KNOWLEDGE CHECK NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS NURS 6501

KNOWLEDGE CHECK NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS NURS 6501

KNOWLEDGE CHECK NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS NURS 6501

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 (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by inflammation, demyelination, and subsequent damage to the myelin sheath that surrounds nerve fibers. This disrupts the normal transmission of nerve impulses, leading to a wide range of neurological symptoms.

In the case of the 28-year-old female patient, her presenting symptoms align with the characteristic manifestations of MS. The complaints of blurry vision, double vision (corrected with prism glasses), and optic neuritis (indicated by edema of the optic nerve) indicate involvement of the optic nerves. Optic neuritis often presents as acute loss of vision, pain with eye movements, and visual field deficits, as observed in this patient.

The difficulty with concentration, focusing, and cognitive impairment can be attributed to the impact of MS on the CNS. In MS, inflammation and demyelination can occur in various regions of the brain, including those responsible for attention, concentration, and memory. These inflammatory processes disrupt the efficient transmission of nerve signals, leading to cognitive difficulties.

The presence of fine tremors in the hands suggests involvement of the motor pathways. MS can cause damage to the nerves responsible for controlling muscle movements, resulting in tremors or unsteady hand movements. This can affect fine motor skills and coordination.

The patient’s difficulty with voiding can be attributed to MS affecting the nerves that control bladder function. MS-related damage to these nerves can lead to urinary symptoms such as urgency, frequency, hesitancy, or even difficulty completely emptying the bladder.

MS is a chronic and unpredictable disease, with symptoms varying widely between individuals and over time. Relapses and remissions are common, where symptoms worsen during acute inflammatory episodes and may partially or completely resolve during periods of remission.

The exact cause of MS remains unknown, but it is believed to involve a combination of genetic and environmental factors that trigger an autoimmune response against the myelin sheath. The resulting inflammation and demyelination lead to the characteristic neurological symptoms experienced by patients with MS.

Managing MS involves a multidisciplinary approach, including medication to modify the course of the disease, symptom management, rehabilitation, and lifestyle modifications. Regular monitoring and follow-up with healthcare providers are essential to tailor treatment plans to individual needs and optimize quality of life.

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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]

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 enmes 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