NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

Walden University NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes-Step-By-Step Guide

 

This guide will demonstrate how to complete the Walden University  NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.

 

How to Research and Prepare for NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

 

Whether one passes or fails an academic assignment such as the Walden University  NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.

 

After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.

 

How to Write the Introduction for  NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes 

 

The introduction for the Walden University  NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.

 

How to Write the Body for  NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes 

 

After the introduction, move into the main part of the  NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.

 

Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.

 

How to Write the Conclusion for  NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes 

 

After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.

 

How to Format the References List for  NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

 

The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.

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Sample Answer for NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

This paper is being written to explain the pathology of cystic fibrosis. I personally have a friend who has this disease and have learned from her. The topics that will be covered are, how cystic fibrosis is created at a cellular level, genetics role in cystic fibrosis, the reasoning for the symptoms that the patient presented with, the description of the cells involved in cystic fibrosis, and how other characteristics would change the child’s response to cystic fibrosis. In short what I remember from nursing school is that cystic fibrosis is a genetic disorder which is an autosomal recessive gene that is carried by both the mother and the father. The abnormality occurs in chromosome 7 which is where creates an inability to transport small molecules across the cell’s membrane, which in turn, dehydrates the cells of the epithelium and this then creates dry secretion. This is a broad overview of what this disease is, but I will go into further detail below.

 The Role Genetics Plays in the Disease

Genetics play an important role in this disease, according to an article published in PubMed titled Cystic fibrosis genetics: from molecular understanding to clinical application states that due to a defective epithelial cell that is defective, this cell is inherited and is an autosomal recessive gene. The genetic information that is in the cell, which is the recipe for the cell to make proteins (Cutting, 2015).  According to Pathophysiology of disease: An introduction to clinical medicine, if a person receives a cystic fibrosis transmembrane conductance regulator gene (CFTCR), or a person can receive two copies of the CFTCR gene. This copy has a mutation of the cystic fibrosis gene, furthermore these two copies of the CFTR gene have stored a mutation which is the on chromosome seven. So, when the recipe is being presented to the cell to be made, the genetic information is then stored into the deoxyribonucleic acid which is known as DNA.  This is part of the twenty-three pairs of chromosomes, but on the seventh chromosome, the cystic fibrosis recipe is stored in that chromosome. In the DNA, where the CFTCR gene recipe lives, if there is one copy of the recipe than the gene will not show up in the person but will be a carrier but if there are two copies of the recipe being stored in the chromosome than the cystic fibrosis gene than the person will have cystic fibrosis (McCance at el., 2019).

Why the Patient is Presenting with the Specific Symptoms Described

The baby’s symptoms included salty skin, a swollen stomach on occasion, and a failure to gain weight normally. According to an article published in the Journal of Cystic Fibrosis titled Inflammation in cystic fibrosis lung disease: Pathogenesis and therapy, epithelia make up the major organ systems. The sweat glands, liver’s bile duct, and intestines in the gastrointestinal tract are all affected in this patient. The article goes on to explain that the patient suffers from malnutrition and does not grow normally as a result of the loss of pancreatic function. As a result, enzyme replacement is critical for this patient in order to prevent cell clogging caused by an inability to breakdown a key nutrient (Cutting, 2015).

The physiologic response to the stimulus presented in the scenario and why you think this response occurred

After reading different sources, I was able to breakdown the pathology behind this patient’s symptoms. This disease starts with the CFTR gene protein being mutated in the chromosome seven, which there are two copies of the recipe, this mutation causes the decrease of chloride acceptance and ion being transported, then this makes the absorption of water to increase which throws off ciliary from completing the job and there is mucus that is dry, this is what causes the skin to be salty of the baby. The stomach inflammation and swelling that is being experienced, is due to the CFTR gene protein not having the right recipe present to the epithelial cell, this is causing malfunction by changing the reabsorption of the sodium, chloride and potassium in the cell, the recipe tells the cell to keep the sodium, chloride and potassium outside of the cell, this causes a back-up of outside of the cell structure and blocks the cell from absorbing the nutrients especially, proteins, fats and vitamins that are fat soluble.

The Cells that are Involved in this Process

The cells involved in this process begin with epithelial membranes found in the digestive tract, pancreas, airways, and reproductive area. According to an article in Apoptosis Journal, cystic fibrosis is caused by epithelial cell dysfunction, which leads to inflammation and an inability to create homeostasis due to the CFTR gene’s constant inflammation. Furthermore, the epithelial cells fail and undergo apoptosis as a result of the inflammation that occurs in the endoplasmic reticulum (Soleti at el., 2013).

How another characteristic (e.g., gender, genetics) would change your response

For cystic fibrosis, it is important to understand that this would not be a disease if the parents did not carry the gene. The

gene is the CFTR gene mutation, mentioned throughout this paper. According to a study done by Harvard Stem Cell Institute, where a lung cell was isolated to examine the function of the CFTR gene. It was shown in the study that if the ionocytes in the cell are not doing their job because it is expressing CFTR gene in increased levels, then the symptoms are created in the cell (Montoro at el., 2018). This occurs in the form of thick mucus and creates the response in the body that does not allow for the patient to regulate sodium, chloride, and potassium in a normal fashion.

Conclusion

During this journey of studying disease in depth and truly understanding how they work will help in the future of my career. I believe that if screening done at the hospitals before they leave would be beneficial. When parents are informed about the possibility of something occurring and what it means, parents will be empowered and get treatment before or if cystic fibrosis symptoms could show up. Also, encouraging parents to come to their baby checkups, will also allow for the medical staff to ask the right questions and treat the baby early, if they see symptoms. Cystic fibrosis is a challenge some patients may struggle with and it is our job as practitioners to catch things before extreme measures need to be taken.

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.

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.

Check Out Also: NURS 6501 Week 1 Discussion Alterations in Cellular Processes

Read a selection of your colleagues’ responses.

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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

Sample Answer 2 for NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

What I have found through researching is that genetics make up more than 50% of substance use disorder/ addiction. One way genetics affects the person is through a predisposition. If an abuser has a close family member (parent, grandparent or sibling) that has struggled with addiction, they may be predisposed of developing an addiction also.  Another way is by their environment. If children are exposed to drugs and alcohol growing up, as they become adults, they are more susceptible to developing a problem. Dopamine receptors play a part in addiction/abuse.  People who have fewer dopamine receptors are more likely to become alcoholics as well as have an increased risk for cocaine or heroin (Ashley Addiction Treatment, 2022).  There are other risk factors that are involved such as environmental, personality traits, mental health, and the age of exposure.

Genes, developmental stage, gender, and ethnicity are among the biological factors that can influence the risk of substance abuse, according to NIDA (2020). Between 40 and 60 percent of a person’s risk of developing an addiction is caused by genes and environmental risk factors. According to NIDA (2020), adolescents and people with mental health issues are more likely than others to use drugs and become addicted. Numerous genes have been linked to addiction in general, as well as genes linked to addiction to particular substances. For instance Alcohol dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (ALDH2; mitochondrial aldehyde dehydrogenase), alcohol metabolism is influenced by these genes. Hereditary contrasts that lead to higher ADH1B movement or lower ALDH2 action can bring about an individual encountering awkward side effects assuming they drink liquor which may lead to a defensive impact against alcohol abuse.  GABRA2 and CHRM2 genes are linked to alcohol use disorder (AUD). CHRNA2 gene has been linked to cannabis use disorder and HIST1H2BD is linked to being associated with cocaine dependence (NIDA, 2020). Chemical substances (opioids or cocaine) alters the dopamine receptors (brain reward center), and will eventually bring about addicitve behaviors characterized by diminished sensitivity to natural rewards. The reward deficiency syndrome has been linked to opioids and other drugs (Gondré-Lewis, et al., 2022).

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References:

Are genetics and substance use related? – ashley treatment. Ashley Addiction Treatment. (2022, August 26). https://www.ashleytreatment.org/rehab-blog/genetics-substance-use-related/#:~:text=Scientists%20have%20found%20that%20genetics,history%20of%20dependence%20or%20addiction

Links to an external site..

Gondré-Lewis, M. C., Elman, I., Alim, T., Chapman, E., Settles-Reaves, B., Galvao, C., … & Blum, K. (2022). Frequency of the dopamine receptor D3 (rs6280) vs. opioid receptor µ1 (rs1799971) polymorphic risk alleles in patients with opioid use disorder: a preponderance of dopaminergic mechanisms?. Biomedicines, 10(4), 870.

NIDA. 2020, July 13. Drug Misuse and Addiction. Retrieved from https://nida.nih.gov/publications/drugs-brains-behavior-science-addiction/drug-misuse-addiction on 2023, May 30

Sample Answer 3 for NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

Millions of Americans are estimated to be sickle cell trait carriers (Linder & McCance, 2019). I agree that sickle cell disease (SCD) is common in those with ancestors from Africa. However, it is a worldwide issue and can be found in those with ancestors such as “Mexican Americans, and white Americans, especially those whose families originally came from Turkey, Italy, Greece, Spain, and other Latin American or Mediterranean countries” (Texas Health and Human Services, n.d.). SCD is transmitted as an autosomal recessive disorder, and few clinical studies have examined how it affects the genders (Ceglie et al., 2019).

The SCD and sickle cell trait (HbAS) run throughout my family. Knowing if one has SCD or HbAS is essential because it can be passed down from parent to child. Typically, infants are tested for SCD during their neonatal screening (Linder & McCance, 2019). One is likely to inherit the disease when both parents are carriers. It is important to note that if both parents have HbAS, they have a one in four chance of having a child with SCD (Texas Health and Human Services, n.d.). If only one parent has HbAS, the child can not have SCD (Texas Health and Human Services, n.d.).

Sickle cell is “characterized by the presence of an atypical form of hemoglobin S (Hbs; sickle hemoglobin) within the erythrocytes.” (Linder & McCance, 2019). The beta chain of the hemoglobin is mutated and causes anemia (Linder & McCance, 2019). The cycle of malformation occurs when the RBC carries the malformed protein deoxygenate (Berkowitz, 2020). The genotypes for SCD include “homozygosity for the βS allele (HbS/S), heterozygosis for the βS allele and β-thalassemia (HbS/β), heterozygosity for the βS allele and some hemoglobin variants: HbS/C, HbS/D, HbS/Lepore-Boston” (Linder & McCance, 2019) (Ceglie et al., 2019). The disease is painful due to the effects on the hemoglobin.

The cell’s sickling, occasional, and intermittent phenomenon causes pain because they clog small blood vessels (Berkowitz, 2020) (Linder & McCance, 2019). Sickling can be triggered by prolonged exposure to stressors such as “hypoxia, acidosis, decreased plasma osmolality, decreased plasma volume, and temperature” (Linder & McCance, 2019). The clogs can cause acute painful crises, ischemia, stroke, and renal ischemia (Berkowitz, 2020). Individuals with SCD have been known to have a yearly crisis that requires a hospital stay (Ceglie et al., 2019). The reduction of stressors can help reduce the amount of SCD attacks one can have. Treatments for crisis include non-steroidal anti-inflammatory drugs (NSAIDs), minor opioids (tramadol or codeine), and significant opioids (morphine) (Ceglie et al., 2019). As you mentioned, SCD can be hard on the patient and the family; therefore, connecting them with support groups can be helpful. Thank you for your post.

References

Berkowitz, A. (2020). Chapter 6. The Hematologic System. In A. Berkowitz, Clinical Pathophysiology Made Ridiculously Simply (p. 122). Miami: MedMaster .

Ceglie, G., Di Mauro, M., Tarissi De Jacobis, I., de Gennaro, F., Quaranta, M., Baronci, C., . . . Palumbo, G. (2019). Gender-Related Differences in Sickle Cell Disease in a Pediatric Cohort: A Single-Center Retrospective Study. Retrieved June 3, 2023, from National Library of Medicine National Center for Biotechnology Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906547/#:~:text=The%20incidence%20of%20sickle%20cell,as%20an%20autosomal%20recessive%20disorder.

Linder, L., & McCance, K. (2019). Chapter 31: Alterations of Hematologic Function in Children. In L. A. Linder, & K. L. McCance, Pathophysiology. The Biologic Basis for Disease in Adults and Children. Eighth Edition (pp. 1000- 1004). Canada: Elsevier.

Texas Health and Human Services. (n.d.). Sickle Cell Disease – So Your Baby Has The Sickle Cell Trait. Retrieved June 3, 2023, from Texas Health and Human Services: https://www.dshs.texas.gov/newborn-screening-program/sickle-cell-disease/sickle-cell-trait/sickle-cell-disease-so#:~:text=If%20only%20one%20parent%20has,of%20having%20sickle%20cell%20anemia.

Sample Answer 4 for NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

Case Scenario 2:

Cystic Fibrosis is an autosomal recessive inherited disease that is caused by a defective epithelial chloride ion transport (McCance & Huether 2019). There are over 2000 different variants of the cystic fibrosis gene that are divided into six different classes. Classes one through three are more severe in nature, where classes four through six are milder pulmonary disease cases. Cystic fibrosis is more prominent in the white race than other races.

Cystic fibrosis is a multi-organ disease affecting the respiratory tract, digestive tract, and reproductive organs (McCance & Huether 2019). Genes within our bodies carry instructions for every part of our genetic make-up. When an error occurs within our genetic make-up, that is when diseases occur. The cystic fibrosis transmembrane conductance regulator (CFTR) is responsible for Cystic Fibrosis. When someone has cystic fibrosis, a change or mutation occurs within two copies of this gene causing the CFTR proteins that are not able to do their job correctly (Vertex 2023). When this occurs, the mucus that lines the organs become really thick, which causes increased infections and damage to those organs.

Children are at a 25% risk for developing cystic fibrosis if both parents are cystic fibrosis carriers and the children are at a 50% risk of being a cystic fibrosis carrier of the gene mutation, however, they do not develop the disease themselves. One in four children will not be carriers or have the disease (Chi & Whelan 2020). Once the parents have had a child that tests positive for cystic fibrosis, they still only have a one in four chance that each additional child may be born with cystic fibrosis. What this also means is that there is a three out of four chance that any additional children that they have may not have cystic fibrosis, but they may end up being cystic fibrosis carriers (Stanford 2023).

Individuals with high levels of chloride, which is part of salt, are present in people with a cystic fibrosis diagnosis. This is to be expected when the mom tastes a salty taste when kissing her child as it is secreted through the sweat glands. Cystic fibrosis causes significant problems within the digestive tract. Thick fluid blocks the ducts within the pancreas that makes enzymes that help the small intestines to break down food. Because the enzymes are not being made to help breakdown food, poor growth, slow weight gain, frequent, greasy, and bulky stools are the result regardless of the amount of food that is eaten. The liver can become inflamed as bile that is excreted is much thicker and can cause the bile ducts to become blocked. The thicker secretions can cause the large intestines to become blocked due to chronic constipation issues which will make the abdomen appear swollen and the child in much discomfort (Vertex 2023).

All children are screened 24 hours post birth by having a metabolic screen done that is then sent to the lab for analysis. Testing is important and further workup would be recommended for the 23-month-old child to make sure they are not affected by cystic fibrosis or to determine if they are a carrier of the disease as this could affect their children years down the road. The chances of the mother having another child with cystic fibrosis holds a 25% probability and a 50% chance of being a carrier without having a cystic fibrosis diagnosis, so it is important that the family knows the risk. As far as the mother wanting to know if she should have more children, if she is aware of the risks that are involved, that is a decision that she and her partner will have to make.

References:

Chi, E., & Whelan, C. (2020). Cystic Fibrosis Carrier: What You Need to Know. Retrieved from https://www.healthline.com/health/cystic-fibrosis-carrier#in-childrenLinks to an external site.

McCance, K., & Huether, S. (2019). Pathophysiology: The Biologic Basis for Disease in Adults and Children. Chapter 13: Alterations of Pulmonary Function in Children.

Stanford Medicine Children’s Health. (2023). The Genetics of Cystic Fibrosis. Retrieved from https://www.stanfordchildren.org/en/topic/default?id=the-genetics-of-cystic-fibrosis-90-PO2933Links to an external site.

Vertex Pharmaceuticals Incorporated. (2023). CF Within the Cells. Retrieved from https://www.cfsource.comLinks to an external site.

Sample Answer 5 for NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

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.

 

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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