A. Acute Inflammation

1. General a. Acute inflammation is an immediate response to injury b. Short duration c. Cardinal signs of inflammation i. Rubor (redness)

iii. Himor (swelling)

v. Functio laesa (loss of function)

2. Hemodynamic changes a. Initial transient vasoconstriction b. Massive vasodilatation mediated by histamine, bradykinin, and prostaglandins c. Increased vascular permeability i. Chemical mediators of increased permeability

■ Vasoactive amines, histamine, and serotonin

• Bradykinin, an end-product of the kinin cascade

ii. Mechanism of increased vascular permeability

■ Endothelial cell and pericyte contraction » Direct endothelial cell injury

• Leukocyte injury of endothelium d. Blood flow slows (stasis) due to increased viscosity, allows neutrophils to marginate

B. Neutrophils

1. Important cells in acute inflammation a. Neutrophils i. Synonyms: segmented neutrophils, polymorphonuclear leukocytes (PMN)

ii. Primary (azurophilic) granules

• Myeloperoxidase

• PhosphoUpase A2

• Acid hydrolases


Important components of acute inflammation

• Hemodynamic changes

• Neutrophils

» Chemical mediators


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