COPD Pathology MCQ — NEET PG Practice Question | NEETPGAI
COPD Pathology
medium
microscope Pathology
A 62-year-old man with a 40 pack-year smoking history presents with progressive dyspnea on exertion, chronic productive cough, and recurrent lower respiratory tract infections over the past 3 years. Spirometry shows FEV₁/FVC ratio of 0.58 with FEV₁ 45% predicted. High-resolution CT chest reveals extensive centrilobular emphysema with bronchial wall thickening. Pathological examination of a lung biopsy shows destruction of alveolar walls with loss of elastic recoil and enlarged air spaces distal to the terminal bronchioles. Which of the following best describes the primary pathological lesion in this patient?
A. Panlobular emphysema with uniform destruction of the acinus
B. Centrilobular emphysema with selective destruction of proximal alveoli while distal alveoli remain relatively preserved
C. Paraseptal emphysema affecting distal alveoli near the pleura and septa
D. Irregular emphysema with patchy destruction associated with scarring
Explanation
Pathological Classification of Emphysema in COPD
Key Point
The distribution and pattern of alveolar destruction defines the morphological subtype of emphysema, which has important etiological and clinical implications.
Centrilobular Emphysema — The Classic COPD Pattern
Centrilobular (centriacinar) emphysema is the hallmark pathological finding in smoking-related COPD. The destruction is:
1.
Selective — affects the proximal portion of the acinus (respiratory bronchioles)
2.
Spares distal alveoli — the terminal alveoli remain relatively intact
3.
Predominantly upper lobe and apical segments — characteristic distribution
4.
Associated with bronchial wall thickening and mucus plugging — explains the productive cough and airway obstruction
High-YieldNEET PG
Centrilobular emphysema is pathognomonic for cigarette smoking. When you see this pattern on histology or imaging in a smoker with COPD, the diagnosis is confirmed.
Comparison with Other Emphysema Types
Table
Feature
Centrilobular
Panlobular
Paraseptal
Irregular
Distribution
Proximal acinus
Entire acinus uniformly
Distal alveoli (near pleura/septa)
Patchy, near scars
Primary association
Cigarette smoking
α₁-AT deficiency
Aging, apical blebs
Scarring, fibrosis
Lobe predominance
Upper lobes
Lower lobes
Apical/subpleural
Variable
Clinical presentation
Airflow obstruction, productive cough
Early-onset dyspnea, basilar disease
Spontaneous pneumothorax
Minimal symptoms
Pathophysiology in This Case
The patient's clinical and pathological findings align perfectly with centrilobular emphysema:
Smoking history (40 pack-years) — the primary risk factor
Productive cough — due to bronchial wall thickening and mucus retention in proximal airways
Airflow obstruction (FEV₁/FVC 0.58) — loss of elastic recoil and airway collapse
Upper lobe predominance on CT — characteristic distribution
Clinical Pearl
The presence of bronchial wall thickening on imaging is a clue to centrilobular emphysema; panlobular emphysema typically shows minimal bronchial changes.
Why Elastic Recoil Is Lost
The destruction of alveolar walls removes the elastic fibers (elastin and collagen) that normally provide elastic recoil. This leads to:
1.
Airway collapse during expiration → air trapping
2.
Increased residual volume and total lung capacity
3.
Flattening of the diaphragm → mechanical disadvantage
