NURS 6501 Concepts of Neurological and Musculoskeletal Disorders – Part 1

NURS 6501 Concepts of Neurological and Musculoskeletal Disorders – Part 1

NURS 6501 Concepts of Neurological and Musculoskeletal Disorders – Part 1

  • Question 2

4 out of 4 points

Scenario 1: Gout

A 68-year-old obese male presents to the clinic with a 3-day history of fever with chills, and Lt. great toe pain that has gotten progressively worse. Patient states this is the first time that this has happened, and nothing has made it better and walking on his right foot makes it worse. He has tried acetaminophen, but it did not help. He took several ibuprofen tablets last night which did give him a bit of relief.

HPI: hypertension treated with Lisinopril/HCTZ .

SH: Denies smoking. Drinking: “a fair amount of red wine” every week. General appearance: Ill appearing male who sits with his right foot elevated.

PE:  remarkable for a temp of 100.2, pulse 106, respirations 20 and BP 158/92. Right great toe (first metatarsal phalangeal [MTP]) noticeably swollen and red. Unable to palpate to assess range of motion due to extreme pain. CBC and Complete metabolic profile revealed WBC 15,000 mm3 and uric acid 9.0 mg/dl.

Diagnoses the patient with acute gout.

Question:

Explain why a patient with gout is more likely to develop renal calculi.
Selected Answer: Most uric acid is eliminated from the body through the kidneys. Urate is filtered at the glomerulus and undergoes reabsorption and excretion within the proximal renal tubules. In primary gout, urate excretion by the kidneys is sluggish. This may be caused by a decrease in glomerular filtration of urate or acceleration in urate reabsorption. This allows for urate crystals to be deposited in the renal tubules.
Correct Answer: Most uric acid is eliminated from the body through the kidneys. Urate is filtered at the glomerulus and undergoes reabsorption and excretion within the proximal renal tubules. In primary gout, urate excretion by the kidneys is sluggish. This may be caused by a decrease in glomerular filtration of urate or acceleration in urate reabsorption. This allows for urate crystals to be deposited in the renal tubules.
Response Feedback: [None Given]

In this exercise, you will complete a 10- to 20-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

Photo Credit: Getty Images/Science Photo Libra

Complete the Knowledge Check By Day 7 of Week 7

To complete this Knowledge Check:

Module 5 Knowledge Check

Next Week

To go to the next week:

Week 8

 Week 7: Concepts of Neurological and Musculoskeletal Disorders – Part 1

Anatomists often use the analogy of a house to explain the human body, with skeletal systems, respiratory systems, and circulatory systems represented as a home’s framing structure, ventilation, and piping, respectively. Such analogies further emphasize the point that relationships between systems can result in complications when issues arise in one system.

With hundreds of diseases that can impact the brain, spine, and nerves, neurological disorders represent a complicated array of issuesNURS 6501 Concepts of Neurological and Musculoskeletal Disorders – Part 1

that present significant health concerns. Disorders such as strokes and Parkinson’s disease not only affect the nervous system, however; they can have secondary impacts in other areas, especially the musculoskeletal system.

This week, you examine fundamental concepts of neurological disorders. You explore common disorders that impact these systems and you apply the key terms and concepts that help communicate the pathophysiological nature of these issues to patients.

Learning Objectives

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Students will:

  • Analyze concepts and principles of pathophysiology across the lifespan

Learning Resources

Required Readings (click to expand/reduce)

 McCance, K. L. & Huether, S. E. (2019). Pathophysiology: the biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.

  • Chapter 15: Structure and Function of the Neurologic System
  • Chapter 16: Pain, Temperature Regulation, Sleep, and Sensory Function (stop at Sleep); Summary Review
  • Chapter 17: Alterations in Cognitive Systems, Cerebral Hemodynamics, and Motor Function (start at Acute confusional states and delirium) (stop at Alterations in neuromotor functions); (Parkinson’s Disease); Summary Review
  • Chapter 18: Disorders of the Central and Peripheral Nervous Systems and the Neuromuscular Junction (stop at Degenerative disorders of the spine); (start at Cerebrovascular disorders) (stop at Tumors of the central nervous system); Summary Review
  • Chapter 44: Structure and Function of the Musculoskeletal System (stop at Components of muscle function); Summary Review
  • Chapter 45: Alterations of Musculoskeletal Function (stop at Bone tumors); (start at Disorders of joints); Summary Review
  • Chapter 47: Structure, Function, and Disorders of the Integument (section on Lyme Disease)

Chin, L. S. (2018). Spinal cord injuries. Retrieved from https://emedicine.medscape.com/article/793582-overview#a4

Required Media (click to expand/reduce)

Module 5 Overview with Dr. Tara Harris 

Dr. Tara Harris reviews the structure of Module 5 as well as the expectations for the module. Consider how you will manage your time as you review your media and Learning Resources throughout the module to prepare for your Knowledge Check and your Assignment. (3m)

Khan Academy. (2019b). Ischemic stroke . Retrieved from https://www.khanacademy.org/science/health-and-medicine/circulatory-system-diseases/stroke/v/ischemic-stroke 

Note: The approximate length of the media program is 8 minutes.

Osmosis.org. (2019, June 12). Osteoporosis  – causes, symptoms, diagnosis, treatment, pathology [Video file]. Retrieved from https://www.youtube.com/watch?v=jUQ_tt_zJDo 

Note: The approximate length of the media program is 9 minutes.

Online Media from Pathophysiology: The Biologic Basis for Disease in Adults and Children

In addition to this week’s media, it is highly recommended that you access and view the resources included with the course text, Pathophysiology: The Biologic Basis for Disease in Adults and Children. Focus on the videos and animations in Chapters 15, 16, 18, and sections of Chapters 44 and 45 that relate to the neurological and musculoskeletal systems. Refer to the Learning Resources in Week 1 for registration instructions. If you have already registered, you may access the resources at https://evolve.elsevier.com/

  • 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.
Response Feedback: [None Given]

  • 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.
Response Feedback: [None Given]