An inflammation may be triggered by several mechanisms. These include: — Noxious physical agents — Noxious chemical agents — Accumulated products of metabolism; — Immunologic tissue injury; — Tissue injury from infection; — Tissue necrosis. <ul><li>INFLAMACION </li></ul><ul><ul><ul><li>AGUDA </li></ul></ul></ul><ul><ul><ul><li>CRONICA </li></ul></ul></ul><ul><ul><ul><li>GRANULOMATOSA </li></ul></ul></ul>
2. Hemodynamic changes a. Initial transient vasoconstriction b. Massivevasodilatation mediated by histamine, bradykinin, and prostaglandins c. Increased vascular permeability i. Chemical mediators of increased permeability . Vasoactiveamines, histamine, and serotonin . Bradykinin, an end-product of the kinin cascade . Leukotrienes (e.g., LTC4,LTD4,LTE4) 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,allowsneutrophils to marginate
Figure 2-2 The major local manifestations of acute inflammation, compared to normal. (1) Vascular dilation and increased blood flow (causing erythema and warmth), (2) extravasation and deposition of plasma fluid and proteins (edema), and (3) leukocyte emigration and accumulation in the site of injury.
B. Neutrophils 1. Important cells in acute inflammation a. Neutrophils i. Synonyms:segmented neutrophils, polymorphonuclear leukocytes (PMN) ii. Primary (azurophilic) granules . Myeloperoxidase . Phospholipase A2 . Lysozyme . Acid hydrolases .Elastase . Defensins . Bactericidal permeability increasing protein (BPI)
iii. Secondary (specific) granules .Phospholipase A2 . Lysozyme . Leukocyte alkaline phosphatase (LAP) . Collagenase . Lactoferrin . Vitamin BI2 binding proteins b. Macrophages i. Acid hydrolases ii. Elastase iii. Collagenase
2. Neutrophil margination and adhesion a. Adhesion is mediated by complementary molecules on the surface of neutrophils and endothelium i. Step 1:at sites of inflammation, the endothelial cellshave increased expression of E-selectin and P-selectin ii. Step 2: neutrophils weakly bind to the endothelial selectins and roll along the surface iii. Step 3: neutrophils are stimulated by chemokines to express their integrins iv. Step 4: binding of the integrins firmly adheres the neutrophil to the endothelial cell
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