What is expected in a premature baby with IRDS? T=alveolar surface tension, C=lung compliance, PaO2=arterial PO2?

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: 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.

Correct Answer: A

Rationale: Work of breathing (WOB) is energy to overcome elastic (compliance) and resistive (airway) forces. Compliance (C = ΔV / ΔP) measures lung stretchability low C (stiff lungs) raises pressure needed, increasing WOB; thus, WOB is inversely related to compliance, true. During exercise, WOB rises with ventilation demand, not constant false. Airway resistance (R) directly increases WOB (e.g., asthma), contradicting not affected' false. In pulmonary fibrosis, low compliance elevates WOB, not reduces it false (emphysema might lower elastic work). The inverse compliance link (WOB = ∫P dV, P rises as C falls) is fundamental, reflecting effort to expand stiff lungs, making it the correct statement, critical for understanding respiratory workload in disease.

Correct Answer: D

Rationale: Inhalation sequence: (5) Diaphragm and intercostals contract, expanding the thorax. (1) Intrapleural pressure drops from -4 mmHg (756 mmHg) to -6 mmHg (754 mmHg), increasing transpulmonary pressure. (3) Lungs expand. (4) Intra-alveolar pressure falls to 759 mmHg (-1 mmHg) per Boyle's law, creating a gradient. (2) Air flows in. Order 5,1,3,4,2 reflects causality: muscle action lowers IPP, expands lungs, drops alveolar pressure, drives airflow. Others disrupt e.g., 5,2,3,4,1 puts flow before pressure; 1,3,4,5,2 starts without muscle action. This aligns with respiratory mechanics, ensuring logical progression for tidal breathing (~500 ml).

Correct Answer: B

Rationale: Nitrogen (N2) is the most abundant gas in Earth's atmosphere, comprising ~78% by volume, due to its chemical stability and geological accumulation. Oxygen (O2) is ~21%, vital for life but secondary. Argon (~0.93%) and carbon dioxide (CO2, ~0.0407%) are trace gases, with CO2 critical for climate despite low abundance. Nitrogen's dominance results from its inert nature and massive release during Earth's formation, per atmospheric composition data (e.g., NOAA). It dilutes other gases, shaping atmospheric pressure (~1013 hPa), making it the correct choice, far exceeding oxygen or trace constituents in prevalence.