Emphysema

Emphysema is a lung disease marked by permanent enlargement of air spaces beyond the smallest airways and destruction of their walls. This loss of elastic tissue impairs airflow and gas exchange.

Alveoli: Microscopic air sacs where oxygen and carbon dioxide move between the lungs and blood. Their walls are destroyed and neighboring air spaces merge in emphysema.
Cigarette smoking: The inhalation of tobacco smoke produced by burning cigarettes. It is the most common cause of emphysema and drives chronic lung inflammation.
Spirometry: A lung-function test that measures the volume and speed of air inhaled and exhaled. It identifies persistent airflow obstruction, though it does not alone show emphysema's structural damage.
Chronic bronchitis: A clinical condition defined by a productive cough lasting at least three months in each of two consecutive years. It is another major COPD phenotype, defined by airway mucus and cough rather than alveolar destruction.
Elastic recoil: The tendency of stretched lung tissue to return toward its resting size during exhalation. Loss of recoil makes small airways more likely to collapse during exhalation.
Alpha-1 antitrypsin deficiency: An inherited disorder in which low or dysfunctional alpha-1 antitrypsin leaves lung tissue vulnerable to protease injury. It can cause emphysema, often at a younger age and with little smoking exposure.
Computed tomography: An imaging method that combines X-ray measurements to create cross-sectional views of the body. Chest CT can show enlarged air spaces and help characterize emphysema distribution.
Asthma: A chronic airway disease involving variable symptoms and often reversible airflow limitation. Its airflow obstruction is often variable and reversible, unlike the persistent structural damage of emphysema.
Air trapping: Retention of excess air in the lungs because exhalation does not fully empty them. Narrowed, unstable airways impede emptying and leave lungs overinflated.
Protease-antiprotease imbalance: Excess protease activity relative to antiprotease defenses, allowing enzymes to damage tissue proteins. This imbalance helps explain how inflammation destroys alveolar walls.

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