Discuss the condition and critique the post written about the following case stu

Discuss the condition and critique the post written about the following case study. Citations: At least one high-level scholarly reference in APA from within the last 5 years
A 19-year-old presents with a deep laceration on the left leg. After sutures are placed the patient is discharged.
The healing of a wound is an intricate process that involves inflammatory mediators and cells interacting with each other. At the point when an injury occurs on our bodies, the healing process begins to take place. When we read into our textbook, Dlugasch & Story (2021) state that the wound healing process occurs in the following stages: the hemostasis, inflammatory, proliferative, and maturation phase.
Following an injury on the skin, vasoconstriction is activated, and hemostasis occurs. During the phase of vascular constriction, platelets are formed, which releases inflammatory markers and cytokines and fibrinolysis. This process then sends signals to start the inflammatory response. It activates inflammatory cells to promote angiogenesis, thrombosis, and epithelialization. Neutrophils, leukocytes, and macrophages migrate toward the wound using the bloodstream. They proceed to clear the damage of foreign bodies and consume the bacteria and dead tissue, leading to pus formation. Macrophages engulf and ingest debris and bacteria through phagocytosis, and they also produce growth factors that aid in the healing of the wound (Demidova-Rice et al., 2012). The end of the inflammatory phase is accompanied by apoptosis of inflammatory cells, which occurs gradually within a few days after the wound. The proliferative phase of healing begins when fibroblast cells enter the area of the wounded tissue. In collagen deposition, the fibroblast cells produce collagen in the wound site that forms connective skin tissue that aids in replacing the fibrin from before the injury (Demidova-Rice et al., 2012). Lastly, maturation is the migration of fibroblasts elastin and collagen to form granulation tissue. Granulation tissue is essential in remodeling, wound healing, and maturation. Depending on the extent of the laceration, the recently created skin and scar tissue can return to 50-80% of their original function (Demidova-Rice et al., 2012).
Williams & Fatima (2021) communicated that the focal aggregate of immune cells is granuloma, developed by the body in reaction to a repeated inflammatory stimulus. Granulomas form in an attempt to isolate and contain the infection. They are made up of macrophages and lymphocytes (Dlugasch & Story, 2021). Occasionally more macrophages are recruited when the initially activated macrophages could not remove the cause of inflammation. This triggers a chronic inflammatory reaction where collective macrophages surround infectious pathogens and stimulate lymphocytes’ release (Williams & Fatima, 2021). In a deep laceration, this is noteworthy because, without the protection provided by macrophages and lymphocytes, an additional infection could ensue. It would be difficult for the wound to heal, but it could lead to something more severe like sepsis. Granulation tissue plays an essential role in remodeling the extracellular matrix in an injury (Demidova-Rice et al., 2012). Granulation tissue is also where the fibroblasts are found that help bring the edges of the dermis together to heal the wound (Demidova-Rice et al., 2012).
The disorder known as graft host disease is an immune condition that usually happens following transplant procedures like bone marrow transplants used to treat blood cancers. The pathophysiology of GVHD is a three-step process: tissue damage to the recipient, donor T-cell activation, and cellular and inflammatory markers (Ferrara & Reddy, 2006). A study states that a donor’s immune cells view the recipient’s tissues as a foreign body, which triggers graft host disease (Saito et al., 2020). What happens is “the immunocompetent graft cells recognize the host cells as foreign due to the host having antigens that are not on the graft and organize a cell-mediated (primarily T-cell) attack. The host is usually immunocompromised and unable to fight the graft cells’ actions.” (Dlugasch & Story, 2021).
References
Demidova-Rice, T. N., Hamblin, M. R., Herman, I. M. (2012). Acute and impaired wound healing: pathophysiology and current methods for drug delivery, part 1: normal and chronic wounds: biology, causes, and approaches to care. Advances in skin & wound care, 25(7), 304–314. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428147/
Dlugasch, L., & Story, L. (2021). Applied pathophysiology for the advanced practice nurse. Burlington, MA: Jones & Bartlett Learning, LLC.
Saito, A., Ichimura, Y., Kubota, N., Tanaka, R., Nakamura, Y., Fujisawa, Y., … & Okiyama, N. (2020). Interferon-γ-stimulated apoptotic keratinocytes promote sclerodermatous changes in chronic graft-versus-host disease. Journal of Investigative Dermatology.
Ferrara, J., & Reddy, P. (2006, January). Pathophysiology of Graft-versus-host Disease. Semin Hematol: DOI: 10.1053/j.seminhematol.2005.09.001
Williams, O., & Fatima, S. (2021, February 17). Granuloma. StatPearls: https://www.ncbi.nlm.nih.gov/books/NBK554586/
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