NR507 Week 6 Discussion Urticaria

1. Discuss the likely cause of the patient’s urticaria.
2. Describe the cellular mechanism of urticaria and how it leads to the signs and symptoms experienced by the patient.
3. Describe the relationship between the patient’s symptoms and the concept of inflammation.
4. What pharmacological and non-pharmacologic treatment options are available?
5. Discuss the complications of urticaria.
6. What teaching would be appropriate to provide the parent and child about urticaria?

Support your response with at least one current evidence based resource.

Example Approach

The primary cells that are involved in the initiation of urticaria are mast cells that are located in and around the dermis and become activated by specific immunoglobulin antibodies such as immunoglobulin E (IgE), immunoglobulin M (IgM), or immunoglobulin G (IgG) (Fine & Bernstein, 2016).  Mast cells are leukocytes that originate from the bone marrow and mature in mucosal and epithelial tissues throughout the body by the influence of stem cell factors and various cytokines that are secreted by endothelial cells and fibroblasts (Krystel-Whittemore, Dileepan, & Wood, 2015).  Mast cells play a pivotal role in the regulation of normal physiological processes and disease states throughout the body.  Some examples of physiological processes and disease states that mast cells contribute to include homeostasis, vasodilation, tissue repair, angiogenesis, innate immunity, adaptive immunity, immune tolerance, allergies, allergic reactions, asthma, anaphylaxis, inflammation, urticaria, Crohn’s disease, autoimmune diseases, mastocytosis, cardiovascular diseases, and cancers (da Silva, Jamur, & Oliver, 2014).

In urticaria, mast cells become activated by IgE antibodies that bind to IgE receptors on the surface of mast cells and results in signaling of secretion of cytokines and membrane phospholipids as well as degranulation of mast cells and the release of histamines, chemotactic factors, and proteases, which contribute to the initiation of inflammation, wheals, and pruritus seen in urticaria (Moon, Befus, & Kulka, 2014).  At the initiation of urticaria, inflammation activates other cells to be released and in return more proinflammatory mediators serve to recruit and activate other cell types, such as basophils, neutrophils, eosinophils, and T-lymphocytes, thereby amplifying the progression and duration of urticaria (Jain, 2014).  What I found interesting during my readings and studying was what differentiates the results of urticaria from angioedema.  While urticaria and angioedema have very similar underlying pathophysiologic mechanisms and require histamines and other vasodilatory mediators to be released from mast cells and basophils in order to develop, if the release occurs in the dermis, it will result I urticaria, whereas if the release occurs in the deeper dermis and subcutaneous tissues, it will result in angioedema (Schaefer, 2017).

References

da Silva, E. Z., Jamur, M. C., & Oliver, C. (2014). Mast cell function: A new vision of an old cell. Journal of Histochemistry and Cytochemistry, 62(10), 698-738. doi:10.1369/0022155414545334

Fine, L. M., & Bernstein, J. A. (2016). Guideline of chronic urticaria beyond. Allergy, Asthma & Immunology Research, 8(5), 396-403. doi:10.4168/aair.2016.8.5.396

Jain, S. (2014). Pathogenesis of chronic urticaria: An overview. Dermatology Research and Practice, 2014(674709). doi:10.1155/2014/674709

Krystel-Whittemore, M., Dileepan, K. N., & Wood, J. G. (2015). Mast cell: A multi-functional master cell. Frontiers in Immunology, 6(620). doi:10.3389/fimmu.2015.00620

Moon, T. C., Befus, A. D., & Kulka, M. (2014). Mast cell mediators: Their differential release and the secretory pathways involved. Frontiers in Immunology, 5(569). doi:10.3389/fimmu.2014.00569

Schaefer, P. (2017). Acute and chronic urticaria: Evaluation and treatment. American Family Physician, 95(11), 717-724. Retrieved from https://www.aafp.org/2017/0601/p717.html