A premature neonate at 28 weeks gestation develops respiratory distress syndrome (RDS). The pathophysiological basis relates directly to the ontogeny of surfactant production. Type II pneumocytes begin producing surfactant in clinically significant amounts beginning at:
- A 24-26 weeks, but maturation accelerates markedly after 34-36 weeks ✓
- B 20-22 weeks (early canalicular stage)
- C 28-30 weeks with mature amounts present by 32 weeks
- D Surfactant production begins at 16 weeks but is not secreted into alveoli until term
Explanation
Type II pneumocyte differentiation and surfactant synthesis begin in the late canalicular/early saccular stage around 20-22 weeks, but clinically adequate surfactant amounts appear from about 24-26 weeks. However, the crucial lecithin/sphingomyelin (L/S) ratio reaches ≥2 (indicating lung maturity) typically after 34-36 weeks; phosphatidylglycerol (PG) also appears at 35-36 weeks as a marker of maturity. Infants between 24-34 weeks have sufficient surfactant to survive with support but remain at risk for RDS. Antenatal corticosteroids accelerate surfactant synthesis by upregulating transcription factors for surfactant proteins in type II cells.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.