A client with a T6 spinal cord injury suddenly develops severe hypertension, headache, flushed skin above the level of injury, and cool, pale lower extremities.
Which pathophysiologic mechanism best explains these findings?
Uncontrolled sympathetic response below the level of injury.
Decreased norepinephrine release causing systemic hypotension.
Increased intracranial pressure causing reflex bradycardia.
Loss of parasympathetic control leading to widespread vasodilation.
The Correct Answer is A
Choice A rationale
Autonomic dysreflexia occurs in patients with injuries at or above the T6 level. A noxious stimulus below the injury triggers an exaggerated sympathetic nervous system response. This causes massive vasoconstriction in the lower body, leading to severe hypertension and pale, cool skin. Because the spinal cord injury blocks descending inhibitory signals from the brain, the sympathetic surge remains uncontrolled. The brain attempts to compensate by increasing parasympathetic activity, causing vasodilation and flushing only above the injury level.
Choice B rationale
Decreased norepinephrine release would result in a reduction of sympathetic tone, which typically leads to systemic hypotension rather than the severe hypertension observed in autonomic dysreflexia. In this clinical scenario, there is actually an excessive release of norepinephrine from the sympathetic postganglionic neurons below the level of the spinal cord lesion. This surge is the primary driver behind the sudden and dangerous rise in blood pressure that characterizes this life-threatening neurological emergency.
Choice C rationale
Increased intracranial pressure can lead to Cushing's triad, which includes hypertension, bradycardia, and irregular respirations. While hypertension and bradycardia are present in both conditions, the specific presentation of autonomic dysreflexia is driven by a spinal cord reflex rather than primary brain pathology. The headache and hypertension in this case are secondary to the massive peripheral vasoconstriction and systemic pressure increase, not a primary increase in intracranial volume or pressure within the cranial vault itself.
Choice D rationale
Loss of parasympathetic control would typically result in tachycardia and an inability to achieve vasodilation. However, in autonomic dysreflexia, the parasympathetic nervous system remains intact above the level of the spinal cord injury. The brain sends signals through the vagus nerve to slow the heart and dilate vessels to lower the blood pressure. This explains why the patient experiences flushing and diaphoresis above the injury level while the lower extremities remain constricted and pale.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
Choice B rationale
A fever of 38.9 degrees Celsius is a classic systemic manifestation of inflammation. This occurs when inflammatory mediators, such as cytokines (interleukin-1 and tumor necrosis factor), enter the bloodstream and travel to the hypothalamus. The hypothalamus then resets the body's internal thermostat to a higher level. Unlike localized signs, a fever affects the entire body and indicates that the inflammatory process is no longer confined to the initial site of injury, involving a coordinated physiological response across multiple systems.
Choice A rationale
Erythema and warmth are part of the classic cardinal signs of inflammation, which also include swelling, pain, and loss of function. However, when these findings are confined strictly to the incision site, they represent a localized inflammatory response. This local reaction is caused by hyperemia from vasodilation and increased blood flow to the injured area to facilitate tissue repair. It does not indicate that the inflammatory mediators have triggered the systemic responses typically seen in widespread or severe inflammation.
Choice C rationale
Serous drainage is a normal finding during the early stages of wound healing and represents the inflammatory exudate that leaks from capillaries during the phase of increased permeability. This fluid contains proteins and white blood cells needed for repair. Since this drainage is noted specifically at the wound edges, it is a localized clinical finding. It provides information about the status of the specific tissue injury but does not provide evidence that the patient is experiencing a body-wide systemic response.
Choice D rationale
Edema and tenderness surrounding the affected tissue are localized symptoms resulting from increased capillary hydrostatic pressure and the release of chemical mediators like bradykinin and prostaglandins that sensitize local nerve endings. While these symptoms can be distressing, they are restricted to the area of injury. A systemic response would require manifestations such as leukocytosis (WBC count > 11,000/mm), malaise, or the aforementioned fever, which demonstrate that the entire organism is reacting to the presence of inflammation or infection.
Correct Answer is D
Explanation
Choice A rationale
A stable blood pressure helps maintain the integrity of the blood-brain barrier. The barrier consists of tight junctions between endothelial cells, astrocytes, and a basement membrane. These structures are designed to regulate the movement of substances into the brain parenchyma. When blood pressure remains within a normal autoregulatory range, the physical pressure against these tight junctions is controlled, preventing the mechanical "stretching" or leaking of fluids and solutes into the delicate neural tissue.
Choice B rationale
Normal oxygen saturations, typically maintained above 95 percent, ensure that the endothelial cells of the blood-brain barrier receive adequate oxygen for metabolic processes. Hypoxia, or low oxygen, is what actually threatens the barrier. Under hypoxic conditions, the tight junction proteins can degrade, and inflammatory mediators are released, leading to increased permeability. Therefore, maintaining high oxygen levels is a protective factor that keeps the barrier sealed and functioning as a selective filter for the CNS.
Choice C rationale
A glucose level of 90 mg/dL is within the normal fasting range of 70 to 99 mg/dL. The brain requires a constant supply of glucose, which is transported across the blood-brain barrier via specific GLUT1 transporters. Normal physiological levels of glucose do not disrupt the structural integrity of the barrier. It is chronic hyperglycemia, seen in uncontrolled diabetes, that eventually damages the microvasculature and increases permeability through the formation of advanced glycation end products.
Choice D rationale
Inflammation and infection are primary causes of increased blood-brain barrier permeability. During an infection such as meningitis, pathogens and immune cells trigger the release of proinflammatory cytokines like tumor necrosis factor and interleukins. These substances cause the tight junctions between endothelial cells to loosen. This increased permeability allows white blood cells and antibiotics to enter the brain, but it also permits the entry of toxins and excess fluid, leading to potentially dangerous cerebral edema.
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