Gross photos of emphysematous lungs as seen on cut surfaces are shown. These overexpanded lungs would take up a lot of space in the thorax. In panacinar emphysema, as shownNoca in both of these photos, the expansion is diffuse throughout each affected acinus, involving respiratory bronchiole, alveolar ducts, and terminal alveoli. In centriacinar (centrilobular) emphysema, the gross changes are less severe; the overexpansion is mostly confined to the respiratory bronchioles in the central portion of the acinus.
Microscopically, one sees greatly enlarged alveoli. For comparison, a few normal-sized alveoli are seen in the upper central portion of the photo. Septa are thin. Because the pores of Kohn are enlarged some septa falsely appear to be unattached to surrounding tissue.
Chronic obstructive lung disease is a large tent which covers emphysema and chronic bronchitis. There is much overlap of these two entities. Only a minority of these patients are nonsmokers. Because of the variable degree of hypoxia and polycythemia, patients with predominant chronic bronchitis are sometimes referred to as “blue bloaters”; patients with predominant emphysema as “pink puffers”.
Theoretically, an imbalance between proteases (mainly elastase) and antiproteases causes alveolar wall destruction. Alpha1-antitrypsin supplies most of the antielastase activity in the lung. Therefore, one cause of emphysema is a1-AT deficiency. Smoking is accompanied by decreased antielastase activity and increased elastase availability, furthering the damage.
From the slide collection of the late Dr. Charles Kuhn