COPD: Change in Definition. COPD Pathology with 3D Interactive. COPD: Definitions of 21st Century 1. COPD Includes Chronic Bronchitis 2

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1 COPD: Change in Definition COPD Pathology with 3D Interactive by Scott Cerreta, BS, RRT Director of Education COPD used to include 5 disease processes 1 1 Chronic Bronchitis 2 Emphysema 3 Asthma 4 Bronchiectasis 5 Cystic fibrosis & fibrosis from Tb Differential diagnosis separates 3 to 5 COPD: Definitions of 21st Century 1 Preventable and treatable Airflow limitation that is not fully reversible Progressive disease Abnormal inflammatory response of the lungs Subsets of patients Chronic bronchitis COPD Asthma Emphysema COPD Includes Chronic Bronchitis 2 Productive cough for 3 months in 2 consecutive years with intermittent wheezing and variable degrees of recurring dyspnea on exertion Inflammation of cells that line the bronchus resulting in excess sputum Mucous glands enlarge and bronchial walls thicken, resulting in a deformed and narrow airway lumen

2 COPD Includes Emphysema 2 COPD: Airway Effects 7 Abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. Destruction occurs in the alveoli and the orderly appearance of the acinus is disturbed. Normal elasticity is lost, air becomes trapped in over-inflated lungs. Structural changes of Emphysema 10 Pathology, Pathogenesis, & Pathophysiology Pathology Characteristics and effects of COPD Pathogenesis Origin and cause of COPD Normal Emphysema Pathophysiology Biologic and physical manifestations of COPD Processes within the body that result in signs and symptoms

3 COPD: Anatomy Review Divisions of lower respiratory tract 1. Trachea cartilage; conducting airway 2. Mainstem bronchi ß 2 smooth muscle; conducting airway 3. Secondary bronchi ß 2 smooth muscle; conducting airway 4. Tertiary bronchi ß 2 smooth muscle; conducting airway 5. Bronchioles ß 2 smooth muscle; conducting airway 6. Terminal bronchioles ß 2 smooth muscle; conducting airway COPD: Pathology COPD Compromises Four Compartments of the Lung 1. Central airways cartilaginous >2mm diameter Bronchial glands hypertrophy increased sputum production Airway epithelium metaplasia changes loss of cilia and cilliary dysfunction, increased smooth muscle and connective tissue Inflammatory cells predominate lymphocytes (CD8+), neutrophils, and macrophages 7. Respiratory bronchioles gas exchange starts here 8. Alveoli gas exchange; septa are alveolar walls COPD: Pathology Inflammatory Cells Involved in COPD 10 COPD Compromises Four Compartments of the Lung Epithelial cells Cigarette smoke (and other irritants) Alveolar macrophage 2. Peripheral airways non-cartilaginous < 2mm diameter Bronchiolitis present in early stages of COPD Increased number of goblet cells and epethilial metaplasia Inflammatory cells predominate lymphocytes (CD8+), neutrophils, and macrophages Advanced disease reveals fibrosis and more collagen in walls Fibroblast Fibrosis (Obstructive bronchiolitis) CD8 + lymphocyte PROTEASES Alveolar wall destruction (Emphysema) Chemotactic factors Neutrophil Monocyte Neutrophil elastase Cathepsins MMPs Mucus hypersecretion

4 COPD: Pathology 1 Changes in the Lung Parenchyma in COPD Patients 10 COPD Compromises Four Compartments of the Lung Alveolar wall destruction 3. Lung parenchyma respiratory bronchioles, alveoli, and capillaries Emphysema enlargement of air spaces distal to terminal bronchioles, Two types 1. Centrolobular dilation and destruction of respiratory bronchioles 2. Panlobular destruction of entire acinus, Alpha1-antitrypisin Loss of alveolar attachments airway collapse Inflammation similar to previous Development of bullae Loss of elasticity Destruction of pulmonary capillary bed Inflammatory cells macrophages, CD8 + lymphocytes COPD: Pathology 1 Changes in Pulmonary Arteries in COPD Patients 10 COPD Compromises Four Compartments of the Lung 4. Pulmonary vasculature Begins early in disease Vessel wall thickening and endothelial dysfunction Increased vascular smooth muscle tone Infiltration of vessel wall with CD8+ and T lymphocytes Advanced stages develop collagen deposition and capillary bed destruction leading to pulmonary hypertension and corpulmonale Endothelial dysfunction Intimal hyperplasia Smooth muscle hyperplasia Inflammatory cells (macrophages, CD8 + lymphocytes)

5 COPD: Key Concept Susceptible Smokers & COPD 14 4 Not everyone that smokes gets COPD FEV1 (liters) Disability Death Age (years) Nonsmoker 10-15ml/yr Average smoker 15-25ml/yr Susceptible smoker 40-80ml/yr COPD: Benefits of Smoking Cessation Lung Health Study Susceptible Smokers & COPD FEV1, liters Sustained quitters Continuous smokers Anthonisen et al, AJRCCM, 2002 Years of followup FEV1 (liters) Disability Death Age (years) Nonsmoker Average smoker Susceptible smoker 70 75

6 COPD: Pathogenesis 1 Tobacco smoking is the main risk factor for COPD Some smokers display an exaggerated protected inflammatory response, which causes tissue destruction, impairs defense and repair mechanisms, thus leading to characteristics of COPD COPD: Pathogenesis 1 Three processes important to Pathogenesis 1. Inflammation cascade Differs from bronchial asthma cascade 2. Proteinase and antiprotease imbalance Released by inflammatory cells 3. Oxidative Stress Oxidizing biological molecules leads to cell dysfunction and/or death COPD: Pathogenesis 10 Inflammation in Asthma & COPD 1 Anti-oxidants Oxidative stress Cigarette smoke Biomass particles Particulates LUNG INFLAMMATION COPD PATHOLOGY Host factors Amplifying mechanisms Anti-proteinases Proteinases Repair mechanisms COPD Macrophages PMNs CD8 T cells proteases LTB4 IL-8, TNF- Asthma Eosinophils Mast cells CD4 T cells mediators LTD4 IL-4, IL-5, Il-13

7 COPD: Pathophysiology 1 Changes in Large Airways of COPD Patients 10 Pathogenic mechanisms produce pathological changes, giving rise to four physiological abnormalities in COPD 1. Mucous hypersecretion and ciliary dysfunction First physiologic abnormality developed in COPD Enlarged mucous glands and epithelial cell metaplasia Mucus hypersecretion Goblet cell hyperplasia Mucus gland hyperplasia Neutrophils in sputum Squamous metaplasia of epithelium No basement membrane thickening Macrophages CD8 + lymphocytes Little increase in airway smooth muscle COPD: Pathophysiology 1 COPD: Pathophysiology 1 2. Airflow limitation and hyperinflation Expiratory (largely irreversible) airflow limitation Physiologic hallmark of COPD Major site is smaller conducting airways <2mm Loss of elastic recoil due to alveolar wall destruction Destruction of alveolar attachments Accumulation of inflammatory cells, mucous and plasma exudate in the bronchi Smooth muscle contraction (tense vagal tone) and dynamic hyperinflation during exercise Major factor affecting exercise limitation in patients 3. Gas exchange abnormalities Occurs in advanced COPD characterized by hypoxemia with or without hypercapnia Abnormal gas exchange as a result of anatomical alterations as described previously 4. Pulmonary hypertension Occurs after severe gas exchange abnormalities Results from hypoxic vasoconstriction, endothelial dysfunction, remodeling of pulmonary arteries and destruction of capillary bed Leads to right sided heart failure cor pulmonale

8 Pulmonary Hypertension in COPD 10 Chronic hypoxia Only Two Things Clinically Proven to Prolong Life for COPD Patients Pulmonary vasoconstriction Pulmonary hypertension Cor pulmonale Muscularization Intimal hyperplasia Fibrosis Obliteration 1. Quitting Tobacco 2. LTOT only for those who qualify Death Edema Pro-Active vs. Passive Referral Pro-Active vs. Passive Referral Fax Referral System 50% enrollment rate 35-45% abstinence at 6mos 25-35% abstinence at 1 year Results = 6mos / 15@yr Leaving it up to the individual to call when ready According to research conducted at San Diego State University only 3% of clients receiving literature containing quit line information made a call to the quit line Results = 6mos / 1@yr

9 QuitFax Referral Form Quick and Easy! COPD: Treatment & Management 10 ASHLine National Quit Line Quit Now Four Components of Care 1. Assess and monitor disease Spirometry is the tool 2. Reduce risk factors 3. Manage stable COPD Pharmacologic and non-pharmacologic 4. Manage acute exacerbations Steroids, antibiotics, ventilation support GOLD Standards COPD Pharmacotherapy 9 Manage Exacerbations: Introduction 1 I: Mild FEV 1 >80% pred II:Moderate FEV % pred FEV 1 / FVC < 70% III: Severe FEV % pred IV: Very Severe FEV 1 < 30% pred Avoidance of risk factor(s); influenza vaccination Add short-acting bronchodilator when needed: ß 2 agonists Add regular treatment with one or more long-acting bronchodilators: ß 2 agonists and anticholinergics Add rehabilitation Add ICS for repeated exacerbations Add LTOT Surgical interventions An exacerbation of COPD is an event in the natural course of the disease characterized by a sudden change in the patients baseline symptoms: dyspnea, cough, and/or sputum that is beyond normal day-to-day variations May warrant a change in regular medication usage

10 COPD Exacerbations: Epidemiology COPD Exacerbations: Epidemiology 1 Exacerbations play a role in decline of FEV 1 Decline in FEV 1 of 46.1 ml/yr with frequent (>1.5) exacerbations per year Decline in FEV 1 of 25.3 ml/yr with infrequent (<1.5) exacerbations per year Greater lung function decline value observed in COPD exacerbations amongst current smokers Seasonality 50% more likely in the winter Recurrent Exacerbations 30% of those hospitalized have another exacerbation within 8 weeks Donaldson et al, Thorax 2002;57;847-52) COPD Exacerbations: Epidemiology 8 The most common causes are: Infection of the tracheobronchial tree Air pollution WORLD COPD DAY November 16, 2011 Cause of 1/3 of severe exacerbations unknown Conditions that mimic exacerbations: pneumonia, CHF, PE, pneumothorax, pleural effusions, arrhythmia Important to Differential Diagnosis Raising COPD Awareness Worldwide

11 Interactive COPD Education System References Click to Launch the COPD Active Learning Module This interactive module is provided by Syandus, Inc. 1. American Thoracic Society European Respiratory Society: Standards for the Diagnosis and Management of Patients with COPD, download manual: 2. Arizona Department of Health Services: Arizona Comprehensive Lung Disease Control Plan, download manual: 3. National Heart Lung and Blood Institute, COPD Learn More Breathe Better: COPD: It has a Name, download provider edition: 4. National Heart Lung and Blood Institute, COPD Learn More Breathe Better: COPD: It has a Name, download consumer edition: 5. National Heart Lung and Blood Institute, COPD Learn More Breathe Better: COPD: Are You at Risk, download handout: 6. National Heart Lung and Blood Institute, COPD Learn More Breathe Better: Breathing Better with a COPD Diagnosis, download handout: References References 7. National Lung Health Education Program: Prevent COPD Now! Information for Patients Who May Be Developing COPD, download Save Your Breath, America!: 8. Global Initiative for Chronic Lung Disease, Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: Executive Summary, download manual: 9. Global Initiative for Chronic Lung Disease, Pocket Guide to COPD Diagnosis, Management, and Prevention: A Guide for Health Care Professionals, download manual: Global Initiative for Chronic Lung Disease, Power Point Presentation with NHLBI diagrams by: Peter J. Barnes, M.D., download manual: National Lung Health Education Program and AlphaMedia, Inc., Simple Office Spirometry, Thomas L. Petty, M.D., and Paul L. Enright, M.D., download manual: SimpleOfficeSpirometryForPrimaryCarePractitioners.pdf 12. American Thoracic Society European Respiratory Society: Standards for the Diagnosis and Management of Individuals with Alpha-1 Antitrypsin Deficiency, download manual: Rau JL: Respiratory Care Pharmacology, Mosby, American Lung Association of Minnesota, COPD Educator Course, Cheryl Sasse; Jeff Rubins, MD; Kathy Schultz, RRT; Charles McArthur, RRT, RPFT; Janet Malkiewicz, RN, PHN; Lynn Sieben, RRT; Dick Stenholz LSW; Bob McVoy, RRT, FAARC; Charlene McEvoy, MD 15. Arizona Department of Health Services, Tobacco Education & Prevention Program, University of Arizona HealthCare Partnership, Basic Tobacco Intervention Skills Certification Guidebook, Medical Reviewer: Dr. David R. Sanderson, M.D., Professor of Medicine: Emeritus Mayo Clinic College of Medicine