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Nursing Pharmacology: Drug Suffixes, Prefixes and Prototypes — quiz

15 multiple-choice questions covering Drug stem concept, Beta blockers (-olol), ACE inhibitors & ARBs, Statins (-statin), PPIs vs H2 blockers. One answer each; you get a score at the end and the explanation for every question. No account needed.

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Updated 2026-11-03. Keys 1–4 pick an answer, Enter moves on. Redo it any time, in order or shuffled.

The questions

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  1. Drug stem concept

    A nursing student encounters a medication she has never studied before, but notices it ends in a familiar syllable shared by other drugs in the same class. What is the main benefit of recognizing this pattern?

    • It guarantees the drug has no interactions with other medications
    • It confirms the exact brand name and manufacturer for the drug
    • It tells her the exact dosage to administer
    • It allows her to predict the drug's class, mechanism, and likely side effects even without prior exposure to that specific drug
  2. Beta blockers (-olol)

    A patient is prescribed metoprolol for hypertension. Before administering the morning dose, what should the nurse prioritize, and why?

    • Check potassium level because beta blockers cause hyperkalemia
    • Check for dry cough because beta blockers commonly cause angioedema
    • Check apical pulse and hold the dose if heart rate is below 60 bpm, since beta blockers slow heart rate
    • Check blood glucose because beta blockers commonly cause hyperglycemia
  3. ACE inhibitors & ARBs

    A patient taking lisinopril develops a persistent dry cough. What is the most likely physiologic explanation, and what would the prescriber likely switch the patient to?

    • Accumulation of bradykinin due to ACE inhibition; switch to an ARB like losartan
    • Direct bronchoconstriction from beta receptor blockade; switch to a calcium channel blocker
    • Decreased potassium excretion; switch to a loop diuretic
    • Increased angiotensin II levels; switch to another ACE inhibitor
  4. Statins (-statin)

    A patient newly started on atorvastatin calls the clinic reporting diffuse muscle aches. Which lab value should the nurse ask the provider about, and what serious complication does this symptom raise concern for?

    • Elevated potassium, concern for hyperkalemia-induced arrhythmia
    • Elevated creatine phosphokinase (CPK), concern for myopathy/rhabdomyolysis
    • Elevated INR, concern for bleeding
    • Decreased platelet count, concern for heparin-induced thrombocytopenia
  5. PPIs vs H2 blockers

    A patient asks why their omeprazole seems to control heartburn better than the famotidine they used previously. What is the best explanation?

    • H2 blockers work on a completely different organ system unrelated to acid secretion
    • PPIs act faster but wear off within hours, unlike H2 blockers
    • PPIs irreversibly block the final step of acid secretion for more complete, longer-lasting suppression, while H2 blockers only block one stimulatory pathway
    • Famotidine is only used for H. pylori eradication, not acid suppression
  6. Antifungals (-azole)

    A patient on fluconazole for a fungal infection is also taking a medication metabolized by the liver. Why is this combination a concern for the nurse to monitor closely?

    • Azoles have no effect on liver enzymes but cause renal toxicity instead
    • Azoles induce CYP450 enzymes, decreasing the effectiveness of other medications
    • Azoles bind to beta-lactam receptors, reducing antifungal effectiveness
    • Azoles inhibit human CYP450 enzymes, increasing the risk of drug interactions and altered drug levels
  7. Penicillins & cephalosporins

    A patient with a documented penicillin allergy is ordered a cephalosporin antibiotic. What should the nurse do first?

    • Refuse to give any antibiotic until an infectious disease consult is obtained
    • Substitute an aminoglycoside automatically without physician input
    • Assess the severity/type of the penicillin allergy, since cephalosporins carry a small but possible cross-allergy risk due to the shared beta-lactam structure
    • Administer the cephalosporin without concern since the two drug classes never cross-react
  8. Aminoglycosides vs macrolides

    Two antibiotics both have names containing '-mycin'-type syllables: gentamicin and azithromycin. How do their mechanisms and toxicity profiles differ?

    • Both are cell-wall synthesis inhibitors with similar beta-lactam structure
    • Gentamicin (aminoglycoside) binds the 30S subunit with nephro/ototoxicity risk; azithromycin (macrolide) binds the 50S subunit with QT prolongation and GI upset as main concerns
    • Gentamicin binds the 50S subunit while azithromycin binds the 30S subunit, but both are equally nephrotoxic
    • Both bind the 50S ribosomal subunit and share the same ototoxicity risk
  9. Fluoroquinolones (-floxacin)

    A 70-year-old on ciprofloxacin reports new heel pain after starting a walking program. What complication should the nurse suspect, and what medication teaching is appropriate regarding administration timing?

    • Peripheral neuropathy; advise taking with dairy products for better absorption
    • Tendon rupture/tendinitis; advise separating dosing from dairy/antacids to preserve drug absorption
    • Tendon rupture/tendinitis; advise taking the drug with dairy products to protect tendons
    • Ototoxicity; advise discontinuing all physical activity permanently
  10. Monoclonal antibodies (-mab)

    Before starting a patient on infliximab, what screening is essential, and why?

    • Screen for G6PD deficiency, because monoclonal antibodies cause hemolysis in deficient patients
    • Screen for latent tuberculosis and other infections, because monoclonal antibodies suppress immune function and can reactivate dormant infections
    • Screen renal function only, since monoclonal antibodies are exclusively nephrotoxic
    • Screen for pregnancy only, since monoclonal antibodies have no other contraindications
  11. Local anesthetics (-caine)

    During administration of IV lidocaine for an arrhythmia, the nurse should monitor for early signs of toxicity. Which symptom cluster indicates this?

    • Hyperglycemia and polyuria
    • Tendon pain and Achilles rupture
    • Tinnitus, metallic taste, and seizures from CNS toxicity
    • Dry cough and angioedema
  12. Benzodiazepine reversal

    A patient who has been taking alprazolam daily for two years is given flumazenil after an overdose. What is an important safety consideration unique to this reversal scenario?

    • Flumazenil is only used for alcohol withdrawal, not benzodiazepine overdose
    • Flumazenil permanently cures benzodiazepine dependence
    • Flumazenil can precipitate seizures in patients who are physically dependent on benzodiazepines
    • Flumazenil is safe at any dose and carries no risk in dependent patients
  13. Heparins (-parin)

    A patient on enoxaparin develops a dropping platelet count several days into therapy. What condition should the nurse suspect, and what is the antidote used for heparin-class bleeding?

    • Disseminated intravascular coagulation; antidote is vitamin K
    • Rhabdomyolysis; antidote is protamine sulfate
    • Heparin-induced thrombocytopenia (HIT); antidote is flumazenil
    • Heparin-induced thrombocytopenia (HIT); antidote is protamine sulfate
  14. SGLT2 inhibitors (-flozin)

    A patient taking empagliflozin presents with nausea, abdominal pain, and a blood glucose that is only mildly elevated, yet is found to be in ketoacidosis. What is this presentation called, and what drug class causes it?

    • Lactic acidosis; caused by metformin
    • Euglycemic diabetic ketoacidosis; caused by SGLT2 inhibitors
    • Hyperosmolar hyperglycemic state; caused by sulfonylureas
    • Euglycemic diabetic ketoacidosis; caused by DPP-4 inhibitors
  15. Beta2 agonists (-terol)

    A patient uses albuterol frequently for asthma symptom relief and reports new tremor and a racing heart. Which mechanism explains these side effects?

    • Leukotriene receptor blockade causing neuropsychiatric effects
    • Corticosteroid receptor binding causing adrenal suppression
    • Mast cell stabilization causing systemic vasodilation
    • Beta2-adrenergic stimulation causing bronchial smooth muscle relaxation also affects beta receptors elsewhere, causing tachycardia and tremor
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