Which of the following is NOT true at FRC?

Correct Answer: B

Rationale: At functional residual capacity (FRC), the lung-thorax system rests (D), with lung recoil inward (C) balanced by chest wall recoil outward (B) . FRC is ~2.5-3 L, roughly 50% of TLC (~6 L), not 75% (A), making A false. At FRC, intrapleural pressure is -5 cm H2O, and alveolar pressure equals atmospheric (0 cm H2O). B's outward chest recoil is true, opposing C's inward lung pull, stabilizing D's rest state. A's exaggeration 75% TLC (~4.5 L) overshoots FRC's role as post-expiratory equilibrium, where diaphragm relaxes and no airflow occurs, per physiology.

Correct Answer: D

Rationale: Intrapleural pressure is always less than atmospheric (D) . At rest (FRC), it's -5 cm H2O (755 mmHg vs. 760 mmHg); inspiration drops it to -7 cm H2O, aiding lung expansion. A's only inspiration' is false it's always negative. B's equality occurs in pneumothorax (Q11). C's definition fits transpulmonary pressure, not intrapleural alone. D's consistency unlike A's limit maintains lung inflation, per pleural mechanics (Q60).

Correct Answer: C

Rationale: Surfactant isn't deficient in term neonates . Type II cells mature by 36 weeks, producing surfactant (Q26). It causes hysteresis (A, true), easing inspiration vs. expiration. It doesn't raise resistance (B, false) it lowers work (Q9). Edema prevention (D) is indirect via stability, not primary. C's term-neonate claim unlike A's lung behavior contradicts physiology; deficiency is preterm (IRDS, Q5).

Correct Answer: D

Rationale: In pulmonary fibrosis, FEV1/FVC is ≥ normal. A 10% diameter increase cuts resistance (R ∝ 1/r^4), not raises it (A, false). COPD is common (B, false). Fibrosis restricts, not obstructs (C, false resistance normal). D's ratio (> 80%) holds as FEV1 and FVC drop evenly (Q1), unlike A's physics error, per restrictive physiology.

Correct Answer: D

Rationale: Chronic emphysema, an obstructive disease, causes CO₂ retention (hypercapnia), lowering pH (acidosis) as HCO₃⁻ rises to compensate respiratory acidosis. Chloride drops (low Cl⁻) via renal compensation, shifting anions, yielding low pH, low chloride, high CO₂ content' (D). High pH (A, E) suggests alkalosis, unfit for chronic CO₂ buildup. Eosinophilia (B) ties to allergy, not emphysema. Low CO₂ (C) fits hyperventilation, not obstruction. This blood gas shift e.g., pH 7.30, PaCO₂ 60 mmHg reflects ventilatory failure, critical in monitoring COPD progression and guiding oxygen or ventilatory support in advanced stages.