The Case: Carlton, who is a six-year-old boy, was having fun on a sandy beach with his mother. He started to run along the shoreline when he, unfortunately, stepped on a shell with a sharp edge, causing him a deep cut on his foot. His mother took the initiative to wash his foot using the lake water and put on his sports shoes to take him home. A day later, Carlton's injured foot seemed worse from the effect of the accident. The gash/wound was red and very painful. The foot was also warm when touched and appeared swollen. Carlton's mother put added to it some gauze and organized to take him to the local community health care.
#1 What is the physiologic technique causing the wound to become swollen, red, hot, and painful? How is this different from the inflammatory reaction that may occur in an internal organ?
Wounds swell, become red, hot, and painful as part of the cardinal acute inflammation process. The feeling of warmth and erythema is due to the vasodilation effects. Inflammation of wound can last from a few minutes to a number of days and usually occurs due to exudation and high vessel permeability that increases plasma and fluid components. The emigration of leucocytes, especially neutrophils also increase in the wounded part, that is, in the extravascular tissue. Therefore, the physiological changes are as a result of high inflammation response and quick vascular changes like vasodilation and increase in capillary permeability, increase in inflammatory cells (neutrophils), which are inflammatory mediators that result into the symptoms such as those observed in Carlton's wound. The primary cells of inflammation include the endothelial cells, monocytes, platelets, and neutrophils. The endothelial cells release the antithrombic and antiplatelet agents that maintain the patency of vessels. They also produce the vasoconstrictors and vasodilators that act as regulators to the blood flow. The activated platelets produce potential inflammatory agents and mediators, hence alters the adhesive, chemotactic, and proteolytic nature of the endothelial cells, and increase vascular permeability (Guo & DiPietro, 2010).
Also, the process of inflammation is the same in the entire body. It entails a release of cytokines chemicals, which attract the molecules of inflammation like TNF alpha. This molecule, as well as other similar ones, activate the immune systems to the cells, causing the blood to dilate and stimulate the pain receptors (Guo & DiPietro, 2010).
The internal inflammation process has a similar effect. The lymph nodes engagements can cause the inflammation of the internal tissues. For instance, myocarditis (inflammation of heart), which can cause fluid retention and chest pain; nephritis (the kidney inflammation), which may result in kidney failure and high blood pressure; large intestines' inflammation (colitis), which may lead to diarrhea and cramps; eye inflammation (uveitis or iritis), which may lead to decreased vision and eye pain; muscles inflammation (polymyositis), which may cause weakness and achiness; blood vessels inflammation or vasculitis, which may result in headaches, rush, and internal damage of organs; and inflammation of lungs (known as brocholosis), which cause asthma attack and breathing problems/shortness (Gantwerker & Hom, 2012).
The internal inflammation is, however, slightly different. The heat is not as rampant as in the external inflammation (due to the maintenance of the internal temperature at the level of homeostasis), and the pains are apparent at the time when the stretch receptors are stimulated (Akira & Kawai, 2012).
#2 What are the immunologic occurrences that are happening at the foundational level during Carlton's severe inflammatory response?
In Carlton's case, that is, an acute reaction, the white blood cells that circulate in the blood around the wound would trigger the process known as leukocytosis, which aids in the immunity response. The white blood cells appear in the injury site due to chemotaxis. The emigration and margination are the events that cause the leukocytes circulation in the injured site. The movement of the leukocytes is mediated or regulated by the tissue swelling and reduced motion of the blood flow (Gantwerker & Hom, 2012).
The predominant cells in the acute cell injury or wound are the neutrophils. The phagocytic leucocytes that will be present just hours after the injury are the neutrophils and macrophages. However, the primary phagocyte to arrive at the inflammation site within ninety minutes of injury is the neutrophil, and it is often known as the polymorphonuclear neutrophil (PMN) or the segmented neutrophil. The neutrophil rises greatly in the blood at the time of inflammation, more particularly the bacterial prone infections (Koh & DiPietro, 2011). The lifespan of this leucocyte is only 10 hours, and therefore, the movement of the white blood cells are extremely high, hence leukocytosis. Increase in demand for neutrophils causes the bone marrows to release the immature neutrophils (phagocytes), which are known as the bands. The mononuclear cells take 24 hours to arrive at the affected site (the wound) and in 48 hours, the macrophages and monocytes become the predominant cells around the wound (Koh & DiPietro, 2011).
The body immune system responds very fast to injuries and infections that cause tissues to sore and turn red. The natural killer cells, the macrophages, and neutrophils provide early and quick response to eliminate the harmful stimuli (Koh & DiPietro, 2011). The immune responses that are adaptive require the microbial antigens mediated by lymphocytes and therefore serve as an amplifier to the acute inflammation. While the inflammation may at times be beneficial, the severe ones can lead to a systematic inflammation reaction syndrome, which can cause organ shock, injury, and sometimes death in its most extreme form.
#3 Nutrition has an important role in the wound the healing process. What stages of the injured body healing would be affected by a lack of enough vitamins A and C?
Nearly all the aspects of wound healing and stages would be affected by the lack and deficiency of vitamins C and A. Most vitamins are very crucial cofactors the body functions. However, vitamins A and C play a critical role in the wound healing process. Collagen synthesis requires vitamin C, and in the deficiency of the same, the wounds would not heal properly, and the previous wounds may fall apart (Stone, 2017). The intake of a lot of vitamin C containing nutrients would rapidly improve the healing process to be normal. Vitamin C helps in collagen synthesis, replacement of blood tissues that damaged, and has the antidioxidizing agents that improve immune systems and protects against wounds. On the other hand, vitamin A has often been depicted to counteract the inflammatory effects of the corticosteroids medications and, therefore, helps in the reversing of the effects in people who experience chronic steroid therapy (Medlin, 2012). Also, from the Nutrition Institute, deficiency of vitamin A can increase the risk of infections on wounds as well as their delayed healing (Medlin, 2012).
Gantwerker, E. A., & Hom, D. B. (2012). Skin: histology and physiology of wound healing. Clinics in plastic surgery, 39(1), 85-97.
Guo, S. A., & DiPietro, L. A. (2010). Factors affecting wound healing. Journal of dental research, 89(3), 219-229.
Koh, T. J., & DiPietro, L. A. (2011). Inflammation and wound healing: the role of the macrophage. Expert reviews in molecular medicine, 13.
Medlin, S. (2012). Nutrition for wound healing. British Journal of Nursing, 21(Sup12), S11-S15.Stone, I. (2017). The Healing Factor-Vitamin C Against Disease: How to live longer and better (Vol. 2357). BoD-Books on Demand.
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