NUR 631 Topic 6 DQ 1

Sample Answer for NUR 631 Topic 6 DQ 1 Included After Question

Select two of the following questions for your discussion response. Indicate which question you have chosen using the format displayed in the “Discussion Forum Sample.”

  1. From a pathophysiological perspective, describe the disease mechanism of spinal trauma. Discuss complications associated with spinal trauma based upon time of injury.
  2. What are some the recent discoveries surrounding the pathophysiology of Alzheimer’s disease, and how could these discoveries lead to new treatments? Include your resources in your response.
  3. What are some of the leading theories that attempt to describe the pathophysiology underlying fibromyalgia? Which ones are best supported? Include your resources in your response.
  4. Differentiate between Alzheimer’s disease, Parkinson’s disease, and vascular dementia.

A Sample Answer For the Assignment: NUR 631 Topic 6 DQ 1

Title: NUR 631 Topic 6 DQ 1

From a pathophysiological perspective, describe the disease mechanism of spinal trauma. Discuss complications associated with spinal trauma based upon time of injury.

Anjum et al in the article Spinal Cord Injury, defines a spinal cord injury (SCI) as a destructive neurological and pathological state which creates severe motor, sensory, and autonomic dysfunctions (2020). Pathophysiology compromises of SCI incorporate a cascade of destructive events including ischemia, oxidative stress, inflammatory events, apoptotic pathways and locomotor dysfunctions (Anjum et al, 2020). Severity of spinal cord injury is determined by the location of initial destruction and duration of spinal cord compression. After a spinal cord injury, the multi-faceted neurological communication is interrupted and disorganized leading to impaired spinal recovery.

Acute SCI often occurs from a traumatic injury to the spine resulting in fractures and vertebrae dislocation. Anjum et al illustrates spinal cord injuries occur in two phases, primary and secondary (2020). Primary injury is associated with bone fragments and spinal ligament tearing. The first phase includes the destruction of neural parenchyma, disruptions of the axonal network, hemorrhage and disruptions of glial membrane (Anjum et al, 2020). Secondary injury initiates a cascade of events activating biochemical, mechanical, and physiological changes within the neural tissues (Anjum et al, 2020). The primary injury triggers secondary injury leading to further chemical and mechanical damage to spinal tissues from neuronal excitotoxicity; this multi-featured pathological secondary injury phase occurs for several weeks (Anjum et al, 2020).

Anjum et al describes clinical manifestations of secondary injury include increased cell permeability, apoptotic signaling, ischemia, vascular damage, excitotoxicity, ionic deregulation, inflammation, lipid peroxidation, free radical formation, demyelination, Wallerian degeneration, fibroglial scar and cyst formation (2020). However, the most vulnerable clinical manifestation of a SCI is the interruption in spinal cord vascular supply leading to hypotension or hypo-perfusion, hypovolemia, neurogenic shock and bradycardia (Anjum et al, 2020). Extensive bleeding and neurogenic shock lead to spinal cord ischemia. Rupturing of small blood vessels and capillaries promote extravasation of leukocytes and red blood cells (RBCs); this formation of immune cells further disrupts the flow of blood creating vasospasms (Anjum et al, 2020). Vascular ischemia, hypovolemia, and hypoperfusion eventually lead to cellular death. 

Differentiate between Alzheimer’s disease, Parkinson’s disease, and vascular dementia.

In accordance with McCance et al, Alzheimer disease is a senile disease complex which is irreversible (2019). Alzheimer disease is the leading cause of dementia in older adults. There is no known cause for Alzheimer’s disease, but risk factors related to the disease are age and a family history. Pathophysiology of Alzheimer’s disease is neurofibrillary tangles, neuritic plaques, and degeneration of basal forebrain cholinergic neurons (McCance et al, 2019). Clinical manifestations include forgetfulness, emotional upset, disorientation, confusion, lack of concentration; declines in abstraction, problem solving, and judgment (McCance et al, 2019). Whereas, vascular dementia is defined as progressive failure of cerebral functions which cause impairment (McCance et al, 2019).

Pathophysiology regarding vascular dementia includes neuron degeneration, compression of brain tissue, atherosclerosis of cerebral vessels, brain drama, genetic predisposition, or central nervous system (CNS) infections (McCance et al, 2019). Clinical manifestations of dementia include impaired memory, language, intelligence, and behavior. There is no specific treatment for vascular dementia or Alzheimer disease, the treatment goal is to slow the progression of symptoms. McCance et al defines Parkinson’s disease as severe degeneration of the basal ganglia (corpus striatum) involving the dopaminergic nigrostriatal pathway (2019).

Pathophysiologic mechanisms include rigidity, bradykinesia and akinesia, resting tremor, postural fixation, and cognitive-affective symptoms and dementia to list a few (McCance et al). Clinical manifestations of parkinson’s disease are staring expression with immobile facial muscles, frequent drooling, slow gait, shuffling steps, flexed and abducted arms, and slightly forward bending trunk (McCance et al, 2019). Pharmacological treatment of the disease includes Levodopa, anticholinergic medications, antihistamines, and amantadine (McCance et al, 2019). Physical, speech, and occupational therapy may also be utilized to retain functionality. 

Anjum, A., Yazid, M. D., Fauzi Daud, M., Idris, J., Ng, A. M. H., Selvi Naicker, A., Ismail, O. H. R., Athi Kumar, R. K., & Lokanathan, Y. (2020). Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms. International journal of molecular sciences21(20), 7533. 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

A Sample Answer 2 For the Assignment: NUR 631 Topic 6 DQ 1

Title: NUR 631 Topic 6 DQ 1

Mechanism of Spinal Trauma and Time of Injury-Related Complications

Spinal cord trauma can be a devastating and life-changing diagnosis for patients with many manifestations. Most spinal trauma patients will require intensive care due to the tendency of neurogenic shock management after injury. Motor vehicle accidents and long-distance falls are the top causes of spinal cord trauma in the U.S. (HHS, n.d). Other mechanisms of spinal trauma are acts of violence (battery, gunshot, etc.), surgical injury, industrial accidents, sports injuries, and medical conditions that damage the spinal cord. Age is a risk factor for people 16-30 years old and over 65 years old (HHS, n.d).

The severity of trauma and its location on the spinal cord will predict the permanence and prognosis. The mechanism of injury and time of injury are important factors when caring for spinal cord injury patients. The tissue destruction from shearing, compression, or penetration is responsible for impaired nerve impulses (McCance et al., 2019). Shearing describes the rotational forces that twist the cord and damage impulse pathways. Compression describes pressure inflicted on the spinal cord due to crushed vertebrae. A spinal hematoma may also lead to a cord compression injury. A penetration injury is from a foreign body’s obstruction in the spinal space and may result in the transection of the cord.

Theories Supporting Fibromyalgia

Fibromyalgia is a condition in which muscles, tendons, and joints are painful, stiff, and tender, often accompanied by restless sleep, fatigue, anxiety, depression, and disturbances in bowel function—widespread pain, cognitive difficulties, and impaired quality of life prompt patients to seek treatment (McCance et al., 2019). Fibromyalgia is a fascinating condition that has evolved over centuries. Medical providers have theorized about widespread pain with no injury since the 1590s (Dellwo, 2022). Fibromyalgia has had many names over the centuries, but it was not until 1904 that these symptoms were named Fibrositis. In the 1930s, medical researchers discovered the interconnectedness of psychological and physiological existence.

Providers began to speculate that the symptoms were primarily psychological and caused by stress. Additionally, connections between post-WWII trauma and what is now called fibromyalgia were validated. The medical community did not fully acknowledge the condition until about 1949, after a chapter was published in the well-regarded textbook, Arthritis and Allied Conditions (Dellwo, 2022). Today, the diagnosis of fibromyalgia may be accepted by a provider, but this does not ensure the provider is prepared to manage the condition without seeking expert consultation. Ongoing research on this condition continues, but many milestones have been in recent years.

This condition is currently understood to involve dysfunctional neurotransmitter systems that influence the body’s endogenous stress response systems (Martins et al., 2021). This results in asynchrony between parasympathetic and sympathetic processes. Based on the polyvagal theory, aberrant vagal tone is being explored as a cause or effect of fibromyalgia. This theory proposes that the nervous system of mammals is a product of evolution and describes the existence of two functionally distinct branches of the vagal nerve, the dorsal and ventral branches. The dorsal branch is demyelinated and delivers impulses more slowly (Martins et al., 2021).

The most evolved ventral branch is myelinated and linked to emotional expression, communication, and self-calming behaviors. As the autonomic nervous system changed throughout the evolution process, so did the interaction between the autonomic nervous system and the other physiological systems that respond to stress, including the cortex, the HPA-axis, the oxytocin and vasopressin neuropeptides, and the immune system (Martins et al., 2021). This theory proposed a biological basis to enhance positive social behavior because behaviors that promote homeostasis of these interdependent systems can provide more quantitative evidence.


Martins, D. F., Viseux, F. J. F., Salm, D. C., Ribeiro, A. C. A., da Silva, H. K. L., Seim, L. A., Bittencourt, E. B., Bianco, G., Moré, A. O. O., Reed, W. R., & Mazzardo-Martins, L. (2021). The role of the vagus nerve in fibromyalgia syndrome. Neuroscience and Biobehavioral Reviews, 131, 1136–1149.

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.

Dellwo, A. (2022, May 23). The history of fibromyalgia. [web article].

U.S. Department of Health and Human Services [HHS]. (n.d.). Spinal Cord Injury. National Institute of Neurological Disorders and Stroke.