The nurse is preparing to administer morning medications to a patient who has been newly diagnosed with tuberculosis. The patient asks, "Why do I have to take so many different drugs?" Which response by the nurse is correct?
Your prescriber hopes that at least one of these drugs will work to fight the tuberculosis.
Using more than one drug can help to reduce side effects.
Using multiple drugs enhances the effect of each drug.
Taking multiple drugs is recommended because more drugs are becoming resistant to TB drug therapy.
The correct answer is: c) Using multiple drugs enhances the effect of each drug.
The Correct Answer is C
Choice A reason: The purpose of multiple drugs in tuberculosis treatment is not to hope one works but to ensure comprehensive bacterial eradication. Combination therapy targets different aspects of Mycobacterium tuberculosis, preventing resistance and ensuring efficacy, as single-drug therapy is ineffective and promotes resistant strains.
Choice B reason: Multiple drugs do not primarily reduce side effects; they increase the likelihood of adverse effects due to cumulative toxicity (e.g., hepatotoxicity from isoniazid and rifampin). The rationale for combination therapy is to enhance efficacy and prevent resistance, not to mitigate side effects, making this incorrect.
Choice C reason: Combination therapy (e.g., isoniazid, rifampin, ethambutol, pyrazinamide) enhances efficacy by targeting different bacterial populations and metabolic states of Mycobacterium tuberculosis. This synergistic approach ensures rapid bacterial killing, prevents resistance, and shortens treatment duration, making it the standard for effective tuberculosis management.
Choice D reason: The use of multiple drugs is not because drugs are becoming resistant but to prevent resistance development. Combination therapy overwhelms Mycobacterium tuberculosis with multiple mechanisms, reducing the chance of resistant mutants surviving. Resistance occurs with inadequate or monotherapy, not as a rationale for combination therapy.
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 A
Explanation
Choice A reason: Gentamicin, an aminoglycoside, causes ototoxicity, manifesting as ringing in the ears (tinnitus). It damages cochlear hair cells, leading to hearing loss or balance issues. Monitoring for tinnitus is critical, as ototoxicity is often irreversible, requiring dose adjustment or discontinuation to prevent further auditory damage.
Choice B reason: Elevated WBC count is not a typical indicator of gentamicin toxicity. Gentamicin’s primary toxicities are nephrotoxicity and ototoxicity. Elevated WBCs suggest infection or inflammation, not a direct effect of gentamicin, which targets bacterial protein synthesis, making this an incorrect monitoring parameter.
Choice C reason: Decreased BUN levels are not associated with gentamicin toxicity. Gentamicin causes nephrotoxicity, increasing BUN and creatinine due to renal tubular damage. Monitoring for elevated, not decreased, BUN is essential to detect kidney injury early, making this an incorrect toxicity indicator.
Choice D reason: Increased body temperature is not a direct indicator of gentamicin toxicity. Fever may indicate infection persistence or a drug reaction, but gentamicin’s primary toxicities are ototoxicity and nephrotoxicity. Monitoring for tinnitus or renal function changes is more relevant than temperature for toxicity assessment.
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