Emphysema, defined as an abnormal enlargement of air spaces distal to the terminal bronchioles, occurs in the lung parenchyma in COPD.
As a result of emphysema there is a significant loss of alveolar attachments, which contributes to peripheral airway collapse .
There are two major types of emphysema, according to the distribution within the acinus: 1) centrolobular (which involves dilatation and destruction of the respiratory bronchioles); and 2) panlobular emphysema (which involves destruction of the whole of the acinus). The former is the most common type of emphysema in COPD and is more prominent in the upper zones, while the latter predominates in patients with α1-antitrypsin deficiency and is more prominent in the lower zones.
In the early stages of the disease, these are microscopic lesions. During the course of the disease, they may progress to macroscopic lesions or bullae (defined as an emphysematous space >1 cm in diameter). Bullous disease can also occur in the absence of COPD.
The inflammatory cell profile in the alveolar walls and the airspaces is similar to that described in the airways and persists throughout the course of the disease . There is some evidence suggesting the persistence of inflammation in the proximal and distal airspaces after smoking cessation [14, 15].
Fig. 3. - a) Common airway with alveolar attachments. b) Loss of alveolar walls, enlargement of alveolar spaces and decreased alveolar wall attachment in emphysema. Printed with kind permission from W. MacNee and D. Lamb.
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