Patient Scenario

A 16-year-old boy comes to clinic with chief complaint of sore throat for 3 days. Denies fever or chills. PMH negative for recurrent colds, influenza, ear infections or pneumonias. NKDA or food allergies. Physical exam reveals temp of 99.6 F, pulse 78 and regular with respirations of 18. HEENT normal with exception of reddened posterior pharynx with white exudate on tonsils that are enlarged to 3+. Positive anterior and posterior cervical adenopathy. Rapid strep test performed in office was positive. His HCP wrote a prescription for amoxicillin 500 mg po q 12 hours x 10 days disp #20. He took the first capsule when he got home and immediately complained of swelling of his tongue and lips, difficulty breathing with audible wheezing. 911 was called and he was taken to the hospital, where he received emergency treatment for his allergic reaction.

As mentioned patient was diagnosed with Strep throat reason the infected stayed localized was cytotoxic T-cells bind to the surface of infected cells (MHC1), disrupt the membranes and destroy it before it can infect other cells. Normal cells (nucleus) contains MHC1, in which lets white blood cells that there is an infection, allowing cytotoxic T-cells bind and recognizing there is an infection and destroys it. Patient has no PMH and with that normal plasma cells are able to make antibodies to destroy bacteria and viruses (Soo, 2018).

Amoxicillin was prescribed and after the first dose he immediately develops a swelling of his tongue, lips and difficulty breathing causing an anaphylactic reaction. An immediate allergic or anaphylactic type of reaction mediated primarily by sensitized and direct activation of mast cells, with that being said mast cells and anaphylaxis are intimately related (Liberman & Garvey, 2916). Patient had a hypersensitivity reaction that can be exaggerated against an antigen or allergen. This particular patient had presented with type I or anaphylactic response antibodies (IgE) that bind to mast cells and basophils, which contain histamine granules that are released in the reactions and cause inflammation (Justiz-Valliant & Zito, 2019). Mast cells release a large amount of histamine and later on leukotrienes (family of eicosanoid inflammatory mediators) causing bronchospasm, largnegeal edema, cyanosis, hypotension and shock. An immunological reaction is termed anaphylactic when antigen reacts with cell-bound antibody, the union of antigen with cell-fixed antibody is linked to histamine release (Schilld & Silva, 2017).

Although it was mentioned that the patient had no PMH or NKDA the development of allergens bind to B-cells and IgE has a strong genetic and hereditary linkage (Soo, 2018) it would be interesting to see if his parents ever has an anaphylactic reaction to the same class of antibiotics or any other type of medication.

References

Galli, S.J. (2016). The mast cell-IgE paradox: from homeostasis to anaphylaxis.

The American Journal of Pathology, 186(2), 212-224.

              https://doi.org/10.1016/j.apath.2015.07.025.

Justiz-Valliant, A.A., Zito, P.M. (2019). Immediate hypersensitivity reactions. In StatPearls.

Treasure Island, FL: StatPearls Publishing. Retrieved from

https://www.ncbi.nlm.nih.gov/books/NBK513315/

Liberman, P., & Garvey, L.H. (2016). Mast cells and anaphylaxis. Current Allery and Asthma

               Reports, 16(3), 1-7.

              https://dx.doi.org.ezp.waldenulibrary.org/10.1007/511882-016-0598-5.

McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children. (8th ed.). St. Louis, MO: Mosby/Elsevier.

Schilld, H.O., Silva, R.E. (2017). Immunopharmacology & Immunotoxicology. (4^th ed).

Headington Hill Hall, Oxford: Pergamon Press Ltd.

Soo, P. (2018, July 28). Pathophysiology CH 10 alterations in immune function

.

Retrieved from https:www.youtube.com/watch?v=JzOwvl-jTds.

Strasser, A., Whittman, H.J. (2017). Histamine and histamine receptors in health and disease.

          Handbook of experimental pharmacology, 241, 31. DOI:10.1007/164_2016_113.

Discussion: Alterations in Cellular Processes

For this Discussion, you examine a case study and explain the disease that is suggested. You examine the symptoms reported and explain the cells that are involved and potential alterations and impacts.

To prepare:

• By Day 1 of this week, you will be assigned to a specific scenario for this Discussion. Please see the “Course Announcements” section of the classroom for your assignment from your Instructor.

By Day 3 of Week 1

Post an explanation of the disease highlighted in the scenario you were provided. Include the following in your explanation:

• The role genetics plays in the disease.
• Why the patient is presenting with the specific symptoms described.
• The physiologic response to the stimulus presented in the scenario and why you think this response occurred.
• The cells that are involved in this process.
• How another characteristic (e.g., gender, genetics) would change your response.

Read a selection of your colleagues’ responses.

By Day 6 of Week 1

Respond to at least two of your colleagues on 2 different days and respectfully agree or disagree with your colleague’s assessment and explain your reasoning. In your explanation, include why their explanations make physiological sense or why they do not

Note: For this Discussion, you are required to complete your initial post before you will be able to view and respond to your colleagues’ postings. Begin by clicking on the “Post to Discussion Question” link and then select “Create Thread” to complete your initial post. Remember, once you click on Submit, you cannot delete or edit your own posts, and you cannot post anonymously. Please check your post carefully before clicking on Submit!

Ding et. al (2020) remind us that most acute pharyngitis is caused by infection, which is consistent with strep presenting as a sore throat with exudate and swelling. In this scenario, the sixteen year old boy’s healthy immune system actually contributed to the problematic symptoms. Having an abundance of T cells attacking the invading bacteria led to swelling.  If he’d been ninety years old, his compromised immune system would not have reacted quite so harshly with regard to the airway compromise. Granted, this patient was having anaphylactic shock as an allergic reaction to amoxicillin. But the other factors named here also contributed.  Genetics plays a significant role in many processes here. Eluded to above, if the boy had been given a weaker genetic makeup, he may have not had as extreme of an immune response, which comes with different implications. If he were immunocompromised, the infection, the culprit here, may have caused him to go into septic shock.  As well, he could’ve gone into vasodilatory shock from the anaphylaxis in a more profound way, costing him his life if at baseline he already was hypotensive and had erratic vitals. A heart susceptible to irritability and subsequent arrythmias, for example, is not a good platform on which to place one’s life when one is undergoing the inner battlefield of white blood cells attacking invaders and causing massive fluid shifts, release of cytokines and hystamine, and subsequent inflammation.  Having sound genetics, with good kidneys and healthy blood pressure, helps tremendously when one goes into shock.  As is stated by Lee et. al (2020)  severe symptoms affecting various organ systems can occur in a short period of time.  If at baseline a patient already has compromised organs due to a genetic disease, there’s even more problems to combat.   In this situation, the initial infection caused inflammation in the airway that then was exacerbated by the allergic response to the drug.  A localized swelling became out of control due to a more global inflammatory allergic reaction, threatening to end the patient’s life.  Regarding this situation, the issue of airway size differences in children and adults is relevant.  According to Fenley, Voorman, Dove, and Greene (2020) in the pediatric population, guidelines for endotracheal tube (ETT) size are primarily based on age, speaking to a correlation between age and airway size. If the patient had a fully developed airway, there’d be less risk.  It comes down to the genetic predisposition of an allergic reaction to the antibiotic as well.  Without the boy’s genetic predisposition of reacting to the antibiotic, big picture there wouldn’t have been as dire a situation.
 

Ding, Y., Yu, S., Wei, Z., Deng, R., Chen, P., Sun, Y., Jia, Q., Li, X., Wu, Y., Chen, W., Zanker, K. S., Wang, A., & Lu, Y. (2020). Relieving Sore Throat Formula Exerts a Therapeutic Effect on Pharyngitis through Immunoregulation and NF-κB Pathway. Mediators of Inflammation, 1–21. https://doi-org.ezp.waldenulibrary.org/10.1155/2020/2929163
 

Fenley, H., Voorman, M., Dove, J. T., & Greene, J. S. (2020). Predicting pediatric tracheal airway size from anthropomorphic measurements. International Journal of Pediatric Otorhinolaryngology, 134. https://doi-org.ezp.waldenulibrary.org/10.1016/j.ijporl.2020.110020 

Lee, W. S., An, J., Jung, Y.-H., Jee, H. M., Chae, K.-Y., Park, Y. A., Han, M. Y., & Lee, K. S. (2020). Characteristics and Treatment of Anaphylaxis in Children Visiting a Pediatric Emergency Department in Korea. BioMed Research International, 1–7. https://doi-org.ezp.waldenulibrary.org/10.1155/2020/2014104