A 32-week preterm neonate is intubated for respiratory distress syndrome (RDS). The primary physiological deficiency causing RDS is:
- A Insufficient pulmonary surfactant from immature type II pneumocytes; surfactant reduces alveolar surface tension, and its absence causes atelectasis, V/Q mismatch, and hypoxemia ✓
- B Absent pulmonary surfactant production due to immature type I pneumocytes
- C Pulmonary vascular immaturity causing right-to-left shunting at the foramen ovale
- D Airway obstruction from underdeveloped cartilaginous bronchi
Explanation
Pulmonary surfactant (primarily dipalmitoylphosphatidylcholine/DPPC with surfactant proteins SP-A, SP-B, SP-C, SP-D) is synthesized and secreted by type II pneumocytes. Surfactant production matures after 34–36 weeks gestation, regulated by cortisol, thyroid hormones, and prolactin. Before this, surfactant deficiency increases alveolar surface tension, causing progressive alveolar collapse (atelectasis) with each expiration, V/Q mismatch, intrapulmonary shunting, and refractory hypoxemia. Type I pneumocytes are involved in gas exchange but do not produce surfactant. Foramen ovale shunting in RDS is a consequence, not the primary cause. Antenatal corticosteroids accelerate fetal lung maturation by inducing surfactant synthesis.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.