1,477 Pharmacology questions written for the NCLEX-RN, each with a rationale explaining why the correct answer is correct and why the others are not. Free, no account required. 10 examples are shown below.
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The correct answer is anaphylactic reaction to penicillin. The timing (symptoms within 5 minutes of first exposure), classic triad of symptoms (cutaneous: urticaria; respiratory: stridor; cardiovascular: hypotension), and lack of alternative explanations confirm anaphylaxis. Even though the patient had no known penicillin allergy, anaphylaxis can occur on first exposure due to prior sensitization from structurally similar compounds. Septic shock would not cause urticaria or stridor. Serum sickness has delayed onset. Anxiety attacks do not cause hypotension or stridor.
Spironolactone is a potassium-sparing diuretic that can cause hyperkalemia. Clients should avoid foods high in potassium, such as bananas, oranges, potatoes, and tomatoes. Monitoring potassium levels is essential while taking this medication.
Guaifenesin is an expectorant that works by thinning and loosening mucus in the airways, making it easier to cough up. Adequate hydration enhances this effect. It does NOT suppress cough (that's an antitussive), and it should not be taken with other cough suppressants unless specifically ordered.
Olanzapine is a second-generation antipsychotic associated with metabolic syndrome, including hyperglycemia and diabetes mellitus. A fasting blood glucose of 145 mg/dL indicates hyperglycemia, which requires prompt intervention. While weight gain is common and dry mouth and sedation can occur, the elevated glucose level poses the most serious risk and requires immediate attention.
Bisphosphonates like alendronate must be taken with a full glass of plain water (not other beverages) while sitting or standing upright, and clients must remain upright for at least 30 to 60 minutes after taking the medication. This prevents esophageal irritation and ulceration. The medication should be taken first thing in the morning, at least 30 minutes before any food, drink, or other medications.
In acute pulmonary edema, furosemide reduces preload by causing rapid diuresis, which decreases left ventricular filling pressure and pulmonary congestion. This leads to improved oxygenation. An increase in oxygen saturation from 88% to 96% indicates improved pulmonary gas exchange and reduced pulmonary edema. While decreased blood pressure and increased urine output are expected effects, improved oxygen saturation is the most direct indicator of therapeutic response in pulmonary edema.
Acetazolamide is a carbonic anhydrase inhibitor and is chemically related to sulfonamides. Patients with sulfonamide allergies may have cross-reactivity and are at risk for severe allergic reactions including Stevens-Johnson syndrome. The nurse should withhold the medication and notify the provider so an alternative medication can be prescribed. This is a contraindication, not just a precaution requiring monitoring.
Amiodarone is a potent inhibitor of the CYP3A4 enzyme, which metabolizes simvastatin. Co-administration can significantly increase simvastatin levels, raising the risk of severe rhabdomyolysis (muscle breakdown). The nurse should notify the provider, who may need to reduce the simvastatin dose significantly or switch to a different statin (such as rosuvastatin or pravastatin, which have less CYP3A4 metabolism). This is a clinically significant drug interaction requiring provider intervention.
The answer: A — Hold the morning dose of repaglinide the day of the procedure Think of it this way: Repaglinide only works when you eat — it stimulates insulin release at mealtime. Give it to a fasting patient with no food coming, and you trigger insulin release with no glucose to absorb. The result is hypoglycemia with nothing to prevent it. Why A is right: Repaglinide (Prandin) is a meglitinide — a short-acting insulin secretagogue taken immediately before each meal. For any NPO (nothing by mouth) procedure, the meglitinide dose for that meal must be withheld to prevent hypoglycemia. This is communicated to the provider and appropriate glucose monitoring is arranged during the procedure. Why the others are wrong: - B: Continuing repaglinide unchanged on the day of a fasting procedure risks hypoglycemia. The dose must be withheld. - C: Giving the medication with a light breakfast violates the NPO requirement before cardiac catheterization and is clinically inappropriate. - D: Doubling the evening dose to 'compensate' would cause dangerous nocturnal hypoglycemia and provides no clinical benefit. Never double doses. Remember: Repaglinide = taken WITH each meal. No meal = no dose. Hold it when the patient is NPO. Technical note: Meglitinides (repaglinide, nateglinide) have very short onset and duration — designed specifically for mealtime use. Without food, they carry the same hypoglycemia risk as sulfonylureas.
The answer: B (Gastrointestinal bleeding) Think of it this way: The stomach has a natural armor — a mucus layer — that protects it from its own acid. That armor is maintained partly by prostaglandins. NSAIDs block the enzyme (COX-1) that makes those protective prostaglandins. Without the armor, the stomach's acid starts eroding through the stomach wall. Long-term NSAID use is like removing that armor and leaving the stomach unprotected day after day. Why B is right: NSAIDs inhibit COX-1, which reduces the synthesis of prostaglandins that normally protect the gastric and intestinal mucosa. Long-term NSAID use leads to a gradual breakdown of this protection, resulting in gastric ulcers and GI bleeding. This is the most common and serious adverse effect of chronic NSAID therapy. Why the others are wrong: - A: Constipation is a classic side effect of opioids (morphine, codeine, oxycodone), not NSAIDs. NSAIDs can cause GI irritation, nausea, and diarrhea — the opposite of constipation. - C: Severe sedation is associated with opioids, benzodiazepines, and other CNS depressants — not NSAIDs. NSAIDs are not sedating. - D: Physical dependence is a feature of opioids and CNS depressants. NSAIDs do not cause physical dependence. Remember: Long-term NSAIDs = GI bleeding risk. Patients at high risk (elderly, history of ulcer, anticoagulant use) should use the lowest effective dose or consider a COX-2 inhibitor with a proton pump inhibitor. Technical note: NSAIDs inhibit both COX-1 (gastroprotective prostaglandins) and COX-2 (inflammatory prostaglandins). COX-2 selective inhibitors (celecoxib) spare COX-1 and have less GI toxicity. Risk of NSAID-induced GI bleeding is increased by concomitant use of corticosteroids, anticoagulants, and aspirin.
