Which of the following statements regarding surfactants is incorrect?

Correct Answer: C

Rationale: Surfactant, from type II alveolar cells, reduces alveolar surface tension, aiding lung function. It causes hysteresis the difference in lung inflation vs. deflation pressure-volume curves by lowering tension more effectively as alveoli expand, a true property. It decreases, not increases, pulmonary resistance by easing expansion and reducing collapse tendency, so that's incorrect but not the queried option. Surfactant deficiency is common in preterm neonates (<37 weeks), causing respiratory distress syndrome (RDS), but in term neonates (≥37 weeks), surfactant production is typically mature, making commonly deficient in term-neonates' incorrect RDS is rare at term unless congenital defects exist. Surfactant prevents pulmonary edema indirectly by maintaining alveolar stability, reducing transudation pressure, though not its primary role. The term-neonate statement is the incorrect one, misaligning with developmental physiology where surfactant sufficiency is expected at full gestation.

Correct Answer: B

Rationale: Infant respiratory distress syndrome (IRDS) in premature babies stems from inadequate surfactant production, critical for reducing alveolar surface tension (T). Without surfactant, T increases, causing alveoli to collapse due to high water-induced tension, unlike normal low-tension stability. This elevates the pressure needed to expand lungs, decreasing lung compliance (C), as stiff lungs resist inflation a hallmark of IRDS. Collapsed alveoli impair gas exchange, reducing arterial PO2 (PaO2) from normal (75-100 mmHg) to hypoxic levels (e.g., 50-60 mmHg), driving respiratory distress. Option B (T increases, C decreases, PaO2 decreases) matches this pathophysiology: high T from surfactant lack, low C from rigidity, and low PaO2 from poor oxygenation. Other options fail e.g., C increasing contradicts stiffness, PaO2 equal ignores hypoxemia. This triad reflects IRDS's core mechanism, where surfactant deficiency cascades into ventilatory and oxygenation failure.

Correct Answer: B

Rationale: Atmospheric air has ~21% oxygen (O2) and ~0.04% carbon dioxide (CO2), so O2's percentage vastly exceeds CO2's, reflecting their natural abundances. Solubility, per Henry's law, depends on the solubility coefficient: O2's is ~0.024 ml/mmHg/L blood, while CO2's is ~0.51 ml/mmHg/L over 20 times higher. Thus, O2 is less soluble than CO2, despite its higher atmospheric presence. In blood, O2 relies on hemoglobin (~98% bound, ~2% dissolved), while CO2 uses dissolved (~7%), bicarbonate (~70%), and hemoglobin (~23%) forms, leveraging its solubility. Option B (higher O2 percentage, lower O2 solubility) fits: 21% vs. 0.04%, and 0.024 vs. 0.51. This contrast drives distinct transport mechanisms O2's hemoglobin dependence vs. CO2's solubility advantage crucial for respiration and acid-base balance, making it the accurate physiological description.

Correct Answer: B

Rationale: Surfactant, from type II alveolar cells, reduces surface tension of alveolar fluid from water's high value (~72 dynes/cm) to ~5-10 dynes/cm, preventing collapse per Laplace's law (P = 2T/r). It doesn't increase pleural pressure, which stays negative (~-4 mmHg at rest) to keep lungs expanded surfactant acts intra-alveolarly. It doesn't lower alveolar pressure (atmospheric at rest, ~760 mmHg); that's muscle-driven. It eases inspiration by reducing tension, not hindering it, countering collapse and aiding neonates especially. Pneumothorax (not listed) involves pleural breach, unrelated to surfactant. Reducing surface tension is its core function, stabilizing alveoli and enhancing compliance, a vital adaptation for efficient breathing, making it the true statement amid pressure or effort misconceptions.

Correct Answer: A

Rationale: Work of breathing (WOB) is energy to overcome elastic (compliance) and resistive (airway) forces. Compliance (C = ΔV / ΔP) measures lung stretchability low C (stiff lungs) raises pressure needed, increasing WOB; thus, WOB is inversely related to compliance, true. During exercise, WOB rises with ventilation demand, not constant false. Airway resistance (R) directly increases WOB (e.g., asthma), contradicting not affected' false. In pulmonary fibrosis, low compliance elevates WOB, not reduces it false (emphysema might lower elastic work). The inverse compliance link (WOB = ∫P dV, P rises as C falls) is fundamental, reflecting effort to expand stiff lungs, making it the correct statement, critical for understanding respiratory workload in disease.