Fick's law depend on multiple factors, which one of them will have the most effect when observing the diffusion of different gases?

Correct Answer: D

Rationale: Fick's law of diffusion states that the rate of gas diffusion across a membrane (e.g., alveolar-capillary) is proportional to the surface area (A), diffusion coefficient (D), and partial pressure gradient (ΔP), and inversely proportional to diffusion distance (d): Rate = (A × D × ΔP) / d. When comparing different gases (e.g., O2 vs. CO2), the diffusion coefficient (D) varies most significantly, as it depends on gas solubility and molecular weight (D ∝ solubility / √MW). CO2's solubility is ~20 times higher than O2's (0.51 vs. 0.024 ml/mmHg/L), though O2's molecular weight is slightly lower (32 vs. 44), making CO2 diffuse ~20 times faster despite similar gradients. Partial pressure gradient drives diffusion but is gas-specific and often comparable (e.g., O2: 100-40 mmHg, CO2: 46-40 mmHg). Temperature and distance affect all gases similarly in the lung. Thus, the diffusion coefficient has the most pronounced effect across different gases, explaining why CO2 equilibrates faster than O2 across the respiratory membrane.

Correct Answer: D

Rationale: Pulmonary fibrosis, a restrictive disease, stiffens lungs with interstitial scarring. The FEV1/FVC ratio is normal or high (≥80%) because both FEV1 and FVC decrease proportionally, unlike obstructive diseases. Increased pulmonary vascular resistance occurs as fibrosis compresses capillaries, raising resistance. Peak expiratory flow (PEF), when corrected for reduced lung volume, can remain normal or above, as airflow isn't obstructed, just limited by volume. However, residual volume (RV) decreases in pulmonary fibrosis (e.g., from 1.5 L to <1 L) due to stiff lungs limiting all volumes, contrasting with obstructive diseases (e.g., COPD) where RV increases from air trapping. Increased RV doesn't fit fibrosis's restrictive pattern, where reduced elasticity shrinks residual air, not expands it, making this the inconsistent value among the set, reflecting the disease's impact on lung mechanics.

Correct Answer: D

Rationale: In a healthy upright individual, regional ventilation varies due to gravity and pleural pressure gradients. At rest, intrapleural pressure (IPP) is more negative at the apex (~-10 cm H2O) than the base (~-2.5 cm H2O) due to lung weight, making apices less compliant (stiffer) and bases more compliant (easier to expand). During quiet breathing (VT = 400 ml, RR = 12/min), the diaphragm's downward pull preferentially ventilates the lower zones, where compliance is higher and initial volume lower, allowing greater volume change (ΔV). Studies (e.g., West) show lower lobes receive ~4 times more ventilation per unit volume than apices. Thus, ventilation is greatest in the lower zones, followed by middle, then upper (Lower > Middle > Upper). Equal ventilation ignores gravity's effect, and Upper > Middle > Lower reverses the gradient. For this boy, VA = (400 - ~120 ml VD) × 12 = ~3.36 L/min, distributed predominantly to the base, making this the best description.

Correct Answer: C

Rationale: Residual volume (RV) is the air left in the lungs after maximal expiration (~1-1.5 L), preventing collapse and measurable only indirectly (e.g., helium dilution). It's not just after tidal expiration that's FRC (~2.5-3 L), including RV plus ERV, making that false. In COPD, RV increases (e.g., to 2-3 L) due to air trapping from obstructed airways and lost elasticity, not decreases. In pulmonary fibrosis, a restrictive disease, RV decreases (e.g., to <1 L) as stiff lungs limit all volumes, including residual air, making this correct. RV doesn't stay constant lifelong aging and disease alter it but in health, it's relatively stable, though this isn't the strongest fit. Fibrosis's reduction reflects restricted lung expansion, contrasting with obstructive hyperinflation, making it the accurate statement amid options misaligned with RV's physiological behavior.

Correct Answer: D

Rationale: Intrapleural pressure (IPP) is the pressure in the pleural space, negative relative to atmospheric (760 mmHg) due to lung (inward) and chest wall (outward) recoil. At FRC, IPP is ~756 mmHg (-4 mmHg); inspiration drops it to ~-6 mmHg, and expiration raises it slightly, but it stays negative in health. It's always less than atmospheric pressure, maintaining lung expansion unless breached (e.g., pneumothorax). It's not just low during inspiration it's consistently subatmospheric. Respiratory muscles adjust IPP but don't equalize it to atmospheric pressure (that's pathological). IPP isn't the alveolar-pleural difference (transpulmonary pressure); it's the pleural cavity's absolute pressure. This constant negativity is vital for lung mechanics, making it the true statement reflecting pleural dynamics.