In a normal human, The total lung capacity (TLC) is approximately equal to?

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: 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.

Correct Answer: B

Rationale: Atmospheric air has ~21% oxygen (O2) and ~0.04% carbon dioxide (CO2), so O2's percentage vastly exceeds CO2's, reflecting their natural abundances. Solubility, per Henry's law, depends on the solubility coefficient: O2's is ~0.024 ml/mmHg/L blood, while CO2's is ~0.51 ml/mmHg/L over 20 times higher. Thus, O2 is less soluble than CO2, despite its higher atmospheric presence. In blood, O2 relies on hemoglobin (~98% bound, ~2% dissolved), while CO2 uses dissolved (~7%), bicarbonate (~70%), and hemoglobin (~23%) forms, leveraging its solubility. Option B (higher O2 percentage, lower O2 solubility) fits: 21% vs. 0.04%, and 0.024 vs. 0.51. This contrast drives distinct transport mechanisms O2's hemoglobin dependence vs. CO2's solubility advantage crucial for respiration and acid-base balance, making it the accurate physiological description.

Correct Answer: B

Rationale: Surfactant, from type II alveolar cells, reduces surface tension of alveolar fluid from water's high value (~72 dynes/cm) to ~5-10 dynes/cm, preventing collapse per Laplace's law (P = 2T/r). It doesn't increase pleural pressure, which stays negative (~-4 mmHg at rest) to keep lungs expanded surfactant acts intra-alveolarly. It doesn't lower alveolar pressure (atmospheric at rest, ~760 mmHg); that's muscle-driven. It eases inspiration by reducing tension, not hindering it, countering collapse and aiding neonates especially. Pneumothorax (not listed) involves pleural breach, unrelated to surfactant. Reducing surface tension is its core function, stabilizing alveoli and enhancing compliance, a vital adaptation for efficient breathing, making it the true statement amid pressure or effort misconceptions.