NUR 635 Topic 7 DQ 2

Sample Answer for NUR 635 Topic 7 DQ 2 Included After Question

Select one of the prompts below to complete this discussion question:

  1. Select a prescription or nonprescription medication and explain the cultural and genetic factors that need to be considered when recommending or prescribing for contraception or hormone replacement. Share the mechanism of action of this medication and hints for monitoring, side effects, and drug interactions, including interactions with CAM. Include the name of the medication in the subject line so that the medications can be followed. Include references using APA format.
  2. Hypogonadism affects many men and is known to be one of the main causes of infertility. Explain the pathophysiology of infertility. Discuss testosterone replacement therapy (TRT), including the benefits, risks, contraindications, potential drug interactions, preparations, and dosing. Explain the cultural and genetic factors that need to be considered when recommending or prescribing TRT. Discuss evidence and treatment guidelines to determine appropriate therapeutic options for a patient with infertility. Use evidence-based, peer-reviewed research to support your answer. Include references using APA format.

American Association of Colleges of Nursing Core Competencies for Professional Nursing Education 

This assignment aligns to AACN Core Competencies 1.2, 2.2, 2.5. 4.2, 6.4, 9.2

A Sample Answer For the Assignment: NUR 635 Topic 7 DQ 2

Title: NUR 635 Topic 7 DQ 2

Medication: Testosterone Replacement Therapy (TRT)

Cultural and Genetic Factors:

When recommending or prescribing Testosterone Replacement Therapy (TRT), healthcare providers should consider cultural and genetic factors that can influence its effectiveness and safety. These factors may include variations in androgen receptor sensitivity, differences in metabolism, and cultural perceptions of masculinity and virility(Hackett, 2017). Genetic variations, such as polymorphisms in the androgen receptor gene, can impact the response to TRT. Additionally, cultural beliefs and expectations around masculinity and sexual health may affect a patient’s willingness to accept TRT as a treatment option.

Mechanism of Action:

TRT involves the administration of exogenous testosterone to replace or supplement the body’s own production. Testosterone acts through the androgen receptor to exert its effects, which include promoting secondary sexual characteristics, increasing muscle mass, and maintaining bone density (Rosenthal, 2022). TRT can be administered through various forms, including gels, injections, patches, and implants, with each method having a different mechanism of release and absorption.

Monitoring, Side Effects, and Drug Interactions:

Regular monitoring of testosterone levels, hematocrit, and lipid profiles is essential to ensure that testosterone levels remain within the therapeutic range and to detect any adverse effects. Common side effects of TRT may include acne, oily skin, increased hematocrit, mood swings, and gynecomastia. More severe side effects may include cardiovascular risks, sleep apnea exacerbation, and worsening of prostate conditions in some cases (Hayes, 2020).

TRT can interact with other medications. For example, TRT may decrease the anticoagulant effect of warfarin, and it can interact with medications like insulin, leading to changes in blood glucose levels. Patients should inform their healthcare provider about all medications and supplements they are taking to minimize potential interactions (Bogehave, 2023).

Contraindications:

TRT is contraindicated in patients with prostate or breast cancer. It is also not recommended for patients with uncontrolled heart failure, severe lower urinary tract symptoms due to benign prostatic hyperplasia (BPH), or those with elevated hematocrit (Bogehave, 2023).

Preparations and Dosing:

Several TRT formulations are available, including intramuscular injections, transdermal gels, patches, buccal systems, and long-acting injections. The choice of preparation and dosing depends on individual patient characteristics, including preferences, lifestyle, and the specific indications for treatment. The dosing regimen should be tailored to maintain testosterone levels within the therapeutic range.

Evidence and Treatment Guidelines:

Treatment guidelines for TRT are typically based on peer-reviewed research and evidence-based practices. Guidelines, such as those from the Endocrine Society, provide recommendations for the diagnosis and treatment of hypogonadism and infertility in men (PaRK, 2019). They emphasize the importance of a thorough evaluation, including clinical symptoms and laboratory testing, before initiating TRT. The decision to prescribe TRT should be based on the presence of clinical symptoms and consistent laboratory evidence of low testosterone.

References:

Rosenthal, L. D., & Burchum, J. R. (2020). Lehne’s pharmacotherapeutics for advanced practice nurses and physician assistants – e-book (2nd ed.). Elsevier Health Sciences.Bhasin, S., Cunningham, G. R., Hayes, F. J., Matsumoto, A. M., Snyder, P. J., & Swerdloff, R. S. (2010).

Barbonetti, A., D’Andrea, S., & Francavilla, S. (2020). Testosterone replacement therapy. Andrology8(6), 1551–1566. https://doi.org/10.1111/andr.12774

Testosterone therapy in men with androgen deficiency syndromes: An Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 95(6), 2536-2559.

Hackett, G., Kirby, M., Edwards, D., Jones, T. H., & Wylie, K. (2017). British Society for Sexual Medicine guidelines on the management of erectile dysfunction in men-2017. The Journal of Sexual Medicine, 14(5), 551-564.

Salonia, A., Rastrelli, G., Hackett, G., Seminara, S. B., Huhtaniemi, I. T., Rey, R. A., … & Tajar, A. (2019). Paediatric and adult-onset hypogonadism: differences in clinical presentation and long-term outcome. European Journal of Endocrinology, 181(6), 585-596.

Bogehave, M., Glintborg, D., Gram, J. B., Bladbjerg, E. M., Andersen, M. S., & Sidelmann, J. J. (2023). Testosterone therapy increases the anticoagulant potential in men with opioid-induced hypogonadism: a randomized, placebo-controlled study. Endocrine connections12(4), e220455. https://doi.org/10.1530/EC-22-0455

Park, H. J., Ahn, S. T., & Moon, D. G. (2019). Evolution of Guidelines for Testosterone Replacement Therapy. Journal of clinical medicine8(3), 410. https://doi.org/10.3390/jcm8030410

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NUR 635 Topic 7 DQ 1

A Sample Answer 2 For the Assignment: NUR 635 Topic 7 DQ 2

Title: NUR 635 Topic 7 DQ 2

According to Leslie, et al. (2023), male infertility is the inability of a guy to conceive a fertile female after at least one year of unprotected sexual activity. Males are primarily responsible for 20% and contribute to 30%–40% of infertility cases. Male and female reasons commonly co-exist, thus both spouses should be tested and treated for infertility. Male component contributes to 50% of infertility cases. Many types of male infertility may be categorized by their general etiology.  Endocrine disorders (usually hypogonadism) account for 2% to 5%, sperm transport disorders (like vasectomy) for 5%, primary testicular defects for 65% to 80%, and idiopathic (where an infertile male has normal sperm and semen parameters) for 10% to 20%.

Hypogonadism was a prevalent cause of male infertility. It may be acquired or congenital and caused by hypothalamic-pituitary-testicular axis abnormalities. The anterior pituitary gland releases pulses of LH into the blood to stimulate testicular Leydig cells to produce testosterone. LH raises cAMP levels via binding to Leydig cell receptors. Increased cAMP levels activate StAR and CYP11A1, the cholesterol sidechain clevage enzyme. StAR moves cholesterol from the outside mitochondrial membrane to the inner mitochondrial membrane, whereas CYP11A1 converts cholesterol to pregnenolone, the precursor of all steroid hormones.

DHEA is produced via 17 alpha-hydroxylation of pregnenolone to 17 OH pregnenolone. DHEA becomes androstenediol to create testosterone.  Primary hypogonadism occurs when testicular steroidogenesis fails to produce enough testosterone, while secondary hypogonadism occurs when LH or GnRH signaling to the testis fails to stimulate Leydig cell testosterone production. It is important to differentiate between primary (testes-based) and secondary (hypothalamus or pituitary gland-based) hypogonadism. Decreased spontaneous erections, nocturnal penile tumescence, libido, and testicular volume imply hypogonadism. 

Testosterone is a crucial hormone in males, playing a vital role in several processes such as differentiation, developmental growth, and the maintenance of phenotypic (Park, et.al. 2019). Sizar O, & Pico J. (2022) state that FDA-approved testosterone replacement treatment is for hypogonadism and low testosterone levels. Testosterone is FDA-approved for congenital or acquired hypogonadotropic hypogonadism caused by tumors, trauma, or radiation. As three hormones, testosterone has various biological impacts. Testosterone may directly act on the androgen receptor or convert to DHT in tissues through 5-alpha reductase. After aromatase conversion to estradiol, testosterone may behave as an estrogen. In many organs, testosterone’s function relies on its conversion to DHT, which binds to cytosol receptor proteins.

Once in the nucleus, this steroid-receptor combination activates transcription and androgen-related cellular changes. Testosterone cypionate IM is slowly absorbed, thus it may be taken every two to four weeks. Most plasma testosterone (98%) is linked to globulin. Free and bound forms rely on plasma testosterone-estradiol binding globulin levels. The half-life is proportional to plasma free testosterone. Eight days is IM testosterone cypionate’s half-life. 90% of testosterone is eliminated in the urine as glucuronic or sulfuric acid conjugates, which the liver converts into inactive form.

There are several testosterone formulations. Transdermal gels and IM injections are preferred choices. When selecting testosterone treatment candidates, differences and side effects must be considered. Oral, buccal, transdermal (gel, patch, solution, pellet), and IM testosterone administration are available.FDA found in 2015 that testosterone usage may raise cardiovascular risk, necessitating labeling changes to alert the public, according to Ponce, et al. (2018). Testosterone usage increases hematocrit-related erythrocytosis and venous thromboembolism risk.  Serum PSA levels may rise with testosterone treatment, thus prostate cancer must be ruled out before treatment to prevent progression.

Three months and one year after starting replacement therapy, prostate cancer patients must be reevaluated. Females and children may contract testosterone from testosterone gels, according to Ponce, et al. (2023). To prevent transmission, patients should cover the application location with garments and wash their skin before skin-to-skin contact. Skin responses and mood, energy, and libido variations may result with testosterone patches and injectables. Furthermore, buccal pills might irritate gums and oral mucosa.

References:

Leslie SW, Soon-Sutton TL, Khan MAB. (2023). Male Infertility. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK562258/

Park, H. J., Ahn, S. T., & Moon, D. G. (2019). Evolution of Guidelines for Testosterone Replacement Therapy. Journal of clinical medicine, 8(3), 410. https://doi.org/10.3390/jcm8030410

Ponce OJ, Spencer-Bonilla G, Alvarez-Villalobos N, Serrano V, Singh-Ospina N, Rodriguez-Gutierrez R, Salcido-Montenegro A, Benkhadra R, Prokop LJ, Bhasin S, Brito JP. (2018). The efficacy and adverse events of testosterone replacement therapy in hypogonadal men: A systematic review and meta-analysis of randomized, placebo-controlled trials. J Clin Endocrinol Metab. 

Sizar O, & Pico J. (2022). Androgen Replacement. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing.  https://www.ncbi.nlm.nih.gov/books/NBK534853/