Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501

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

 

This guide will demonstrate how to complete the Walden University Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501 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 Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501                     

 

Whether one passes or fails an academic assignment such as the Walden University Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501 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 Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501                     

The introduction for the Walden University Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501 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 Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501                     

 

After the introduction, move into the main part of the Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501 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 Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501                     

 

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 Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501                     

 

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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Knowledge Check: Neurological And Musculoskeletal Disorders NURS 6501

KNOWLEDGE CHECK: NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS NURS 6501

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. 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

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	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

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 1 Scenario 1: Syndrome of Antidiuretic Hormone (SIADH) A 77-year-old female was brought to the clinic by her daughter who stated that her mother had become slightly confused over the past several days. She had been stumbling at home and had fallen twice but was able to walk with some difficulty. She had no other obvious problems and had been eating and drinking. The daughter became concerned when she forgot her daughter’s name, so she thought she better bring her to the clinic. HPI: Type II diabetes mellitus (DM) with peripheral neuropathy x 30 years. Emphysema. Situational depression after death of spouse 6-months ago SHFH: – non contributary except for 40 pack/year history tobacco use. Meds: Metformin 1000 mg po BID, ASA 81 mg po qam, escitalopram (Lexapro) 5 mg po q am started 2 months ago Labs-CBC WNL; Chem 7- Glucose-102 mg/dl, BUN 16 mg/dl, Creatinine 1.1 mg/dl, Na+116 mmol/L, K+4.2 mmol/L, CO237 m mol/L, Cl–97 mmol/L. The APRN refers the patient to the ED and called endocrinology for a consult for diagnosis and management of syndrome of inappropriate antidiuretic hormone (SIADH). Question: Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH      SIADH is characterized by less than maximally dilute urine with serum hypo-osmolality in patients with normal thyroid, adrenal, renal, hepatic, and cardiac function and who do not have volume depletion, hypotension, or other physiologic causes affecting ADH secretion. Low plasma osmolality impedes ADH secretion, causing the kidneys to produce dilute urine (Mentrasti et al., 2020). Inappropriate vasopressin secretion is associated with central nervous system disorders, pulmonary disorders, and certain malignancies. Some drugs also trigger ADH secretion, particularly analgesics (opioids and NSAIDs), antiseizure drugs (carbamazepine), hypoglycemic (metformin) Prostaglandin synthetase inhibitors, antidepressants (SSRIs and venlafaxine), antipsychotics, and cytotoxics (Mentrasti et al., 2020). Therefore, patient factors contributing to SIADH are emphysema (pulmonary disorder) and medications like escitalopram (SSRI), aspirin, and Metformin. QUESTION 2 Scenario 2: Type 1 Diabetes A 14-year-old girl is brought to the pediatrician’s office by his parents who are concerned about their daughter’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with her school activities. She had been seemingly healthy until about 4 months ago when her parents started noticing these symptoms. She admits to sleeping more and gets tired very easily. PMH: noncontributory. Allergies-NKDA FH:- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process SH: denies alcohol, tobacco or illicit drug use. Not sexually active. Labs: random glucose 244 mg/dl. DIAGNOSIS: Diabetes Mellitus type 1 and refers to an endocrinologist for further work up and management plan. Question Explain the pathophysiology of the three P’s for (polyuria, polydipsia, polyphagia)” with the given diagnosis of Type I DM. Insulin deficiency in the body results in blood glucose build-up and, eventually, hyperglycemia. Hyperglycemia causes an imbalance in fluid and electrolytes that contribute to the classic features of diabetes: polyuria, polydipsia, and polyphagia. Increased glucose levels in the urine create an osmotic dieresis that results in increased and excessive urination (polyuria) (DiMeglio et al., 2018). The osmotic dieresis contributes to the excretion of electrolytes, particularly potassium, sodium, and chloride, through the urine, causing severe water loss and eventually dehydration that results in acute thirst (polydipsia) (DiMeglio et al., 2018). Lack of glucose in body cells causes them to starve, which causes increased hunger (polyphagia) even when one consumes large amounts of food since there is deficient insulin to facilitate the movement of glucose into body cells. QUESTION 3 Scenario 2: Type 1 Diabetes A 14-year-old girl is brought to the pediatrician’s office by his parents who are concerned about their daughter’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with her school activities. She had been seemingly healthy until about 4 months ago when her parents started noticing these symptoms. She admits to sleeping more and gets tired very easily. PMH: noncontributory. Allergies-NKDA FH:- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process SH: denies alcohol, tobacco or illicit drug use. Not sexually active. Labs: random glucose 244 mg/dl. DIAGNOSIS: Diabetes Mellitus type 1 and refers to an endocrinologist for further work up and management plan. Question Explain the genetics relationship and how this and the environment can contribute to Type I DM. The overall risk of developing Type 1 diabetes (T1DM) is higher in individuals with close relatives having the disease. Redondo et al. (2018) explain that siblings of diabetic patients have an average of 6-7% lifetime risk. Besides, the offspring of a female patient with T1DM have a 1.3-4% risk, while that of a male patient is 6-9%. Genetic factors directly involved in controlling beta cell function and immune response are attributed to the development of T1DM. In addition, some environmental factors damage the beta cells, including cytotoxins, toxic chemicals, and viruses like enterovirus, mumps, and rubella (Redondo et al., 2018). Therefore, the client’s family history of diabetes and environmental factors could have contributed to T1DM. QUESTION 4 Scenario 3: Type II DM A 55-year-old male presents with complaints of polyuria, polydipsia, polyphagia, and weight loss. He also noted that his feet on the bottom are feeling “strange” “like ants crawling on them” and noted his vision is blurry sometimes. He has increased an increased appetite, but still losing weight. He also complains of “swelling” and enlargement of his abdomen. PMH: HTN – well controlled with medications. He has mixed hyperlipidemia, and central abdominal obesity. Physical exam unremarkable except for decreased filament test both feet. Random glucose in office 333 mg/dl. Diagnosis: Type II DM and prescribes oral medication to control the glucose level and also referred the patient to a dietician for dietary teaching. Question: How would you describe the pathophysiology of Type II DM?   Type 2 diabetes mellitus (T2DM) occurs due to the resistance of body cells to insulin. It is caused by inadequate insulin secretion when a person develops insulin resistance, primarily due to obesity. Hepatic insulin resistance causes an inability to curb hepatic glucose production (Banday et al., 2020). Besides, peripheral insulin resistance hinders peripheral glucose uptake. The combination results in fasting and postprandial hyperglycemia. Hyperglycemia impairs insulin secretion in persons with T2DM since elevated glucose levels desensitize beta cells, causing beta-cell dysfunction. As a result, insulin secretion reduces later in the disease, worsening hyperglycemia. QUESTION 5 Scenario 4: Hypothyroidism A patient walked into your clinic today with the following complaints: Weight gain (15 pounds), however has a decreased appetite with extreme fatigue,  cold intolerance, dry skin, hair loss, and falls asleep watching television. The patient also tearfulness with depression, and with an unknown cause and has noted she is more forgetful.  She does have blurry vision. PMH: Non-contributory. Vitals: Temp 96.4˚F, pulse 58 and regular, BP 106/92, 12 respirations. Dull facial expression with coarse facial features. Periorbital puffiness noted. Diagnosis: hypothyroidism. Question: What causes hypothyroidism? Hypothyroidism is characterized by thyroid hormone deficiency. It occurs when thyroid cells fail to produce adequate amounts of thyroid hormone. This is usually due to abnormal functioning of thyroid cells, destruction of thyroid cells, or limited dietary intake of iodine and tyrosine, which play a major role in the synthesis of thyroid hormones (Chiovato et al., 2019). The consumption of lithium can also cause hypothyroidism since it hinders the release of thyroid hormone by the thyroid. It can also occur in persons taking medications, including amiodarone, iodine-containing drugs, interferon-alfa, and tyrosine kinase inhibitors for cancer. References Banday, M. Z., Sameer, A. S., & Nissar, S. (2020). Pathophysiology of diabetes: An overview. Avicenna Journal of Medicine, 10(4), 174–188. https://doi.org/10.4103/ajm.ajm_53_20 Chiovato, L., Magri, F., & Carlé, A. (2019). Hypothyroidism in Context: Where We’ve Been and Where We’re Going. Advances in Therapy, 36(Suppl 2), 47–58. https://doi.org/10.1007/s12325-019-01080-8 DiMeglio, L. A., Evans-Molina, C., & Oram, R. A. (2018). Type 1 diabetes. Lancet (London, England), 391(10138), 2449–2462. https://doi.org/10.1016/S0140-6736(18)31320-5 Mentrasti, G., Scortichini, L., Torniai, M., Giampieri, R., Morgese, F., Rinaldi, S., & Berardi, R. (2020). Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): Optimal Management. Therapeutics and Clinical Risk Management, 16, 663–672. https://doi.org/10.2147/TCRM.S206066 Redondo, M. J., Steck, A. K., & Pugliese, A. (2018). Genetics of type 1 diabetes. Pediatric Diabetes, 19(3), 346–353. https://doi.org/10.1111/pedi.12597

NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS

this exercise, you will complete a 5-essay type question Knowledge Check to gauge your understanding of this module’s content.  

Possible topics covered in this Knowledge Check include:

• Stroke
• Multiple sclerosis
• Transient Ischemic Attack
• Myasthenia gravis
• Headache
• Seizure disorders
• Head injury
• Spinal cord injury
• Inflammatory diseases of the musculoskeletal system
• Osteoporosis
• Osteopenia
• Bursitis
• Tendinitis
• Gout
• Lyme Disease
• Spondylosis
• Fractures
• Parkinson’s
• Alzheimer’s

Three basic bone-formations:

• Osteoblasts
• Osteocytes
• Osteoclasts

RESOURCES

Be sure to review the Learning Resources before completing this activity.
Click the weekly resources link to access the resources. 

WEEKLY RESOURCES

BY DAY 7 OF WEEK 7

Complete the Knowledge Check by Day 7 of Week 7.

Attempt History

	Attempt	Time	Score
LATEST	Attempt 1	5,980 minutes	20 out of 20

Score for this quiz: 20 out of 20

Submitted Jan 15 at 8:56am

This attempt took 5,980 minutes.

Question 1

4 / 4 pts

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 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.

Question 2

4 / 4 pts

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.

Your Answer:

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.

Question 3

4 / 4 pts

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? 

Your Answer:

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.

Question 4

4 / 4 pts

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? 

Your Answer:

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. 

Question 5

4 / 4 pts

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?

Your Answer:

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.

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 hepariis 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