Upon completion of the chapter, the reader will be able to:
Describe the pathophysiology of chronic obstructive pulmonary disease (COPD).
Identify signs and symptoms of COPD.
List the treatment goals for a patient with COPD.
Design an appropriate COPD maintenance treatment regimen based on patient-specific data.
Design an appropriate COPD exacerbation treatment regimen based on patient-specific data.
Develop a monitoring plan to assess effectiveness and adverse effects of pharmacotherapy for COPD.
Formulate an appropriate education plan for a patient with COPD.
Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by airflow limitation that is not fully reversible. Previous definitions of COPD included chronic bronchitis and emphysema. Chronic bronchitis is defined clinically as a chronic productive cough for at least 3 months in each of two consecutive years in a patient in whom other causes have been excluded.1 Emphysema is defined pathologically as destruction of alveoli.1 The major risk factor for both conditions is cigarette smoking, and many patients share characteristics of each one. Therefore, current guidelines focus instead on chronic airflow limitation.
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) is an expert panel of health professionals who developed consensus guidelines for the diagnosis and care of patients with COPD that are updated annually.1 Clinical practice guidelines for the diagnosis and management of stable COPD have also been published by several medical organizations.2
EPIDEMIOLOGY AND ETIOLOGY
COPD is a major cause of morbidity and mortality and a significant cause of disability worldwide. In 2011, 12.7 million US adults were estimated to have COPD.3 COPD is the third leading cause of death in the United States; in 2010, 134,676 adults died from the disease. Its estimated cost to the United States in 2010 was $49.9 billion, with direct medical costs accounting for $29.5 billion of the total.3
COPD is caused by repeated inhalation of noxious particles or gases, most commonly cigarette smoke. Marijuana and other forms of tobacco, including secondhand smoke, are also risk factors.1 Not all smokers develop clinically significant COPD, which suggests that genetic susceptibility plays a role. The best documented genetic factor is a rare hereditary deficiency of α1-antitrypsin (AAT). Severe deficiency of this enzyme results in premature and accelerated development of emphysema. Other COPD risk factors include occupational exposure to dusts and chemicals (vapors, irritants, and fumes), biomass smoke inhalation, asthma, bronchial hyperresponsiveness, maternal smoking, childhood asthma, and severe childhood respiratory infections.4 Environmental air pollution has been implicated as a cause, but its exact role is unclear.
Repeated exposure to noxious particles and gases causes chronic inflammation, resulting in pathologic changes in the central and peripheral airways, lung parenchyma, and pulmonary vasculature that lead to obstruction.1,5,6 An imbalance ...