NAPLEX Quiz: Pharmacology

What this quiz covers

This quiz focuses on Pharmacology, 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. Selective β1 blockade in the heart causing reflex tachycardia
2. Nonselective β blockade inhibiting β2-mediated bronchodilation, potentially worsening bronchospasm (correct answer)
3. α1 agonism causing increased peripheral vasoconstriction and hypertension
4. Muscarinic receptor antagonism causing urinary retention

Explanation: This question tests understanding of beta-blocker receptor selectivity and contraindications. The key patient-specific factor is the history of asthma requiring albuterol use in a patient started on propranolol. Nonselective β blockade inhibiting β2-mediated bronchodilation (B) is correct - propranolol blocks both β1 and β2 receptors, antagonizing β2-mediated bronchodilation and potentially triggering severe bronchospasm in asthmatic patients. Selective β1 blockade causing reflex tachycardia (A) is incorrect as propranolol is nonselective and actually causes bradycardia. α1 agonism (C) and muscarinic antagonism (D) are not mechanisms of propranolol. The clinical framework is that nonselective beta-blockers (propranolol, nadolol, timolol) are contraindicated in asthma and COPD; if beta-blockade is necessary for anxiety in asthmatic patients, highly β1-selective agents like atenolol or metoprolol at low doses may be cautiously tried with close monitoring.

Question 2

1. Increase levothyroxine to 150 mcg daily
2. Continue levothyroxine 125 mcg daily and recheck TSH in 2–3 days
3. Decrease levothyroxine to 100 mcg daily and recheck TSH in 6–8 weeks (correct answer)
4. Stop levothyroxine permanently and start methimazole

Explanation: This question tests levothyroxine dose adjustment based on thyroid function tests. The key patient-specific factors are the suppressed TSH (0.05 mIU/L) and elevated free T4 (2.3 ng/dL) indicating iatrogenic hyperthyroidism after a recent dose increase. Decreasing levothyroxine to 100 mcg daily and rechecking TSH in 6-8 weeks (C) is correct - the patient is over-replaced with symptoms of hyperthyroidism requiring dose reduction back to the previous dose. Increasing to 150 mcg (A) would worsen hyperthyroidism. Continuing current dose with early recheck (B) is inappropriate as TSH takes 6-8 weeks to equilibrate after dose changes. Stopping levothyroxine and starting methimazole (D) is incorrect as this is medication-induced, not primary hyperthyroidism. The clinical framework is that levothyroxine has a half-life of 7 days, requiring 6-8 weeks to reach steady state; elderly patients often require 20-30% lower doses; and calcium supplements should be separated by 4 hours to avoid chelation.

Question 3

1. HLA-B*57:01 positivity increasing risk of abacavir hypersensitivity (correct answer)
2. CYP2C19 poor metabolizer status increasing clopidogrel response
3. SLCO1B1 decreased function increasing warfarin sensitivity
4. CYP2D6 ultrarapid metabolizer status decreasing simvastatin exposure

Explanation: This question tests knowledge of pharmacogenetic testing in HIV treatment. The key patient-specific factor is the family history of severe reaction to abacavir and the plan to start an abacavir-containing regimen. HLA-B57:01 positivity (A) is correct - this genetic variant is strongly associated with abacavir hypersensitivity syndrome, occurring in about 5-8% of patients, with nearly 100% negative predictive value when absent. CYP2C19 polymorphisms (B) affect clopidogrel activation, not abacavir. SLCO1B1 variants (C) affect statin myopathy risk, not warfarin sensitivity. CYP2D6 status (D) doesn't significantly affect simvastatin, which is primarily metabolized by CYP3A4. The clinical framework is that HLA-B57:01 testing is mandatory before starting abacavir per HIV treatment guidelines, and patients who test positive should never receive abacavir due to risk of potentially fatal hypersensitivity reaction.

Question 4

1. Obtain a random lithium level 1 hour after the next dose and adjust based on peak level
2. Obtain a 12-hour post-dose (trough) lithium level and monitor renal function closely (correct answer)
3. Monitor only liver function tests because lithium is primarily hepatically cleared
4. Monitor INR weekly because lithium potentiates warfarin anticoagulation

Explanation: This question tests lithium monitoring principles in the setting of drug-induced toxicity. The key patient-specific factors are the toxic lithium level (1.9 mEq/L), acute kidney injury (SCr 1.6 mg/dL), and recent NSAID initiation. Obtaining a 12-hour post-dose trough level and monitoring renal function (B) is correct - lithium levels must be drawn 12 hours post-dose for accurate interpretation, and renal function monitoring is crucial as lithium is 100% renally eliminated. Random levels 1 hour post-dose (A) are not standardized and will be falsely elevated. Liver function monitoring (C) is incorrect as lithium undergoes no hepatic metabolism. INR monitoring (D) is irrelevant as lithium doesn't affect coagulation. The clinical framework is that NSAIDs reduce renal lithium clearance by 20-60% through prostaglandin inhibition; lithium toxicity presents with GI, neurologic, and renal symptoms; management includes holding lithium and NSAIDs, IV hydration, and serial lithium levels every 6-12 hours.

Question 5

1. Start lisinopril and add potassium chloride supplementation to prevent hypokalemia
2. Start lisinopril but reduce furosemide to minimize ACE inhibitor cough
3. Avoid adding lisinopril until hyperkalemia is corrected and/or spironolactone is reduced/held (correct answer)
4. Start lisinopril and increase spironolactone to improve blood pressure control

Explanation: This question tests understanding of the dangerous drug interaction between ACE inhibitors and potassium-sparing diuretics. The key patient-specific factor is the baseline hyperkalemia (K 5.6 mEq/L) in a patient already on spironolactone, a potassium-sparing diuretic. Avoiding lisinopril until hyperkalemia is corrected (C) is the safest approach because adding an ACE inhibitor to spironolactone significantly increases hyperkalemia risk through dual mechanisms of reducing potassium excretion. Starting lisinopril with potassium supplementation (A) would dangerously worsen hyperkalemia. Reducing furosemide (B) is inappropriate as it helps promote potassium excretion and ACE inhibitor cough is unrelated to diuretic dose. Increasing spironolactone (D) would further elevate potassium levels. The clinical framework is to always check baseline potassium before starting ACE inhibitors/ARBs in patients on potassium-sparing diuretics, and consider temporarily holding or reducing the potassium-sparing agent when initiating RAAS blockade.

Question 6

1. Competitive inhibition of HMG-CoA reductase leading to reduced cholesterol synthesis
2. Prostaglandin-mediated vasodilation from increased PGD2/PGE2 release in the skin (correct answer)
3. Chelation of bile acids in the gut leading to increased bile acid excretion
4. Activation of PPAR-α increasing lipoprotein lipase activity and fatty acid oxidation

Explanation: This question tests understanding of niacin's mechanism for causing flushing, a common side effect. The key patient-specific factor is the timing of symptoms (30 minutes after first dose) and the characteristic presentation of facial flushing and itching. Prostaglandin-mediated vasodilation from increased PGD2/PGE2 release in the skin (B) is the correct mechanism - niacin activates GPR109A receptors on epidermal Langerhans cells, triggering prostaglandin release and cutaneous vasodilation. Competitive inhibition of HMG-CoA reductase (A) describes statins' mechanism, not niacin's side effect profile. Bile acid chelation (C) describes bile acid sequestrants like cholestyramine. PPAR-α activation (D) describes fibrates' mechanism of action. The clinical takeaway is that pre-treatment with aspirin 325 mg 30 minutes before niacin can reduce flushing by inhibiting prostaglandin synthesis, and extended-release formulations cause less flushing than immediate-release.

Question 7

1. Continue warfarin and TMP-SMX; recheck INR at the next routine visit
2. Hold warfarin doses and arrange prompt INR recheck; consider alternative antibiotic if feasible (correct answer)
3. Increase warfarin dose by 10–20% to overcome antibiotic effects
4. Add aspirin 325 mg daily to reduce thrombotic risk while INR is elevated

Explanation: This question tests management of a significant warfarin drug interaction. The key patient-specific factor is the dangerously elevated INR of 5.8 (goal 2.5-3.5) after starting TMP-SMX, without active bleeding. Holding warfarin and arranging prompt INR recheck (B) is correct - TMP-SMX inhibits CYP2C9, reducing warfarin metabolism and dramatically increasing INR, requiring immediate dose adjustment to prevent bleeding. Continuing both drugs (A) risks major bleeding with INR 5.8. Increasing warfarin (C) would worsen the supratherapeutic INR. Adding aspirin (D) would increase bleeding risk without addressing the elevated INR. The clinical framework is that TMP-SMX typically increases INR by 2-3 fold within 3-5 days through CYP2C9 inhibition; proactive warfarin dose reduction by 25-50% when starting TMP-SMX, with INR checks every 2-3 days, can prevent this dangerous interaction.

Question 8

1. No adjustment; use 300 mg PO TID
2. Avoid gabapentin because it is hepatically cleared
3. Use a reduced total daily dose with extended dosing interval (e.g., 300 mg PO once daily to BID) (correct answer)
4. Increase the dose due to reduced absorption in CKD

Explanation: This question tests the pharmacokinetic adjustment of gabapentin in renal impairment, as it is primarily renally excreted unchanged. The key patient-specific factor is the patient's CKD stage 4 with CrCl 22 mL/min, which reduces gabapentin clearance and increases toxicity risk. Using a reduced total daily dose with extended dosing interval (e.g., 300 mg PO once daily to BID) is the best choice to maintain efficacy while preventing accumulation and side effects like sedation. No adjustment is incorrect as it ignores renal dosing guidelines, and avoiding gabapentin due to hepatic clearance is wrong since it is renally cleared; increasing the dose would worsen toxicity. Clinically, calculate CrCl and consult renal dosing resources for gabapentin, typically reducing to 100–300 mg daily for CrCl <30 mL/min. In practice, monitor for CNS side effects and titrate slowly in CKD patients to optimize neuropathy management.

Question 9

1. Decrease warfarin dose because rifampin increases INR
2. Continue warfarin unchanged and recheck INR in 3 months
3. Increase warfarin dose with very frequent INR monitoring during rifampin therapy (correct answer)
4. Add fluconazole to counteract rifampin induction

Explanation: This question tests the pharmacokinetic induction of warfarin metabolism by rifampin, a potent CYP3A4 and CYP2C9 inducer, reducing anticoagulant effect. The key patient-specific factor is the subtherapeutic INR of 1.4 after 2 weeks of rifampin in a patient with a mechanical valve requiring higher INR goals. Increasing warfarin dose with very frequent INR monitoring during rifampin therapy is the best approach to restore therapeutic anticoagulation and prevent thrombosis. Decreasing warfarin is incorrect as it would further lower INR, and continuing unchanged or adding fluconazole ignores the induction effect. Clinically, anticipate up to 2–3 fold warfarin dose increases with rifampin, monitoring INR weekly initially. In practice, consider alternative anticoagulants like DOACs if induction interactions are unavoidable to maintain efficacy.

Question 10

1. Inhibition of SGLT2 in the proximal tubule causing glucosuria and osmotic diuresis (correct answer)
2. Blockade of DPP-4 causing antidiuretic hormone suppression
3. Activation of PPAR-$\gamma$ causing sodium retention
4. Stimulation of insulin release causing free-water loss

Explanation: This question tests the diuretic side effects of SGLT2 inhibitors like empagliflozin, promoting urinary glucose excretion. The key patient-specific factor is type 2 diabetes with recent empagliflozin start, causing polyuria and thirst from osmotic diuresis. Inhibition of SGLT2 in the proximal tubule causing glucosuria and osmotic diuresis is the correct mechanism, explaining the symptoms despite improving glucose control. DPP-4 blockade or PPAR-γ activation cause different effects like edema, not diuresis; insulin stimulation does not directly cause water loss. Clinically, counsel on transient volume depletion and monitor for dehydration. In practice, assess electrolytes and encourage hydration to manage SGLT2i side effects in diabetes care.

Question 11

1. Continue current regimen and recheck digoxin level in 6 months
2. Obtain a digoxin level 30 minutes after the next dose to confirm toxicity
3. Hold digoxin, correct electrolytes, and recheck a trough digoxin level (≥6 hours post-dose) (correct answer)
4. Switch to immediate IV digoxin and monitor peak levels daily

Explanation: This question tests digoxin toxicity monitoring, focusing on trough levels and electrolyte influences. The key patient-specific factor is hypokalemia (K 3.1 mEq/L) and elevated digoxin level (2.4 ng/mL), exacerbating toxicity symptoms like nausea and visual changes in heart failure. Holding digoxin, correcting electrolytes, and rechecking a trough level (≥6 hours post-dose) is the best strategy to confirm and manage toxicity while preventing arrhythmias. Continuing without change ignores toxicity, and checking 30 minutes post-dose measures peak, not trough; switching to IV increases risk without benefit. Clinically, digoxin toxicity is potentiated by hypokalemia, so replete potassium and monitor levels 5–7 days after changes. In practice, use lower doses (0.125 mg) in renal impairment and educate on toxicity signs for safe digoxin use in HF and AF.

Question 12

1. Rely only on total phenytoin level because it reflects free drug in hypoalbuminemia
2. Obtain a free phenytoin concentration (or adjust for albumin) and assess for toxicity (correct answer)
3. Measure INR weekly to monitor phenytoin effect
4. Monitor serum potassium due to phenytoin-induced hyperkalemia

Explanation: This question tests the monitoring of phenytoin in the context of hypoalbuminemia and drug interactions, where total levels may not reflect free (active) drug. The key patient-specific factor is low albumin (2.5 g/dL) and recent TMP-SMX initiation, which displaces phenytoin from protein binding and inhibits its metabolism, increasing free levels and toxicity symptoms like nystagmus. Obtaining a free phenytoin concentration (or adjusting for albumin) and assessing for toxicity is the best strategy to accurately evaluate active drug exposure. Relying only on total levels is incorrect as they underestimate free drug in hypoalbuminemia, while INR or potassium monitoring is irrelevant to phenytoin toxicity. Clinically, use the Winter-Tozer equation to correct total phenytoin: corrected = total / [(0.2 x albumin) + 0.1]. In practice, always measure free levels in altered protein states or interactions to guide dosing and prevent adverse effects.

Question 13

1. Continue both drugs; add coenzyme Q10 to prevent myopathy
2. Hold simvastatin during clarithromycin therapy and use an alternative antibiotic if possible (correct answer)
3. Increase simvastatin dose to maintain LDL lowering during infection
4. Add gemfibrozil to reduce muscle symptoms

Explanation: This question tests the pharmacokinetic interaction where clarithromycin inhibits CYP3A4, increasing simvastatin levels and rhabdomyolysis risk. The key patient-specific factor is concurrent use leading to elevated CK and myopathy symptoms in a patient with infection. Holding simvastatin during clarithromycin therapy and using an alternative antibiotic if possible is the best approach to prevent further muscle damage. Continuing both or adding coenzyme Q10 ignores the severe interaction, increasing dose worsens toxicity, and adding gemfibrozil compounds myopathy risk. Clinically, limit simvastatin to 10 mg with strong inhibitors or hold during short courses. In practice, check for CYP interactions and consider pravastatin alternatives to manage lipids safely during antibiotics.

Question 14

1. Continue glyburide; hypoglycemia is unrelated to renal function
2. Increase glyburide dose because reduced kidney function lowers effect
3. Discontinue glyburide and switch to an agent safer in CKD (e.g., glipizide) with appropriate dosing (correct answer)
4. Add insulin sliding scale and keep glyburide unchanged

Explanation: This question tests sulfonylurea adjustments in renal impairment, where glyburide's active metabolites accumulate, causing prolonged hypoglycemia. The key patient-specific factor is CKD stage 3 with CrCl ~35 mL/min, increasing hypoglycemia risk as seen with glucose 42 mg/dL. Discontinuing glyburide and switching to a safer agent in CKD (e.g., glipizide) with appropriate dosing is the best choice due to glipizide's hepatic metabolism. Continuing or increasing glyburide worsens risk, and adding insulin without change ignores the cause. Clinically, avoid glyburide if CrCl <50 mL/min and monitor glucose closely. In practice, prefer short-acting sulfonylureas or alternatives like DPP-4 inhibitors in renal patients to prevent hypoglycemic events.

Question 15

1. Inhibition of monoamine oxidase leading to decreased tyramine breakdown and excess catecholamines (correct answer)
2. Blockade of dopamine D2 receptors causing hypertensive crisis
3. Inhibition of COMT leading to serotonin depletion
4. Activation of GABA-A receptors causing sympathetic overactivity

Explanation: This question tests the pharmacodynamic interaction of monoamine oxidase inhibitors (MAOIs) like phenelzine with tyramine-rich foods, leading to hypertensive crisis. The key patient-specific factor is recent phenelzine initiation and ingestion of aged cheese/pepperoni, which contain tyramine that MAOIs prevent from being metabolized. Inhibition of monoamine oxidase leading to decreased tyramine breakdown and excess catecholamines is the correct mechanism, explaining the headache, palpitations, and hypertension. Dopamine D2 blockade or COMT inhibition do not involve tyramine, and GABA activation causes sedation, not sympathetic overactivity. Clinically, counsel patients on tyramine-restricted diets when starting MAOIs to avoid crises. In practice, consider MAOI washout periods and emergency treatments like phentolamine for similar interactions.

Question 16

1. Continue both agents and add ondansetron for nausea
2. Discontinue tramadol and use a non-serotonergic analgesic alternative (correct answer)
3. Increase tramadol dose to overcome reduced analgesic effect
4. Switch duloxetine to fluoxetine to reduce serotonergic toxicity

Explanation: This question tests the pharmacodynamic interaction of serotonin syndrome from combining duloxetine (an SNRI) and tramadol (a weak serotonin reuptake inhibitor and opioid). The key patient-specific factor is the recent addition of tramadol to duloxetine therapy, leading to symptoms like nausea, sweating, tremor, and agitation indicative of serotonergic excess. Discontinuing tramadol and using a non-serotonergic analgesic alternative is the best choice as it resolves the interaction while managing pain without risking severe serotonin syndrome complications. Continuing both with ondansetron is incorrect as it may mask symptoms without addressing the root cause, and increasing tramadol would exacerbate serotonergic effects. Switching to fluoxetine worsens the risk due to its strong serotonergic profile. Clinically, screen for serotonergic agents before adding new medications and educate patients on syndrome symptoms. In practice, prefer non-serotonergic options like acetaminophen or gabapentin for pain in patients on SNRIs to avoid similar interactions.

Question 17

1. Stop amiodarone and continue warfarin at the same dose
2. Increase warfarin dose by 10–20% due to reduced anticoagulant effect
3. Hold 1–2 doses of warfarin and reduce the maintenance dose with closer INR monitoring (correct answer)
4. Add aspirin 81 mg daily to stabilize anticoagulation control

Explanation: This question tests the pharmacokinetic interaction between amiodarone and warfarin, where amiodarone inhibits CYP2C9 and CYP1A2, potentiating warfarin's anticoagulant effect. The key patient-specific factor is the recent initiation of amiodarone 10 days ago in a patient with CKD stage 3, which may further impair drug clearance and elevate INR. Holding 1–2 doses of warfarin and reducing the maintenance dose with closer INR monitoring is the best choice because it addresses the supratherapeutic INR of 4.6 to prevent bleeding while maintaining anticoagulation. Stopping amiodarone and continuing warfarin is incorrect as amiodarone is likely necessary for atrial fibrillation rhythm control, and increasing the warfarin dose would worsen the elevated INR and bleeding risk. Adding aspirin is suboptimal as it increases bleeding risk without addressing the interaction, and continuing without adjustment ignores the clear interaction evidence. Clinically, always monitor INR closely when starting CYP inhibitors with warfarin, anticipating a 30–50% dose reduction. In practice, use interaction checkers and patient education on bleeding signs to guide management in similar drug-drug interactions.

Question 18

1. No adjustment; morphine is safe in severe renal impairment
2. Increase morphine dose because clearance is reduced and analgesia will be inadequate
3. Avoid or reduce morphine and consider an alternative opioid with less renally cleared active metabolites (correct answer)
4. Switch to extended-release morphine at the same total daily dose to reduce sedation

Explanation: This question tests opioid dosing adjustments in renal impairment, where morphine's active metabolite (M6G) accumulates, causing toxicity. The key patient-specific factor is CKD stage 4 with CrCl 18 mL/min, leading to sedation and confusion from metabolite buildup. Avoiding or reducing morphine and considering an alternative opioid with less renally cleared active metabolites is the best choice to ensure safe analgesia without prolonged effects. No adjustment ignores accumulation risks, increasing dose worsens toxicity, and switching to ER form does not mitigate metabolite issues. Clinically, prefer opioids like fentanyl or hydromorphone in severe CKD due to hepatic metabolism. In practice, assess CrCl before opioid selection and monitor for CNS depression to guide therapy in renal patients.

Question 19

1. Continue clozapine and monitor liver enzymes weekly
2. Stop clozapine and follow ANC monitoring per protocol due to severe neutropenia (correct answer)
3. Reduce clozapine dose by 10% and recheck ANC annually
4. Switch to lithium immediately to treat agranulocytosis without further labs

Explanation: This question tests clozapine's risk of agranulocytosis, requiring strict ANC monitoring per REMS protocols. The key patient-specific factor is the severely low ANC of 420/mm³ with symptoms like fever, indicating agranulocytosis in schizophrenia treatment. Stopping clozapine and following ANC monitoring per protocol due to severe neutropenia is the best strategy to prevent life-threatening infections. Continuing or reducing dose ignores guidelines mandating discontinuation below 1000/mm³, and switching to lithium is inappropriate without addressing neutropenia. Clinically, monitor ANC weekly for 6 months, then biweekly, and hold for ANC <1500/mm³. In practice, rechallenge only after hematology consult and consider alternatives like olanzapine for psychosis if clozapine is discontinued.

Question 20

1. Stimulation of muscarinic receptors in the detrusor muscle
2. Inhibition of muscarinic receptors leading to decreased bladder detrusor contraction (correct answer)
3. Blockade of beta-2 receptors causing bronchoconstriction and urinary retention
4. Inhibition of alpha-1 receptors causing increased sphincter tone

Explanation: This question tests the anticholinergic side effects of ipratropium, a muscarinic antagonist used in COPD management. The key patient-specific factor is the patient's BPH, which predisposes him to urinary retention exacerbated by anticholinergic effects on bladder detrusor muscle. Inhibition of muscarinic receptors leading to decreased bladder detrusor contraction is the correct mechanism as it explains the urinary retention and dry mouth from systemic absorption of nebulized ipratropium. Stimulation of muscarinic receptors would increase contraction, not cause retention, while beta-2 receptor blockade is unrelated to ipratropium's action and alpha-1 inhibition would decrease sphincter tone. Clinically, monitor for anticholinergic effects in patients with BPH or glaucoma when using inhaled antimuscarinics. In practice, consider dose reduction or alternatives like tiotropium alone if side effects persist, and educate on symptoms like urinary hesitancy.