Inflammation
Dr. Cándido L. Otero is a retired pathologist in Orlando, Florida. Dr. Otero is a doctor who specializes in the study of bodily fluids and tissues. As a pathologist, Dr. Otero did two Fellowships, the first Fellowship was Cytopathology, the study of the cell, at Shans Jacksonville, Florida and the second Felllowship, Oncological... more
Inflammation is a response to injury of vascularized tissue. This tissue inflammation response could be classified as acute or chronic. Acute response is composed of three major reactions which are increase blood flow and vascular diameter if the vessels, microvascular changes permitting extravasation of blood plasma proteins and leukocytes to produce the inflammatory exudate, and leukocytes accumulation at the site of tissue injury. The classic sign of inflammation are heat (color), redness (color), edema (tumor), and pain (dolor).
There are vascular changes that occurs in the process that are increase flow and caliber of the vessels. At the beginning, there is vasoconstriction of the vessels around the injury site followed by vasodilation increasing the blood flow. This process causes redness in the injury area. Subsequently, blood stasis occurs due to the vasodilation permitting permeability of the the plasma proteins and leukocytes to confine the area of tissue injury. This reaction causes edema.
The permeability and normal fluid exchange depend mainly on the Starling's law and a normal endothelial cell wall. It is compose of two forces, the hydrostatic pressure (move fluid out of the vessels), and the plasma colloid osmotic pressure (move the fluid into the vessels). Inflammation is the results of an increase hydrostatic pressure and a decrease of the osmotic pressure.
In reality, there are six common mechanism that causes edema or inflammation of the endothelial cells. They are the endothelial cells contraction in venules, producing a gap between cells to create a leak from the vessels, and leading to protein plasma and leukocytes infiltration to tissue. This is most commonly produced by histamines. another reaction is caused by an endothelial retraction due to the cytoskeletal and cell junction organization. They results in widened inter-endothelial junctions. It is a delayed, long live response that is produced by cytokines.
Direct endothelial injury can cause endothelial cell necrosis and rupture affecting all levels of microcirculation including arterioles venules, and capillaries. This reaction provoke a sustained lineage in the area if injury.
Leukocyte-mediated endothelial injury resulting from the aggregate of leukocytes, adhesion to the endothelial cells and immigration across those endothelial cells. they cause release of toxins (oxygen radicals), proteolytic enzymes, causing damage and resulting in increase permeability of plasma substances . Increase transcytosis through vacuoles and vesicles. Also, leakage through the regenerating capillaries. Leukocyte extravasation and phagocytosis are also occurring at the same time, and is an important function of the inflammatory process. After encapsulation and digestion of the toxic microorganism or substance, the process of repair continues.
