At the end of quiet respiration, muscles are relaxed and lungs content represents.

Correct Answer: C

Rationale: At the end of quiet expiration, respiratory muscles (diaphragm, intercostals) relax, and the lungs reach functional residual capacity (FRC), typically 2.5-3 liters. FRC is the resting volume where lung inward recoil balances chest wall outward recoil, maintaining equilibrium without active effort. Residual volume (RV, ~1-1.5 L) is the air left after maximal expiration, not quiet breathing. Expiratory reserve volume (ERV, ~1-1.5 L) is the extra air forcibly exhaled beyond quiet expiration, not present at rest. Inspiratory reserve volume (IRV, ~2-3 L) is additional air inhaled beyond a normal breath, irrelevant post-expiration. Total lung capacity (TLC, ~6 L) includes all volumes, not the resting state. FRC's role as the baseline volume after passive expiration reflects the natural relaxation point, critical for continuous gas exchange, distinguishing it from volumes tied to forced maneuvers or inspiration.

Correct Answer: D

Rationale: Normal inhalation follows a mechanical sequence. (5) Contraction of the diaphragm and external intercostals starts it, expanding the thoracic cavity. (1) This lowers intrapleural pressure (IPP) from -4 mmHg (756 mmHg) to -6 mmHg (754 mmHg), increasing transpulmonary pressure. (3) Lung size increases as the lungs expand with the chest wall. (4) Intra-alveolar pressure drops to 759 mmHg (-1 mmHg) as volume rises (Boyle's law), creating a gradient from atmospheric pressure (760 mmHg). (2) Air flows in from higher to lower pressure. The order 5,1,3,4,2 reflects causality: muscle action lowers IPP, expands lungs, drops alveolar pressure, and drives airflow. Alternatives disrupt this: 5,2,3,4,1 puts flow before pressure changes; 1,3,4,5,2 starts with IPP drop without muscle action; 5,4,3,2,1 misplaces alveolar pressure before lung expansion. The correct sequence mirrors respiratory physiology's step-by-step process.

Correct Answer: B

Rationale: Idiopathic pulmonary fibrosis (IPF) scars the lung interstitium, reducing elasticity and volumes. Total lung capacity (TLC) decreases (e.g., from 6 L to 4 L) as stiff lungs resist expansion. FEV1 and FVC both drop due to restricted capacity, though their ratio (FEV1/FVC) stays normal or high (≥80%). Arterial PO2 (PaO2) falls (e.g., from 75-100 mmHg to 60 mmHg) due to impaired diffusion across thickened alveoli, causing hypoxemia. However, total pulmonary vascular resistance (PVR) increases as fibrosis compresses and obliterates capillaries, narrowing the vascular bed and raising resistance to blood flow. This can strain the right heart, potentially leading to cor pulmonale, a known IPF complication. Among these, only PVR exceeds normal levels, reflecting the disease's vascular impact, while volumes and oxygenation decline, aligning with IPF's restrictive pattern and distinguishing it from healthy physiology.

Correct Answer: D

Rationale: Per Fick's law (Rate = A × D × ΔP / d), diffusion decreases if surface area (A) drops (e.g., emphysema destroys alveoli, halving A halves rate), diffusion distance (d) increases (e.g., pulmonary edema doubles d from 0.5 to 1 μm, halving rate), or partial pressure gradient (ΔP) falls (e.g., hypoventilation lowers alveolar PO2). Decreased pressure coefficient' likely means ΔP; reducing it (e.g., from 60 to 30 mmHg) slows diffusion. Increased lung fluid thickens the barrier, adding resistance beyond distance (e.g., protein debris). All factors reduced A, increased d, lowered ΔP independently and collectively cut diffusion, as seen in hypoxemia from edema or fibrosis. Diffusion coefficient (D) is unchanged here. Each aligns with clinical scenarios impairing O2 transfer, making all the above' correct, reflecting multiple pathways to reduced gas exchange efficiency.

Correct Answer: B

Rationale: The PAO2-PaO2 gradient (alveolar-arterial O2 difference) is normally ~5-10 mmHg due to efficient diffusion. In pulmonary fibrosis, thickened alveolar walls impair O2 transfer, dropping PaO2 (e.g., to 60 mmHg) while PAO2 (~100 mmHg, per alveolar gas equation) stays closer to normal, widening the gradient (e.g., 40 mmHg). During exercise, a normal person's ventilation and perfusion match, keeping the gradient small despite higher O2 use. Anemia lowers O2-carrying capacity, not diffusion, so PaO2 ≈ PAO2, maintaining a normal gradient. At 5000 m, low atmospheric PO2 reduces both PAO2 and PaO2 (e.g., 50 vs. 45 mmHg), keeping the gradient small. Fibrosis's diffusion barrier creates the largest gradient, as O2 struggles to cross, a hallmark of restrictive disease affecting gas exchange, unlike other scenarios.