Chronic obstructive pulmonary disease (COPD) is a progressive lung condition defined by persistent airflow limitation that is not fully reversible. It typically combines chronic bronchitis, characterized by long term cough and mucus production, and emphysema, in which the alveoli are destroyed and lose elasticity. The main cause is long term exposure to inhaled irritants, especially tobacco smoke. Other contributors include biomass fuel smoke, occupational dusts and chemicals, air pollution, and genetic factors such as alpha‑1 antitrypsin deficiency.

Pathophysiologically, COPD involves chronic inflammation of the airways, lung parenchyma, and pulmonary vasculature. This inflammation leads to airway narrowing, mucus hypersecretion, ciliary dysfunction, and destruction of alveolar walls, which together reduce airflow and impair gas exchange. Hyperinflation of the lungs increases the work of breathing and contributes to dyspnea. Exacerbations, often triggered by respiratory infections or pollutants, accelerate lung function decline, worsen symptoms, and increase mortality.

Diagnosis relies on clinical assessment plus spirometry, which demonstrates a reduced ratio of forced expiratory volume in one second to forced vital capacity that persists after bronchodilator use. Disease severity is evaluated using spirometric grades, symptom scores, and exacerbation history.

Management aims to relieve symptoms, reduce exacerbations, and improve quality of life. Key strategies include smoking cessation, vaccinations, pulmonary rehabilitation, inhaled bronchodilators, and inhaled corticosteroids for selected patients, as well as oxygen therapy in cases with chronic hypoxemia. For advanced disease, surgical and interventional options such as lung volume reduction procedures or transplantation may be considered. Ongoing research targets inflammation, structural remodeling, and regenerative therapies to slow or reverse disease progression.