Emphysema
Emphysema is a type of chronic obstructive lung disease. It is often caused by exposure to toxic chemicals or long-term exposure to tobacco smoke.
In normal breathing, air is drawn in through the bronchial passages and down into the increasingly fine network of tubing in the lungs called the alveoli, which are many millions of tiny sacs surrounded by capillaries. These absorb the oxygen and transfer it into the blood. 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.
After a prolonged period, hyperventilation becomes inadequate to maintain high enough oxygen levels in the blood. The body compensates by vasoconstricting appropriate vessels. This leads to pulmonary hypertension, which places increased strain on the right side of the heart, the one that pumps unoxygenated blood to the lungs, fails. The failure causes the heart muscle to thicken to pump more blood. Eventually, as the heart continues to fail, it becomes larger and blood backs up in the liver.
Emphysema occurs in a higher proportion in patients with decreased alpha 1-antitrypsin (A1AT) levels (alpha 1-antitrypsin deficiency, A1AD). In A1AD, inflammatory enzymes (such as elastase) are able to destroy the alveolar tissue (the elastin fibre, for example). Most A1AD patients do not develop clinically significant emphysema, but smoking and severely decreased A1AT levels (10-15%) can cause emphysema at a young age. In all, A1AD causes about 2% of all emphysema. However, smokers with A1AD are in the highest risk category for emphysema.