Which of the following is a major factor in the pathogenesis of bronchopulmonary dysplasia (BPD)?

Enhance your readiness for the MEDNAX Neonatal Nurse Practitioner Exam. Utilize flashcards, multiple-choice questions, and detailed explanations. Equip yourself for success!

Multiple Choice

Which of the following is a major factor in the pathogenesis of bronchopulmonary dysplasia (BPD)?

Explanation:
Oxygen toxicity is a central driver of bronchopulmonary dysplasia because prolonged exposure to high oxygen levels in the immature lung creates oxidative stress that disrupts normal lung development. In preterm infants, excess oxygen generates reactive oxygen species that damage alveolar and vascular cells, trigger inflammation, and impair the process of alveolarization and pulmonary vascular development. This injury leads to fewer and larger alveoli, abnormal airway architecture, and persistent respiratory dysfunction characteristic of BPD. While ventilator-related injury and inflammation also contribute—especially historically—the initiating and most influential factor in many cases is oxygen toxicity from high FiO2 exposure. The other options reflect treatments or contributing factors, not the primary pathogenesis.

Oxygen toxicity is a central driver of bronchopulmonary dysplasia because prolonged exposure to high oxygen levels in the immature lung creates oxidative stress that disrupts normal lung development. In preterm infants, excess oxygen generates reactive oxygen species that damage alveolar and vascular cells, trigger inflammation, and impair the process of alveolarization and pulmonary vascular development. This injury leads to fewer and larger alveoli, abnormal airway architecture, and persistent respiratory dysfunction characteristic of BPD. While ventilator-related injury and inflammation also contribute—especially historically—the initiating and most influential factor in many cases is oxygen toxicity from high FiO2 exposure. The other options reflect treatments or contributing factors, not the primary pathogenesis.

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