INFI^AMMATION. PHI.OGOSIS. PHI^EGMASIA. 



Definitions. Relations to active hypersemia. Redness. Heat. Pain. 

 Swelling. Forms : in vascular tissues : in non-vascular. Changes in tissue 

 elements. Death of cells. Cloudy swelling. Granular degeneration. Cell 

 proliferation. Karyokinesis. Embryonic cells. Amoeboid functions. 

 Migration of leucocytes. Red cells escaping. Changes in innervation. 

 Vaso-motor disorders. Fever. Changes in circulation. Contraction of 

 capillaries, dilatation, rapid flow, tardy flow, stasis, oscillations, thrombus, 

 collecting of white globules in periphery of current, migration of leucocytes, 

 blood plates, and red globules, massing of red globules, exudation, soften- 

 ing of the capillary walls, nutrient artery more rigid and transmits more 

 blood, heart contracts more forcibly, increase of fibrine, increase of waste 

 products. Buffy coat, physiological causes. Haemolysis Microbes. Pto- 

 maines. Toxins. Chemiotaxis. Phagocytosis. Polynuclear and mononuclear 

 leucocytes. Exudates, unlike dropsies. Mucous exudate, Serous exudate. 

 Fibrinous exudate. Blood exudations. Croupous exudation. Chyliform 

 exudate. Results and Products. Resolution. Deletescence. Metastasis. 

 New formations. Suppuration. Pus microbes. Pus. Healing by ist in- 

 tention. Healing by 2nd intention, granulation. Granule corpuscles. In- 

 terstitial neoplasia. Degenerations in lymph. Fatty degeneration, 

 melanotic. Softening. Ulceration. Gangrene. 



Inflammation has been variously defined as ' ' perverted nutri- 

 tion, " as a " protective reaction of the organism against irritant 

 agents' ' and in other terms that express at once too much and too 

 little, without actually defining the morbid process. Older defini- 

 tions dealt with the manifest disorders of circulation", of innerva- 

 tion or of tissue change too often exalting the importance of one 

 set of changes at the expense of another and thus giving in the 

 main a one sided view of the morbid process. 



Some modern bacteriologists are inclined to refuse the title to 

 any morbid process that is not caused by the presence of microbes 

 or their toxic products. To them the changes occurring in an 

 aseptic wound or in a simple fracture in process of healing are 

 purely reparatory and partake no more of the nature of inflamma- 

 tion than do the developmental changes in the growing embryo. 

 While to a large extent true, this exclusive view implies excep- 

 tions, since if the chemical poisons derived from the bacteria can 

 ■develope inflammation, the same must be admitted as possible for 

 chemical irritants drawn from other sources. 



39 



