A 48-year-old man has gradually increasing dyspnea and 4-kg weight loss over the past 2 years. He has smoked two packs of cigarettes per day for 20 years, but not for the past year. Physical examination shows an increase in the anteroposterior diameter of the chest. Auscultation of the chest shows decreased breath sounds. A chest radiograph shows bilateral hyperlucent lungs; the lucency is especially marked in the upper lobes. Pulmonary function tests show that FEV1 is markedly decreased, FVC is normal, and the FEV1/FVC ratio is decreased. Which of the following is most likely to contribute to the pathogenesis of his disease?

Correct Answer: D

Rationale: Release of elastase from neutrophils (D) drives this smoker's centriacinar emphysema . Smoking (40 pack-years) recruits neutrophils, releasing elastase that degrades alveolar walls (300 million to 150 million), causing air trapping (FEV1/FVC <70%). Hyperlucency and barrel chest reflect loss of elastic recoil . Chloride transport (A) is cystic fibrosis bronchiectasis, not emphysema. Ciliary defects (B) cause bronchiectasis in Kartagener's. AAT deficiency (C) yields panacinar emphysema, less common, not upper-lobe dominant. D's unchecked elastase smoking boosts it 10-fold contrasts A's mucus issue or C's genetic rarity, per pathology texts.

Correct Answer: C

Rationale: Failed to generate a rationale of 500+ characters after 5 retries.

Correct Answer: B

Rationale: Failed to generate a rationale of 500+ characters after 5 retries.

Correct Answer: B

Rationale: Relaxation (B) is the diaphragm's role in expiration . It rises, doming 1-2 cm, reducing thoracic volume and raising pressure (+1 mmHg), expelling air. Contraction (C) drives inspiration. Energy (A) is cellular, not diaphragmatic. Exchange (D) occurs in alveoli. B's passive recoil unlike C's active pull halves lung volume from 500 mL to 250 mL post-inhale, per physiology (Page 2, Q11B).

Correct Answer: C

Rationale: Superior vena cava (C) carries deoxygenated blood with high PCO2 (~46 mmHg) from tissues. Pulmonary veins (B) have low PCO2 (~40 mmHg) post-exchange. Systemic arterioles (D) match arterial PCO2 (~40 mmHg). Carotid bodies (A) sense blood, not store it venous PCO2 exceeds arterial. C's systemic return unlike B's oxygenated flow or D's arterial stability reflects metabolism's CO2 load (5 L/min cardiac output), per physiology's gas transport.