NUR-631 Topic 13 DQ 1 - Assignment Helper

Sample Answer for NUR-631 Topic 13 DQ 1 Included After Question

Answer all of the following questions for your discussion response. Use the format displayed in the “Discussion Forum Sample.”

A 28-year-old woman was admitted to the general internal medicine service with a 3-day history of malaise and cough that progressed to include myalgia, generalized weakness, and dark-colored urine. Three days before admission, she had an abrupt onset of a dry nonproductive cough, malaise, and anorexia that resulted in a prolonged period of fasting. On the second day of the illness, she awoke with diffuse muscle pain and progressive weakness, culminating in an inability to walk. She subsequently noted dark urine and presented to the emergency department, leading to this admission. She had no recent trauma, exercise, rash, joint pain, or foreign travel. She was taking a multivitamin supplement but no prescription medication.

At presentation, she was mildly distressed but oriented. Her vital signs were within normal limits, apart from mild tachycardia (heart rate, 104 beats/min). Physical examination revealed grade 3/5 limb muscle strength, although testing was associated with obvious discomfort. Muscle bulk and tone, tendon reflexes, and sensation were normal. Notably, there was no rash, and cardiorespiratory examination yielded unremarkable findings. Initial chest radiography revealed a left lower lobe infiltrate most consistent with pneumonia. Urinalysis was strongly positive for hemoglobin. Initial laboratory analysis (reference ranges provided parenthetically) revealed that her creatine kinase (CK) level was markedly elevated at 118,342 U/L (38-176 U/L).

What is the most appropriate next step to confirm the diagnosis of rhabdomyolysis in this patient? Provide an explanation for your answer.

What is the most likely etiology of this patient’s recurrent rhabdomyolysis?

Rhabdomyolysis is a rapid breakdown of muscle. Detail the pathophysiology behind rhabdomyolysis.

What are the possible complications of rhabdomyolysis?

Which medications may cause rhabdomyolysis?

A Sample Answer For the Assignment: NUR-631 Topic 13 DQ 1

Title: NUR-631 Topic 13 DQ 1

DQ RESPONSE

CAT Pediatric Musculoskeletal disorders.

Please discuss the pathophysiology, clinical manifestations, and evaluation/treatment of one of the many pediatric musculoskeletal disorders.

Duchenne Muscular Dystrophy Pathophysiology: Duchenne Muscular Dystrophy (DMD) is an X-linked inherited muscular disease primarily affecting males. It is caused by deletion of one or more exons of the DMD gene on the X chromosome or, by a rare nonsense mutation (McCance et al., 2019). The DMD gene is responsible for dystrophin production, a membrane-stabilizing protein absent in DMD. Dystrophin mediates the anchorage of the actin cytoskeleton of skeletal muscle fibers to the basement membrane. Without adequate anchorage of the basement membrane, these poorly organized fat and connective tissue strands cannot develop normal musculoskeletal anatomy. The contraction physiology leads to unorganized forces exerted on disease muscle cells and destroys them. Free calcium is released and causes muscle cell death. Children under three generally can regenerate some muscle cells and sustain some normal functions until the muscle cell death rate exceeds regeneration. Clinical onset of DMD is rapid and occurs around three to four years old.

Clinical Manifestations:  Difficulty walking, gait instability, waddling, frequent falls, and difficulting standing are signs that parents will seek care for. Significant lumbar and gluteal muscle weakness presents as a child that rises from standing by bracing on their own legs and thighs to stand (Gower sign). The shoulders also become affected but typically after lower body manifestations. A hallmark pathology sign of DMD is pseudohypertrophic calf muscles consisting of fat and connective tissue rather than muscle tissue (McCance et al., 2019). The feet assume equinovarus positioning, and ambulatory children tend to walk on their toes. It is typical for loss of ambulation to occur around 12 to 15 years old. Intellectual disability is a common component, although learning disability is thought to contribute to lower-than-average IQs. The life expectancy for DMD has been increasing, but patients often have high mortality with respiratory complications. Scoliosis and kyphosis are common complications, resulting in respiratory insufficiency, pneumonia, and chronic aspiration risk. The average life expectancy of DMD is around 20 to 25 years old. Patients with Becker muscular dystrophy, a less severe variation of DMD have a life expectancy of 30 to 40 years old. Cardiac complications also accompany many inherited diseases.

Evaluation and Treatment Options:

Prenatal diagnosis is now possible and female carriers can be identified, especially if there is a known genetic defect in another family member (McCance et al., 2019). Due to rapid muscle breakdown and death, serum enzymes (CPK, LDH, SGOT, aldolase) are often elevated. CK increase can be 100 to 1,000x normal and CK elevation in infants is indicative of DMD. Patients may require ventilatory support throughout their life, and multidisciplinary care models are required to optimize health and quality of life for these patients.

References

McCance, K. L., Huether, S. E., Brashers, V. L., Rote, N. S., & McCance, K. L. (2019). Pathophysiology: The biologic basis for disease in adults and children. Elsevier.

Developmental dysplasia of the hip (DDH), also known as congenital hip dysplasia (CHD), is one of the commonest musculoskeletal pathologies in the newborn (Nievelstein, 2021). It is a developmental (and not a congenital!) disease of the hip as newborns with normal hips at birth can be affected later during infancy (Nievelstein, 2021). Therefore, CHD is a misnomer and should be avoided (Nievelstein, 2021).

DDH occurs in approximately 1:1000 live births with a female predominance (Nievelstein, 2021). The left hip is more commonly involved than the right hip, and it can occur bilaterally (Nievelstein, 2021). Risk factors include breech position during pregnancy (girls 12%, boys 2.6%) and a positive family history (girls 4.4%, boys 0.9%) (Nievelstein, 2021). Clubfoot has been thought to be a risk factor but this no longer holds true (Nievelstein, 2021).

Ultrasound (US) is the imaging technique of first choice in infants younger than 6–9 months of age with suspicion of DDH (Nievelstein, 2021). After this age the physiological ossification of the femoral epiphyses usually obscures an adequate overview of the entire hip joint and a pelvic X-ray is preferred (Nievelstein, 2021). With US we are looking at the same anatomic structures as on a pelvic X-ray, with the advantage of also displaying the cartilaginous structures of the hip joint (Nievelstein, 2021). DDH on US is classified according to the Graf classification in types I–IV based on the morphology of the iliac bone, including the shape of the acetabulum, the bony and cartilaginous acetabular rim, labrum, and position of the femoral head (Nievelstein, 2021). It has been shown that US can also be used for guidance and follow-up of manually as well as operatively reduced dislocated dysplastic hips (Nievelstein, 2021).

Nievelstein, R. A. (2021). Non-traumatic musculoskeletal diseases in children. In IDKD Springer series (pp. 283–292). https://doi.org/10.1007/978-3-030-71281-5_20

CAT 2 Calcium Metabolism

As we are talking about musculoskeletal disorders this week let’s review the calcium metabolism.

What organs, hormones, electrolytes, factors, etc. are involved and how do they work together

The intricate interactions of numerous systems are necessary for normal calcium control. By acting on bone, kidney, and intestine, the calcium-regulating hormones parathyroid hormone, calcitriol, and calcitonin regulate calcium and phosphorus concentration and delivery (Matikainen et al., 2021). In addition to controlling these hormones, the fluctuating ion concentration and supply may also have a direct impact on the function of the target organs, particularly bone. Systemic hormones that interact with calcium regulators are crucial for skeletal growth and development, including thyroid hormone, growth hormone, somatomedins, glucocorticoids, and sex hormones (Matikainen et al., 2021). In the local control of bone, prostaglandins and osteoclast activating factor may be significant. Hypercalcemia is a common disorder of calcium control, but tests of parathyroid hormone are not yet accurate and the causes of hypercalcemia in malignancy have not been discovered. It is debatable how calcium-regulating hormones affect osteoporosis pathogenesis and treatment. The identification of other components that affect mineral metabolism may be necessary to find a solution to these issues (Matikainen et al., 2021).

Reference

Matikainen, N., Pekkarinen, T., Ryhänen, E. M., & Schalin-Jäntti, C. (2021). Physiology of Calcium Homeostasis: An Overview. Endocrinology and metabolism clinics of North America, 50(4), 575–590. https://doi.org/10.1016/j.ecl.2021.07.005

Calcium serves a vital role in skeletal muscle mineralization. Greater than 99% of the calcium in the body is stored in the bone. Calcium exists in the serum in three forms: protein-bound, ionized or free, and complexed or chelated. There are three primary hormones that regulate calcium transport in the gut, kidneys, and bone. These hormones are parathyroid hormone, 1,25-dihydroxyvitamin D-3, and calcitonin. Parathyroid is released by the parathyroid glands when there is a decrease in serum calcium. Parathyroid works in the kidneys causing an increase in calcium reabsorption. In response to parathyroid hormone, the kidney also increases the secretion of Vitamin D-e that then stimulates calcium absorption through the gut. In the bone, parathyroid stimulates osteoclasts involved in bone reabsorption and the release of free calcium. The sum of these actions is a rise of serum calcium. When there is an increase in serum calcium, calcitonin is released by the thyroid parafollicular cells. Calcitonin stimulates osteoblasts in the bone to deposit calcium into the bone. In the kidneys, calcitonin causes the decrease in reabsorption of calcium, increasing urinary calcium excretion. In the gut, calcitonin also causes a decrease in calcium absorption. This leads to a decrease in serum calcium.

Yu, E., Sharma, S. (2022). Physiology, Calcium. StatPearls Internet. Retrieved on August 2, 2023, from https://www.ncbi.nlm.nih.gov/books/NBK482128/

CAT 1 Fractures

What are the defining characteristics of the following types of fractures;

Oblique, Occult, Open, Pathologic, Segmented, Spiral, Transverse, Greenstick, and Impacted

CAT 1 Fractures

What are the defining characteristics of the following types of fractures;

Oblique: the fracture is slanted on the shaft of the bone.

Occult: the fracture is often hidden on X-ray imaging

Open: (previously compound fracture) It is a fracture that breaks the skin at the site of the fracture.

Pathologic: The fracture is due to a different disease process and occurs where the bone is weaker due to said disease. 

Segmented: The bone is broken into two or more pieces or segments

Spiral: A spiral fracture encircles the bone; can become displaced by a twist

Transverse: The fracture line goes straight across the bone

Greenstick: An incomplete fracture; the break is only in the cortex of the bone. This is usually caused by minor direct or indirect energy

Impacted: (Also called Buckle fracture) A fracture with one end wedged into the other end of the fractured bone (Like a belt buckle). 

***All information obtained from McCance et al., 2019

McCance, K. L., Huether, S. E., Brashers, V.L., & Rote, N.S. (2019). Pathophysiology the biological basis for disease in adults and children (8th ed.). Elsevier Health Sciences. ISBN-13:9780323402811

Good. Can anyone share images of the above fractures.

You will find attached oblique, occult, open, and pathological fracture imaging.

Characteristics of each type of fracture include:

Oblique: Fracture of the bone shaft which is slanted (McCance, 2019)

Occult: Fracture does not show up on X-rays (McCance, 2019)

Open: Bone fracture protrudes through skin (McCance, 2019)

Pathological: Fracture occurs at the site of a preexisitng abnormality (McCance, 2019)

Children’s Mercy Kansas City. 2023. Elbow Fractures. Retrieved on August 1, 2023 from: elbow-fractures

Kemp, A. Pathological Fracture Treatment Detroit. Retrieved on August 1, 2023 from: pathological-fractures-orthopaedic-oncologist-detroit-mi.html

Oblique Fracture: Symptoms, Causes & Treatments. Cleveland Clinic. Retrieved on August 1, 2023 from: 22185-oblique-fracture

Servier Medical Art. Retrieved on August 1, 2023 from: https://smart.servier.com/smart_image/arm-bone-fracture-ov/

Attachments

open fracture.png

oblique-fracture.jpg

pathological fracture.jpg

occult fracture.jpg

According to the Journal of the American Podiatric Medical Association, spiral fractures mainly occur in the tibia and are a result of torsion trauma, these types of fractures are frequently complicated by posterior malleolus fractures (2018). Spiral fractures occur when the bone is broken in a twisted motion, the Cleveland Clinic describes it as a corkscrew (Cleveland Clinic, 2021). A spiral fracture can occur in the femur, fibula, humerus, ankle, forearm, fingers and hands. The main causes of spiral fractures are trauma, car accidents, sports injuries, and falls (Cleveland Clinic, 2021). Treatment of a spiral fracture includes surgery, immobilization of the bone, and both external and internal fixation.

References:

Chen, Q., Song, L., Fang, J., Qin, X., Lv, T., & Li, X. (2018). Effectiveness of Diagnosis and Treatment of Spiral Fracture of the Distal Third of the Tibia Combined with Posterior Malleolus Fracture A Series of Ten Cases. Journal of the American Podiatric Medical Association, 108(2), 106–114. https://doi.org/10.7547/15-181

Spiral Fracture (2021, December 27). Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/22241-spiral-fracture

Image of spiral fracture:

https://my.clevelandclinic.org/health/diseases/22241-spiral-fracture

Kimberly Mendoza-Maxcy

Jul 29, 2023, 11:37 PM

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What is the most appropriate next step to confirm the diagnosis of rhabdomyolysis in this patient? Provide an explanation for your answer.

Creatine kinase (CK) is the most commonly used and most clinically useful value in diagnosing rhabdomyolysis. Normal CK levels are 5-25 units/L in women and 5-35 units/L in men. Above 5000 units/L, kidney failure is likely (McCance & Huether, 2019). 

What is the most likely etiology of this patient’s recurrent rhabdomyolysis?

The most likely etiology of this patient’s rhabdomyolysis would be an infectious cause considering her initial symptoms were indicative of some type of viral infection. Her initial symptoms were malaise, cough, and myalgia. Infectious causes of rhabdomyolysis include viruses such as influenza, parainfluenza, adenovirus, coxsackievirus, echovirus, herpes simplex virus, cytomegalovirus, Epstein-Barr virus, and HIV. Bacterial infections include Streptococcus, Salmonella, Legionella, Staphylococcus, and Listeria (McCance & Huether, 2019). 

Rhabdomyolysis is a rapid breakdown of muscle. Detail the pathophysiology behind rhabdomyolysis.

In the setting of muscle injury and ATP depletion, there is an excessive intracellular influx of Na+ and Ca++. This increase in intracellular Na+ also draws water into the cell and disrupts the intracellular space. The increase in intracellular Ca++ leads to sustained myofibrillar contraction and further depletes ATP. The increased calcium also activates proteases and phospholipases, leading to lysis of the cellular membrane and further damage to the ion channels. The cumulative result of these changes to the cell is a myolytic cascade that leads to necrosis of the muscle fibers and release of the contents of the muscle into the extracellular space and blood stream (Torres, et al., 2015). 

What are the possible complications of rhabdomyolysis?

Rhabdomyolysis leads to hyperkalemia due to the release of intracellular potassium into the circulation, metabolic acidosis due to the release of intracellular phosphorus and sulfate, acute renal failure from myoglobin precipitating in the tubules of the kidney obstructing flow through the nephron, and even DIC from the activation of the clotting cascade by the release of intracellular components from the damaged muscle (McCance & Huether, 2019). 

Which medications may cause rhabdomyolysis?

Medications that can lead to rhabdomyolysis include anesthetic and paralytic agents, antihistamines, anti-hyperlipidemic agents including statins, antipsychotics and antidepressants, hypnotics and sedatives, and methadone. Other toxins that may cause rhabdomyolysis include cocaine, amphetamines, LSD, MDMA, and heroin (McCance & Huether, 2019). 

McCance, K., Huehter, S. (2019). Pathophysiology: The Biologic Basis for Disease in Adults and Children, (8thed.). Elsevier. 

Torres, P., Helmstetter, J., Kaye, A.M., Kaye, A.D.  (2015). Rhabdomyolysis: Pathogenesis, diagnosis, and treatment. The Oschner Journal, 15(1), 58-69. Retrieved on July 29, 2023, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4365849/.

Sample Answer for NUR-631 Topic 13 DQ 1 Included After Question

A Sample Answer For the Assignment: NUR-631 Topic 13 DQ 1

Title: NUR-631 Topic 13 DQ 1

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