| Pathophysiology of Inflammation |  |
| Inflammation occurs in 3 distinct phases—acute, subacute, and chronic (or proliferative). The acute response to tissue injury occurs in the microcirculation at the site of injury. Initially there is a transient constriction of arterioles; however, within several minutes, chemical mediators released at the site cause relaxation of arteriolar smooth muscle, vasodilation, and increased capillary permeability. Protein-rich fluid then exudes from capillaries into the interstitial
space. This fluid contains many of the components of plasma, including fibrinogen, kinins, complement, and immunoglobulins that mediate the inflammatory response. The subacute phase is characterized by movement of phagocytic cells to the site of injury. In response to adhesion molecules released from activated endothelial cells, leukocytes, platelets, and RBC in injured vessels become sticky and adhere to the endothelial cell surfaces. Polymorphonuclear leukocytes such as neutrophils
are the first cells to infiltrate the site of injury. Basophils and eosinophils are more prevalent in allergic reactions or parasitic infections. As the inflammatory process continues, macrophages predominate, actively removing damaged cells or tissue. If the cause of injury is eliminated, acute inflammation may be followed by a period of tissue repair. Blood clots are removed by fibrinolysis, and damaged tissues are regenerated or replaced with fibroblasts, collagen, or endothelial
cells. However, inflammation may become chronic, leading to further tissue destruction and fibrosis. |
