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
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. 

This page contains the Learning Resources for this week. Be sure to scroll down the page to see all of this week’s assigned Learning Resources. To access select media resources, please use the media player below. 

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:  

Fuerst, M. (2015). How common is gout in the united states, really? Rheumatology Network. Retrieved from: 

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). 


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. 


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. 

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. 


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. 


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. 



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: 

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 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 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.  


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 of pain pathways.  Tramadol should only be prescribed for short periods, as it has a potential for dependence.  Tramadol is not associated with GI symptoms nor renal disease and does not affect hypertension or congestive heart failure.  Most common side effects are nausea, dizziness, drowsiness with a potential to cause constipation, and respiratory depression.  Tapentadol  has similar effects as tramadol and  should be avoided in patients  with impaired respiratory function, combination with other serotonergic agents, ingestion of alcohol should also be avoided.  


Geriatric Considerations 

NSAID’s are contraindicated for patients on cardiovascular medications such as the older population, along with those who have impaired hepatic and renal function.  NSAID’s with a shorter half-life or COX2 inhibitor should be prescribed for patients over 65, due to the adverse GI effects.  The addition of a proton pump inhibitor should also be considered in this population 


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. 

Drahl, C. (2014). How Does Acetaminophen Work? Researchers Still Aren’t Sure. Chemical & Engineering News, 92(29), 31-32. Retrieved January 2, 2019, from 

National Institute of Health. (n.d.). National Center for Biotechnology Information. PubChem Compound Database; CID=3672.  Retrieved from 

Saliba, S. W., Marcotegui, A. R., Fortwängler, E., Ditrich, J., Perazzo, J. C., Muñoz, E., … Fiebich, B. L. (2017). AM404, paracetamol metabolite, prevents prostaglandin synthesis in activated microglia by inhibiting COX activity. Journal of Neuroinflammation, 14, 1–11. 

Chronic Gout    Acute Gout   




100 mg, daily, PO. Titrate by 100 mg until reaching uric acid level of less than 6 mg/dL. Max 800 mg/day. Contraindicated with the concurrent use of pegloticase since it can cause anaphylaxis. Common side effects: rash, arthralgias, GI upset. Take with food. Avoid using with ACE inhibitors, thiazide, and loop diuretics since it can increase allopurinol levels.  NSAID’s 




Initial dose of 750 mg, PO, then 250 mg Q 8 hours until attack subsides 

50 mg, PO, TID, then reduce the dose 

200 mg, PO, daily 



Inhibitors) Febuxostat 

 40 mg daily, PO. Max dose 80 mg/day. Contraindicated with the concurrent use of pegloticase since it can cause anaphylaxis.   (Systemic Corticosteroids) 



0.5 mg/kg for 5-10 days and taper down 


Use with caution in diabetic and suppressed immune system patients. Side effects: hyperglycemia, HTN, fluid retention 

Probenecid  Used when XOI are contraindicated. 250 mg PO, BID, increase the dose to 500 mg PO, BID if needed for a max of 2g/day. Not to be given during acute gout attacks. Side effects: hemolytic anemia, hepatic necrosis, anaphylaxis. Avoid penicillin, cephalosporins, and fluoroquinolones since it can increase their concentration.  Colchicine  1.2 mg at first sign of gout flare, 0.6 mg 1 hr later, and 0.6 mg PO daily or BID. The dose is reduced to 0.3 mg daily in renal failure patients. Use with caution in hepatic and renal patients. Side effects: GI upset, fatigue and headache  
Pegloticase  Last-line therapy. 8 mg IV infusion every 2 weeks. Side effects: bruising and redness and urticaria on infusion site.     


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

Title: NURS 6521 Week 6: Endocrine and Musculoskeletal System 


In the United States, a majority of people are affected by endocrine and musculoskeletal disorders. The process of managing the disease requires long-term treatment and care. Also, there is an increasing need for extensive patient education. Consistent education of the patients originates from advanced practice nurses and helps in managing the disorders. In the clinical environment, patients that suffer from endocrine and musculoskeletal disorders usually seek treatment for symptoms that tend to threaten their everyday lives. This is because the disease may interfere with the ordinary tasks of an individual. Some of the complexities associated with these disorders include difficulties in walking short distances, preparing meals and even managing day-to-day activities. Healthcare professionals aim at reducing these symptoms and additional health risks by developing appropriate drug therapy plans and considering specific patient factors.  

Major Musculoskeletal Disorder: Gout 

In this discussion, the selected endocrine or musculoskeletal disorder is gout. The treatment of gout requires various drug prescriptions that target the gout symptoms. Treatment procedures also depend on specific patient features such as age, gender or behaviour. This discussion will concentrate on age as the predominant factor.  

Gout is among the significant resultants of musculoskeletal disorder. Gout originates from effects of accumulated fluids such as water, fatty materials, lymph, ions that are in between the cells of any organ or between the interstitial space and organ spaces. These accumulations typically lead to increased volume along oedema. Also, gout results from the increased levels of uric acid crystals in between the bones (Robinson, 2018).  

Major Musculoskeletal disorder and Genetics 

Genetic factors of patients may contribute to the adverse effects of gout and mainly originate from the familial inheritance of gout genes such as SLC2A9 and SLC22A12. In most cases, NSAIDs produce hepatotoxicity whereas colchicine may cause abnormal cell division implications that result from changes in the number of chromosomes. 

This disorder affects people of advanced age typically. The age factor for gout patients is predominantly significant among older adults due to the formation of uric acid crystals in the synovial fluid. The acid originates from the hyperuricemia inside the blood (Arcangelo, Peterson, Wilbur & Reinhold, 2017). It is these deposits of uric acid crystals that infect the joints and tendons that connect bones to muscles, subjecting them to severe inflammation that usually results in inflammatory arthritis. Also, the severity of gout is higher in older people who drink a lot of beer, meat and fructose-sweetened drinks. The impacts of gout are profoundly manifested in older people of above fifty years compared to young persons of between twenty to thirty-five years. Gout produces potential adverse effects that undermine the lifestyle of elders. This includes the deposition of uric acid crystals in their joints that renders the patients unable to walk. 

Drug Therapy 

The treatment of gout and other musculoskeletal disorder symptoms require specific drug prescriptions some of which could have negative implications on the patient. One of the drugs responsible is the Allopurinol which is a suicide inhibitor that works against the xanthine oxidase (Robinson, 2018).  

The preferred treatments for gout include drugs such as allopurinol and non-steroidal anti-inflammatory drugs (NSAIDs) (Arcangelo, Peterson, Wilbur & Reinhold, 2017). Other treatments include the corticosteroids and loop diuretics that enhance the uric acid dieresis.  

Measures to Reduce Side Effects 

On the third day, the adverse effects of gout are eliminated by using supplements of vitamin C and diuretics that also get rid of excess deposits of drugs in the hepatic metabolism through the renal filtrate (Arcangelo, Peterson, Wilbur & Reinhold, 2017). Also, the absorption of high amounts of drinking water is vital in eliminating excess drug deposits from the patient’s body.  


Essentially, nurses should consider factors that cause side effects before prescribing drugs that treat musculoskeletal disorders such as gout. Minimal adverse effects improve patient’s functionality and suppress chances or impacts of gout. Also, nurses should review the patients’ health history and prescribed medications for appropriate intervention.  



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. 

Robinson, J. (2018, May 15). What Medicines Treat Gout? Retrieved December 31, 2018, from Web MD: 

A Sample Answer 7 For the Assignment: NURS 6521 Week 6: Endocrine and Musculoskeletal System 

Title: NURS 6521 Week 6: Endocrine and Musculoskeletal System 

     Thyroid disease is commonly seen in primary care with hypothyroidism representing the most common hormone deficit (Halawani et al., 2017). Other thyroid disorders include hyperthyroidism (Graves disease), thyroid nodules, thyroiditis, myxedema coma, and thyroid cancer (Arcangelo, Peterson, Wilbur, & Reinhold, 2017). A short pharmacological discussion of the types of medications that are used to treat hypothyroidism, hyperthyroidism, and transient thyroiditis in a primary care setting follows as well as the impact age has on treatment. The presence of a goiter or nodule requires a referral to an endocrinologist (Sheeran, 2016). 

     The thyroid produces thyroxine (T4) and triiodothyronine (T3) through a negative feedback loop governed by the hypothalamus and pituitary glands (Hammer & McPhee, 2014). Medications used to treat disorders of the thyroid are focused on replacing deficient hormone, reducing the production of thyroid hormones, and treating potential side effects (in thyroiditis).   

     Levothyroxine, liothyronine, liotrix, and desiccated thyroid are all medications that replace T4, T3, or a combination of both to treat hypothyroid disease (Arcangelo et al., 2017). Levothyroxine is synthetically produced T4 which is orally administered, and ninety-nine percent protein bound; seventy percent is metabolized to T3 and reverse triiodothyronine by deiodination (DrugBank, n.d.). Thyroid hormones are excreted mostly by the kidneys but also in the stool after enterohepatic circulation and reabsorption and excretion of its hydrolyzed conjugates (DrugBank, n.d.). 

     Absorption of levothyroxine and other thyroid hormone replacement can be altered by the coadministration of cholestyramine, sucralfate, calcium, and antacids containing aluminum and must be taken two hours apart from them and on an empty stomach thirty minutes to one hour before the first meal of the day (Arcangelo et al., 2017). 

     Pharmacological treatment of hyperthyroidism consists of the use of radioactive iodine as a first-line treatment and antithyroid medications (Arcangelo et al., 2017). Iodine is an essential piece to the proper function of the thyroid; it is changed into iodide in the gastrointestinal tract and absorbed into the follicular cells of the thyroid (Arcangelo et al., 2017). Oxidated iodine is assimilated into tyrosine residues and forms monoiodothyronine (MIT) and diiodothyronine (DIT)which combine to form T4 and T3 (Arcangelo et al., 2017). When radioiodine is used as a treatment for hyperthyroidism, it is absorbed into the follicular cells and destroys the thyroid over a period to decrease the amount of hormone it produces. RI is not used in pregnant, lactating or women expecting to get pregnant within six months (Arcangelo et al., 2017). 

     Methimazole and propylthiouracil inhibit iodine organification, in other words, they do not allow the thyroid to absorb iodine which makes the production of MIT and DIT impossible, and they block peripheral conversion of T4 to T3 (Arcangelo et al., 2017). Both drugs will need to be used for 12-24 months; methimazole has a longer duration that propylthiouracil and can be administered only one time per day (Arcangelo et al., 2017). Methimazole interrupts the normal production of T4 and T3 in the very beginning by acting as a substrate for thyroid peroxidase, and is absorbed into the follicular cells instead of oxidized iodine (Prescribers Digital Reference [PDR], n.d.). It is metabolized by the liver and excreted in the urine, has a duration of forty hours, and does not affect T4 and T3 that has been produced and stored in the thyroid (PDR, n.d.). Once the patient is euthyroid treatment can be tapered and eventually discontinued (Arcangelo et al., 2017). 

     Lithium is indicated for the treatment of hyperthyroid disease only in those patients who cannot tolerate antithyroid meds, and beta blockers such as propranolol or atenolol can decrease the stimulation of adrenergic receptors to prevent atrial fibrillation until the patient is euthyroid (Arcangelo et al., 2017). A beta blocker is the treatment of choice for post-partum and de Quervain thyroiditis to treat tachycardia and nervousness; the symptoms are temporary since they are the result of the thyroid releasing more than normal of stored T3 and T4 but not producing more (Arcangelo et al., 2017). In the primary care setting, patients with new-onset hyperthyroidism should be prescribed a beta- blocker and referred to endocrinology (Hammer & McPhee, 2014). 

     It had been determined that there is no reason to treat subclinical hyperthyroid disease (TSH 0.1 to 0.4 mIU/L) except for the patient who is older than 65 years of age, or one who is under 65 who also have heart disease or osteoporosis (Donangelo & Suh, 2017). Treatment of hypothyroid disease in the elderly consists of a lower levothyroxine dose, typically 25 to 50 mcg of levothyroxine daily and titrated up in 12.5 mcg adjustments until TSH is within normal ranges (Gaitonade, Rowley, & Sweeney, 2012).  Children should always be referred to an endocrinologist for treatment of thyroid disorders (Gaitonade et al., 2012). 


Arcangelo, V. P., Peterson, A. M., Wilbur, V., & Reinhold, J. A. (Eds.). (2017). Pharmacotherapeutics for advanced practice a practical  

     approach (4th ed.). Philadelphia, PA: Wolters Kluwer. 

Donangelo, I., & Suh, S. Y. (2017). Subclinical hyperthyroidism: When to treat. American Family Physician, 95(11), 710-716. Retrieved 


DrugBank. (n.d.). Levothyroxine. Retrieved January 1, 2019, from 

Gaitonade, D. Y., Rowley, K. D., & Sweeney, L. B. (2012). Hypothyroidism: An update. American Family Physician, 1(86), 244-251. 

Halawani, M. S., Nughays, R. O., Altemani, A. F., Mubarak, N., Hussein, M., Alghamdi, N. M., … Siraj, M. M. (2017). Causes, diagnosis, and 

     management of hypothyroidism. The Egyptian Journal of Hospital Medicine, 71(1), 2250-2252. 

Hammer, G. D., & McPhee, S. J. (2014). Pathophysiology of disease: An introduction to clinical medicine (7th ed.). New York, NY: McGraw 

     Hill Education. 

Prescribers Digital Reference. (n.d.). methimazole- Drug summary. Retrieved January 2, 2019, from 


Sheeran, M. T. (2016). Biochemical testing of the thyroid: TSH is the best and, oftentimes, only test needed- a review for primary care. 

     Clinical Medicine & Research, 14(2), 83-92. 

A Sample Answer 8 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 joint disease characterized by loss and damage of articular cartilage, inflammation, new bone formation of joint margins, bone changes, synovitis, and thickening of the joint capsule (Huether & McCance, 2017, p. 1009).  This disease can lead to chronic pain, restricted range of motion, and muscle weakness with the most common joints affected being the knees, hips, cervical and lumbar spine, and joints of the hand (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 591).  Primary OA results from the normal aging process whereas secondary OA results from traumatic injuries, mechanical stress on the joints and excess fat on articular cartilage due to obesity, and inherited conditions (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 591).   

When selecting a treatment plan for patients with OA, appropriate non-pharmacological interventions should be instated such as physical therapy and weight loss if necessary.  Interventions such moist heat to diminish muscle spasm and joint stiffness, exercising and the use of assistive devices with activities of daily living can help manage some symptoms of OA (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 593).  “The goals of drug therapy for OA are to maintain function, prevent further joint damage, and diminish associated pain” (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 593).   There is no cure for OA, and the standards of treatment are limited to pain management, steroids, other anti-inflammatory drugs, physical therapy, and eventual joint replacement (Cho, Walker, Williams, & Hasty, 2015).  The types of drugs that are often prescribed for patients with OA include acetaminophen, nonsteroidal anti-inflammatory drugs, nonacetylated salicylates, analgesics, topical agents, and corticosteroids.  

Drug Treatment for OA 

            When selecting pharmacotherapy for patients with OA, it is important to consider many factors such as the severity of the disease, the age of the patient, underlying illnesses, and current medications. American College of Rheumatology (ACR), the European League Against Rheumatism (EULAR), and the Osteoarthritis Research Society International (OARSI) have all published guidelines for the treatment of OA.   

Acetaminophen has historically been used as the first-line treatment for OA due to its cost-effectiveness, relative safety, and effectiveness in reducing pain within 4 weeks and lasting up to 2 years (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 600).  Acetaminophen is thought to act primarily in the central nervous system, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin synthesis (Acetaminophen, 2018).  The absorption of acetaminophen is rapid and almost complete, 25% bound to protein, metabolized in the liver, has a half-life of one to four hours and is excreted in the urine with approximately 80% conjugated and 3% excreted unchanged. The recommended dose of acetaminophen is 650 mg every 4 to 6 hours or 1,000 mg every 6 to 8 hours around the clock and should be taken regularly, regardless of the patients’ pain to be most effective (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 593).  Higher doses (over 4,000 mg per day) have been associated with hepatotoxicity and patients with a history of liver disease or chronic alcohol use should not take more than 2,000 mg per day (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 593).  Aside from the potential of overdose and toxicity, acetaminophen is typically well tolerated with the most common adverse events being dizziness and rash (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 593).   

Nonsteroidal anti-inflammatory (NSAID) medications should be considered for second-line therapy, monotherapy, or in combination with acetaminophen if acetaminophen fails to provide relief as a first-line therapy.  “The anti-inflammatory effects of NSAIDs are mainly due to their ability to inhibit cyclooxygenase (COX), impairing production of prostaglandins, which are important mediators of both pain and the inflammatory response” (Cho, Walker, Williams, & Hasty, 2015, p. 1).  Ibuprofen is a common and cost-effective NSAID used to treat pain and inflammation associated with OA.  Pain relief of ibuprofen is attributed to “peripheral affected regions and central nervous system effects in the pain transmission mediated by the dorsal horn and higher spinothalamic tract” (Ibuprofen, 2018).  Ibuprofen inhibits the activity of both COX-1 and COX-2 decreasing the synthesis of prostaglandins involved in mediating inflammation, pain, fever, and swelling as well as causing side effects of GI ulceration (Ibuprofen, 2018).  The usual dose of ibuprofen is 400 mg four times daily.  Ibuprofen is well absorbed with a peak concentration in one to two hours, more than 99% bound to plasma proteins, rapidly metabolized and biotransformed in the liver and oxidized by the cytochrome P450, with a half-life of 1.2 to 2 hours (Ibuprofen, 2018).  Ibuprofen is rapidly metabolized and eliminated in the urine and is completely eliminated in 24 hours after the last dose with nearly all of the dose metabolized, representing about 99% of the eliminated dose (Ibuprofen, 2018).   

Nonacetylated salicylates such as diflunisal is a treatment option for patients who cannot take NSAIDs due to GI irritation as it is an effective COX-1 inhibitor with anti-inflammatory and analgesic properties (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 596).  Difunisal is a nonsteroidal drug with analgesic and anti-inflammatory properties. The dosage is 500 to 1000 mg per day in two divided doses, not to exceed 1500 mg per day.  The mechanism of action appears to be associated with the inhibition of prostaglandin synthesis via the arachidonic acid pathway, relieving pain accompanied by inflammation due to a decrease in prostaglandins in peripheral tissues (Diflunisal, 2018).  Diflunisal is rapidly and completely absorbed with a bioavailability of 80-90% with peak concentrations 2 to 3 hours after oral administration (Diflunisal, 2018). This drug is 99% bound to proteins, metabolized in the liver, excreted in the urine as two soluble glucuronide conjugates, and a half-life of 8 to 12 hours (Diflunisal, 2018).   

Opioid or nonopioid analgesics can be considered as third-line therapy for patients who have not achieved pain control with acetaminophen or NSAIDs or for whom acetaminophen or NSAIDs are not an option. Tramadol is a narcotic analgesic pain medication often prescribed for pain associated with OA.  The analgesic properties of Tramadol can be attributed to norepinephrine and serotonin reuptake blockade in the CNS, which inhibits pain transmission in the spinal cord (Tramadol, 2018).  Tramadol binds to the mu opioid receptor, inhibits ascending pain pathways, and results in decreased pain sensation (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 597).  The usual adult dose for pain is 50 to 100 mg orally every 4 to 6 hours of the immediate release form as needed for pain with a maximum daily dose of 400 mg.  This form begins to work for pain control as soon as 1 hour after taking, with the maximum effect at 2 hours (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 597).  The extended-release dosage for chronic pain is 100 mg orally once per day with an increase every 5 days if needed to a maximum of 300 mg per day with pain control maximum effect at about 12 hours (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 597).  Tramadol is rapidly and almost completely absorbed after oral administration with the mean absolute bioavailability of a 100mg dose being 75%, peak plasma concentration at 2 to 3 hours, with 20% bound to plasma proteins, and a half-life of 6 to 7 hours (Tramadol, 2018).  Tramadol is metabolized in the liver and excreted primarily by the kidneys with 30% of the dose unchanged in the urine and 60% excreted as metabolites (Tramadol, 2018).  The most common side effects of tramadol include nausea, dizziness, drowsiness, and sweating and can also lead to constipation, dependency, euphoria, and respiratory depression (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 597).   

Duloxetine is also used in some patients with OA as it is a serotonin and norepinephrine reuptake inhibitor (SSRI) which acts to enhance serotonin and norepinephrine in the central nervous system to reduce pain transmission (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 598).  SSRIs are typically used to treat depression, but the neurobiology of depression and chronic pain shares the specific neurotransmitters of serotonin and norepinephrine and can reduce chronic pain when interacting with cytokines, serotonin, and norepinephrine to modulate the pain response (Saccomano, 2018, p. 53).  The FDA approved dose for chronic pain is 30 mg orally per day for 7 days and then increased to 60 mg daily (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 598).  Duloxetine is well absorbed, greater than 90% protein bound, with peak plasma concentrations in about 6 hours, and a half-life of approximately 12 hours (Duloxetine, 2018).  Duloxetine is extensively metabolized by CYP isoenzymes into numerous metabolites, excreted mainly in the urine as metabolites (about 70%) and in feces (20%) (Duloxetine, 2018).  This medication should not be taken with a monoamine oxidase inhibitor (MAOI) and should not be stopped abruptly.  Risks associated with this medication include hepatotoxicity, orthostatic hypotension, serotonin syndrome, abnormal bleeding and mania (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 598).    

Topical agents such as capsaicin and topical diclofenac are also treatment options for the pain associated with OA. Capsaicin is effective for pain control through the depletion of substance P.  Substance P is a chemomediator responsible for pain transmission from the periphery to the CNS (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 598).  Initially, capsaicin releases substance P from the peripheral sensory neurons, and with repeated use, substance P becomes depleted and capsaicin prevents reaccumulation of substance P (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 598).  Capsaicin’s mechanism of action is also attributed to “defunctionalization” of nociceptor fibers by inducing a topical hypersensitivity reaction on the skin (Capsaicin, 2018).  This medication can be used as a patch, cream, gel, liquid, or lotion and should be applied at least three times per day, with the patch applied to the affected area three to four times per day (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 598).  There is low systemic absorption of capsaicin and the onset of action is two to four weeks of continuous therapy with a half-life of 1.64 hours (Capsaicin, 2018).  

Long-term oral corticosteroids are typically only prescribed for intermittent flare-ups as they can lead to adverse reactions such as oral infection, embolism, and bone disorders (Saccomano, 2018, p. 53).  Intra-articular corticosteroid injections may be helpful for patients who have not responded to first- or second-line treatment or when a joint effusion and local inflammation are present although this treatment varies in benefit and duration of pain control.  Intra-articular injections are not suggested more than every 3 to 4 months and preferred corticosteroid injections include triamcinolone acetonide and methylprednisolone acetate (Saccomano, 2018, p. 53).  Corticosteroids work to suppress the inflammatory process and the dose of these medications depend on the site of the joint to be injected.   

Age as a Factor 

“For elderly patients, the practitioner usually prescribes an NSAID with a shorter half-life in a smaller dosage than for a younger adult” (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 600).  For patients over 75 years and older, the ACR recommends topical NSAIDS over oral NSAIDs.  Gastric ulceration, kidney dysfunction, and increased bleeding times are some adverse reactions of NSAIDs and have been known to increase the risk of cardiovascular thrombotic events, including myocardial infarction and stroke (Saccomano, 2018, p. 53).  Since NSAIDs are frequently used in treating the pain of OA, caution must be used when these medications are prescribed to older adults as they are at increased risk for these adverse reactions.  Acetaminophen and ibuprofen can affect the INR of patients on warfarin, which is why it is important to know other medications patients are currently taking as older adults are often on multiple medications.  Older adults on NSAIDs should have periodic kidney function monitoring and should not be used in patients with decreased creatinine clearance levels (Saccomano, 2018, p. 53).  One study shares that despite reports of pain, older adults with osteoarthritis did not take their pain medications as they did other prescribed medications (Merkle & McDonald, 2009).  This incorporates both age and behavior as factors for adherence to a pain management program.   

Measures to Reduce Negative Side Effects 

NSAIDs are associated with more adverse effects, such a GI disorders and may be coupled with a proton pump inhibitor to provide gastric protection (Arcangelo, Peterson, Wilbur, & Reinhold, 2017, p. 600).  NSAIDs should also be taken with food to avoid GI disturbance.  Using a combination of drugs with different actions can lower drug doses, essentially minimizing adverse reactions while maximizing relief (Saccomano, 2018, p. 53). Alternative treatment for patients who are at risk for adverse reactions to oral NSAIDs have the option of using topical NSAIDs for treatment and are recommended for patients over the age of 75 (Saccomano, 2018, p. 53).  Narcotic medications should be taken with food to avoid an upset stomach, and if taken regularly, a stool softener could be taken to avoid constipation.   



Acetaminophen. (2018). Retrieved January 1, 2019, from 

Arcangelo, V.P., Peterson, A.M., Wilbur, V., & Reinhold, J.A. (Eds.). (2017). Pharmacotherapeutics for advanced practice: A practical approach(4thed.). Ambler, PA: Lippincott Williams & Wilkins. 

Capsaicin. (2018). Retrieved January 2, 2019, from 

Cho, H., Walker, A., Williams, J., Hasty, K. (2015). Study of Osteoarthritis Treatment with Anti-Inflammatory Drugs: Cyclooxygenase-2 Inhibitor and Steroids.BioMed Research International, 2015, p. 1–10. doi:10.1155/2015/595273. 

Diflunisal. (2018).  Retrieved January 1, 2019, from 

Huether, S.E., & McCance, K.L. (2017). Understanding pathophysiology (6thed.). St. Louis, MO: Mosby. 

Ibuprofen. (2018).  Retrieved January 1, 2019, from 

Merkle, D. & Mcdonald, D.D. (2009).  Use of recommended osteoarthritis pain treatment by older adults. Journal of Advanced Nursing 65(4): 828-835. doi: 10.1111/j.1365-2648.2008.04940.x 

Saccomano, S.J. (2018). Osteoarthritis treatment: Decreasing pain, improving mobility. The Nurse Practitioner, 43(9): 49-55. doi: 10.1097/01.NPR.0000544281.05010.86 

A Sample Answer 10 For the Assignment: NURS 6521 Week 6: Endocrine and Musculoskeletal System 

Title: NURS 6521 Week 6: Endocrine and Musculoskeletal System 

“Osteoarthritis is a progressive disease that can result in chronic pain, restricted range of motion and muscle weakness, especially if a weight bearing joint is affected”(Arcangelo, Peterson, Wilbur & Reinhold, 2017). Joints that are mainly affected by osteoarthritis include, hips, knees, hands, cervical and lumbosacral spine ( Arcangelo, Peterson, Wilbur & Reinhold, 2017). In  2012, the ACR published guidelines for the treatment of osteoarthritis depending on the location ( Arcangelo, Peterson, Wilbur & Reinhold, 2017). 


Depending on the location of the individuals osteoarthritis will then depend on the appropriate treatment. First line pharmacotherapy  to treat osteoarthritis is geared to analgesia ( Arcangelo, Peterson, Wilbur & Reinhold, 2017).Acetaminophen is used as first line therapy as treatment for individuals with osteoarthritis of the hip and knees. Acetaminophen is a pain reliever and  fever reducer used to treat muscle aches and arthritis (, 2017). Current limits of acetaminophen is four grams daily, however, some experts recommend three grams daily when used for long- term therapy (, 2017). ” Acetaminophen is thought to act primarily in the central nervous system, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2 and COX-3 enzymes involved in prostaglandin synthesis”( Drug Bank, 2018).  Acetaminophen is primarily metabolized in the liver, approximately 80% is excreted in the urine, with 3% being unchanged ( Drug Bank, 2018). 

Second line treatment in osteoarthritis of the hip and knee include the use of oral NSAIDs. Oral NSAIDs are also used as the third line therapy for osteoarthritis of the hand ( Arcangelo, Peterson, Wilbur & Reinhold, 2017). Non steroidal anti-inflammatories are classified according to their chemical structure which include: Acretic Acid NSAIDs, Enolic Acid NSAIDs, Fenamic Acid NSAIDs, Phenylacetic Acid NSAIDs, Propionic Acid NSAIDs, Salicylic Acid NSAIDs and COX-2 selective NSAIDs ( Arcangelo, Peterson, Wilbur & Reinhold, 2017). These drugs may be prescribed to individuals that do not respond well to acetaminophen. 

Indomethacin is a non steriodal anti inflammatory that is classified as an acetic acid (, 2018). Initial dose to treat osteoarthritis is 25 mg two to three times daily and  may be increased by 25 mg at weekly intervals (, 2018). Indomethacin is well absorbed from the GI tract and is metabolized in the liver, 60% is excreted in the urine as an unchanged drug and metabolites (, 2018). 

Meclofenamate is an anti inflammatory and is classified as an anthranilic acid  and is used for the relief of mild to moderate pain ( RX List, 2018). In the treatment of osteoarthritis the recommended dose is 200 -400 mg daily divides into three doses ( RX List, 2018).” The mode of action like that of other non steriodal anti inflammatories is unknown, it is rapidly absorbed following administration and is extensively metabolized to an active metabolite and approximately 70% of the dose is excreted in the kidneys” ( RX List, 2018). 

Diclofenac sodium is a benzene acetic deriviative used for the relief of osteoarthritis symptoms ( RX List, 2018). Diclofenac is a topical NSAID used to treat osteoarthritis of the hand as second line therapy and third line therapy in the treatment of osteoarthritis of the knee ( Arcangelo, Peterson, Wilbur & Reinhold, 2017). The mechanism of action of diclofenac is not completely understood but involves inhibition of cyclooxygenase ( RX List, 2018). 

Ibuprofen is a non steriodal anti inflammatory in the propionic acid category used to treat pain and inflammation (, 2017). Ibuprofen is well absorbed, with pain relief achieved within one hour (, 2017). Ibuprofen is extensively metabolized and excreted mainly in the urine as metabolites (, 2017). 

Celecoxib is  selective inhibitor of cclooxygenase-2 ( COX-2) used to treat the symptomatic treatment of osteoarthritis (, 2018). Celecoxib is well absorbed following administration and peak plasma concentrations are usually attained within three hours, distribution is not well characterized(, 2017). Celecoxib is metabolized in the liver and excreted in the urine (, 2017). 

When the pain with osteoarthritis is no longer receptive to acetaminophen or NSAIDs, tramadol is the next option in the treatment of osteoarthritis of the hip and knees ( Arcagelo, Peterson Wilbur & Reinhold, 2017). Tramadol is used to treat moderate to moderately severe pain ( Mayo Clinic, 2018). Patients may feel a relief of pain as soon as one hour after administration and maximum effect at two hours ( Arcangelo, Peterson, Wilbur & Reinhold, 2017). It is a muopioid receptor agonist similar to other opioids, by binding to the mu opioid receptor, ascending pain pathways are inhibited, resulting in decreased pain sensation ( Arcangelo, Peterson, Wilbur & Reinhold, 2017). 

Topical agents such as capsaicin are used as the first line therapy for treatment of osteoarthritis of the hand ( Arcangelo, Peterson, Wilbur & Reinhold, 2017). Capsaicin releases the depletion of substance P, from the peripheral sensory neurons ( Arcangelo, Peterson, Wilbur & Reinhold, 2017). 

” If symptoms of osteoarthritis are restricted to one or two joints that have not responded to first or second line therapy intra- articular corticosteriods may be helpful ( Arcangelo Peterson, Wilbur & Reinhold, 2017).” Intra- articular cirticosteriods have been used for the past decade in the treatment of osteoarthritis. Corticosteriods have an anti infalmmatory effect due to the inhibition of inflammatory cytokines, as well as the inhibition of the pathways that lead to their functioning ( Wang & He, 2015). “Hyalonic acid injections have also been demonstrated to be beneficial in the treatment of osteoarthritis by improving joint lubrication and synovial fluid viscosity, however, the safety of hyalurinc acid remains controversial” ( Wang & He, 2015). 

Genetic Factors 

Researchers believe that multiple gene factor influence the progression and severity of osteoarthritis ( Thomas, 2014). Estimates are that osteoarthritis has a 50% genetic influence ( Thomas, 2014). Some epidemiologist studies show 40% probablity of inheriting osteoarthritis of the knee and 45% probabliltiy of inheriting in hips and hands ( Thomas, 2014). 


Arcangelo, V.P, Peterson, A.M., Wilbur, V. & Reinhold, J.A. (2017). Pharmacotherapeutics for advanced practice: A practical approach. ( 4th ed). Ambler, PA: Lippincott, Williams & Wilkins 

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Thomas, M. (2014). Osteoarthritis and our genes. Retrieved from: 

Wang, F. & He, X.  Intra- Articular Hyraluronic Acid and Corticosteriods in the Treatment of Knee Osteoarthritis. Exp Ther Med. 205 Feb; 9(2): 493 

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

Title: NURS 6521 Week 6: Endocrine and Musculoskeletal System 

Explain the Differences between Types of Diabetes Including Type One and Type Two, Gestational and Juvenile Diabetes 

Diabetes is a condition that occurs when glucose in the blood becomes too high (Vygotsky, Fonda, Chellappa, Walker, & Ehrhardt, 2011)). Type 1 diabetes is a condition when people not to produce any insulin. In type 2 diabetes, patients produce inadequate insulin or in small quantities that cannot work effectively. Gestational diabetes occurs during pregnancy and causes high sugar levels that are detrimental to mother and baby. Juvenile diabetes affects children under eighteen years. The most common form in juveniles is typed one diabetes which affects 90% of the young people (Juvenile Diabetes, 2019).   

One of the typical class of drugs for the treatment of diabetes is Alpha-glucosidase inhibitors (de Camargo, Regitano-d’Arce, Biasoto & Shahidi, 2016)). They are also known as “starch blockers.” The medications aid the body to break down food rich in starches and sugar. Consequently, lowering the level of blood sugar in the body. Examples include acarbose, voglibose, and miglitol. Alpha-glucosidase acts as enzyme inhibitors. From the three, miglitol is the one that is completely and rapidly absorbed by the upper side of the small intestine. Hence having an immediate effect on the reduction of glucose levels. They have a mechanism of action of pancreatic center. The group of medicine acts by delaying the absorption of carbohydrates by the gastrointestinal tract.   

Alpha-glucosidase is administered orally. They are best taken before meals or immediately before intake of the first bite of food. They help in preventing the rapid rise of blood sugar after food intake. Since the drug avoids breakdown of starches to form monosaccharides, they are absorbed in the gastrointestinal tract. Therefore allowing beta cells in the body to produce enough insulin for the body. The drug is friendly thus can be used in combination with other classes of diabetes medications. And, since alpha-glucosidase do not lower blood sugar in themselves, they have to be used together with other medicines for diabetes.  

Because they prevent absorption of carbohydrates in the small intestines, some patients experience bloating, nausea diarrhea as well as flatulence. Thus for beginner patients, doctors prescribe Alpha-glucosidase in small doses. As the patient gets used to the medication, the dose gets increased. However, the symptoms diminish with time. The medicine is a booster to other treatment plans.  

Though the drug is designed to minimize the absorption of carbohydrates and simple sugars into the body, diabetes patients still need to check on the intake of these types of food. Patients who have diabetes should eat a balanced diet just like anyone else. However, they should check on quantities and dietary patterns of the food they take especially the carbohydrates and the sugars. Natural and unprocessed foods are preferable for diabetic patients. They should eat more nuts, avocado, fruits and vegetables, a diet rich in fiber fish, cereals, white meat and proteins like beans, unsweetened yogurt, and eggs. They should eat less of animal fats packaged and processed foods, white bread, and red meat.  

 Explain Short Term and Long-Term Impact on This Diabetes Including Effects of Drug Treatment 

The short term and long- term effects of diabetes may be mild or severe. Excessive release of sugars into the blood may lead to dehydration. When sugars are released into the urine for some time may lead to weight loss. Patients may also experience blurred vision, headache, nausea, and fatigue. Elevated levels of blood sugar can negatively impact the immune system. Therefore, patients are prone to infections. During periods of sugar elevation, patients are susceptible to fungal and bacterial infections. Other conditions that are associated with high blood sugar are poor circulation colonization of pathogens in the skin and weakening the nervous system. Hence patients commonly experience fungal, urinary tract infections and skin or foot conditions. Other conditions include sexual problems in men and women, heart and stroke.  

If heightened blood sugar is not managed immediately, it can be life-threatening. It can lead to acute diabetes known as Diabetic Ketoacidosis. In this case, there is severe dehydration as well as electrolyte imbalances. Hence, the levels of acid in the blood rise significantly leading to vomiting and low blood pressure. In more severe cases, a patient experiences kidney failure, coma, and death. Diabetes can cause peripheral arterial disease neuropathy. It leads to nerve damage, which in turn cause numbness. Hence, pausing a risk to a patient since they cannot feel foot injury. Wounds, cuts, and scrapes may heal slowly. In severe cases, where there is damage to the blood vessel, the wound may become severe and lead to amputation. In some cases, long-term diabetes could result in retinopathy, which is retina damage.  

Diabetes drugs are essential for treating blood sugar, but they can also have adverse reactions to the human body.  Some of the common effects include nausea, gas, bloating, diarrhea, and stomach upset. However, different types of medicine may have varying side effects. For instance, sulfonylureas may lead to low blood sugar, skin rash as well as weight gain. Alpha-glucosidase may cause bloating, stomach gas and diarrhea and thiazolidinediones could cause weight gain, liver disease, anemia and swelling of the feet.  


Diabetes is a disease that can be avoided by intake of less carbohydrate and simple sugars. However, if a person has the condition, they should take medication as prescribed. Therefore, patients must inform the physician of any side effects from the drugs since no patient should experience discomforts from treatment that are unavoidable. And by following appropriate dietary advice, the disease is manageable, and the patients live a normal life.  


de Camargo, A. C., Regitano-d’Arce, M. A. B., Biasoto, A. C. T., & Shahidi, F. (2016). Enzyme-assisted extraction of phenolics from winemaking by-products: Antioxidant potential and inhibition of alpha-glucosidase and lipase activities. Food chemistry, 212, 395-402. 

Juvenile Diabetes. (2019.). Retrieved from 

Vygotsky, R. A., Fonda, S. J., Chellappa, M., Walker, M. S., & Ehrhardt, N. M. (2011). Short- and long-term effects of real-time continuous glucose monitoring in patients with type 2 diabetes. Diabetes care, 35(1), 32-8.