All of the following are true about bone marrow EXCEPT:

Correct Answer: D

Rationale: Red marrow (A) contains hematopoietic cells, producing blood cells. Yellow marrow (B) is mostly adipocytes, storing fat. Yellow can convert to red marrow (C) in anemia to boost hematopoiesis. Yellow marrow lacks significant hematopoietic cells (D), unlike red, making D false. Its fat-dominated composition contrasts with red marrow's active blood cell production, and while conversion occurs, yellow marrow itself doesn't house hematopoietic cells unless transformed, making D the exception.

Correct Answer: D

Rationale: Diffusion rate, per Fick's law, depends on surface area (choice A), concentration gradient (choice B), solubility (choice C), and membrane thickness (choice E), but not directly on molecular weight of gas (choice D), making D correct. Surface area increases diffusion by providing more space for gas exchange, as seen in alveoli. The concentration gradient (partial pressure difference) drives diffusion, e.g., Oâ‚‚ from alveoli to blood. Solubility affects how easily gases dissolve in the membrane, with COâ‚‚ diffusing faster than Oâ‚‚ due to higher solubility. Thickness inversely affects rate; thinner alveolar walls enhance diffusion. Molecular weight influences diffusion speed in free gas (Graham's law), but in the lung's aqueous environment, solubility dominates over molecular weight for Oâ‚‚ and COâ‚‚ exchange across membranes. Studies show diffusion capacity correlates with solubility and pressure gradients, not molecular weight, in physiological contexts, confirming D as the factor least affecting diffusion rate here.

Correct Answer: D

Rationale: With ventilation halved (e.g., from 6 L/min to 3 L/min) and CO₂ output unchanged, arterial pCO₂ rises to 80 mmHg (choice D). Normally, pCO₂ = (V̇CO₂ × K) / V̇A, where V̇CO₂ is CO₂ production, K is a constant (≈863), and V̇A is alveolar ventilation. If pCO₂ is 40 mmHg at 6 L/min, V̇CO₂ = (40 × 6) / 863 ≈ 0.278 L/min. Halving ventilation to 3 L/min, new pCO₂ = (0.278 × 863) / 3 ≈ 80 mmHg. Choice A (50) underestimates doubling; B (60) fits a 33% drop; C (70) is arbitrary. Barbiturates depress respiratory drive, reducing V̇A without altering metabolism (V̇CO₂), doubling pCO₂ as ventilation inversely governs it. Thus, D is correct.

Correct Answer: D

Rationale: Alveolar ventilation (V̇A) = (tidal volume - dead space) × respiratory rate. With TV = 600 ml, dead space ≈ 150 ml, and rate = 10/min, V̇A = (600 - 150) × 10 = 4500 ml/min (choice D). Choice A (1000 ml) fits a lower TV or rate (e.g., 250 ml × 4). Choice B (1750 ml) suggests miscalculation (e.g., 325 ml × 5). Choice C (3000 ml) aligns with TV = 450 ml at 10/min. Choice E (6000 ml) ignores dead space (600 × 10). Dead space (150 ml) is air not reaching alveoli; only 450 ml/breath ventilates gas exchange zones. At 10 breaths, 4500 ml/min reflects effective CO₂ removal and O₂ uptake, matching physiological norms for a resting adult, confirming D.

Correct Answer: D

Rationale: Choice D is likely correct (no answer provided); vagal afferents, via pulmonary stretch receptors (Hering-Breuer reflex), can prolong inspiration (‘breath-holding') if the pneumotaxic center, which limits inspiration, is destroyed. Choice A is false; vagal input (stretch) inhibits inspiration, not expiration. Choice B is wrong; it doesn't directly excite expiratory neurons. ' vagotomy causes deeper, slower breathing, not gasping (medullary damage does). Choice E (shallow rapid breathing) contradicts vagotomy's effect. Vagal afferents signal lung inflation, inhibiting inspiratory neurons via the medulla. Without pneumotaxic modulation, this can lock inspiration, mimicking breath-holding. Physiologically, D aligns with reflex disruption, making it the most consistent vagal influence description.