Respiratory System MCAT Practice Question
A 58-year-old man with a 40 pack-year smoking history presents with progressive dyspnea and chronic cough. Pulmonary function tests show FEV1 of 45% predicted with an FEV1/FVC ratio of 0.62 and markedly elevated residual volume. High-resolution CT demonstrates basilar predominant emphysema with loss of normal lung architecture. Laboratory studies reveal normal serum α1-antitrypsin levels and activity. Bronchoscopic biopsy shows extensive elastin fiber fragmentation with increased neutrophil infiltration and elevated neutrophil elastase activity in bronchoalveolar lavage fluid. Which of the following best explains the mechanism of lung destruction in this patient?
Answer choices
- AQuantitative α1-antitrypsin deficiency preventing adequate neutralization of neutrophil elastase
- BReduced synthesis of elastin by lung fibroblasts secondary to smoking-induced oxidative stress
- COverwhelming neutrophil elastase activity that exceeds the functional capacity of normal protease inhibitors to neutralizeCorrect answer
- DLoss of elastin cross-linking due to defective lysyl oxidase activity independent of protease imbalance
- EDirect cigarette smoke-induced toxic injury to elastic fibers with secondary neutrophilic inflammation
- FAlveolar macrophage production of matrix metalloproteinase-9 as the primary mechanism of elastin degradation
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