A nurse is assessing a client with a suspected neurologic injury.
Which finding is most consistent with an upper motor neuron (UMN) lesion?
Loss of voluntary movement.
Increased muscle tone with exaggerated deep tendon reflexes.
Progressive muscle atrophy with fasciculations.
Hyporeflexia with decreased muscle tone.
The Correct Answer is B
Choice A rationale
While the loss of voluntary movement, or paralysis, can occur in both upper and lower motor neuron lesions, it is not the most specific or defining characteristic of a UMN injury. UMN lesions occur in the brain or spinal cord, affecting the descending motor pathways. Although voluntary control is lost, the reflexive arcs remain intact and often become overactive because the inhibitory influence from the primary motor cortex is removed by the injury.
Choice B rationale
Upper motor neuron lesions are characterized by spasticity, which is an increase in muscle tone, and hyperreflexia, which is exaggerated deep tendon reflexes. This occurs because the UMNs normally provide inhibitory signals to the lower motor neurons in the spinal cord. When the UMN pathway is damaged, such as in a stroke or spinal cord injury, the LMNs become hyper-excitable. This results in the classic clinical presentation of increased resistance to passive stretch and hyperactive reflexes.
Choice C rationale
Progressive muscle atrophy and fasciculations are hallmark signs of a lower motor neuron (LMN) lesion, not an upper motor neuron lesion. LMNs are the final common pathway connecting the central nervous system to the muscles. When these neurons are damaged, the muscle loses its trophic support and nerve stimulation, leading to significant wasting and spontaneous twitching of muscle fibers. In contrast, UMN lesions typically cause minimal disuse atrophy and no fasciculations.
Choice D rationale
Hyporeflexia, which refers to diminished reflexes, and decreased muscle tone, or flaccidity, are classic indicators of a lower motor neuron lesion. This occurs because the reflex arc is physically interrupted at the level of the peripheral nerve or the anterior horn cell of the spinal cord. In an acute UMN injury, such as spinal shock, there may be temporary flaccidity, but the long-term consistent finding of a UMN lesion is the development of hypertonicity.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is ["2"]
Explanation
63 Step 1 is 10 mg ÷ 5 mg.
Step 2 is 2 × 1 mL. The final calculated answer is 2 mL.
Correct Answer is B
Explanation
Choice A rationale
Respiratory alkalosis is caused by the excessive loss of carbon dioxide through hyperventilation, resulting in a pH above 7.45. While confusion can occur with any significant acid-base imbalance, the pathophysiology of prolonged vomiting involves the direct loss of hydrochloric acid and potassium from the stomach. This loss of acid leads to an accumulation of bicarbonate in the blood, which is a metabolic process rather than a primary respiratory issue related to CO2 clearance.
Choice B rationale
Metabolic alkalosis is the anticipated imbalance because vomiting results in the significant loss of hydrogen ions and chloride from gastric secretions. As the body loses acid, the serum bicarbonate level increases, raising the pH above 7.45. Confusion arises from electrolyte shifts and reduced cerebral perfusion. Shallow respirations, or hypoventilation, occur as a compensatory respiratory mechanism to retain carbon dioxide, which acts as an acid to help lower the elevated systemic pH.
Choice C rationale
Metabolic acidosis involves a decrease in pH and bicarbonate, often due to the gain of acid or the loss of base, such as in diarrhea or renal failure. Prolonged vomiting has the opposite effect because it removes acid from the body. While severe dehydration from vomiting could eventually lead to poor tissue perfusion and lactic acidosis, the initial and most direct consequence of losing gastric contents is the development of an alkalotic state.
Choice D rationale
Respiratory acidosis is characterized by the retention of carbon dioxide due to hypoventilation, leading to a pH below 7.35. Although the client is currently exhibiting shallow respirations, this is a compensatory response to the primary metabolic alkalosis caused by vomiting. In a primary respiratory acidosis, the client would usually have a history of lung disease or respiratory depression rather than the active loss of acidic gastric fluids seen in this clinical scenario.
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