Chronic Obstructive Pulmonary Disease

1. Chronic Obstructive Pulmonary Disease Hou-haifeng

2. LUNG STRUCTURE

3. NORMAL VENTILATORY FUNCTION • Diaphragm contracts and descends, rib cage moves upwards and outward. • Pressure in the thorax is less than in the mouth so air flow into the lungs occurs. • In expiration diaphragm relaxes and moves upwards, the rib cage moves inward. • Expiration is passive so no muscular contraction is needed. • Lung tissue is intrinsically elastic and has a natural ability to recoil. • During exercise expiration is aided by the contraction of abdominal and thoracic expiratory muscles. • Contractions generate positive pressure in the thorax pushing air out.

4. COPD DISORDERS • Chronic Bronchitis • Emphysema • Asthma (?) Although not strictly a COPD disorder ASTHMA is often linked with being a COPD disorder.

5. DEFINITION • Progressive, non-reversible, obstructive airway disease leading to damaged alveolar walls and inflammation of the conducting airways • Some part of the airway becomes obstructed or no longer functions efficiently

6. CHRONIC OBSTRUCTIVE PULMONARY DISEASE:

8. Pathogenesis of COPD NOXIOUS AGENT(tobacco smoke, pollutants, occupational agent) COPD Genetic factors Respiratory infection Other

10. MECHANISMS Bronchial glands / cells inflame Increased secretions Inflammation spreads to smooth muscle (bronchiole) Airway obstruction, decreased ciliary action Air trapping / Collapse of small airways Further air trapping Hyperventilation Increased pressure in airways Weakened airway walls / wall destruction Alveolar destruction Overstressed right ventricle

11. MECHANISMS II Increases in RBC, Blood viscosity, BP Ventilation / Perfusion imbalances Hypoxemia Carbon dioxide retention Bronchial hyperreactivity Hyperinflation

12. CHRONIC BRONCHITIS • Chronic bronchitis is defined as "persistent cough with sputum production for at least 3 months in at least two consecutive years". • The most important cause of chronic bronchitis is recurrent irritation of the bronchial mucosa by inhaled substances, as occurs in cigarette smokers. • The pathological hallmarks of chronic bronchitis are congestion of the bronchial mucosa and a prominent increase in the number and size of the bronchial mucus glands. Copious mucus may be seen within airway lumens. The terminal airways are most susceptible to obstruction by mucus.

13. CHRONIC BRONCHITIS Aetiology • Characterised by a chronic cough and excessive sputum production. • There is an enlargement and an increased density of mucous glands. • The airway becomes thickened and the surface irregular • Bronchial inflammation. (ACSM, 1998) • Reduced number of ciliated cells • Causes an increase in air flow resistance • In chronic severe cases right heart failure occurs • Plugged airways and decreased ciliary action encourages stagnant bronchial secretions and an increased risk of infection.

14. CHRONIC BRONCHITIS • Inflammatory cells produce elastase • Destroys connective tissue of alveolar walls • Alpha-1 anti-trypsin (or alpha-1 protease inhibitor) is a protein produced by the liver that circulates in the blood and limits the action of elastase

15. MUCUS PRODUCTION

16. MUCUS PRODUCTION

17. CHANGES IN LUNG VOLUMES

18. VENTILATION COST • In COPD work of breathing is greater for any given level of ventilation than normal. SEVERE COPD The cost of work at a given ventilation for ‘normal’ and COPD patients (ACSM, 1998) WORK OF BREATHING MODERATE COPD NORMAL COPD VENTILATION

19. EMPHYSEMA AETIOLOGY • Can be caused by smoking, air pollution and environmental and occupational hazards • Main characteristic is loss of lung elasticity and reduction of elastic recoil due to alveolar destruction • Destruction of elastic tissue leads to loss of elastic recoil of lungs during expiration and forced expiration necessitated • Eventual destruction of airway / capillary membranes • Destruction due to increased protease production or a deficiency in anti-protease

21. EFFECTS OF EMPHYSEMA ON HEALTH • Reduction in expiratory flow level • Patients are thin with general muscle wastage. • Lung diffusion capacity is reduced due to loss of alveolar capillary units • Lactic acid threshold is much lower in COPD patients • Exercise tolerance impaired

22. Diagnosis of COPD EXPOSURE TO RISK FACTORS SYMPTOMS cough tobacco sputum occupation dyspnea indoor/outdoor pollution è SPIROMETRY

23. Spirometry: Normal and COPD

24. MEDICAL THERAPY • BRONCHODILATORS Adrenergic agents • Beta-agonists bind to B2 receptors on airway and result in smooth muscle relaxation and bronchodilation • Inhaled route is preferred • Acute relief of symptoms Anti-cholinergic agents • Bind to acetylcholine receptors and result in bronchodilation (of mostly larger airways) • Reduces sputum production • Inhaled route is preferred Methylxanthines (i.e. theophylline) • Weak bronchodilator • Delays respiratory muscle fatigue • Reduces trapped lung gas • Improves respiratory muscle mechanics

25. MEDICAL THERAPY • Corticosteroids • Reduce airway inflammation • Mucolytics • Alter viscosity of sputum • May reduce symptoms in some patients • Must be used carefully (i.e. avoiding hypotension)

26. EXERCISE • Increase exercise tolerance • Increase quality of life • Improve co-ordination and efficiency of movement • Improve strength particularly respiratory muscles • Encourage relaxation • Confidence in physical abilities • Flexibility

27. What we want to do • As we all know there is so much data on the patients deposited in the hospital,however,that is not well exploited • So we want to use these data to make a disease model to help doctors to make a appropriate diagnostic and therapeutic scheme for the patients with COPD • We also can use this model to predict the progress of the disease and the prognosis

28. mathematics, statistics, cybernetics, system theory, computer science COPD Disease Model The information from the data base in the hospital The information from the data base in the hospital Disease progress prognosis The knowledge of medicine(Pathology Physiology Pharmacology…) therapeutic scheme doctor