G O L D lobal Initiative for Chronic bstructive ung isease.

G O L D lobal Initiative for Chronic bstructive ung isease

GOLD Executive Committee
GOLD Structure GOLD Executive Committee Sonia Buist, MD – Chair Roberto Rodriguez-Roisin, MD – Co-Chair Science Committee Klaus Rabe, MD, PhD - Chair Dissemination/Implementation Task Group Christine Jenkins, MD - Chair

N. Khaltaev, Switzerland WHO M. Lopez, Uruguay ALAT E. Nizankowska, Poland K. Rabe, Netherlands R. Rodriguez-Roisin, Spain T. van der Molen, Netherlands C. Van Weel, Netherlands WONCA S. Buist, Chair, US A. Anzueto, US ATS P. Calverley, UK T. DeGuia, Philippines Y. Fukuchi, Japan APSR C. Jenkins, Australia J. Kiley, US NHLBI A. Kocabas, Turkey

GOLD Science Committee
K. Rabe, Chair A. Agusti, A. Anzueto P. Barnes S. Buist P. Calverley M. Decramer Y. Fukuchi P. Jones R. Rodriguez-Roisin J. Vestbo J. Zielinski

Description of Levels of Evidence
Evidence Category Sources of Evidence A Randomized controlled trials (RCTs). Rich body of data B Randomized controlled trials (RCTs). Limited body of data C Nonrandomized trials Observational studies. D Panel consensus judgment

GOLD Structure GOLD Executive Committee Sonia Buist, MD – Chair Roberto Rodriguez-Roisin, MD – Co-Chair Science Committee Klaus Rabe, MD, PhD - Chair Dissemination/Implementation Task Group Christine Jenkins, MD - Chair GOLD National Leaders - GNL

GOLD National Leaders Israel Slovenia Germany Ireland Australia
Bangladesh Saudi Arabia Slovenia Germany Ireland Australia Yugoslavia Croatia Canada Philippines Brazil Austria Taiwan ROC United States Portugal Thailand Norway Malta Greece Moldova China Syria South Africa United Kingdom Hong Kong ROC Italy New Zealand Nepal Chile Israel Argentina Mexico Pakistan Russia United Arab Emirates Japan Peru GOLD National Leaders Poland Korea Netherlands Egypt Switzerland India Venezuela Georgia France Macedonia Iceland Czech Republic Denmark Turkey Slovakia Belgium Singapore Spain Romania Columbia Ukraine Uruguay Sweden Albania Kyrgyzstan Vietnam

GOLD Website Address

G O L D lobal Initiative for Chronic bstructive ung isease

GOLD Objectives Increase awareness of COPD among health professionals, health authorities, and the general public. Improve diagnosis, management and prevention of COPD. Stimulate research in COPD.

Global Strategy for Diagnosis, Management and Prevention of COPD
Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Practical Considerations

Definition of COPD COPD is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.

Classification of COPD Severity
by Spirometry Stage I: Mild FEV1/FVC < 0.70 FEV1 > 80% predicted Stage II: Moderate FEV1/FVC < 0.70 50% < FEV1 < 80% predicted Stage III: Severe FEV1/FVC < 0.70 30% < FEV1 < 50% predicted Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure

“At Risk” for COPD COPD includes four stages of severity classified by spirometry. A fifth category--Stage 0: At Risk--that appeared in the 2001 report is no longer included as a stage of COPD, as there is incomplete evidence that the individuals who meet the definition of “At Risk” (chronic cough and sputum production, normal spirometry) necessarily progress on to Stage I: Mild COPD. The public health message is that chronic cough and sputum are not normal remains important - their presence should trigger a search for underlying cause(s).

Burden of COPD: Key Points
COPD is a leading cause of morbidity and mortality worldwide and results in an economic and social burden that is both substantial and increasing. COPD prevalence, morbidity, and mortality vary across countries and across different groups within countries. The burden of COPD is projected to increase in the coming decades due to continued exposure to COPD risk factors and the changing age structure of the world’s population.

Burden of COPD: Prevalence
Many sources of variation can affect estimates of COPD prevalence, including e.g., sampling methods, response rates and quality of spirometry. Data are emerging to provide evidence that prevalence of Stage I: Mild COPD and higher is appreciably higher in: - smokers and ex-smokers - people over 40 years of age - males

COPD Prevalence Study in Latin America
The prevalence of post-bronchodilator FEV1/FVC < 0.70 increases steeply with age in 5 Latin American Cities Source: Menezes AM et al. Lancet 2005

Burden of COPD: Mortality
COPD is a leading cause of mortality worldwide and projected to increase in the next several decades. COPD mortality trends generally track several decades behind smoking trends. In the US and Canada, COPD mortality for both men and women have been increasing. In the US in 2000, the number of COPD deaths was greater among women than men.

Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998
Proportion of 1965 Rate 3.0 Coronary Heart Disease Stroke Other CVD COPD All Other Causes 2.5 2.0 1.5 1.0 0.5 –59% –64% –35% +163% –7% Source: NHLBI/NIH/DHHS

Of the six leading causes of death in the United States, only COPD has been increasing steadily since 1970 Source: Jemal A. et al. JAMA 2005

COPD Mortality by Gender, U.S., 1980-2000
Number Deaths x 1000 Source: US Centers for Disease Control and Prevention, 2002

Risk Factors for COPD Genes Lung growth and development
Exposure to particles Tobacco smoke Occupational dusts, organic and inorganic Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings Outdoor air pollution Lung growth and development Oxidative stress Gender Age Respiratory infections Socioeconomic status Nutrition Comorbidities

Risk Factors for COPD Aging Populations Nutrition Infections
Socio-economic status Aging Populations

Amplifying mechanisms
Pathogenesis of COPD Cigarette smoke Biomass particles Particulates Host factors Amplifying mechanisms LUNG INFLAMMATION Anti-oxidants Anti-proteinases Oxidative stress Proteinases Repair mechanisms COPD PATHOLOGY Source: Peter J. Barnes, MD

Alveolar wall destruction
Changes in Lung Parenchyma in COPD Alveolar wall destruction Loss of elasticity Destruction of pulmonary capillary bed ↑ Inflammatory cells macrophages, CD8+ lymphocytes Source: Peter J. Barnes, MD

Pulmonary Hypertension in COPD
Chronic hypoxia Pulmonary vasoconstriction Muscularization Intimal hyperplasia Fibrosis Obliteration Pulmonary hypertension New Cor pulmonale Edema Death Source: Peter J. Barnes, MD

COPD ASTHMA Airflow Limitation Small airway narrowing
Alv macrophage Ep cells CD8+ cell (Tc1) Neutrophil Cigarette smoke Small airway narrowing Alveolar destruction COPD ASTHMA Allergens Y Ep cells Mast cell CD4+ cell (Th2) Eosinophil Bronchoconstriction AHR Airflow Limitation Reversible Irreversible Source: Peter J. Barnes, MD

Four Components of COPD Management
Assess and monitor disease Reduce risk factors Manage stable COPD Education Pharmacologic Non-pharmacologic Manage exacerbations

GOALS of COPD MANAGEMENT
VARYING EMPHASIS WITH DIFFERING SEVERITY Relieve symptoms Prevent disease progression • Improve exercise tolerance • Improve health status • Prevent and treat complications • Prevent and treat exacerbations • Reduce mortality

Assess and Monitor COPD: Key Points
Management of Stable COPD Assess and Monitor COPD: Key Points A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. The diagnosis should be confirmed by spirometry. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. Comorbidities are common in COPD and should be actively identified.

indoor/outdoor pollution
Diagnosis of COPD EXPOSURE TO RISK FACTORS SYMPTOMS cough tobacco sputum occupation shortness of breath indoor/outdoor pollution A diagnosis of COPD should be considered in any patient who has cough, sputum production, or dyspnea and/or a history of exposure to risk factors. The diagnosis is confirmed by spirometry. To help identify individuals earlier in the course of disease, spirometry should be performed for patients who have chronic cough and sputum production even if they do not have dyspnea. Spirometry is the best way to diagnose COPD and to monitor its progression and health care workers to care for COPD patients should have assess to spirometry. è è è SPIROMETRY

Assess and Monitor COPD: Spirometry
Management of Stable COPD Assess and Monitor COPD: Spirometry Spirometry should be performed after the administration of an adequate dose of a short- acting inhaled bronchodilator to minimize variability. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. Where possible, values should be compared to age-related normal values to avoid overdiagnosis of COPD in the elderly.

Spirometry: Normal and Patients with COPD

Differential Diagnosis: COPD and Asthma
Onset in mid-life Symptoms slowly progressive Long smoking history Dyspnea during exercise Largely irreversible airflow limitation Onset early in life (often childhood) Symptoms vary from day to day Symptoms at night/early morning Allergy, rhinitis, and/or eczema also present Family history of asthma Largely reversible airflow limitation

COPD and Co-Morbidities
COPD patients are at increased risk for: Myocardial infarction, angina Osteoporosis Respiratory infection Depression Diabetes Lung cancer

COPD and Co-Morbidities
COPD has significant extrapulmonary (systemic) effects including: Weight loss Nutritional abnormalities Skeletal muscle dysfunction

Reduce Risk Factors: Key Points
Management of Stable COPD Reduce Risk Factors: 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 in most people to reduce the risk of developing COPD and stop its progression (Evidence A).

Brief Strategies to Help the Patient Willing to Quit Smoking
ASK Systematically identify all tobacco users at every visit. ADVISE Strongly urge all tobacco users to quit. ASSESS Determine willingness to make a quit attempt. ASSIST Aid the patient in quitting. ARRANGE Schedule follow-up contact. 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. Brief tobacco dependence treatment is effective, and every tobacco user should be offered at least this treatment at every visit to a health care provider. Three types of counseling are especially effective: practical counseling, social support as part of treatment, and social support arranged outside of treatment.

Reduce Risk Factors: Smoking Cessation
Management of Stable COPD Reduce Risk Factors: Smoking Cessation Counseling delivered by physicians and other health professionals significantly increases quit rates over self-initiated strategies. Even a brief (3-minute) period of counseling to urge a smoker to quit results in smoking cessation rates of 5-10%. Numerous effective pharmacotherapies for smoking cessation are available and pharmacotherapy is recommended when counseling is not sufficient to help patients quit smoking.

Reduce Risk Factors: Indoor/Outdoor Air Pollution
Management of Stable COPD Reduce Risk Factors: Indoor/Outdoor Air Pollution Reducing the risk from indoor and outdoor air pollution is feasible and requires a combination of public policy and protective steps taken by individual patients. Reduction of exposure to smoke from biomass fuel, particularly among women and children, is a crucial goal to reduce the prevalence of COPD worldwide.

Manage Stable COPD: Key Points
Management of Stable COPD Manage Stable COPD: Key Points The overall approach to managing stable COPD should be individualized to address symptoms and improve quality of life. For patients with COPD, health education plays an important role in smoking cessation (Evidence A) and can also play a role in improving skills, ability to cope with illness and health status. None of the existing medications for COPD have been shown to modify the long-term decline in lung function that is the hallmark of this disease (Evidence A). Therefore, pharmacotherapy for COPD is used to decrease symptoms and/or complications.

Pharmacotherapy: Bronchodilators
Management of Stable COPD Pharmacotherapy: Bronchodilators Bronchodilator medications are central to the symptomatic management of COPD (Evidence A). They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms and exacerbations. The principal bronchodilator treatments are ß2- agonists, anticholinergics, and methylxanthines used singly or in combination (Evidence A). Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators (Evidence A).

Pharmacotherapy: Glucocorticosteroids
Management of Stable COPD Pharmacotherapy: Glucocorticosteroids The addition of regular treatment with inhaled glucocorticosteroids to bronchodilator treatment is appropriate for symptomatic COPD patients with an FEV1 < 50% predicted (Stage III: Severe COPD and Stage IV: Very Severe COPD) and repeated exacerbations (Evidence A). An inhaled glucocorticosteroid combined with a long-acting ß2-agonist is more effective than the individual components (Evidence A).

Pharmacotherapy: Glucocorticosteroids
Management of Stable COPD Pharmacotherapy: Glucocorticosteroids The dose-response relationships and long-term safety of inhaled glucocorticosteroids in COPD are not known. Chronic treatment with systemic glucocorticosteroids should be avoided because of an unfavorable benefit-to-risk ratio (Evidence A).

Pharmacotherapy: Vaccines
Management of Stable COPD Pharmacotherapy: Vaccines In COPD patients influenza vaccines can reduce serious illness (Evidence A). Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years and older and for COPD patients younger than age 65 with an FEV1 < 40% predicted (Evidence B).

Management of Stable COPD All Stages of Disease Severity
Avoidance of risk factors - smoking cessation - reduction of indoor pollution - reduction of occupational exposure Influenza vaccination

Therapy at Each Stage of COPD
I: Mild II: Moderate III: Severe IV: Very Severe FEV1/FVC < 70% FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure FEV1/FVC < 70% 30% < FEV1 < 50% predicted FEV1/FVC < 70% 50% < FEV1 < 80% predicted FEV1/FVC < 70% FEV1 > 80% predicted Active reduction of risk factor(s); influenza vaccination Add short-acting bronchodilator (when needed) This provides a summary of the recommended treatment at each stage of COPD. Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation Add inhaled glucocorticosteroids if repeated exacerbations Add long term oxygen if chronic respiratory failure. Consider surgical treatments

Other Pharmacologic Treatments
Management of Stable COPD Other Pharmacologic Treatments Antibiotics: Only used to treat infectious exacerbations of COPD Antioxidant agents: No effect of n-acetylcysteine on frequency of exacerbations, except in patients not treated with inhaled glucocorticosteroids Mucolytic agents, Antitussives, Vasodilators: Not recommended in stable COPD

Non-Pharmacologic Treatments
Management of Stable COPD Non-Pharmacologic Treatments Rehabilitation: All COPD patients benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue (Evidence A). Oxygen Therapy: The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival (Evidence A).

Revised 2006 Assess and monitor disease Reduce risk factors Manage stable COPD Education Pharmacologic Non-pharmacologic Manage exacerbations

Key Points An exacerbation of COPD is defined as:
Management COPD Exacerbations Key Points An exacerbation of COPD is defined as: “An event in the natural course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.”

Key Points Management COPD Exacerbations
The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified (Evidence B). Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased sputum purulence) may benefit from antibiotic treatment (Evidence B).

Key Points Manage COPD Exacerbations
Inhaled bronchodilators (particularly inhaled ß2-agonists with or without anticholinergics) and oral glucocorticosteroids are effective treatments for exacerbations of COPD (Evidence A).

Key Points Management COPD Exacerbations
Noninvasive mechanical ventilation in exacerbations improves respiratory acidosis, increases pH, decreases the need for endotracheal intubation, and reduces PaCO2, respiratory rate, severity of breathlessness, the length of hospital stay, and mortality (Evidence A). Medications and education to help prevent future exacerbations should be considered as part of follow-up, as exacerbations affect the quality of life and prognosis of patients with COPD.

Translating COPD Guidelines into Primary Care KEY POINTS
Better dissemination of COPD guidelines and their effective implementation in a variety of health care settings is urgently required. In many countries, primary care practitioners treat the vast majority of patients with COPD and may be actively involved in public health campaigns and in bringing messages about reducing exposure to risk factors to both patients and the public.

Translating COPD Guidelines into Primary Care KEY POINTS
Spirometric confirmation is a key component of the diagnosis of COPD and primary care practitioners should have access to high quality spirometry. Older patients frequently have multiple chronic health conditions. Comorbidities can magnify the impact of COPD on a patient’s health status, and can complicate the management of COPD.

Global Strategy for Diagnosis, Management and Prevention of COPD SUMMARY

COPD is increasing in prevalence in many countries of the world.
Global Strategy for Diagnosis, Management and Prevention of COPD: Summary COPD is increasing in prevalence in many countries of the world. COPD is treatable and preventable. The GOLD program offers a strategy to identify patients and to treat them according to the best medications available.

Global Strategy for Diagnosis, Management and Prevention of COPD: Summary
COPD can be prevented by avoidance of risk factors, the most notable being tobacco smoke. Patients with COPD have multiple other conditions (comorbidities) that must be taken into consideration. GOLD has developed a global network to raise awareness of COPD and disseminate information on diagnosis and treatment.

GOLD National Leaders Israel Slovenia Germany Ireland Australia
Bangladesh Saudi Arabia Slovenia Germany Ireland Australia Yugoslavia Croatia Canada Philippines Brazil Austria Taiwan ROC United States Portugal Thailand Norway Malta Greece Moldova China Syria South Africa United Kingdom Hong Kong ROC Italy New Zealand Nepal Chile Israel Argentina Mexico Pakistan Russia United Arab Emirates Japan Peru GOLD National Leaders Poland Korea Netherlands Egypt Switzerland India Venezuela Georgia France Macedonia Iceland Czech Republic Denmark Turkey Slovakia Belgium Singapore Spain Romania Columbia Ukraine Uruguay Sweden Albania Kyrgyzstan Vietnam

WORLD COPD DAY November 14, 2007 Raising COPD Awareness Worldwide

GOLD Website Address

ADDITIONAL SLIDES WITH NOTES PREPARED BY:
PROFESSOR PETER J. BARNES, MD NATIONAL HEART AND LUNG INSTITUTE LONDON, ENGLAND

Squamous metaplasia of epithelium No basement membrane thickening
Changes in Large Airways of COPD Patients Mucus hypersecretion Neutrophils in sputum Squamous metaplasia of epithelium No basement membrane thickening Goblet cell hyperplasia ↑ Macrophages ↑ CD8+ lymphocytes Changes in large airways of COPD patients. The epithelium often shows squamous metaplasia and there is goblet cell and submucosal gland hyperplasia, resulting in mucus hypersecretion. The airway wall is infiltrated with macrophages and CD8+ lymphocytes, whereas neutrophils predominate in the airway lumen and around submucosal glands. Airway smooth muscle and basement membrane are minimally increased compared to the findings in asthma. Mucus gland hyperplasia Little increase in airway smooth muscle Source: Peter J. Barnes, MD

Changes in Small Airways in COPD Patients
Inflammatory exudate in lumen Disrupted alveolar attachments Changes in small airways in COPD patients. The airway wall is thickened and infiltrated with inflammatory cells, predominately macrophages and CD8+ lymphocytes, with increased numbers of fibroblasts. In severe COPD there are also lymphoid follicles. The lumen is often filled with an inflammatory exudate and mucus. There is peribronchial fibrosis and airway smooth muscle may be increased, resulting in narrowing of the airway. Thickened wall with inflammatory cells - macrophages, CD8+ cells, fibroblasts Peribronchial fibrosis Lymphoid follicle Source: Peter J. Barnes, MD

Alveolar wall destruction
Changes in the Lung Parenchyma in COPD Patients Alveolar wall destruction Loss of elasticity Changes in the lung parenchyma in COPD patients. There is loss of elasticity and alveolar wall destruction, and accumulation of inflammatory cells, predominantly macrophages and CD8+ lymphocytes. The destructive changes reduce the pulmonary capillary bed. The left panel shows a scanning electron micrograph of a patient with emphysema demonstrating the enlargement of alveoli and destruction of the alveolar walls. Destruction of pulmonary capillary bed ↑ Inflammatory cells macrophages, CD8+ lymphocytes Source: Peter J. Barnes, MD

Endothelial dysfunction Smooth muscle hyperplasia
Changes in Pulmonary Arteries in COPD Patients Endothelial dysfunction Intimal hyperplasia Smooth muscle hyperplasia Changes in pulmonary arteries in COPD patients. There is dysfunction of endothelial cells (reduced vasodilator release), intimal thickening, hyperplasia of smooth muscle and infiltration with inflammatory cells, predominantly macrophages and CD8+ lymphocytes. ↑ Inflammatory cells (macrophages, CD8+ lymphocytes) Source: Peter J. Barnes, MD

Amplifying mechanisms
Pathogenesis of COPD Cigarette smoke Biomass particles Particulates Host factors Amplifying mechanisms LUNG INFLAMMATION Anti-oxidants Anti-proteinases Oxidative stress Pathogenesis of COPD, illustrating the central role of inflammation Proteinases Repair mechanisms COPD PATHOLOGY Source: Peter J. Barnes, MD

PROTEASES Fibrosis Inflammatory Cells Involved in COPD CD8+ Neutrophil
Cigarette smoke (and other irritants) Epithelial cells Alveolar macrophage Chemotactic factors CD8+ lymphocyte Fibroblast Neutrophil Monocyte Inflammatory cells involved in COPD. Cigarette smoke activates macrophages and epithelial cells to release chemotactic factors that recruit neutrophils, monocytes and CD8+ T-lymphocytes from the circulation. They also release factors that activate fibroblasts leading to small airway obstruction (obstructive bronchiolitis). Proteases released from neutrophils and macrophages may cause mucus hypersecretion and emphysema. Neutrophil elastase Cathepsins MMPs PROTEASES Fibrosis (Obstructive bronchiolitis) Alveolar wall destruction Mucus hypersecretion (Emphysema) Source: Peter J. Barnes, MD

↓ HDAC2 ↑Inflammation Steroid resistance
Oxidative Stress in COPD Macrophage Neutrophil Anti-proteases SLPI 1-AT NF-B Proteolysis IL-8 TNF- ↓ HDAC2 ↑Inflammation Steroid resistance O2-, H202 OH., ONOO- Neutrophil recruitment Oxidative stress in COPD has several detrimental consequences, including activation of the transcription factor nuclear factor-κB (NF-κB), reduction in antiproteases, plasma leakage and mucus hypersecretion. In addition it reduces histone deacetylase-2, resulting in amplified inflammation and reduced anti-inflammatory response to corticosteroids. Isoprostanes Bronchoconstriction Plasma leak  Mucus secretion Source: Peter J. Barnes, MD

COPD ASTHMA Airflow Limitation
Differences in Inflammation and its Consequences: Asthma and COPD Alv macrophage Ep cells CD8+ cell (Tc1) Neutrophil Cigarette smoke Small airway narrowing Alveolar destruction COPD ASTHMA Allergens Y Ep cells Mast cell CD4+ cell (Th2) Eosinophil Bronchoconstriction AHR Airflow Limitation Irreversible Reversible Source: Peter J. Barnes, MD

Air Trapping in COPD Mild/moderate COPD Normal Severe COPD ↓ Health
Inspiration small airway alveolar attachments loss of elasticity loss of alveolar attachments Expiration closure Air trapping in COPD. During expiration small airways narrow but closure is prevented by the elasticity of alveolar attachments. In COPD patients there is a loss of elasticity with greater narrowing in small airways, which may close completely when there is loss of alveolar attachments as a result of emphysema. This results in air trapping and hyperinflation, leading to dyspnea and reduced exercise capacity. ↓ Health status Dyspnea ↓ Exercise capacity Air trapping Hyperinflation Source: Peter J. Barnes, MD

Pulmonary Hypertension in COPD
Chronic hypoxia Pulmonary vasoconstriction Muscularization Intimal hyperplasia Fibrosis Obliteration Pulmonary hypertension Cor pulmonale Edema Death Source: Peter J. Barnes, MD

Inflammation in COPD Exacerbations
Bacteria Viruses Non-infective Pollutants Macrophages Epithelial cells TNF- IL-8 IL-6 Inflammation in COPD exacerbations induced by several causal mechanisms. Increased numbers of inflammatory cells, particularly neutrophils, are seen with increased concentrations of inflammatory mediators and oxidative stress. Neutrophils Oxidative stress Source: Peter J. Barnes, MD

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