All the following laboratory values are consistent with pulmonary fibrosis EXCEPT?

Correct Answer: A

Rationale: Pulmonary fibrosis stiffens lungs, reducing compliance (D) and total lung capacity (TLC), not residual volume (RV) . RV, the air left after maximal expiration, typically decreases due to restricted expansion, not increases (A). Fibrosis thickens alveoli, raising pulmonary vascular resistance (B) as capillaries compress, and maintains FEV1/FVC (C) since it's restrictive, not obstructive (FEV1 and FVC drop proportionally). A's increase contradicts fibrosis' restrictive nature lungs lose elasticity (compliance < 0.2 L/cm H2O vs. normal 0.5), trapping less air. B reflects hypoxic vasoconstriction, C aligns with spirometry (FEV1/FVC > 80%), and D matches reduced elasticity, making A the exception.

Correct Answer: D

Rationale: Residual volume (RV, D) remains after forced exhalation (~1.2 L) . Tidal volume (A) is quiet breathing (~500 mL). ERV (B) is expirable reserve (~1.3 L). Vital capacity (C) is max exhale (~4.8 L, Q26). RV, unmeasurable by spirometry, stays due to chest wall recoil and airway closure. D's permanence unlike A's cycle or C's total defines post-effort air, per lung volume physiology (Q13).

Correct Answer: D

Rationale: Physiological dead space isn't just alveolar dead space . It's anatomic (~150 mL) plus alveolar dead space (A, true). Lung disease (B) and high V/Q (C) increase it (e.g., embolism, Q34). D's equation misses anatomic part alveolar dead space varies (0 to >150 mL), while physiological sums both. Bohr's method (Q12) confirms. D's error unlike A's baseline misdefines total wasted ventilation, per physiology (Q3).

Correct Answer: A

Rationale: Cough suppressants aren't indicated in asthma. Resistance rises (B) via bronchoconstriction (Q8). FEV1/FVC falls (< 80%, C, true) in attacks (Q15). Bronchodilators (D) relieve spasms. Allergies trigger it. A's suppression cough clears mucus worsens obstruction, unlike B's mechanics or D's therapy, per asthma management (opposite Q13's bronchitis).

Correct Answer: D

Rationale: All (D) are true for rheumatoid lung disease. Rheumatoid arthritis (RA) raises idiopathic pulmonary fibrosis risk (A) interstitial inflammation scars lungs, a known extra-articular feature. Nodular lesions (B), akin to subcutaneous rheumatoid nodules, appear in lung parenchyma, histologically identical (necrobiotic centers). Progressive fibrosis in coal miners with RA and positive rheumatoid factor (C) Caplan's syndrome combines pneumoconiosis and RA's immune response. These manifestations, from fibrosis to nodules, reflect RA's systemic nature, complicating lung function (restrictive patterns), key in rheumatology-pulmonology overlap for diagnosis (e.g., HRCT) and management (e.g., immunosuppression).