Discursion Involving Inflammation Tissue Repair and Wound Healing Term Paper

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1) Inflammation, Tissue Repair, and Wound Healing

Case study on a 6-year old

Six-year-old, Carlton, suffered a deep gash on his foot when playing with his mom along the beachside. His mom washed the injured foot and took him home. The next day, Carlton’s foot worsened, with the gash growing pink, inflamed, warm and painful. So his mom put gauze on the wound before taking him to their community healthcare center.

· 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?

An injured tissue starts healing instantly. Tissue destruction directly injures numerous soft tissue cells which leads to metabolism alteration, with chemical mediator liberation initiating inflammatory reaction (Tissue Response to Injury, n.d). The body’s intrinsic defense mechanism mediates acute inflammatory reaction against pathogen invasion at the skin’s entry portal or systemically in case of infection of internal organs, propagating inflammation. Acute inflammatory reaction leads to the creation of a harmful microenvironment through increased leucocyte and plasma movement (particularly granulocytes) between the blood and injured tissues, for localizing and destroying specific pathogens and initiating healing. It propagates inflammation, which forms part of a complex vascular tissue reaction to all harmful stimuli (like damaged cells or invading pathogens). As such, acute inflammation represents a stereotyped primary cellular and biochemical reaction occurring only in vascularized tissues where microbial pathogens and other harmful stimuli cause cell invasion, injury, or death. Further, its mediators include a torrent of biomedical occurrences furthering and maturing acute inflammatory reaction involving the immune and vascular systems, and several cells in the affected tissue.

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Acute inflammation’s key signs on the skin include swelling, redness; warmness; function loss; and pain. Acute internal organ inflammation might not produce all aforementioned key signs (e.g., pain may occur only if the inflamed spot has sensory nerve endings). Meanwhile, systemic inflammation impacts all body organs, manifesting as general infection (marked by pyrexia, cardiovascular and hematological changes, intensified metabolic functioning, and impaired renal, brain and liver function) (Berg, 2014).

· What are the immunologic events that are happening at the local level during Carlton’s acute inflammatory response?

Leukotrienes, cytokines and histamine are the chemical mediators vital to limiting exudate extent and, hence, extent of swelling, following injury. Histamine, which is secreted by damaged mast cells, results in vasodilation, increasing cell permeability because of endothelial cell swelling and separation. Prostaglandins and leukotrienes cause margination, where leukocytes (macrophages and neutrophils) stick to cell walls. Further, they improve local cell permeability, thereby impacting fluid, neutrophil, and protein passage across cell walls through diapedesis for forming exudate within extravascular spaces. Hence, active hyperemia and vasodilation prove critical to plasma (exudate) formation and to the supply of neutrophils to damaged regions. With increased swelling and extravascular pressure, lymphatic and vascular flow decreases. The extent of swelling is associated directly with vessel damage levels. Cytokines, especially interleukin and chemokines, largely regulate leukocyte traffic, facilitating phagocyte attraction to the inflammation site. In response to chemokine presence, leukocytes and macrophages move to the inflammation….....

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