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The basic pathologic changes of inflammation in the site of injury are alteration, exudation, and proliferation. 1. Alteration (1) Definition: The tissues or cells in the inflammatory site become degeneration and/or necrosis. (2) Causes and mechanism: Be damaged by inflammatory factors directly. Local blood circulation disturbance Be affected by inflammatory mediators. (3) Morphology Parenchyma cells: edema, fatty change, necrosis etc. Interstitium: edema, mucoid degeneration, fibrinoid degeneration, necrosis, etc. 2. Vascular changes (hyperemia and exudation) (1) Changes in vascular flow and caliber ① Changes in caliber Transient arteriolar constriction Persistent vasodilatation ② Changes in flow a. Initially rapid as a result of vasodilatation (active hyperemia) b. Slowing and disturbance of axial flow as a result of increased blood viscosity secondary to loss of plasma into the tissue (congestion and edema) ③ Changes in the endothelium Increased vascular permeability leading to the escape of a protein-rich fluid (exudates) into the interstitium. a. Endothelial cell contraction, or increased transcytosis across the endothelial cytoplasm. b. Direct endothelial injury, resulting in endothelial cell necrosis and detachment c. Leakage from regenerating capillaries (2) Fluid exudate Normally the walls of small blood vessels are freely permeable to water and crystalloids but relatively impermeable to plasma proteins. The formation of protein-rich fluid exudates is facilitated by separation of the intercellular junction of the endothelium. The fluid exude carries into the inflamed area the following important constituents: ① Serum bactericidal factors a. Antibodies which act by opsonising bacteria prior to phagocytosis and by neutralizing exotoxins b. Components of the complement system ② Interferon: a non-specific antiviral agent ③ Fibrinogen which is converted to fibrin. Fibrin is important in providing: a. Cement subs
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