CHRONIC OBSTRUCTIVE PULMONARY DISEASE ( COPD )_2024.pptx

CHRONIC OBSTRUCTIVE PULMONARY DISEASE ( COPD )_2024.pptx

1. CHRONIC OBSTRUCTIVE LUNG DISEASE PRESENTER EMMANUEL J MKUYE

2. OBJECTIVES Introduction Epidemiology Etiology/Risk Factors Pathophysiology Clinical Presentation Diagnosis Investigations Treatment Preventions

3. DEFINITION COPD is a common progressive disorder characterized by airway obstruction that is not full reversible . The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases .

4. COPD includes, Chronic bronchitis
Emphysema Chronic bronchitis is defined as a chronic productive cough over a defined period, classically for at least three months in each of two successive years Emphysema describes enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls

5. EPIDEMIOLOGY US , In smokers, two thirds of men and one fourth of women have emphysema and about 15 million individuals. It is notable that many more have never been formally diagnosed . In east A frica COPD pooled prevalence in the different countries was 18.994%, 7%, 15.745%,9.032%, 15.026% and 11.266% in ethiopia , uganda , tanzania , malawi , sudan and kenya

6. Epidemiology cont ….

7. RISK FACTORS ENVIRONMENT/EXPOSURE Tobacco smoking (active and passive) Biomass solid fuel fires (wood, animal dung, crop residue, coal) Occupation: coal miners Air pollution (indoor and outdoor) Low socio economic status Nutrition

8. Risk factors cont.. HOST FACTORS Alpha-1 antitrypsin (alpha 1 antiproteinase ) deficiency Airway hyper- reactivity

9. Host factors Environmental exposures Genetic 10–20% of heavy smokers develop COPD Siblings of patients with severe COPD have increased risk of airways obstruction α1-AT deficiency, ZZ allele Cigarette smoking 95% of cases More than 20 pack-years of smoking Mucus hypersecretion and chronic airflow obstruction Atopy and airway hyperresponsiveness Air pollution Sulfur dioxide and particulates (black smoke or particulate matter < 10 μ m Indoor air pollution from biomass fuel. More women?? Nutrition and lung growth Vitamin A, C and E Fish oil Flavonoids Alcohol consumption Occupational dust and chemicals Dust (coal, silica, quartz) Isocyanate fumes These may interact with cigarette smoking Gender Female more susceptible Infection Chest infections in the first year of life Adenovirus may amplify inflammation HIV smokers more susceptible to emphysema

10. Progression of COPD is characterized by the accumulation of inflammatory mucous exudates in the lumens of small airways and the thickening of their walls. These walls become infiltrated by adaptive and innate inflammatory immune cells. Infiltration of the airways with substances such as polynuclear and mononuclear phagocytes and CD4 T cells increases with each stage of disease progression. PATHOPHYSIOLOGY

11. This is also true for B cells and CD8 T cells, which organize into lymphoid follicles. This chronic inflammatory process is associated with tissue repair and remodeling that ultimately determines the pathologic type of COPD. It appears that smoking may overcome the body's natural mechanisms for limiting this immune response. This process can continue in susceptible individuals even after smoking cessation. Even if the original noxious insults are removed, COPD is still characterized by progressive accumulation of cells of the immune system, fibrosis, and mucus hypersecretion

12. Clinical Presentation

13. In the chronic bronchitis group, classic symptoms include the following Productive cough, with progression over time to intermittent dyspnea Frequent and recurrent pulmonary infections Progressive cardiac/respiratory failure over time, with edema and weight gain

14. In the emphysema group,may include the following set of classic symptoms A long history of progressive dyspnea with late onset of nonproductive cough Occasional mucopurulent relapses Eventual cachexia and respiratory failure

15. Physical Examination Chronic bronchitis (blue bloaters) findings may be as follows: Frequent cough and expectoration are typical . Use of accessory muscles of respiration is common . Coarse rhonchi and wheezing may be heard on auscultation . Patients may have signs of right heart failure ( ie , cor pulmonale ), such as edema and cyanosis.

16. Emphysema (pink puffers) findings may be as follows: Patients may be very thin with a barrel chest . They typically have little or no cough or expectoration . Breathing may be assisted by pursed lips and use of accessory respiratory muscles ; May adopt the tripod sitting position. In this manner, the patient is trying to maintain a certain amount of positive end-expiratory pressure (PEEP) at the end of expiration, to help keep their lungs open, owing to the loss of lung structure from the disease.

17. The chest may be hyperresonant , and wheezing may be heard; heart sounds are very distant . Overall appearance is more like classic COPD exacerbation.

18. Acute exacerbations The hallmarks of an exacerbation of COPD include
increased cough,
greater volumes of purulent sputum,
increased dyspnea, and sometimes perceptible wheezing

19. exacerbations are often attributed to, viral upper respiratory infections acute bacterial bronchitis, exposure to respiratory irritants . As COPD progresses, acute exacerbations tend to become more frequent, averaging about 1 to 3 episodes/year. Acute exacerbations cont …

20. Differential Diagnosis

21. Diagnosis of COPD Diagnosis is suggested by, history physical examination chest imaging findings confirmed by pulmonary function tests

22. LAB INVESTGATIONS Sputum: C/s and cytology FBP: Polycythemia Measure arterial blood gases, PaO2 and PaCO2 INVESTIGATIONS

23. Chest Xray Chronic bronchitis Features increased bronchovascular markings cardiomegaly .

24. Emphysema features Hyperinflation flat hemidiaphragms possible bullous changes

25. Pulmonary function test Spirometry Forced expiratory volume in 1 second (FEV1 ) is decreased, with concomitant reduction in FEV1/forced vital capacity (FVC) ratio. Patients have poor/absent reversibility with bronchodilators. FVC is normal or reduced .

26. a forced expiratory volume in one second/forced vital capacity [FEV1/FVC] ratio less than 0.7 Total lung capacity (TLC) is normal or increased. Residual volume (RV) is increased. Diffusing capacity is normal or reduced Cont …

27. SPIROMETER

28. Cont …

29. Treatment of COPD Treatment of chronic stable COPD aims to prevent exacerbations and improve lung and physical function. Relieve symptoms rapidly with primarily short-acting beta-adrenergic drugs and decrease exacerbations with inhaled corticosteroids, long-acting beta-adrenergic drugs, long-acting anticholinergic drugs, or a combination

30. Smoking cessation Inhaled bronchodilators, corticosteroids , or both Supportive care ( eg , oxygen therapy, pulmonary rehabilitation) Treatment cont …

31. BRONCHODILATORS

32. Examples of bronchodilator

33. Muscarinic antagonist Decrease contractility of smooth muscle in the lung, inhibit bronchoconstriction and mucus secretions Examples SAMA: IPRATROPIUM BROMIDE LAMA: TIOTROPIUM BROMIDE

34. Chronic bronchitis

35. Emphysema

36. COPD EXACERBATION

37. Pulmonary rehabilitation includes structured and supervised exercise training nutrition counseling self-management education Treatment of exacerbations ensures adequate oxygenation and near-normal blood pH, reverses airway obstruction, and treats any cause TREATMENT CONT….