2. Classification:
Chronic bronchitis is defined as cough or sputum production for at least three months per year for two or more years. Sputum production, which predominantly reflects inflammation of the medium and large airways, tends to be directly related to the irritating effects of ongoing smoke or dust exposure. Many studies suggest that smokers with chronic bronchitis and normal lung function are more likely to progress to COPD than are those without chronic bronchitis. Smoking cessation may result in resolution of chronic bronchitis and reduction in the risk of progression to COPD. Compared to COPD patients without chronic bronchitis, patients with chronic bronchitis have a greater risk of exacerbations and disease progression and tend to be current smokers.
Emphysema is defined as permanent enlargement of alveolar spaces because of the destruction of alveolar walls. The pathologic changes are irreversible and are due to proteolytic destruction of the matrix framework of the alveoli. The loss of alveoli structure reduces lung elastic recoil, decreases the ability of the lung to tether open the small airways, and obliterates the pulmonary microcirculation involved in gas exchange. Patients with the emphysematous form of COPD generally have more dyspnea and weight loss and a greater risk for development of lung cancer than do COPD patients without emphysema.
Smoking-induced bronchiolitis is defined as inflammation of the small airways associated with smoke exposure. Smoke-induced bronchiolitis spans a spectrum from modest changes in small airway function to respiratory bronchiolitis-interstitial lung disease (RB-ILD). The small airways appear to be the first site of inflammation in young, otherwise healthy smokers; they also appear to be the initial area of airway remodeling in COPD. Functional loss of small airways probably occurs prior to development of emphysema.
Alpha-1 anti-trypsin (A1AT)-deficient emphysema is due to deficiency of the most abundant serum protease inhibitor (A1AT), resulting in significant increased risk for both smoke- and occupation-induced COPD. A1AT deficiency commonly occurs at a younger age (the fourth or fifth decades) than typical COPD and results in a more homogeneous pattern of emphysema. A1AT deficiency may present with symptoms of asthma (in the absence of atopy) or bronchiectasis, even when emphysema is not severe. A1AT deficiency is easily excluded by testing serum A1AT levels.
Although each of these entities may be considered separate and distinct, they usually occur together, with one or more predominating in affected individuals.
Reposted with permission from Decision Support in Medicine, LLC.