time becomes more pronounced “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, tremors, confusion of speech, etc.) “Pink puffers” “Pink puffers” do not look cyanotic, low nutrition. When examined, signs of pulmonary emphysema predominate. The cough is minor, and the main complaint is shortness of breath when physical activity. Job respiratory muscles significantly increased. Changes in gas composition arterial blood at the same time 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

By 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 - deterioration of 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 of modern anticholinergic drugs (anticholinergic bronchodilators), (long-acting β2-agonists and inhaled glucocorticosteroids (GCS). Treatment should begin with monotherapy with an anticholinergic or long-acting β2-agonist. β2-agonists). agonists of inhaled glucocorticosteroids anticholinergic β2-agonist BASIC TREATMENT

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Diagnosis of internal diseases Topic 2.1 Acute bronchitis, COPD. Bronchial asthma.

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease that occurs in people over 35 years of age under the influence of various environmental aggression factors (risk factors), the main one of which is tobacco smoking, which occurs with predominant damage to the distal respiratory tract. and lung parenchyma, the formation of emphysema, characterized by partially reversible rate limitation air flow induced inflammatory reaction, which differs from inflammation in bronchial asthma and exists regardless of the severity of the disease. The disease develops in predisposed individuals and is manifested by cough, sputum production and increasing shortness of breath, and has a steadily progressive nature with the outcome in chronic respiratory failure and chronic cor pulmonale. Chronic obstructive disease today is distinguished as an independent lung disease and is distinguished from a number of chronic processes of the respiratory system that occur with obstructive syndrome (obstructive bronchitis, secondary pulmonary emphysema, bronchial asthma, etc.).

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ICD - 10 J44 Other chronic obstructive pulmonary disease J44.0 Chronic obstructive pulmonary disease with acute respiratory infection of the lower respiratory tract Excluded: with influenza (J10-J11) J44.1 Chronic obstructive pulmonary disease with exacerbation, unspecified J44.8 Other specified chronic obstructive pulmonary disease disease Chronical bronchitis: . asthmatic (obstructive) NOS (not otherwise specified"). emphysematous NOS. obstructive NOS J44.9 Chronic obstructive pulmonary disease, unspecified Chronic obstructive: ... respiratory tract disease NOS. lung disease NOS

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EXAMPLE OF FORMULATION OF DIAGNOSIS Nosology – COPD Severity (disease stage): Mild (stage I); Moderate course (stage II); Severe course (stage III); Extremely severe (stage IV). Clinical form (in severe disease): bronchitis, emphysematous, mixed (emphysematous-bronchitis). Progression phase: exacerbation, subsiding exacerbation, stable course. There are two types of course: With frequent exacerbations (3 or more per year); With rare exacerbations. Complications: Chronic respiratory failure; Acute respiratory failure against the background of chronic respiratory failure; Pneumothorax; Pneumonia; Thromboembolism; If bronchiectasis is present, indicate its location; Pulmonary heart; The degree of circulatory failure. Specify index smoking man(in units of “pack/years”). Diagnosis: Chronic obstructive pulmonary disease, severe course, bronchitis form, exacerbation phase. Complications of the main diagnosis: Respiratory failure of the 3rd degree. Chronic cor pulmonale. Stage II heart failure. IR 25 (pack/years).

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ETIOLOGY Smoking (both active and passive). Long-term exposure to occupational irritants (dust, chemical pollutants, vapors of acids and alkalis). Atmospheric and domestic air pollution. Particular importance in the development of COPD is given to disturbances in the ecology of the home. Infectious diseases respiratory tract. Genetic predisposition. The disease can significantly increase in its manifestations when several risk factors are combined in the same patient.

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PATHOGENESIS Inflammatory changes, which are caused by the pathological action of inhalation damaging factors, lead to changes in the wall of the bronchial tree, disrupting mucociliary clearance and changing the elastic properties of the bronchi. This leads to reversible (bronchospasm, swelling of the bronchial wall, quantitative and qualitative violation bronchial secretions, dynamic hyperinflation during physical activity) and irreversible (sclerosation of the bronchial wall, expiratory collapse of small bronchi during exhalation, emphysema) changes.

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CLASSIFICATION Stage I – mild COPD (FEV1≥80%). Stage II - moderate COPD (50≥FEV1≤80%). Stage III – severe COPD (30% ≥FEV1≤50%). Stage IV – extremely severe COPD (FEV1≤ 30%). DEGREES OF RESPIRATORY INSUFFICIENCY (RF) RD I stage - shortness of breath during physical exertion RD II stage - shortness of breath with minimal physical activity DN III stage. - shortness of breath at rest

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CLINIC Main clinical signs of COPD: Cough Sputum production Shortness of breath Signs of bronchial obstruction Swelling of the neck veins Breathing through closed lips or a “tube” Wheezing in the lungs expressed in a lying position

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PHASES OF COPD 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. Two types of exacerbation can be distinguished: exacerbation, characterized by an inflammatory syndrome (increased body temperature, increased quantity and viscosity of sputum, increased purulence of sputum). exacerbation, manifested by an increase in shortness of breath, increased remote wheezing, a feeling of constriction in the chest, decreased tolerance to physical activity, the occurrence of hypoxemia and hypercapnia (increased carbon dioxide content in arterial blood and body tissues), increased extrapulmonary manifestations COPD (weakness, fatigue, headache, bad dream, depression); participation in the act of breathing of auxiliary muscles, paradoxical movements of the chest, the appearance or worsening of central cyanosis and peripheral edema.

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Clinical forms of COPD In patients with moderate and severe disease, two clinical forms of COPD can be distinguished: emphysematous (panacinar emphysema, “pink puffers”) and bronchitis (centroacinar emphysema, “blue puffers”).

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Characteristics of clinical forms of COPD Symptoms Bronchitic form Emphysematous form Correlation of the main symptoms Cough is more pronounced than shortness of breath Dyspnea is more pronounced than cough Bronchial obstruction Pronounced Pronounced Hyperinflation of the lungs (increased airiness according to radiography) Weakly expressed Strongly expressed Color of the skin and visible mucous membranes Diffuse blue Pink- gray Cough With hypersecretion of sputum Unproductive Changes on the radiograph Diffuse pneumosclerosis Pulmonary emphysema Cor pulmonale In middle and old age, earlier decompensation In old age, later decompensation Polycythemia, erythrocytosis Often pronounced, increased blood viscosity Not typical Cachexia Not typical Often present Weight of the patient Obese patients Weight loss Functional disorders Signs of progressive respiratory failure and congestive heart failure Decreased diffusion capacity of the lungs for carbon monoxide. Prevalence of respiratory failure Gas exchange disorders paO2 less than 60 mm Hg. Art. paCO2 more than 45 mm Hg. Art. paO2 less than 60 mm Hg. Art. paCO2 more than 45 mm Hg. Art. death In middle age In old age

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DIAGNOSIS COPD should be considered in all patients who have cough and sputum production and/or shortness of breath and who have risk factors for developing the disease. Chronic cough and sputum production often precede airflow limitation leading to shortness of breath. If any of the above symptoms are present, spirometry should be performed. These signs are not diagnostic individually, but the presence of several of them increases the likelihood of having COPD.

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ANAMNESIS When talking with a patient, you need to remember that the disease begins to develop long before the appearance of severe symptoms. COPD long time proceeds without clear clinical symptoms: at least, patients do not complain. It is advisable to clarify what the patient himself associates with the development of symptoms of the disease and their increase. When studying the anamnesis, it is advisable to establish the frequency, duration and characteristics of the main manifestations of exacerbations and evaluate the effectiveness of previously carried out treatment measures. Find out if there is a hereditary predisposition to COPD and other pulmonary diseases. In cases where the patient underestimates his condition, and the doctor, during a conversation with him, cannot determine the nature and severity of the disease, special questionnaires should be used. As the disease progresses, COPD is characterized by a steadily progressive course.

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COMPLAINTS Analysis of complaints (their severity depends on the stage of the disease phase). Cough (it is necessary to establish its frequency and intensity). Cough most early symptom, manifesting itself by 40-50 years of age. By this time, during cold seasons, episodes of respiratory infection begin to occur, which at first are not associated by the patient and the doctor into one disease. The cough is observed daily or is intermittent. Most often observed during the day, rarely at night. Sputum (it is necessary to find out the nature and quantity). Sputum, as a rule, is released in small quantities in the morning (rarely > 50 ml per day) and is mucous in nature. The purulent nature of sputum and an increase in its quantity are signs of exacerbation of the disease. The appearance of blood in the sputum deserves special attention, which suggests another cause of cough (lung cancer, tuberculosis and bronchiectasis). Shortness of breath (it is necessary to evaluate its severity and its relationship with physical activity). Dyspnea is a cardinal sign of COPD and is the reason why the majority of patients consult a doctor. As the disease progresses, shortness of breath can vary widely: from a feeling of lack of air during habitual physical activity to severe respiratory failure. Shortness of breath, felt during physical activity, occurs on average 10 years later than cough (extremely rarely, the onset of the disease can begin with shortness of breath). As pulmonary function declines, shortness of breath becomes more severe. Dyspnea in COPD is characterized by: progression (constant increase, persistence (every day), intensification with physical activity, increase with respiratory infections. Dyspnea can be described by the patient in different ways: “increasing effort during breathing,” “heaviness,” “air starvation,” “ labored breathing".

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PHYSICAL EXAMINATION Examination of the patient: Assessment appearance the patient, his behavior, the reaction of the respiratory system to a conversation, movement around the office. The lips are gathered in a “tube”, the forced position is orthopnea, signs of severe COPD. Color assessment skin determined by a combination of hypoxia, hypercapnia and erythrocytosis. Central gray cyanosis is usually a manifestation of hypoxemia. Acrocyanosis detected at the same time is usually a consequence of heart failure. Examination of the chest: its shape is deformed, “barrel-shaped”, inactive during breathing, paradoxical retraction (retraction) of the lower costal spaces during inspiration and participation in the act of breathing of the auxiliary muscles of the chest and abdominal muscles; significant expansion of the chest in the lower sections are signs of severe COPD. Percussion of the chest: a boxy percussion sound and drooping lower borders of the lungs are signs of emphysema. Auscultatory picture: Hard or weakened vesicular breathing in combination with a low diaphragm confirms the presence of pulmonary emphysema. Dry wheezing, aggravated by forced exhalation, in combination with increased exhalation - obstruction syndrome.

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LABORATORY AND INSTRUMENTAL STUDIES 1. Functional studies external respiration Spirography. Peak flowmetry. 2. X-ray studies: Chest X-ray CT scan of the chest 3. Blood tests: Clinical analysis blood Pulse oximetry 4. Sputum cytology 5. Electrocardiography EchoCG Bronchoscopic examination

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Bronchial asthma Signs of COPD Asthma Age of onset of the disease Typically over 35-40 years of age More often in children and young people (bronchial asthma can begin in middle and old age.) Smoking history Characteristic Not typical Extrapulmonary manifestations of allergy ( allergic rhinitis, conjunctivitis, atopic dermatitis, urticaria) Not typical Typical Symptoms (cough and shortness of breath) Constant, progressing slowly Clinical variability, appear in paroxysms; during the day, day by day, seasonally Compounded heredity for asthma Not typical Bronchial obstruction Slightly reversible or not reversible Daily variability of peak expiratory flow Less than 10% More than 20% Bronchodilator test Negative Positive Presence of cor pulmonale Characteristic in severe cases Not typical Type of inflammation (cytological examination of sputum and fluid obtained from bronchoalveolar lavage). Neutrophils predominate, increase in macrophages (++), increase in CD8+ lymphocytes Eosinophils predominate, increase in macrophages (+), increase in CD4+ lymphocytes, activation mast cells Inflammatory mediators Leukotriene B, interleukin (IL) 8, tumor necrosis factor -ά Leukotriene D, IL 4, 5, 13 Efficacy of glucocorticoid therapy Low high

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Other diseases Heart failure. Wheezing in the lower parts of the lungs on auscultation. Significant decrease in left ventricular ejection fraction. Dilation of the heart. The x-ray shows expansion of the contours of the heart, congestion (up to pulmonary edema). When studying pulmonary function, disorders of the restrictive type are determined (the restrictive type of ventilation disorder develops with a decrease in the elasticity and ability of the lungs to expand and collapse during the act of breathing) without restricting the air flow. Consultation with a cardiologist. Bronchiectasis. Large volumes of purulent sputum. Frequent communication with bacterial infection. Rough moist rales of various sizes on auscultation. "Drumsticks". An X-ray or CT scan shows dilation of the bronchi and thickening of their walls. If suspected, consult a pulmonologist. Tuberculosis. Starts at any age. X-ray demonstrates pulmonary infiltration or focal lesions. If suspected, consult a phthisiatrician. Obliterating bronchitis. Development in at a young age. No connection with smoking has been established. Contact with vapors, smoke. CT scan reveals areas of low density during exhalation. Often rheumatoid arthritis. If suspected, consult a pulmonologist.

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PROGNOSIS Continued smoking usually contributes to the progression of airway obstruction, leading to early disability and shortened life expectancy. After quitting smoking, the decrease in forced expiratory volume in 1 second and the progression of the disease slow down. To alleviate the condition, many patients are forced to take drugs in gradually increasing doses for the rest of their lives, and also use additional drugs during exacerbations.

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Chronic bronchitis Chronic obstructive pulmonary disease

Propaedeutics of internal diseases

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Chronical bronchitis

Chronic bronchitis is a diffuse progressive lesion of the bronchial tree caused by prolonged irritation and inflammation of the airways

Bronchitis is considered chronic if the patient coughs up sputum for at least three months a year for two years, excluding other diseases of the bronchopulmonary apparatus

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Chronic bronchitis is characterized by a restructuring of the secretory apparatus of the mucous membrane with quantitative and qualitative changes in bronchial secretions with the development of degenerative-inflammatory and sclerotic changes in the bronchial wall.
This is accompanied by hypersecretion, disruption of the cleansing function of the bronchi with coughing and sputum production, and if the small bronchi are affected, shortness of breath

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Men get sick more often
The disease develops between 20 and 40 years of age
The disease remains latent for a long time, with maximum manifestations occurring between 50 and 70 years of age.
Occurs in 3 - 8% of the adult population

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risk factors for chronic bronchitis

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Pathogenesis of chronic bronchitis

Structural changes in the mucosa (hyperplasia of goblet cells, metaplasia and atrophy of the epithelium, hypertrophy of the tracheobronchial glands)

Increased amount of bronchial mucus (hypercrinia),
Changes in its rheological properties (discrimination),
Mucociliary clearance disorders,
Decreased local immunity (decrease in interferon, lysozyme, surfactant, phagocytic activity of alveolar macrophages, increase in neutrophils)

Colonization of microorganisms and
activation of respiratory infection

Inflammation of the bronchial mucosa

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The key point in pathogenesis is the development of chronic inflammation,
the morphological marker of which is NEUTROPHILS (in sputum)

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Mechanisms of bronchial obstruction

REVERSIBLE
Bronchospasm
Inflammatory swelling of the bronchial mucosa
Breath obstruction. mucus paths

IRREVERSIBLE
Sclerotic changes in the walls of the bronchi
Expiratory collapse of small airways. pathways due to developing emphysema

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Classification of chronic bronchitis

By functional characteristics(taking into account the presence of shortness of breath, FEV1 indicators):
1.Non-obstructive
2.Obstructive
According to the clinical and laboratory characteristics of the presence and severity of inflammation:
1. Catarrhal
2. Mucopurulent
3. Purulent
According to the phase of the disease:
1. Exacerbation
2.Remission
For complications of bronchial obstruction:
1. Chronic cor pulmonale
2.Respiratory (pulmonary) failure

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Chronic bronchitis (mechanism of development)

Non-obstructive
The central airways are affected
Bronchial obstruction is reversible

Obstructive
Are affected
peripheral airways
Bronchial obstruction is irreversible and progressive
Pulmonary emphysema, pneumosclerosis, and pulmonary insufficiency are formed pulmonary hypertension, "pulmonary heart"

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Clinic of chronic non-obstructive bronchitis

Cough (morning cough with a small amount of sputum; during exacerbations, mucopurulent and purulent sputum, malaise, sweating, tachycardia, low-grade fever, shortness of breath)
Auscultation of the lungs reveals vesicular breathing; during exacerbation - dry “buzzing” and silent moist rales
There are no violations of physical activity

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Principles of treatment of non-obstructive bronchitis

Eliminating risk factors, quitting smoking
In case of exacerbation - antibiotics, mucolytics, bronchodilators

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Chronic obstructive bronchitis

Has an unfavorable prognosis due to the progression of shortness of breath, symptoms of respiratory failure, emphysema and the development of “cor pulmonale”

Currently chronic. obstructive bronchitis is associated with the concept of chronic obstructive pulmonary disease (COPD)

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COPD: definition

COPD is a disease characterized by incompletely reversible airflow limitation (bronchial obstruction), which is usually progressive and caused by an inflammatory response. lung tissue to exposure to pathogenic particles or gases.

GOLD, updated 2015

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COPD: prevalence in the world

The prevalence of COPD in the world is ~1% of the population, and in people over 40 years of age – up to 10%.
COPD is often underdiagnosed - only 25-30% of cases are detected.
The prevalence of COPD is steadily increasing.

Chapman, 2006; Pauwels RA, Rabe KF. 2004;
Murray CJ et al., 1997; Murray CJ et al., 2001; WHO, 2002

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Although the prevalence of COPD in men is still higher than in women, the incidence of COPD among women is increasing faster, approaching the prevalence among men

Prevalence (%)

Women

Men

Soriano et al. Thorax 2000; 55: 789-94 UK GPRD, 1990 to 1997.

QPRD – 3.4 million patients

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Facts about women's health in Russia

19% of women are exposed to the harmful habit of smoking. According to the forecast, after some time 40% of all women in Russia will smoke.
A third of girls aged 15-16 smoke.
Women are less likely to quit smoking, and nicotine replacement therapy for women is less effective.

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COPD: mortality

In the 1990s. COPD was the 5th leading cause of death worldwide and 4th in developed countries.
By 2020, COPD will become the 3rd leading cause of death and will account for 4.7 million deaths per year.

ERS/ELF. European Lung White Book 2003; Murray & Lopez, Harvard University Press 1996 Chapman, 2006; Pauwels RA, Rabe KF. 2004. Murray CJ et al., 1997; Murray CJ et al., 2001.

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COPD: the role of smoking

Beginning of the 20th century

The main cause of COPD is smoking.
2006 – about 1.1 billion people smoke in the world
2025 – 1.6 billion people will smoke in the world
WHO, 2002

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COPD: a multicomponent disease

Airway inflammation

Mucociliary dysfunction

Bronchial obstruction

System component

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Bronchial obstruction

Contraction of bronchial smooth muscles
Increased cholinergic tone
Bronchial hyperreactivity
Loss of the elastic “frame”

Parenchymal “framework” that “stretches” the bronchi and prevents their collapse

Loss of the parenchymal “framework” - a tendency to collapse of the bronchi, especially during the expiratory phase

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Inflammation
respiratory tract

Increased number of inflammatory cells
Activation of inflammatory mediators
Increased activity of enzymes that destroy tissue
Swelling of the mucous membrane

Neutrophil-
main inflammatory cell
for COPD

COPD: features of pathophysiology

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COPD: features of pathophysiology

Structural changes in the airways

Destruction of the alveoli
Thickening of the epithelial layer
Gland hypertrophy
Goblet cell changes
Airway fibrosis

Emphysema

An increase in the size of air cells due to the destruction of the alveoli - a decrease in the gas exchange surface area

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COPD: features of pathophysiology

Mucociliary dysfunction

Increased mucus secretion
Increased mucus viscosity
Slowing mucus transport (clearance)
Damage to the mucous membrane

H. influenzae infection

Cilia

Bacteria

Damaged eyelashes

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COPD: features of pathophysiology

System component

Dysfunction of skeletal muscles (including respiratory muscles
Decline muscle mass and BMI
Osteoporosis
Anemia
Increased risk of cardiovascular disease

Similowski et al., Eur Respir J 2006; 27: 390–396; Sin et al. Am J Med. 2003; 114: 10–14; Sin et al. Chest 2005; 127: 1952-59

Inflammation in COPD is systemic, affecting many organs and tissues (hypoxemia,
hypercapnia,
pulmonary hypertension,
"pulmonary heart")

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www.goldcopd.org

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COPD: objective examination

Central cyanosis
Barrel-shaped chest with widened intercostal spaces
Participation in the act of breathing of auxiliary muscles
Resting respiratory rate >20/min
Edema of the lower extremities (due to right ventricular failure)
Liver prolapse upon palpation
Narrowing of the zone of cardiac dullness during percussion
Reducing breath sounds
Dry wheezing during quiet breathing
Muffled heart sounds due to emphysema

There may be no objective signs of COPD!
They usually occur after significant impairment of lung function and may include:

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SPIROMETRY

To confirm the diagnosis and determine the severity of the disease, spirometry is necessary

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Spirometry
Assessing the reversibility of bronchial obstruction
Chest X-ray (to exclude other diseases of the respiratory system)
Arterial blood gas analysis
Determination of α1-antitrypsin level
Sputum examination

Additional research methods

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Spirometry

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Obstruction reversibility study (bronchodilator test)

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 of the terminal bronchioles. extrapulmonary changes (osteoporosis, anemia, myopathy, etc.) COPD is complicated by gradual and steady: decreased bronchial patency, increased airiness of the lungs; the increase in chronic respiratory failure (CRF) and the formation of chronic pulmonary heart disease (CHP).

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 of the 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 (in pure form are rare).

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; mucociliary transport disorders, airway obstruction, 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, a respiratory infection is not main reason 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: the impact of exo- and/or endogenous AH on healthy person, which can cause “gaps” in the local protection of the respiratory tract. Stage 2. Pre-illness state - symptoms appear pathological process V different options: 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 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). Gradual evolution of COPD and major compensatory possibilities young organism 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 is excluded: due to inhalation of chemicals, 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 (without apparent reason), an increase in RR or HR >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, accompanying illnesses, 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 a day, 50 mcg) with fluticasone (ICS 500 mcg, 2 times a 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