NR 507Week 1 case study: Allergic Rhinitis Paper

NR 507Week 1 case study: Allergic Rhinitis Paper

 

Pathophysiology & Clinical Findings of the Disease

1. Identify the correct hypersensitivity reaction:

The most appropriate diagnosis for the patient is allergic rhinitis (AR), a type I hypersensitivity reaction related to her environment. The patient reported a history of nasal secretion, sneezing, and nasal congestion for the last 12 months, which she claims have persisted. To make a diagnosis of AR, a comprehensive history can be taken from the patient, a physical examination conducted extensively with a special focus on the HEENT (head, eyes, ears, neck, and throat), and other laboratory tests to confirm the diagnosis. Patients will report symptoms that persist throughout the year when they are in a specific environment or symptoms that are noticed during a particular season only. From history, environmental factors promoting AR may include pollen from any source like trees and grass, dust mites, and dander from animals. The latter are responsible for perennial allergens, which are present throughout the year. To diagnose AR, various diagnostic tests can be conducted. Nasal smears depict large numbers of eosinophils. Skin tests can help determine specific allergens, including prick, scratch, and intradermal tests (Akhouri & House, 2023). Other tests include the Radioallergosorbent (RAST) and nasal provocation tests (Akhouri & House, 2023). Upon initiating medications such as oral antihistamines on patients with AR, they respond positively, and this can also be a modality of confirming the diagnosis.

2. Explain the pathophysiology associated with the chosen hypersensitivity reaction:

AR is an IgE-mediated immunological response that develops following exposure to allergens (Liva et al., 2021). It is characterized by a watery discharge from the nose, sneezing, nasal obstruction, and itchiness of the nose (Akhouri & House, 2023). Upon inhalation of allergens, specific IgE antibodies are produced by the immune system of individuals who have a genetic predisposition. The antibodies secreted become fixed to basophils found in blood or mast cells within tissues using their Fc ends. On the next exposure to allergens, the antigen will combine with the IgE antibodies at their Fab ends. This reaction causes mast cell degranulation and the production of chemical mediators such as histamine. The inflammatory mediators produced are responsible for the symptomatic presentation of AR (Akhouri & House, 2023). Depending on tissue involvement, effects include vasodilatation, eosinophil infiltration, mucosal edema, excessive nasal gland secretion, or contraction of smooth muscles. Clinically, the response of AR among affected individuals occurs in two phases: early and late phases (Akhouri & House, 2023). In the acute or early phase, the reaction takes place immediately within 5-30 minutes after allergen exposure, and there is IgE production that binds to mast cells resulting in their degranulation. Histamine and leukotriene release causes local inflammation. The action of histamine on the trigeminal nerve causes sneezing and mucus production upon acting on the mucous glands. Other features include bronchospasm due to the vasoactive amines released (Akhouri & House, 2023).

The late phase/delayed response occurs after 2-8 hours of allergen exposure. The mast cells produce interleukins 4 and 13 which cause cellular infiltration like eosinophils, neutrophils, monocytes, basophils, and CD4+ T cells into the mucosal tissues (Akhouri & House, 2023). These cells infiltrate at sites where antigens deposit, and the consequence includes nasal edema, congestion, and the production of a thick secretion.

3. Identify at least three subjective findings from the case:

The woman reported experiencing nasal stuffiness, sneezing, and rhinorrhea that have been persistent. She also reported of recurrent nasal infections.

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4. Identify at least three objective findings from the case:

The features observed on the patient by the Nursing Practitioner upon examination include allergic shiners, erythematous and swollen conjunctiva, red and swollen eyelids, allergic creases, and inflamed nares. Objective findings are the features that can be obtained from physical examination, and they include allergic salute, allergic crease, edematous nasal mucosa, allergic shiners, and Dennie-Morgan lines.  The lateral crease on the nose (allergic crease) is a consequence of constant rubbing of the nose. Allergic shiners manifested as lower lid venous swelling are due to obstruction of lymphatic and venous drainage, chronic obstruction of the nose, and orbital edema.

Management of the Disease

*Utilize the required Clinical Practice Guideline (CPG) to support your treatment recommendations.

1. Identify two strongly recommended medication classes for the treatment of the condition and provide an example (drug name) for each:

According to Seidman et al. (2015), as published in the Clinical Practice Guideline for Allergic Rhinitis, the first strong recommendation for treatment is the use of topical steroids. Clinicians should recommend the use of intranasal steroids among patients who have a clinical diagnosis of allergic rhinitis and whom the symptoms of the condition are affecting their quality of life. The second strong recommendation is the use of oral antihistamines. Clinicians should advise patients to use oral second-generation antihistamines or antihistamines that are less sedating among patients who have allergic rhinitis and primarily complain of sneezing and itching (Seidman et al., 2015).

2. Describe the mechanism of action for each of the medication classes identified above:

Intranasal steroids act on genomic and non-genomic pathways like transactivation, histone medication, transrepression, and Src kinase signaling in reducing the severity of allergic inflammation (Watts et al., 2019). Through the reduction of the influx of inflammatory cells into the nasal mucosa in response to allergic stimuli through fewer eosinophils, neutrophils, basophils, and monocyte cells, they limit the secretion of vasoactive amines and causation of bronchial hyperresponsiveness (Watts et al., 2019). They also antagonize the antigen-induced hyperresponsiveness of the nasal mucosa against reacting with the allergen, thus minimizing symptoms of AR. The action of onset of intranasal steroids is within 3-5 hours following administration of the first dose; however, it may go up to 36 hours before patients report of positive response to therapy. Examples of intranasal steroids for AR include budesonide, fluticasone propionate, and beclomethasone dipropionate (Daley-Yates et al., 2021).

Oral antihistamines cause blockage of histamine towards its receptor (H1 receptor). The antihistamine medications act on the H1 receptor, thus ameliorating the effects of histamine by stabilizing the receptor in an inactive conformation (Watts et al., 2019). Histamine is associated with lowering a high level of vascular permeability which can cause the dissemination of fluid to distant body parts, where the fluid accumulates and causes vessel dilatation and selling. By antagonizing histamine receptors, antihistamine medications prevent this. The onset of action of the second-generation antihistamines in managing AR takes place for 12-24 hours (Watts et al., 2019). Examples of 2nd generation antihistamines include cetirizine, loratadine, and fexofenadine (Kawauchi et al., 2019). Antihistamines are effective in controlling sneezing, itchiness, and rhinorrhea.

3. Identify two treatment options that are NOT recommended (I.e., recommended against):

According to the Clinical Practice Guideline for AR, it has recommended against the following two in the management of AR: imaging and oral leukotriene receptor antagonists (LTRA). For imaging, clinicians should not routinely conduct sinonasal imaging modalities on patients who come with symptoms that are consistent with a diagnosis of AR (Seidman et al., 2015). For LTRAs, clinicians are advised against prescribing oral leukotriene receptor antagonists as the mainstay therapy intervention among patients with AR (Seidman et al., 2015).

References

Akhouri, S., & House, S. A. (2023). Allergic Rhinitis. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK538186/#:~:text=Objectives%3A%201%20Identify%20the%20abnormal%20immune%20response%20in

Daley-Yates, P. T., Larenas-Linnemann, D., Bhargave, C., & Verma, M. (2021). Intranasal Corticosteroids: Topical Potency, Systemic Activity and Therapeutic Index. Journal of Asthma and Allergy, Volume 14, 1093–1104. https://doi.org/10.2147/jaa.s321332

Kawauchi, H., Yanai, K., Wang, D.-Y., Itahashi, K., & Okubo, K. (2019). Antihistamines for Allergic Rhinitis Treatment from the Viewpoint of Nonsedative Properties. International Journal of Molecular Sciences, 20(1), 213. https://doi.org/10.3390/ijms20010213

Liva, G. A., Karatzanis, A. D., & Prokopakis, E. P. (2021). Review of Rhinitis: Classification, Types, Pathophysiology. Journal of Clinical Medicine, 10(14), 3183. https://doi.org/10.3390/jcm10143183

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. (Whit) W., Omole, F. S., Reddy, W. D., Wallace, D. V., Walsh, S. A., Warren, B. E., & Wilson, M. N. (2015). Clinical Practice Guideline: Allergic Rhinitis. Otolaryngology–Head and Neck Surgery, 152(1_suppl), S1–S43. https://doi.org/10.1177/0194599814561600

Watts, A. M., Cripps, A. W., West, N. P., & Cox, A. J. (2019). Modulation of allergic inflammation in the nasal mucosa of allergic rhinitis sufferers with topical pharmaceutical agents. Frontiers in Pharmacology, 10, 294. https://doi.org/10.3389/fphar.2019.00294

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Preparing the Assignment

Content Criteria:

Read the case study listed below.

Refer to the rubric for grading requirements.

Utilizing the Week 1 Case Study TemplateLinks to an external site., provide your responses to the case study questions listed below.

You must use at least one scholarly reference to provide pathophysiology statements. For this class, use of the textbook for pathophysiology statements is acceptable. You may also use an appropriate evidence-based journal.

You must use the Clinical Practice Guideline (CPG) for the management of allergic rhinitis to answer the treatment recommendation questions. The guideline can be found at the following web address: https://journals.sagepub.com/doi/10.1177/0194599814561600Links to an external site..You may also use a medication administration reference such as Epocrates to provide medication names.

Proper APA format (in-text citations, reference page, spelling, English language, and grammar) must be used.

Case Study Scenario

A 35-year-old woman presents to the primary care office with a history of nasal congestion that has worsened over time and recurrent sinus infections. She considered herself healthy until about 12 months ago when she began experiencing rhinorrhea, sneezing, and nasal stuffiness that “seems to never go away”. She noticed that her rhinorrhea greatly improved when she attended her family reunion on a two-week Caribbean cruise but returned after being home a few days. She lives with her husband and 5- year-old child. They have two household pets: a dog that has lived with them for the last 4 years and a cat who joined the family 1 year ago. Upon exam, the NP observed eyelid redness and swelling, conjunctival swelling and erythema, allergic shiners (lower lid venous swelling), Allergic crease (lateral crease on the nose) and inflamed nares.

Case Study Questions

Pathophysiology & Clinical Findings of the Disease

Identify the correct hypersensitivity reaction.

Explain the pathophysiology associated with the chosen hypersensitivity reaction.

Identify at least three subjective findings from the case.

Identify at least three objective findings from the case.

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.

Describe the mechanism of action for each of the medication classes identified above.

Identify two treatment options that are NOT recommended (I.e., recommended against).