Lippincott CHAPTER 2 Drug receptor interactions and pharmacodynamics Flashcards by Lovely jane Luchavez

Action of a drug on the body ?

a. pharmacodynamic
b. pharmacokinetic

a. pharmacodynamic

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bind to a site on a receptor protein and activates it to initiate a series of reactions that ultimately result in a specific intracellular response.

a. agonist
b. antagonist

a. agonist

note: Second messenger or effector molecule are part of the cascade of events that translates agonist binding into a cellular response.

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what receptor of the cardiac cells respond to epinephrine?

a. B- adrenergic receptor
b. Muscarinic

a. B- adrenergic receptor

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what receptor of the cardiac cells respond to norephineprine?

a. B- adrenergic receptor
b. Muscarinic

a. B-adrenergic receptor

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what receptor of the cardiac cells respond to Acetylcholine?

a. B- adrenergic receptor
b. Muscarinic

b. Muscarinic

note: the magnitude of the cellular response is proportional to the number of drug- receptor complexed.

Not all drugs exert effects by interacting with a receptor.

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what are the two states of receptor

(R) inactive
(R*) active

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are drugs that bind to the receptor but do not increase the fraction R* , instead stabilizing from R to R*.

a. agonist
b. antagonist

b. antagonist

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shift the equilibrium

a. full agonist
b. partial agonists

b. partial agonist

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is defined as any biologic molecule to which a drug binds and produces a measurable response.

receptor

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what are the four receptor families

ligand gated ion channels
2.G protein coupled receptors
Enzyme lined receptors
intracellular receptors

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interacts with the receptor s that are found on the cell surface

a. hydrophilic ligand
b. hydrophobic ligands

a. hydrophilic ligand

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enters through the lipid bilayers of the cell membrane to interact with receptors found inside cells

a. hydrophilic ligand
b. hydrophobic ligands

b. hydrophobic ligands

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cholinergic nicotinic receptors

a. ligand gated ion channels
b. g protein coupled receptors
c. enzyme linked receptors
d. intracellular receptors

a. ligand gated ion channels

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a nd b adrenoceptors

a. ligand gated ion channels
b. g protein coupled receptors
c. enzyme linked receptors
d. intracellular receptors

b. g protein coupled receptors

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insulin receptor

a. ligand gated ion channels
b. g protein coupled receptors
c. enzyme linked receptors
d. intracellular receptors

c. enzyme linked receptors

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steroid receptors

a. ligand gated ion channels
b. g protein coupled receptors
c. enzyme linked receptors
d. intracellular receptors

d. intracellular receptors

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what receptor does an ion uder go ?
a. ligand gated ion channels
b. g protein coupled receptors
c. enzyme linked receptors
d. intracellular receptors

a. ligand gated ion channels

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what receptor changes in membrane potential or ionic concentration within the cell

a. ligand gated ion channels
b. g protein coupled receptors
c. enzyme linked receptors
d. intracellular receptors

a. ligand gated ion channel

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what receptor undergo protein phosphorylation

a. ligand gated ion channels
b. g protein coupled receptors
c. enzyme linked receptors
d. intracellular receptors

b. g protein coupled receptor

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what receptor undergo protein and receptor phosphorylation

a. ligand gated ion channels
b. g protein coupled receptors
c. enzyme linked receptors
d. intracellular receptors

c. enzyme linked receptor

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what receptor undergoes protein phosphorylation and altered gene expression

a. ligand gated ion channels
b. g protein coupled receptors
c. enzyme linked receptors
d. intracellular receptors

d. intracellular receptor

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what are the signal transduction

a. transmembrane ligand gated ion channels
b. transmembrane g protein coupled receptor
c. enzyme linked receptor
d. intracellular receptor

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what receptor will be stimulated using the acetylcholine

a. nicotinic recptor
b. gaba receptor

a. nicoinic receptor

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waht will happen if the nicotinic recptor will be simulated?

sodium influx and potassium outflux. this change in ionic concentration across the membrane generates an action potential in a neuron and contraction in skeletal muscle and cardiac muscle.

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what is the result when gaba is simulated

increase chloride influx , resulting in hyperpolarization of neurons and less chances of generating an action potential.

what are the kinds of G protein

Gs, Gq,G

what are three proteins subunit of G protein

alpha, beta gamma.

what protein subunit binds to guanosine triphosphate (GTP) a. alpha b. beta c. gamma

a. alpha

waht protein subuni anchor the G protein in the cell membrane a. alpha b. beta c. gamma

b. beta c. gamma

what is activated by Gs and inhibited by G

adenylyl cyclase

it produces the second messenger cyclic adenosine monophosphate (cAMP)

adenylyl cyclase

this effector when activated by Gg , generated two second messengers : inositol 1,4,5 -triphosphate (IP3) and diacylglycerol (DAG) a. adenylyl cylcase b. phospholipase C

b. phospholipase C

what second messenger increases intracellular calcium concentration , which in turn activates protein kinases? a. inositol 1,4,5-triphosphate (IP3) b. diacylglycerol (DAG)

b. diacylglycerol (DAG)

when alpha subunit dissociates, it also activates what ? a. adenylyl cyclase b. phopholipase C

a. adenylyl cyclase

what is the target of the drug placlitaxel a. tubulin b. dihydrofolate reductase c. 50s subunit

a. ubulin tubulin is the target of antineoplastic agent such as placitaxel

what is the target of trimethoprim a. tubulin b. dihydrofolate reductase c. 50s subunit

b. dihydrofolate reductase dihydrofolate reductase is the target of antimicrobial such as trimethoprim

what is the target of erythomyin a. tubulin b. dihydrofolate reductase c. 50s subunit

c. 50s subunit 50s subunit of the bacterial ribosome is the target of the macrolide antibiotics such as erythromycin

paclitaxel a. ligand gated ion channel b. G protein coupled receptors c. enzyme linked receptor d. intracellular receptor

d. intracellular receptor

trimethoprim a. ligand gated ion channel b. G protein coupled receptors c. enzyme linked receptor d. intracellular receptor

d. intracellular receptor

erythromcin a. ligand gated ion channel b. G protein coupled receptors c. enzyme linked receptor d. intracellular receptor

d. intracellular receptor

what are the two important drug characteristic that can be determined by graded dose response curve

potency, efficacy

therapeutic dose rang of candesartan is 4 to 32 mg . therapeutic dose range of irbesarta in 75 to 300 mg. which is more potent?

candesartn because it has lower EC 50 value than irbesartan.

is a measure of tha amount of drug necessary to produce an effect. a. potency b. efficacy

a. potency

the concentration of the drug necessary of the maximum effect a. EC50 b. Emax

a. EC50

is often used to determine potency a. EC50 b. Emax

a. EC50

is the magnitude of response a drug causes when it interacts wih a receptor . a.potency b. efficacy

a. potency

efficacy is _____ on the number of drug-receptor complexes formed and the intrinsic activiy of the drug a. dependnt b. independent

a. dependent

assumes that the drug occupies all receptors and no increase in response is observed in response to higher concentration of drug. a. EC50 b. Emax

b. Emax ( maximal efficacy of a drug)

which is more useful in clinically a. efficacy b. potency

a. efficacy drug with greater efficacy is more therapeutically beneficial

true or false the lower the EC50 the more potent the drug

true

describe the lenght of interaction (binding) between a ligand and its receptor a. efficacy b. affinity

b. affinity

it further determines its ability to fully or partially activate the receptors a. affinity b. intrinsic activity

b. intrinsic activity

what are the intrinsic activities of a drug?

a. full agonist B. partial agonist c. inverse agonist D. antagonist

drug binds to a receptor and produces a maximal biological response that mimics the reaponse to the endogenous ligand a. full agonist B. partial agonist c. inverse agonist D. antagonist

a. full agonist

phenyleprine a. full agonist B. partial agonist c. inverse agonist D. antagonist

a. full agonist

is a full agonist at alpha 1 adrenoceptors because it produces the same Emax as the endogenous ligand, norepinephrine a. aripiprazole b. phenylephrine

b. phenylephrine

produces complete activation of a receptor at high drug concentrations. a. full agonist b. partial agonist c. inverse agonist

a. full agonist

binding results in less than 1 00% activation, even at very high concentrations. a. full agonist b. partial agonist c. inverse agonist

b. partial agonist

produce a response below the base- line response measured in the absence of drug. a. full agonist b. partial agonist c. inverse agonist

c. inverse agonist

what will happen when norepinephrine or phenylephrine binda to alpha 1 adrenoceptors on vascular smooth muscle

Upon binding to a1-adrenoceptors on vascular smooth muscle, both norepinephrine and phenylephrine stabilize the recep- tor in its active state, thereby increasing Gq activation. Activation of Gq increases intracellular Ca2 +, causing interaction of actin and myo- sin filaments and shortening of the muscle cells. The diameter of the arteriole decreases, causing an increase in resistance to blood flow through the vessel and an increase in blood pressure. Thus, effects of agonists on intracellular molecules, cells, tissues, and intact organ- isms are all attributable to interaction of the drug with the receptor. For full agonists, the dose-response curves for receptor binding and each of the biological responses should be comparable.

have intrinsic activities greater than zero but less than one a. full agonist b. partial agonist c. inverse agonist

b. partial agonist

Even when all the receptors are occupied, it cannot produce the same Emax as a full agonist. a. full agonist b. partial agonist c. inverse agonist

b. partial agonist

. A partial agonist may also act as a partial antagonist of a full agonist true or false

true As the number of receptors occupied by the partial agonist increases, the number of receptors that can be occupied by the full agonist decreases and therefore Emax would decrease until it reached the Emax of the partial agonist.

aripriprazole a. full agonist b. partial agonist c. inverse agonist

b. partial agonist

binds to selected dopamine receptor a. phenylephrine b. aripiprazole

aripiprazole

atypical antipsychotic a. phenylephrine b. aripiprazole

b. aripiprazole Overactive dopaminergic pathways tend to be inhibited by aripiprazole, whereas underactive pathways are stimulated.

unlike full agonists, stabilize the inac- tive R form and cause R* to convert to R. a. full agonist b. partial agonist c. inverse agonist

c. inverse agonist

intrinsic activity less than zero, reverse the activation state of receptors, and exert the opposite pharmacological effect of agonists. a. full agonist b. partial agonist c. inverse agonist

answer: c. inverse agonist

bind to a receptor with high affinity but possess zero intrinsic activity. a. full agonist b. partial agonist c. antagonist

answer: c. antagonist

has no effect on biological function in the absence of an agonist, but can decrease the effect of an agonist when present. a. full agonist b. partial agonist c. antagonist

answer: c. antagonist note:Antagonism may occur either by blocking the drug's ability to bind to the receptor or by blocking its ability to activate the receptor.

What are the different kind of antagonist?

answer: a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

If the antagonist binds to the same site on the receptor as the agonist in a reversible manner a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer: a. competitive antagonist

interferes with an agonist bind- ing to its receptor and maintains the receptor in its inactive state. a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer: a. competitive antagonist

terazocin + norepinephrine (at alpha 1 adrenoceptor)= a. decreasing vascular smooth muscle tone and reducing blood pres- sure b. increasing vascular smooth muscle tone and increasing blood pres- sure

answer:a. decreasing vascular smooth muscle tone and reducing blood pres- sure

8. characteristically shift the agonist dose-response curve to the right (increased EC50) without affecting Emax a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer: a. competitive antagonist

bind cova- lently to the active site of the receptor, thereby permanently reducing the number of receptors available to the agonist a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer: irreversible antagonist

causes a downward shift of the Emax. with no shift of EC50 values a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer: b. irreversible antagonist

are considered noncompetitive antagonists. a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer:b and c

reduce agonist potency (increase EC50) a.competitive antagonist b. non competitive antagonist

answer: a. competitive antagonist

reduce agonist efficacy (decrease Emax). a.competitive antagonist b. non competitive antagonist

answer: b. noncompetitive antagonist

binds to a site other than the agonist-binding site and prevents receptor activation by the agonist a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer: c. allosteric antagonist

causes a downward shift of the Emax of an agonist, with no change in the EC50 value a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer: c. allosteric antagonist

picrotoxin a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer: c. allosteric antagonist

where does picrotoxin binds?

answer:binds to the inside of the GABA-controlled chloride chan- nel. When picrotoxin binds inside the channel, no chloride can pass through the channel, even when GABA fully occupies the receptor.

An antagonist may act at a completely separate receptor, initiating effects that are functionally opposite those of the agonist a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer: d. functional antagonist

Epinephrine + histamine a. competitive antagonist b. irreversible antagonist c. allosteric antagonist d. functional antagonist

answer: d. functional antagonist note: A classic example is the functional antago- nism by epinephrine to histamine-induced bronchoconstriction. Histamine binds to H1 histamine receptors on bronchial smooth muscle, causing bronchoconstriction of the bronchial tree. Epinephrine is an agonist at P2-adrenoceptors on bronchial smooth muscle, which causes the muscles to relax.

is defined as a fall of at least 5 mm Hg in diastolic blood pressure. a. quantal dose response curve b. positive response c. ED 50

answer: b. positive response

is the drug dose that causes a therapeutic response in half of the population. a. quantal dose response curve b. positive response c. ED 50

answer: c. ED50

note: The presence of partial agonist displaces some agonist. resulting In diminished receptor response.

note: At high concentration of partial agonist, the agonist is completely displaced, and receptor activity Is determined by the Intrinsic activity of the partial agonist.

what is the meaning of TI ?

answer : Therapeutic Index

of a drug is the ratio of the dose that pro- duces toxicity in half the population {TD50) to the dose that produces a clinically desired or effective response (ED50) in half the population:

answer : Therapeutic Index

what is the formula of Therapeutic Index

answer TI =TD50/ ED 50

low therapeutic index a. warfarin b. penicillin

answer: a. warfarin

high therapeutic index a. warfarin b. penicillin

answer :b. penicillin note:safe and com- mon to give doses in excess of that which is minimally required to achieve a desired response without the risk of adverse effects.

Which of the following best describes how a drug that acts as an agonist at the A subtype of GABA receptors affects signal transduction in a neuron? A. Activation of this receptor subtype alters transcription of DNA in the nucleus of the neuron. B. Activation of this receptor subtype opens ion chan- nels that allow sodium to enter cells and increases the chance of generating an action potential. C. Activation of this receptor subtype opens ion chan- nels that allow chloride to enter cells and decreases the chance of generating an action potential. D. Activation of this receptor subtype results in G protein activation and increased intracellular second mes- senger levels.

Correct answer= C. The GABA-A receptor is a ligand-gated ion channel selective for chloride. Agonlsts for the GABA-A receptor Increase opening of channels, resulting in chloride entry Into the neuron, hyperpolarization, and decreased action potential events.

If 1 mg of lorazepam produces the same anxiolytic response as 10 mg of diazepam, which is correct? A. Lorazepam is more potent than is diazepam. B. Lorazepam is more efficacious than is diazepam. C. Lorazepam is a full agonist, and diazepam is a partial agonist. D. Lorazepam is a better drug to take for anxiety than is diazepam.

Correct answer = A. A drug that causes the same effect at a lower dose is more potent. B and C are incorrect because without information about the maximal effect of these drugs, no conclusions can be made about efficacy or Intrin- sic activity. D Is Incorrect because the maximal response obtained Is often more important than the amount of drug needed to achieve it.

If 1 0 mg of oxycodone produces a greater analgesic response than does aspirin at any dose, which is correct? A. Oxycodone is more efficacious than is aspirin. B. Oxycodone is less potent than is aspirin. C. Aspirin is a full agonist, and oxycodone is a partial agonist. D. Oxycodone and aspirin act on the same drug target.

Correct answer = A. Drugs with greater response at maxi- mally effective concentrations are more efficacious than drugs with a lower maximal response. Choice B is incorrect since no Information Is given about the half maximal con- centrations of either drug. Choices C and Dare Incorrect since It Is not known if both drugs bind to the same receptor population.

In the presence of propranolol, a higher concentration of epinephrine is required to elicit full antiasthmatic activity. Propranolol has no effect on asthma symptoms. Which is correct regarding these medications? A. Epinephrine is less efficacious than is propranolol. B. Epinephrine is a full agonist, and propranolol is a par- tial agonist. C. Epinephrine is an agonist, and propranolol is a com- petitive antagonist. D. Epinephrine is an agonist, and propranolol is a non- competitive antagonist.

Correct answer = C. Since propranolol decreases the effect of epinephrine but the inhibition can be overcome by giv- ing a higher dose of epinephrine, propranolol must be a competitive antagonist. If D were correct, even very high concentrations of epinephrine would not be able to elicit a maximal effect in the presence of propranolol. Since pro- pranolol has no effect by ltseH, A and B are Incorrect.

In the presence of picrotoxin, diazepam is less efficacious at causing sedation, regardless of the dose. Picrotoxin has no sedative effect, even at the highest dose. Which of the following is correct regarding these agents? A. Picrotoxin is a competitive antagonist. B. Picrotoxin is a noncompetitive antagonist. C. Diazepam is less efficacious than is picrotoxin. D. Diazepam is less potent than is picrotoxin.

Correct answer = B. Since picrotoxin decreases the maxi- mal effect of diazepam regardless of the diazepam dose, it is a noncompetitive antagonist. Picrotoxin has no efficacy alone, so C is incorrect. No information is provided about potency of either drug.

Haloperidol, chlorpromazine, and clozapine are antipsy- chotic medications that bind to the D2 subtype of dopa- mine receptors, with a binding affinity of haloperidol > chlorpromazine > clozapine. Which statement would have to be correct to conclude that the mechanism of antipsychotic effects for these drugs is via binding to D2 receptors? A. Haloperidol should have the lowest potency of the three antipsychotic drugs. B. D2 receptor binding should also be related to the potency of these drugs in causing Parkinson's-like adverse effects. C. A positive correlation should exist between the affin- ity of these drugs to bind to D2 receptors and their potency for antipsychotic actions. D. Clozapine would have to be more potent than chlor- promazine for decreasing psychosis.

Correct answer = C. To conclude that the mechanism of antipsychotic effect for these drugs is via binding to D2 receptors, there should be a positive correlation between the affinity of the drugs for D2 receptors and their potency for antipsychotic actions. Haloperidol should have the high- est antipsychotic potency and clozaplne the lowest. There Is no guarantee the therapeutic effects and adverse effects are mediated by the same receptor population; therefore, a different correlation may exist for the adverse effects and D2 receptor affinity.

If there were spare fl1-adrenergic receptors on cardiac muscle cells, which statement would be correct? A. The number of spare fl1-adrenergic receptors deter- mines the size of the maximum effect of the agonist epinephrine. B. Spare fl1 adrenergic receptors make the cardiac tis- sue less sensitive to epinephrine. C. A maximal effect of epinephrine is seen when only a portion of fl1 adrenergic receptors are occupied. D. Spare receptors are active even in the absence of epinephrine.

Correct answer = C. Only a fraction of the total receptors need to be bound to elicit a maximum cellular response when spare receptors are present. The other choices do not accurately describe the effects of having spare receptors.

Which of the following up-regulates postsynaptic a1- adrenergic receptors? A. Daily use of amphetamine that causes release of norepinephrine B. A disease that causes an increase in the activity of norepinephrine neurons C. Daily use of phenylephrine, an a1 receptor agonist D. Daily use of prazosin, an a1 receptor antagonist

Correct answer= D. Up-regulation of receptors occurs when receptor activation is lower than normal, such as when the receptor Is continuously exposed to an antagonist for that receptor. Down-regulation of receptors occurs when recep- tor activation Is greater than normal because of continuous exposure to an agonist, as described in A, B, and C.

Methylphenidate helps patients with attention deficit hyperactivity disorder (ADHD) maintain attention and perform better at school or work, with an EDso of 10 mg. However, methylphenidate can also cause significant nausea at higher doses (TD50 "' 30 mg). Which is correct regarding methylphenidate? A. The therapeutic index of methylphenidate is 3. B. The therapeutic index of methylphenidate is 0.3. C. Methylphenidate is more potent at causing nausea than treating ADHD. D. Methylphenidate is more efficacious at causing nau- sea than treating ADHD.

Correct answer = A. Therapeutic Index Is calculated by divid- ing TD50 by ED50 (30/10), making B incorrect. Cis incorrect because methylphenidate is more potent at treating ADHD (it takes a lower dose) than causing n

Which is correct concerning the safety of using warfarin (with a small therapeutic index) versus penicillin (with a large therapeutic index)? A. Warfarin is a safer drug because it has a low thera- peutic index. B. Warfarin treatment has a high chance of resulting in dangerous adverse effects if bioavailability is altered. C. The high therapeutic index makes penicillin a safe drug for all patients. D. Penicillin treatment has a high chance of causing dangerous adverse effects if bioavailability is altered.

Correct answer = B. Agents with a low n (that is, drugs for which dose is critically important) are those drugs for which bioavailability critically alters the therapeutic and adverse effects. A is incorrect, because a drug with a low Tl is not generally considered to be safe. C Is Incorrect because a high Tl does not ensure safety across the entire patient population. D Is Incorrect because the hi!1J Tl makes it unlikely that bioavailability alters the incidence of therapeu- tic or adverse effects.