Which of the following drugs is most effective in converting a patient with atrial fibrillation into sinus rhythm?

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ATI RN Pharmacology Online Practice 2019 A Questions

Question 1 of 5

Which of the following drugs is most effective in converting a patient with atrial fibrillation into sinus rhythm?

Correct Answer: B

Rationale: Converting atrial fibrillation (AF) to sinus rhythm requires cardioversion or antiarrhythmics. Digoxin controls rate, not rhythm, ineffective for conversion. Atenolol, a beta-blocker, and diltiazem, a calcium channel blocker, manage rate, not rhythm restoration. Lidocaine treats ventricular arrhythmias. Amiodarone, a class III antiarrhythmic, prolongs repolarization, effectively converting AF to sinus rhythm, especially in acute settings, outperforming others. Its broad-spectrum action is key in AF management, balancing efficacy and safety.

Question 2 of 5

A client has benign prostatic hyperplasia (BPH) and hypertension. Which medication could the client safely receive for hypertension?

Correct Answer: A

Rationale: Terazosin, an alpha-1 blocker, treats hypertension and benign prostatic hyperplasia (BPH) by relaxing vascular and prostate smooth muscle, lowering blood pressure and easing urinary flow. Sildenafil, for erectile dysfunction, doesn't address hypertension or BPH and may drop blood pressure, risking complications. Finasteride shrinks the prostate for BPH but doesn't affect hypertension, missing the dual need. Tamsulosin, also for BPH, can cause hypotension but isn't used routinely for hypertension management. Terazosin's dual efficacy makes it safe and suitable, addressing both conditions without worsening either, unlike alternatives lacking hypertensive benefits or posing risks.

Question 3 of 5

The nursing instructor prepares to teach student nurses about how mean effective doses of medications are related to clinical practice. As a result of the instruction, what is the best understanding of the student nurses?

Correct Answer: D

Rationale: Mean effective dose (ED50) affects 50% of a population, but individuals vary-some need more or less due to metabolism, weight, or genetics, a clinical reality. Severe side effects aren't 50%-that's toxicity. Ethnic differences influence response, but dose variation is broader. No effect in 50% misreads ED50. Dose adjustment reflects individual pharmacokinetics, key to practice.

Question 4 of 5

The patient is receiving the benzodiazepine clonazepam (Klonopin) for the treatment of panic attacks. What is an important medication outcome for this patient as it relates to safety?

Correct Answer: D

Rationale: Clonazepam, a benzo, risks withdrawal (e.g., seizures) if stopped abruptly-patients knowing this ensures safe taper, per safety. Stevens-Johnson isn't linked-rash is rare. No diet restrictions apply (unlike MAOIs). Blood work isn't routine for benzos. Abrupt cessation's danger is key, protecting against rebound.

Question 5 of 5

A 6-year-old boy presents to his pediatrician for followup of recurrent hay fever and asthma. He usually has two to three attacks per week. For symptom control, he uses an albuterol inhaler, but his parents would like to try something more. They would like him to take something that would lessen the amount of attacks he has. Although corticosteroids would probably work best for prophylaxis, they are contraindicated in children. Which of the following drugs would decrease the amount of asthma attacks by preventing an arachidonic acid derivative from binding to its receptor?

Correct Answer: D

Rationale: Asthma attacks in this case are driven by inflammation, often mediated by leukotrienes, which are arachidonic acid derivatives. The goal is to reduce the frequency of attacks by targeting this pathway. Aspirin inhibits cyclooxygenase (COX), reducing prostaglandins but not leukotrienes, and may even worsen asthma in some patients. Celecoxib is a selective COX-2 inhibitor, also irrelevant to leukotrienes. Ipratropium is an anticholinergic bronchodilator, effective for acute symptom relief but not prophylaxis via arachidonic acid pathways. Montelukast is a leukotriene receptor antagonist, directly preventing leukotrienes from binding to their receptors, thus reducing inflammation and attack frequency. Zileuton (E), while a leukotriene synthesis inhibitor, isn't the best choice here as the question specifies receptor binding prevention, not synthesis inhibition. Montelukast aligns perfectly with the mechanism described, making it the correct answer.

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