Serum sickness proteins to form immune complexes. These complexes precipitate, enter the walls of blood vessels, and activate the complement cascade, initiating an inflammatory response and consuming much of the available complement component 3 (C3). The result is a leukocytoclastic vasculitis. This results in hypocomplementemia, a low C3 level in serum. They can also cause more reactions resulting in typical symptoms of serum sickness. Serum sickness can be developed as a result of exposure to antibodies derived from animals. These sera or antitoxins are generally administered to prevent or treat an infection or envenomation. Some of the drugs associated with serum sickness
Sweat gland cell are actually pinched off, and disintegrate later to excrete sweat. In both apocrine and eccrine sweat glands, the sweat is originally produced in the gland's coil, where it is isotonic with the blood plasma there. When the rate of sweating is low, salt is conserved and reabsorbed by the gland's duct; high sweat rates, on the other hand, lead to less salt reabsorption and allow more water to evaporate on the skin (via osmosis) to increase evaporative cooling. Secretion of sweat occurs when the myoepithelial cell cells surrounding the secretory glands contract. Eccrine sweat increases the rate of bacterial