Wk1 Discussion 6501
The 16-year-old boy in the discussion scenario presented to the clinic with specific complaints that are common in Strep Throat infection. He complained of a sore throat for 3 days. He denied recent cold, influenza, ear infections, or allergies. Redness, +3 tonsil edema, positive anterior and posterior cervical adenopathy, low-grade temperature, and pharyngeal exudate were noted by the practitioner on the exam. A diagnosis of Strep Throat was confirmed by a positive rapid strep throat culture. Penicillin was prescribed.
Strep Throat is not a genetic disorder, but an infectious one caused by A. Streptococcus bacteria. It is not gender-specific. Strep throat most commonly occurs during the late winter or early spring months as a direct result of people being grouped closely together indoors allowing it to spread easily via direct contact (American Academy of Family Physicians, 2016).
The patient’s symptomology and positive culture confirm that he was infected by A. Streptococcus bacteria. His body’s response to A. Streptococcus bacteria is the body’s initial inflammatory response to this bacteria; redness, swelling, heat, and pain (Kahn Academy, 2010). The patient’s anaphylactic response to penicillin was mediated by ‘IgE antibodies that are produced by the immune system in response to an environmental allergen’ (Justiz-Vaillant & Zito, 2019). These allergens include pollens, animal dander, dust mites or fungi (Justiz-Vaillant & Zito, 2019). The patient’s anaphylactic response to penicillin, a fungus, was unknown prior to its administration.
When a bacterial infection occurs, the body releases mast cells that are activated by chemokines to attack the infection (Kahn Academy, 2010). Histamine is released causing vasodilation (Kahn Academy, 2010). Endothelial cells are pushed apart and capillaries become larger and dilated, causing swelling to occur (Kahn Academy, 2010). The capillary walls become more porous allowing more cells to pass through them (Kahn Academy, 2010). Neutrophils act as the first responders and are attracted to the chemokines (Kahn Academy, 2010). They roll along the endothelial wall, squeezing through to eat up bacteria and damaged cells (Kahn Academy, 2010). Specific action via B and T cells are also activated to attack and destroy the bacteria (Kahn Academy, 2010).
The patient’s anaphylactic response, Type I hypersensitivity reaction, to IgE antibodies is produced by the ‘immune system in response to environmental allergens’ (Justiz-Vaillant & Zito, 2019). If left untreated, it can result in a life-threatening or irreversible injury that includes death (Justiz-Vaillant & Zito, 2019). While the patient did not have a known allergy and it was disclosed that he had none, Type I hypersensitivity reactions occur after a previous sensitization (Justiz-Vaillant & Zito, 2019). In a Type I hypersensitivity reaction, mast cells quickly release a large amount of ‘histamine and later on leukotrienes’ after encountering an allergen (Justiz-Vaillant & Zito, 2019). This reaction can lead to ‘bronchospasm, laryngeal edema, cyanosis, hypotension, and shock’ in the most severe cases (Justiz-Vaillant & Zito, 2019).
References
American Academy of Family Physicians. (2016). Strep Throat. Retrieved February 23, 2020 from https://eds-a-ebscohost-com.ezp.waldenulibrary.org/eds/pdfviewer/pdfviewer?vid=5&sid=040cd3d9-4ef6-4b25-872f-592f1c7c030c%40sessionmgr4006
Khan Academy (2010, February 24). Inflammatory Response/Human Anatomy and Physiology/Health & Medicine [Video File]. Retrieved February 23, 2020 from https://www.youtube.com/watch?v=FXSuEIMrPQk%20%20
Justiz-Vaillant, A.A., & Zito, P.M. (2019). Immediate Hypersensitivity Reactions. In StatPearls. Treasure Island, FL: StatPearls Publishing. Retrieved February 23, 2020 from https://class.content.laureate.net/f6bf9251ee3c3f606fefa59546a98a32.pdf
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
Soo, P. (2018, July, 28). Pathophysiology Ch 10 alterations in immune function [Video File]. Retrieved February 23, 2020 from https://www.youtube.com/watch?v=Jz0wx1-jTds
Sonia – Discussion Week 1 – Scenario 1
COLLAPSE
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Main Question Post
In an attempt to treat this patient’s symptoms of strep throat, the provider prescribed amoxicillin, an antibiotic, to treat the bacteria that causes strep throat and manage the signs that the patient is experiencing. According to Lockett, Huoman, and Holloway, a family history of allergies is a risk factor for individuals developing allergic reactions (2015). Mothers with a history of hypersensitivity increase their child’s risk factor of producing the same allergies as them (Lockett, Huoman, & Holloway, 2015). However, parents having an allergic reaction does not mean that the child will have the same allergy or experience the same response when exposed to allergens (Cleveland Clinic, 2015). It appears that although it is common for children to experience allergies when inherited from a parent, an allergic response can decrease and diminish over time (Shenoy et al., 2019). The patient in this scenario had a genetically-linked anaphylactic reaction to the amoxicillin prescribed.
According to the patient’s medical history, there was no history of known food or drug allergies and the patient was negative for frequent infections as a child. This suggests that the patient had no experience receiving penicillin-like antibiotics, so there was no recent exposure to amoxicillin that would have allowed the provider to anticipate the patient’s response. This patient experienced a severe allergic reaction because several body systems displayed an immediate reaction to a drug with swollen lips and tongue, difficulty breathing, and audible wheezes, which are signs of anaphylaxis (Cleveland Clinic, 2015). Anaphylactic reactions to amoxicillin, as a beta-lactam antibiotic, is a standard Type 1 hypersensitivity reaction that is IgE-mediated. IgE is an antibody that affects mast cells upon exposure to the antigen, but the effect decreases over time (Reber, Hernandez, & Galli, 2017). According to Patterson and Stankewicz, the patient may have a less severe reaction to amoxicillin in the future if this antibiotic is avoided for an extended time (2019).
Conclusion
If this patient scenario reported an adverse family history of allergies to penicillin-like drugs, although the research has found a connection, I would not stress the significant risk of inheriting drug allergies from parents. I believe this was a Type 1 hypersensitivity response to amoxicillin (Reber, Hernandez, & Galli, 2017). If the patient had a prior history of taking this antibiotic, I would not maintain my belief that this was a Type 1 response due to the critical nature of this reaction without prior warning.
References
Cleveland Clinic. (2015). Allergies in children. Retrieved from https://my.clevelandclinic.org/health/diseases/13080-allergies-in-children
Lockett, G. A., Huoman, J., & Holloway, J. W. (2015). Does allergy begin in utero? Pediatric Allergy and Immunology, 26, 394–402. doi: 10.1111/pai.12408
Patterson, R. A., & Stankewicz, H. A. (2019). Penicillin allergy. StatPearls [Internet]. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK459320/
Reber, L. L., Hernandez, J. D., & Galli, S. J. (2017). The pathophysiology of anaphylaxis. The Journal of Allergy and Clinical Immunology, 140(2), 335–348. http://dx.doi.org/doi: 10.1016/j.jaci.2017.06.003
Shenoy, E. S., Macy, E., Rowe, T., & Blumenthal, K. G. (2019). Assessment and management of penicillin allergy: A review. Journal of the American Medical Association, 321(2), 188-199. http://dx.doi.org/doi: 10.1001/jama.2018.19283
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