A patient tells the nurse that she takes aspirin for menstrual cramps, but she does not feel that it works well. What will the nurse suggest?
The patient should increase the dose until pain is controlled.
The patient should use a first-generation nonsteroidal anti-inflammatory medication instead.
The patient should use acetaminophen because of its anti-inflammatory effects.
The patient should avoid any type of COX inhibitor because of the risk of Reye’s syndrome.
The Correct Answer is B
Choice A reason: Increasing aspirin dosage without medical guidance risks toxicity, including gastrointestinal bleeding and ulceration, as aspirin inhibits COX enzymes, reducing prostaglandin production. Prostaglandins mediate pain and inflammation, but excessive inhibition can damage the stomach lining. This approach is unsafe and not recommended for managing menstrual cramps effectively, as it may exacerbate adverse effects without ensuring better pain relief.
Choice B reason: First-generation NSAIDs, like ibuprofen, are more effective for menstrual cramps due to their stronger inhibition of COX-1 and COX-2 enzymes, which reduce prostaglandin synthesis responsible for uterine contractions and pain. Unlike aspirin, ibuprofen offers better pain relief with a more favorable dosing profile, making it a suitable alternative for dysmenorrhea management in most patients.
Choice C reason: Acetaminophen lacks significant anti-inflammatory effects, as it primarily inhibits COX enzymes in the central nervous system, not peripherally. It reduces pain and fever but does not effectively target prostaglandin-mediated inflammation in menstrual cramps. Therefore, it is less effective than NSAIDs like ibuprofen for dysmenorrhea, making it an inappropriate substitute in this context.
Choice D reason: Avoiding COX inhibitors due to Reye’s syndrome risk is unwarranted here, as Reye’s syndrome is primarily associated with aspirin use in children with viral infections. Menstrual cramps are unrelated to this condition, and COX inhibitors like NSAIDs are standard treatment. This choice is overly restrictive and not clinically justified for managing dysmenorrhea.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
Choice A reason: Inhaled glucocorticoids, like budesonide, reduce airway inflammation over time but don’t act quickly enough to abort acute asthma attacks. Short-acting beta-agonists (e.g., albuterol) are used for acute relief, as glucocorticoids lack immediate bronchodilatory effects, making this choice incorrect for chronic asthma management.
Choice B reason: Using inhaled glucocorticoids only in emergencies is ineffective for chronic asthma. These drugs prevent inflammation and exacerbations through consistent use, not acute intervention. Emergency use is reserved for rescue inhalers like albuterol, making this choice inappropriate for long-term asthma control.
Choice C reason: Inhaled glucocorticoids require daily use to maintain anti-inflammatory effects, reducing airway hyperresponsiveness and preventing asthma exacerbations. Consistent dosing ensures steady suppression of chronic inflammation, improving lung function and reducing symptoms, making this the correct choice for managing chronic asthma effectively.
Choice D reason: A 2-week on/off schedule disrupts the consistent anti-inflammatory action of inhaled glucocorticoids needed for chronic asthma control. Intermittent use reduces efficacy, allowing inflammation to rebound, increasing exacerbation risk. Daily use is standard to maintain therapeutic benefits, making this choice incorrect.
Correct Answer is C
Explanation
Choice A reason: Synthesis of more receptor sites (upregulation) typically occurs with receptor antagonists, not agonists, as the body compensates for blocked receptors. This would increase drug sensitivity, not decrease effectiveness. For most medications, continuous exposure leads to desensitization, not receptor proliferation, making this choice incorrect for explaining tolerance.
Choice B reason: Decreased receptor selectivity implies a drug binding to unintended receptors, causing varied effects, not reduced efficacy. Tolerance results from receptor desensitization, not altered selectivity. This mechanism doesn’t explain the patient’s “immunity” to the drug’s therapeutic effects, making this choice scientifically inaccurate for the scenario.
Choice C reason: Desensitization occurs when continuous drug exposure reduces receptor responsiveness, leading to tolerance. For example, opioid receptors downregulate or internalize with prolonged agonist exposure, decreasing drug efficacy. This explains the patient’s perception of “immunity” as the drug’s effect diminishes over time, making this the correct choice.
Choice D reason: The body does not produce antagonists to compete with drugs for receptor sites. Tolerance arises from receptor desensitization or metabolic changes (e.g., enzyme induction), not endogenous antagonist production. This mechanism is not a recognized pharmacological process for reduced drug effectiveness, making this choice incorrect.
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