Chat with us, powered by LiveChat Carlton, a 6-year-old boy, was playing on a sandy - Writedi

Carlton, a 6-year-old boy, was playing on a sandy

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.  The physiologic mechanism causing Carlton’s signs and symptoms is anacute inflammatory process.Given the suddenness of Carlton’s signs and symptoms, injury on the beach and the site of this injury, it is likely his symptoms are the result of his injuredfootand his body is attempting to restore physiologic hemostasis. Rubor, swelling, heat, and pain are all the cardinal signs of inflammation(Grossman & Porth, 2013).There is a series of normal vascular changes occurring at the site of tissue injury that is meant to repair, restoreand protect injured tissue from microorganisms.Inflammatory mediators involved in this mechanism include complement, tumor necrosis factor alpha, vascular endothelial growth factor (VEGF), neutrophils, and serum amyloid(Grossman & Porth, 2013). These mediators are contributing to the redness, heat, swelling and tenderness.It is possible that the acute inflammatory process could be caused by tissue trauma and/or invasion of infectious microbes during tissue injury.How is this different than the inflammatory response that might occur in an internal organ?The inflammatory response of an internal organ is perceived and manifests differently.Carlton’s signs and symptoms are reminiscent of a local inflammatory response. Internal organ inflammation can result in systemic manifestations as mediators are not confined to small areas. When inflammation involves an internal organ , there is potential for activation of the acute-phase inflammatory response. Leukocyte counts are affected,the whole body may be feverish rather than a localized area, and physical signs like enlarged lymph nodes may be seen (Grossman & Porth, 2013). Sepsis and septic shock are also prominent systemic manifestations of inflammation. Pain during inflammation of internal organs is sensed as a result of activation of organ stretch receptorswith inflammation or enlargement (McKean, Ross, Dressler, Brotman, 2012)  What are the immunologic events that are happening at the local level during Carlton’s acute inflammatory response?The acute inflammatory response occurs before the adaptive immune response has time to kick in. It is nonspecific and generally meant to eliminate altered cells, microbes and antigens. The inflammatory phase happens in two phases: the vascular phase and the cellular phase.The vascular phase leads to vasodilation of localized small blood vessels. This allows rapid blood flow to the site then moves out of the vessels. Clotting of blood occurs as a result of the cascade of events leading to the complement pathway and blood flow begins to slow in the area. Slowed blood flow will help localize any possible infection. The resultant increased blood volume due to vasodilation causes the warmth and redness Carlton is experiencing. Increased microvascular permeability leads to loss of plasma proteins from the capillary intravascular space reducing osmotic pressure, thus causing intravascular fluid to also flow from the vascular space to surrounding tissue. This process explains Carlton’s pain caused by increased pressure from swelling.The cellular phase starts with delivery of granulocytes, including the most abundant of them called the neutrophils and monocytes, to the site. Granulocytes are part of the innate immune system. They are white blood cells (or leukocytes) that contain cytoplasmic granules. These leukocytes migrate from the within the vascular system to the extravascular space to the site of injury by margination, adhesion, transmigration and then chemotaxis for phagocytosis and killing of the target cell (Grossman & Porth, 2013). ReferencesGrossman, S. & Porth, C.M. (2013). Porth’s pathophysiology: Concepts of altered health states (9th ed.). Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams &Wilkins. McKean, S.C., Ross, J.J, Dressler, D.D.,Brotman, B.J.(2012). Principles and practice of hospital medicine. https://accessmedicine.mhmedical.com/book.aspx?bookid=496

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