A nurse teaches a patient who takes daily low-dose aspirin for protection against myocardial infarction and stroke to avoid also taking which medication?
Diphenhydramine [Benadryl]
Loratadine [Claritin]
Ibuprofen [Motrin]
Multivitamin
The Correct Answer is C
Choice A reason: Diphenhydramine, an antihistamine, does not significantly interact with aspirin’s antiplatelet effects. It primarily blocks histamine receptors, affecting allergies, not platelet aggregation. While it may cause drowsiness, it doesn’t increase bleeding risk or counteract aspirin’s cardiovascular benefits, making it safe to use concurrently with low-dose aspirin.
Choice B reason: Loratadine, a second-generation antihistamine, targets histamine receptors to relieve allergy symptoms. It has no known interaction with aspirin’s antiplatelet mechanism or bleeding risk. Its minimal side effect profile makes it compatible with low-dose aspirin for cardiovascular protection, so avoiding it is unnecessary in this context.
Choice C reason: Ibuprofen, an NSAID, competes with aspirin for COX-1 binding sites, reducing aspirin’s antiplatelet effect critical for preventing myocardial infarction and stroke. It also increases gastrointestinal bleeding risk when combined with aspirin, making it contraindicated for patients on low-dose aspirin therapy, thus the correct choice to avoid.
Choice D reason: Multivitamins do not interfere with aspirin’s antiplatelet action or increase bleeding risk. They provide supplemental nutrients without affecting COX-1 inhibition or platelet aggregation. There’s no pharmacological basis for avoiding multivitamins with low-dose aspirin, making this choice irrelevant for the patient’s cardiovascular regimen.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
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.
Correct Answer is B
Explanation
Choice A reason: Lipid-soluble drugs cross cell membranes quickly due to their affinity for lipid bilayers, leading to predictable, rapid absorption. Their onset is not unpredictable but typically faster than water-soluble drugs, especially via routes like intravenous or transdermal, making this choice incorrect for lipid-soluble drugs.
Choice B reason: Lipid-soluble drugs, like fentanyl, rapidly cross lipid-rich cell membranes, including the blood-brain barrier, leading to quick onset of action. This is due to their high partition coefficient, allowing fast diffusion into tissues, making rapid effect onset the correct expectation for the nurse.
Choice C reason: Lipid-soluble drugs have faster onset than water-soluble drugs due to easier membrane penetration. Slow effects are more typical of water-soluble or poorly absorbed drugs. Lipid solubility enhances rapid distribution and action, making this choice incorrect for the expected effect timeline.
Choice D reason: Osmosis refers to water movement across membranes, not drug absorption. Lipid-soluble drugs diffuse through lipid bilayers, not via osmosis, which is irrelevant to their pharmacokinetics. This choice is scientifically inaccurate for describing the onset of lipid-soluble drug effects.
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