Essay on Acute Inflammation

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Acute Inflammation
The survival of all organisms requires that they eliminate foreign invaders, such as infectious pathogens, and damaged tissues. These functions are mediated by a complex host response called inflammation.
Definition of inflammation Inflammation is fundamentally a protective response, the ultimate goal of which is to rid the organism of both the initial cause of cell injury (e.g., microbes, toxins) and the consequences of such injury (e.g., necrotic cells and tissues)
The process of inflammation is usually described by the suffix “itis”

[The components of the inflammatory reaction that destroy and eliminate microbes and dead tissues are capable of also injuring normal tissues. Therefore, injury may accompany
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As stasis develops, leukocytes, primarily neutrophils, accumulate along the vascular endothelium, stick to the endothelium and eventually escape into the interstitial tissue via the vascular wall.

Normal fluid exchange and microvascular permeability are critically dependent on an intact endothelium. How then does the endothelium become leaky in acute inflammation?
Following mechanisms have been proposed: 1. Gaps due to endothelial contraction Endothelial cell contraction leads to intercellular gaps in venules. It is the most common form of increased vascular permeability and is elicited by histamine, bradykinin, leukotrienes and many other classes of chemical mediators. Its action is fast and short lived. 2. Direct Injury Direct endothelial injury results in vascular leakage by causing endothelial cell necrosis and detachment. This effect is usually seen after severe injuries like burns, toxins and chemicals. Venules, arterioles, and capillaries can all be affected depending on site of injury. Its action is fast and may be long lived (hours to days).

3. Leukocyte-dependent injury Leukocyte dependant endothelial injury usually happens in venules and pulmonary capillaries,

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