Regarding surfactants, one is true?

Correct Answer: B

Rationale: Surfactant, a phospholipid-protein mix from type II alveolar cells, lines alveoli and reduces surface tension of the fluid layer, preventing collapse and easing lung expansion. Normally, water's high surface tension (~72 dynes/cm) pulls alveolar walls inward, but surfactant lowers it (to ~5-10 dynes/cm), stabilizing smaller alveoli per Laplace's law (P = 2T/r). It doesn't increase pleural pressure, which remains negative (~-4 mmHg at rest) to keep lungs expanded surfactant affects intra-alveolar dynamics, not pleural space. It doesn't directly decrease alveolar pressure (typically atmospheric at rest, ~760 mmHg); that's a muscle-driven effect. It makes inspiration easier, not harder, by reducing the work needed to overcome tension, countering collapse tendencies. Pneumothorax relates to pleural breach, not surfactant. Reducing surface tension is the true function, critical for neonatal lung maturation and preventing atelectasis, distinguishing it from pressure or effort-related misconceptions.

Correct Answer: A

Rationale: Functional residual capacity (FRC) is the volume in the lungs after a normal expiration, equaling expiratory reserve volume (ERV) plus residual volume (RV). The spirogram shows maximal inhalation to total lung capacity (TLC) and exhalation to RV, with VC (vital capacity) as TLC - RV. RV is given as 1.0 L via helium dilution. FRC = ERV + RV, but without the figure, assume a typical female FRC (~2-3 L). If VC is ~4 L (normal for a young woman) and TLC ~5 L, then after maximal exhalation to RV (1 L), the difference from TLC to FRC includes ERV. Standard ERV is ~1-1.5 L; with RV = 1 L, FRC = 1 + 1 = 2.0 L fits option A, plausible for a smaller female frame. Higher values (2.5-3.5 L) align with larger individuals or males (~3 L). Without exact spirogram data, 2.0 L is reasonable, matching RV + minimal ERV, consistent with helium-derived RV and typical physiology.

Correct Answer: C

Rationale: A stab wound causing pneumothorax allows air into the pleural space, disrupting the negative intrapleural pressure (~-4 to -6 mmHg) that keeps lungs expanded. This equalizes pleural pressure to atmospheric (760 mmHg), eliminating the force opposing lung elastic recoil, which pulls the lung inward to collapse toward the hilum, reducing its volume. Meanwhile, the chest wall's outward recoil, no longer countered by lung tension, causes it to expand outward, increasing thoracic diameter. Thus, the lung collapses and the chest wall expands, a classic pneumothorax feature. Both expanding defies recoil mechanics, fixing at FRC ignores pressure loss, and collapse-collapse misrepresents chest wall behavior. This dynamic reflects the opposing elastic properties unleashed by pleural breach, critical for understanding respiratory compromise and interventions like chest tube placement.

Correct Answer: D

Rationale: Inspiration relies on Boyle's law: expanding the thorax lowers intrapulmonary pressure (e.g., 760 to 758 mmHg) below atmospheric, creating a pressure difference driving air in. Diaphragm and intercostal contraction generate this ~1-2 mmHg gradient for tidal breathing (~500 ml). Atmospheric pressure (760 mmHg) is static, not a force its difference with intrapulmonary pressure matters. Muscular spasm implies involuntary action, unlike controlled respiratory muscle contraction. Reduced surface tension (via surfactant) eases expansion but isn't the force pressure difference is. Muscle relaxation drives expiration, not inspiration. This gradient, directly linking mechanics to airflow, is the primary force, quantifiable and fundamental to ventilation, distinguishing it from secondary factors like surfactant or muscle state.

Correct Answer: D

Rationale: Restrictive lung disease (e.g., fibrosis) stiffens lungs, reducing expansion. Forced vital capacity (FVC) drops (e.g., from 4-5 L to 2-3 L) due to limited volume. FEV1 also falls (e.g., 3-4 L to 1.5-2 L) proportionally, but the FEV1/FVC ratio stays normal or high (≥80%), as both decrease similarly, unlike obstructive disease (<70%). Ventilation/perfusion (V/Q) ratio may rise in fibrosis (ventilation falls more than perfusion), not remaining normal. FEV1 and FVC individually are reduced, not normal. The FEV1/FVC ratio's preservation is a restrictive hallmark volume-limited, not airflow-obstructed making it the relatively normal value, key for spirometric diagnosis and distinguishing restrictive from obstructive patterns.