COPD is a chronic inflammatory disease of the airways and lung parenchyma driven most often by tobacco smoke, but also by biomass fuel exposure, occupational dusts and fumes, air pollution, recurrent childhood infection, and genetic susceptibility. The inhaled insult provokes a neutrophil- and macrophage-predominant inflammatory response that persists even after exposure stops, which is why quitting smoking slows but does not reverse established disease. Two overlapping structural processes result, and although most patients have features of both, the dominant pattern shapes the clinical picture. In the chronic bronchitis pattern, inflammation of the conducting airways produces mucus gland hyperplasia, excess secretions, and airway wall thickening. The clinical hallmark, defined by convention as a productive cough for at least three months in two consecutive years, is chronic sputum production, and these patients classically retain carbon dioxide, become hypoxemic, and develop cor pulmonale earlier. In the emphysema pattern, the destructive process falls on the alveolar walls and the elastic recoil of the lung, enlarging airspaces and destroying the capillary bed. These patients lose the tethering that holds small airways open, so airways collapse...