All of the following lab-values are consistent with Pulmonary fibrosis except?

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: 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.

Correct Answer: D

Rationale: Physiological dead space (VDphys) comprises anatomic dead space (VDanat, ~150 ml, airways) and alveolar dead space (VDalv, non-perfused alveoli). Normally, VDphys ≈ VDanat, but in disease, it's ≥ VDanat due to added VDalv true. Lung diseases (e.g., PE) increase VDphys via VDalv true. High V/Q (ventilation > perfusion, e.g., PE) raises VDphys, as ventilated alveoli lack blood flow true. However, VDphys isn't just alveolar dead space; it's VDanat + VDalv, so equating it to VDalv alone is wrong, omitting the anatomic component always present. This misdefinition skews VDphys's scope, critical for assessing total ventilatory waste, not just alveolar inefficiency, making it the false statement amid accurate descriptions.

Correct Answer: A

Rationale: Bronchial asthma features reversible airway obstruction from inflammation and bronchoconstriction. Airway resistance rises due to narrowed bronchi true. During attacks, FEV1/FVC falls below 80% (e.g., 50-60%) as FEV1 drops more true. Bronchodilators (e.g., albuterol) relieve constriction true. Allergies (not listed) often trigger attacks true. However, cough suppressants aren't indicated asthma's productive cough clears mucus; suppressing it risks obstruction and infection false. Treatment prioritizes bronchodilation and inflammation control (e.g., steroids), not cough suppression, which could worsen symptoms. This exception contradicts asthma management, distinguishing it from true statements reflecting pathophysiology and therapy.