NR 566: ADVANCED PHARMACOLOGY EXAM READY - VERIFIED QUESTIONS
AND ANSWERS - COMPREHENSIVE LATEST VERSION 2026/2027
Q1. What are the four pharmacokinetic processes?
ANSWER : ADME: Absorption (drug moves from site of administration into
bloodstream), Distribution (drug moves through body compartments),
Metabolism (drug is biotransformed, mainly by liver), Excretion
(drug/metabolites eliminated, mainly by kidney).
Q2. What is the first-pass effect?
ANSWER : First-pass (presystemic) metabolism: Oral drugs absorbed from
GI tract pass through the portal circulation to the liver before reaching
systemic circulation. Extensive hepatic metabolism reduces bioavailability.
Example: nitroglycerin is nearly 100% metabolized on first pass and must be
given sublingually or transdermally.
Q3. Define bioavailability.
ANSWER : The fraction (percentage) of an administered dose that reaches
the systemic circulation unchanged. IV bioavailability = 100%. Oral
bioavailability is reduced by incomplete absorption and first-pass metabolism.
Clinically important when switching routes or formulations.
Q4. What is the volume of distribution (Vd)?
ANSWER : Vd = Total drug in body / Plasma concentration. Low Vd (~5 L) =
drug stays in plasma (e.g., warfarin). High Vd (hundreds of liters) = drug
extensively distributes to tissues (e.g., chloroquine). High Vd means drug is
not easily dialyzable.
Q5. What is a drug's half-life and why is it clinically important?
ANSWER : Half-life (t1/2) is the time for plasma concentration to decrease by
50%. It determines dosing frequency, time to steady state (~4-5 half-lives),
and time to drug elimination. Example: fluoxetine has a t1/2 of 1-4 days -
takes weeks to reach steady state and weeks to wash out.
Q6. What is steady state?
NR 566 Advanced Pharmacology Midterm Study Guide | Page 1 of 60
, ANSWER : The point at which drug input equals drug elimination, reached
after approximately 4-5 half-lives of continuous dosing. At steady state,
plasma concentration fluctuates between a predictable peak and trough.
Loading doses can accelerate achievement of steady state.
Q7. What are CYP450 enzymes and why do they matter?
ANSWER : Cytochrome P450 enzymes (mainly CYP3A4, CYP2D6, CYP2C9,
CYP2C19) are hepatic and intestinal enzymes responsible for phase I drug
metabolism. Inhibition raises drug levels (toxicity risk); induction lowers drug
levels (therapeutic failure). Key to predicting drug-drug interactions.
Q8. Name three major CYP3A4 inhibitors.
ANSWER : Inhibitors increase drug levels: Ketoconazole/fluconazole (azole
antifungals), erythromycin/clarithromycin (macrolides), grapefruit juice, and
ritonavir. Mnemonic: GNERK - Grapefruit, Nelfinavir/ritonavir, Erythromycin,
Ritonavir, Ketoconazole.
Q9. Name three major CYP3A4 inducers.
ANSWER : Inducers decrease drug levels: Rifampin (strongest), phenytoin,
carbamazepine, St. John's Wort, and phenobarbital. Mnemonic: SCAR GP -
St. John's Wort, Carbamazepine, Antiretrovirals (rifampin), Rifampin,
Griseofulvin, Phenobarbital/Phenytoin.
Q10. What is protein binding and how does it affect drug action?
ANSWER : Most drugs bind to plasma proteins (mainly albumin). Only free
(unbound) drug is pharmacologically active. Low albumin (malnutrition, liver
disease, elderly) increases free drug fraction leading to toxicity risk. Highly
protein-bound drugs can displace each other (e.g., warfarin + aspirin).
Q11. Explain zero-order vs. first-order kinetics.
ANSWER : First-order: A constant fraction of drug is eliminated per unit time
(most drugs). Rate is proportional to concentration. Zero-order: A constant
amount eliminated per unit time (saturation kinetics). Examples: ethanol,
phenytoin, aspirin at high doses. Zero-order kinetics make dose adjustments
unpredictable.
Q12. What is renal clearance and how is eGFR used clinically?
ANSWER : Renal clearance = glomerular filtration + tubular secretion minus
tubular reabsorption. eGFR estimates kidney function. Drugs primarily renally
NR 566 Advanced Pharmacology Midterm Study Guide | Page 2 of 60
, excreted (metformin, digoxin, aminoglycosides) require dose adjustment when
eGFR is reduced to prevent toxicity.
Q13. What is the therapeutic index (TI)?
ANSWER : TI = Toxic dose 50 / Effective dose 50 (TD50/ED50). A narrow TI
means small changes in dose can cause toxicity or sub-therapeutic effect.
Examples of narrow TI drugs: lithium, digoxin, warfarin, phenytoin,
aminoglycosides, and theophylline. These require therapeutic drug monitoring
(TDM).
Q14. What is a loading dose and when is it used?
ANSWER : A loading dose rapidly achieves therapeutic concentrations
without waiting 4-5 half-lives. Used for drugs with long half-lives in urgent
situations. Formula: LD = (Target Cp x Vd) / Bioavailability. Examples: digoxin,
amiodarone, and vancomycin loading doses.
Q15. How does hepatic disease affect drug metabolism?
ANSWER : Liver disease reduces CYP450 enzyme activity, decreases
albumin production (increased free drug), and reduces first-pass metabolism
leading to higher bioavailability of oral drugs. May also cause portosystemic
shunting (bypasses liver). Dose reductions needed for hepatically metabolized
drugs (opioids, benzodiazepines, statins).
Q16. How does aging affect pharmacokinetics?
ANSWER : Absorption: delayed gastric emptying. Distribution: decreased
lean body mass increases Vd for lipophilic drugs; decreased albumin
increases free drug. Metabolism: reduced hepatic blood flow and CYP activity.
Excretion: reduced GFR. Result: drugs stay in body longer - start low, go slow.
Q17. What is pharmacodynamics?
ANSWER : The study of what the drug does to the body - mechanism of
action, receptor binding, dose-response relationships, and drug effects.
Contrasts with pharmacokinetics (what the body does to the drug). Includes
concepts like efficacy, potency, agonism, antagonism, and therapeutic effect.
Q18. Define agonist vs. antagonist.
ANSWER : Agonist: binds receptor and activates it (produces effect).
Antagonist: binds receptor but does not activate it; blocks agonist. Partial
NR 566 Advanced Pharmacology Midterm Study Guide | Page 3 of 60
, agonist: activates receptor but with less efficacy than full agonist (e.g.,
buprenorphine). Inverse agonist: binds receptor and produces opposite effect.
Q19. What is the difference between potency and efficacy?
ANSWER : Potency: the dose required to produce a given effect - lower dose
= more potent. Efficacy: the maximum effect a drug can produce regardless of
dose. A drug can be highly potent but have low efficacy. Clinically, efficacy
matters more than potency for most treatment decisions.
Q20. What is drug tolerance?
ANSWER : Diminished drug effect with repeated use, requiring higher doses
to achieve same effect. Mechanisms: receptor downregulation, enzyme
induction (pharmacokinetic tolerance), or cellular adaptation. Examples: opioid
tolerance, nitrate tolerance, benzodiazepine tolerance.
Q241. What is the significance of the P-glycoprotein (P-gp) transporter?
ANSWER : P-glycoprotein is an efflux transporter (ABC family) that pumps
drugs out of cells. Found in intestinal epithelium, blood-brain barrier, liver,
kidney, and cancer cells. Limits oral absorption and CNS penetration of many
drugs. P-gp inhibitors (cyclosporine, verapamil, quinidine) increase drug
levels. Inducers (rifampin) decrease levels. Major mechanism of multidrug
resistance in cancer.
Q242. What are the phases of drug metabolism?
ANSWER : Phase I: Oxidation, reduction, hydrolysis (mainly CYP450) - adds
or unmasks functional groups; products often still active or toxic. Phase II:
Conjugation (glucuronidation, sulfation, acetylation, methylation, glutathione
conjugation) - attaches large polar molecules causing inactive, water-soluble
products more easily excreted. Some drugs undergo only phase I or only
phase II.
Q243. What is the concept of pharmacogenomics?
ANSWER : The study of how genetic variants affect drug response.
Examples: CYP2D6 poor metabolizers (codeine to morphine conversion fails
causing reduced analgesia; also at risk with tamoxifen); CYP2D6 ultrarapid
metabolizers (codeine causes excess morphine and fatal respiratory
depression reported in children). TPMT variants affect thiopurine
(azathioprine) toxicity. G6PD deficiency affects hemolysis with primaquine and
TMP-SMX.
NR 566 Advanced Pharmacology Midterm Study Guide | Page 4 of 60
AND ANSWERS - COMPREHENSIVE LATEST VERSION 2026/2027
Q1. What are the four pharmacokinetic processes?
ANSWER : ADME: Absorption (drug moves from site of administration into
bloodstream), Distribution (drug moves through body compartments),
Metabolism (drug is biotransformed, mainly by liver), Excretion
(drug/metabolites eliminated, mainly by kidney).
Q2. What is the first-pass effect?
ANSWER : First-pass (presystemic) metabolism: Oral drugs absorbed from
GI tract pass through the portal circulation to the liver before reaching
systemic circulation. Extensive hepatic metabolism reduces bioavailability.
Example: nitroglycerin is nearly 100% metabolized on first pass and must be
given sublingually or transdermally.
Q3. Define bioavailability.
ANSWER : The fraction (percentage) of an administered dose that reaches
the systemic circulation unchanged. IV bioavailability = 100%. Oral
bioavailability is reduced by incomplete absorption and first-pass metabolism.
Clinically important when switching routes or formulations.
Q4. What is the volume of distribution (Vd)?
ANSWER : Vd = Total drug in body / Plasma concentration. Low Vd (~5 L) =
drug stays in plasma (e.g., warfarin). High Vd (hundreds of liters) = drug
extensively distributes to tissues (e.g., chloroquine). High Vd means drug is
not easily dialyzable.
Q5. What is a drug's half-life and why is it clinically important?
ANSWER : Half-life (t1/2) is the time for plasma concentration to decrease by
50%. It determines dosing frequency, time to steady state (~4-5 half-lives),
and time to drug elimination. Example: fluoxetine has a t1/2 of 1-4 days -
takes weeks to reach steady state and weeks to wash out.
Q6. What is steady state?
NR 566 Advanced Pharmacology Midterm Study Guide | Page 1 of 60
, ANSWER : The point at which drug input equals drug elimination, reached
after approximately 4-5 half-lives of continuous dosing. At steady state,
plasma concentration fluctuates between a predictable peak and trough.
Loading doses can accelerate achievement of steady state.
Q7. What are CYP450 enzymes and why do they matter?
ANSWER : Cytochrome P450 enzymes (mainly CYP3A4, CYP2D6, CYP2C9,
CYP2C19) are hepatic and intestinal enzymes responsible for phase I drug
metabolism. Inhibition raises drug levels (toxicity risk); induction lowers drug
levels (therapeutic failure). Key to predicting drug-drug interactions.
Q8. Name three major CYP3A4 inhibitors.
ANSWER : Inhibitors increase drug levels: Ketoconazole/fluconazole (azole
antifungals), erythromycin/clarithromycin (macrolides), grapefruit juice, and
ritonavir. Mnemonic: GNERK - Grapefruit, Nelfinavir/ritonavir, Erythromycin,
Ritonavir, Ketoconazole.
Q9. Name three major CYP3A4 inducers.
ANSWER : Inducers decrease drug levels: Rifampin (strongest), phenytoin,
carbamazepine, St. John's Wort, and phenobarbital. Mnemonic: SCAR GP -
St. John's Wort, Carbamazepine, Antiretrovirals (rifampin), Rifampin,
Griseofulvin, Phenobarbital/Phenytoin.
Q10. What is protein binding and how does it affect drug action?
ANSWER : Most drugs bind to plasma proteins (mainly albumin). Only free
(unbound) drug is pharmacologically active. Low albumin (malnutrition, liver
disease, elderly) increases free drug fraction leading to toxicity risk. Highly
protein-bound drugs can displace each other (e.g., warfarin + aspirin).
Q11. Explain zero-order vs. first-order kinetics.
ANSWER : First-order: A constant fraction of drug is eliminated per unit time
(most drugs). Rate is proportional to concentration. Zero-order: A constant
amount eliminated per unit time (saturation kinetics). Examples: ethanol,
phenytoin, aspirin at high doses. Zero-order kinetics make dose adjustments
unpredictable.
Q12. What is renal clearance and how is eGFR used clinically?
ANSWER : Renal clearance = glomerular filtration + tubular secretion minus
tubular reabsorption. eGFR estimates kidney function. Drugs primarily renally
NR 566 Advanced Pharmacology Midterm Study Guide | Page 2 of 60
, excreted (metformin, digoxin, aminoglycosides) require dose adjustment when
eGFR is reduced to prevent toxicity.
Q13. What is the therapeutic index (TI)?
ANSWER : TI = Toxic dose 50 / Effective dose 50 (TD50/ED50). A narrow TI
means small changes in dose can cause toxicity or sub-therapeutic effect.
Examples of narrow TI drugs: lithium, digoxin, warfarin, phenytoin,
aminoglycosides, and theophylline. These require therapeutic drug monitoring
(TDM).
Q14. What is a loading dose and when is it used?
ANSWER : A loading dose rapidly achieves therapeutic concentrations
without waiting 4-5 half-lives. Used for drugs with long half-lives in urgent
situations. Formula: LD = (Target Cp x Vd) / Bioavailability. Examples: digoxin,
amiodarone, and vancomycin loading doses.
Q15. How does hepatic disease affect drug metabolism?
ANSWER : Liver disease reduces CYP450 enzyme activity, decreases
albumin production (increased free drug), and reduces first-pass metabolism
leading to higher bioavailability of oral drugs. May also cause portosystemic
shunting (bypasses liver). Dose reductions needed for hepatically metabolized
drugs (opioids, benzodiazepines, statins).
Q16. How does aging affect pharmacokinetics?
ANSWER : Absorption: delayed gastric emptying. Distribution: decreased
lean body mass increases Vd for lipophilic drugs; decreased albumin
increases free drug. Metabolism: reduced hepatic blood flow and CYP activity.
Excretion: reduced GFR. Result: drugs stay in body longer - start low, go slow.
Q17. What is pharmacodynamics?
ANSWER : The study of what the drug does to the body - mechanism of
action, receptor binding, dose-response relationships, and drug effects.
Contrasts with pharmacokinetics (what the body does to the drug). Includes
concepts like efficacy, potency, agonism, antagonism, and therapeutic effect.
Q18. Define agonist vs. antagonist.
ANSWER : Agonist: binds receptor and activates it (produces effect).
Antagonist: binds receptor but does not activate it; blocks agonist. Partial
NR 566 Advanced Pharmacology Midterm Study Guide | Page 3 of 60
, agonist: activates receptor but with less efficacy than full agonist (e.g.,
buprenorphine). Inverse agonist: binds receptor and produces opposite effect.
Q19. What is the difference between potency and efficacy?
ANSWER : Potency: the dose required to produce a given effect - lower dose
= more potent. Efficacy: the maximum effect a drug can produce regardless of
dose. A drug can be highly potent but have low efficacy. Clinically, efficacy
matters more than potency for most treatment decisions.
Q20. What is drug tolerance?
ANSWER : Diminished drug effect with repeated use, requiring higher doses
to achieve same effect. Mechanisms: receptor downregulation, enzyme
induction (pharmacokinetic tolerance), or cellular adaptation. Examples: opioid
tolerance, nitrate tolerance, benzodiazepine tolerance.
Q241. What is the significance of the P-glycoprotein (P-gp) transporter?
ANSWER : P-glycoprotein is an efflux transporter (ABC family) that pumps
drugs out of cells. Found in intestinal epithelium, blood-brain barrier, liver,
kidney, and cancer cells. Limits oral absorption and CNS penetration of many
drugs. P-gp inhibitors (cyclosporine, verapamil, quinidine) increase drug
levels. Inducers (rifampin) decrease levels. Major mechanism of multidrug
resistance in cancer.
Q242. What are the phases of drug metabolism?
ANSWER : Phase I: Oxidation, reduction, hydrolysis (mainly CYP450) - adds
or unmasks functional groups; products often still active or toxic. Phase II:
Conjugation (glucuronidation, sulfation, acetylation, methylation, glutathione
conjugation) - attaches large polar molecules causing inactive, water-soluble
products more easily excreted. Some drugs undergo only phase I or only
phase II.
Q243. What is the concept of pharmacogenomics?
ANSWER : The study of how genetic variants affect drug response.
Examples: CYP2D6 poor metabolizers (codeine to morphine conversion fails
causing reduced analgesia; also at risk with tamoxifen); CYP2D6 ultrarapid
metabolizers (codeine causes excess morphine and fatal respiratory
depression reported in children). TPMT variants affect thiopurine
(azathioprine) toxicity. G6PD deficiency affects hemolysis with primaquine and
TMP-SMX.
NR 566 Advanced Pharmacology Midterm Study Guide | Page 4 of 60
