PHARM 271: PRINCIPLES OF PHARMACOLOGY EXAM
2025-2026 QUESTIONS AND ANSWERS A+ GUARANTEED
PASS
Q. pharmacokinetics
A. relationship between drug dosage and concentration in plasma over time, determines onset,
duration, and intensity of drug
Q. pharmacodynamics
A. relationship between drug concentration over time and therapeutic response
Q. chemical specificity for receptors
A. specificity between receptors and bonds, EX strict structural requirements for binding
Q. receptor saturability
A. only a finite number of receptors that can be occupied
Q. receptor affinity
A. measure of attraction between drug and receptor
Q. drug potency
A. dose required to have certain effect, related to affinity of receptor
Q. ED50
,A. dose which produces 50% of maximum effect, used to compare drugs in terms of potency
Q. drug efficacy
A. maximal effect achievable for a drug, related to number of receptor/complexes formed, intrinsic
activity of drug in activating receptor
Q. full agonist
A. affinity to, and full activator, of receptor (high intrinsic activity/efficacy), increases activity above
basal level of receptor where receptor has a constitutive (intrinsic basal) level of activity in the
absence of a ligand
Q. inverse agonist
A. affinity to, and full activator of receptor (high intrinsic activity/efficacy), but has exact opposite
effect of full agonist (metoprolol), decreases activity below basal level of receptor where receptor
has a constitutive (intrinsic basal) level of activity in the absence of a ligand
Q. partial agonist
A. affinity to receptor but only partially activates a receptor, produces less than the ceiling effect of a
full agonist
Q. pure antagonist
A. affinity to receptor but produces no activation, dose curve is a straight line across the bottom of
an XY graph (EX oraverse vasodilates, overcoming the vasocontriction of the LA)
Q. neutral antgonist
A. has no activity in the absence of an agonist or inverse agonist but can block either's activity
, Q. competitive antagonist
A. lacks efficacy, competes with agonists for binding sites, inhibitory effect can be overcome by
increasing concentration of competing agonist
Q. physiological antagonism
A. stimulates competing/opposite physiological responses which counteract the effects of a
therapeutic drug, the inhibitory effect can NOT be overcome by increasing the agonist dosage (EX
epi is used during anaphylaxis to produce physiological responses instead of an antihistamine which
is only a competing antagonist)
Q. therapeutic index
A. the difference between a dose that produces a therapeutic effect and a dose that produces a
lethal toxicity, this has to do with a population
Q. which drug is a safer drug? a drug with a
A. therapeutic index of 2
or
therapeutic index of 10
the therapeutic index of 10 is safer, there is a larger range of dosages we can give without toxicity
Q. therapeutic window
A. difference between ineffective and effective dose range, drugs like penicillin has a large window
where others have a small one (more dangerous), some DDIs happen to decrease or increase
metabolism/reception of the drug and therefore increase or decrease plasma conc. causing toxicity
or ineffectiveness depending on the type of DDI
2025-2026 QUESTIONS AND ANSWERS A+ GUARANTEED
PASS
Q. pharmacokinetics
A. relationship between drug dosage and concentration in plasma over time, determines onset,
duration, and intensity of drug
Q. pharmacodynamics
A. relationship between drug concentration over time and therapeutic response
Q. chemical specificity for receptors
A. specificity between receptors and bonds, EX strict structural requirements for binding
Q. receptor saturability
A. only a finite number of receptors that can be occupied
Q. receptor affinity
A. measure of attraction between drug and receptor
Q. drug potency
A. dose required to have certain effect, related to affinity of receptor
Q. ED50
,A. dose which produces 50% of maximum effect, used to compare drugs in terms of potency
Q. drug efficacy
A. maximal effect achievable for a drug, related to number of receptor/complexes formed, intrinsic
activity of drug in activating receptor
Q. full agonist
A. affinity to, and full activator, of receptor (high intrinsic activity/efficacy), increases activity above
basal level of receptor where receptor has a constitutive (intrinsic basal) level of activity in the
absence of a ligand
Q. inverse agonist
A. affinity to, and full activator of receptor (high intrinsic activity/efficacy), but has exact opposite
effect of full agonist (metoprolol), decreases activity below basal level of receptor where receptor
has a constitutive (intrinsic basal) level of activity in the absence of a ligand
Q. partial agonist
A. affinity to receptor but only partially activates a receptor, produces less than the ceiling effect of a
full agonist
Q. pure antagonist
A. affinity to receptor but produces no activation, dose curve is a straight line across the bottom of
an XY graph (EX oraverse vasodilates, overcoming the vasocontriction of the LA)
Q. neutral antgonist
A. has no activity in the absence of an agonist or inverse agonist but can block either's activity
, Q. competitive antagonist
A. lacks efficacy, competes with agonists for binding sites, inhibitory effect can be overcome by
increasing concentration of competing agonist
Q. physiological antagonism
A. stimulates competing/opposite physiological responses which counteract the effects of a
therapeutic drug, the inhibitory effect can NOT be overcome by increasing the agonist dosage (EX
epi is used during anaphylaxis to produce physiological responses instead of an antihistamine which
is only a competing antagonist)
Q. therapeutic index
A. the difference between a dose that produces a therapeutic effect and a dose that produces a
lethal toxicity, this has to do with a population
Q. which drug is a safer drug? a drug with a
A. therapeutic index of 2
or
therapeutic index of 10
the therapeutic index of 10 is safer, there is a larger range of dosages we can give without toxicity
Q. therapeutic window
A. difference between ineffective and effective dose range, drugs like penicillin has a large window
where others have a small one (more dangerous), some DDIs happen to decrease or increase
metabolism/reception of the drug and therefore increase or decrease plasma conc. causing toxicity
or ineffectiveness depending on the type of DDI
