Chronic obstructive pulmonary disease, etiology, pathophysiology and it's management

Brief discussion about chronic obstructive pulmonary disease

1. CHRONIC OBSTRUCTIVE PULMONARY DISEASES Poovarasan.A PHARM.D Intern KLE College of Pharmacy, Bengaluru-10 Mail.Id : [email protected]

2. DEFINITION Chronic Obstructive Pulmonary disease (COPD) is a lung disease characterized by longstanding obstruction of lung airways that interferes with normal breathing and is not fully reversible. There are 2 forms of COPD Chronic Bronchitis and Emphysema Sufferers of COPD tend to have a bit of both

3. Chronic bronchitis is defined as presence of a chronic cough that is accompanied by sputum production for at least 3 months in 2 consecutive years. Emphysema is abnormal enlargement of air spaces within the lungs.

4. STAGES Stage 1 – Mild COPD: This is the first stage where it is difficult for the patient to identify an abnormality in their lungs because of very mild difficulty in airflow. Some might also experience coughing sputum, a mixture of mucus and saliva. Stage 2 – Moderate COPD: Stage two is where people tend to have some unusual breathlessness during exercising and airflow in the lungs starts worsening. In usual cases, a patient seeks medical assistance at this point.

5. CONTD… Stage 3 – Severe COPD: As the name goes, the condition and the quality of life of the patient start depleting. Recurring episodes of shortness of breath with minimal exertion, greater restriction to their airflow, and increased tolerance to exercise lead to a miserable condition. Stage 4- Very severe COPD: This is the extreme situation where breathing becomes so restrictive that it seems life-threatening and an immediate external oxygen supply is required. The patient’s body is almost intolerable to any kind of physical strain and immediate treatment is to be given.

6. EPIDEMIOLOGY 1.5 million emergency room visits in 2000 726,000 hospitalizations in 2000 Total estimated cost of COPD in 2002 was $32.1 billion $18 billion in direct costs
$14.1 billion in indirect costs

7. ETIOLOGY Dyspnea on exertion
Progressive
Persistent
Worse with exercise
Worse during respiratory infections Not all patients with these symptoms develop COPD

8. RISK FACTORS History of exposure to risk factors
Tobacco smoke
Occupational dusts and chemicals
Cigarettes Smoke from home cooking and heating fuels

9. Contd …. Occupational dusts and chemicals
Vapours, irritants, fumes
Need sufficiently intense or prolonged exposure
Indoor air pollution
Biomass fuel used for cooking and heating in poorly vented dwellings

10. Outdoor air pollution
Minor risk factor Passive cigarette smoke exposure
Respiratory infections in early childhood
Lower socioeconomic status
Association with COPD
May be secondary to crowding, poor nutrition, etc

11. SEVERITY Stage Characteristics 0: At Risk Normal spirometry Chronic symptoms (cough, sputum) I: Mild FEV 1 /FVC < 70% FEV 1 >= 80% predicted Usu. Chronic cough and sputum production II: Moderate 50% <= FEV 1 < 80% predicted Progression of symptoms; dyspnea on exertion III: Severe 30%<= FEV 1 < 50% predicted ↑ dyspnea; repeated exacerbations which have an impact on patients’ quality of life IV: Very severe FEV1< 30% predicted OR FEV1<50% predicted + chronic respiratory failure Quality of life is appreciably impaired Exacerbations may be life-threatening

12. DIAGNOSTIC TESTS Chest X-ray
Flattened diaphragms
Use to exclude other diagnoses
ABG
Spirometry

13. High resolution CT Not routinely recommended
If in doubt about diagnosis of COPD
If considering bullectomy or lung volume reduction surgery

14. SPIROMETRY Best performed with the patient seated
Optimal results
Patient breathes in fully
Patient must seal their lips around the mouthpiece
Have the patient force the air out of their chest as hard and fast as they can until their lungs are completely “empty”

15. ABG Respiratory Failure: PaO2 < 60 mm Hg with or without PaCO2 > 45 mm Hg while breathing air

16. OTHER’S TESTS Alpha-1 antitrypsin
Consider in patients with COPD < age 45
Strong family history of early COPD or with alpha-1 antitrypsin deficiency

17. DIFFERENTIAL DIAGNOSIS Asthma Symptoms vary day to day Reversible airflow limitation
Early onset (childhood) Congestive heart failure Volume restriction, NOT airflow limitation
CXR with dilated heart, pulmonary edema

18. Contd … Tuberculosis Onset at all ages
Chest x-ray with infiltrate or nodular lesions Obliterative bronchiolitis
Younger patients/non-smokers
May have a history of rheumatoid arthritis or fume exposure
CT shows hypodense areas with expiration

19. Contd … Diffuse panbronchiolitis Male/non-smokers
Chronic sinusitis
CXR and high resolution CT show diffuse small centrilobular nodular opacities and hyperinflation Bronchiectasis Large volumes of purulent sputum
Commonly associated with bacterial infection
Bronchial dilation and bronchial wall thickening on CXR or CT

20. PATHOPHYSIOLOGY Abnormal Inflammatory response Of the lungs Due to toxic gases Response occurs in the Airways, parenchyma and Pulmonary vasculature Narrowing of the airway takes place Destruction of parenchyma leads to Emphysema

21. CLINICAL MANIFESTATIONS Cough usually worse in the morning and is accompanied by sputum production Breathlessness which is seen more in the patients 60 and above. Wheezing which is usually worse after physical activity Other symptoms that might be seen include tightness in the chest, swelling of the legs and also weight loss in the patient

22. GOALS Prevent disease progression Relieve symptoms Improve exercise tolerance Improve health status Prevent and treat complications Prevent and treat exacerbations Reduce mortality Prevent or minimize side effects from treatment Cessation of cigarette smoking

23. Non-Pharmacologic Therapy Improves both exercise tolerance and symptoms of dyspnea and fatigue Comprehensive program should include several types of health professionals: Exercise training Nutrition counseling Education Minimum effective length of time = 2 months Setting: inpatient OR outpatient OR home

24. PHARMACOTHERAPY Short-acting beta2-agonist (SABA) Salbutamol ATP to cAMP leads to relaxation of bronchial smooth muscle, inhibition of release of mediators of immediate hypersensitivity from cells, especially mast cells.

25. Long-acting beta2-agonists (LABA) Salmeterol Formeterol Both remain in the lung tissue for longer Provide long lasting bronchodialation (> 12hrs)

26. CONTD… Long-acting beta2-agonists (LABA) Beta2-receptors are the predominant receptors in bronchial smooth muscle Stimulate ATP- cAMP which leads to relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity Inhibits release of mast cell mediators such as histamine, leukotrienes, and prostaglandin-D2

27. ANTICHOLINERGICS Ipratropium and Tiotropium Generally produce further improvement in lung function (10 – 15%) instead of B2 agonists alone In patients with FEV1 < 30% of predicted (at baseline) may produce reduced hospitalization rate C ombination bronchodilators Fenoterol /ipratropium ( Duovent ) Salbutamol/ipratropium ( Combivent )

28. GLUCOCORTICOIDS Does not modify the long-term decline in FEV 1 BUT does reduce the frequency of excacerbations and improves health status The combination of a long-acting beta2-agonist and an inhaled glucocorticosteroid is more effective than the individual components Long-term treatment with oral glucocorticoids is NOT recommended Treatment trial of inhaled glucocorticosteroids for 6 to 12 weeks then repeat spirometry with and without bronchodilators

29. INHALED GLUCOCORTICOIDS Beclomethasone ( Vanceril ) Budesonide ( Pulmicort ) Fluticasone ( Flovent ) Triamcinolone ( Azmacort )

30. VACCINES Influenza yearly Reduces serious illness and death in COPD patients by approximately 50% Give once yearly: autumn OR twice yearly: autumn and winter Pneumovax Sufficient data to support its general use in COPD is lacking, but it is commonly used

31. OTHER MEDICATIONS Alpha-1 Antitrypsin Augmentation Therapy Only if this deficiency is present in an individual should they undergo treatment Antibiotics Prophylactic use is NOT recommended Can be used in the treatment of infectious exacerbations of COPD

32. OTHER MEDICATIONS Mucolytic agents Overall benefits are small, so currently not recommended for widespread use Types: Ambroxol Erdosteine ( Erdostin , Mucotec ) Carbocysteine ( Mucodyne ) Iodinated gylerol ( Expigen )

33. OTHER MEDICATIONS Antioxidant agents N-acetylcysteine ( Bronkyl , Fluimucil , Mucomyst ) Have been shown to reduce the frequency of exacerbations and could have a role in the treatment of patients with recurrent exacerbations Immuno regulators Not recommended at this time No reproducible studies are available

34. OTHER MEDICATIONS Antitussives Regular use is contraindicated in stable COPD since cough has a significant protective role Vasodilators Inhaled nitric oxide Can worsen gas exchange because of altered hypoxic regulation of ventilation-perfusion balance and is contraindicated in stable COPD

35. THANK YOU….