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NURS 6501 Knowledge Check: Neurological And Musculoskeletal Disorders

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
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.

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  • NURS 6501 Knowledge Check: Neurological And Musculoskeletal DisordersQuestion 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.

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  • Question 3

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NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders
NURS 6501 Knowledge Check: Neurological and Musculoskeletal Disorders

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.

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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

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

Question 2 of 2:

 

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

Selected Answer:  

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

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

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

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