<unk>  is caused by loss of elasticity of the lung tissue, from  destruction of structures supporting the alveoli, and destruction of capillaries feeding the alveoli. The result is that the  small airways collapse during exhalation (although alveolar  collapsability has increased), leading to an obstructive form of lung disease (airflow is impeded and air is generally "trapped" in the lungs in obstructive lung diseases). When toxins such as smoke are breathed into the lungs, the particles are trapped and cause a localized inflammatory response. Chemicals released during the inflammatory response (e.g., elastase) can break down the walls of alveoli (alveolar septum). This leads to fewer but larger alveoli, with a decreased surface area and a decreased ability to absorb oxygen and exude carbon dioxide by diffusion. The activity of another molecule called alpha 1-antitrypsin normally neutralizes the destructive action of one of these damaging molecules.
Emphysema pathophysiology
Pulmonary edema pathophysiology
Atelectasis pathophysiology
Bronchitis pathophysiology
Bronchiolitis pathophysiology
Pneumoconiosis pathophysiology
Acute bronchitis pathophysiology
Air embolism pathophysiology