Alveolar tissue is destroyed in the chronic, progressive condition called emphysema, which results in fewer but larger alveoli (fig. 16.18). This reduces the surface area for gas exchange and decreases the ability of the bronchioles to remain open during expiration. Collapse of the bronchioles as a result of the compression of the lungs during expiration produces air trapping, which further decreases the efficiency of gas exchange in the alveoli.
Among the different types of emphysema, the most common occurs almost exclusively in people who have smoked cigarettes heavily over a period of years. A component of cigarette smoke apparently stimulates the macrophages and leukocytes to secrete proteolytic (protein-digesting) enzymes that destroy lung tissues. A less common type of emphysema results from the genetic inability to produce a plasma protein called aj-antitrypsin. This protein normally inhibits proteolytic enzymes such as trypsin, and thus normally protects the lungs against the effects of enzymes that are released from alveolar macrophages.
Chronic bronchitis, asthma, and emphysema, the most common causes of respiratory failure, are together called chronic obstructive pulmonary disease (COPD). In addition to the more direct obstructive and restrictive aspects of these conditions, other pathological changes may occur. These include edema, inflammation, hyperplasia (an increase in the number of cells), zones of pulmonary fibrosis, pneumonia, pulmonary emboli (traveling blood clots), and heart failure. Patients with severe chronic bronchitis or
■ Figure 16.18 Emphysema destroys lung tissue. These are photomicrographs of tissue (a) from a normal lung and (b) from the lung of a person with emphysema. The destruction of lung tissue in emphysema results in fewer and larger alveoli.
emphysema may develop cor pulmonale—pulmonary hypertension with hypertrophy and the eventual failure of the right ventricle. COPD is the fifth leading cause of death in the United States.
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