NURS 6051 Discussion Alterations in Cellular Processes

NURS 6051 Discussion Alterations in Cellular Processes

In the given scenario, the young boy received treatment with amoxicillin following a positive rapid strep test and the manifestation of symptoms. Common symptoms of strep throat include fever, red and swollen tonsils, purulent tonsils, pain during swallowing, petechiae, odynophagia, and swollen lymph nodes (CDC, 2021). The localized inflammatory response involves vascular changes and fluid leakage into the tissues (McCance & Huether, 2019). The redness and swelling result from increased blood flow through vasodilation, allowing white blood cells to infiltrate the infected area. The pain is attributed to heightened pressure on the tissues caused by fluid accumulation. The purulent exudate is the consequence of phagocytic cell death in the region, expelled through the epithelial tissue in the throat. These cells, having reached maturity, can no longer replicate and are sensitive to the body’s acidic environment, leading to their demise after fulfilling immunological duties (McCance & Huether, 2019).

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The lymphatic system plays a pivotal role in the manifestation of anterior and posterior cervical adenopathy. Lymphatic channels transport body fluids from the infection site to nodules, causing swelling due to fluid shifts. These nodes act as processing centers, introducing invaders to B-cells, T-cells, and macrophages residing within the nodes (NCBI, 2021). The immune system analyzes the invaders and fine-tunes its response.

Upon administration of amoxicillin, the physiologic response exhibited a type 1 hypersensitivity reaction. Cells in the body perceived amoxicillin as a threat, initiating an inflammatory immune response. This process begins with mast cells, strategically located in skin, blood vessels, and lung tissue. Mast cells can be activated by various stimuli, including injury, chemicals, adaptive immune responses, or molecular patterns of viruses and bacteria (McCance & Huether, 2019). Immunoglobulin E (IgE), present in blood plasma, binds to mast cells, prompting the release of prostaglandins, interleukins, leukotrienes, and histamine through degranulation. Histamine, a crucial chemical in this reaction, binds to the H1 receptor, causing hives, vasodilation, bronchoconstriction, hypotension, and increased mucous production. This facilitates the entry of phagocytes like neutrophils, eosinophils, and dendritic cells into the injured area. The ensuing influx of red blood cells, other body fluids, and white blood cells induces edema in affected areas. The excess fluid response to the threat led to edema in the tongue, lips, airway, and increased secretion of lung tissues, posing an urgent concern due to the potential for airway compromise, which is life-threatening.

Strep throat is more prevalent in children, particularly those aged five to 15, with crowded areas such as schools and daycare centers posing an increased risk of transmission (CDC, 2018). The recent quarantine measures may have contributed to slowing the spread by keeping children at home. Despite being on the higher age range for children with strep throat, the boy’s social situation could still influence the likelihood of contracting the infection.

nurs 6051 discussion alterations in cellular processes

NURS 6051 Discussion Alterations in Cellular Processes

NURS 6051 Discussion Alterations in Cellular Processes

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Genetic factors also contribute significantly to the scenario. About ten percent of all U.S. patients have reported past allergies to penicillin-class antibiotics (CDC, n.d.). The transmission of allergies from parents to children through genetics is a well-documented phenomenon (NCBI, 2014). Consequently, it is advisable to conduct allergy testing in children at a young age. This proactive measure allows for the anticipation of severe allergic reactions, helping to avoid potentially life-threatening situations.

Thanks,

Centers for Disease Control (CDC). (n.d.) Is it really a penicillin allergy? https://www.cdc.gov/antibiotic-use/community/pdfs/penicillin-factsheet.pdf

Centers for Disease Control (CDC). (2021, January 12) Strep throat: all you need to know. https://www.cdc.gov/groupastrep/diseases-public/strep-throat.html

Centers for Disease Control (CDC). (2018, November) Group A streptococcal (gas) disease. https://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html

McCance, K., & Huethe, S. (2019) Pathophysiology the biologic basis for disease in adults and children (8thed.). St. Louis, MO: Elsevier

National Center for Biotechnology Information (NCBI). (2021). Adenopathy. https://www.ncbi.nlm.nih.gov/books/NBK513250/

National Center for Biotechnology. (2014) Genetics of allergic diseases. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4415518/

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Discussion: Alterations in Cellular Processes

Photo Credit: Getty Images

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, 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.

In this week’s case study, the patient presents with a chief complaint of a sore throat and multiple other

In this week’s case study, the patient reported a chief complaint of a sore throat along with various other symptoms, leading to a positive strep test. Strep throat, also termed bacterial pharyngitis, is caused by Streptococcus group A bacteria, primarily transmitted through respiratory droplets, and stands as the predominant cause of pharyngitis in children (Chauhan et al., 2016). A recent meta-analysis revealed that 37% of children under 18 years were diagnosed with Group A Strep, seeking outpatient treatment for a sore throat, compared to only 15% of adults (Ashurst & Edgerley-Gibb, 2022).

Clinical presentation included a sore throat, a reddened posterior pharynx with white exudate, and enlarged 3+ tonsils—all attributed to the presence and colonization of Streptococcus bacteria. The observed anterior and posterior cervical adenopathy signifies the body’s response to combat the infection. The prescribed ten-day course of amoxicillin led to immediate adverse reactions in the patient, characterized by swelling of the tongue and lips, difficulty breathing, and wheezing—an anaphylaxis reaction to the antibiotics. Anaphylaxis, an IgE-mediated response, involves mast cells releasing a substantial amount of histamine and leukotrienes, resulting in bronchospasm and edema (Vaillant, Vashisht, & Zito, 2022).

Despite antibiotic treatment, some children experience recurrent strep throat due to genetic factors. A study by Dr. Shane Crotty and Dr. Jennifer Dan (2019) explored germinal centers in children with a normal infection rate versus those with recurrent tonsillitis. Their findings indicated that children with recurring strep throat had smaller germinal centers with fewer B and helper T cells, responsible for antibody production and combating invading pathogens. Further research identified a genetic component, specifically two variants in the HLA genomic region, associated with increased susceptibility to recurrent tonsillitis and protective against the disease. In cases of recurring group A streptococcus pharyngitis, a different approach, such as referral to an Ear, Nose, and Throat (ENT) specialist for a tonsillectomy, might be warranted rather than relying solely on antibiotic treatment.

NURS 6051 Discussion 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

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.

Discussion: Alteration in Cellular Processes

Malnutrition, a pervasive issue globally, exhibits varying prevalence in different regions such as third-world countries and the United States of America. While malnutrition is commonly observed in children, its prevalence is notably higher among the elderly in the United States. Symptoms often go unnoticed due to subtle signs, further complicated by the challenge of recognizing symptoms, often attributed to the aging process (Alliance for Aging Research, 2016).

This discussion centers around a brief scenario involving an 83-year-old individual presenting with generalized edema of the extremities and abdomen. The patient, with a history of malabsorption syndrome and difficulty eating due to a lack of dentures, receives a diagnosis of Protein Malnutrition. This disease will be explored comprehensively, delving into the presented symptoms, the cells responsible for the illness, and potential variations and effects of protein malnutrition.

Role of Genetics in the Disease

The formation and reproduction of deoxyribonucleic acid (DNA) within the nucleus’s cell result in the formation of proteins in the cytoplasm, involving two phases known as transcription and translation, with the intervention of ribonucleic acid (RNA) (McCance & Huether, 2019). Transcription, facilitated by the RNA polymerase enzyme, involves bonding to a specific DNA region, forming a gene. Transcription factor binding sites, originating from the DNA segment, regulate specific genes for transcription, influencing the timing of the process. Enhancers often enhance transcription by creating or inhibiting genes. The RNA polymerase generates mRNA nucleotides, guiding the cycle of mRNA nucleotides. Transcription concludes when the DNA cycle, known as the termination sequence, is achieved.

Subsequently, RNA polymerase detaches from the DNA, allowing the transcribed mRNA to exit the nucleus into the cytoplasm (McCance & Huether, 2019). The second step, translation, involves the transition from a gene to the formation of a protein in the cytoplasm. Translation engages with transfer RNA (tRNA) for amino acids, accommodating amino acids due to tRNA’s structure. Anticodon, a combination of three nucleotides, pairs with the correct codon in the mRNA, determining the order of amino acids. The communication between mRNA and tRNA, facilitated by ribosomes in the cytoplasm, leads to the formation of a bond adjacent to amino acids, resulting in polypeptide production. At the terminal stage, the ribosome signals the cessation of mRNA sequence, translation, and polypeptide growth, after which they separate. The polypeptide is then transported into the cytoplasm to perform its function (McCance & Huether, 2019).

Reasons for the Patient’s Specific Symptoms

Protein deficiency contributes to the accumulation of intestinal mucosa, reducing absorption rates and impairing functionality. Low levels of protein in the blood lead to protein malnutrition. Additionally, reduced albumin levels result in diminished intravascular osmotic pressure, causing the retention of fluid in the extravascular space, manifesting in the patient’s symptoms of tissue edema and ascites (McConnell, 2014).

The Physiologic Response to the Stimulus and Why the Response Occurred

A decline in plasma oncotic pressure, attributed to the loss of albumin production, leads to the escape of fluid from capillaries into the interstitial space, causing edema in the extremities. The combination of decreased plasma protein composition and reduced osmotic pressure culminates in the patient’s diagnosis of protein malnutrition (McCance & Huether, 2019). Increased capillary permeability is another physiologic response, where an excess of fluids exits the plasma into the interstitial space, causing swelling as observed in the patient’s symptoms. This challenging situation arises due to protein loss from the vascular area, leading to decreased osmotic pressure and increased fluid in the interstitial oncotic pressure, facilitating the entry of free fluids into the interstitial space (McCance & Huether, 2019). The patient’s physiologic response includes localized edema of the abdomen, reflecting an excess accumulation of fluid in this region (McCance & Huether, 2019).

Cells Involved in this Process

Cells exhibit diverse specializations based on differentiation or maturity, performing various functions such as muscle movement, conductivity, absorption, secretion, excretion, respiration, reproduction, and communication (McCance & Huether, 2019). In this scenario, the focus is on cells involved in metabolic absorption, with cells in the intestine and kidney responsible for the absorption and re-absorption of fluids and protein synthesis. Specifically, cells from the intestinal epithelium play a crucial role in reabsorbing fluids and protein enzymes. The endoplasmic reticulum (ER) is involved in synthesizing and transporting protein and lipid constituents of cell organelles (McCance & Huether, 2019).

How Gender Changed My Response

Gender differences contribute to variations in protein levels, particularly in the context of c-reactive protein (CRP). Research indicates that blacks tend to have higher CRP levels compared to whites, and women tend to have higher CRP levels than men (Khera et al., 2005). Understanding these gender and race-related disparities in protein levels becomes crucial, as it may impact the assessment tools and approaches used by healthcare providers. This information adds an essential dimension to the evaluation of protein malnutrition, considering its prominence in different racial and gender groups.

Review a Selection of Colleague 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!

The Impact of Genetics on the Disease:

The human body comprises approximately 20,000 to 25,000 genes that dictate its structure and function. Any errors in these genes can result in genetic diseases, which may be passed on to subsequent generations (McCance & Huether, 2019, p.133). The genetic code stored in DNA instructs the synthesis of proteins, composed of polypeptides. With the body consisting of 20 different amino acids and four bases (Thymine, Adenine, Guanine, and Cytosine), the complementary base pairing mechanism is crucial for DNA replication. Mutations, occurring when base pairs substitute, represent inherited alterations in genetic material (McCance & Heuther, 2019, p.137).

Understanding the Patient’s Specific Symptoms:

The patient is undergoing an anaphylactic reaction following the ingestion of amoxicillin. With a temperature of 99.6 F, the body’s response is triggered by either the positive strep test or the amoxicillin itself. This immediate reaction falls under type 1 hypersensitivity, with anaphylaxis symptoms manifesting within 24 hours. Amoxicillin, belonging to the penicillin antibiotic group, can commonly induce anaphylaxis, which is IgE-mediated. The IgE production characterizes a type I hypersensitivity reaction, capable of initiating anaphylaxis. Symptoms such as swelling of the tongue and lips and difficulty breathing are indicative of the anaphylactic response (Justiz & Zito, 2019).

Physiological Response to the Stimulus and Its Rationale:

The patient is undergoing a type I hypersensitivity reaction, where immunoglobulin IgE is produced and binds to Fc receptors on mast cells and basophils. Upon encountering the allergen, in this case, amoxicillin, cytophilic IgE cells are triggered, leading to the activation of mast cells and their degranulation, releasing histamine and other mediators. This allergic reaction results in edema, bronchoconstriction, and inflammation (Justiz & Zito, 2019).

Cells Involved in the Process:

Histamine and lipid mediators, including PAF, LTC4, and PGD2, are key players in type I hypersensitivity reactions. Tumor necrosis factor (TNF) induces inflammation, while eosinophils release cationic granule proteins and eosinophil peroxidase, contributing to tissue remodeling. IgE antibodies, produced by the immune system in response to allergens, bind to mast cells and basophils, which contain histamine granules, initiating inflammation. The symptoms, such as lip edema and bronchoconstriction, are outcomes of this hypersensitivity reaction (Justiz & Zito, 2019).

Impact of Other Characteristics on the Response:

Type 1 hypersensitivity reactions can have both genetic and environmental predispositions. Testing can identify type I hypersensitivity allergies, and avoiding triggers is the most effective preventive measure. Genetic factors, including certain genes and elevated levels of IgE antibodies, can contribute to a higher susceptibility to type 1 reactions. Although environmental factors may influence sensitivity, the fundamental immune response to type 1 hypersensitivity reactions remains consistent and would not change based on gender or genetics (Abbas et al., 2022).

NURS 6051 Discussion Alterations in Cellular Processes References

Abbas, M., Moussa, M., & Akel, H. (2022, July 18). Type I hypersensitivity reaction. Retrieved February 27, 2023, from https://www.ncbi.nlm.nih.gov/books/NBK560561/

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/

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

Submission and Grading Information

Grading Criteria

To access your rubric:

Week 1 Discussion Rubric

Post by Day 3 of Week 1 and Respond by Day 6 of Week 1

To Participate in this Discussion:

Week 1 Discussion

Assignment Practicum Manual Acknowledgment

The Practicum Manual describes the structure and timing of the classroom-based and practicum experiences and the policies students must follow to be successful in the nurse practitioner (NP) specialties.

Click here and follow the instructions to confirm you have downloaded and read the entire MSN Nurse Practitioner Practicum Manual and will abide by the requirements described in order to successfully complete this program.

What’s Coming Up in Week 2?

Photo Credit: [BrianAJackson]/[iStock / Getty Images Plus]/Getty Images

Next week, you will examine alterations in the immune system and the resultant disease processes. You will also consider patient characteristics, including racial and ethnic variables, that may impact altered physiology.

Practicum – Upcoming Deadline

In the Nurse Practitioner programs of study (FNP, AGACNP, AGPCNP, and PMHNP) you are required to take several practicum courses. If you plan on taking a practicum course within the next two terms, you will need to submit your application via Meditrek .

For information on the practicum application process and deadlines, please visit the Field Experience: College of Nursing: Application Process – Graduate web page.

Please take the time to review the Appropriate Preceptors and Field Sites for your courses.

Please take the time to review the practicum manuals, FAQs, Webinars and any required forms on the Field Experience: College of Nursing: Student Resources and Manuals web page.

Next Week

To go to the next week:

Week 1: Cellular Processes and the Genetic Environment

One of the more common biology analogies refers to cells as the “building blocks” of life. This rightfully places an emphasis on understanding cells, cellular behavior, and the impact of the environment in which they function.

Such an understanding helps explain how healthy cell activity contributes to good health. Just as importantly, it helps explain how breakdowns in cellular behavior and alterations to cells lead to health issues.

This week, you examine cellular processes that are subject to alterations that can lead to disease. You evaluate the genetic environments within which these processes exist as well as the impact these environments have on disease.

Learning Objectives

Students will:

  • Evaluate cellular processes and alterations within cellular processes
  • Evaluate the impact of the genetic environment on disease

Learning Resources

Required Readings (click to expand/reduce)

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

  • Chapter 1: Cellular Biology; Summary Review
  • Chapter 2: Altered Cellular and Tissue Biology: Environmental Agents (pp. 46-61; begin again with Manifestations of Cellular Injury pp. 83-97); Summary Review
  • Chapter 3: The Cellular Environment: Fluids and Electrolytes, Acids, and Bases
  • Chapter 4: Genes and Genetic Diseases (stop at Elements of formal genetics); Summary Review
  • Chapter 5: Genes, Environment-Lifestyle, and Common Diseases (stop at Genetics of common diseases); Summary Review
  • Chapter 7: Innate Immunity: Inflammation and Wound Healing
  • Chapter 8: Adaptive Immunity (stop at Generation of clonal diversity); Summary Review
  • Chapter 9: Alterations in Immunity and Inflammation (stop at Deficiencies in immunity); Summary Review
  • Chapter 10: Infection (pp. 289–303; stop at Infectious parasites and protozoans); (start at HIV); Summary Review
  • Chapter 11: Stress and Disease (stop at Stress, illness & coping); Summary Review
  • Chapter 12: Cancer Biology (stop at Resistance to destruction); Summary Review
  • Chapter 13: Cancer Epidemiology (stop at Environmental-Lifestyle factors); Summary Review

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/

Credit Line: Immediate Hypersensitivity Reactions – StatPearls – NCBI Bookshelf. (2019, June 18). Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK513315/. Used with permission of Stat Pearls

Required Media (click to expand/reduce)

Module 1 Overview with Dr. Tara Harris 

Dr. Tara Harris reviews the structure of Module 1 as well as the expectations for the module. Consider how you will manage your time as you review your media and Learning Resources throughout the module to prepare for your Discussion and Assignment. (4m)

Foundational Concepts of Cellular Pathophysiology – Week 1 (14m)

Immunity and Inflammation

Khan Academy (2010, February 24). Inflammatory response | Human anatomy and physiology | Health & medicine [Video file]. Retrieved from https://www.youtube.com/watch?v=FXSuEIMrPQk  

Note: The approximate length of the media program is 14 minutes.

Soo, P. (2018, July 28). Pathophysiology Ch 10 alterations in immune function [Video file]. Retrieved from https://www.youtube.com/watch?v=Jz0wx1-jTds   

Note: The approximate length of the media program is 37 minutes.

Acid-Base Balance #1

MedCram. (2012, April 28). Medical acid base balance, disorders & ABGs explained clearly [Video file]. Retrieved from https://www.youtube.com/watch?v=4wMEMhvrQxE 

Note: The approximate length of the media program is 13 minutes.

Acid-Base Balance #2

MedCram. (2012, April 29). Medical acid base balance, disorders & ABGs explained clearly | 2 of 8 [Video file]. Retrieved from https://www.youtube.com/watch?v=GmEeKVTpOKI  

Note: The approximate length of the media program is 15 minutes.

Hyponatremia

MedCram. (2017, December 23). Hyponatremia explained clearly (remastered) – Electrolyte imbalances [Video file]. Retrieved from https://www.youtube.com/watch?v=bLajK5Vy55M 

Note: The approximate length of the media program is 15 minutes.

Online Media from Pathophysiology: The Biologic Basis for Disease in Adults and Children

In addition to this week’s media, it is highly recommended that you access and view the resources included with the course text, Pathophysiology: The Biologic Basis for Disease in Adults and Children. Focus on the videos and animations in Chapters 3, 7, and 8 that relate to alterations in immunity, hyponatremia, and acid/base balance.

Note: To access the online resources included with the text, you need to complete the FREE online registration that is located at https://evolve.elsevier.com/cs/store?role=student

To Register to View the Content

  1. Go to https://evolve.elsevier.com/cs/store?role=student
  2. Enter the name of the textbook, Pathophysiology: The Biologic Basis for Disease in Adults and Children, or ISBN 9780323654395 (name of text without the edition number) in the Search textbox.
  3. Complete the registration process.

To View the Content for This Text

  1. Go to https://evolve.elsevier.com/
  2. Click on Student Site.
  3. Type in your username and password.
  4. Click on the Login button.
  5. Click on the plus sign icon for Resources on the left side of the screen.
  6. Click on the name of the textbook for this course.
  7. Expand the menu on the left to locate all the chapters.
  8. Navigate to the desired content (checklists, videos, animations, etc.).

Note: Clicking on the URLs in the APA citations for the Resources from the textbook will not link directly to the desired online content. Use the online menu to navigate to the desired content.

Kidney transplant is an effective treatment for patients suffering from end-stage renal disease. However, some patients develop adverse effects including kidney rejection. The management of kidney transplant rejection depends on the type and patient factors. Therefore, this paper examines why a patient with acute kidney transplant developed the described symptoms, genes associated with kidney transplant rejection and process of immunosuppression.

Reasons for the Patient’s Symptoms:

The patient exhibited symptoms such as weight gain, decreased urinary output, fatigue, and a temperature of up to 101 F. The weight gain can be attributed to an elevated body fluid volume, with impaired kidney function hindering the proper regulation of fluids, leading to their accumulation and subsequent weight gain. Additionally, the decline in renal function affected normal urine output, resulting in reduced urine production, as observed in the case study. The compromised renal function also impacted the elimination of toxins, including excess ammonia, contributing to symptoms like fatigue, poor concentration, acidosis, and anemia. Patients experiencing kidney transplant rejection or end-stage renal disease often face immunosuppression, making them more susceptible to infections, thus explaining the patient’s fever (Rauen et al., 2020).

Genetic Factors in Disease Development:

Several genes have been linked to kidney transplant rejection, including cytochrome p450 2EI (CYP2EI), CYP3A5, cytotoxic T-lymphocyte-associated protein 4 (CTLA4), C-X-C motif chemokine ligand 8 (CXL8), epoxy hydrolase 2, coagulation factor II thrombin, and coagulation factor V genes. Additionally, Forkhead box P3, Fc fragment of IgG receptor IIA, major histocompatibility complex class II, I, DO alpha, interleukin 1 beta, 2, 2-receptor subunit beta genes play roles in rejection development. Interleukin genes, inflammatory cytokines, regulate inflammatory processes post-allograft, but they also hinder antigen and cell maturation, impacting the host’s immunity post-transplant. ATP-binding genes enhance the body’s resistance to immunosuppressive drugs used post-transplant (Arnold et al., 2022; Spicer & Runkel, 2019; van Vugt et al., 2022).

Understanding Immunosuppression:

Immunosuppression refers to the state where the body’s ability to combat infections is diminished, achieved through medications or conditions like cancer. Medications for cancer and treatments like radiotherapy and chemotherapy induce immunosuppression, rendering patients more susceptible to infections. The consequences of immunosuppression include heightened vulnerability to infections, increased healthcare costs due to frequent hospitalizations, a negative impact on the quality of life through prolonged infections, and potential mortality in severe cases of compromised immune systems (Gupta et al., 2021).

Conclusion on Alterations in Cellular Processes:

In summary, the patient’s symptoms stemmed from diminished renal function, with genetic factors playing a crucial role in kidney transplant rejection. This rejection can lead to immunosuppression, introducing adverse health effects and complicating the patient’s overall well-being.

NURS 6051 Discussion Alterations in Cellular Processes References

Arnold, M.-L., Heinemann, F. M., Oesterreich, S., Wilde, B., Gäckler, A., Goldblatt, D., Spriewald, B. M., Horn, P. A., Witzke, O., & Lindemann, M. (2022). Correlation of Fc Receptor Polymorphisms with Pneumococcal Antibodies in Vaccinated Kidney Transplant Recipients. Vaccines, 10(5), Article 5. https://doi.org/10.3390/vaccines10050725

Gupta, R., Woo, K., & Yi, J. A. (2021). Epidemiology of end-stage kidney disease. Seminars in Vascular Surgery, 34(1), 71–78. https://doi.org/10.1053/j.semvascsurg.2021.02.010

Rauen, T., Wied, S., Fitzner, C., Eitner, F., Sommerer, C., Zeier, M., Otte, B., Panzer, U., Budde, K., Benck, U., Mertens, P. R., Kuhlmann, U., Witzke, O., Gross, O., Vielhauer, V., Mann, J. F. E., Hilgers, R.-D., Floege, J., Floege, J., … Hilgers, R.-D. (2020). After ten years of follow-up, no difference between supportive care plus immunosuppression and supportive care alone in IgA nephropathy. Kidney International, 98(4), 1044–1052. https://doi.org/10.1016/j.kint.2020.04.046

Spicer, P., & Runkel, L. (2019). Costimulatory pathway targets for autoimmune and inflammatory conditions: Clinical successes, failures, and hope for the future. Expert Opinion on Investigational Drugs, 28(2), 99–106. https://doi.org/10.1080/13543784.2019.1557146

van Vugt, L. K., Schagen, M. R., de Weerd, A., Reinders, M. E., de Winter, B. C., & Hesselink, D. A. (2022). Investigational drugs for the treatment of kidney transplant rejection. Expert Opinion on Investigational Drugs, 31(10), 1087–1100. https://doi.org/10.1080/13543784.2022.2130751

This 16-year-old patient presented to the Primary Care Physician (PCP) and was diagnosed with strep throat. The cells, having traversed the extracellular matrix (McCance & Huether, 2019), are now injured due to the infection. In response, the PCP prescribed antibiotics to reverse the cellular damage. The infection-induced damage is evident in the patient’s symptoms, including a reddened pharynx and enlarged tonsils with white patches. Additionally, the cells in the 16-year-old are undergoing hypertrophy, leading to an increase in the size of the tonsils.

After taking two doses of amoxicillin 500mg, the patient experienced swelling of the tongue and lips, difficulty breathing, and audible wheezing—indicative of anaphylaxis. This is an IgE-mediated reaction, where IgE antibodies produced by the immune system trigger mast cells and basophils through the binding of Fc receptors, leading to an allergic response. Enzymes such as tryptase contribute to tissue damage, while TNF induces inflammation (Justiz-Vaillant & Zito, 2019).

Initially, the patient had no known drug allergies. The emergence of a new drug allergy, particularly in the context of a recurrent infection, raises questions. To confirm the amoxicillin allergy as a true allergy, the PCP can utilize an allergic test known as a radioallergosorbent test (RAST) (Justiz-Vaillant & Zito, 2019).

It’s noteworthy that the patient’s anaphylaxis is generalized and not systemic. Studies indicate that penicillin accounts for 40.7% of antibiotics causing anaphylaxis, with a higher likelihood in females and those with comorbidities or other medications (Regateiro, Marques, & Gomes, 2020).

Reference:

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/

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

Regateiro, F. S., Marques, M. L., & Gomes, E. R. (2020). Drug-Induced Anaphylaxis: An Update on Epidemiology and Risk Factors. International Archives of Allergy and Immunology, 181(7), 481–487. https://doi.org/10.1159/000507445

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