中国医科大学病理学英文.pptxVIP

2. Mediators from plasma;2) Complement System:;C3a, 5a increase vascular permeability cause vasodilation by releasing histamine from mast cells C5a A powerful chemotactic agent for neutrophils basophils, eosinophils, monocytes Activates the lipoxygenase pathway of AA metabolism in monocytes, neutrophils → release of mediators ;3) Clotting and fibrinolytic system;ii) Factor Xa increased V permeability leukocyte exudation ② Activated fibrinolytic system C3 C3a increase v permeability vasodilation Fibrin to fibrin products: increase v permeability;Sources of mediators;3. Summary of inflammatory mediators;V. Types and morphology of  acute inflammation; Serous inflammation 1. Common sites loose CT, serosa mucosa and skin 2. Lesions: Serous exudation blood serum (main) secretion of mesothelial C LM albumin: 3~5% fibrin, neutrophils, epithelial cell;3. Common causes:;Serous inflammation of skin;The skin blister resulting from a burn or viral infection represents a large accumulation of serous fluid, either within or immediately beneath the epidermis of the skin ; Fibrinous inflammation;3. Favor sites and features;Diphtheria of trachea;Mucosa of colon is covered by exudates. Bran-like substances surface the mucosal folds Mucosa appears thickened due to edema Constitutes of the mixture of fibrin, mucus, injured tissue, neutrophils, RBCs, bacilli.;(2) Serosa fibrinous inflammation:;Fibrinous pericarditis. Pericardial cavity has been opened to reveal a fibrious pericarditis with strands of stringy pale fibrin between viseral and parietal pericardium. Deposits of fibrin on the pericardium. Fine villose