A nurse is caring for a client who has a prescription for acyclovir IV three times daily.
Which of the following actions should the nurse take?
Assess for an increase in creatinine.
Administer oxygen prophylactically.
Assess for a decrease in Hgb and Hct.
Administer the medication over 30 min.
The Correct Answer is A
Choice A rationale
Acyclovir is primarily excreted renally, and its metabolism can lead to crystal formation in the renal tubules, particularly if the client is dehydrated or the infusion is too rapid. Monitoring for an increase in creatinine (normal range 0.6-1.2 mg/dL) is crucial as it indicates decreased glomerular filtration rate and potential nephrotoxicity or acute kidney injury, necessitating dose adjustment or hydration.
Choice B rationale
Administering oxygen prophylactically is not a standard or scientifically indicated action for acyclovir administration. Acyclovir does not inherently cause respiratory depression or compromise oxygenation. Its primary adverse effects are typically related to renal function, central nervous system, or gastrointestinal system, not respiratory compromise.
Choice C rationale
While some antiviral medications can affect hematopoiesis, acyclovir is not commonly associated with significant decreases in hemoglobin (normal range 12-18 g/dL) and hematocrit (normal range 37-52%). These parameters are generally monitored in clients with pre-existing hematological conditions or those on long-term, high-dose therapy, but it's not a primary immediate concern for IV administration.
Choice D rationale
Administering acyclovir IV over 30 minutes is the recommended infusion duration. Rapid intravenous infusion can increase the risk of renal tubular damage and crystal formation, leading to nephrotoxicity. A slower infusion rate allows for proper dilution and minimizes the concentration of the drug in the renal tubules, thus protecting kidney function and reducing adverse effects.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Choice A rationale
Allopurinol is a xanthine oxidase inhibitor. This enzyme is crucial in the purine catabolism pathway, converting xanthine and hypoxanthine into uric acid. By inhibiting xanthine oxidase, allopurinol effectively decreases the de novo synthesis of uric acid, thereby lowering serum uric acid levels. This reduction prevents the formation of uric acid crystals in joints and tissues, which are responsible for the painful manifestations of gout.
Choice B rationale
Tophus formation is a direct consequence of chronic hyperuricemia, where uric acid crystals accumulate in soft tissues, leading to palpable nodules. Allopurinol's primary mechanism of action is to reduce uric acid levels. By achieving this, it prevents further crystal deposition and can even lead to the regression of existing tophi over time. Therefore, it does not increase tophus formation.
Choice C rationale
Allopurinol's mechanism of action is specifically related to uric acid metabolism. It does not directly influence calcium homeostasis in the body. Calcium levels are primarily regulated by parathyroid hormone, calcitonin, and vitamin D, which are distinct physiological pathways unrelated to xanthine oxidase inhibition. Therefore, it does not lower calcium levels.
Choice D rationale
While allopurinol ultimately helps relieve joint inflammation in gout, it does so indirectly. Its primary action is to reduce uric acid production, which then prevents the formation of inflammatory uric acid crystals. The direct reduction of inflammation is typically achieved by anti-inflammatory drugs like NSAIDs or colchicine, which act on inflammatory mediators or pathways, not directly by allopurinol.
Correct Answer is B
Explanation
Choice A rationale
Nystagmus, an involuntary rhythmic eye movement, is not a recognized or common adverse effect of oral albuterol. Albuterol is a beta-2 adrenergic agonist primarily acting on bronchial smooth muscle to cause bronchodilation. Its side effects are typically related to sympathetic nervous system stimulation, not oculomotor dysfunction.
Choice B rationale
Tachycardia is a common adverse effect of oral albuterol due to its systemic absorption and stimulation of beta-1 adrenergic receptors in the heart, in addition to its primary beta-2 effects on the lungs. This leads to an increased heart rate (normal range 60-100 bpm) and can cause palpitations, especially in sensitive individuals or with higher doses.
Choice C rationale
Drowsiness is not a typical adverse effect of oral albuterol. In fact, due to its stimulant properties, albuterol is more likely to cause central nervous system excitation, leading to insomnia, nervousness, or tremors rather than sedation. Its action is to activate adrenergic pathways, which generally promote alertness.
Choice D rationale
Oral fungal infections, such as oral candidiasis (thrush), are commonly associated with inhaled corticosteroids, not oral albuterol. Inhaled corticosteroids suppress the local immune response in the oral cavity, allowing opportunistic fungal growth. Oral albuterol does not have immunosuppressive effects on the oral mucosa.
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