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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
EPIDEMIOLOGY AND ETIOLOGY
COPD is a major cause of morbidity and mortality and a significant cause of disability worldwide. In 2013, 15.7 million US adults were estimated to have COPD.2 Chronic lower respiratory diseases are the third leading cause of death in the United States. In 2014, more than 151,000 adults died from COPD.3 Personal health care spending in the United States on COPD was estimated to be $53.8 billion in 2013.4
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. Factors that potentially reduce maximal attained lung function (eg, maternal smoking, preterm birth, early childhood lung infections, air pollution, childhood asthma, and active smoking during adolescence) increase the risk of COPD.1,5 Other COPD risk factors include occupational exposure to dusts and chemicals (vapors, irritants, and fumes), biomass smoke inhalation, asthma, and bronchial hyperresponsiveness. Outdoor air pollution has been implicated as a cause, but its exact role is unclear.
Repeated exposure to noxious particles and ...