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

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 letters, 29(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 science, 27(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 Safety, 9(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 neuroscience, 13, 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 Management, 11(1), 35-48. https://doi.org/10.2217/nmt-2020-0052

Sample Answer 2 for NURS 6501 Knowledge Check: Neurological And Musculoskeletal Disorders

Question 1

4 out of 4 points

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

NURS 6501 Knowledge Check Neurological And Musculoskeletal Disorders

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:

A gout is a complex form of arthritis, that is having swollen and painful joints due to the accumulation of urate crystals in the joints. in other words, Gout is an inflammatory response to too much uric acid in the bloodstream causing hyperuricemia.

Pathophysiology; Urate crystals are formed when the body breaks down purines a naturally occurring substance in the body and found in red meat and mostly raised when high fructose sugar is ingested having hypertension and being obese. Formation of uric acid occurs and this substance is excreted by the kidney, in this case, the kidney may have failed to eliminate the uric acid and what happens next is that the uric acid dissolves in blood and is transported in the body. When this acid reaches the joints, it forms sharp urate crystals in the joint tissues. this causes pain, swelling, and inflammation of the joint hence the symptoms that are brought in by the patient.

Gout depends on metabolic processes. Purines must first be available and then breaking down leads to the formation of way too much uric acid that the kidneys. Kidneys are then overwhelmed in excreting, and, therefore, leading to retention in the blood that leads to urate crystals forming.

in summary: 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 levels.

Correct Answer:

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:

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Question 2

4 out of 4 points

Scenario 1: Gout

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.

Diagnoses the patient with acute gout.

Question:

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

Selected Answer:

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.

Correct Answer:

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Question 3

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4 out of 4 points

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:

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 such as hyperparathyroidism, hyperthyroidism, diabetes mellitus, also certain medications like 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 the bone to be 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 allow the osteoblasts to form new bone.

Osteoclasts are responsible for the 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 contribute 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.

Correct Answer:

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.

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Question 4

4 out of 4 points

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:

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 the 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 is a non-inflammatory disease process

Correct Answer:

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

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Question 5

4 out of 4 points

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:

MS is a chronic inflammatory disease involving degeneration of CNS myelin, scarring sclerosis, 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. 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.

Correct Answer:

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.

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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.
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Question 17

Needs Grading

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.

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

Alzheimer’s is one of the most common types of dementia among the elderly. It is a progressive disorder that starts presenting with mild memory loss (Shah, & Bennett, 2020). This disorder affects parts of the brain which control an individual’s thoughts, memory, and language. It can seriously impair the patient’s ability to conduct routine daily activities.

Summarize the Patient Case Study

The patient in the case study provided is 76 years old who was presented to the clinic by his eldest son as a result of strange behaviors. He started displaying symptoms of Alzheimer’s about two years ago. He lost interest in religious activities and started getting confused and forgetful. When Mini-Mental State Exam was administered, his score suggested moderate dementia.

Treatment Decisions

The first decision was to start Exelon (rivastigmine) 1.5 mg orally twice a day, which was to be increased to 3mg twice a day in two weeks. Based on the treatment outcome, the dose of Exelon was increased to 4.5 mg orally twice a day after 4 weeks. The last decision was to increase the dose further to 6 mg twice a day and observe the clinical outcome for the next four weeks. Rivastigmine is a cholinesterase inhibitor approved by the FDA as the first-line medication for managing symptoms of Alzheimer’s disease (Morant, Vestergaard, Lassen, & Navikas, 2020). Studies show that the recommended starting dose of Exelon is 1.5mg, to assess the patient’s tolerance, after which the dose can be increased to 3mg in two weeks. The dosage can however be increased to 4.5 mg then 6 mg depending on the patient’s tolerance and treatment outcome.

Expected Outcome

With the first decision, the patient was expected to display more than 50% remission of Alzheimer’s symptoms (Grossberg, Tong, Burke, & Tariot, 2019). Increasing the dosage in the second intervention was even expected to display further management of symptoms, as the last decision was expected for the patient’s symptoms to be completely managed.

Difference Between Expected and Actual Outcome

The first treatment outcome was quite different from what was expected as the patient’s symptoms did not improve. The second and last outcomes were exactly as expected as the patient displayed no side effects with well-controlled symptoms (Atri, 2019).

References

Morant, A. V., Vestergaard, H. T., Lassen, A. B., & Navikas, V. (2020). US, EU, and Japanese regulatory guidelines for development of drugs for treatment of Alzheimer’s disease: Implications for global drug development. Clinical and Translational Science, 13(4), 652-664. https://doi.org/10.1111/cts.12755

Grossberg, G. T., Tong, G., Burke, A. D., & Tariot, P. N. (2019). Present algorithms and future treatments for Alzheimer’s disease. Journal of Alzheimer’s Disease, 67(4), 1157-1171. DOI: 10.3233/JAD-180903

Atri, A. (2019). The Alzheimer’s disease clinical spectrum: Diagnosis and management. Medical Clinics, 103(2), 263-293. DOI: 10.1016/j.mcna.2018.10.009.

Shah, R. C., & Bennett, D. A. (2020). Physicians and Alzheimer dementia: past, present, and future. Annals of internal medicine, 172(10), 695-696. https://doi.org/10.7326/M20-1500