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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NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

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.
	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: [None Given]

Question 2

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. 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: 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

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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: 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 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. Response Feedback: [None Given]

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 Response Feedback: [None Given]

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. Response Feedback: [None Given]

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

Your Answer:

Patients with gout are highly likely to develop renal calculi and renal failure. Normally, kidneys excrete excess fluids and wastes from the body. The kidneys also excrete excess urates from the body, which is dissolved in the blood. Optimum renal function is essential for the elimination of excess urates from the body. Patients suffering from gout have hyperuricemia. The main mechanisms in which urates are regulated are through the kidneys and gout (Estiverne & Mount, 2020).

            The buildup of urates in the body may affect the kidneys. Accordingly, the buildup of urates with reduced excretion through the kidneys results in the formation of urate crystals. The kidneys rare excrete large urate particles with urine, which results in the formation or kidney stones. Over time, the progressive kidney stones cause damage to the kidneys resulting in kidney disease and failure if responsive treatments for gout are not adopted (Wu et al., 2022).

            The kidneys excrete the excess urates in the form or uric acid in the kidneys. Conditions such as gout result in elevated levels of uric acid that is be excreted through the kidneys. The filtration of blood in the kidneys coupled with the high levels of uric acid cause urate crystals formation, which cause renal stones and obstruction as urine is excreted (He et al., 2022). These mechanisms result in the development of renal complications such as stones and kidney disease and failure.

References

Estiverne, C., & Mount, D. B. (2020). The Management of Gout in Renal Disease. Seminars in Nephrology, 40(6), 600–613. https://doi.org/10.1016/j.semnephrol.2020.12.007

He, Y., Xue, X., Terkeltaub, R., Dalbeth, N., Merriman, T. R., Mount, D. B., Feng, Z., Li, X., Cui, L., Liu, Z., Xu, Y., Chen, Y., Li, H., Ji, A., Ji, X., Wang, X., Lu, J., & Li, C. (2022). Association of acidic urine pH with impaired renal function in primary gout patients: A Chinese population-based cross-sectional study. Arthritis Research & Therapy, 24(1), 32. https://doi.org/10.1186/s13075-022-02725-w

Wu, B., Chen, L., Xu, Y., Duan, Q., Zheng, Z., Zheng, Z., & He, D. (2022). The Effect of Allopurinol on Renal Outcomes in Patients with Diabetic Kidney Disease: A Systematic Review and Meta-Analysis. Kidney and Blood Pressure Research, 47(5), 291–299. https://doi.org/10.1159/000522248

Discuss what is osteoporosis and how does it develop pathologically? 

Your Answer:

Osteoporosis is a musculoskeletal disorder characterized by low bone mass and density and increase fragility of the skeleton. The affected patients have impaired quality of bones, propensity to fracture, and reduced bone mass. The rate of bone resorption in these patients is higher than bone formation, which leads to bone degeneration (Rosen, 2020). Osteoporosis has high prevalence in women as compared to males.

            Several pathological processes contribute to osteoporosis. One of them is an increase in the level of osteoclastogenesis and osteoclasts. Osteoclasts are bone cells that are involved in bone loss. Patients with osteoporosis have an elevated number of osteoclasts that stimulate osteoclastogenesis. Ineffective bone repair and microdamage accumulation, which cause bone structural deterioration characterize osteoclastogenesis. The other pathogenesis contributing to osteoporosis is lack of estrogen. Decrease in estrogen levels as seen in postmenopausal increases the release of proinflammatory cytokines that signal the RANKL signaling pathways involved in bone resorption(Al Saedi et al., 2020). There is also the enhanced formation of osteoclasts, which accelerate bone resorption.

            Osteoporosis also develops from reduced osteoblastogenesis and bone formation. Patients with osteoporosis have decreased number of osteoblasts, which are essential in bone formation. Reduction in osteoblastogenesis also lowers the maturation of osteoblasts, hence, increased bone loss than formation. Osteocytes also play a role in the development of osteoporosis. Osteocytes are crucial cells that regulate bone remodeling. A reduction of osteocytes and osteoblasts levels is prevalent in osteoporosis, which increase bone resorption rate. Bone formation is also largely dependent on supplementation of essential minerals such as calcium and vitamins, that include vitamin D. Dietary supplementation of these essential minerals and vitamins are crucial for bone health. However, inadequate intake of calcium and vitamin D affects the rate of bone formation. As a result, patients develop bones with low mass and density, leading to the formation of osteoporosis(Al Saedi et al., 2020; Rosen, 2020). Lifestyle factors such as smoking and dietary restriction as seen in athletes predispose patients to developing osteoporosis.

References

Al Saedi, A., Stupka, N., & Duque, G. (2020). Pathogenesis of Osteoporosis. Handbook of Experimental Pharmacology, 262, 353–367. https://doi.org/10.1007/164_2020_358

Rosen, C. J. (2020). The Epidemiology and Pathogenesis of Osteoporosis. In Endotext [Internet]. MDText.com, Inc. https://www.ncbi.nlm.nih.gov/books/NBK279134/

A Sample Answer For the Assignment: NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

Title: NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

The patient in the case study has been diagnosed with rheumatoid arthritis. Rheumatoid arthritis refers to an inflammatory disorder affecting mostly the joints and other regions of the body. The patient in the case study developed the disorder due to risk factors associated with rheumatoid arthritis such as genetics, hormonal imbalances with the advancing age, and diet. The patient reports that her grandmother had crippling arthritis. Genetics increase the risk of rheumatoid arthritis to individuals born to families with a history. The patient may be menopausal due to her age. As a result, she currently experiences estrogen imbalances, which predispose her to developing rheumatoid arthritis (Radu &Bungau, 2021). The additional risk factors that predispose her to the disease include dietary habits, obesity, and gender.

            The patient presents the hospital with a range of symptoms that include generalized joint pain, swelling, and stiffness. She also reports difficulty in grasping things and fatigue. These symptoms are attributable to the proinflammatory processes that affect different body joints making it difficult to move and engage in activities(Scherer et al., 2020). The inflammation also causes damage to the joints, lowering individual’s functioning abilities.

Rheumatoid arthritis differs from osteoarthritis. Rheumatoid arthritis is an autoimmune disease affecting the joints and other organs while osteoarthritis is a degenerative disease of the bones and joints. Rheumatoid arthritis has an early stage of development and rapid progression while osteoarthritis develops at the later stages of life with slow profession. Rheumatoid arthritis also affects joints of the writs, hands, and feet while osteoarthritis may affect any body joint and often seen at finger tips (Radu &Bungau, 2021; Scherer et al., 2020). Osteoarthritis also has asymmetrical pattern of affecting the joints while rheumatoid arthritis demonstrates a symmetrical pattern in affecting the joints.

References

Radu, A.-F., &Bungau, S. G. (2021). Management of Rheumatoid Arthritis: An Overview. Cells, 10(11), Article 11. https://doi.org/10.3390/cells10112857

Scherer, H. U., Häupl, T., & Burmester, G. R. (2020). The etiology of rheumatoid arthritis. Journal of Autoimmunity, 110, 102400. https://doi.org/10.1016/j.jaut.2019.102400

An APRN working in an anticoagulation clinic has been asked by the local college to present a lecture on platelets and their role in blood clotting to the graduate pathophysiology nursing students.     Question:   What key concepts should the APRN include in the presentation?

Selected Answer: The endothelia cells that line blood vessels control the activation of platelets. When a blood vessel is damaged, the platelets fill endothelial gaps and their adhesion is prompted by endothelial cell loss that expose adhesive glycoproteins. Through receptors that bind to adhesive glycol proteins, the platelets adhere to the sub endothelium then activation begins which results in receptor changes.  There ae changes that occur in the shape of platelets, with the formation of pseudopods and activation of arachidonic pathways. The aggregation of platelets is influenced by thromboxane A2 (TXA2) release which also causes adhesive glycoproteins to bind simultaneously to two different platelets and fibrin, coagulation factors. And thrombin are activated to stabilize the platelet plug which is formed when platelets and RBCs enmesh in fibrin. Clots are formed when heparin is neutralized. Correct Answer: Platelet activation is primarily under the control of the endothelial cells lining the blood vessels. Damage to the vessel causes platelets to fill in the endothelial gaps. Platelet adhesion is initiated by the loss of endothelial cells (or ruptures or erosions of atherosclerotic plaque) which exposes adhesive glycoproteins. Platelets adhere to the subendothelium through receptors that bind to the adhesive glycoproteins. Platelet activation begins after platelet adhesion and undergoes an activation process that leads to changes in receptors, resulting in their ability to bind adhesive proteins. There are changes in the platelet shape, formation of pseudopods and activation of arachidonic pathways. Platelet aggregation is induced by the release of thromboxane A2 (TXA2). Adhesive glycoproteins bind simultaneously on 2 different platelets. Stabilization of the platelet plug (blood clot) occurs by activation of coagulation factors, thrombin, and fibrin. Heparin neutralization factor enhances clot formation. Platelet plug formation occurs when red blood cells and platelets become enmeshed in fibrin. Clot retraction and clot dissolution -clot retraction, using large numbers of platelets, join the edges of the injured vessel. Clot dissolution is regulated by thrombin and plasminogen activators. Response Feedback: [None Given]

 

 

Gout refers to chronic inflammatory arthritis characterized by the deposition of monosodium urate monohydrate crystals in tissues. Gout is relatively common with an estimated global prevalence of 1 to 4% (Dehlin et al., 2020). In the United States, gout affects more than 2 million adults (Dehlin et al., 2020). The incidence of gout increases with age as well as a family history of gout. Additionally, gout is slightly male preponderance with up to 2 to 6 times higher in males than females. The pathophysiology of gout is considered complex and multifactorial.

Factors implicated in the development of gout include alcohol, medications, hypertension, hyperlipidemia, obesity, diabetes mellitus, cardiovascular disease, diet, chronic kidney disease, advanced age, ethnicity, family history, and male gender (Dehlin et al., 2020). Gout is contemplated as a disorder of metabolism resulting in the accumulation of urate and uric acid in blood and tissues. Consequently, tissues become supersaturated leading to the precipitation of urate salts forming monosodium urate crystals. The deposition of these crystals occurs in an array of tissues although the synovium, kidney, bone, ligament, skin, tendon, and cartilage are among the most common sites. Uric acid is less soluble under low temperatures and acidic conditions. Finally, microcrystals may be shed from preexisting tophi initiating an inflammatory response.

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

Individuals with gout have high levels of urate and uric acid in their plasma. Uric acid is a weak organic acid. It exists in a less soluble non-ionized form in acid conditions such as in urine. Physiologically, uric acid production is from purine metabolism in the liver with a slight contribution from the small intestines. Similarly,  the glomerulus filters almost all the urate. As a result, the entire pool of urate is managed by renal excretion in steady-state conditions. Hyperuricemia increases the urate pool which causes supersaturation and precipitation of uric acid and the formation of uric acid calculi.

According to Cicerello (2018),  hyperuricemia,  diminished fractional excretion of uric acid, and constantly low urinary pH levels are common in patients with gout which leads to uric acid nephrolithiasis. For instance, a reduction in pH induces alterations in uric acid dissolution and acid-base status while a reduction in urine output leads to highly concentrated urinary solutes resulting in precipitation (Cicerello, 2018). Finally, individuals with gout may also develop renal calculi due to hyperuricosuria and a decrease in crystallization inhibitors such as urinary glycosaminoglycans.

Discuss what is osteoporosis and how it develops pathologically

Osteoporosis refers to low bone mineral density as a result of altered bone microstructure. Osteoporosis predisposes patients to fragility and low-impact fractures. Globally, osteoporosis affects over 200 million individuals with its incidence increasing with age. Generally, women are more affected. Osteoporosis can be primary or secondary. According to Pouresmaeili et al. (2018), primary osteoporosis is a consequence of aging and a reduction in sex hormones while other disease processes cause secondary osteoporosis.

Osteoporosis develops from an imbalance between bone formation and resorption. An interplay of several factors including genetic, lifestyle, intrinsic and exogenous factors interact to cause an imbalance between bone resorption and formation leading to decreased skeletal mass (Pouresmaeili et al., 2018). For instance, with aging, bone resorption exceeds bone formation. Physiologically, bone mass peaks in the third decade. Consequently, factors that cause osteoporosis result in failure to achieve a normal peak bone mass as well as an acceleration of bone loss.

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

The patient had articular manifestations of rheumatoid arthritis such as polyarthralgia, morning stiffness, swelling of joints, ulnar deviation of her hands, and boggy proximal interphalangeal joints. According to Bullock et al. (2018),  rheumatoid arthritis mostly affects metacarpophalangeal joints and proximal interphalangeal joints but rarely distal interphalangeal joints. Additionally, rheumatoid arthritis is a systemic disorder and hence commonly presents with constitutional symptoms such as fatigue. Rheumatoid arthritis refers to a chronic inflammatory autoimmune disorder that principally affects the joints but also causes extraarticular features (Bullock et al., 2018). On the other, osteoarthritis is a degenerative disease that results from the biochemical breakdown of articular cartilage.  Osteoarthritis typically involves weight-bearing joints such as the hip, knee, and lower back while rheumatoid arthritis can affect any joint although common in hands, wrists, and feet. Similarly, osteoarthritis develops gradually over several years while rheumatoid arthritis develops acutely. 

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

Multiple sclerosis is a chronic autoimmune disease of the central nervous system distinguished by demyelination, inflammation, neuronal loss, and gliosis (Lane & Yadav, 2020). The exact etiology of multiple sclerosis is unknown although environmental, immune, and genetic factors are involved in its pathogenesis. In multiple sclerosis, there is focal inflammation that is injurious to the blood-brain barrier and causes macroscopic plaques (Lane & Yadav, 2020). Similarly, there is microscopic injury as a result of the degeneration of various CNS components such as neurons, axons, and synapses. The aforementioned processes explain the multifocal nature of injury in multiple sclerosis and the neurological symptoms observed in this patient such as blurring of vision, tremors, difficulty concentrating, memory impairment, weakness, and difficulty voiding (Lane & Yadav, 2020). Finally, the course of multiple sclerosis varies considerably and can be remitting, relapsing, or progressive.

References

Bullock, J., Rizvi, S. A. A., Saleh, A. M., Ahmed, S. S., Do, D. P., Ansari, R. A., & Ahmed, J. (2018). Rheumatoid arthritis: A brief overview of the treatment. Medical Principles and Practice: International Journal of the Kuwait University, Health Science Centre, 27(6), 501–507. https://doi.org/10.1159/000493390

Cicerello, E. (2018). Uric acid nephrolithiasis: An update. Urologia, 85(3), 93–98. https://doi.org/10.1177/0391560318766823

Dehlin, M., Jacobsson, L., & Roddy, E. (2020). Global epidemiology of gout: prevalence, incidence, treatment patterns, and risk factors. Nature Reviews. Rheumatology, 16(7), 380–390. https://doi.org/10.1038/s41584-020-0441-1

Lane, M., & Yadav, V. (2020). Multiple Sclerosis. In Textbook of Natural Medicine (pp. 1587-1599.e3). Elsevier. https://doi.org/10.1016/b978-0-323-43044-9.00199-0

Pouresmaeili, F., Kamalidehghan, B., Kamarehei, M., & Goh, Y. M. (2018). A comprehensive overview of osteoporosis and its risk factors. Therapeutics and Clinical Risk Management, 14, 2029–2049. https://doi.org/10.2147/TCRM.S138000