Es EPOC o Asma? Dr. Cristian Ibarra Duprat. Hospital Clínico Universidad de Chile. Definición de EPOC

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1 Es EPOC o Asma? Hospital Clínico Universidad de Chile Definición de EPOC Enfermedad prevenible y tratable. Con efectos extrapulmonares significativos que pueden contribuir a su gravedad en pacientes individuales. Su componente pulmonar se caracteriza por limitación al flujo aéreo que no es completamente reversible.

2 Definición de EPOC La limitación al flujo aéreo es generalmente progresiva y asociada con una respuesta inflamatoria anormal del pulmón a partículas o gases nocivos (humo de tabaco y polución ambiental). GLOBAL STRATEGY FOR THE DIAGNOSIS, MANAGEMENT, AND PREVENTION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE UPDATED 2007 Definición de Asma! Proceso inflamatorio crónico de las vías aéreas.! Diversas células y elementos celulares desempeñan un rol.! La inflamación crónica está asociada con hiperreactividad de las vías aéreas que conduce a episodios recurrentes de sibilancias, disnea, opresión toráxica y tos.! Limitación generalizada, variable, y a menudo reversible del flujo aéreo.

3 Risk Factors for COPD Host Factors Exposure chemicals Genes (e.g. alpha1-antitrypsin deficiency) Hyperresponsiveness Lung growth Tobacco smoke Occupational dusts and Infections Socioeconomic status

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

5 Noxious particles and gases Anti-oxidants Lung inflammation Host factors Anti-proteinases Oxidative stress Proteinases Repair mechanisms COPD pathology Asthma of 9 months duration Budesonide 600µg BID for 3 months Laitinen et al., J Allergy Clin Immunol 1992; 90:32-42

6 Mild allergic asthma loss of surface epithelium homogeneous thickening of the reticular basement membrane COPD ( heavy smoker, FEV 1 = 40% pred) intact epithelium with squamous metaplasia the basement membrane is relatively thin Jeffery pk. Chest, 117(5) Suppl S-260S

7 Changes in inflammatory cells: Comparison of smokers with chronic bronchitis, COPD, and asthma vs healthy control subjects leukocytes that are CD8 + leukocytes that are CD4+ Bronchial biopsy from a smoker with chronic bronchitis In contrast to asthma, the predominant T-cell in COPD is the CD8 phenotype

8 Neutrophil elastase in chronic bronchitis ASTHMA Sensitizing agent COPD Noxious agent Asthmatic airway inflammation CD4 + T-lymphocytes Eosinophils COPD airway inflammation CD8 + T-lymphocytes Macrophages Neutrophils Completely reversible Completely irreversible (Airflow limitation)

9 Characteristics of Inflammation in Asthma and COPD Cells Mediaters Consequences Response to therapy Asthma Eosinophils Small increase in macrophages Activation of mast cells LTD4 IL4, IL5 and many others Fragile epithelium Thickening of basement membrane Mucus metaplasia Glandular enlargement Glucocorticoids inhibit inflammation COPD Neutrophils Large increase in macrophages Increase in CD8 + lymphocytes LTB4 IL-8 TNF-! Squamous metaplasia of epithelium Parenchymal destruction Mucus metaplasia Glandular enlargement Glucocorticoids have little or no effect Bronchial Hyperresponsiveness Reversible Airway Obstruction Asthma Airway Inflammation

10 Inflammation of COPD Small airway disease Airway inflammation Airway remodeling Parenchymal destruction Loss of alveolar attachments Decrease of elastic recoil Airflow Limitation Causes of Irreversible Airflow Limitation in COPD Fibrosis and narrowing of the airways Loss of elastic recoil due to alveolar destruction Destruction of alveolar support that maintains patency of small airways

11 Causes of Reversible Airflow Limitation in COPD Accumulation of inflammatory cells, mucus, and plasma exudate in bronchi Smooth muscle contraction in peripheral and central airways Dynamic hyperinflation during exercise

12 Reversible and variable airway limitation in Asthma 1. PEF increases more than 15 % mins after inhalation of a rapid acting bronchodilator 2. PEF varies more than 20 % from morning measurement upon arising to measurement 12 hrs later in P t taking a bronchodilator ( more than 10% in P ts who are not taking a bronchodilator ) 3. PEF decrease more than 15 % after 6 minutes of sustained running or exercise.

13 Diagnosis of COPD SYMPTOMS cough sputum dyspnea EXPOSURE TO RISK FACTORS tobacco occupation indoor/outdoor pollution " SPIROMETRY Características clínicas de Asma y EPOC

14 Stage Characteristics 0: At risk Normal spirometry Chronic symptoms (cough, sputum) I: Mild FEV 1 /FVC < 70%; FEV 1 # 80% predicted With or without symptoms (cough, sputum) II: Moderate lll: Severe Classification of COPD by Severity dyspnea) FEV 1 /FVC < 70%; 50% $ FEV 1 < 80% predicted; With or without symptoms (cough, sputum, dyspnea) FEV1/FVC < 70%; 30% $ FEV 1 < 50% predicted) With or without chronic symptoms (cough, sputum, IV: Very SevereFEV 1 /FVC < 70%; FEV 1 < 30% predicted or FEV 1 < 50%predicted plus respiratory failure or clinical signs of right heart failure

15 GOLD Workshop Report Four Components of COPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD " Education " Pharmacologic " Non-pharmacologic 4. Manage exacerbations

16 Reduce Risk Factors of COPD Key Points Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD. Smoking cessation is the single most effective-and cost-effective- intervention to reduce the risk of developing COPD and stop its progression (Evidence A). 100 COPD risk and smoking cessation FEV 1 (% of value at age 25) Disability Death Smoked regularly and susceptible to effects of smoke Age (years) Never smoked or not susceptible to smoke Stopped smoking at 45 (mild COPD) Stopped smoking at 65 (severe COPD) Adapted from Flecher CM, Peto R. The Natural History of Chronic Airflow Obstruction. Brit Med J. 1977;1:

17 The Aim of Treatment is Control of Asthma Step 4: Severe persistent CONTROLLER Daily multiple medications Inhaled corticosteroid Long-acting bronchodilator Oral corticosteroid Avoid or control triggers Step 3: Moderate persistent CONTROLLER Daily medications Inhaled corticosteroid Long-acting bronchodilator Avoid or control triggers Step 2: Mild persistent RELIEVER Inhaled beta 2 - agonist p.r.n. CONTROLLER RELIEVER Daily medications Inhaled beta 2 - Select one controller medication agonist p.r.n. Possibly add long-acting bronchodilator Avoid or control triggers Step 1: Intermittent Avoid or control triggers Treatment RELIEVER Inhaled beta 2 - agonist p.r.n. RELIEVER Inhaled beta 2 - agonist p.r.n. Step down when controlled Reduce therapy if controlled at least 3 months Continue monitoring Step up if not controlled Classification of anti-asthma medication Reliever treat acute symptoms % Inhaled short acting & 2 -agonist % Inhaled anticholinergics % Systemic corticosteroids Controller maintain long term control % Inhaled corticosteroid % Cromolyn sodium (Intal) % Long acting & 2 agonist % Slow releasing theophylline % Leukotriene modifiers

18 Reliever Short acting &2-agonists (cold color) Controller Inhaled corticosteroids (warm color) Bronchodilators in Stable COPD Bronchodilator medications are central to symptom management in COPD Inhaled therapy is preferred Long-acting inhaled bronchodilators are more convenient Combining bronchodilators may improve efficacy and decrease the risk of side effects compared to increasing the dose of a single bronchodilator

19 Steroid in Stable COPD Indication of Inhaled glucocorticosteroids: FEV 1 < 50% predicted with repeated exacerbations Chronic treatment with systemic glucocortico-steroids should be avoided Non-pharmacological Management of Stable COPD Exercise training programs can improve the exercise tolerance and symptoms of dyspnea and fatigue The long-term administration of oxygen (> 15 hours per day) increase survival

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21 Common Causes of Acute Exacerbations of COPD Primary Tracheobronchial infection Air pollution Secondary Penumonia Pulmonary embolism Pneumothorax Rib fracture/chest trauma Inappropriate use of sedatives, narcotics, & blockers LVF/RVF or arrhythmias Manage of COPD Exacerbations 1/3 causes unknown Inhaled bronchodilators, theophylline, and oral steroids are effective Antibiotics for airway infection NIIPPV: ' ABG and ph, ( mortality, ( the need for intubation and mechanical ventilation, ( the length of hospital stay

22 CONCLUSIONES Similitudes CONCLUSIONES Diferencias