NU 451 ALTERATIONS IN CELLULAR PROCESSES
The Role Genetics Plays in the Disease
I believe this individual has Strep throat also called streptococcal pharyngitis. Genetics play a role in the disease process because genes provide a specific set of instructions that dedicate the way cells form, grow and multiply. According to Cho et al. (2019), the Streptococcus pyogenes can determine the virulence impact of strep throat infection and the factors to the pathogenesis that affect the interventions and recurrence of the disease (Cho et al., 2019). Some individuals are more susceptible to bacterial infections caused by the Group A streptococcus bacteria, due to their genetics and their cellular response. The infections target the immune system and the genetic susceptibility to this disease allows the bacteria to target the immune system, thus preventing some individuals from developing immunity.
Why the patient is presenting with the specific symptoms described.
The pharyngitis or sore throat in this scenario is likely caused by group A streptococcus bacteria. These bacteria attach the tissue and cause inflammation of the pharynx and tonsils, which explains his enlarged tonsils. The blood vessels in the throat are covered with endothelial cells, which maintain normal blood flow (Dan, J. M et al., 2019). During the inflammatory response “the vascular endothelium becomes a principal coordinator of blood clotting and the passage of cells and fluid into the tissue. The tissue close to the vessels contains mast cells, which are.
probably the most important activators of inflammation” (Dan, J. M et al., 2019). This inflammation can also manifest into adenopathy and redden posterior. The white exudate on the tonsils is a result of the purulent forming from the white blood cells fighting off the infection. The low-grade fever of 99.6f was also a sign of infection because it indicates that the body increases in overall temperature as a mechanism to fight off infection.
The physiologic response to the stimulus presented in the scenario and why you think this response occurred.
The stimulus-response in this scenario is anaphylaxis caused by an allergy to amoxicillin. Anaphylaxis reactions to amoxicillin that caused life-threatening reactions such as difficulty breathing, and swelling of the tongue and lips can be attributed to an immune-mediated drug reaction at a cellular level. Anaphylaxis is a reaction that can occur when allergens are exposed to the systems, causing a release of mediators’ basophils and mast cells. The airway obstruction was a direct result of an inflammatory histamine response to the immunologic and vascular environments, which is impacted by cellular communication. (Nuñez-Borque et al., 2022). I understand that this physiologic response could have resulted in the death of the 16-year-old boy in this scenario luckily, he recognized the signs and called 911.
The Cells Involved in this Process.
The communication between resident cells and the immune underlies the pathologic response of anaphylaxis. Mast cells are viewed as key players as well as IgE and IgG antibodies, the effector cells, and mediators by the reactions of allergens with antigen-specific antibodies. Endothelial cells, vascular cells, and cell injury pathways contribute to this cellular communication. The researcher suggests that the body recognizes allergens as foreign evaders thus, “promoting the activation of downstream signaling events that lead to the secretion of several biologically active products thought to be implicated in allergic reactions, such as histamine and various cysteinyl leukotrienes” (Reber et al.,2017). The endothelial receptors activate phospholipase C and histamine which can cause vascular leakage and severe bronchoconstriction. The cells in the cardiovascular system have a significant role in the most severe symptoms that obstruct the airway and “the most common symptoms of anaphylaxis, involve vascular fluid extravasation and are characterized by temporary localized swelling” (Nuñez-Borque et al., 2022).
How Another Characteristic (e.g., gender, genetics) Would Change the Response
Certain characteristics can change a response to a medication or disease process, such as gender and age. In a study that compared gender and age responses to allergen hypersensitivity, Lateef ( 2022), tested the hypersensitivity reaction of amoxicillin injections in females and males in two different age groups. The higher sensitivity rate in males was 37% compared to that of females whose sensitivity rate to amoxicillin was 18.5% Lateef ( 2022),. Research suggests that males have a higher incidence of hypersensitivity to reactions due to allergens and perhaps genetics as well.
References
Cho, K. H., Port, G. C., & Caparon, M. (2019). Genetics of Group A Streptococci. Microbiology spectrum, 7(2), 10.1128/microbiolspec.GPP3-0056-2018. https://doi.org/10.1128/microbiolspec.GPP3-0056-2018Links to an external site.
Dan, J. M., Havenar-Daughton, C., Kendric, K., Al-Kolla, R., Kaushik, K., Rosales, S. L., … & Crotty, S. (2019). Recurrent group A Streptococcus tonsillitis is an immunosusceptibility disease involving antibody deficiency and aberrant TFH cells. Science translational medicine, 11(478), eaau3776.
Lateef, N. (2022). Investigation on the Effect of Age and Gender on Hypersensitivity Reactions due to Allergens Injection in Iraqi Population. Archives of Razi Institute, 77(1), 359.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9288604/Links to an external site.
Nuñez-Borque, E., Fernandez-Bravo, S., Yuste-Montalvo, A., & Esteban, V. (2022). Pathophysiological, Cellular, and Molecular Events of the Vascular System in Anaphylaxis. Frontiers in immunology, 13, 836222. https://doi.org/10.3389/fimmu.2022.836222Links to an external site.
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. https://doi.org/10.1016/j.jaci.2017.06.003Links to an external site.
NU 451 ALTERATIONS IN CELLULAR PROCESSES
At its core, pathology is the study of disease. Diseases occur for many reasons. But some, such as cystic fibrosis and Parkinson’s Disease, occur because of alterations that prevent cells from functioning normally.
Understanding of signals and symptoms of alterations in cellular processes is a critical step in diagnosis and treatment of many diseases. For the Advanced Practice Registered Nurse (APRN), this understanding can also help educate patients and guide them through their treatment plans.
For this Discussion NU 451 ALTERATIONS IN CELLULAR PROCESSES , 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.
RESOURCES
Be sure to review the Learning Resources before completing this activity.
Click the weekly resources link to access the resources.
WEEKLY RESOURCES
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 NU 451 ALTERATIONS IN CELLULAR PROCESSES , you are required to complete your initial post before you will be able to view and respond to your peers’ posting. 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!
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In this week’s case study, the patient presents with a chief complaint of a sore throat and multiple other symptoms that resulted
in a positive strep test. Strep throat, also known as bacterial pharyngitis, is caused by the presence of Streptococcus group A bacteria that is spread by respiratory droplets and is the most common cause of pharyngitis in children (Chauhan, et al., 2016). In a recent meta-analysis, 37% of children less than 18 years old were diagnosed with Group A Strep and presented to an outpatient center for treatment for a sore throat in comparison to only 15% of adults (Ashurst & Edgerley-Gibb, 2022).
The patient presented with a sore throat, reddened posterior pharynx with white exudate, and 3+ tonsils- all due to the presence and colonization of the streptococcus bacteria. The positive sign of anterior and posterior cervical adenopathy is due to the infection and the body’s response to try and fight the infection. The patient was prescribed ten days’ worth of amoxicillin and after consumption, immediately experienced swelling of the tongue and lips, difficulty breathing, and wheezing. The patient was having an anaphylaxis reaction to the antibiotics. An anaphylaxis response is IgE mediated and results in mast cells releasing a large amount of histamine and leukotrienes that cause bronchospasm and edema (Vaillant, Vashisht, & Zito, 2022).
Even after antibiotic treatment, some children get recurrent strep throat due to a genetic basis. A study performed by Dr. Shane Crotty and Dr. Jennifer Dan (2019), explored the germinal centers of both children with a normal rate of infection and those with recurrent tonsillitis. Their findings suggested that children with recurring strep throat had smaller germinal centers with fewer B and helper T cells which are responsible for producing antibodies and fighting invading pathogens. Upon further research, it was discovered that the genetic component was identified as two variants in the HLA genomic region which are associated with increased susceptibility to recurrent tonsillitis as well as protecting against the disease. If a child presented with recurring group A streptococcus pharyngitis, it may warrant a different response than treating with just antibiotics, such as referring them to an ENT for a tonsillectomy.
NU 451 ALTERATIONS IN CELLULAR PROCESSES References
Ashurst, J. V., & Edgerley-Gibb, L. (2022). Streptococcal Pharyngitis. National Library of Medicine. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK525997/
Chauhan, S., Kashyap, N., Kanga, A., Thakur, K., Sood, A., & Chandel, L. (2016). Genetic diversity among group A streptococcus isolated from throats of healthy and symptomatic children. Journal of Tropical Pediatrics, 62(2), 152-157. doi:10.1093/tropej/fmv092
Crotty, S., & Dan, J. (2019). Recurrent group A streptococcus tonsillitis is an immunosusceptibility disease involving antibody deficiency and aberrant TFH cells. Science Translational Medicine, 11(478). doi:DOI: 10.1126/scitranslmed.aau3776
Vaillant, A. A., Vashisht, R., & Zito, P. M. (2022). Immediate hypersensitivity reactions. StatPearls. doi:https://www.ncbi.nlm.nih.gov/books/NBK513315/
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Case Discussion 1
In this scenario, an otherwise healthy 16-year-old boy is diagnosed with strep pharyngitis (strep throat) via an in-office rapid strep test, which tests for group A streptococcus bacteria (Cohen et al., 2016). He was prescribed penicillin, which is the antibiotic of choice for a patient with no known allergy to penicillin given that there is no strain of group A streptococcus bacteria that is resistant to it (“Centers for Disease Control,” 2022). Unfortunately for this young man, upon taking his first dose of penicillin he experienced an anaphylactic response, as evidenced by lip and oral swelling and breathing difficulties. This response is the most rapid and severe, and characteristic of a Type I hypersensitivity reaction, or IgE-mediated response resulting from the sensitization of mast cells by the binding of IgE to Fc protein receptors on the plasma membranes (McCance & Huether, 2019). Once sensitized, further exposure results in degranulation and release of histamine causing bronchial constriction and increased vascular permeability producing the breathing difficulties and lip and oral swelling respectively seen in this patient (Patterson & Stankewicz, 2020; McCance & Huether, 2019). Though type IV (IgG-mediated) hypersensitivity reactions are found in penicillin allergies, the primary result of this would be related to a delayed hypersensitivity mechanism resulting in dermatologic symptoms, not reported in this case (McCance & Huether, 2019).
Of note, Type I allergic responses can only occur with prior sensitization of the Fc proteins on mast cells. This patient was presented as having no known drug allergies, and while he could have taken penicillin in the past, which could have resulted in sensitization without evidence of allergic reaction, consideration should be given to the possibility that the patient carries a genetic erroneous beta (b)-lactam allergy. This could result in the allergic reaction without previously having taken the drug (Bhattacharya, 2010). Knowing the patient has a serious sensitivity to penicillins, the clinician should be aware of a cross-sensitivity to cephalosporins due to similarities in the chemical structure (Patterson & Stankewicz, 2020). Though research has shown females have a greater predisposition to penicillin allergy than males, the case presentation demonstrates a clear hypersensitivity reaction in this patient (Park et al., 2007).
NU 451 ALTERATIONS IN CELLULAR PROCESSES References
Bhattacharya, S. (2010). The Facts About Penicillin Allergy: A Review. Journal of Advanced Pharmaceutical Technology and Research, 1(1), 11–17.
Centers for Disease Control and Prevention. (2022, June 27). Pharyngitis (strep throat): Information for clinicians. Centers for Disease Control and Prevention. https://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html#:~:text=Penicillin%20or%20amoxicillin%20is%20the,that%20is%20resistant%20to%20penicillin.
Cohen, J. F., Bertille, N., Cohen, R., & Chalumeau, M. (2016). Rapid antigen detection test for group A streptococcus in children with pharyngitis. Cochrane Database of Systematic Reviews. https://doi.org/10.1002/14651858.cd010502.pub2
McCance, K., & Huether, S. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier.
Park, M. A., Matesic, D., Markus, P. J., & Li, J. T.-C. . (2007). Female sex as a risk factor for penicillin allergy. Annals of Allergy, Asthma & Immunology, 99(1), 54–58. https://doi.org/10.1016/s1081-1206(10)60621-7
Patterson, R. A., & Stankewicz, H. A. (2020). Penicillin Allergy. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK459320/
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Great explanation of the type I hypersensitivity presented in this week’s case study. I was interested to learn about the genetic component and the possibility of the beta (b)-lactam allergy you spoke of and did not consider it when I was reviewing this patient. My assumption was that the patient likely took penicillin before making him hypersensitive to it now. Upon further research, I found an article that studied the prediction of penicillin allergy through genome mapping. This study researched 387 patients with immediate allergic reactions to B-lactams and found significant associations between gene variants HLA-DRA and an allergy to penicillin (Gueant, et al., 2015). It is important to note that this study confirmed predictors of penicillin allergies but not to cephalosporins. Although rare, it is interesting to understand that there could be a genetic component to those with allergies to penicillin. Another aspect to consider with this case study is how recurring strep throat could be a genetic component. Germinal centers of individuals with recurrent strep were found to be smaller, there were fewer B and helper T cells and two variants in the HLA genomic region could make them more susceptible to tonsillitis (Crotty & Dan, 2019).
NU 451 ALTERATIONS IN CELLULAR PROCESSES References
Crotty, S., & Dan, J. (2019). Recurrent group A streptococcus tonsillitis is an immunosusceptibility disease involving antibody deficiency and aberrant TFH cells. Science Translational Medicine, 11(478). doi:DOI: 10.1126/scitranslmed.aau3776
Gueant, J.-L., Romano, A., Cornejo-Garci, J.-A., Oussalah, A., Chery, C., Blanca-Lopez, N., . . . Gaeta, F. (2015). HLA-DRA variants predict penicillin allergy in genome-wide fine-mapping genotyping. Journal of Allergy and Clinical Immunology, 135(1), 253-259. doi:https://doi.org/10.1016/j.jaci.2014.07.047
Collapse SubdiscussionMercy Wendy Muthoni
YesterdayNov 28 at 11:23pm
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The role genetics plays in the disease.
According to McCance (2019), humans have approximately 20,000-25,000 genes. An error in one of the genes can be the cause of an identifiable genetic disease (McCance et al., 2019). Variations in DNA and differences in how DNA functions on its own or in combination with the environment can be a contributing factors to disease processes (Jackson et al., 2018).
Why the patient is presenting with the specific symptoms described
The patient is presenting the symptoms of a reddened posterior pharynx with white exudate on tonsils that are enlarged to 3+. Positive anterior and posterior cervical adenopathy. A rapid strep test performed in the office was positive. The patient has been infected either through a respiratory droplet or by direct contact with someone who had the disease. The symptoms the patient is presenting are from a bacteria called group A Streptococcus (group A strep). Among the symptoms presented by a patient infected by Streptococcus are Sore throat, fever, pain when swallowing, red and swollen tonsils, headache swollen lymph nodes.
The physiologic response to the stimulus presented in the scenario and why you think this response occurred.
The physiologic response to the stimulus in this case is the way the body reacted to amoxicillin 500 mg when the patient took it. The patient complained of difficulty breathing with audible wheezing. He had an allergic reaction to amoxicillin. This may have happened because the patient’s immune system became hypersensitive to the drug and mistook the drug as a harmful substance or as if the amoxicillin was a viral or bacterial infection. Seems the patient had never been exposed to the medication before
The cells that are involved in this process
The cells involved are Helper T-cells αβT cells. These cells can be divided into, CD4+ and CD8+ T cells. T cell-mediated immunity can be invoked upon recognition of foreign or non-self peptides (eg viral) presented by the human leukocyte antigen (HLA) molecules of an antigen-presenting cell (APC) (Goh et al, 2021). This was a type 1 hypersensitivity reaction.
How another characteristic (e.g., gender, genetics) would change your response?
Genetics would change my response by analyzing how immunodeficiency may affect this patient. Immunodeficiency emerges from the absence of elements of the immune system, such as the phagocytes, lymphocytes, and the complement system. These are classified as primary and secondary immunodeficiencies. The primary immunodeficiency cause deficiencies such as T-cell deficiency, B-cell deficiency, phagocyte deficiency, immunoglobulin A deficiency, and complement deficiency. The secondary immunodeficiency is caused by obesity, steroids, AIDS, nutrient deficiency, and viral infections. If this patient lacks the Helper T-cells due to immunodeficiency, this would be a life-or-death situation.
NU 451 ALTERATIONS IN CELLULAR PROCESSES References:
Goh, SJR, Tuomisto, JEE, Purcell, AW, Mifsud, NA, Illing, PT. (2021). The complexity of T cell–mediated penicillin hypersensitivity reaction Allergy. 76: 150– 167. https://doi.org/10.1111/all.14355Links to an external site.
Jackson M, Marks L, May GHW, Wilson JB. (2018). The genetic basis of disease. Biochem. ;62(5):643-723. doi: 10.1042/EBC20170053. Erratum in: Essays Biochem. 2020 Oct 8;64(4):681. PMID: 30509934; PMCID: PMC6279436.
McCance K. L. Huether S. E. Brashers V. L. & Rote N. S. (2019). Pathophysiology : the biologic basis for disease in adults and children (Eighth). Elsevier.
7:22amNov 29 at 7:22am
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The patient was diagnosed with group A streptococcus (strep) pharyngitis, also known as strep throat, after complaining of a sore throat for three days and a positive rapid strep test. A physical exam revealed a reddened posterior pharynx, white exudate on the tonsils, tonsils enlarged to 3+, and cervical adenopathy. Strep throat is a bacterial infection caused by streptococcus pyogenes, gram-positive cocci that grow in chains in the throat and tonsils (Centers for Disease Control and Prevention, 2022). Streptococcus pyogenes are called group A streptococcus (Centers for Disease Control and Prevention, 2022). Group A streptococcus is contagious and spreads through respiratory droplets or direct contact (Centers for Disease Control and Prevention, 2022). It usually takes two to five days for someone exposed to group A streptococcus bacteria to become ill with strep throat (Centers for Disease Control and Prevention, 2022). Acute pharyngitis commonly presents with a sore throat, painful swallowing, fever, pharyngeal and tonsillar erythema, tonsillar hypertrophy with or without exudate, palate petechiae, and cervical lymphadenopathy due to colonization in the throat and tonsils (Centers for Disease Control and Prevention, 2022).
Strep throat is more common in children 5 to 15 years old, rare in children less than three-year-old, and most common during the winter and spring in the United States (Centers for Disease Control and Prevention, 2022). Adults are at increased risk for strep if they have school-aged children or are in frequent contact with children (Centers for Disease Control and Prevention, 2022). Close contact with infected individuals is the most common risk factor for illness (Centers for Disease Control and Prevention, 2022). Infection typically spreads in large groups of people, such as schools, daycares, or military facilities (Centers for Disease Control and Prevention, 2022). Since this patient is 16 years old, he likely attends school, and this is likely where he contracted the illness. If this were an adult that works from home with grown children, he would be less susceptible to contracting the infection. There appears to be no genetic component to strep throat; however, conditions associated with recurrent strep susceptibility run in families, suggesting a genetic component (Dan et al., 2019). Dan et al. (2019) found that children with recurrent tonsillitis had smaller germinal centers and reduced antibacterial antibodies revealing that altered adaptive immune responses to group A streptococcus may make an individual susceptible to recurrent infection (Dan et al., 2019). Since this patient denies a history of recurrent colds, influenza, ear infections, or pneumonia, we can presume this is an isolated occurrence.
Because the patient reported no know drug allergies, amoxicillin was ordered. However, the patient quickly complained of swollen lips and tongue, difficulty breathing, and wheezing. These symptoms signify a type I immediate hypersensitivity reaction to amoxicillin. Hypersensitivity reactions are exaggerated immune responses to an antigen or allergen (Justiz-Vaillant & Zito, 2019). Immediate hypersensitivity reactions are types I, II, and III, and they occur within 24 hours of exposure (Justiz-Vaillant & Zito, 2019). Type I hypersensitivity reactions exhibit a response mediated by immunoglobulin E (IgE) antibodies produced by the immune system in response to allergens and typically occur within 15 to 30 minutes of exposure to the antigen (Justiz-Vaillant & Zito, 2019; Soo, 2018). Anaphylaxis is the most rapid and severe immediate hypersensitivity reaction occurring within minutes of re-exposure to the allergen; symptoms of generalized anaphylaxis include breathing problems, gastrointestinal upset, headaches, erythema, bronchial constriction, laryngeal edema, vascular collapse, hypotension, and itching (McCance & Huether, 2019).
This response occurred because this patient likely had a previous exposure to amoxicillin. With the first exposure, the allergen binds to B cells which stimulate the production of IgE antibodies against this allergen; the IgE antibodies bind to Fc receptors on mast cells (Soo, 2018). When exposed to the allergen again, the allergen binds to the antibodies attached to the mast cells causing the mast cells to degranulate and release chemicals that are proinflammatory mediators (Soo, 2018). These histamines include prostaglandins, interleukins, and leukotrienes (Soo, 2018). This is a form of adaptive immunity. Adaptive immunity attacks specific antigens with a slow initial response but a more rapid response with the second exposure (Soo, 2018). Mediators include histamine and lipid mediators such as PAF, LTC4, and PGD2, causing bronchoconstriction, inflammation, vascular leak, and intestinal hypermotility (Justiz-Vaillant & Zito, 2019). Tumor necrosis factor causes inflammation (Justiz-Vaillant & Zito, 2019). Basophils can be found in the nose, lungs, skin, or gut during a hypersensitivity reaction, and mast cells are found in the mucosa and connective tissue (Justiz-Vaillant & Zito, 2019). This causes symptoms including wheezing, airway inflammation, tachycardia, tachypnea, itchy eyes and nose, sneezing, dermatitis, gastrointestinal upset, increased vascular permeability, vasodilation, hypotension, hives, bronchoconstriction, and increased mucous secretions (Justiz-Vaillant & Zito, 2019; Soo, 2018). This allergic response is why this patient presents with wheezing, difficulty breathing, and swelling of the lips and tongue. IgE initiates inflammatory and allergic reactions (Soo, 2018). In type I hypersensitivity reactions, the allergens are proteins with a molecular weight of 10 to 40 kDa; allergens include drugs, plants, fungi, rats, grass, German cockroaches, dust mites, and cats (Justiz-Vaillant & Zito, 2019). β-lactam antibiotics, including penicillin and amoxicillin, are associated with various immune-mediated or hypersensitivity reactions, including immediate type I reactions (Nicoletti et al., 2021).
Hypersensitivity reactions are common, affecting 15% of the world’s population at some point (Justiz-Vaillant & Zito, 2019). Type I hypersensitivity reactions have a strong genetic or hereditary linkage regarding IgE response to the antigen or allergens (Soo, 2018). Risk factors for immediate hypersensitivity reactions to β-lactam antibiotics are family history, concurrent virus infections, and the route of administration (Nicoletti et al., 2021). An analysis of single nucleotide polymorphisms identified that the HLA-DRA locus might protect against penicillin-induced immediate hypersensitivity reactions (Nicoletti et al., 2021). Wong et al. (2019) conducted a study that found that females account for most hypersensitivity reactions. The study also revealed that white patients accounted for most immediate and delayed hypersensitivity reactions (Wong et al., 2019). Penicillin also accounted for one of the most significant proportions of drug hypersensitivity reactions (Wong et al., 2019).
NU 451 ALTERATIONS IN CELLULAR PROCESSES References
Centers for Disease Control and Prevention. (2022, June 27). Group A streptococcus: Information for clinicians. Centers for Disease Control and Prevention. Retrieved November 28, 2022, from https://www.cdc.gov/groupastrep/diseases-hcp/index.html
Dan, J. M., Havenar-Daughton, C., Kendric, K., Al-kolla, R., Kaushik, K., Rosales, S. L., Anderson, E. L., LaRock, C. N., Vijayanand, P., Seumois, G., Layfield, D., Cutress, R. I., Ottensmeier, C. H., Lindestam Arlehamn, C. S., Sette, A., Nizet, V., Bothwell, M., Brigger, M., & Crotty, S. (2019). Recurrent group A Streptococcus tonsillitis is an immunosusceptibility disease involving antibody deficiency and aberrant TFH cells. Science Translational Medicine, 11(478). https://doi.org/10.1126/scitranslmed.aau3776Links to an external site.
Justiz-Vaillant, 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/Links to an external site.
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
Nicoletti, P., Carr, D. F., Barrett, S., McEvoy, L., Friedmann, P. S., Shear, N. H., Nelson, M. R., Chiriac, A. M., Blanca-López, N., Cornejo-García, J. A., Gaeta, F., Nakonechna, A., Torres, M. J., Caruso, C., Valluzzi, R. L., Floratos, A., Shen, Y., Pavlos, R. K., Phillips, E. J., … Pirmohamed, M. (2021). Beta-lactam-induced immediate hypersensitivity reactions: A genome-wide association study of a deeply phenotyped cohort. The Journal of Allergy and Clinical Immunology, 147(5), 1830–1837. https://doi.org/10.1016/j.jaci.2020.10.004Links to an external site.
Soo, P. (2018, July 28). Pathophysiology Ch 10 alterations in immune function [Video file]. Retrieved fromhttps://www.youtube.com/watch?v=Jz0wx1-jTdsLinks to an external site.
Wong, A., Seger, D. L., Lai, K. H., Goss, F. R., Blumenthal, K. G., & Zhou, L. (2019). Drug Hypersensitivity Reactions Documented in Electronic Health Records within a Large Health System. The Journal of Allergy and Clinical Immunology: In Practice, 7(4), 1253–1260. https://doi.org/10.1016/j.jaip.2018.11.023Links to an external site.
Collapse SubdiscussionCammeo Rose Deboutez
2:12pmNov 29 at 2:12pm
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Discussion
In this scenario, the patient has swelling of the tongue and lips, difficulty breathing and audible wheezing after taking amoxicillin. I believe that this is an anaphylactic reaction as symptoms include constriction of the bronchial smooth muscle which would explain the difficulty breathing and wheezing, as well as laryngeal edema which he is also experiencing (McCance & Huether, 2019, p.256). Anaphylaxis is a type I hypersensitivity reaction which has a strong genetic hereditary linkage regarding IgE response to antigens (Soo, 2018). IgE binds to receptors on mast cells, which cells which release pro-inflammatory mediators including prostaglandins, interleukins, and leukotrienes. I believe this is why the edema is occurring with this scenario. Histamine is also released which causes increased vascular permeability, vasodilation, hypotension, urticaria, bronchoconstriction, and increased mucus secretion which I would expect to see if this patient did not receive treatment. This would eventually lead to shock and death. There is limited research on the interaction between strep throat, the use of penicillin, and the occurrence of anaphylaxis, but there has been a connection between rheumatic fever and penicillin allergies with or without history of the allergy and the impact of using secondary antibiotic prophylaxis in these cases (Sanyahumbi et. al., 2019). Allergies, specifically type I allergies can be passed down from parent to child, and this is called an atopic individual. These individuals “produce higher quantities of IgE” and “have more Fc receptors for IgE on their mast cells” which will increase the severity of their reaction (McCance & Huether, 2019, p.264). These individuals are also more likely to have a heightened reaction in the airway and skin as well. Treatment would include antihistamines to block the inflammatory effects of histamine, beta-adrenergics to decrease bronchoconstriction, corticosteroids to decrease inflammatory response, anticholinergics to block the parasympathetic system and block bronchoconstriction, IgE therapy which inhibits binding of IgE to mast cells, and epinephrine for acute allergic reactions (Soo, 2018). If the patient had a family history of anaphylactic reactions to medications, or in general, I might suggest taking the first dose of the medication while in a clinic and waiting 15-30 minutes after that dose to ensure that the medication is safe, or include teaching of what to do if certain symptoms present. My response would not change based on gender, age, or other demographics based on the knowledge that I have at this time, but I would be interested to learn if the strep infection had a bigger role in the reaction that I previously thought.
NU 451 ALTERATIONS IN CELLULAR PROCESSES References
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
Sanyahumbi, A., Ali, S., Benjamin, I. J., Karthikeyan, G., Okello, E., Sable, C. A., Taubert, K., Wyber, R., Zuhlke, L., Carapetis, J. R., Beaton, A. Z., & n American Heart Association (2022). Penicillin Reactions in Patients With Severe Rheumatic Heart Disease: A Presidential Advisory From the American Heart Association. Journal of the American Heart Association, 11(5), e024517. https://doi.org/10.1161/JAHA.121.024517
Soo, P. (2018, July 28). Pathophysiology Ch 10 alterations in immune function Links to an external site.Links to an external site.[Video file]. Retrieved from https://www.youtube.com/watch?v=Jz0wx1-jTds
3:18pmNov 29 at 3:18pm
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Response 1
Genetics plays a significant role in the disease when assessing and treating the patient. Therefore, in confirming that the patient had a positive strep test. The next step would have been to ask if the family or siblings had a history of recurrent positive strep tests, and once confirmed, the provider should have asked what was the initiated treatment. According to Brashers and Rote (2019), family members share genes. This concept can also go for an allergy reaction, for an individual’s genetic makeup determines the degree of resultant immune response from the effects of the insult (Brashers & Rote, 2019). Therefore, in evaluating and assessing more, the allergic reaction could have been prevented.
The patient presented with specific symptoms because a streptococcus bacterial microorganism had invaded the body of the 16-year-old boy, and he had a type 1 hypersensitivity reaction due to an allergic reaction from taking amoxicillin to treat the positive strep.
A physiologic response occurs because a microorganism invades the body, destroys cells, produces toxins, and produces damaging hypersensitivity reactions (Brashers & Rote, 2019). The physiologic responses are the increased temperature of 99.6, enlarged reddened posterior pharynx with white exudate on tonsils, and positive anterior and posterior cervical adenopathy. The cells creating this response are the T cells, macrophages, and neutrophils.
The physiologic response also occurred when he had a drug allergy related to taking amoxicillin. The symptoms are swollen tongue and lips, difficulty breathing, and audible wheezing. The IgE B cells, basophils, and mast cells are the cells involved in creating this response. According to Justiz-Vaillant and Zito (2019), immunoglobulin (Ig) E is produced and binds to Fc receptors on mast cells and basophils. Therefore, when the patient ingests amoxicillin, it causes an activation of these cells that causes physiological responses.
Factors that could have changed the response is assessing the patient genetic makeup and looking at environmental factors. Gathering more information on the client’s family and assessing for allergies within the family can change the response. Evaluating the child’s environment, looking at who is living with the child, assessing if anyone is sick in the home and educating the family on the importance of cleaning the home in the winter and spring months are also preventative.
NU 451 ALTERATIONS IN CELLULAR PROCESSES Reference
Brashers, V. L., & Rote, N. S. (2019). Pathophysiology: The Biologic Basis for Disease in Adults and Children (8th ed.). Elsevier
Justiz-Vaillant, A. A., & Zito, P. M. (2019). Immediate hypersensitivity reactions Download Immediate hypersensitivity reactions. In StatPearls. Treasure Island, FL: StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK513315/
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The Role that Genetics Plays in the Disease-
Every person has 46 chromosomes inheriting 23 from each parent and individual genes are copied to messenger RNA. The proteins produced in a cell determine the phenotype. According to Casey, G, an individual’s DNA code is known as their genotype and the type and number of proteins produced to determine a cell’s and an organism’s phenotype (2016). If the gene is on one of the first 22 pairs of chromosomes (autosomes), the genetic disorder is called an autosomal condition. If the gene is on the X chromosome, the disorder is called X-linked. Some mutations can be passed down from a parent to a child while others can happen in the sperm or the egg. Genetic disorders can be grouped by dominant or recessive, depending on how they are passed down from a family. Genetics plays an important role in the susceptibility of strep throat. Children with a genetically poor immune response to group A strep bacteria are at higher risk of receiving the infection. Children with a family history of frequent streptococcus throat infections are also at high risk of a streptococcus infection. In other words, children with a large familial history of strep throat usually have reoccurring episodes more often than those without (Cho KH, et al. 2019).
Why is the Patient Presenting with the Symptoms-
The patient is presenting with enlarged tonsils due to adaptive immunity. Our bodies attack bacteria and toxins when present. Inflammation and redness occur as a part of innate immunity and our bodies’ role in defending against strep bacteria. The fever serves as a protective role as cellular components of the immune system drive temperature response. DCS, macrophages, neutrophils, T and B lymphocytes, NK cells, and vascular endothelial cells play a role in hyperthermic temperatures and febrile response.
The physiologic response to the stimulus presented in the scenario and why you think this response occurred.
The patient had an anaphylactic response (or type 1 reaction) as evidenced by wheezing, angioedema and difficulty breathing, and bronchoconstriction. This hypersensitivity can occur with dust, allergens, and proteins. Antibiotics are the leading cause of anaphylaxis and in this particular case, Amoxicillin caused the reaction. “Anaphylactic Response is mediated by IgE antibodies that are produced by the immune system in response to environmental proteins” Justiz-Vaillant, A. A., & Zito, P. M. (2019). This is the most severe response as the cell releases large amounts of histamine and could potentially cause death. This type of reaction is mediated by antibodies produced by b lymphocytes.
The Cells that are Involved in this Process-
Type I reactions are the most severe of all and can cause anaphylaxis and death. “In type I hypersensitivity reactions after a previous sensitization, the immunoglobulin (Ig) E is produced and binds to Fc receptors on mast cells and basophils” (Soo, P. 2018). Histamine and tryptase are mediators stored in the mast cells and released by basophils and mast cell degranulation. “The mediators that participate in this type of hypersensitivity reaction include histamine and lipid mediators such as PAF, LTC4, and PGD2 that cause a vascular leak, bronchoconstriction, inflammation, and intestinal hypermotility” (Soo, P. 2018).
How another characteristic (e.g., gender, genetics) would change your response?
It is known that women may have an increased risk of having an immune response. In addition, a history of increased bacterial infections may also increase the risk of a patient developing an immune response as well. Stress can contribute to this happening in an older individual as well. Anaphylaxis may be more common if someone has had a repeat virus or exposure to bacteria. Type 1 response may be linked to a strong heredity component (Soo, P. 2018). For example, my husband, and both my sons are allergic to penicillin. Most of the men on my husband’s side of the family are also allergic to this medication. “We also recently reported that immediate allergic reactions to BLs were associated with the rs11125 variant in the gene coding for the β-galactoside–binding lectin galectin-3, LGALS3” (Jurado-Escabor, 2022). Some studies have found that patients with low to undetectable IgE levels may experience anaphylaxis more often (Jeanana et al. 2019).
NU 451 ALTERATIONS IN CELLULAR PROCESSES References
Casey, G. (2016). Genetics, epigenetics and disease. Kai Tiaki Nursing New Zealand, 22(9), 20–24.
Centers for Disease Control and Prevention. (2021, June 24). Genetics basics. Centers for Disease Control and Prevention. November 29, 2022
https://www.cdc.gov/genomics/about/basics.htm
Jurado-Escobar R;Perkins JR;García-Martín E;Isidoro-García M;Doña I;Torres MJ;Cornejo-García JA; (n.d.). Update on the genetic basis of drug
hypersensitivity reactions. Journal of investigational allergology & clinical immunology. Retrieved November 29, 2022, from https://pubmed.ncbi.nlm.nih.gov/29199960/
Jenana H. Maker, Cassandra M. Stroup, Vanthida Huang, & Stephanie F. James. (2019).
Antibiotic Hypersensitivity Mechanisms. Pharmacy, 7(3), 122. https://doi.org/10.3390/pharmacy7030122
Justiz-Vaillant, A. A., & Zito, P. M. (2019). Immediate hypersensitivity reactions Download
Immediate hypersensitivity reactions. In StatPearls. Treasure Island, FL: StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK513315/Links to an external site.
Jurado-Escobar R;Perkins JR;García-Martín E;Isidoro-García M;Doña I;Torres MJ;Cornejo-García JA; (n.d.). Update on the genetic basis of drug
hypersensitivity reactions. Journal of investigational allergology & clinical immunology. Retrieved November 29, 2022, from https://pubmed.ncbi.nlm.nih.gov/29199960/
Kim SH, Ye YM, Palikhe NS, Kim JE, Park HS. Genetic and ethnic risk factors associated
with drug hypersensitivity. Curr Opin Allergy Clin Immunol. 2010 Aug;10(4):280-90. doi: 10.1097/ACI.0b013e32833b1eb3. PMID: 20485159.Soo, P. (2018, July 28).
Pathophysiology Ch 10 alterations in immune function Links to an external site.Links to an external site.[Video file].
https://www.youtube.com/watch?v=Jz0wx1-jTds
Cho KH, Port GC, Caparon M. Genetics of Group A Streptococci. Microbiol Spectr. 2019
Mar;7(2). doi: 10.1128/microbiolspec.GPP3-0056-2018. PMID: 30825299.
10:35pmNov 29 at 10:35pm
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Alterations in Cellular Processes
This week’s case study focuses on a 16-year-old male presenting with a three-day history of sore throat. The patient denied any fever or chills. There was no past medical history of pneumonia, or ear, nose, or throat infections. In the objective examination, the patient had a temperature of 99.6 F, a pulse rate of 78, and a respiratory rate of 18. The patient had enlarged erythematous tonsils of grade 3+ which had a white exudate. There was cervical adenopathy of the posterior and anterior cervical lymph nodes. The rapid streptococcus test was positive and Amoxicillin was initiated. The patient had an allergic reaction to amoxicillin after taking the first dose. Acute tonsilitis is fairly common at the school-going age (Dhingra & Dhingra, 2021). The most implicated organisms in the etiology of acute tonsilitis are viruses and the hemolytic streptococci. The distinction of the cause of acute tonsilitis is crucial to prevent the misuse of antibiotics that would ultimately result in antibiotic resistance (Bulut et al., 2020). The positive rapid streptococcal test indicates that acute tonsilitis in this patient is caused by hemolytic streptococci. The purpose of this paper is to discuss acute tonsilitis (Acute membranous tonsilitis) under the subheadings of; the role of genetics in the disease process, symptoms, physiologic response to stimuli in acute tonsilitis, the cells involved in the pathophysiologic process, and individual characteristics that affect physiologic responses in acute tonsilitis.
Role of Genetics
There is limited evidence on the role of genNetics in acute tonsilitis. Genetics has a role in the occurrence of recurrent tonsilitis. Genetic clustering is essential in cases of the severe tonsillar disease. People with at least a copy of the IL1B-31*C allele have a higher propensity to develop tonsillar inflammation (Bulut et al., 2020). Genetic polymorphisms in complement factor H and Toll-Like Receptor 4-T399I are implicated in Group A hemolytic streptococci infection and inflammation of the tonsils (Bulut et al., 2020). Several immunological mechanisms have also been proposed.
Physiologic Responses, Cells involved in the Response, and Reason for the Symptoms,
Group A beta-hemolytic streptococci adhere to the pharyngeal mucosa through the adhesins. Microorganisms invade the mucosa by releasing proteases and cytolysins which mediate an inflammatory reaction. Inflammation is marked by swelling, redness, pain, and heat. These cardinal features explain the symptoms of fever, sore throat, tonsillar exudates, and difficulty in swallowing secondary to swelling of the tonsils.
Inflammation is a physiologic response to noxious stimuli. Tonsils are part of the lymphoid tissue that form Waldeyer’s ring. White blood cells have a role in combating both viral and bacterial infections. Lymphocytes are produced in the lymphoid tissues. The lymphatic system also mediates the production of pro-inflammatory cytokines. The lymphatic vessels are enlarged to help drain the extravasated fluid resulting from the increased permeability of blood vessels (Schwager & Detmar, 2019). This explains the physiologic hyperplasia and enlargement of the lymph nodes. This response occurs to signal and enable the body to clear the disease-causing organisms. Another physiologic process in this case study is an allergy to amoxicillin. Allergy is predominantly mediated by IgE. Eosinophils and basophils cause inflammation and mediate tissue damage (Pichler, 2019). Mast cell degranulation and release of Ig E cause activation of type 2 T-helper cells. This process culminates with the accumulation of basophils and eosinophils.
The Impact of Gender on Inflammation
The male gender has a worse prognosis in acute inflammatory conditions. Males have a higher risk of morbidity, complications, and mortality from acute inflammatory conditions (Casimir et al., 2018). However, for chronic inflammatory conditions, females have a worse prognosis.
NU 451 ALTERATIONS IN CELLULAR PROCESSES References
Bulut, F., Cumbul, A., & Ballica, B. (2020). Clinical importance of family history in recurrent chronic tonsillitis pediatric patients: Mini-review. Journal of Pediatrics and Pediatric Medicine, 4(3). https://www.pediatricsresearchjournal.com/articles/clinical-importance-of-family-history-in-recurrent-chronic-tonsillitis-pediatric-patients-mini-review.htmlLinks to an external site.
Casimir, G. J., Lefèvre, N., Corazza, F., Duchateau, J., & Chamekh, M. (2018). The acid–base balance and gender in inflammation: A mini-review. Frontiers in Immunology, 9. https://doi.org/10.3389/fimmu.2018.00475Links to an external site.
Dhingra, P. L., & Dhingra, S. (2021). Diseases of Ear, Nose & Throat and Head & Neck Surgery – E-Book. Elsevier India.
Pichler, W. J. (2019). Immune pathomechanism and classification of drug hypersensitivity. Allergy. https://doi.org/10.1111/all.13765Links to an external site.
Schwager, S., & Detmar, M. (2019). Inflammation and lymphatic function. Frontiers in Immunology, 10. https://doi.org/10.3389/fimmu.2019.00308Links to an external site.
NU 451 ALTERATIONS IN CELLULAR PROCESSES Grading Rubric
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