cigar, and environmental tobacco smoke), occupational dusts and chemicals (vapors, irritants, and fumes), indoor air pollution from biomass fuel used for cooking and heating (in poorly vented dwellings), outdoor air pollution, and any factor that affects lung growth during gestation and childhood (low birth weight, respiratory tract infections). 80 Genetic susceptibilities have been identified, including polymorphisms of genes that code for tumor necrosis factor, surfactant, proteases, antiproteases, and risks for lung cancer. The clinical phenotypes of COPD are chronic bronchitis and emphysema. 82 An inherited mutation in theα1 -antitrypsin gene results in the development of COPD (emphysema) at an early age, even in nonsmokers. 83,84 The pathologic changes of COPD occur in large central airways, small peripheral airways, and the lung parenchyma, the dominant features of chronic bronchitis and emphysema. Chronic irritant exposure recruits macrophages, neutrophils, and lymphocytes to the lung, resulting in progressive damage from oxidative stress, inflammation, extracellular matrix proteolysis, and apoptotic and autophagic cell death. 85,86 Systemic abnormalities, such as renal and hormonal abnormalities, malnutrition, muscle wasting, osteoporosis, and anemia, are associated with COPD. 87 Chronic Bronchitis. Chronic bronchitis is defined as hypersecretion of mucus and chronic productive cough that continues for at least 3 months of the year (usually the winter months) for at least 2 consecutive years. Initially chronic bronchitis affects only the larger bronchi, but eventually all airways are involved. The thick mucus and bronchial smooth muscle narrow the airways and lead to obstruction, particularly during expiration when the airways are constricted. Obstruction eventually leads to ventilation-perfusion mismatch with hypoxemia. The airways collapse early in expiration, trapping gas in the distal portions of the lung (Figure 35-15).Air trapping expands the thorax, putting the respiratory muscles at a mechanical disadvantage. This leads to decreased tidal volume, hypoventilation, and hypercapnia. CLINICAL MANIFESTATIONS. The common symptoms of chronic bronchitis include decreased exercise tolerance, wheezing, and shortness of breath. Individuals usually have a productive cough (“smoker’s cough”), and evidence of airway obstruction (decreased FEV1 ) is shown by spirometry. Hypoxemia may occur with exercise. As the disease progresses, copious amounts of sputum are produced, accompanied by frequent pulmonary infections. 90 FVC and FEV1 values become markedly reduced, and FRC and residual volume (RV) measurements are increased as airway obstruction and air trapping become more pronounced.
Airway obstruction results in decreased alveolar ventilation and increased Paco2 . Marked hypoxemia leads to polycythemia (overproduction of erythrocytes) and cyanosis. If not reversed, hypoxemia leads to pulmonary hypertension and eventually results in cor pulmonale (see p. 1278) and can lead to severe disability or death. (Table 35-3 lists the common clinical manifestations of chronic bronchitis.)
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