text: what is the pathophysiology of emphysema?   what do you need this for?  background: the word emphysema is derived from greek and means "to blow into," hence "air containing" or "air inflated." the term emphysema was initially applied to air within the tissues (ie, subcutaneous emphysema). in 1721, ruysch described large air spaces in lung specimens of humans as emphysema. in 1799, matthew bailey subsequently provided the first clear illustration and description of emphysema as enlarged air spaces. laennec contributed considerably to the understanding of emphysema and recognized that emphysema is associated with chronic bronchitis. in 1939, cournand introduced the notion that emphysema causes airflow obstruction.  emphysema is defined as abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of the walls and without obvious fibrosis. the 3 described morphological types of emphysema are centriacinar, panacinar, and paraseptal.  the first type, centriacinar emphysema, begins in the respiratory bronchioles and spreads peripherally. also called centrilobular emphysema, this form is associated with long-standing cigarette smoking and predominantly involves the upper half of the lungs.  the second type is panacinar emphysema, which destroys the entire alveolus uniformly and is predominant in the lower half of the lungs. this type of emphysema generally is observed in patients with homozygous alpha1-antitrypsin (aat) deficiency. in people who smoke, focal panacinar emphysema at the lung bases may accompany centriacinar emphysema.  the third type, distal acinar emphysema (also known as paraseptal emphysema), preferentially involves the distal airway structures, alveolar ducts, and alveolar sacs. the process is localized around the septae of the lungs or pleura. although airflow frequently is preserved, the apical bullae may lead to spontaneous pneumothorax. giant bullae occasionally cause severe compression of adjacent lung tissue.  pathophysiology: emphysema commonly presents with chronic bronchitis, and the pathological changes occur not only in the lung parenchyma but also in the large and small airways. chronic bronchitis is characterized by mucous gland enlargement, focal squamous metaplasia, ciliary abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, and bronchial wall thickening. the respiratory bronchioles display a mononuclear inflammatory process, lumen occlusion by mucus plugging, goblet cell metaplasia, smooth muscle hyperplasia, and distortion due to fibrosis. these changes, combined with loss of supporting alveolar attachments, cause airflow limitation by allowing airway walls to deform and narrow the airway lumen.  emphysema, on the other hand, is characterized by focal destruction limited to the airspaces distal to the respiratory bronchioles. both emphysematous destruction and small airway inflammation often are found in combination in individual patients. when emphysema is moderate or severe, loss of elastic recoil, rather than bronchiolar disease, is the mechanism of airflow limitation. by contrast, when emphysema is mild, bronchiolar abnormalities are most responsible for the airflow limitation. although air flow obstruction in emphysema is virtually irreversible, bronchoconstriction due to inflammation accounts for a limited amount of reversibility.  pathogenesis  pathologically, various lesions may be found in the airways of emphysematous lungs. some are the lesions of chronic bronchitis; others affect the small airways. the vascular changes develop simultaneously. abnormal longitudinal muscle appears in the intima of arterioles and arteries; these may show intimal fibrosis and thickening of the muscular media. enlargement of bronchial arteries and veins occurs in some patients. bronchial venous enlargement may cause shunting of systemic venous blood to the left atrium.  cigarette smoking  cigarette smoking leads to neu