In healthy tissue each bronchiole leads to a group of small thin-walled alveoli. Patients with emphysema have smaller number of larger air sacs with thicker walls. This reduces the total surface area for gas exchange and the distance over which the diffusion of gases happens is increased, making gas exchange less effective and ventilation becomes more difficult.
Molecular mechanisms involve:
Usually phagocytes in the alveoli prevent lung infections by engulfing bacteria and producing elastase, a protein that digests lung tissue, killing bacteria inside the vesicles formed by endocytosis.
Alpha 1-antitrypsin, an enzyme inhibitor,usually prevents elastase and other proteases from digesting any lung tissues. But for smokers, the number of phagocytes in the lungs increases, producing more elastase. Genetic factors will also contribute to the quantity and effectiveness of this enzyme inhibitor produced in the lungs.
Emphysema is chronic disease as the damage caused is irreversible, causing low oxygen saturation in blood and abnormally high CO2 levels. This causes symptoms such as fatigue, shortness of breath and ventilation is quicker than usual.
Molecular mechanisms involve:
Usually phagocytes in the alveoli prevent lung infections by engulfing bacteria and producing elastase, a protein that digests lung tissue, killing bacteria inside the vesicles formed by endocytosis.
Alpha 1-antitrypsin, an enzyme inhibitor,usually prevents elastase and other proteases from digesting any lung tissues. But for smokers, the number of phagocytes in the lungs increases, producing more elastase. Genetic factors will also contribute to the quantity and effectiveness of this enzyme inhibitor produced in the lungs.
Emphysema is chronic disease as the damage caused is irreversible, causing low oxygen saturation in blood and abnormally high CO2 levels. This causes symptoms such as fatigue, shortness of breath and ventilation is quicker than usual.