Share a DM level mcq question with 4 options for a pulmonary medicine resident Topic of mcq is tropical pulmonary eosinophilia
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"tropical pulmonary eosinophilia" diagnosis treatment
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I now have excellent source material from Murray & Nadel's Textbook of Respiratory Medicine and Fishman's Pulmonary Diseases and Disorders. Here is a DM-level MCQ:
DM Pulmonary Medicine - MCQ
A 32-year-old man from Tamil Nadu presents with a 3-month history of nocturnal paroxysmal cough, exertional dyspnea, and low-grade fever. Examination reveals bilateral wheeze. Investigations show: absolute eosinophil count 5,800/μL (5.8 × 10⁹/L), serum IgE 6,400 IU/mL, strongly positive antifilarial IgG, and negative blood microfilaria smear. HRCT chest shows bilateral reticulonodular opacities. He is started on diethylcarbamazine (DEC) 6 mg/kg/day for 3 weeks with significant symptomatic improvement. However, at 18-month follow-up, he reports recurrent dyspnea on exertion and spirometry now shows an FVC of 68% predicted with FEV1/FVC of 0.82.
Which of the following best explains his current spirometric pattern and its pathological basis?
(A) Ongoing eosinophilic airway inflammation causing irreversible bronchoconstriction, representing a fixed obstructive defect from filarial antigen-driven remodeling
(B) Pulmonary fibrosis with histiocytic infiltration developing as a consequence of inadequately treated or late/recurrent TPE, resulting in a restrictive ventilatory defect
(C) Development of allergic bronchopulmonary aspergillosis (ABPA) triggered by the prior eosinophilic milieu, causing central bronchiectasis with mixed obstruction
(D) DEC-induced obliterative bronchiolitis causing air-trapping and a pseudo-restrictive pattern on spirometry
Answer: (B)
Explanation:
Cases of TPE left untreated for 5 years or more - or with inadequate treatment - eventually develop pulmonary fibrosis with histiocytic infiltration. This results in a restrictive ventilatory defect (reduced FVC, normal or elevated FEV1/FVC), which is exactly the pattern seen here (FVC 68%, FEV1/FVC 0.82).
The restrictive fibrotic end-stage is a well-recognized long-term complication of chronic or recurrent TPE, caused by persistent localized eosinophil degranulation in the lung vasculature and interstitium even after the acute phase resolves. Clinically important points tested here:
- Why (A) is wrong: TPE can cause a reversible obstructive defect acutely (wheezing, hyperinflation), but the classic late complication is restrictive, not obstructive
- Why (C) is wrong: ABPA is caused by Aspergillus fumigatus sensitization, not filarial antigens; the high IgE here is filarial in origin, and there is no mucoid impaction or central bronchiectasis described
- Why (D) is wrong: DEC is not associated with obliterative bronchiolitis; it is the definitive treatment for TPE
Key DM-level teaching point: Murray & Nadel notes that both a reversible obstructive defect (early, from bronchospasm) AND a restrictive defect (late, from fibrosis) can occur in TPE - distinguishing the chronological stage and the mechanism is the discriminating knowledge expected at the DM level.
Source: Murray & Nadel's Textbook of Respiratory Medicine, Chapter 58 - Tropical Pulmonary Eosinophilia (lines 2064-2066); Fishman's Pulmonary Diseases and Disorders, Chapter 71
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