All the following laboratory values are consistent with pulmonary fibrosis EXCEPT?

Correct Answer: A

Rationale: Pulmonary fibrosis is a restrictive lung disease characterized by the deposition of excessive collagen in the lung interstitium, leading to stiff, non-compliant lungs. This stiffness results in decreased lung compliance, making it difficult for the lungs to expand during inspiration. Additionally, the fibrotic tissue compresses pulmonary blood vessels, increasing pulmonary vascular resistance. The forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) are both reduced due to the restricted lung expansion, but the FEV1/FVC ratio remains normal or above normal because the reduction is proportional, distinguishing it from obstructive diseases where the ratio decreases. Residual volume (RV), however, is the amount of air remaining in the lungs after a maximal expiration. In pulmonary fibrosis, RV is typically decreased because the stiff lungs cannot hold as much air at the end of expiration, unlike in obstructive diseases like COPD where air trapping increases RV. Therefore, increased residual volume is not consistent with pulmonary fibrosis and stands out as the exception among the listed values, which align with the pathophysiology of this condition.

Correct Answer: A

Rationale: Total lung capacity (TLC) is the maximum volume of air the lungs can hold after a maximal inspiration, encompassing all lung volumes: residual volume (RV, ~1-1.5 L), expiratory reserve volume (ERV, ~1-1.5 L), tidal volume (VT, ~0.5 L), and inspiratory reserve volume (IRV, ~2-3 L). In a normal adult, TLC averages around 6 liters (5-7 L, varying by age, sex, and size), widely accepted in physiology (e.g., Guyton, West). The 2 L option might confuse with FRC (~2.5-3 L), the resting volume after normal expiration. Four liters approximates vital capacity (VC, ~4-5 L), excluding RV. Nine liters exceeds typical human capacity, possibly a misestimate, and 15 L is implausible without pathology (e.g., hyperinflation). The 6 L value aligns with standard measurements (e.g., spirometry plus RV via helium dilution), reflecting the full extent of lung expansion in a healthy individual, making it the most accurate approximation.

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: D

Rationale: Pulmonary function tests (PFTs) differentiate lung diseases. Obstructive diseases (e.g., COPD) reduce airflow, decreasing FEV1 (<80% predicted) due to airway narrowing, with increased residual volume (RV) and total lung capacity (TLC) from air trapping. Restrictive diseases (e.g., fibrosis) limit expansion, also reducing FEV1 (<80% predicted) due to lower volumes, but RV and TLC decrease. Decreased FEV1 is common to both obstructive from airflow limitation, restrictive from reduced capacity making it consistent across types. Decreased RV fits restriction, not obstruction (increased RV). Normal or above TLC fits obstruction, not restriction (decreased TLC). Vascular resistance isn't a PFT metric; it rises in fibrosis, not decreases. Decreased FEV1's shared reduction reflects impaired exhalation, a unifying feature despite differing mechanisms, distinguishing it as the overlapping value.

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.