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3 main components of acute inflammation

1) Dilation of vessels to allow increased blood flow
2) Structural changes in microvascular to permit migration of plasma proteins and leukocytes into tissue
3) Emigration of leukocytes and their accumulation at the site of injury, and their activation to eliminate the harmful agent


4 stimuli for acute inflammation

-foreign material
-tissue necrosis (e.g. from hypoxia, injury, etc)
-immune reactions (hypersensitivity)


Examples of opsonins

IgG, complement (especially C3b), mannan-binding lectin


Types of mediators of inflammation

1) Cell-produced ones (e.g. from neutrophils, macrophages, endothelial cells, and other cells)
2) Plasma-derived mediators (e.g. complement, kinins) produced by the liver that must be activated by cleavage once in the circulation


Possible outcomes of acute inflammation

-complete resolution
-healing by fibrosis
-progression to chronic inflammation


When might a fibrinous exudate occur?

-large vascular leaks (permitting migration of fibrin)
-local procoagulant stimulus (e.g. cancer)


Causes of chronic inflammation

-chronic infection
-immune mediated disease (both prolonged immune reaction against microbes and autoimmune reponses)
-chronic exposures to toxins (e.g. silica)