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Pathology · Respiratory: neonatal respiratory distress syndrome
Sample itemA neonate born at 30 weeks develops grunting, cyanosis and chest wall retractions within hours of birth. Radiograph shows a ground-glass pattern with air bronchograms. Which cell fails to produce enough of the deficient substance, and which antenatal intervention reduces the risk?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Type II pneumocytes; antenatal betamethasone
Surfactant is synthesised by type II pneumocytes and lowers alveolar surface tension, and production matures at about 34 to 36 weeks. A deficiency causes atelectasis, hypoxia and hyaline membranes composed of fibrin and necrotic cells. Antenatal corticosteroids given to mothers at risk of preterm delivery accelerate surfactant synthesis.
Option by option
A. Type I pneumocytes; antenatal betamethasone
Type I pneumocytes form the thin gas-exchange surface and do not make surfactant.
B. Type II pneumocytes; antenatal betamethasone (correct)
Correct. Surfactant comes from type II cells, and antenatal steroids induce its production.
C. Alveolar macrophages; tocolysis with nifedipine
Alveolar macrophages clear debris and do not secrete surfactant, and tocolysis does not mature the lung.
D. Club cells; postnatal indomethacin
Club cells secrete protective proteins in bronchioles, and indomethacin is used to close a ductus arteriosus.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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