ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara , Nepal

1. C O P D ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara, Nepal

2. . DEFINATION Chronic obstruction of lung airflow which ispermanent& progressive over time

3. . COPD is comprised primarily of Chronic bronchitis Emphysema

4. . • Asthma also is a pulmonary disease in which there is obstruction to the flow of air out of the lungs • obstruction in asthma usually is reversible • Between "attacks" of asthma the flow of air through the airways usually is good (With execptions)

5. are two ends of spectrum of COPD with various shades in between . Emphysema and Ch.Bronchitis

6. EMPHYSEMA a result of a loss of elastic recoil due to lung tissue destruction Pathology starts beyond terminal bronchioles CHR. BRONCHITIS increase in resistance of the conducting airways due to accumulation of inflammatory mucous exudates in the lumens of small airways Thickening of their walls Pathology confined up to terminal bronchioles Defining feature of COPD isirreversible airflow limitation during forced expirationFEV1(<80%) & FEV1/FVC (<70%) are reduced

7. Ch. Bronchitis Emphysema

8. Chronic Bronchitis Inflammation & swelling of the airways lining narrowing and obstruction of airways due to • Hyperplasia of mucus-producing glands • Over production of mucous - further obstruction of the airways - increases likelihood of bacterial lung infections

10. Reid index - chronic bronchitis Ratio of the thickness of mucous gland layer to thickness of wall between epithelium & cartilage. Normal Reid index is less than 0.4 is increased in chronic bronchitis.

11. . • Pulmonary capillary bed relatively undamaged • Centrilobular Emphysema present to a variable degree

12. Centrilobular emphysema Normal Pulmonary vessels in between alveoli are undamaged

13. Compared to Emphysema • Air way narrowing is more • Pulmonary circulation is less affected • Body responds by decreasing ventilation and increasing cardiac output. • due to rapid circulation in a poorly ventilated lung – increase in physiological shunt leading to • Hypoxemia • Polycythemia V/Q mismatch

14. Eventually, hypercapnia and respiratory acidosis develop • Leading to pulmonary artery vasoconstriction and pulmonary hypertension with corpulmonale • Patients have signs of right heart failure and are known as “Blue bloaters"

15. Emphysema Permanent enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls • reduces the elasticity of the lung • collapse of the bronchioles • obstructing airflow out of the alveoli Inspiration Expiration

16. . • Air trapping in the alveoli • Inability of the lung to shrink during exhalation • Amount of air inhaled is reduced • Less air for the exchange of gasses in lungs • Trapped air compress adjacent less damaged lung tissue compromising their function

17. Panacinar emphysema Destruction of the alveoli – blood vessels obstrcted/destroyed reduced diffusing capacity of the lung for carbon monoxide (DLCO)

18. Now identify them

19. Normal lung

20. Emphysematous lung

21. . Destruction of the alveolar walls decreases the number of capillaries gas exchange decreases (decreased DLCO) • due to relatively limited blood flow through a fairly well oxygenated lung – increase in physiological dead space with normal blood gases and pressures in the lung, (in contrast to the blue bloaters.) • The body compensates with • lowered cardiac output • hyperventilation V/Q mismatch

22. Normally expiration is passive process- effortless • extra effort required to exhale due to collapse of airways • Lungs are already inflated due to air trapping so more effort required to inhale further • Work of breathing is increased • Reduced gaseous exchange increase the Breathing rate

23. Because of low cardiac output, rest of body suffers from tissue hypoxia and pulmonary cachexia. Eventually, develop muscle wasting and weight loss and are identified as “Pink puffers"

24. Causes for cachexia in emphysema • Increased work of breathing • Low cardiac out put • Increase in TNF alpha and other mediators of inflammation

25. EMPHYSEMA Pulmonary capillary bed relatively damaged V/Q mismatch - relatively limited blood flow through a fairly well oxygenated lung with normal blood gases & pressures in the Lung - Dead Space Body compensates with lowered cardiac output and Hyperventilation CHR. BRONCHITIS Pulmonary capillary bed relatively undamaged V/Q mismatch – rapid circulation in a poorly ventilated lung, leading to hypoxemia and Polycythemia Shunt Body responds by increasing cardiac output & decreasing ventilation .

26. Chronic Asthma Obstruction to the flow of air is due to • inflammation of the airways -thickening of the airway walls lead to scarring and fixed airway obstruction • spasm of smooth muscles - bronchospasm reversible • subsides spontaneously or • with the use of bronchodilators

27. Etiology

28. Smoking responsible for 90% of COPD • not all cigarette smokers develop COPD-15% will (don’t tell this to smokers) • Smokers with COPD have higher death rates than non smokers with COPD • Have more frequent respiratory symptoms • coughing, • shortness of breath passive smoking – equally harmful

29. MECHANISM • Irritation of cigarette smoke attracts cells to the lungs that promote inflammation. They releaseelastase -breaks down the elastic fibers in lung tissue • Increases mucus production • Decreases ciliary motility

30. 2. Air pollution Role of outdoor air pollution – unclear most common cause of COPD in non industrialized world is indoor air pollution due to indoor stoves used for cooking – biomass fuel 3. Occupational pollutants: Cadmium & Silica - increase the risk of COPD

31. . Alpha-1 antitrypsin deficiency • Genetic disorder • Accounts for less than 1% of the COPD Enzyme elastase is found normally in lungs.It can break down the elastin and damage the airways and alveoli Alpha-1 antitrypsin produced by liver block the damaging effects of elastase on elastin.

32. . Alpha-1 antitrypsin deficiency causes 1. Early on set of emphysema- homozygos 2. Accelerated emphysema in smokers- hetrozygos 3. Chronic liver disease leading to cirrhosis due to their defective release leading to intra hepatic accumulation

33. Clinical features of COPD

34. . Patients with COPD present with a combination of signs and symptoms of chronic bronchitis emphysema Symptoms • Worsening dyspnea • Progressive exercise intolerance • Alteration in mental status • In addition, some important clinical and historical differences exist between the types of COPD Common symptoms

35. Chronic bronchitis Productive cough, with progression over time to intermittent dyspnoea Cough and sputum on most days -at least 3 consecutive months for at least 2 successive years Morning headache – CO2 retention Hemoptysis – usually small Frequent & recurrent pulmonary infections Progressive cardiac/respiratory failure over time, with oedema and weight gain Emphysema A long history of progressive dyspnea with late onset of nonproductive cough Occasional mucopurulent relapses Eventual cachexia and respiratory failure .

36. . 19.29 MODIFIED MRC DYSPNOEA SCALE Grade Degree of breathlessness 0 No breathlessness except with strenuous exercise 1 Breathlessness when hurrying on the level or walking up a slight hill

37. 2 Walks slower than contemporaries on level ground because of breathlessness or has to stop for breath when walking at own pace 3 Stops for breath after walking about 100 m or after a few minutes on level ground 4 Too breathless to leave the house, or breathless when dressing or undressing

38. Haemoptysis may complicate exacerbations of COPD but should not be attributed to COPD without thorough investigation Exclude Infection malignancy & other causes

39. Physical Examination

40. Barrel shaped chest • sternum more arched • spine unduly concave • AP diam > Trans diamt (5 : 7) • horizontal ribs

41. Emphysema

42. Normal Compare it with Previous one

43. COPD • Movement of chest wall diminished & reduced expansion < 2 cm (from neutral to maximum inspiration) Normal TLC IRV TLC IC VT ERV FRC RV

44. Laboured breathing – pursed lip breathing • Increased hollow in supraclavicular & suprasternal space • Indrawing of intercostal spaces • Accessory muscles of inspiration / expiration active

45. Tracheal span reduced - < 2 c.m. • Tracheal tug – may be present • Indicates the severity of disease • Apical impulse/Apex beat – not visible/palpable

46. Hyper resonant note, liver & cardiac dullness diminished or obliterated • Breath sounds –diminished, vesicular with prolonged expiration • Ronchi or wheeze during expiration • Crepitations may be present more during inspiration

47. Inspiration: • result of active contraction • Diaphragm • External intercoastals • pump handle action of the upper 8 ribs • increases the AP diameter of the chest • bucket handle action of the lower 4 ribs • increases the transverse diameter of the chest • resulting in costal elevation & lateral expansion

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50. Hutchison's Clinical Methods (22E)page 55 • Movement of the chest Body: Look at the chest movements. Are they symmetrical? If they seem to be diminished on one side, that is likely to be the side on which there is an abnormality. Intercostal recession - a drawing-in of the intercostal spaces with inspiration - may indicate severe upper airways obstruction, as in laryngeal disease, or tumours of the trachea. In COPD the lower ribs often move inwards on inspiration instead of the normal outwards movement