Chronic obstructive pulmonary disease (COPD) is a preventable chronic disease of the airways characterized by gradual, progressive loss of lung function. COPD patients have airflow limitation that is not fully reversible. The airflow limitation is associated with an abnormal inflammatory response of the lung to noxious particles or gases. Emphysema and chronic bronchitis are often present in COPD, but patients must also have abnormal spirometry to be formally diagnosed with COPD. Emphysema is an abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without fibrosis. Chronic bronchitis is inflammation of the bronchioles with mucus hypersecretion and chronic productive cough. Because most patients exhibit some features of emphysema and chronic bronchitis, the appropriate emphasis of COPD pathophysiology is on small airway disease and parenchymal damage that contributes to chronic airflow limitation.
The most common risk factor for COPD is cigarette smoking; however, not all smokers develop COPD. Inhalation exposure risk factors include occupational dusts and chemicals (chemical agents and fumes), indoor air pollution (wood, animal dung, crop residues, and coal burned in open fires), and outdoor air pollution. A rare genetic disorder called alpha 1 antitrypsin (AAT) deficiency is also a risk factor for COPD. AAT deficiency causes patients to develop COPD at an early age (20-50 years). Patients presenting with COPD at an early age or a strong family history should be screened for this disorder. Another potential risk factor is impaired lung growth during gestation, birth, and childhood. Oxidative stress, or a depletion of antioxidants in the lungs plays a role in the development of COPD and can initiate lung inflammation and injury. Respiratory infections (viral and bacterial) may contribute to the pathogenesis of COPD and are considered a risk factor.
COPD is caused by amplification of the normal inflammatory response to chronic irritants such as cigarette smoke. Inflammatory mediators increased in COPD patients include neutrophils, macrophages, and lymphocytes. Oxidative stress generated by oxidants released by cigarette smoke and other inhaled substances and a reduction in endogenous antioxidants also contribute to lung inflammation. An imbalance between the proteases that break down connective tissue in the lung and the antiproteases that protect against this is also seen in COPD. These characteristics lead to airflow limitation and air trapping, resulting in hyperinflation of the lungs. This reduces the capacity of the lungs to fill during inspiration, resulting in dyspnea, particularly during exertion. Gas exchange abnormalities also result, with hypoxemia and hypercapnia common in COPD. Finally, mucus hypersecretion and chronic productive cough are often present due to chronic irritation of the airway.
Symptoms characteristic of COPD are dyspnea, chronic cough, and sputum production. Dyspnea is usually present every day, worsened by exertion, and progressively worsens over time. Patients describe an increased effort to breathe or gasping. Patients with symptoms of COPD and exposure to risk factors should be tested with spirometry to confirm a ...