This is a real-world medical entrance exam question, please give the true answer based on the question and selection. Topic name: None, Subject name: Pathology
[{'content': 'Antitrypsin deficiency is associated with- (a) (b) \nSelect and explain. \nA. Restrictive lung pathology, B. Cystric fibrosis, C. Emphysema, D. Carcinoma', 'role': 'user'}, {'content': 'Answer: C \nExplanation: Pathogenesis of Emphysema\n\nThe most accepted theory in the pathogenesis of emphysema is protease - antiprotease mechanism which is responsible in the pathogenesis of two common forms of emphysema, i.e. centriacinar and panacinar.\nThe alveolar wall destruction results from an imbalance between proteases (mainly elastase) and antiproteases in the lung.\nProteases (elastase) cause the destruction of alveolar wall, while antiproteases prevent this damage.\nα1\xa0- antitrypsin is the major antiprotease (anti elastase) secreted by neutrophils during inflammation\n\nA. Pathogenesis of panacinar emphysema\n\nPanacinar emphysema is associated with congenital deficiency of α1 -\xa0antitrypsin.\nThis results in unchecked overactivity of neutrophil elastase that causes the destruction of alveolar wall.\nAs α1\xa0- antitrypsin is deficient throughout the acinus, the acini are uniformly involved from the respiratory bronchiole to the terminal blind alveoli.\nNeutrophils are the major cells in the pathogenesis of panacinar emphysema\n\nB. Pathogenesis of centriacinar emphysema\n\nCentriacinar emphysema is associated with smoking.\nNicotine acts as a direct chemoattractant for neutrophils and macrophages.\nSo, in centriacinar emphysema, both neutrophils and macrophages play a central role.\nSmoking enhances the activity of neutrophil and macrophage elastase.\nMacrophage elastase is not inhibited by a1\xa0- antitrypsin and indeed can proteolytically digest this antiprotease.\nBeside protease - antiprotease mechanism, oxidant-antioxidant imbalance also plays an important role in the pathogenesis of smoking-related emphysema.\nNormally, the lung contains a healthy complement of antioxidants (superoxide dismutase, glutathione).\nTobacco smoke contains abundant reactive oxygen species (free radicals) which deplete these antioxidant mechanisms.\nFree radicals cause tissue damage, as well as they, inactivate α1\xa0- antitrypsin, resulting in functional α1\xa0- antitrypsin deficiency even in patients without enzyme deficiency.\n\nWhy smoking-related emphysema involves centriacinar portion?\nThe impaction of smoke particles occurs predominantly at the bifurcation of respiratory bronchioles, resulting in the influx of neutrophils and macrophages, both of which secrete proteases. An increase in protease activity localized in the centriacinar region, together with the smoke-induced oxidative damage, causes the centriacinar pattern of emphysema that is seen in smokers.', 'role': 'assistant'}]