The inflammations of the lung vary considerably according to cause, distribution, and the structures specially affected. The irritant which leads to the inflammation may have its seats primarily in the bronchi, in the lung alveoli, or in the pulmonary arteries. In the first case it will probably happen that the agent will affect certain bronchi and their connected alveoli so as to produce a Lobular distribution. In the second case there may be a general diffusion over a wide tRact of lung, such as a whole lobe or more, so as to give a Lobar distribution, whilst in the third case there is likely to be an Embolic distribution.

The character of the inflammation will depend on the nature of the irritant as well as on its distribution. We have acute inflammations, with excessive exudation, sometimes going on to suppuration; and we have chronic inflammations with new-formation of connective tissue. We have also inflammations mainly affecting the lining membranes of bronchi and alveoli, and others involving the deeper structures. In nearly all inflammations the epithelium of the alveoli is more or less-involved. In acute inflammations it is soon shed, while in the chronic forms it proliferates and yields large cells (catarrhal cells) which may accumulate in the alveoli.'

The chief forms of inflammation may be considered under four headings, namely, acute lobar pneumonia, acute broncho-pneumonia, embolic pneumonia, and chronic or interstitial pneumonia. In phthisis pulmonalis many of the lesions are inflammatory, but, as we have here a true tuberculosis, the inflammatory manifestations will be considered along with the tubercular.