Final answer:
Centriacinar emphysema is primarily observed in smokers and is caused by the destruction of alveolar walls, leading to reduced gas exchange and breathing difficulties. It is a form of COPD, and individuals with a₁ antitrypsin deficiency are also at increased risk of developing this disease.
Step-by-step explanation:
Centriacinar emphysema is most commonly observed in individuals who have a history of smoking. This form of emphysema involves the central or proximal parts of the acini, which are the smallest respiratory units of the lungs composed of air ducts and alveoli. In centriacinar emphysema, the alveoli are destroyed due to the breakdown of their walls, leading to decreased gas exchange and shortness of breath.
People with an a₁ antitrypsin deficiency are at a higher risk of developing emphysema because a₁ antitrypsin acts as an important inhibitor of neutrophil elastase. Without enough of this inhibitor, neutrophil elastase can destroy the elastin in the alveolar walls, contributing to emphysema.
Emphysema is a type of chronic obstructive pulmonary disease (COPD), and its development is closely linked to the breakdown of connective tissue in the lungs. This deterioration diminishes lung elasticity and capacity, causing air to become trapped in the alveoli and hampering efficient gas exchange. Primary risk factors include smoking and genetic factors such as a₁ antitrypsin deficiency.