NURS 6521 Week 6: Endocrine and Musculoskeletal System 

Sample Answer for NURS 6521 Week 6: Endocrine and Musculoskeletal System Included After Question

Patients with endocrine and musculoskeletal disorders often require long-term treatment and care resulting in the need for extensive patient education. By appropriately educating patients, advanced practice nurses can assist patients with the management of their disorders. In clinical settings, patients with endocrine and musculoskeletal disorders typically seek treatment for symptoms that pose problems to their everyday lives as ordinary tasks may become difficult to complete. For instance, patients might have difficulty walking short distances, preparing meals, or even running errands. To reduce these symptoms and additional health risks, it is essential to develop drug therapy plans with individual patient factors in mind. 

To prepare: 
Select one of the following endocrine or musculoskeletal disorders: thyroid disease, osteoarthritis, rheumatic arthritis, gout, multiple sclerosis, or fibromyalgia. Consider the types of drugs that would be prescribed to patients to treat symptoms associated with this disorder. 
Select one of the following factors: genetics, gender, ethnicity, age, or behavior. Reflect on how this factor might impact the effects of prescribed drugs, as well as any measures you might take to help reduce negative side effects. 

With these thoughts in mind: 

By Day 3 

Post a description of the endocrine or musculoskeletal disorder you selected including types of drugs that would be prescribed to patients to treat associated symptoms. Then, explain how the factor you selected might impact the effects of prescribed drugs, as well as any measures you might take to help reduce negative side effects. 

By Day 6 

Read a selection of your colleagues’ responses and respond to at least two of your colleagues on two different days who selected a different endocrine or musculoskeletal disorder than you did. Provide recommendations for alternative drug treatments and patient education strategies for treatment and management. 

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! 

Submission and Grading Information 

Grading Criteria  

The endocrine and musculoskeletal systems play important roles in the regulation and coordination of activities throughout the body. When alterations of these systems occur, many patients require long-term drug therapies. In addition to drugs prescribed by their health care providers, patients with these disorders also often take herbal and dietary supplements. According to the American Diabetes Association, 22 percent of diabetic patients use herbal therapy and 31 percent use dietary supplements (American Diabetes Association, 2009). This may impact the effects of prescribed drugs, as well as pose a concern of adverse drug reactions in patients. When treating patients with endocrine and musculoskeletal disorders, it is important to educate patients on associated risks. As an advanced practice nurse prescribing drugs, you must carefully consider all drug, herbal, and dietary therapies prior to finalizing treatment plans. 

This week you examine types of drugs prescribed to patients with endocrine and musculoskeletal disorders, as well as the impact of patient factors on the effects of drugs. You also explore ways to improve patient treatment plans including suggested drug therapies. Finally, you examine types of diabetes and the impact of diabetes drugs on patients. 

Learning Objectives 

By the end of this week, students will: 

Analyze types of drugs prescribed to treat endocrine and musculoskeletal disorders 
Evaluate the impact of patient factors on the effects of prescribed drugs for endocrine and musculoskeletal disorders 
Evaluate drug therapy plans to treat endocrine and musculoskeletal disorders 
Analyze patient education strategies for treatment and management of endocrine and musculoskeletal disorders 
Differentiate types of diabetes 
Evaluate the impact of diabetes drugs on patients 
Understand and apply key terms, concepts, and principles related to prescribing drugs to treat endocrine and musculoskeletal disorders 

Photo Credit: Mark Hatfield/iStock / Getty Images Plus/Getty Images 

NURS 6521 Week 6: Endocrine and Musculoskeletal System
Learning Resources 

Note: To access this week’s required library resources, please click on the link to the Course Readings List, found in the Course Materials section of your Syllabus. 

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A Sample Answer For the Assignment: NURS 6521 Week 6: Endocrine and Musculoskeletal System 
Title: NURS 6521 Week 6: Endocrine and Musculoskeletal System 

In the United States there is and average of 3.9% of the adult population that report gout symptoms each year (Fuerst, 2015). Gout occurs due to an elevated level of urate that eventually leaves deposits of monosodium urate crystals in the joints. This deposit causes an inflammatory reaction within the joints. This condition is called gouty arthritis (Schumacher, 2008). The inflammatory response is a result of macrophages phagocyting the urate crystals within the joint space. This in turn cause the release and activation of the IL-1B that bind to the synovial endothelium. This binding causes the release of proinflammatory cytokines and additional IL-1B (Arcangelo et al, 2017). While patients may be treated with anti-inflamatories to manage the pain and inflammation, the only real treatment is to lower the urate levels (Fuerst, 2015).  

Gout occurs acutely and chronically. Treatment of the condition will vary based on which form of the condition is needing to be treated. When treating chronic gout, the goal is to maintain a urate level less than 6 mg/dL or 5 mg/dL in patients with frequent gout attacks. The acute gout goal is to manage pain and inflammation. Maintaining joint function as well as stopping the attack is the predominant focus in acute gout.  

Chronic gout medications: 

Xanthine oxidase inhibitors work in just the way they sound, they inhibit xanthine oxidase. By doing so, the conversion of hypoxanthine into uric acid does not occur. With this medication, it will take at least 2 weeks to see results. Patients on this medication will need to have uric acid levels drawn every 2-5 weeks to titrate the medication to maintain a therapeutic level. Patients with liver dysfunction of any kind should not take this medication. Those with healthy liver function should be monitored throughout the therapy for any increases in liver enzymes. The medication should not be given to those who are also taking azathioprine and mercaptopurine due to it’s inhibiting of the metabolization of those drugs that could lead to toxic levels of them. Elevated levels of allopurinol can occur if taken with ACE inhibitors, thiazide and loop diuretics (Arcangelo et al, 2017). The medication can also interact with many antineoplastic. Increased risk of bleeding can occur in patients taking warfarin due to its interference in warfarin metabolization.   

Probenecid inhibits the reabsorption of uric acid causing it to be excreted instead at the convoluted tubule. This medication begins to diminish uric acid levels within 2 weeks of initiation (Arcangelo et al, 2017). This medication is often used with colchichine so both the chronic and acute condition is treated. Metabolism of warfarin may be increased when taken with this medication. When taken with thiazoldinedione, the therapeutic effects of the thiazoldinedione can be increased (Drugbank, 2018). Patients with a history of uric acid kidney stones should not take this medication. Children over two and adults may take this medication. With patients who have a G6PD deficiency, anaphylaxis, or hepatic necrosis should not take this medication due to the risk of aplastic and hemolytic anemia. Increased concentrations of penicillins, cephalosporins and fluoroquinolones can occur when taken concurrently with probenecid. Prolonged QT waves can occur if taken with citalopram. Lorazepam toxicity can occur if taken together. When taken with aspirin or other salicylates, the effects of probenecid may be reversed. It should not be taken with pegloticase due to the increased risk of anaphylaxis (Arcangelo et al, 2017).  

Pegloticase is only used if all other interventions to treat chronic gout have been unsuccessful due to being available only in intravenous form. It functions by introducing uricase to the system that then converts uric acid into allantoin rendering it water-soluble and inactive so that may be easily excreted by the kidneys. Results are seen on day one and can remain effective for up to 6 months. Patients with G6PD deficiencies should not be given this medication. Increased levels of pegloticase occur when given with any other gout medication. If this treatment is started, all other gout medications should be discontinued. Since the enzyme this medication introduces to the body is not found in the human body, 92% of patients receiving the medication will develop antipegloticase antibodies. The development of the antibodies can render the treatment ineffective as early as 4 months (Arcangelo et al, 2017). 

Acute gout medications: 

NSAIDs function to control and diminish pain and inflammation that occur during gout attacks. Patients taking this medication during a gout attack will need to continue the medication for an additional 24 hours after symptoms disappear (Arcangelo et al, 2017). Patients with renal dysfunction or transplantation should not take NSAIDs (Horl, 2010). 

Systemic corticosteroids decrease inflammation that occurs during a gout attack by the suppression of the migration of the polymorphonuclear leukocytes. There is a diminished systemic effect in patients with uncontrolled hypertension, diabetes, immunosuppressed, psychiatric disorders, and cardiovascular disease (Arcangelo et al, 2017). Patients with diabetes who take this medication should expect elevations in their blood glucose levels that may require additional treatments to maintain normal levels while on this medication (Tamez-Perez et al, 2015). Due to the effect of this medication and fluid retention, patients with HTN, CHF and edema issues need to be monitored for exacerbation of these conditions (Arcangelo et al, 2017). 

Colchicine works by inhibiting the migration, degranulation, and the activation of neutrophils in the joints that are having the acute attack. Relief with use of this medication come within 18-24 hours. Caution should be used when given to patients with renal or hepatic dysfunction. Patients with either of these conditions and taking either a P-gp or CYP3A4 inhibitor should not be given this medication. When given with these meds, a fatal toxicity level of colchicine can occur.  

Evaluation of patient needs when prescribing treatment is important. Monitoring for medications interactions when initiating therapy is incredibly important and should be done careful to prevent any harm to the patient. Lifestyle changes should be addressed such as exercise and diet in relation to treating the condition and diminishing the number of attacks. The use of vitamin C may be beneficial for patient to diminish their levels of uric acid so as to avoid taking medications that may interact with other conditions or medications. Each patient is different and will need to have a treatment plan specially tailored to them and monitored for effectiveness.  

Arcangelo, V., Peterson, A., Wilbur, V., and Reinhold, J. (2017). Pharmacotherapeutics for advanced practice: A practical approach. (4th edition). Philadelphia, PA: Wolters      Kluwer 

DrugBank (2018). Probenecid. DrugBank. Retrieved from: https://www.drugbank.ca/drugs/DB01032  

Fuerst, M. (2015). How common is gout in the united states, really? Rheumatology Network. Retrieved from: http://www.rheumatologynetwork.com/gout/how-common-gout-united-states-really 

Horl, W. (2010). Nonsteroidal anti-inflammatory drugs and the kidney. Pharmaceuticals. 3(7): 2291-2321 

Schumacher, R. (2008). The pathogenesis of gout. Cleveland Clinic Journal of Medicine. 75(5): 2-4 

Tamez-Perez, H., Quinranilla-Flores, D., Rodriquez-Gutierrez, R., Gonzalez-Gonzalez, J., and Tamez-Pena, A. (2015). Steroid hyperglycemia: Prevalence, early detection and therapeutic recommendation: A narrative review. World Journal of Diabetes. 6(8): 1073-1081 

A Sample Answer 2 For the Assignment: NURS 6521 Week 6: Endocrine and Musculoskeletal System 
Title: NURS 6521 Week 6: Endocrine and Musculoskeletal System 
Thyroid Disease 

Thyroid disease is a malfunction of the thyroid gland that causes hormonal imbalances in the body.  The gland can make to little or too much of the hormone.  Depending on which end of the spectrum that the thyroid is producing the hormone will determine what symptoms the patient will experience.  In hypothyroidism, the individual produces too little hormone, so they experience symptoms such as fatigue, constipation, weight gain, and change in their menstrual cycle along with other symptoms (Arcangelo, Peterson, Wilbur & Reinhold, 2017, p.810).  When free T4 is deficit causing hypothyroidism the hormone must be replaced synthetically.  Also, malfunction of the pituitary gland or hypothalamus can cause low thyroid levels, but they are a less likely cause. 

Hyperthyroidism is when the hormone level is high.  According to Arcangelo et al. 2017, the presence of increased amounts of thyroid hormone that can result in thyrotoxicosis (p.814).  Individual with elevated levels exhibit symptoms of opposite of patients with low levels.  The symptoms include palpitations, heat intolerance, weight loss, sweating, rapid heart rate, increased blood pressure and bruit over the thyroid gland (Arcangelo, Peterson, Wilbur & Reinhold, 2017, p.815). Treating hyperthyroidism is not as straightforward as treating low thyroid levels.  Hyperthyroidism can be treated in different three ways with antithyroid drugs, radioactive iodine ablation, or surgery (Arcangelo, Peterson, Wilbur & Reinhold, 2017, p.815). 

Treatment 

In hypothyroidism, the only treatment is to replace the hormone.  The medication used to replace the hormone is called levothyroxine.  Kizior 2018 states that levothyroxine classification is a synthetic isomer of thyroxine, it works to convert T3 then binds to thyroid receptor proteins exerting metabolic effects through DNA and protein synthesis (p. 667). Levothyroxine has met its desired therapeutic effect when the individual has achieved normal metabolism, growth, and development (Kizior, 2018, p.667).  Blood levels need to be drawn frequently to ensure that the patient is receiving the correct dose because if it is too high the patient will experience hyperthyroid symptoms and if it is to low their current symptoms will not be corrected. According to Kizior 2018, the pharmacokinetics are variable with incomplete absorption from the GI tract. Protein binding is greater than 99%, widely distributed.  Iodine is removed in the peripheral tissues and slightly broken down in the liver. The body rids the drug through biliary excretion and has a long half-life of 6-7 days (Kizior, 2018, p.667).   

 To decrease thyroid hormone antithyroid drugs are used.  These medications consist of methimazole and propylthiouracil (Arcangelo, Peterson, Wilbur & Reinhold, 2017, p.816).  The goal of treatment is to return the patient to normal thyroid levels and to decrease the uncomfortable side effects that accompany the disease.  Arcangelo et al. 2017, states that the drug works by preventing iodine organification and by blocking T4 and T3 at the periphery level (p.816).  Methimazole has a longer half-life only needing to be taken once a day while propylthiouracil has to be taken multiple times a day. 

Factor: Gender 

Gender can impact the effect of medications prescribed for thyroid disease. Thyroid disease has a higher prevalence in woman than men.  When taking levothyroxine estrogens can cause a decrease in serum free thyroxine (Kizior, 2018, p.668).  Woman produce Estrogens naturally and are often prescribed estrogens to help regulate other hormones.  Men often require a lower dose of levothyroxine (LT4) than women because menstrual cycles and maintain a healthy weight play a role in achieving a serum TSH within the normal range ( Devdhar, Drooger, Pehlivanoca, Singh, and Jonklass, 2011, p.821).  

Negative Side Effects 

With medications prescribed for hypothyroidism, the patient needs to be educated on the correct way to take the medication.  The medication should be taken at the same time in the morning to help promote proper absorption.  Taking too much levothyroxine or thyroid replacement will cause the patient to have drug-induced hyperthyroidism and put them at risk for arrhythmias and osteoporosis (Arcangelo, Peterson, Wilbur & Reinhold, 2017, p.814). Drug-induced hyperthyroidism will cause the patient to fall ill, and they may stop taking the medications altogether. 

 Antithyroid drugs can cause common side effects such as rash, arthralgias, itching, and hepatic abnormalities (Arcangelo, Peterson, Wilbur & Reinhold, 2017, p.817).  Patients being prepared for what side effects they might develop will help them better cope with the side effects and report them promptly.  There is a fatal condition that can arise as a result of taking antithyroid drugs that are seen more with PTU called agranulocytosis.  To help reduce chances of developing agranulocytosis the provider orders routine blood work to check the patients complete blood count and the patient who develop symptoms of fever or a sore throat must have a white blood cell count checked immediately (Arcangelo, Peterson, Wilbur & Reinhold, 2017, p.817).  Encouraging patients to be active in their care will help to decrease negative effects. 

Reference: 

Arcangelo, V. P., Peterson, A. M., Wilbur, V., & Reinhold, J. A. (Eds.). (2017).  

Pharmacotherapeutics for advanced practice: A practical approach (4th ed.). Ambler, PA: Lippincott Williams & Wilkins. 

Devdhar, M., Drooger, R., Pehlivanova, M., Singh, G., & Jonklaas, J. (2011). Levothyroxine  

replacement doses are affected by gender and weight, but not age. Thyroid : official journal of the American Thyroid Association, 21(8), 821-7. 

Kizior, R. (2018). Saunders Nursing Drug Handbook 2019. Elsevier – Health Sciences Division. 

Małgorzata Gietka-Czernel. (2017). The thyroid gland in postmenopausal women: physiology  

and diseases. Menopause Review, Vol 16, Iss 2, Pp 33-37 (2017), (2), 33. https://doi-org.ezp.waldenulibrary.org/10.5114/pm.2017.68588 

A Sample Answer 3 For the Assignment: NURS 6521 Week 6: Endocrine and Musculoskeletal System 
Title: NURS 6521 Week 6: Endocrine and Musculoskeletal System 

Gout is an inflammatory arthritis (Arcangelo, Peterson, & Reinhold, 2017), both disabling and painful, that is prevalent in developing countries (Hill-McManus, Marshall, Soto, Lane, & Hughes, 2018). Dietary overindulgence was thought to be the sole cause of Gout, which resulted in it being called the “Disease of the King;” however, studies have indicated other causes (Arcangelo, Peterson, & Reinhold, 2017). This post will review a description of the disease, discuss drugs prescribed to treat the symptoms, explore how behavior impacts the treatment plan, and identify measures to reduce negative side effects. 

Description 

Gout results from the deposition of monosodium uric acid crystals in the joints and surrounding tissues (Khanna, et al., 2015). The deposition occurs as a result of excess uric acid, which results in the inflammatory arthritis (Khanna, et al., 2015). During acute attacks joints become swollen, painful, and recurrent attacks or flare ups lead to joint damage and disability (Khanna, et al., 2015). Clinical symptoms and uric acid levels greater than 6mg/dL are the diagnostic indications for Gout. Treatment objectives are to decrease the uric acid level to less than 6 mg/dL and manage associated symptoms through non-pharmacological and pharmacological methods (Hill-McManus, Marshall, Soto, Lane, & Hughes, 2018). 

Drugs Prescribed to Treat Symptoms 

The first line of treatment is medications classified as Xanthine Oxidase Inhibitors (such as Allipurinol), which inhibits xanathine oxidase selectively resulting in a decrease in the uric acid (Arcangelo, Peterson, & Reinhold, 2017). Xanathine oxidase is the enzyme responsible for converting hypoxanthine to xanthine and subsequently to uric acid (Arcangelo, Peterson, & Reinhold, 2017). Allopurinol dosing starts at 100 mg by mouth once daily (QD), which can be increased by 100mg weekly (max dose of 800mg/day) until desired uric acid levels are reached (Arcangelo, Peterson, & Reinhold, 2017). Caution is recommended in individuals with hepatic or renal impairments, requiring monitoring of Liver Function Panels (LFTs) and dosing based on Creatinine Clearance (CrCl) is required respectively (Arcangelo, Peterson, & Reinhold, 2017). Adverse reactions include gastrointestinal symptoms, rashes, and arthralgia (Arcangelo, Peterson, & Reinhold, 2017). Consumption of Allopurinol with food helps to decrease the gastrointestinal symptoms. It can take up to two weeks for the desired effects to take place (Arcangelo, Peterson, & Reinhold, 2017). Monitoring of uric acid levels are indicated every 2-5 weeks during titration and should be continued every 6 months after the goal is achieved (Arcangelo, Peterson, & Reinhold, 2017). Interactions exist with Angiotensin Converting Enzyme (ACE) inhibitors, thiazide diuretics, and loop diuretics which can increase the allopurinol levels. Allopurinol also impacts the effects of antineoplastic agents. 

If Allopurinol is not effective, the next line of treatment is Probenecid, which increases uric acid excretion by competitively inhibiting uric acid reabsorption at the convoluted tube proximally (Arcangelo, Peterson, & Reinhold, 2017). Dosing usually begins at 250mg twice daily (BID) and then increased to 500mg BID if needed after one week (Connective Rx, 2018). It can be increased in 500mg increments every four weeks to a maximum dosage of 2grams per day (Connective Rx, 2018). It can take 2 weeks up to 6 months to reach the maximum therapeutic effect (Arcangelo, Peterson, & Reinhold, 2017). It should not be given during acute attacks, it can exacerbate the symptoms, and caution should be utilized in individuals with blood dyscrasias, uric acid kidney stones, and it should not be used in conjunction with ketorolac (Arcangelo, Peterson, & Reinhold, 2017). Adverse reactions can include hemolytic anemia in patients with gastrointestinal reflux disease, hepatic necrosis, nausea, vomiting, and dizziness (Connective Rx, 2018). Allopurinol interacts with antibiotics classified as penicillin derivatives, cephalosporin, and fluoroquinolones which increase the concentration of the antibiotics (Arcangelo, Peterson, & Reinhold, 2017). Concurrent usage with methotrexate, citalopram, and lorazepam can cause toxic levels of allopurinol (Arcangelo, Peterson, & Reinhold, 2017). 

Pegloticase is the last line therapy, when other options have not been successful, due to the expense and monitoring required for this medication. It costs $5,000 per dose and requires close monitoring during and two hours after the infusion for anaphylaxis (Arcangelo, Peterson, & Reinhold, 2017). Pegloticase converts uric acid into an inactive water-soluble metabolite of uric acid, called allantoin, which allows uric acid to be easily excreted by the kidneys (Arcangelo, Peterson, & Reinhold, 2017). Pegloticase is a pegylated recombinant form of an enzyme, uricase (usually absent in humans but found in increased levels in primates) (Arcangelo, Peterson, & Reinhold, 2017). Dosing starts at 8mg intravenously over at least two hours every 2 weeks (Arcangelo, Peterson, & Reinhold, 2017). At least one week prior to the infusion, preventative medications ( a Non-Steroidal Anti-inflammatory Drug and Cholchicine), should be started (Arcangelo, Peterson, & Reinhold, 2017). Therapeutic response time is one day and the reduction of the uric acid levels can be maintained up to 6 months (Arcangelo, Peterson, & Reinhold, 2017). Adverse reactions include gout flare ups, injection reactions (urticarial, bruising, pruritis, and erythema), nausea, vomiting, and constipation can occur. 

Non-Steroidal Anti-inflammatory Drugs (NSAIDs) are utilized to decrease the inflammation and pain on initial onset of the symptoms and up to 24 hours after. Dosing is contingent on the NSAID chosen. Adverse effects can include gastrointestinal symptoms which can be decreased by taking them with food. Caution should be utilized in patients with hypertension secondary to the ability for the NSAIDs to cause increased hypertension. 

Systemic Corticosteroids (SC) can be used to decrease inflammation by suppressing the migration of the polymorphonuclear leukocytes (Arcangelo, Peterson, & Reinhold, 2017). Dosing of prednisone and methyprednisone can be 0.5 mg/kg for 5-10 days or 2-5 days with tapering from day 7-10 days (Arcangelo, Peterson, & Reinhold, 2017). Therapeutic effects can take 1-2 days and caution should be utilized in patients that are immunosuppressed, have uncontrolled hypertension, and have heart disease. SC therapy timeframes should be limited due to the increased possibilities of side effects the longer the therapy continues (Arcangelo, Peterson, & Reinhold, 2017). 

Colchicine is prescribed to decrease the inflammation and pain associated with Gout attacks by inhibiting the activation, migration, and degranulation of neutrophils to the area of the attack (Arcangelo, Peterson, & Reinhold, 2017). It should be administered within 24 hours of the symptoms and will not be effective after 36 hours of the symptom onset (Arcangelo, Peterson, & Reinhold, 2017). Dosing is 1.2 mg  initially, 0.6mg one hour after the initial dose, 0.6mg QD or BID 12 hours after the second dose, and continues at 0.6mg until symptoms subside (Arcangelo, Peterson, & Reinhold, 2017). It can also be utilized prophylactically at 0.6 mg QD or BID after achieving levels (Arcangelo, Peterson, & Reinhold, 2017). Cautions should be utilized in the renal ad hepatic impaired patient. A common adverse reaction is diarrhea. 

How Behavior Impacts the Treatment Plan 

In addition to pharmacological treatment, patients are taught to avoid purine rich food (such as red meat, seafood, and high fructose corn syrup), sweetened beverages, and alcohol (Arcangelo, Peterson, & Reinhold, 2017). Patients should also be encouraged to increase vegetables, water, and non-fat dairy (Arcangelo, Peterson, & Reinhold, 2017). If patients chose not to be compliant with dietary recommendations it can increase the frequency of flare ups, increase the pharmacological needs, and increasing the possibility for more adverse symptoms. This possibility causes the need to ensure patients are provided adequate education on the condition and management of the condition. 

Measures to Reduce Negative Side Effects 

Side effects can be reduced through ensuring medication reconciliation, minimizing drug-drug interaction. Many of these medications can be taken with food to minimize the possibility of gastrointestinal symptoms. Frequent follow-up and communication with the patient about taking the medications as prescribed and reporting adverse effects as soon as possible can allow the patient and the practitioner to ensure the most appropriate treatment regime is prescribed. 

Summary 

In summary, gout is an inflammatory arthritis resulting in the deposition of uric acid in joint tissue due to an increase of uric acid in the body. Treatment can include multiple pharmacological and nonpharmacological methods. Dietary modification is the most significant behavior aspect that can impact the efficacy of the treatment plan. Education, medication reconciliation, and frequent follow-up can help reduce adverse effects from the treatment plans. 

Reference 

Arcangelo, V. P., Peterson, A. M., & Reinhold, J. A. (2017). Pharmacotherapeutics for Advanced Practice: A Practical Approach. Ambler, PA: Lippincott Williams & Wilkins. 

Connective Rx. (2018). Allopurinol. Retrieved from PDR: https://www.pdr.net/drug-summary/Zyloprim-allopurinol-816.988 

Hill-McManus, D., Marshall, S., Soto, E., Lane, S., & Hughes, D. (2018). Impact of non-adherence and flare recolution on the cost-effectiveness of trratments for gout: Application of linked pharmacometric/pharmacoeconomic model. Value in Health, 1373-1381. 

Khanna, P. P., Shiozawa, A., Walker, V., Bancroft, T., Essoi, B., Akhras, K. S., & Khanna, D. (2015). Health-related quality of life and treatment satisfaction in patientes with gout: Results from s cross-sectional study in a managed care setting. Patient Preference and Adherence, 971-981. 

A Sample Answer 4 For the Assignment: NURS 6521 Week 6: Endocrine and Musculoskeletal System 
Title: NURS 6521 Week 6: Endocrine and Musculoskeletal System 

Osteoarthritis (OA) is a progressive disease affecting the hip and knee joints, causing chronic pain in individuals over 65.  OA is the deterioration of cartilage and connective tissue within the joints, resulting in remodeling of the bones causing osteophyte formation and diminished amounts of synovial fluid.  The individual is left with chronic pain and possible debilitating joint damage.  Initial drug treatment begins with acetaminophen, followed by non-steroidal anti-inflammatory drugs (NSAID’s), and as a last resort an analgesic.  

Acetaminophen 

Acetaminophen acts within the central nervous system (CNS) inhibiting central cyclooxygenase (COX) which decreases prostaglandin synthesis (Arcangelo, Peterson, Wibur, & Reinhold, 2017).  Acetaminophen should be taken on a regular schedule to achieve maximum effects within one week.  Individuals who have hepatic disease or consume alcohol should not take acetaminophen, as hepatic failure may result.  It is otherwise safe with the most common adverse effects of dizziness and rash. According to Drahl (2014), research indicates that some are still unsure how acetaminophen works, one theory is that there is a COX3 which resides mostly in the brain and seemed more sensitive to acetaminophen.  According to Saliba et al. (2014) acetaminophen is converted into p-aminophenol in the liver and CNS, which is then conjugated with arachidonic acid to produce N- arachidonoylphenolamine (AM404), which is responsible for the analgesic response. 

NSAID’s 

NSAID’s such as ibuprofen, celecoxib and diclofenac may be orders for individuals not responding to acetaminophen therapy or requiring anti-inflammatory relief, these medications exert a similar mechanism of action by inhibiting COX.  There are two types of COX enzymes (COX1 and COX2), COX1 enzymes reside in the gastrointestinal (GI) tract and kidney and secrete a protective enzyme, while COX2 is produced at sites of inflammation.  Ibuprofen and diclofenac may select COX1 or COX2, which may cause GI upset.  Celecoxib is selective for COX2, which allows for inflicting analgesic and anti-inflammatory relief without causing GI symptoms (Arcangelo, Peterson, Wilbur & Reinhold, 2017).   NSAID’s may cause bleeding in patients on anticoagulant therapy by decreasing the formation of thromboxane (National Institute of Health, n.d.).  Other major adverse effects are GI upset and impaired renal function.  

Analgesics 

For individuals not tolerating acetaminophen or NSAID’s, analgesics such as tramadol or tapentadol may be prescribed.  These medications are only effective against pain and have no anti-inflammatory properties.  These analgesics inhibit pain by binding to mu receptors which blocks the uptake of serotonin and norepinephrine inhibiting the activation