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Quizzes > Health & Medicine > Human Anatomy & Medicine

Take the ATI Pharmacology Quiz and Master Drug Knowledge

Think you can ace these pharmacology practice questions? Dive into our drug knowledge quiz now!

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art illustration of pill syringe and test tube icons with quiz title text on sky blue background.

Use this ATI Pharmacology Quiz to practice drug actions, side effects, and safe dosing so you can spot gaps before the exam. Questions cover analgesics, antibiotics, and antivirals, with a focus on therapeutic use and key interactions. When you finish, keep practicing with more practice questions.

Which class of antibiotic inhibits bacterial cell wall synthesis?
Aminoglycosides
Tetracyclines
Penicillins
Macrolides
Penicillins inhibit the transpeptidase enzyme required for peptidoglycan cross-linking in the bacterial cell wall, leading to cell lysis. This beta-lactam mechanism is distinct from protein synthesis inhibitors like tetracyclines. Macrolides and aminoglycosides act on the ribosome rather than the cell wall.
Which diuretic acts primarily on the distal convoluted tubule to inhibit sodium-chloride symporters?
Hydrochlorothiazide
Spironolactone
Furosemide
Mannitol
Hydrochlorothiazide inhibits the Na?/Cl? symporter in the distal convoluted tubule, reducing sodium reabsorption. Furosemide works on the ascending loop of Henle, spironolactone is an aldosterone antagonist, and mannitol is an osmotic diuretic. This site specificity explains their differing effects and electrolyte changes.
Which medication is a selective beta-1 adrenergic blocker used to reduce heart rate?
Metoprolol
Carvedilol
Labetalol
Propranolol
Metoprolol selectively blocks ?? receptors in the heart, decreasing heart rate and contractility. Propranolol blocks both ?? and ?? receptors, while labetalol and carvedilol also block ? receptors. This selectivity makes metoprolol preferable in asthma patients to avoid bronchoconstriction.
Which drug class reduces angiotensin II production by inhibiting angiotensin-converting enzyme?
ACE inhibitors
Loop diuretics
Calcium channel blockers
Beta blockers
ACE inhibitors such as lisinopril block the conversion of angiotensin I to angiotensin II, lowering blood pressure and reducing aldosterone release. Beta blockers work on heart rate, calcium channel blockers on calcium influx, and loop diuretics on the loop of Henle. ACE inhibitors also decrease preload and afterload.
Which drug is a proton pump inhibitor used to reduce gastric acid secretion?
Magnesium hydroxide
Omeprazole
Ranitidine
Sucralfate
Omeprazole irreversibly inhibits the H?/K? ATPase in gastric parietal cells, profoundly reducing acid secretion. Ranitidine blocks H? receptors, sucralfate forms a protective barrier, and magnesium hydroxide neutralizes acid directly. PPIs provide more sustained acid suppression.
Which antihyperlipidemic agent inhibits HMG-CoA reductase?
Simvastatin
Niacin
Cholestyramine
Ezetimibe
Simvastatin competitively inhibits HMG-CoA reductase, reducing cholesterol synthesis in the liver. Cholestyramine binds bile acids, ezetimibe blocks intestinal absorption, and niacin reduces VLDL secretion. Statins also upregulate LDL receptors for increased clearance.
Which drug is an opioid antagonist used in opioid overdose?
Naltrexone
Naloxone
Buprenorphine
Methadone
Naloxone is a competitive opioid receptor antagonist that rapidly reverses respiratory depression in overdose. Naltrexone is used for maintenance, methadone is an agonist, and buprenorphine is a partial agonist. Naloxone's rapid onset makes it ideal for emergency reversal.
Which antihistamine is a first-generation H? blocker known for causing sedation?
Cetirizine
Loratadine
Fexofenadine
Diphenhydramine
Diphenhydramine crosses the blood - brain barrier and antagonizes central H? receptors, causing sedation. Second-generation antihistamines like loratadine, fexofenadine, and cetirizine have less CNS penetration. This difference reduces drowsiness.
Which inhaled bronchodilator is a short-acting ?? agonist?
Ipratropium
Albuterol
Theophylline
Salmeterol
Albuterol selectively stimulates ?? receptors in bronchial smooth muscle, causing rapid bronchodilation. Salmeterol is long-acting, ipratropium blocks muscarinic receptors, and theophylline is a phosphodiesterase inhibitor. Short-acting agents are used for acute relief.
Which medication is classified as a loop diuretic?
Acetazolamide
Chlorthalidone
Amiloride
Furosemide
Furosemide inhibits the Na?-K?-2Cl? cotransporter in the thick ascending limb of the loop of Henle, causing significant diuresis. Chlorthalidone is a thiazide, amiloride is a K?-sparing diuretic, and acetazolamide is a carbonic anhydrase inhibitor. Loop diuretics are potent and used in edema.
Which insulin is rapid-acting and used around meal times?
Insulin NPH
Insulin lispro
Insulin detemir
Insulin glargine
Insulin lispro has an altered amino acid sequence that prevents dimerization, allowing rapid absorption and onset. Glargine and detemir are long-acting, and NPH is intermediate-acting. Lispro's quick action matches postprandial glucose rise.
Which anticoagulant directly inhibits thrombin (factor IIa)?
Rivaroxaban
Enoxaparin
Warfarin
Dabigatran
Dabigatran is a direct thrombin inhibitor that prevents conversion of fibrinogen to fibrin. Rivaroxaban inhibits factor Xa, enoxaparin potentiates antithrombin III, and warfarin inhibits vitamin K - dependent synthesis of clotting factors. Direct thrombin inhibitors act independently of antithrombin.
Which medication is used as emergency treatment for anaphylaxis by stimulating ? and ? adrenergic receptors?
Epinephrine
Dopamine
Norepinephrine
Phenylephrine
Epinephrine acts on ?? receptors to constrict blood vessels and ?? receptors to bronchodilate, reversing anaphylaxis. Norepinephrine has minimal ?? effect, dopamine works on dopaminergic receptors, and phenylephrine is ?? selective. Epinephrine's broad adrenergic action makes it first-line.
Which class of drugs is first-line therapy for type II diabetes by increasing insulin sensitivity?
Biguanides (metformin)
Sulfonylureas
Alpha-glucosidase inhibitors
Meglitinides
Metformin (a biguanide) reduces hepatic gluconeogenesis and increases insulin sensitivity in peripheral tissues. Sulfonylureas and meglitinides increase insulin secretion, while alpha-glucosidase inhibitors slow carbohydrate absorption. Metformin's efficacy and safety make it first-line.
Which antiplatelet drug irreversibly inhibits cyclooxygenase-1 in platelets?
Aspirin
Abciximab
Ticlopidine
Clopidogrel
Aspirin acetylates and irreversibly inhibits COX-1, preventing thromboxane A? synthesis and reducing platelet aggregation. Clopidogrel and ticlopidine inhibit the P2Y?? receptor, while abciximab blocks the GPIIb/IIIa receptor. The irreversible action of aspirin lasts for the platelet's lifespan.
Which nonsteroidal anti-inflammatory drug (NSAID) reversibly inhibits both COX-1 and COX-2?
Aspirin
Celecoxib
Ibuprofen
Acetaminophen
Ibuprofen reversibly inhibits both COX-1 and COX-2, reducing prostaglandin synthesis and inflammation. Celecoxib selectively inhibits COX-2, aspirin irreversibly inhibits COX enzymes, and acetaminophen has minimal anti-inflammatory effect. The reversible inhibition reduces GI side effects compared to irreversible agents.
What is the primary adverse effect associated with angiotensin-converting enzyme (ACE) inhibitors?
Bradycardia
Dry cough
Hypokalemia
Hyperglycemia
ACE inhibitors increase bradykinin levels, which can lead to a persistent dry cough in some patients. They can cause hyperkalemia rather than hypokalemia due to decreased aldosterone. Bradycardia and hyperglycemia are not typical primary effects.
Which laboratory value must be monitored most closely during heparin therapy?
Activated partial thromboplastin time (aPTT)
Prothrombin time (PT)
International normalized ratio (INR)
Platelet count
Heparin potentiates antithrombin III and is monitored by measuring aPTT to ensure therapeutic anticoagulation. PT/INR is used for warfarin monitoring. Although platelet count should be checked for heparin-induced thrombocytopenia, aPTT guides dosing.
Which sign is most indicative of digoxin toxicity?
Visual disturbances (yellow halos)
Tinnitus
Hypertension
Hyperreflexia
Digoxin toxicity can cause color vision changes or yellow-green halos around lights. Hypertension is not a typical feature, and hyperreflexia and tinnitus are not specific to digoxin. Early recognition of visual symptoms is key.
Lithium toxicity is often accompanied by which electrolyte disturbance?
Hypernatremia
Hypokalemia
Hyponatremia
Hypercalcemia
Lithium is reabsorbed in the proximal tubule alongside sodium; states of hyponatremia increase lithium reabsorption and risk toxicity. Hypernatremia reduces lithium reabsorption. Potassium and calcium disturbances are less directly related.
Which adverse effect is most commonly associated with aminoglycoside antibiotics?
Nephrotoxicity
Pulmonary fibrosis
Hepatotoxicity
Bone marrow suppression
Aminoglycosides can accumulate in renal proximal tubule cells, causing nephrotoxicity. They can also cause ototoxicity, but hepatotoxicity, pulmonary fibrosis, and bone marrow suppression are not common. Monitoring renal function is essential.
Metformin's major rare but serious adverse effect is:
Lactic acidosis
Hypertension
Pancreatitis
Severe hypoglycemia
Metformin can rarely cause lactic acidosis, especially in renal impairment or hypoxic states. It does not typically cause hypoglycemia when used alone. Hypertension and pancreatitis are not primary concerns with metformin.
Which drug interaction can lead to serotonin syndrome?
Metformin + insulin
SSRI + MAOI
Digoxin + furosemide
Warfarin + aspirin
Combining SSRIs with MAO inhibitors can lead to excessive serotonin activity and serotonin syndrome. The other combinations pose bleeding risk, electrolyte changes, or hypoglycemia but not serotonin toxicity. Monitoring and washout periods reduce risk.
Which antifungal agent is associated with infusion-related rigors and nephrotoxicity?
Amphotericin B
Terbinafine
Fluconazole
Ketoconazole
Amphotericin B binds ergosterol, causing fungal cell death but also renal tubular damage and cytokine release leading to infusion-related rigors. Azoles like fluconazole are less nephrotoxic. Terbinafine works on squalene epoxidase.
Tamoxifen acts as an estrogen receptor antagonist in which tissue?
Liver
Breast
Uterus
Bone
Tamoxifen blocks estrogen receptors in breast tissue, reducing tumor growth in ER-positive breast cancer. It can act as an agonist in the uterus and bone. Its mixed agonist-antagonist profile explains tissue-specific effects.
Methotrexate inhibits which enzyme to exert its antimetabolite effect?
DNA polymerase
Dihydrofolate reductase
Thymidylate synthase
Topoisomerase II
Methotrexate competitively inhibits dihydrofolate reductase, preventing tetrahydrofolate formation and DNA synthesis. Thymidylate synthase is inhibited by 5-fluorouracil, and DNA polymerase/topoisomerase II by other agents. Folinic acid rescue is used to reduce toxicity.
Allopurinol lowers uric acid levels by inhibiting which enzyme?
Adenine phosphoribosyltransferase
Uricase
Xanthine oxidase
Hypoxanthine guanine phosphoribosyltransferase
Allopurinol is a xanthine oxidase inhibitor that prevents conversion of xanthine to uric acid, reducing gout flares. The other enzymes are involved in purine salvage or degradation pathways. This reduces urate burden.
Atropine exerts its effect by antagonizing which receptor type?
Beta-adrenergic receptors
Nicotinic acetylcholine receptors
Alpha-adrenergic receptors
Muscarinic acetylcholine receptors
Atropine is a competitive antagonist at muscarinic receptors, reducing parasympathetic effects like bradycardia and bronchoconstriction. It does not block nicotinic, adrenergic, or beta receptors. This antimuscarinic action is used in bradyarrhythmias.
A patient requires a loading dose. Which formula calculates the loading dose?
Loading dose = Half-life × clearance
Loading dose = Clearance × dosing interval
Loading dose = Clearance / Vd
Loading dose = Vd × target plasma concentration
The loading dose compensates for volume of distribution (Vd) to rapidly achieve target plasma concentration. Clearance and dosing interval are used for maintenance dosing. Half-life and clearance together define steady-state but not loading dose.
Which kinetic order does phenytoin follow at therapeutic concentrations?
First-order kinetics
Nonlinear enzyme induction
Zero-order kinetics
Mixed-order kinetics
Phenytoin exhibits zero-order kinetics at therapeutic levels because its metabolic enzymes become saturated, leading to a constant amount metabolized per time. First-order kinetics metabolizes a constant fraction. Mixed-order applies to drugs like ethanol at variable doses.
How is volume of distribution (Vd) calculated?
Half-life multiplied by clearance
Amount of drug in body divided by plasma concentration
Clearance divided by elimination rate constant
Maintenance dose multiplied by dosing interval
Vd = Amount of drug in the body ÷ Plasma concentration, indicating distribution into tissues versus plasma. Clearance/elimination rate constant gives Vd only if you know k. Maintenance dose and half-life relate to steady state but not direct Vd.
What effect does a cytochrome P450 inducer have on drug metabolism?
Blocks renal excretion
Decreases metabolism, raising plasma levels
Increases metabolism, lowering plasma levels
Alters drug absorption
P450 inducers increase enzyme synthesis, accelerating drug metabolism and reducing plasma concentrations. Inhibitors have the opposite effect. This does not directly affect renal excretion or absorption.
Which calculation determines maintenance dose for a constant infusion?
Vd × target concentration
Clearance × target concentration
Dose × bioavailability
Half-life × dosing interval
Maintenance infusion rate equals clearance × target plasma concentration to replace drug eliminated per unit time. Vd relates to loading dose, half-life and dosing interval to accumulation, and bioavailability to oral dosing.
Steady-state concentration is reached after how many half-lives?
Approximately 4 - 5 half-lives
Half-life is not relevant
10 half-lives
1 half-life
It takes about 4 - 5 half-lives for a drug to reach ~95% of steady-state concentration under first-order kinetics. One half-life reaches only 50%. Ten would be >99%, and half-life is directly relevant.
Which phase II metabolism reaction involves acetyl group transfer?
Glutathione conjugation
Glucuronidation
Sulfation
N-acetylation
N-acetylation transfers an acetyl group to drugs or metabolites, often via N-acetyltransferase enzymes. Glucuronidation adds glucuronic acid, sulfation adds sulfate, and glutathione conjugation protects against oxidative damage. Acetylation rates vary genetically.
P-glycoprotein in the gut affects drug therapy by:
Facilitating drug absorption into cells
Metabolizing drugs into inactive forms
Pumping drugs back into the intestinal lumen
Binding to plasma proteins
P-glycoprotein is an efflux transporter that pumps substrates out of enterocytes back into the gut lumen, reducing oral bioavailability. It does not metabolize drugs or bind plasma proteins.
Upregulation of receptors in response to chronic antagonist exposure is called:
Receptor super-sensitivity
Desensitization
Tachyphylaxis
Downregulation
Receptor super-sensitivity or upregulation occurs when cells increase receptor number after prolonged antagonist exposure. Downregulation and desensitization occur with excess agonist. Tachyphylaxis is a rapid decrease in response to repeated dosing.
A drug with a narrow therapeutic index requires:
Only clinical monitoring
No monitoring if dose is standard
Peak levels only
Frequent plasma level monitoring
Narrow therapeutic index drugs have small margins between therapeutic and toxic doses, necessitating frequent plasma monitoring. Clinical signs alone may be insufficient. Both peak and trough levels may be important.
Bioavailability (F) of an oral drug is calculated as:
Dose oral ÷ Dose IV
Cmax oral ÷ Cmax IV
AUC oral ÷ AUC IV × (Dose IV ÷ Dose oral)
AUC IV ÷ AUC oral
F = (AUC oral / AUC IV) × (Dose IV / Dose oral), correcting for dose differences. AUC ratios alone do not account for dose. Cmax ratios reflect peak concentrations but not total exposure.
A patient has a Cl of 5 L/hr and a target concentration of 10 mg/L. What is the maintenance infusion rate?
5 mg/hr
50 mg/hr
0.5 mg/hr
100 mg/hr
Maintenance rate = Clearance × target concentration = 5 L/hr × 10 mg/L = 50 mg/hr. The other options do not match the formula.
A patient is a CYP2D6 poor metabolizer. Which drug's efficacy is most impacted?
Digoxin
Metformin
Codeine
Warfarin
Codeine is converted by CYP2D6 into morphine for analgesia. Poor metabolizers experience reduced effect. Warfarin is affected by CYP2C9, metformin is not P450 metabolized, and digoxin is renally excreted.
Which targeted therapy blocks the JAK-STAT pathway in rheumatoid arthritis?
Etanercept
Methotrexate
Adalimumab
Tofacitinib
Tofacitinib is a JAK inhibitor that prevents STAT signaling, reducing cytokine-mediated inflammation. Etanercept and adalimumab are TNF inhibitors, and methotrexate is a folate antimetabolite. JAK inhibition offers an oral alternative.
Which monoclonal antibody is an immune checkpoint inhibitor targeting PD-1?
Bevacizumab
Infliximab
Pembrolizumab
Rituximab
Pembrolizumab blocks PD-1 on T cells, enhancing anti-tumor immunity. Infliximab targets TNF-?, rituximab targets CD20, and bevacizumab targets VEGF. Checkpoint inhibitors have revolutionized oncology.
Which agent is a small-molecule EGFR tyrosine kinase inhibitor used in non - small cell lung cancer?
Cetuximab
Erlotinib
Trastuzumab
Imatinib
Erlotinib reversibly inhibits the EGFR tyrosine kinase domain in NSCLC with activating mutations. Trastuzumab and cetuximab are monoclonal antibodies; imatinib targets BCR-ABL. Small molecules penetrate cells to block kinase activity.
Which biologic DMARD targets IL-6 receptors in rheumatoid arthritis?
Tocilizumab
Abatacept
Etanercept
Rituximab
Tocilizumab is a monoclonal antibody against the IL-6 receptor, reducing inflammation in RA. Etanercept targets TNF-?, abatacept modulates T-cell costimulation, and rituximab depletes B cells. IL-6 blockade addresses acute-phase responses.
Pharmacokinetic profiling of monoclonal antibodies differs from small molecules primarily because they:
Are catabolized by proteolysis rather than hepatic enzymes
Have high oral bioavailability
Undergo extensive renal filtration
Are metabolized by cytochrome P450
Monoclonal antibodies are degraded by proteolytic pathways in reticuloendothelial cells, not by CYP450 or renal filtration. They have negligible oral bioavailability and rely on parenteral administration. This results in long half-lives.
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Study Outcomes

  1. Understand Drug Mechanisms -

    Explain the pharmacodynamics and pharmacokinetics of common medications to build solid foundational knowledge for your ATI Pharmacology Quiz.

  2. Analyze NCLEX Pharmacology Practice Questions -

    Break down question stems and answer choices to improve test-taking strategies and confidence on pharmacology practice questions.

  3. Calculate Accurate Dosages -

    Perform dosage calculation practice with precision, ensuring safe and effective medication administration in clinical scenarios.

  4. Apply Drug Classification Principles -

    Use drug classes and mechanisms to categorize medications and predict their therapeutic uses and side effects.

  5. Differentiate Adverse Effects and Contraindications -

    Identify common side effects, warnings, and contraindications to anticipate patient responses and ensure safe care.

  6. Evaluate Drug Interactions -

    Assess potential interactions between medications to mitigate risks and optimize patient outcomes in your drug knowledge quiz practice.

Cheat Sheet

  1. Pharmacokinetic Fundamentals -

    Pharmacokinetics covers absorption, distribution, metabolism, and excretion; key formulas include Vd=Amount of drug in body/Plasma concentration and half-life (t1/2)=0.693×(Vd/CL). Remember that changes in clearance (CL) directly affect t1/2, so doubling CL halves the half-life - critical for dosing intervals (Goodman & Gilman, 2018).

  2. Pharmacodynamic Principles -

    Pharmacodynamics explores how drugs produce effects via receptor binding, agonism, and antagonism; dose - response curves and EC50 values help predict potency. Use the therapeutic index (TI=TD50/ED50) to gauge safety - warfarin's narrow TI underscores the need for regular INR monitoring (Rang & Dale, 2020).

  3. Dosage Calculation Techniques -

    Master dimensional analysis and the formula "D/H×V" (Desired dose/On-hand dose×Volume) for accurate IV and PO calculations; for example, (250 mg ordered ÷ 500 mg on hand)×10 mL=5 mL. Practice converting units (mcg to mg) to avoid errors, a common focus in NCLEX pharmacology practice questions (University of Washington Nursing).

  4. Common Drug Interactions -

    Many interactions stem from cytochrome P450 modulation; inhibitors like ketoconazole increase substrate levels, while inducers like rifampin reduce efficacy. Use the mnemonic "G PACMAN" (Grapefruit, Protease inhibitors, Azoles, Cimetidine, Macrolides, Amiodarone, Non-DHP CCBs) to recall major CYP3A4 inhibitors (FDA Drug Development & Drug Interactions, 2021).

  5. NCLEX Pharmacology Strategy Tips -

    Use the "ADPIE" approach (Assessment, Diagnosis, Planning, Implementation, Evaluation) when answering NCLEX-style pharmacology questions and eliminate clearly wrong options first. Build confidence with timed quizzes - our ATI Pharmacology Quiz provides immediate feedback to reinforce high-yield drug facts and dosage calculations.

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