A 38-year-old man presents with a 3-year history of asthma diagnosed at age 35, now complicated by recurrent sinusitis with nasal polyps, a 2-week history of wrist drop, and a petechial rash on the lower extremities. Laboratory work shows peripheral eosinophilia of 2200/μL and p-ANCA positivity. Spirometry reveals an obstructive pattern with FEV1/FVC ratio of 0.68 and 15% improvement in FEV1 post-salbutamol, as marked **A** in the diagram. Which of the following best explains the pathophysiology of the airway obstruction pattern shown at **A**?
A. Emphysematous destruction with loss of elastic recoil from cigarette smoking
B. Reversible small-airway obstruction due to eosinophilic infiltration and smooth-muscle contraction in the prodromal-to-eosinophilic phase of EGPA
C. Fixed airway narrowing from tracheal stenosis secondary to granulomatous inflammation
D. Restrictive physiology from diffuse pulmonary fibrosis caused by chronic vasculitis
Explanation
Why "Reversible small-airway obstruction due to eosinophilic infiltration and smooth-muscle contraction in the prodromal-to-eosinophilic phase of EGPA" is right
The pattern marked A (FEV1/FVC <0.7 with >12% reversibility post-bronchodilator) is the hallmark spirometric finding in EGPA during the prodromal and eosinophilic phases. The clinical presentation—late-onset asthma (age 35), nasal polyposis, peripheral eosinophilia >1500/μL, and p-ANCA positivity—confirms EGPA diagnosis. The reversibility (≥12% and ≥200 mL improvement) indicates active bronchospasm from eosinophilic infiltration of small airways and bronchial smooth-muscle contraction, not fixed structural damage. This obstructive pattern with bronchodilator response is pathognomonic for the asthmatic phase of EGPA and is a major diagnostic criterion (ACR/EULAR 2022). Per Harrison's 21e Ch 363 and the MIRRA trial framework, this reversible obstruction responds to glucocorticoids and IL-5 antagonists (mepolizumab), confirming the eosinophilic-inflammatory mechanism.
Why each distractor is wrong
Fixed airway narrowing from tracheal stenosis secondary to granulomatous inflammation: EGPA is a small-vessel necrotizing vasculitis, not a granulomatous disease (that is granulomatosis with polyangiitis, GPA). Tracheal stenosis is not a feature of EGPA, and fixed obstruction would NOT show ≥12% reversibility.
Restrictive physiology from diffuse pulmonary fibrosis caused by chronic vasculitis: Restrictive patterns (low FVC, normal or high FEV1/FVC) are not typical of EGPA; the diagram shows obstructive pattern (A, not B). Pulmonary fibrosis is rare in EGPA and would not produce reversibility.
Emphysematous destruction with loss of elastic recoil from cigarette smoking: There is no smoking history in the vignette. Emphysema causes fixed obstruction without reversibility and is not part of EGPA pathophysiology.
High-YieldNEET PG
EGPA spirometry = obstructive pattern with ≥12% bronchodilator reversibility in the prodromal/eosinophilic phase; reversibility distinguishes it from fixed airway disease and guides use of bronchodilators and steroid-sparing agents like mepolizumab.
