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INTRODUCTION

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  • Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation that is not fully reversible. Two principal conditions (referred to as phenotypes) include:

    • Chronic bronchitis: chronic or recurrent excess mucus secretion with cough that occurs on most days for at least 3 months of the year for at least 2 consecutive years.

    • Emphysema: abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls, without fibrosis.

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PATHOPHYSIOLOGY

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  • Chronic inflammatory changes lead to destructive changes and chronic airflow limitation. The most common cause is exposure to tobacco smoke.

  • Inhalation of noxious particles and gases activates neutrophils, macrophages, and CD8+ lymphocytes, which release chemical mediators, including tumor necrosis factor-α, interleukin-8, and leukotriene B4. Inflammatory cells and mediators lead to widespread destructive changes in airways, pulmonary vasculature, and lung parenchyma.

  • Oxidative stress and imbalance between aggressive and protective defense systems in the lungs (proteases and antiproteases) may also occur. Oxidants generated by cigarette smoke react with and damage proteins and lipids, contributing to tissue damage. Oxidants also promote inflammation and exacerbate protease–antiprotease imbalance by inhibiting antiprotease activity.

  • The protective antiprotease α1-antitrypsin (AAT) inhibits protease enzymes, including neutrophil elastase. In presence of unopposed AAT activity, elastase attacks elastin, a major component of alveolar walls. Hereditary AAT deficiency increases risk for premature emphysema. In emphysema from cigarette smoking, imbalance is associated with increased protease activity or reduced antiprotease activity.

  • Inflammatory exudate in airways leads to increased number and size of goblet cells and mucus glands. Mucus secretion increases and ciliary motility is impaired. There is thickening of the smooth muscle and connective tissue in airways. Chronic inflammation leads to scarring and fibrosis. Diffuse airway narrowing occurs and is more prominent in small peripheral airways.

  • Smoking-related COPD usually results in centrilobular emphysema that primarily affects respiratory bronchioles. Panlobular emphysema is seen in AAT deficiency and extends to the alveolar ducts and sacs.

  • Vascular changes include thickening of pulmonary vessels that may lead to endothelial dysfunction of pulmonary arteries. Later, structural changes increase pulmonary pressures, especially during exercise. In severe COPD, secondary pulmonary hypertension leads to right-sided heart failure (cor pulmonale).

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CLINICAL PRESENTATION

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  • Initial symptoms include chronic cough and sputum production; patients may experience cough for several years before dyspnea develops.

  • Physical examination is normal in most patients in milder stages. When airflow limitation becomes severe, patients may have cyanosis of mucosal membranes, development of a “barrel chest” due to hyperinflation of the lungs, increased resting respiratory rate, shallow breathing, pursing of lips during expiration, and use of accessory respiratory muscles.

  • Patients experiencing COPD exacerbation may have worsening dyspnea, increased sputum volume, or increased sputum purulence. Other features of exacerbation include chest tightness, increased need for bronchodilators, malaise, fatigue, and decreased exercise tolerance.

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DIAGNOSIS

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  • Diagnosis is based in part on patient symptoms ...

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