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| Centriacinar Emphysema |
| Etiology • Cigarette smoking responsible for vast majority of centriacinar emphysema |
| Pathogenesis • At terminal bronchiole level air flow suddenly diminishes dropping particulates into adjacent alveoli • Neutrophil and macrophage elastases turned on by particulates or other components of smoke • Septal destruction secondary to excess elastase and protease activity, |
| Epidemiology • Men>women; heavy smokers • Develops over many years becoming clinically significant in later life |
| General Gross Description • Centrilobular or smoker's emphysema shows air space enlargement mixed with normal airspaces • Largest spaces found in upper portions of all lobes • Black discoloration of walls of spaces • Bronchovascular structures stand out from the parenchyma due to loss of parenchymal tissue • Pillowy soft lungs that may cover the heart |
| General Microscopic Description • Enlarged air spaces with broken septae in the central portion of the acinus around the terminal bronchiole • Septal tips have blunt ends • Little fibrosis • Many carbon laden macrophages |
| Clinical Correlation • Patients with pure emphysema develop progressive dyspnea and weight loss due to loss of oxygen delivery to periphery. • "Pink puffer" with slowed forced expirations |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th edition. Philadelphia, W.B. Saunders, 1994, pp. 683-7. |
| Centriacinar Emphysema |
| Synopsis by: Melinda Sanders M.D. (T28000M32800)[118] |
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