1. The theme of the lecture: “Bronchial asthma. Chronic obstructive pulmonary disease. The syndrome of hyperinflation of lungs. Pulmonary emphysema" Ass-prof.N.Bilkevych

3. The syndrome of bronchial obstruction  Obstructio (lat.) – barrier, obstracle.  Causes of bronchial obstruction: - accumulation of fluid in fine bronchi; - accumulation of fluid in fine bronchi; - edema of bronchial mucosa; - edema of bronchial mucosa; - spasm of bronchial smooth muscles; - spasm of bronchial smooth muscles; - poor elasticity of lungs. - poor elasticity of lungs.

4. Pulmonary emphysema

5. Respiratory system anatomy

6. Bronchial obstruction may be:  Transient: - bronchial asthma, - bronchial asthma, - pneumonia. - pneumonia.  Permanent: - chronic obstructive bronchitis, - chronic obstructive bronchitis, Pulmonary emphysema. Pulmonary emphysema.

7. Bronchial asthma Asthma is a bronchial hypersensitivity disorder characterized by reversible airway obstruction, produced by a combination of mucosal edema, constriction of the bronchial musculature, and excessive secretion of viscid mucus, causing mucous plugs. Essentials of Diagnosis: Recurrent acute attacks of dyspnea, cough, and mucoid sputum, usually accompanied by wheezing. Recurrent acute attacks of dyspnea, cough, and mucoid sputum, usually accompanied by wheezing. Prolonged expiration with generalized wheezing and musical rales. Prolonged expiration with generalized wheezing and musical rales. Bronchial obstruction reversible by drugs Bronchial obstruction reversible by drugs

8.  Ethiology  40-80 % of patients has heredital predisposition  Acquired ethiological factors  Domestic allergens  ( dust, insect allergens, fungi, animal wool, epidermis)  Environmental allergens  ( fungi, insect allergens, pollen etc)  Food allergy  ( milk, flour, fish, chemical admixtures to food)  drugs  ( antibiotics, enzymes, aspirin)  bacterial allergens  ( neisseria, Staphylococcus aureus, Candida albicans, mycoplasma, helmints)

17. Pathogenesis  Bronchial asthma is a complex inflammatory condition involving many inflammatory cells, which release a wide variety of mediators. These mediators act on cells of the airway leading to smooth muscle contraction, mucus hypersecretion, plasma leakage, oedema, activation of cholinergic reflexes and activation of sensory nerves, which can lead to amplifiaction of the ongoing inflammatory response. Chronic inflammation also leads to structural changes, such as subepithelial fibrosis and smooth muscle hypertrophy and hyperplasia, which are less easy to reverse than acute processes. Inadequately treated chronic asthma is thus associated with structural changes in the lungs

31. Immunological mechanisms Caused by: Іg Е basophils mast cells Mediators: Mediators:histamineprostaglandinesleukotriens

33.  Bronchial obstruction in bronchial asthma is caused by: spasm of bronchial smooth muscles; spasm of bronchial smooth muscles; swelling of bronchial mucosa; swelling of bronchial mucosa; Hypersecretion of teniacious mucoid sputum. Hypersecretion of teniacious mucoid sputum.

34. Clinical Findings Asthma is characterized by recurrent attacks of dyspnea, cough, and expectoration of tenacious mucoid sputum, and usually wheezing. Symptoms may be mild and may occur only in association with respiratory infection, or they may occur in various degrees of severity to the point of being life-threatening. Classic allergic (atopic) asthma usually begins in childhood and becomes progressively more severe throughout life, although spontaneous remissions may occur in adulthood. Hay fever often accompanies atopic asthma.

36.  The acute attack is characterized by dyspnea usually associated with expiratory wheezing that may be heard without a stethoscope. Cough may be present but is usually not the predominant symptom. There is a small group of patients with asthma in whom paroxysmal cough may be the predominant symptom.

37. Clinical pattern

39. Appearance of a patient during attack of asthma

42. Status asthmaticus  This is a complication of asthma.  When asthma becomes prolonged, with severe intractable wheezing, it is known as status asthmaticus.  Status asthmaticus is attack af asthma which lasts for more than 24 hours. Patients are not sensitive to β-agonists. Corticosteroids are used for treatment.

45. Дослідження харкотиння

46. спірограма

49. Chest X-ray in asthma

50. X-ray shows pulmonary emphysema

51. Endoscopic findings: hyperemia, edema of bronchial mucosa, hypersecretion

52. Allergic tests allow to determine allergens

53. Positive reaction

56. Usage of inhaler

57. Solotvino (salt caves)

61. Physiotherapy

62. Climatotherapy

63. Elimination of risk-factors

65. Bronchoscopy is used if it is necessary

66. Chronic obstructive pulmonary disease (COPD)  The common combination of chronic bronchitis and emphysema has also been termed chronic obstructive airways disease (COAD) or chronic obstructive pulmonary disease (COPD).  This is a morbid condition characterized by non-reverseble bronchial obstruction caused by deformation and sclerosis of bronchial tree due to persistent inflammation.  Up to 20% of adults worldwide have the disease, and this proportion is higher in heavily industrialized countries. Chronic bronchitis occurs in the majority of heavy smokers, but significant airway obstruction or emphysema, or both occurs in only a minority.  It is the third most common cause of death in men over 65 years (60 per 100.000), and is more common in men (8%) than women (3%). COPD develops in at least 80% of smokers.

67. Chronic bronchitis  This is a clinical syndrome in which there is excess mucous secretion by bronchial gob let cells.  This stimulates the cough so that sputum is produced daily for at least 3 months of the year. There are often episodes of superimposed viral or bacterial infection in which the sputum may be yellow or green and often contains a fleck of blood. Many patients also have an intermittent wheeze with objective evident: of airways obstruction on pulmonary function tests am some may have acute severe bronchoconstriction ii response to respiratory infections or to irritants or allergens (asthmatic bronchitis).

68. Emphysema  This is a syndrome which include symptoms of lung overfilling with air (air hyperinflation).  Emphysema is characterized by enlargement of the airspaces distal to the terminal bronchioles, either from dilatation or destruction of their walls.  It is a pathological or radiological rather than a clinical diagnosis and is commonly associated with chronic bronchitis.  Destruction of the alveolar septae results in the formation of multiple bullae in the lungs, with hyperinflation of the chest and impaired respiratory function.  The PA chest X-ray usually shows hyperinflation of both lung fields, producing depression of both diaphragms and a characteristic long, thin mediastinum. At the right lateral chest X-ray may show a marked increase in the posteroanterior diameter of the chest.  CT scan may demonstrate bullous areas and reduced density of the lung structure on thin slices of lung. The measurements of lung dencity correlate well with histological findings.

69. Causes of COPD  I.Localized  A.Congenital  B.Compensatory due to lung collapse, scarring or resection  C.Partial bronchial obstruction  Neoplasm  Foreign body  D.MacLeod'syndrome  II.Generalized  A.Idiopathic  B.Senile  C.Familial (alpha-1-anti-trypsin deficiency)  D.Associated with chronic bronchitis, asthma or pneumoconiosis.

74. Clinical pattern  The characteristic clinical features of chronic bronchitis and emphysema are cough, productive of thick yellow-green sputum, wheeze and progressive breathlessness.  The symptoms are usually in winter and exacerbated by atmospheric pollution, dry air, intercurrent infections and industrial exposure to irritant gases or dusts.

78. Treatment  The most important step in management is to persuade the patient to stop smoking.  Bronchodilators may achieve some reversal of airways obstruction  Corticosteroids have a role in some patients.  Surgical removal of large bullae is occasionally helpful.  Oxygen is usually given via nasal cannulae. Occasionally transtracheal oxygen therapy (TTOT) via a small polyethylene catheter introduced directly into the trachea. Long-term oxygen therapy from cylinders or an oxygen concentrator may be of value in patients with chronic stable respiratory failure. The flow rate and concentration are adjusted to relieve arterial hypoxaemia while avoiding carbon dioxide narcosis.  Infections are frequent, and it is important to educate patients in the early recognition of symptoms and signs, for example change of sputum colour and quality, fever or increasing wheeze. Many patients should be given a supply of antibiotics to keep at home for self- medication.