Pathophysiology, Adaption, Injury and Inflammation
Inflammation is a protective way of the body whenever there is cell injury. It is a way of removing the causative pathogen and what it can do to the body. Inflammation is an important step for the tissue repair. Inflammation has two phases that involve the vascular and cellular reaction. That is the reason why redness, swelling, tenderness in the area of injury occur and why a good blood supply is necessary for its healing to progress.
The process of tissue repair involves inflammation in the early process. Various cells and tissues participate in these events which include fluid and proteins of plasma, circulating cells, blood vessels and cellular and extracellular constituents of connective tissues. In the vascular reaction, the participative cells are the circulating cells that include neutrophils, basophils, eosinophils, lymphocytes and platelets. These circulating cells travel in the blood vessels toward the injurious part of the body where they proliferate and fight of the causative pathogen and perform antibody functions.
Blood vessels in the body also undergo changes during inflammation. These changes occur to maximize the movement of leukocytes, antibodies and platelets towards the injury site. It undergoes vasodilation, causing increase redness and heat because this process increases blood flow. The blood vessels become more permeable which causes the swelling or edema from the extravasated protein-rich fluid. This is a means of the body to bring the antibodies and other cells to the exact site of injury and perform their function. The changes in the blood vessels are mediated by a number of chemical mediators that cause this vascular leakage. They assert their function in the endothelial cells causing contraction, therefore letting the protein-rich, antibody containing fluid to escape toward the site of injury, and prevent further damage to the body.
Reference:
Kumar, Vinay, et. al. Robbin and Cotran Pathologic Basis of Disease. 7th ed. Philadelphia: Elsevier, 2005.
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