IM28.1-7 | Obstructive Airway Disease Foundations — Summary & Reflection

KEY TAKEAWAYS

Obstructive airway disease encompasses conditions where airflow is limited by airway narrowing or collapse. Asthma (GINA): chronic eosinophilic/mast-cell inflammation with variable, reversible obstruction (≥12% and ≥200 mL FEV1 rise after bronchodilator); COPD (GOLD): persistent, progressive, not-fully-reversible obstruction (post-bronchodilator FEV1/FVC < 0.70), caused by chronic bronchitis or emphysema, predominantly from tobacco or biomass smoke.

Key distinctions: asthma has marked diurnal variability, atopic basis, and reversibility; COPD is progressive with irreversible obstruction. GOLD 1–4 grades COPD by FEV1 % predicted; GINA classifies asthma by severity and control.

Acute exacerbations are triggered by viral infections (50%), bacterial infections (H. influenzae, S. pneumoniae), air pollution, allergens (asthma), drugs (NSAIDs in AERD), and non-compliance. Hypoxia results from V/Q mismatch (dominant mechanism); hypercapnia develops from alveolar hypoventilation when respiratory muscles are overwhelmed — creating type-2 respiratory failure (↑PaCO₂, ↑HCO₃⁻, compensated respiratory acidosis). Safe O₂ target in chronic CO₂ retainers: SpO₂ 88–92%.

AAT deficiency (PiZZ, SERPINA1): autosomal co-dominant; serum AAT <15% of normal; uninhibited neutrophil elastase destroys alveolar walls → panacinar emphysema (basal predominance) at age 40–50; screen all COPD patients <45 years or non-smokers with emphysema.

Environmental causes: tobacco (dominant COPD), biomass fuel smoke (Indian women), occupational dusts/chemicals. Allergic triggers (IgE-mediated): house dust mite, cockroach, Aspergillus, pollen; non-allergic: exercise, cold air, NSAIDs (AERD mechanism = COX-1 block → excess leukotrienes), respiratory infections, air pollutants.

REFLECT

Return to Rajan and his son from the opening scenario. Rajan has COPD from 35 pack-years of smoking — persistent obstruction with daily sputum, progressive dyspnoea, and GOLD 2–3 disease. His son has allergic asthma from atopy — fully reversible, triggered by dust and cold air, responsive to salbutamol. They share 'airway obstruction' as a physiological finding but differ in every meaningful clinical, pathophysiological, and prognostic dimension. Reflect on this: if you saw Rajan in clinic today and he asked whether he could 'take the same inhaler as my son', what would you say — and why? And what single non-pharmacological intervention, if Rajan were willing, would most powerfully alter his disease trajectory?