NR 507 Week 1: Case Study
Chamberlain University NR 507 Week 1: Case Study– Step-By-Step Guide
This guide will demonstrate how to complete the Chamberlain University NR 507 Week 1: Case Study 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 NR 507 Week 1: Case Study
Whether one passes or fails an academic assignment such as the Chamberlain University NR 507 Week 1: Case Study 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 NR 507 Week 1: Case Study
The introduction for the Chamberlain University NR 507 Week 1: Case Study 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.
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How to Write the Body for NR 507 Week 1: Case Study
After the introduction, move into the main part of the NR 507 Week 1: Case Study 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 NR 507 Week 1: Case Study
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 NR 507 Week 1: Case Study
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 NR 507 Week 1: Case Study
Pathophysiology and Clinical Findings of the Disease
Hypersensitivity Reaction
The patient is likely suffering from allergic rhinitis (AR). AR is a chronic respiratory illness that affects the quality of life for 40% of the global population (Zheng et al., 2022). The physician can utilize various diagnostic techniques to confirm the patient’s symptoms are due to allergy. The doctor may examine the history and identify clues in lifestyle to explain the cause of the symptoms. For instance, the practitioner may ask about work and home environments, including the presence of a pet (American College of Allergy, Asthma, and Immunology [ACAAI], 2020). Engaging the 35-year-old woman is crucial since it helps provide an accurate diagnosis of AR. Additionally, a skin prick or intradermal test can be done to determine AR. The procedure involves introducing a small amount of a potential allergen into the skin through a prick. The health practitioner can check the injection site for a reaction after about 20 minutes (ACAAI, 2020). Allergists can use these tests and history and physical review to confirm AR diagnosis and distinguish it from non-allergic types of rhinitis. Confirming an IgE-mediated process guides the use of avoidance measures and appropriate pharmacologic therapy (Wise et al., 2018). Therefore, these procedures can help diagnose AR, in addition to physical examination and medical or family history.
Pathophysiology of AR
AR is caused by the immune system’s overreaction to specific environmental allergens. It is mediated by immunoglobulin E (IgE) antibodies. Feng et al. (2021) suggest that irritants trigger AR by causing IgE-related inflammation in the nasal membranes. An individual’s first exposure leads the immune system to produce IgE antibodies that bind to the surface of mast cells. Upon re-exposure, these sensitized mast cells release histamine and other chemicals that cause acute nasal symptoms, such as nasal congestion, sneezing, and recurrent sinus infections. Over time, these signs become less severe, but inflammation and infiltration of immune cells occur in the final phases of the hypersensitivity. Additionally, following the development of mucosal inflammation, the nose becomes more responsive to subsequent allergen exposure and sensitive to other irritants and changes in atmospheric conditions. In the case study, the patient reported experiencing the AR symptoms, which significantly improved when she avoided the cat that joined her family around the same time her symptoms began. Thus, the woman can feel relieved in the absence of the cat, which seems the irritant.
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Subjective Findings
The patient may report itching on the throat and sinus, experiencing recurrent sinus infections, sneezing, and chronic nasal congestion.
Objective Findings
The objective assessment includes swelling or discoloration of the nasal mucosa, mouth breathing, rubbing the nose, sniffling or clearing the throat, rhinorrhea, and eye-related issues, such as watery discharge and swollen conjunctivae.
Management of the Disease
Recommended Medication Classes
The primary suggested medication classes for treatment of AR are intranasal steroids, such as budesonide, beclomethasone, triamcinolone, and fluticasone propionate, and H1-receptor antihistamines. Intranasal corticosteroids are considered effective medication for treating AR. They can significantly decrease nasal congestion, sneezing, itching, and nasal discharge (ACAAI, 2020). These medications have anti-inflammatory effects, which reduce swelling, edema, rhinorrhea, and congestion (May & Dolen, 2019). Conversely, H1-receptor antagonists work against histamine. These drugs comprise first-generation and second-generation H-1 medications (Farzam et al., 2022). They are present in eye drops, nasal sprays, oral tablets, and syrups. Second-generation oral histamine antagonists include fexofenadine (Allegra), cetirizine (Reactine), loratadine (Claritin), and desloratadine (Aerius) (Jagtap & More, 2020). They are effective pharmacological treatments for AR patients, especially when administered before an allergen exposure. For instance, fexofenadine is authorized as an oral tablet and a liquid suspension to alleviate symptoms of AR (Meltzer et al., 2021). Moreover, first-generation sedating medicines, such as diphenhydramine and chlorpheniramine, relieve AR signs (Jagtap & More, 2020). However, they negatively affect patients’ functioning and cognition and are not suggested for routine treatment of AR. Overall, intranasal corticosteroids and antihistamines are highly recommended medications for AR management.
The Mechanism of Action for the Medication Classes
Intranasal steroids reduce the release of mediators and cytokines in the nasal passages, decreasing nasal secretions through fewer neutrophils, eosinophils, basophils, and mononuclear cells. Accordingly, reducing the presence of these cells decreases cytokines in the nasal mucosa. Moreover, intranasal steroids prevent the mucosa’s hyperresponsiveness to allergens. The medicines takes effect approximately 3 to 36 hours after administering the first dose. However, the patient may experience some side effects, such as irritation and nasal bleeding.
On the other hand, oral antihistamines work by blocking histamine from binding to H1 receptors. Histamine, a naturally occurring chemical messenger, causes an increase in the permeability of blood vessels, leading to fluid accumulation in surrounding tissues (Farzam et al., 2022). As a result, these changes cause inflammation and enlargement of the vascular system. Antihistamines counteract this effect by binding to H-1 receptors. First-generation H-1 medications can cross the blood-brain barrier and reach the nervous system, while second-generation ones have limited access to the system. Consequently, the former binds to central and peripheral histamine-1 receptors, while the latter attach to peripheral histamine-1 receptors only. This difference leads to various therapeutic actions and side effects (Farzam et al., 2022). The impact of first and second-generation drugs lasts for approximately 4 to 6 hours and 12 to 24 hours respectively. These medicines can alleviate nasal allergy symptoms, such as itchiness, red eyes, sneezing, and nasal discharge (ACAAI, 2020). The liver metabolizes the histamine-inhibiting drugs using the P450 cytochrome system. The benefit of these medicines is a decrease in AR symptoms.
Wrong Treatment Options
The treatment options not recommended are oral leukotriene antagonists and sinonasal imaging. The clinical practice guidelines for treating the disease suggest second-generation oral antihistamines. However, these rules do not recommend leukotriene receptor antagonists (LTRAs) as the primary therapy for AR patients (Feng et al., 2021). The benefits of avoiding this treatment method are that it enables the patient to avoid ineffective or less effective therapy, saves costs, and reduces care variations. Although the scan is a choice for patients with inflammatory paranasal sinus illness symptoms, they are not advisable. For instance, routinely conducting sinonasal imaging to diagnose AR is not recommended. The primary aim of imaging the nasal sinuses is to approve the diagnosis, contain the illness, and describe the level of pathology and any anatomical differences. Imaging is not suggested for diagnosing AR since it may trigger the development of chronic diseases in the long run, such as cancer. The harm resulting from this imaging is exposure to unnecessary radiation, which may lead to tumor development (Wise et al., 2018). Accordingly, the long-term risks of excessive ionizing radiation exposure outweigh the possible benefits. Although routine imaging is not a suitable treatment option for AR, physicians can use it to rule out other medical conditions, such as rhinosinusitis. These treatment plans can aggravate the symptoms of AR.
References
American College of Allergy, Asthma, and Immunology. (2020, June 17). Hay fever. https://acaai.org/allergies/types/hay-fever-rhinitis
Farzam, K., Sabir, S., & O’Rourke, M. C. (2022, July 15). Antihistamines. National Library of Medicine. https://www.ncbi.nlm.nih.gov/books/NBK538188/
Feng, Y., Meng, Y.-P., Dong, Y.-Y., Qiu, C.-Y., & Cheng, L. (2021). Management of allergic rhinitis with leukotriene receptor antagonists versus selective H1-antihistamines: A meta-analysis of current evidence. Allergy, Asthma & Clinical Immunology, 17, Article 62. https://doi.org/10.1186/s13223-021-00564-z
Jagtap, V., & More, P. (2020). A review on diagnosis and treatment of allergic rhinitis. The Pharma Innovation Journal, 9(1), 307-311.
May, J. R., & Dolen, W. K. (2019). Evaluation of intranasal corticosteroid sensory attributes and patient preference for fluticasone furoate for the treatment of allergic rhinitis. Clinical Therapeutics, 41(8), 1589–1596. https://doi.org/10.1016/j.clinthera.2019.05.017
Meltzer, E. O., Rosario, N. A., Van Bever, H., & Lucio, L. (2021). Fexofenadine: Review of safety, efficacy and unmet needs in children with allergic rhinitis. Allergy, Asthma & Clinical Immunology, 17, Article 113. https://doi.org/10.1186/s13223-021-00614-6
Wise, S. K., Lin, S. Y., Toskala, E., Orlandi, R. R., Akdis, C. A., Alt, J. A., Azar, A., Baroody, F. M., Bachert, C., Canonica, G. W., Chacko, T., Cingi, C., Ciprandi, G., Corey, J., Cox, L. S., Creticos, P. S., Custovic, A., Damask, C., DeConde, A., … Zacharek, M. (2018). International consensus statement on allergy and Rhinology: Allergic rhinitis. International Forum of Allergy & Rhinology, 8(2), 108–352. https://doi.org/10.1002/alr.22073
Zheng, M., Wang, X., Latiff, A. H. A., Shah, A., Pham, D. L., Kim, D. Y., Oh, J. W., Wang, J. Y., Ruxrungtham, K., Recto, M., Poerbonegoro, N. L., Logi, N., Munkhbayarlakh, S., Leung, T. F., Shimizu, T., Chiang, W. C., Kamchaisatian, W., Pawankar, R., & Zhang, L. (2022). An online survey of clinical practice for allergic rhinitis among the Asia-Pacific representatives. Asian Pacific Journal of Allergy and Immunology. https://doi.org/10.12932/ap-310322-1361
Sample Answer 2 for NR 507 Week 1: Case Study
Pathophysiology & Clinical Findings of the Disease
- Identify the correct hypersensitivity reaction:
Type I hypersensitivity reaction Allergic Rhinitis. “Disease is caused by an IgE-mediated inflammatory response of the nasal mucous membranes after exposure to inhaled allergens” (Seidman et al., 2015). Patient presents with complaints of rhinorrhea, sneezing and nasal stuffiness. The patient reported her symptoms started about 12 months ago, which is also when she acquired her cat. I think the patient is experiencing a type 1 Immunoglobulin E (IgE) Mediated hypersensitive reaction as a result of being allergic to her cat (McCance et al., 2019). Her symptoms greatly improved when she was on a cruise for two weeks, subsequently away from the cat.
- Explain the pathophysiology associated with the chosen hypersensitivity reaction:
The majority of type 1 reactions are directed against environmental antigens, indicating their allergic nature, which are the primary cause of IgE (McCance et al., 2019). The primary cause of IgE production in the human body is exposure to an environmental antigen, with repeated exposure required to “sensitize” the person so that subsequent exposures elicit an allergic response (McCance et al., 2019). Upon subsequent encounters with the particular antigen to which the individual has developed sensitivity, the antigen attaches to IgE-Fc receptors situated on the surface of mast cells, a process referred to as cross-linking which leads to the initiation of intracellular signals and the degranulation of mast cells, causing the release of biochemical mediators (McCance et al., 2019). Histamine, the most potent among these mediators, causes bronchial muscle constriction, increased vascular permeability, vasodilation, and enhances eosinophil attraction and retention in inflamed areas (McCance et al., 2019). Mast cells trigger the production of slower-acting bioactive lipid-derived mediators, like leukotrienes, platelet-activating factor, and prostaglandins, which can lead to prolonged clinical symptoms such as increased inflammation, bronchoconstriction, and more histamine release (McCance et al., 2019). Animal dander is a typical Type I hypersensitivity antigen (McCance et al., 2019). Allergic inflammatory symptoms are related to where the antigen enters the body, inhaled antigen results in respiratory tract symptoms (McCance et al., 2019).
- Identify at least three subjective findings from the case:
The three subjective findings the patient reported were 1. Rhinorrhea, 2. Sneezing, 3. Nasal stuffiness.
- Identify at least three objective findings from the case:
Three of the objective findings were 1. Eyelid redness and swelling, 2. Conjunctival swelling and erythema, 3. Allergic shiners (low lid venous swelling)
Management of the Disease
*Utilize the required Clinical Practice Guideline (CPG) to support your treatment recommendations.
- Identify two strongly recommended medication classes for the treatment of the condition and provide an example (drug name) for each:
Intranasal Steroids and Second-Gen Oral Antihistamines are two strongly recommended medication classes. Intranasal corticosteroid (INS) medications are prescribed for individuals with allergic rhinitis whose symptoms impact their quality of life, the medications encompass options like fluticasone propionate (Flonase) and mometasone furoate (Nasonex) available through prescription, while triamcinolone acetonide (Nasacort Allergy 24 hr) is an over-the-counter alternative (Seidman et al., 2015). For patients experiencing mild to moderate symptoms like sneezing, runny nose, nasal congestion, and itching, second-generation oral antihistamines are advisable, they are a cost-effective solution with a quick onset of action. The preference for second-generation oral antihistamines is attributed to their limited ability to enter the central nervous system, resulting in reduced sedation-related side effects often observed with first-generation oral antihistamines. Over-the-counter choices encompass cetirizine (Zyrtec) and loratadine (Claritin), while levocetirizine (Xyzal) is available by prescription (Seidman et al., 2015).
- Describe the mechanism of action for each of the medication classes identified above:
Intranasal steroids (INS), like Flonase, function by suppressing mast cells, macrophages, and other biological agents to generate anti-inflammatory and effects of vasoconstricting (Wolters Kluwer, 2019). INS medications are highly effective as they directly modulate the pathophysiology of allergic rhinitis by inhibiting mast cell mediators, preventing WBC recruitment, and reduce hyperresponsiveness to allergens and histamine release (Seidman et al., 2015). Second-generation oral antihistamines, known as H1 receptor antagonists, block histamine’s inflammatory response by competing for cellular receptor binding (Wolters Kluwer, 2019). The second-gen were created to be less sedating and anticholinergic side effect that first-gen meds such as Benadryl had.
- Identify two treatment options that are NOT recommended (I.e., recommended against):
Two treatment choices not advised for allergic rhinitis are the utilization of imaging procedures and oral leukotriene receptor antagonists (LTRAs). The absence of radiological findings exclusive to allergic rhinitis, the potential harm from radiation exposure exceeding the advantages of radiological findings, and the financial burden on the patient associated with imaging studies (Seidman et al., 2015). Oral leukotriene receptor antagonists (LTRAs) are discouraged because they’re more costly than oral antihistamines and primarily effective for nasal symptoms, some benefit has been observed in patients with comorbid allergic rhinitis and asthma (Seidman et al., 2015).
References
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The Biologic Basis for Disease in Adults and Children (8th ed.).
Elsevier.Seidman, M. D., Gurgel, R. K., Lin, S. Y., Schwartz, S. R., Baroody, F. M., Bonner, J. R.,Dawson, D. E., Dykewicz, M. S., Hackell, J. M., Han, J. K., Ishman, S. L., Krouse, H. J.,Malekzadeh, S., Mims, J. W. W., Omole, F. S., Reddy, W. D., Wallace, D. V., Walsh, S.A., Warren, B. E., . . . Nnacheta, L. C. (2015). Clinical Practice Guideline. Otolaryngology-Head and Neck Surgery,152(1_suppl), S1- S43.https://doi.org/10.1177/0194599814561600
Wolters Kluwer. (2019). Nursing 2019 Drug Handbook (39th ed.). Wolters Kluwer.
NR 507 Week 2 Discussion 1
- What is the etiology of cystic fibrosis?
This topic is of great interest to me because of this subject that I will be doing my presentation on, so I did a detailed search. The peer review article revealed that according to Munder& Tummler (2015), cystic fibrosis lung disease result from impaired chloride and bicarbonate epithelial transport, defective mucociliary transport, and acidification of the airway-surface liquid. In many ways, the pathophysiological process differs according to the different evidenced-based practice. “The pathophysiology of cystic fibrosis is deduced from the loss or dysfunction of CFTR in the apical epithelial membrane” Stoltz, (2015). The contributing factor is an attenuated bacteria-killing capability has reported in monocytes and macrophages isolated from people with cystic fibrosis.
The response to the peer review is” We agree with Munder and Tümmler that abnormal function in myeloid cells (i.e., neutrophils, monocytes, or macrophages) may contribute to impaired host defense in cystic fibrosis.” Stoltz, 2015. The article contains other pertinent information to describe the depth of this disease. “Specific cell types involved (monocytes, neutrophils, or macrophages) and proposed mechanisms for defects (e.g., organelle acidification, complement-mediated phagocytosis, and intraphagosomal production of hypochlorous acid) vary substantially among studies.” Stoltz (2015).
- Describe in detail the pathophysiological process of cystic fibrosis.
Cystic fibrosis is the abnormal secretions that obstruct the respiratory, digestive, and reproductive tract. According to (McCance et al., 2013) research shows that there may be additional CF-associated primary defects, such as a natural proinflammatory state and abnormal local immune defenses in the lungs. “Cystic fibrosis is also associated with cystic fibrosis transmembrane conductance regulator (CFTCR) gene mutation results in the abnormal expression of cystic fibrosis transmembrane conductance regulator (CFTCR) protein, which is a cyclic adenosine monophosphate (cAMP)–activated chloride channel present on the surface of many types of epithelial cells.” (McCance et al., 2013). These cells include the lining of the airways, bile ducts, the pancreas, sweat glands, and the vas deferens. Even though cystic fibrosis affects multisystem it ultimately most often affects the lung, which is the most critical site of involvement that leads to respiratory failure and death.
- Identify hallmark signs identified from the physical exam and symptoms.
Cystic fibrosis often occurs primarily in the white population; it affects 1 in 29 whites in the united states. The symptoms typically start with the respiratory and digestive systems. Respiratory symptoms include a persistent cough or wheeze, sputum production, and recurrent or severe pneumonia, and chronic sinusitis and nasal polyps. “Persistence of infection incites chronic local inflammation, airway damage, bronchiectasis, microabscess formation, and foci of hemorrhagic pneumonia.
- Describe the pathophysiology of complications of cystic fibrosis.
There is progressive damage to the typical architecture of the lung with a decline in pulmonary function.” (McCance et al., 2013. CF causes reduced hydration of airway mucus which results in increased adherence of mucus to the epithelium, making it easier for bacteria to stick to and increasing the chances of infection (McCance et al., 2013)
- What teaching related to her diagnosis would you provide the parents?
Due to the severity of the disease, it will be overwhelming and devastating to the parents, as an advanced clinical nurse I will provide them with all the information and videos available. I would also refer them to join a group of parents with children of a similar diagnosis. Advising the patient to prevent infection, adequate nutrition, and an increase in caloric intake is the primary goal to maintain a healthy lifestyle. Lastly, I would provide them with my information for them to call with any further questions.
Ingrid
References:
Antje Munder, M.D. Burkhard Tümmler, M.D., Ph.D. Hanover Medical School, Hannover, Germany (2015)
tuemmler.burkhard@mh-hannover.de
David A. Stoltz, M.D., Ph.D. David K. Meyerholz, D.V.M., Ph.D. Michael J. Welsh, M.D.
University of Iowa Carver College of Medicine, Iowa City, IA (2015)
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby