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kaps > Lippincott CHAPTER 2 Drug receptor interactions and pharmacodynamics > Flashcards

Lippincott CHAPTER 2 Drug receptor interactions and pharmacodynamics Flashcards

1
Q

Action of a drug on the body ?

a. pharmacodynamic
b. pharmacokinetic

A

a. pharmacodynamic

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2
Q

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

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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3
Q

what receptor of the cardiac cells respond to epinephrine?

a. B- adrenergic receptor
b. Muscarinic

A

a. B- adrenergic receptor

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4
Q

what receptor of the cardiac cells respond to norephineprine?

a. B- adrenergic receptor
b. Muscarinic

A

a. B-adrenergic receptor

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5
Q

what receptor of the cardiac cells respond to Acetylcholine?

a. B- adrenergic receptor
b. Muscarinic

A

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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6
Q

what are the two states of receptor

A

(R) inactive
(R*) active

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7
Q

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

a. agonist
b. antagonist

A

b. antagonist

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8
Q

shift the equilibrium

a. full agonist
b. partial agonists

A

b. partial agonist

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9
Q

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

A

receptor

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10
Q

what are the four receptor families

A
  1. ligand gated ion channels
    2.G protein coupled receptors
  2. Enzyme lined receptors
  3. intracellular receptors
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11
Q

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

a. hydrophilic ligand
b. hydrophobic ligands

A

a. hydrophilic ligand

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12
Q

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

a. hydrophilic ligand
b. hydrophobic ligands

A

b. hydrophobic ligands

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13
Q

cholinergic nicotinic receptors

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

A

a. ligand gated ion channels

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14
Q

a nd b adrenoceptors

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

A

b. g protein coupled receptors

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15
Q

insulin receptor

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

A

c. enzyme linked receptors

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16
Q

steroid receptors

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

A

d. intracellular receptors

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17
Q

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

a. ligand gated ion channels

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18
Q

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

a. ligand gated ion channel

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19
Q

what receptor undergo protein phosphorylation

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

A

b. g protein coupled receptor

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20
Q

what receptor undergo protein and receptor phosphorylation

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

A

c. enzyme linked receptor

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21
Q

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

A

d. intracellular receptor

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22
Q

what are the signal transduction

A

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

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23
Q

what receptor will be stimulated using the acetylcholine

a. nicotinic recptor
b. gaba receptor

A

a. nicoinic receptor

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24
Q

waht will happen if the nicotinic recptor will be simulated?

A

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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25
Q

what is the result when gaba is simulated

A

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

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26
Q

what are the kinds of G protein

A

Gs, Gq,G

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27
Q

what are three proteins subunit of G protein

A

alpha, beta gamma.

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28
Q

what protein subunit binds to guanosine triphosphate (GTP)

a. alpha
b. beta
c. gamma

A

a. alpha

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29
Q

waht protein subuni anchor the G protein in the cell membrane

a. alpha
b. beta
c. gamma

A

b. beta
c. gamma

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30
Q

what is activated by Gs and inhibited by G

A

adenylyl cyclase

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31
Q

it produces the second messenger cyclic adenosine monophosphate (cAMP)

A

adenylyl cyclase

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32
Q

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

A

b. phospholipase C

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33
Q

what second messenger increases intracellular calcium concentration , which in turn activates protein kinases?

a. inositol 1,4,5-triphosphate (IP3)
b. diacylglycerol (DAG)

A

b. diacylglycerol (DAG)

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34
Q

when alpha subunit dissociates, it also activates what ?

a. adenylyl cyclase
b. phopholipase C

A

a. adenylyl cyclase

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35
Q

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

A

a. ubulin

tubulin is the target of antineoplastic agent such as placitaxel

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36
Q

what is the target of trimethoprim

a. tubulin
b. dihydrofolate reductase
c. 50s subunit

A

b. dihydrofolate reductase

dihydrofolate reductase is the target of antimicrobial such as trimethoprim

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37
Q

what is the target of erythomyin

a. tubulin
b. dihydrofolate reductase
c. 50s subunit

A

c. 50s subunit

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

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38
Q

paclitaxel

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

A

d. intracellular receptor

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39
Q

trimethoprim

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

A

d. intracellular receptor

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40
Q

erythromcin

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

A

d. intracellular receptor

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41
Q

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

A

potency, efficacy

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42
Q

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

which is more potent?

A

candesartn because it has lower EC 50 value than irbesartan.

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43
Q

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

A

a. potency

44
Q

the concentration of the drug necessary of the maximum effect

a. EC50
b. Emax

A

a. EC50

45
Q

is often used to determine potency

a. EC50
b. Emax

A

a. EC50

46
Q

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

a.potency
b. efficacy

A

a. potency

47
Q

efficacy is _____ on the number of drug-receptor complexes formed and the intrinsic activiy of the drug

a. dependnt
b. independent

A

a. dependent

48
Q

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

A

b. Emax ( maximal efficacy of a drug)

49
Q

which is more useful in clinically

a. efficacy
b. potency

A

a. efficacy

drug with greater efficacy is more therapeutically beneficial

50
Q

true or false

the lower the EC50 the more potent the drug

A

true

51
Q

describe the lenght of interaction (binding) between a ligand and its receptor

a. efficacy
b. affinity

A

b. affinity

52
Q

it further determines its ability to fully or partially activate the receptors

a. affinity
b. intrinsic activity

A

b. intrinsic activity

53
Q

what are the intrinsic activities of a drug?

A

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

54
Q

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

a. full agonist

55
Q

phenyleprine

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

A

a. full agonist

56
Q

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

a. aripiprazole
b. phenylephrine

A

b. phenylephrine

57
Q

produces
complete activation of a receptor at high drug
concentrations.

a. full agonist

b. partial agonist

c. inverse agonist

A

a. full agonist

58
Q

binding
results in less than 1 00%
activation, even at very
high concentrations.

a. full agonist

b. partial agonist

c. inverse agonist

A

b. partial agonist

59
Q

produce a response below the base-
line response measured
in the absence of drug.

a. full agonist

b. partial agonist

c. inverse agonist

A

c. inverse agonist

60
Q

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

A

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.

61
Q

have intrinsic activities greater than zero but less than
one

a. full agonist

b. partial agonist

c. inverse agonist

A

b. partial agonist

62
Q

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

A

b. partial agonist

63
Q

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

true or false

A

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.

64
Q

aripriprazole

a. full agonist

b. partial agonist

c. inverse agonist

A

b. partial agonist

65
Q

binds to selected dopamine receptor

a. phenylephrine

b. aripiprazole

A

aripiprazole

66
Q

atypical antipsychotic

a. phenylephrine

b. aripiprazole

A

b. aripiprazole

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

67
Q

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

A

c. inverse agonist

68
Q

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

A

answer: c. inverse agonist

69
Q

bind to a receptor with high affinity but possess zero
intrinsic activity.

a. full agonist
b. partial agonist
c. antagonist

A

answer: c. antagonist

70
Q

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

A

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.

71
Q

What are the different kind of antagonist?

A

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

72
Q

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

A

answer:
a. competitive antagonist

73
Q

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

A

answer:
a. competitive antagonist

74
Q

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

A

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

75
Q
  1. 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

A

answer: a. competitive antagonist

76
Q
A
77
Q

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

A

answer: irreversible antagonist

77
Q

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

A

answer: b. irreversible antagonist

78
Q

are considered noncompetitive antagonists.

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

A

answer:b and c

79
Q

reduce agonist potency (increase
EC50)

a.competitive antagonist
b. non competitive antagonist

A

answer: a. competitive antagonist

80
Q

reduce agonist efficacy
(decrease Emax).

a.competitive antagonist
b. non competitive antagonist

A

answer: b. noncompetitive antagonist

81
Q

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

A

answer: c. allosteric antagonist

82
Q

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

A

answer: c. allosteric antagonist

83
Q

picrotoxin

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

A

answer: c. allosteric antagonist

84
Q

where does picrotoxin binds?

A

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.

85
Q

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

A

answer: d. functional antagonist

86
Q

Epinephrine + histamine

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

A

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.

87
Q

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

A

answer: b. positive response

88
Q

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

A

answer: c. ED50

89
Q

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

A
90
Q

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.

A
91
Q

what is the meaning of TI ?

A

answer : Therapeutic Index

92
Q

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:

A

answer : Therapeutic Index

93
Q

what is the formula of Therapeutic Index

A

answer TI =TD50/ ED 50

94
Q

low therapeutic index

a. warfarin
b. penicillin

A

answer: a. warfarin

95
Q

high therapeutic index

a. warfarin
b. penicillin

A

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.

96
Q

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.

A

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.

97
Q

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.

A

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.

98
Q

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.

A

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.

99
Q

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.

A

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.

100
Q

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.

A

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.

101
Q

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.

A

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.

102
Q

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.

A

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.

103
Q

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

A

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.

104
Q

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.

A

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

105
Q

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.

A

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.

kaps (16 decks)

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