Using Cellular Process
In the case scenario, the 16-year-old boy presented with a sore throat for 3 days. Sore throat. Sore throat caused by pharyngitis is not uncommon in outpatient settings. For instance, Sykes et al. (2020) state that sore throat and pharyngitis account for more than 2% and 5% of all outpatient primary care visits for adult and pediatric populations, respectively.
Pharyngitis is marked by the inflammation of the pharynx and the surrounding tissues. It is predominantly infectious and can be caused by viral, bacterial, or fungal etiologies. Viral pharyngitis is self-limiting, while bacterial and fungal pharyngitis requires antimicrobial therapy.
Among the bacterial infections, group A streptococcus is the most common etiology and accounts for up to 30 % and 15% of pediatric and adult sore throats, respectively (Sykes et al., 2020). Group A streptococcal infections bear a potential risk of life-threatening complications.
Consequently, the detection of strep in this patient necessitated the initiation of antibiotics, particularly amoxicillin, which is recommended for the eradication of this pathogen (Sykes et al., 2020). However, the boy develops anaphylaxis upon taking the first dose of amoxicillin. The subsequent paragraphs will discuss the role of genetics, manifestations, cells involved, and the process of this allergic reaction.
The boy in the case scenario develops anaphylaxis. Anaphylaxis is a systemic life-threatening allergic reaction that predominantly involves IgE-mediated degranulation of mast cells and the release of large amounts of mediators (Fischer et al., 2018).
Several antigens, including foods such as milk, eggs, and nuts, and drugs such as penicillin, can trigger anaphylaxis. The exact cause of anaphylaxis is unknown; however, interaction of environmental, geographical, and genetic factors has been implicated. Genetic predisposition plays a crucial role in allergic reactions.
For instance, according to Varney et al. (2019), gene polymorphisms of ACE, angiotensinogen (AGT-M235T), and chymase (CMA-1 A1903G) have been linked to IgE-mediated systemic anaphylaxis. Additionally, alterations of the PHF11 gene on chromosome 13q14 have been associated with drug hypersensitivity reactions.
Specific Symptomatology and Physiologic Response
Anaphylaxis is a generalized reaction encompassing skin, neurologic, cardiorespiratory, and gastrointestinal manifestations. The patient developed swelling of the lips and tongue as well as difficulty in breathing with audible wheezing. Swelling of the lips and tongue is a manifestation of allergic angioedema. It is a result of an exaggerated immune response toward amoxicillin.
Meanwhile, difficulty in breathing and wheezing are consequences of severe bronchoconstriction following the massive release of inflammatory mediators. Other manifestations of anaphylaxis include nausea, vomiting, dizziness, confusion, anxiety, tachycardia, and hypotension. Physiologically, the immune response plays a vital role in protecting the body against invasion by pathogens. However, an abnormality in the functionality of the immune system predisposes these exaggerated responses.
The Process and Cells Involved
Drug hypersensitivity reactions are immediate hypersensitivity reactions and are principally IgE-mediated responses to drug allergens. This process encompasses two stages, namely sensitization and effector stages (McCance & Huether, 2019). The sensitization phase involves asymptomatic contact with the allergen, while the effector phase consists of the release of inflammatory mediators.
Immune cells involved are the helper T cells of types 1, 2, and 17 (McCance & Huether, 2019). According to Justiz Vaillant et al. (2022), the drug antigen is presented to T cells by dendritic cells, binds to T cells via TCR, and subsequently activates these immune cells.
Several characteristics influence the distribution and response to immediate hypersensitivity reactions. Such characteristics include genetics, gender, geographical location, age, and socioeconomic status. Additionally, medications and comorbidities affect the severity and response to treatment for these allergic reactions. In the case scenario following the stabilization of the patient, alternatives to amoxicillin, such as cephalosporins, can be used to eradicate the infection.
Fischer, D., Vander Leek, T. K., Ellis, A. K., & Kim, H. (2018). Anaphylaxis. Allergy, Asthma, and Clinical Immunology: Official Journal of the Canadian Society of Allergy and Clinical Immunology, 14(Suppl 2), 54. https://doi.org/10.1186/s13223-018-0283-4
Justiz Vaillant, A. A., Vashisht, R., & Zito, P. M. (2022). Immediate hypersensitivity reactions. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK513315/
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children. Elsevier.
Sykes, E. A., Wu, V., Beyea, M. M., Simpson, M. T. W., & Beyea, J. A. (2020). Pharyngitis: Approach to diagnosis and treatment. Canadian Family Physician Medecin de Famille Canadien, 66(4), 251–257. https://www.ncbi.nlm.nih.gov/pubmed/32273409
Varney, V. A., Nicholas, A., Warner, A., & Sumar, N. (2019). IgE-mediated systemic anaphylaxis and its association with gene polymorphisms of ACE, angiotensinogen and chymase. Journal of Asthma and Allergy, 12, 343–361. https://doi.org/10.2147/JAA.S213016
Assignment Description: Cellular Processes and the Genetic Environment