2. Basic level of training

№п/п	The names of previous courses	The obtained skills
1.	Normal anatomy	To know the anatomical structure of the organs of respiratory system, their topography, blood supply and innervation.
2.	Histology	Aware of the cellular structure of the organs of respiratory system.
3.	Biochemistry	To have an understanding of the mechanisms of gas exchange through the alveolar-capillary membrane, the biochemical structure of the surfactant and the importance of its structure for performing the functions; the biochemical composition of bronchial mucus.
4.	Normal physiology	To know the basic functions of respiratory tract; have an idea about the process of gas exchange, how respiratory system take part in the elimination of metabolic products, in thermoregulation, in maintaining acid-base balance; know neuro-hormonal mechanisms of regulation of respiration. Understand the importance of protective elements of respiratory system - mucocilliar clearance, surfactant, immune mechanisms (alveolar macrophages, neutrophils, lymphocytes, immunoglobulins, complement system, lysozyme, lactoferrin).
5.	Physiopathology	To know etiological factors of development of COPD. To know reversible and nonreversibe mechanism of obstractive disorders in COPD. To have an understanding pathogenic mechanisms of various disorders of the respiratory tract in case of COPD: cough, shortness of breath, respiratory discomfort.
6.	Pharmacology	To know the mechanism of action, indications and contraindications of medicines, wyich is used in treating of pneumonia and be able to write them in the form of recipes.
8.	Propaedeutic therapy	Demonstrate skills in examination of patients with COPD (collecting complaints, history of disease and life, doing an objective examination, analyzing the results diagnostic testing (chest X-ray, functional tests, CBC, general analysis of sputum).

3. Contents of the training materials

Subject of the lesson:

Aetiology

The single most important cause of COPD is cigarette smoking although in developing countries exposure to smoke from biomass and solid fuel fires is also important. Smoking is thought to have its effect by inducing persistent airway inflammation and causing a direct imbalance in oxidant/antioxidant capacity and proteinase/antiproteinase load in the lungs. Individual susceptibility to smoking is, however, very wide, with only 15% of smokers likely to develop clinically significant COPD. Recent studies have also emphasised the strong familial risks associated with the development of COPD, with the incidence of disease in an individual who smokes and has an affected sibling being 4.7 times that of matched controls. A small additional contribution to the severity of COPD has been reported in patients exposed to dusty or polluted air. An association also exists between low birth weight, bronchial hyper-responsiveness and the development of COPD. Alpha1-antitrypsin deficiency can cause emphysema in non-smokers but this risk is increased dramatically in enzyme-deficient patients who smoke. Stopping smoking slows the average rate of the decline in FEV1 from 50-70 ml/year to 30 ml/year (i.e. equal to non-smokers). Interestingly, there is no evidence that acute exacerbations or drug therapy affect the rate of decline of the FEV1

Pathogenesis of the disease.

COPD leads to chronic airflow obstruction, which is defined as a persistent decrease in the rate of airflow from the lungs when the person breathes out (exhales). This airflow obstruction is partially reversible in most people, either spontaneously or with treatment. COPD includes the diagnoses of chronic obstructive bronchitis and emphysema. Many people have both disorders. Chronic bronchitis is defined as cough that produces sputum repeatedly during two successive years. When chronic bronchitis involves airflow obstruction, it qualifies as chronic obstructive bronchitis. Emphysema is defined as widespread and irreversible destruction of the alveolar walls (the cells that support the air sacs, or alveoli, that make up the lungs) and enlargement of many of the alveoli.

The small airways (bronchioles) of the lungs contain smooth muscles and are normally held open by their attachments to alveolar walls. In emphysema, the destruction of alveolar wall attachments results in collapse of the bronchioles, causing permanent airflow obstruction.

In emphysema, the destruction of alveolar wall attachments results in collapse of the bronchioles, causing permanent airflow obstruction. In chronic bronchitis, the glands lining the larger airways (bronchi) of the lungs enlarge and increase their secretion of mucus. Inflammation of the bronchioles develops and causes smooth muscle to contract (spasm), further obstructing airflow. Inflammation also causes airflow to be blocked by secretions. Asthma is also characterized by airflow obstruction. However, in contrast with the airflow obstruction of COPD, the airflow obstruction of asthma is completely reversible in most people, either spontaneously or with treatment. The airflow obstruction of COPD causes air to become trapped in the lungs after a full exhalation, increasing the effort required to breathe. Also in COPD, the number of capillaries in the walls of the alveoli decreases. These abnormalities impair the exchange of oxygen and carbon dioxide between the alveoli and the blood. In the earlier stages of COPD, oxygen levels in the blood may be decreased, but carbon dioxide levels remain normal. In the later stages, carbon dioxide levels increase and oxygen levels fall.

The decrease in oxygen levels in the blood stimulates the bone marrow to send more red blood cells into the bloodstream, a condition known as secondary polycythemia. The decrease in oxygen levels in the blood also increases the pressure in the artery through which blood flows from the heart to the lungs (pulmonary artery). As a result of the increased pressure, pulmonary hypertension and cor pulmonale can occur.

Role of inflammation in COPD

In contrast to the eosinophil, which is the most prominent inflammatory cell in asthma, the cellular composition of the airway inflammation in COPD is predominantly mediated by the neutrophils. Cigarette smoking induces macrophages to release neutrophil chemotactic factors and elastases, thus unleashing tissue destruction. Severity of airflow obstruction has correlated with greater induced sputum neutrophilia that is also more prevalent in patients with chronic cough and sputum production and is associated with an accelerated decline in lung function.

Macrophages also play an important role through macrophage-derived matrix metalloproteinases (MMPs). Cigarette smoke causes neutrophil influx and is required for the secretion of MMPs, therefore suggesting that both neutrophils and macrophages are required for the development of emphysema.

Clinical features

The clinical state is dictated largely by the severity of disease. The initial symptoms are usually repeated attacks of productive cough, usually after colds during the winter months, which show a steady increase in severity and duration with successive years until cough is present all the year round. Thereafter, patients suffer recurrent respiratory infections, exertional breathlessness, regular morning cough, wheeze and occasionally chest tightness. Sputum may be scanty, mucoid, tenacious and occasionally streaked with blood during infective exacerbations. Frankly purulent sputum is indicative of bacterial infection, which often occurs in these patients. Breathlessness is aggravated by infection, excessive cigarette smoking and adverse atmospheric conditions.

In patients with mild to moderate disease the respiratory examination may be normal. However, variable numbers of inspiratory and expiratory rhonchi, mainly low- and medium-pitched, are audible in most patients. Crepitations (crackles) which usually, but not always, disappear after coughing may be audible over the lower zones.

Physical signs associated with severe disease reflect pulmonary hyperinflation, hypoxaemia, the development of cor pulmonale (pulmonary hypertension and right heart failure) and polycythaemia

Clinical classification

Stage I: Mild COPD - Characterized by mild airflow limitation (FEV1/FVC < 0.70; FEV1 . 80% predicted). Symptoms of chronic cough and sputum production may be present, but not always. At this stage, the individual is usually unaware that his or her lung function is abnormal.

Stage II: Moderate COPD - Characterized by worsening airflow limitation (FEV1/FVC < 0.70; 50% . FEV1 < 80% predicted), with shortness of breath typically developing on exertion and cough and sputum production sometimes also present. This is the stage at which patients typically seek medical attention because of chronic respiratory symptoms or an exacerbation of their disease.

Stage III: Severe COPD - Characterized by further worsening of airflow limitation (FEV1/FVC < 0.70; 30% . FEV1 < 50% predicted), greater shortness of breath, reduced exercise capacity, fatigue, and repeated exacerbations that almost always have an impact on patients’ quality of life.

Stage IV: Very Severe COPD - Characterized by severe airflow limitation (FEV1/FVC < 0.70; FEV1 < 30% predicted or FEV1 < 50% predicted plus the presence of chronic respiratory failure). Respiratory failure is defined as an arterial partial pressure of O2 (PaO2) less than 8.0 kPa (60 mm Hg), with or without arterial partial pressure of CO2 (PaCO2) greater than 6.7 kPa (50 mm Hg) while breathing air at sea level. Respiratory failure may also lead to effects on the heart such as cor pulmonale (right heart failure). Clinical signs of cor pulmonale include elevation of the jugular venous pressure and pitting ankle edema. Patients may have Stage IV: Very Severe COPD even if the FEV1 is > 30% predicted, whenever these complications are present. At this stage, quality of life is very appreciably impaired and exacerbations may be life threatening.

Complications

Pulmonary bullae are thin-walled airspaces created by rupture of alveolar walls. They may be single or multiple, large or small, and tend to be situated subpleurally. Rupture of subpleural bullae may cause pneumothorax, and occasionally bullae increase in size, compress functioning lung tissue and further embarrass pulmonary ventilation. Respiratory failure and cor pulmonale are generally late complications in COPD patients.