What advantage does loratadine have compared with traditional antihistamines such as diphenhydramine?
Decreased risk of cardiac dysrhythmias
Minimal gastrointestinal upset
Less sedative effect
Increase in bronchodilation
The Correct Answer is C
Choice A reason: Loratadine has no significant advantage in reducing cardiac dysrhythmias compared to diphenhydramine. Both are H1 receptor antagonists, with minimal cardiac effects at therapeutic doses. Older antihistamines like terfenadine had dysrhythmia risks, but loratadine and diphenhydramine are not primarily associated with this issue.
Choice B reason: Loratadine causes minimal gastrointestinal upset, but this is not its primary advantage over diphenhydramine. Both antihistamines have low gastrointestinal side effects, with diphenhydramine’s anticholinergic effects causing more dry mouth. Loratadine’s key benefit is reduced CNS penetration, minimizing sedation.
Choice C reason: Loratadine, a second-generation antihistamine, has less sedative effect than diphenhydramine, a first-generation antihistamine. Its reduced ability to cross the blood-brain barrier minimizes H1 receptor blockade in the CNS, decreasing drowsiness, making it ideal for daytime use in allergic conditions.
Choice D reason: Neither loratadine nor diphenhydramine significantly increases bronchodilation. Antihistamines block histamine-mediated allergic responses, not beta-2 receptors responsible for bronchodilation. Bronchodilation is achieved with beta-agonists like albuterol, making this an incorrect advantage for loratadine over traditional antihistamines.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A reason: Drowsiness is not a systemic effect of inhaled albuterol, a beta-2 agonist. Albuterol stimulates beta-adrenergic receptors, increasing cyclic AMP, which can cause CNS stimulation, not sedation. Drowsiness is more associated with antihistamines or other CNS-depressant drugs, not bronchodilators like albuterol.
Choice B reason: Bradycardia is unlikely with albuterol, which activates beta-2 receptors and, to a lesser extent, beta-1 receptors in the heart, potentially causing tachycardia. Systemic absorption of inhaled albuterol can increase heart rate, not decrease it, as it stimulates sympathetic activity, making this incorrect.
Choice C reason: Heartburn is not a recognized systemic effect of inhaled albuterol. While gastrointestinal irritation may occur with oral beta-agonists, inhaled albuterol has minimal systemic absorption, targeting airway smooth muscle. Its side effects are primarily cardiovascular or neurological, not gastrointestinal, making this an incorrect choice.
Choice D reason: Palpitations are a possible systemic effect of inhaled albuterol due to its beta-adrenergic stimulation. Even with low systemic absorption, albuterol can stimulate cardiac beta-1 receptors, increasing heart rate and causing palpitations. This is a known side effect, particularly in sensitive patients or with overuse.
Correct Answer is D
Explanation
Choice A reason: Fibric acid derivatives, like fenofibrate, lower triglycerides by activating PPAR-alpha, reducing VLDL production. They are not commonly associated with myopathy, though gastrointestinal upset or liver enzyme elevation may occur. Myopathy is more characteristic of statins, making this an incorrect class for monitoring.
Choice B reason: Niacin lowers lipids by inhibiting VLDL synthesis but is not significantly linked to myopathy. Its primary side effects include flushing and hepatotoxicity due to prostaglandin release and metabolic stress. Muscle pain is a hallmark of statins, not niacin, making this incorrect.
Choice C reason: Bile acid sequestrants, like cholestyramine, bind bile acids, reducing cholesterol absorption. They cause gastrointestinal side effects like constipation but not myopathy. Their mechanism does not affect muscle tissue, unlike statins, which inhibit HMG-CoA reductase, making this class irrelevant for myopathy monitoring.
Choice D reason: Statins, like simvastatin, inhibit HMG-CoA reductase, reducing cholesterol synthesis. They can cause myopathy by disrupting muscle cell membranes or mitochondrial function, leading to muscle pain or rare rhabdomyolysis. Monitoring for myopathy is critical, as it can progress to severe muscle damage, making this the correct class.
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