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Correct Answer: bullae are not present.
emphysema is a chronic pulmonary condition characterized by the destruction of the air spaces distal to the terminal bronchioles, leading to impaired respiratory function. panlobular emphysema, also known as panacinar emphysema, is a subtype of this disease that involves the entire acinus (the functional respiratory unit consisting of bronchioles, alveolar ducts, and alveoli). this type of emphysema is uniformly distributed across the lobules, affecting all parts equally.
one of the distinguishing features of panlobular emphysema is the significant loss of lung parenchyma. the lung parenchyma, which includes the alveoli where gas exchange occurs, undergoes extensive destruction. this leads to a decrease in the surface area available for oxygen and carbon dioxide exchange, severely impacting respiratory efficiency.
in panlobular emphysema, the destruction also extends to the alveoli. alveolar walls break down, leading to the formation of larger air spaces known as bullae. contrary to the statement that "bullae are not present," the presence of bullae is indeed a characteristic feature of panlobular emphysema. these bullae can occupy significant portions of the lungs and can even compress adjacent healthy tissue, further impairing lung function.
this type of emphysema is frequently associated with a genetic condition known as α1-antitrypsin deficiency. α1-antitrypsin is a protease inhibitor that protects the lung parenchyma from damage by enzymes like neutrophil elastase. in individuals with α1-antitrypsin deficiency, unchecked enzyme activity leads to excessive tissue destruction, manifesting prominently as panlobular emphysema.
in conclusion, the statement that "bullae are not present" in panlobular type emphysema is incorrect. the presence of bullae, along with the destruction of alveoli and significant loss of lung parenchyma, are defining characteristics of this condition. this type of emphysema impacts the entire acinus and is particularly severe due to its association with α1-antitrypsin deficiency, which accelerates lung tissue damage.
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