Carlton, a 6-year-old boy, was playing on a sandy beach with his mother. He began to run along the shoreline when he stepped on the sharp edge of a shell, giving himself a deep cut on his foot
His mother washed his foot in the lake and put on his running shoe to take him home. One day later, Carlton's foot looked worse. The gash was red and painful. The foot was warm to touch and appeared swollen. Carlton's mom put some gauze over the wound and prepared to take him to the local community health clinic.
What is the physiologic mechanism causing the wound to become red, hot, swollen, and painful? How is this different than the inflammatory response that might occur in an internal organ?
What are the immunologic events that are happening at the local level during Carlton's acute inflammatory response?
Nutrition plays an important factor in wound healing. What stages of wound healing would be affected by a deficiency in vitamins A and C?
Carlton's signs are typical of acute inflammation. Local vasodilation creates erythema and warmth. The edema is a result of increased vessel permeability and migration of exudate into the surrounding tissue. The engorgement of fluid at the area of injury contributes to the sensation of pain.
Visceral inflammation has a slightly different presentation: heat is less likely to occur because core temperature is preserved at a homeostatic level, and pain becomes apparent only when stretch receptors on the surfaces of the viscera are stimulated.
In an acute response, leukocytosis occurs to increase the number of circulating white blood cells to support the immune response. The movement of white blood cells to the site of injury occurs as a result of chemotaxis. Margination and emigration are the events that describe the movement of circulating leukocytes from the blood to the injured tissue; local blood stasis allows leukocytes to move to the perimeter of vessels and pass (or emigrate) through capillary walls. Neutrophils arrive early to phagocytose microbes and cellular debris. Monocytes travel in the blood and migrate to injured tissue where they become macrophages. These cells are capable of engulfing greater quantities of foreign material and are able to move to the lymphatic system, where they prime specific immunity.
While the components of nutritional intake are valuable to all stages of wound healing, some have more specific qualities. Both vitamin A and C assist collagen synthesis, but vitamin C has a direct influence on collagen assembly and the removal of by-products that result from collagen manufacturing. A deficiency in vitamin C would therefore affect the onset of the proliferation stage and the effectiveness of the remodeling phase where collagen production and lay down are critical. Vitamin A stimulates capillary growth and epithelialization. A deficiency in vitamin A would hinder angiogenesis in the inflammatory phase of wound healing and epithelialization in the latter component of the proliferation phase.
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