A patient who has started drug therapy for tuberculosis wants to know how long he will be on the medications. Which response by the nurse is correct?
Drug therapy will last until the symptoms have stopped.
You will be on this drug therapy for the rest of your life.
You should expect to take these drugs for 6 to 9 months or more.
Drug therapy will continue until the tuberculosis develops resistance.
The Correct Answer is C
Choice A reason: Tuberculosis therapy does not stop when symptoms resolve, as residual bacteria may persist, leading to relapse. Standard regimens (e.g., isoniazid, rifampin) last 6-9 months to ensure complete eradication of Mycobacterium tuberculosis, guided by sputum cultures and imaging, not just symptom cessation.
Choice B reason: Lifelong tuberculosis therapy is not typical for active disease. Standard treatment lasts 6-9 months for drug-susceptible tuberculosis, achieving cure in most cases. Lifelong therapy may apply to certain chronic infections, but for tuberculosis, finite regimens are effective, making this statement incorrect.
Choice C reason: Standard treatment for active tuberculosis involves a 6- to 9-month regimen of first-line drugs (isoniazid, rifampin, ethambutol, pyrazinamide). This duration ensures complete bacterial eradication, preventing relapse or resistance. Longer durations may be needed for resistant strains or extrapulmonary disease, aligning with clinical guidelines.
Choice D reason: Therapy does not continue until resistance develops, as this would indicate treatment failure. The goal is to eradicate Mycobacterium tuberculosis before resistance emerges, using combination therapy for 6-9 months. Continuing until resistance occurs is counterproductive and increases the risk of multidrug-resistant tuberculosis.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A reason: Dehydration is not a primary concern with intravenous dexamethasone, a corticosteroid. While corticosteroids can cause fluid retention due to mineralocorticoid effects, leading to edema, they do not typically cause dehydration. Monitoring fluid status is important, but hypokalemia is a more direct electrolyte imbalance associated with corticosteroid use.
Choice B reason: Hypoglycemia is not a common side effect of dexamethasone. This corticosteroid increases blood glucose levels by promoting gluconeogenesis and insulin resistance, potentially causing hyperglycemia, especially in diabetic patients. Monitoring for elevated glucose is more relevant than hypoglycemia, which is not typically induced by corticosteroids.
Choice C reason: Hyponatremia is less likely with dexamethasone, which has minimal mineralocorticoid activity compared to drugs like hydrocortisone. It may cause fluid retention, but significant sodium depletion is rare. Hypokalemia is a more prominent electrolyte disturbance due to potassium excretion induced by corticosteroid effects on renal tubules.
Choice D reason: Hypokalemia is a known side effect of dexamethasone, as corticosteroids enhance renal potassium excretion by stimulating mineralocorticoid receptors. This disrupts electrolyte balance, potentially causing muscle weakness, arrhythmias, or fatigue. Monitoring serum potassium levels is critical during intravenous administration to prevent complications from hypokalemia in patients receiving dexamethasone.
Correct Answer is A
Explanation
Choice A reason: Garlic can enhance warfarin’s anticoagulant effect by inhibiting platelet aggregation and potentially increasing INR, raising bleeding risk. Its sulfur compounds may also induce hepatic enzymes, affecting warfarin metabolism. Patients on warfarin should avoid high garlic intake to maintain stable anticoagulation and prevent hemorrhage.
Choice B reason: Acetaminophen has no significant interaction with garlic. Acetaminophen is metabolized by the liver, primarily via glucuronidation, and garlic’s effects on platelet function or enzymes do not notably affect its pharmacokinetics or analgesic efficacy, making this an unlikely interaction concern.
Choice C reason: Phenytoin, an anticonvulsant, is metabolized by hepatic CYP450 enzymes, but garlic’s weak enzyme induction does not significantly alter phenytoin levels. Garlic’s primary interaction is with anticoagulants like warfarin, not anticonvulsants, making this drug less relevant for garlic-related concerns.
Choice D reason: Digoxin has no major interaction with garlic. Digoxin’s pharmacokinetics are primarily renal, and garlic’s effects on platelets or minor enzyme induction do not significantly alter digoxin levels or cardiac effects. Warfarin’s bleeding risk is more impacted by garlic’s antiplatelet properties.
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