Clinical meaning
COPD is characterized by persistent airflow limitation caused by a combination of small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema). Cigarette smoke and other noxious particles trigger an abnormal inflammatory response involving neutrophils, macrophages, and CD8+ T lymphocytes. Neutrophils release elastase and matrix metalloproteinases (MMPs) that degrade elastin and collagen in lung parenchyma. Alpha-1 antitrypsin (AAT) normally inhibits neutrophil elastase, but the protease-antiprotease balance is overwhelmed by ongoing inflammation or genetically deficient in AAT deficiency (PiZZ phenotype). Emphysema results from alveolar wall destruction, loss of elastic recoil, and air trapping. Chronic bronchitis involves goblet cell hyperplasia, mucus hypersecretion, and squamous metaplasia of ciliated epithelium. Pulmonary hypertension develops from hypoxic vasoconstriction of pulmonary arteries, eventually leading to cor pulmonale.
Diagnosis & workup
Diagnostics & workup: - Post-bronchodilator spirometry: FEV1/FVC < 0.70 confirms airflow limitation - GOLD staging by FEV1 % predicted: 1 (>= 80%), 2 (50-79%), 3 (30-49%), 4 (< 30%) - ABCD assessment using mMRC dyspnea scale and exacerbation history - Alpha-1 antitrypsin level for all newly diagnosed COPD patients (CTS guideline) - 6-minute walk test for functional capacity assessment - CT chest to evaluate emphysema distribution and rule out lung malignancy