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NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

Walden University NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders-Step-By-Step Guide

 

This guide will demonstrate how to complete the Walden University  NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.

 

How to Research and Prepare for NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

 

Whether one passes or fails an academic assignment such as the Walden University  NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.

 

After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.

 

How to Write the Introduction for  NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders 

 

The introduction for the Walden University  NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.

 

How to Write the Body for  NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders 

 

After the introduction, move into the main part of the  NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.

 

Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.

 

How to Write the Conclusion for  NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders 

 

After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.

 

How to Format the References List for  NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

 

The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.

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Sample Answer for NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

A 28-year-old woman presents to the clinic with a chief complaint of hirsutism and irregular menses. She describes irregular and infrequent menses (five or six per year) since menarche at 12 years of age. She began to develop dark, coarse facial hair when she was 14 years of age, but her parents did not seek treatment or medical opinion at that time. The symptoms worsened after she gained weight in college. She got married 3 years ago and has been trying to get pregnant for the last 2 years without success. Height 66 inches and weight 198. BMI 32 kg.m2. Moderate hirsutism without virilization noted.  Laboratory data reveal CMP within normal limits (WNL), CBC with manual differential (WNL), TSH 0.9 IU/L SI units (normal 0.4-4.0 IU/L SI units), a total testosterone of 65 ng/dl (normal 2.4-47 ng/dl), and glycated hemoglobin level of 6.1% (normal value ≤5.6%). Based on this information, the APRN diagnoses the patient with polycystic ovarian syndrome (PCOS) and refers her to the Women’s Health APRN for further workup and management.

Question 2 of 2:

 

How does PCOS affect a woman’s fertility or infertility? 

Selected Answer: The main cause of infertility in women with PCOS are problems in ovulation. Ovulation may be hindered by increased production of testosterone or failure of ovarian follicles to mature. When hormones fail to balance, an individual may experience irregular ovulation and menstruation. Since the main characteristic feature in the pathology of PCOS is a hyperandrogenic state, in excess, androgens   affect the growth of follicles while insulin suppresses apoptosis which declines follicular growth. There are also dysfunctions that occur in the development of ovarian follicles. In other instances, inappropriate secretion of gonadotropin triggers the start of a vicious cycle which perpetuates anovulation.
Correct Answer: Ovulation problems are usually the primary cause of infertility in women with PCOS. Ovulation may not occur due to an increase in testosterone production or because follicles on the ovaries do not mature. Due to unbalanced hormones, ovulation and menstruation can be irregular. A hyperandrogenic state is a cardinal feature in the pathogenesis of PCOS. Excessive androgens affect follicular growth, and insulin affects follicular decline by suppressing apoptosis and enabling follicle to persist. There is dysfunction in ovarian follicle development. Inappropriate gonadotropin secretion triggers the beginning of a vicious cycle that perpetuates anovulation.
Response Feedback: [None Given]

Question 1

4 out of 4 points

Correct

Scenario 1: Gout

A 68-year-old obese male presents to the clinic with a 3-day history of fever with chills, and Lt. great toe pain that has gotten progressively worse. Patient states this is the first time that this has happened, and nothing has made it better and walking on his right foot makes it worse. He has tried acetaminophen, but it did not help. He took several ibuprofen tablets last night which did give him a bit of relief.

HPI: hypertension treated with Lisinopril/HCTZ .

SH: Denies smoking. Drinking: “a fair amount of red wine” every week. General appearance: Ill appearing male who sits with his right foot elevated.

PE:  remarkable for a temp of 100.2, pulse 106, respirations 20 and BP 158/92. Right great toe (first metatarsal phalangeal [MTP]) noticeably swollen and red. Unable

to palpate to assess range of motion due to extreme pain. CBC and Complete metabolic profile revealed WBC 15,000 mm3 and uric acid 9.0 mg/dl.

Diagnoses the patient with acute gout.

Osteoporosis is a condition in which an individual’s bone is brittle. This is due to the bone unable to keep up with the process of new bone formation in balance with bone mineral removal. There are many risks involved with having this disease process such as easy fractures, and severe back issues like compression of vertebras. Risk factors for osteoporosis include family history, female, excessive alcohol, diet deficient in calcium and vitamin D, and many more. The nurse may educate patient on the disease process as well as screen the patient for complications. The nurse can educate the patient on a diet low in caffeine, alcohol, provide resources for exercises for bone strength as well as a diet that supports healthy bone.

Question:

Explain the pathophysiology of gout.

Selected Answer:

Gout is an inflammatory response due to persistently excessive elevation of uric acid in the blood, and in other body fluids. The response of reaction results in the deposition of monosodium urate (MSU) crystals in the joints of patients. When the uric acid is elevated it crystallizes and the crystals are deposited on the joints, tendons, and surrounding tissues, resulting in a gout attack, Prolong accumulation of crystallizing results in joint damage and a condition known as gouty arthritis. crystal deposition in the subcutaneous tissues developed after a long time causing the formation of small, white nodules that are visible all over the body. Hyperuricemia is also associated with hypertension, heart disease, genetic, obesity, certain medications, alcoholism, kidney problem, eating foods that cause the build-up of uric acid such as red meat, sea food, foods rich purine -rich foods such asorgan meats, porks, More common in men that woman.The signs and symptoms severe pain in one or different joints, tenderness, swelling around the affectected area,reddness.

Correct Answer:

Correct 

Gout is an inflammatory response to excessive quantities of uric acid in the blood and other body fluids including synovial fluid. The elevated level of uric acid lea to the formation of monosodium urate crystals in and around joints. When the uric acid levels exceed approximately 6.8 mg/dl, it crystalizes and forms an insoluble precipitate that are deposited into connective tissue through the body. When crystallization occurs in synovial fluid, it triggers Tumor Necrosis Factor (TNF)-α, which causes the release of inflammatory cytokines and interleukins. The result is an acute inflammatory response within the joint.

Gout is caused by a defect in purine metabolism and kidney function. Uric acid is a byproduct of purine nucleotides. People with gout may have an elevated level of purine synthesis accompanied by a rise in uric acid level.

Response Feedback: [None Given]
  • Question 2

    Correct

    Scenario 1: Gout

    A 68-year-old obese male presents to the clinic with a 3-day history of fever with chills, and Lt. great toe pain that has gotten progressively worse. Patient states this is the first time that this has happened, and nothing has made it better and walking on his right foot makes it worse. He has tried acetaminophen, but it did not help. He took several ibuprofen tablets last night which did give him a bit of relief.

    HPI: hypertension treated with Lisinopril/HCTZ .

    SH: Denies smoking. Drinking: “a fair amount of red wine” every week. General appearance: Ill appearing male who sits with his right foot elevated.

    PE:  remarkable for a temp of 100.2, pulse 106, respirations 20 and BP 158/92. Right great toe (first metatarsal phalangeal [MTP]) noticeably swollen and red. Unable to palpate to assess range of motion due to extreme pain. CBC and Complete metabolic profile revealed WBC 15,000 mm3 and uric acid 9.0 mg/dl.

    Diagnoses the patient with acute gout.

    Question:

    Explain why a patient with gout is more likely to develop renal calculi.

    Selected Answer:

    Patients with gout are more at risk for uric acid stone formation due to the low urine PH of less than 5, which makes the environment conducive for uric acid precipitation. and also can increase the risk of calcium oxalate stone formation. If there is excessive uric acid in the blood, and it builds up over time  because the kidney was not able to remove, it  can cause  kidney stones which  can lead to infection scarring, and finally kidney failure

    Correct Answer:

    Correct 

    Most uric acid is eliminated from the body through the kidneys. Urate is filtered at the glomerulus and undergoes reabsorption and excretion within the proximal renal tubules. In primary gout, urate excretion by the kidneys is sluggish. This may be caused by a decrease in glomerular filtration of urate or acceleration in urate reabsorption. This allows for urate crystals to be deposited in the renal tubules.

    Response Feedback: [None Given]
  • Question 3

    4 out of 4 points

    NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

    Correct

    Scenario 2: Osteoporosis

    A 78-year-old female was out walking her small dog when her dog suddenly tried to chase a  rabbit and made her fall. She attempted to try and break her fall by putting her hand out and she landed on her outstretched hand. She immediately felt severe pain in her right wrist and noticed her wrist looked deformed. Her neighbor saw the fall and brought the woman to the local ER for evaluation. Radiographs revealed a Colles’ fracture (distal radius with dorsal displacement of fragments) as well as radiographic evidence of osteoporosis. A closed reduction of the fracture was successful, and she was placed in a posterior splint with ace bandage wrap and instructed to see an orthopedist for follow up.

    Question:

    Discuss what is osteoporosis and how does it develop pathologically? 

    Selected Answer:

    Osteoporosis is a  bone disease that develops when bone mineral density and mass are reduced and the quality or structure of the bone changes that can increase the risk of fractures.  There are no symptoms of osteoporosis, it is considered a silent disease. It is more common in women in their menopausal stage and older. It can affect any part of the body. But most affect  the bones of the hip, vertebrae in the spine, and wrist, There are risk factors for osteoporosis which include, sex, age, body size race, family history, changes to hormones, Medications, other medical conditions such as rheumatoid arthritis, cancer, HIV/AIDS

    Correct Answer:

    Correct 

    Osteoporosis is considered a metabolic bone disease. Osteoporosis, also called porous bone, is the most common bone disease in humans. Its main features include low bone mineral density, impaired structural integrity of bone, decreased bone strength and increased risk of fractures. The two types of osteoporosis are primary and secondary. Primary osteoporosis, the most common is hormone mediated where bone loss is accelerated by declining levels of estrogen in women and testosterone in men. Secondary osteoporosis is caused by other conditions including endocrine disorders (hyperparathyroidism, hyperthyroidism, diabetes mellitus) and certain medications such as heparin, corticosteroids, phenytoin, barbiturates, and lithium) as well as tobacco and alcohol. There are three major bone cells that are involved in the formation, maintenance, and reabsorption of bone. Osteoblasts are immature bone cells that under ideal circumstances allow bone to formed and laid down. Osteocytes are cells that are responsible for the normal maintenance, or the cycle, of bone. Osteocytes removed old bone cells which allows the osteoblasts to form new bone. Osteoclasts are responsible for reabsorption of bone. Hormonal influences remain important in maintaining bone health, but new research has demonstrated that genetic factors and the role of oxidative stress also contributes to the development of osteoporosis. Reactive oxygen species (ROS) serve as signaling molecules for osteoblasts, osteocytes, and osteoclasts. An imbalance between osteoblast formation and osteoclast reabsorption is the primary cause of osteoporosis.

    Response Feedback: [None Given]
  • Question 4

    4 out of 4 points

    Correct

    Scenario 3: Rheumatoid Arthritis

    A 48-year-old woman presents with a five-month history of generalized joint pain, stiffness, and swelling, especially in her hands. She states that these symptoms have made it difficult to grasp objects and has made caring for her grandchildren problematic. She admits to increased fatigue, but she thought it was due to her stressful job.

    FH: Grandmothers had “crippling” arthritis.

    PE: remarkable for bilateral ulnar deviation of her hands as well as soft, boggy proximal interphalangeal joints. The metatarsals of both of her feet also exhibited swelling and warmth.

    Diagnosis: rheumatoid arthritis.

    Question:

    The pt. had various symptoms, explain how these factors are associated with RA and what is the difference between RA and OA? 

    Selected Answer:

    The  symptoms of this patient are associated with rheumatoid  arthitis,because stiffness, swelling especially in the hands, RA  usually attacks the bones of the small joints in the hands and feets,  and she also present with stiffness,as well as boggy proximal interphalageal  The   main cause between  Osteo arthritis and  rheumatoid arthritis is the  caused . Rheuatoid arthritis is an autoimmune disease  and Osteo arthritis is caused by mechanical osteoarthritis is caused by wear and tear on the joints

    Correct Answer:

    Correct 

    Rheumatoid arthritis is an inflammatory, systemic disease that is autoimmune in nature. Symptoms are mediated by antibodies against self-antigens and inflammatory cytokines, especially CD4+ T cells that promote inflammation. Multiple inflammatory cells are involved, and TNF and Interleukin-1 stimulate the synovial cells to secrete protease that damages the hyaline cartilage. The inflammatory cytokines convert the synovium into an abnormally thick layer of granulation tissue called pannus. The pannus acts like a locally invasive tumor. Pannus is the tissue responsible for destruction of the articular cartilage. The other inflammatory mediators affect the soft tissue structures like the tendons, ligaments, and even the valves of the heart, especially the aortic valve. Long standing inflammation causes interstitial fibrosis of the lungs which reduces pulmonary function. Osteoarthritis (OA) is localized destruction of articular cartilage which can either be idiopathic or secondary. Secondary OA is due to a prior injury or infectious process that may affect the normal cartilage. Primary OA is very common in people >65 years of age and there is a strong correlation between obesity and the development of OA. OA in a non-inflammatory disease process

    Response Feedback: [None Given]

Question 5

4 out of 4 points

Correct

Scenario5: Multiple Sclerosis (MS)

A 28-year-old obese, female presents today with complaints for several weeks of vision problems (blurry) and difficulty with concentration and focusing. She is an administrative para-legal for a law firm and notes her symptoms have become worse over the course of the addition of more attorneys and demands for work. Today, she noticed that her symptoms were worse and were accompanied by some fine tremors in her hands. She has been having difficulty concentrating and has difficulty voiding. She went to the optometrist who recommended reading glasses with small prism to correct double vision. She admits to some weakness as well. No other complaints of fevers, chills, URI or UTI

PMH: non-contributory

PE: CN-IV palsy. The fundoscopic exam reveals edema of right optic nerve causing optic neuritis. Positive nystagmus on positional maneuvers. There are left visual field deficits. There was short term memory loss with listing of familiar objects.

DIAGNOSIS: multiple sclerosis (MS).

Question:

Describe what is MS and how did it cause the above patient’s symptoms?

Selected Answer:

Multiple sclerosis is a chronic inflammatory autoimmune disease that affect the brain, the nerves fibers in the central nervous system,causing degeneration and sclerosis, loss of axons, causing damage  and may cause symptoms such as numbness,  pain, problems with vision, arm and leg movement, It can  cause permant disablity. More common in woman than man. The loss of myelin  inhered the nerve conduction leading  to symptoms presention of the symptoms

Correct Answer:

Correct

MS is a chronic inflammatory disease involving degeneration of CNS myelin, scarring (or sclerosis or plaque formation) and loss of axons. It is caused by an autoimmune response to self or microbial antigens in genetically susceptible people. The usual age of onset is between 20 and 40 years of age and is more common in women. When reviewing the demyelinating lesions in the spinal cord and brain of patients with MS shows myelin loss, destruction of oligodendrocytes, and reactive astrogliosis, often with relative sparing of the axon cylinder. In some MS patients, however, the axon is also aggressively destroyed. One of the earliest steps in lesion formation is the breakdown of the blood-brain barrier. Enhanced expression of adhesion molecules on the surface of lymphocytes and macrophages seems to underlie the ability of these inflammatory cells to penetrate the blood-brain barrier. The elevated immunoglobulin G (IgG) level in the cerebrospinal fluid, which can be shown by an oligoclonal band pattern on electrophoresis, suggests an important humoral (i.e., B-cell activation) component to. Variable degrees of antibody-producing plasma cell infiltration have been demonstrated in MS lesions. The patient’s symptoms are directly related to the inflammation and demyelination of the nerve sheath. The short- term memory loss indicates that there may be demyelinating lesions in the brain as well.

Response Feedback: [None Given]
  • Question 16

Needs Grading

A 22-year-old male is in the Surgical Intensive Care Unit (SICU) following a motor vehicle crash (MVC) where he sustained multiple life-threatening injuries including a torn aorta, ruptured spleen, and bilateral femur fractures. He has had difficulty maintaining his mean arterial pressure (MAP) and has required various vasopressors. He has a triple lumen central venous catheter (CVC) for monitoring his central venous pressure, administration of medications and blood products, as well as total parenteral nutrition. Per hospital protocol, he is receiving an unfractionated heparin 1:1000 flush after administration of each of the triple antibiotics that have been ordered to maintain patency of the lumens.  Seven days post injury, the APRN in the SICU is reviewing the patient’s morning labs and notes that his platelet count has dropped precipitously to 50,000 /mm3 from 148,000/mm3 two days ago. The APRN suspects the patient is developing heparin induced thrombocytopenia (HIT).

 

Question 1 of 2:

 

What is underlying pathophysiology of heparin induced thrombocytopenia? 

Selected Answer: Antibodies which bind to platelet factor 4 (PF4), and heparin complexes promote the development of HIT since they activate platelets and trigger a prothrombotic state. However, HIT occurs commonly with unfractionated heparin (UFH) as compared to low molecular weight heparin (LMWH). It is often an adverse drug reaction mediated by IgG antibodies against heparinplatelet factor 4 complexes leading to the activation of platelets. This increases the consumption of platelets and reduces the platelets counts within 5-10 days after unfractionated heparin. Has been administered.
Correct Answer: Heparin-induced thrombocytopenia (HIT) is caused by antibodies that bind to complexes of heparin and platelet factor 4 (PF4), activating the platelets and promoting a prothrombotic state. HIT is more frequently encountered with unfractionated heparin (UFH) than with low molecular weight heparin (LMWH). It is an immune mediated adverse drug reaction caused by IgG antibodies against the heparinplatelet factor 4 complex leading to platelet activation through platelet FcyIIa receptors. The release of additional platelet factor 4 from activated platelets and activation of thrombin lead to increased platelet consumption and a decrease in platelet counts beginning 5-10 days after administration of unfractionated heparin.
Response Feedback: [None Given]
  • Question 17

Needs Grading

A 22-year-old male is in the Surgical Intensive Care Unit (SICU) following a motor vehicle crash (MVC) where he sustained multiple life-threatening injuries including a torn aorta, ruptured spleen, and bilateral femur fractures. He has had difficulty maintaining his mean arterial pressure (MAP) and has required various vasopressors. He has a triple lumen central venous catheter (CVC) for monitoring his central venous pressure, administration of medications and blood products, as well as total parenteral nutrition. Per hospital protocol, he is receiving an unfractionated heparin 1:1000 flush after administration of each of the triple antibiotics that have been ordered to maintain patency of the lumens.  Seven days post injury, the APRN in the SICU is reviewing the patient’s morning labs and notes that his platelet count has dropped precipitously to 50,000 /mm3 from 148,000/mm3 two days ago. The APRN suspects the patient is developing heparin induced thrombocytopenia (HIT).

Question 2 of 2:

 

The APRN assesses the patient and notes there is a decreased right posterior tibial pulse with cyanosis of the entire foot. The APRN recognizes this probably represents arterial thrombus formation. How does someone who is receiving heparin develop arterial and venous thrombosis? 

Selected Answer:  

After platelets are activated, procoagulant platelet microparticles are released, and thrombocytopenia occurs. This is followed by the production of thrombin, and activation of inflammatory cells, and injury to the endothelium which produce the arterial and venous thrombus features observed in HIT. The ris of HIT increases with continued use of thrombophylaxis post-operatively. However, it can also develop even with minor exposure to heparin through intravascular flushes especially when trying to maintain patency of an indwelling venous catheter. The platelets usually collect in the micro-circulation to form an emboli or thrombus. In large arteries of lower and upper extremities, the formation of arterial emboli can lead to necrosis if not promptly identified.

Correct Answer: Platelet activation results in the release of procoagulant platelet microparticles, platelet consumption, and thrombocytopenia. Marked generation of thrombin, activation of monocytes and other inflammatory cells, and endothelial injury and activation follow, producing the characteristic venous and arterial thromboses of HIT. The risk of HIT is highest with prolonged use of heparin for postoperative thrombophylaxis. However, case studies have also demonstrated the possibility of developing HIT with minimal heparin exposure via intravascular flushes to maintain the patency of indwelling arterial or venous catheters.

The platelets aggregate in the microcirculation, leaving to systemic thrombocytopenia but the platelets clump together and form thrombi and emboli. Arterial emboli usually form in the larger arteries of the upper and lower extremities and if not identified quickly, limb necrosis occurs. Treatment is not warfarin which could lead to skin necrosis but rather withdrawal of the heparin and the use of thrombin inhibitors such as argatroban.

Response Feedback: [None Given]

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Sample Answer 3 for NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

Alzheimer’s is one of the most common progressive neurological disorders among the elderly caused by dementia. Patients will present with mild to moderate cognitive signs and symptoms at the onset of the disorder, which will progress to severe memory loss with time, as they grow much older (Li et al., 2019). However, several treatment options have been proven to be effective in the management of Alzheimer’s disorder among the elderly. The purpose of this discussion is to illustrate the decision process in selecting the most effective drug, based on pharmacokinetic and pharmacodynamic factors, for treating an elderly patient diagnosed with Alzheimer’s disease.

Patient Case Study Summary

The assigned case study demonstrates a 76-year-old Iranian male with symptoms of Alzheimer’s disorder. The patient displays strange behavior upon arrival at the clinic reporting symptoms of memory loss, forgetfulness, confusion, and diminished interest in religious activities for the last 2 years. Pharmacokinetic and pharmacodynamic patient factors which contributed to the selection of drugs for this patient include his advanced age, male gender, Iranian race, and presenting symptoms in addition to the mini-mental exam results of moderate dementia. the patient’s diagnosis of Alzheimer’s disorder will also be considered.

Treatment Decisions

Based on the patient history and the pharmacokinetic and pharmacodynamic factors mentioned above, the most appropriate intervention is to initiate Exelon 1.5mg twice daily. Exelon (rivastigmine) is an FFDA-approved drug for treating mild to moderate Alzheimer’s disease (Fish et al., 2019). Previous studies support great effectiveness, and safety profile for use of the drug among the elderly diagnosed with Alzheimer’s (Khoury et al., 2018). The second decision was to increase the dose of Exelon to 4.5 mg twice daily as recommended by most clinical practice guidelines for patients who have displayed great tolerance but with minimal effectiveness. The last decision was to increase the dose further to 6mg twice daily, to promote optimal effectiveness as the patient still displayed limited remission of symptoms with the previous intervention.

Expected Outcome

Studies show that Exelon when administered appropriately takes between 8 to 12 weeks to completely manage symptoms of Alzheimer’s among elderly patients. As such, with the initial intervention of 1.5mg Exelon twice daily, the patient was expected to display approximately 50% remission of symptoms (Nguyen et al., 2021). The dose was however to be titrated to obtain the optimum outcome, not exceeding 6mg twice daily. The same results were expected with the second and third interventions with no side effects expected.

Difference Between Expected Outcome and Actual Outcome

Just like expected, the patient displayed a minimal reduction of symptoms of Alzheimer’s with no side effects reported with the first intervention. After the dose was increased in the second intervention, the patient reported further remission of symptoms, but at a slow rate, hence increasing the dose in the last intervention, which led to optimal remission of Alzheimer’s symptoms just as expected (Huang et al., 2020).

Conclusion

Alzheimer’s is a common disorder among the elderly compromising their quality of life and well-being. For the patient in the provided case study, it was necessary to administer Exelon at a starting dose of 1.5 mg which was titrated to 4.5mg then 6.5mg twice daily. The patient displayed great effectiveness with this medication in the management of his Alzheimer’s symptoms, with no side effects reported.

 

References

Fish, P. V., Steadman, D., Bayle, E. D., & Whiting, P. (2019). New approaches for the treatment of Alzheimer’s disease. Bioorganic & medicinal chemistry letters29(2), 125-133. https://doi.org/10.1016/j.bmcl.2018.11.034

Huang, L. K., Chao, S. P., & Hu, C. J. (2020). Clinical trials of new drugs for Alzheimer’s disease. Journal of biomedical science27(1), 1-13. https://doi.org/10.1186/s12929-019-0609-7

Khoury, R., Rajamanickam, J., & Grossberg, G. T. (2018). An update on the safety of current therapies for Alzheimer’s disease: focus on rivastigmine. Therapeutic Advances in Drug Safety9(3), 171-178. https://doi.org/10.1177/2042098617750555

Li, D. D., Zhang, Y. H., Zhang, W., & Zhao, P. (2019). Meta-analysis of randomized controlled trials on the efficacy and safety of donepezil, galantamine, rivastigmine, and memantine for the treatment of Alzheimer’s disease. Frontiers in neuroscience13, 472. https://doi.org/10.3389/fnins.2019.00472

Nguyen, K., Hoffman, H., Chakkamparambil, B., & Grossberg, G. T. (2021). Evaluation of rivastigmine in Alzheimer’s disease. Neurodegenerative Disease Management11(1), 35-48. https://doi.org/10.2217/nmt-2020-0052

Sample Answer 4 for NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

Question 1

Scenario 1: Gout

A 68-year-old obese male presents to the clinic with a 3-day history of fever with chills, and Lt. great toe pain that has gotten progressively worse. Patient states this is the first time that this has happened, and nothing has made it better and walking on his right foot makes it worse. He has tried acetaminophen, but it did not help. He took several ibuprofen tablets last night which did give him a bit of relief.

HPI: hypertension treated with Lisinopril/HCTZ .

SH: Denies smoking. Drinking: “a fair amount of red wine” every week. General appearance: Ill appearing male who sits with his right foot elevated.

PE:  remarkable for a temp of 100.2, pulse 106, respirations 20 and BP 158/92. Right great toe (first metatarsal phalangeal [MTP]) noticeably swollen and red. Unable to palpate to assess range of motion due to extreme pain. CBC and Complete metabolic profile revealed WBC 15,000 mm3 and uric acid 9.0 mg/dl.

Diagnoses the patient with acute gout.

Question:

Explain the pathophysiology of gout.

 

Your Answer:

Gout is caused by disorders of purine metabolism, increased uric acid production, and reduced uric acid excretion, causing increased serum uric acid (sUA) levels. This forms monosodium urate (MSU) crystals deposited in the joints, kidneys, and other tissues. Gout occurs following the precipitation of monosodium urate crystals in a joint space (Clebak et al., 2020). The deposition of the urate crystals elicits activation of the immune system, causing the release of various inflammatory cytokines and the recruitment of neutrophils. Over time, the joint space becomes irreversibly damaged, causing chronic pain and disability with grossly deformed joints. Tophi may also form at the joint space. These are subcutaneous nodules containing monosodium urate crystals in a matrix of lipids, proteins, and mucopolysaccharides (Clebak et al., 2020). The first metatarsophalangeal joint is mostly affected.

 

Reference

Clebak, K. T., Morrison, A., & Croad, J. R. (2020). Gout: Rapid evidence review. American family physician102(9), 533-538.