NAPLEX Quiz: Errors Omissions And Duplication

What this quiz covers

This quiz focuses on Errors Omissions And Duplication, giving you a quick way to practice the rules, question types, and explanations that matter most for NAPLEX.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

Question 1

1. Therapeutic duplication because immediate-release and extended-release oxycodone should never be used together
2. Omission of a bowel regimen escalation; add a stimulant laxative (e.g., senna) due to chronic opioid use (correct answer)
3. Contraindication because sertraline cannot be used with any opioid analgesic
4. Formulation error because oxycodone extended-release should be changed to immediate-release 10 mg every 12 hours

Explanation: This question tests recognition of inadequate constipation prophylaxis in chronic opioid therapy. The patient is on scheduled extended-release oxycodone plus immediate-release for breakthrough pain but only has docusate (a stool softener) for constipation prevention. Chronic opioid use requires a stimulant laxative (like senna or bisacodyl) in addition to a stool softener for adequate bowel regimen. Option A is incorrect as combining long-acting and short-acting opioids is appropriate pain management. Option C is false as sertraline can be used with opioids. Option D suggests an inappropriate formulation change. The clinical pearl is that all patients on chronic opioids require both a stool softener AND a stimulant laxative; docusate alone is insufficient for opioid-induced constipation prevention.

Question 2

1. Check potassium and serum creatinine within 3–7 days of initiation and again at 1 month, then periodically (correct answer)
2. Check INR weekly because spironolactone increases warfarin effect
3. Check hemoglobin A1c in 2 weeks to monitor for spironolactone-induced hyperglycemia
4. No lab monitoring is needed for spironolactone at 25 mg daily

Explanation: This question assesses appropriate laboratory monitoring for aldosterone antagonists like spironolactone in patients with heart failure with reduced ejection fraction (HFrEF). The key patient-specific factors include the initiation of spironolactone at 25 mg daily alongside an ACE inhibitor (lisinopril), with baseline potassium at 4.9 mEq/L (upper normal limit) and serum creatinine at 1.3 mg/dL indicating potential renal impairment risk. Choice A is the best monitoring plan as it checks potassium and serum creatinine within 3–7 days, at 1 month, and periodically thereafter to detect hyperkalemia or worsening renal function early, which are common risks with this combination. Choice B is incorrect because the patient is not on warfarin, so INR monitoring for a spironolactone-warfarin interaction is irrelevant; choice C is suboptimal as spironolactone does not typically cause significant hyperglycemia requiring A1c checks in 2 weeks. Choice D is inappropriate because spironolactone requires routine monitoring due to its potassium-sparing effects, especially in HFrEF patients on renin-angiotensin system inhibitors. A transferable clinical pearl is that in heart failure management, aldosterone antagonists necessitate close electrolyte and renal function surveillance to prevent life-threatening complications like hyperkalemia. This framework involves tailoring monitoring frequency based on baseline labs and concurrent medications that affect potassium or renal clearance.

Question 3

1. Stop apixaban and continue warfarin 5 mg by mouth daily with international normalized ratio monitoring (correct answer)
2. Continue both apixaban and warfarin because atrial fibrillation requires dual anticoagulation
3. Add aspirin 81 mg by mouth daily to improve stroke prevention in atrial fibrillation
4. Switch metoprolol succinate extended-release to metoprolol tartrate 50 mg by mouth twice daily to reduce fatigue

Explanation: This question tests recognition of therapeutic duplication with anticoagulants. The patient is receiving both apixaban (a direct oral anticoagulant) and warfarin (a vitamin K antagonist) for atrial fibrillation, which represents dangerous duplication. Using two anticoagulants simultaneously significantly increases bleeding risk without additional benefit, as evidenced by the patient's low hemoglobin suggesting possible bleeding. Option A correctly identifies the need to stop one anticoagulant and continue monotherapy. Option B is incorrect because dual anticoagulation is not indicated for atrial fibrillation. Option C would further increase bleeding risk by adding antiplatelet therapy. Option D addresses a non-critical issue. The clinical pearl is that anticoagulant monotherapy is standard for atrial fibrillation; combining anticoagulants is rarely indicated and significantly increases bleeding risk.

Question 4

1. Clopidogrel 75 mg by mouth daily for secondary stroke prevention
2. Aspirin 81 mg by mouth daily for secondary stroke prevention (correct answer)
3. Warfarin with an international normalized ratio goal of 2–3 for secondary stroke prevention
4. Dipyridamole/aspirin extended-release 25 mg/200 mg by mouth twice daily for secondary stroke prevention

Explanation: This question tests knowledge of secondary stroke prevention after transient ischemic attack (TIA). The patient experienced a TIA 2 weeks ago and requires antiplatelet therapy for secondary prevention. Aspirin 81 mg daily is the first-line antiplatelet agent for secondary stroke prevention and is notably absent from her regimen. Clopidogrel 75 mg daily (option A) is an alternative first-line option but not superior to aspirin. Warfarin (option C) is not indicated for TIA without atrial fibrillation or other cardioembolic source. Dipyridamole/aspirin (option D) is an alternative but not preferred over aspirin monotherapy due to increased side effects. The clinical pearl is that all patients with TIA or ischemic stroke require antiplatelet therapy unless anticoagulation is indicated for another reason.

Question 5

1. Therapeutic duplication of alpha-1 blockers (tamsulosin and doxazosin) increasing hypotension risk (correct answer)
2. Sildenafil should be increased to 100 mg by mouth as needed due to urinary symptoms
3. Hydrochlorothiazide should be replaced with furosemide to improve benign prostatic hyperplasia symptoms
4. Tamsulosin should be switched to finasteride because alpha-1 blockers are contraindicated in men over 60 years

Explanation: This question tests identification of therapeutic duplication with alpha-1 blockers. The patient is receiving both tamsulosin and doxazosin, which are both alpha-1 blockers used for benign prostatic hyperplasia (BPH). This duplication increases the risk of orthostatic hypotension, as evidenced by the patient's low blood pressure (102/64 mmHg). Using two alpha-1 blockers provides no additional benefit for BPH symptoms while significantly increasing adverse effects. Option B incorrectly suggests increasing sildenafil dose for urinary symptoms. Option C incorrectly relates diuretic choice to BPH. Option D contains false information about age contraindications. The clinical pearl is that combining alpha-1 blockers for BPH is inappropriate and increases hypotension risk; if monotherapy is inadequate, add a 5-alpha reductase inhibitor instead.

Question 6

1. Continue sitagliptin 100 mg by mouth daily because the hemoglobin A1c is near goal
2. Reduce sitagliptin to 25 mg by mouth daily due to creatinine clearance 28 mL/min (correct answer)
3. Increase metformin to 1500 mg by mouth twice daily to improve glycemic control
4. Reduce atorvastatin to 10 mg by mouth nightly due to elevated serum creatinine

Explanation: This question tests the ability to identify inappropriate dosing in chronic kidney disease. The patient has severe renal impairment with a creatinine clearance of 28 mL/min, requiring dose adjustment for renally eliminated medications. Sitagliptin requires dose reduction to 25 mg daily when CrCl is <30 mL/min to prevent drug accumulation and potential hypoglycemia. Metformin is contraindicated when eGFR <30 mL/min due to lactic acidosis risk, making option C incorrect. Atorvastatin does not require dose adjustment for renal impairment, making option D incorrect. The clinical pearl is to always calculate creatinine clearance and adjust doses of renally eliminated drugs accordingly, particularly DPP-4 inhibitors which accumulate in kidney disease.

Question 7

1. Unnecessary duplication of proton pump inhibitors; use a single PPI at an appropriate dose and evaluate ongoing need (correct answer)
2. Calcium carbonate should be stopped because it causes GERD
3. Add ranitidine 150 mg by mouth twice daily in addition to both PPIs
4. Switch both PPIs to esomeprazole 20 mg every other day to improve control

Explanation: This question tests recognition of therapeutic duplication in acid-suppressive therapy for GERD. The key patient-specific factor is concurrent omeprazole and pantoprazole, both PPIs, leading to hypomagnesemia and potential overuse without improved control. Using a single PPI and evaluating need is the best choice to reduce risks and costs. Stopping calcium carbonate ignores its antacid role, adding ranitidine adds redundancy, and switching to esomeprazole maintains duplication. These distractors perpetuate overlap or introduce unnecessary agents. A clinical pearl is that dual PPI therapy offers no benefit over single and increases adverse effects like hypomagnesemia or infections. In GERD management, de-escalate to the lowest effective dose or H2RA if possible, assessing symptoms periodically.

Question 8

1. Docusate 100 mg by mouth twice daily as the only agent needed
2. A stimulant or osmotic laxative regimen (e.g., senna or polyethylene glycol) for opioid-induced constipation prophylaxis (correct answer)
3. Loperamide 2 mg by mouth daily for constipation prevention
4. Diphenhydramine 25 mg by mouth nightly to improve bowel motility

Explanation: This question tests prophylaxis for opioid-induced constipation in chronic pain management. The key patient-specific factor is chronic opioid use without a laxative, increasing constipation risk in an elderly patient. Adding a stimulant or osmotic laxative like senna or polyethylene glycol is the best choice for effective prophylaxis. Docusate alone is often insufficient, loperamide would worsen constipation, and diphenhydramine has no role in motility. These distractors are ineffective or counterproductive for OIC. A clinical pearl is that all patients on scheduled opioids should receive prophylactic laxatives, preferring stimulants over stool softeners for OIC. Use a decision framework of assessing bowel regimen in opioid users and escalating to osmotics if stimulants fail.

Question 9

1. Advise to continue lisinopril because blood pressure control is most important in pregnancy
2. Recommend stopping lisinopril and contacting the prescriber promptly to switch to a pregnancy-compatible antihypertensive (correct answer)
3. Reduce lisinopril to 5 mg daily and continue during pregnancy
4. Add potassium chloride 20 mEq daily to prevent lisinopril adverse effects

Explanation: This question tests recognition of teratogenic contraindications in pregnancy. The key patient-specific factor is the 10-week pregnancy, making lisinopril contraindicated due to fetal renal and cardiovascular risks. Recommending to stop lisinopril and contact the prescriber for a safer alternative like labetalol is the best choice for maternal-fetal safety. Continuing or reducing lisinopril exposes the fetus to harm, and adding potassium is irrelevant. These distractors prioritize BP over fetal risks inappropriately. A clinical pearl is that ACE inhibitors are pregnancy category D/X, requiring immediate discontinuation upon pregnancy confirmation. Use a framework of reviewing all medications for teratogenicity in reproductive-age women and switching to pregnancy-safe options promptly.

Question 10

1. Aspirin 81 mg by mouth daily (or another appropriate antiplatelet) for secondary stroke prevention (correct answer)
2. Rivaroxaban 20 mg by mouth daily for all stroke patients
3. Clonidine 0.3 mg by mouth twice daily for long-term prevention
4. Prednisone 10 mg by mouth daily to reduce vascular inflammation

Explanation: This question tests secondary prevention strategies after ischemic stroke. The key patient-specific factor is the history of ischemic stroke without atrial fibrillation, necessitating antiplatelet therapy for recurrence prevention. Adding aspirin 81 mg daily is the best choice as it reduces stroke risk by about 20% in non-cardioembolic cases. Rivaroxaban is not indicated without AF, clonidine lacks preventive evidence, and prednisone can increase vascular risks. These alternatives are inappropriate or harmful for secondary prevention. A clinical pearl is that aspirin monotherapy is first-line for secondary stroke prevention in non-AF patients, with dual therapy considered for high-risk cases. Use a decision framework of assessing stroke etiology (e.g., TOAST classification) to select antiplatelet vs. anticoagulant therapy.

Question 11

1. Dispense as written and counsel to take with food to reduce nausea
2. Contact prescriber to change to nitrofurantoin 100 mg by mouth twice daily for 5 days (if appropriate) due to penicillin anaphylaxis (correct answer)
3. Recommend adding diphenhydramine 25 mg by mouth every 6 hours as needed and dispense amoxicillin-clavulanate
4. Reduce amoxicillin-clavulanate to 500/125 mg by mouth twice daily and dispense

Explanation: This question tests recognition of contraindications due to drug allergies in antibiotic selection. The key patient-specific factor is the history of penicillin anaphylaxis, making amoxicillin-clavulanate contraindicated due to cross-reactivity risks. Contacting the prescriber to change to nitrofurantoin (if appropriate) resolves the contraindication while treating the UTI effectively. Dispensing as written or adding diphenhydramine ignores the severe allergy risk, and reducing the dose does not eliminate the contraindication. These alternatives could lead to anaphylaxis or inadequate treatment. A clinical pearl is that beta-lactam antibiotics like amoxicillin share cross-reactivity in true penicillin allergies, necessitating alternatives like nitrofurantoin for uncomplicated UTIs. Use a decision framework of verifying allergy history and selecting non-cross-reactive agents for safety.

Question 12

1. Stop one levothyroxine product and confirm the intended single daily dose with the prescriber; counsel on separating from calcium (correct answer)
2. Continue both levothyroxine doses and add propranolol 10 mg three times daily long term
3. Stop calcium carbonate and continue both levothyroxine products to normalize TSH
4. Switch levothyroxine to liothyronine 25 mcg by mouth twice daily and continue both levothyroxine products

Explanation: This question tests identification of therapeutic duplication in thyroid hormone replacement. The key patient-specific factor is the use of two levothyroxine doses concurrently, leading to overdose symptoms and suppressed TSH, compounded by calcium interference. Stopping one product, confirming the dose, and counseling on separation is the best choice to normalize thyroid function. Continuing both or adding propranolol risks thyrotoxicosis, stopping calcium ignores its need, and switching to liothyronine is unnecessary. These options perpetuate overdose or introduce unneeded drugs. A clinical pearl is to administer levothyroxine on an empty stomach, separating from calcium by 4 hours to optimize absorption. In hypothyroidism management, verify total daily dose and monitor TSH every 6-8 weeks after changes.

Question 13

1. Incorrect directions; fluticasone/salmeterol should be used as scheduled maintenance (e.g., 1 puff twice daily), not as needed (correct answer)
2. Duplication with albuterol; stop albuterol and use fluticasone/salmeterol as needed only
3. Dose is too low; increase to fluticasone/salmeterol 500/50 mcg every 4 hours as needed
4. Contraindication; inhaled corticosteroids are contraindicated in asthma

Explanation: This question tests appropriate use and directions for asthma controller medications. The key patient-specific factor is the prescription of fluticasone/salmeterol as 'as needed,' which is incorrect for a maintenance combination inhaler. Correcting to scheduled use (e.g., 1 puff BID) is the best choice to provide consistent control for persistent asthma. Stopping albuterol removes necessary rescue, increasing the dose promotes overuse, and inhaled corticosteroids are essential in asthma. These distractors lead to poor control or misuse. A clinical pearl is that ICS/LABA combinations like fluticasone/salmeterol are for daily maintenance, not PRN, to reduce exacerbations. In asthma management, distinguish controllers (scheduled) from relievers (PRN) using GINA guidelines for stepwise therapy.

Question 14

1. Wrong formulation dispensed; correct to bupropion sustained-release 150 mg by mouth twice daily as prescribed (correct answer)
2. Dose is too low; increase to bupropion immediate-release 300 mg twice daily
3. Therapy is duplicated; add sertraline 50 mg daily and stop bupropion
4. Contraindication exists; bupropion is contraindicated in all patients with insomnia

Explanation: This question tests identification of dispensing errors in antidepressant formulations. The key patient-specific factor is the dispensing of immediate-release bupropion instead of the prescribed sustained-release, leading to peak-related side effects like insomnia and anxiety. Correcting to sustained-release 150 mg BID is the best choice to restore the intended regimen and mitigate adverse effects. Increasing the dose or adding sertraline worsens risks, and bupropion is not contraindicated in insomnia but formulation matters. These alternatives either escalate side effects or misattribute the issue. A clinical pearl is that bupropion formulations differ in pharmacokinetics; sustained-release reduces peak effects compared to immediate-release. In dispensing, always verify formulation against the prescription to prevent errors in release profiles.

Question 15

1. Lisinopril 10 mg by mouth daily (or other ACE inhibitor/ARB/ARNI) as guideline-directed therapy (correct answer)
2. Diltiazem extended-release 240 mg by mouth daily for rate control
3. Ibuprofen 600 mg by mouth three times daily for inflammation
4. Digoxin 0.25 mg by mouth daily for all patients with HFrEF

Explanation: This question tests guideline-directed medical therapy for heart failure with reduced ejection fraction. The key patient-specific factor is the absence of an ACE inhibitor, ARB, or ARNI despite HFrEF with LVEF 30% and no contraindications. Adding lisinopril or similar is the best choice to improve survival and reduce hospitalizations. Diltiazem is not indicated without rate control needs, ibuprofen can worsen heart failure, and digoxin is not first-line for all HFrEF patients. These alternatives may cause fluid retention or lack evidence for broad use. A clinical pearl is that ACE inhibitors/ARBs/ARNIs are foundational in HFrEF unless contraindicated, titrated to target doses. Use a decision framework of the 'four pillars': beta-blocker, RAAS inhibitor, MRA, and SGLT2i for optimal HFrEF management.

Question 16

1. Discontinue one alpha-1 blocker (tamsulosin or doxazosin) and reassess symptoms and blood pressure (correct answer)
2. Add finasteride 5 mg by mouth daily and continue both alpha-1 blockers indefinitely
3. Increase doxazosin to 8 mg nightly to reduce dizziness
4. Stop lisinopril and continue both tamsulosin and doxazosin for blood pressure control

Explanation: This question tests identification of therapeutic duplication in alpha-1 blocker use for BPH and hypertension. The key patient-specific factor is concurrent tamsulosin and doxazosin, both alpha-1 blockers, causing hypotension and falls as seen with low BP and dizziness. Discontinuing one and reassessing is the best choice to minimize orthostatic risks while addressing symptoms. Adding finasteride maintains duplication, increasing doxazosin worsens hypotension, and stopping lisinopril removes needed BP control. These options exacerbate adverse effects or inadequately manage conditions. A clinical pearl is to avoid combining non-selective (doxazosin) and selective (tamsulosin) alpha-1 blockers due to additive hypotensive effects. In BPH regimens, prefer monotherapy and monitor for orthostasis, especially in hypertensives.

Question 17

1. Monitor renal function (serum creatinine/estimated creatinine clearance) and assess nephrotoxic NSAID use while on tenofovir (correct answer)
2. Monitor INR weekly because tenofovir increases warfarin effect
3. Monitor serum digoxin concentration due to interaction with tenofovir
4. No monitoring is needed once hepatitis B therapy is started

Explanation: This question tests monitoring for nephrotoxicity in antiviral therapy. The key patient-specific factor is the rising serum creatinine on tenofovir, exacerbated by concurrent nephrotoxic ibuprofen in a patient with declining CrCl. Monitoring renal function and assessing NSAID use is the best choice to prevent further kidney damage. Monitoring INR or digoxin is irrelevant as tenofovir does not interact with warfarin or digoxin significantly, and assuming no monitoring risks progression to CKD. These distractors overlook the primary toxicity concern. A clinical pearl is that tenofovir can cause Fanconi syndrome and renal impairment, worsened by NSAIDs; monitor CrCl every 3-6 months. Use a framework of baseline and periodic renal assessments, calculating CrCl trends to guide continuation or switching.

Question 18

1. Check INR within 3–5 days after starting trimethoprim-sulfamethoxazole and adjust warfarin as needed (correct answer)
2. Check hemoglobin A1c in 3 months to assess antibiotic response
3. Check troponin in 24 hours to monitor for warfarin toxicity
4. No additional monitoring is needed because the interaction is not clinically significant

Explanation: This question tests monitoring for drug interactions in anticoagulation therapy. The key patient-specific factor is the addition of trimethoprim-sulfamethoxazole, which potentiates warfarin's effect by inhibiting metabolism and vitamin K-producing bacteria. Checking INR within 3-5 days and adjusting warfarin is the best choice to prevent bleeding complications. Monitoring A1c or troponin is irrelevant to this interaction, and assuming no significance ignores the well-documented risk. These distractors fail to address the potential for supratherapeutic INR. A clinical pearl is that sulfonamides like TMP-SMX can increase INR by 20-50%, necessitating proactive monitoring. Use a framework of anticipating INR changes with interacting antibiotics and scheduling checks based on interaction onset, typically 3-7 days.

Question 19

1. Alendronate 70 mg by mouth once weekly (if no contraindications) for fracture risk reduction (correct answer)
2. Prednisone 20 mg by mouth daily to strengthen bones
3. Omeprazole 40 mg by mouth daily to improve calcium absorption
4. Furosemide 40 mg by mouth daily to increase bone density

Explanation: This question tests pharmacologic management of osteoporosis in postmenopausal women. The key patient-specific factor is the history of fragility fracture and low vitamin D, warranting antiresorptive therapy beyond supplements. Adding alendronate 70 mg weekly is the best choice for fracture risk reduction if no esophageal issues. Prednisone weakens bones, omeprazole does not aid calcium absorption, and furosemide can cause calcium loss. These alternatives worsen osteoporosis or lack benefit. A clinical pearl is that bisphosphonates like alendronate are first-line for high-risk osteoporosis, with vitamin D optimization to ≥30 ng/mL. Use a decision framework of assessing fracture risk (e.g., FRAX score) and initiating therapy if T-score ≤-2.5 or prior fracture.

Question 20

1. Colchicine hourly dosing is inappropriate and increases toxicity risk; recommend standard low-dose flare regimen with renal considerations (correct answer)
2. Allopurinol should be doubled during an acute flare to 600 mg daily
3. Lisinopril should be stopped because it causes gout flares
4. Colchicine should be replaced with probenecid due to kidney disease

Explanation: This question tests appropriate dosing for acute gout flare management in renal impairment. The key patient-specific factor is the CKD stage 3 with CrCl 38 mL/min, making hourly colchicine dosing excessive and toxic. Recommending a standard low-dose regimen (e.g., 1.2 mg followed by 0.6 mg in 1 hour) is the best choice to safely manage the flare. Doubling allopurinol during flares is incorrect and risky, stopping lisinopril ignores its minimal gout impact, and replacing with probenecid may not suit CKD. These distractors could worsen hyperuricemia or fail to address dosing error. A clinical pearl is to limit colchicine to 1.8 mg total over 1 hour in acute flares, with further reductions in CKD to avoid GI and neuromuscular toxicity. For gout therapy, use a framework of low-dose colchicine or NSAIDs for flares, avoiding dose escalations in renal compromise.