Pharmacology Basics Flashcards

1
Q

actions of the biological system on the drug
What the body does to the drug

A

Pharmacokinetics

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2
Q

Pharmacokinetics describes:

A

What the body does to the drug

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3
Q

study of the undesired effects of chemicals on biological systems

A

Toxicology

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4
Q

action of drugs on the biological system
What the drug does to the body

A

Pharmacodynamics

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5
Q

Pharmacodynamics describes:

A

What the drug does to the body

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6
Q

Molecules whose interaction with receptor causes cellular responses

A

Agonists

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7
Q

Molecules whose interaction with receptor does not cause cellular response

A

Antagonists
But can prevent action of an agonist

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8
Q

Difference between agonists and antagonists

A

Agonists cause cellular responses; antagonists do not

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9
Q

3 general types of drug targets

A

Cell surface membrane receptors
Membrane ion channels
Other macromolecules

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10
Q

Type of drug-target binding that is rare for drug-receptor interactions and irreversible

A

Covalent bonds

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11
Q

Drug-target binding for aspirin

A

Aspirin forms covalent (irreversible) bond with cyclooxygenase

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12
Q

Aspirin forms this type of bond with cyclooxygenase

A

Covalent (irreversible)

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13
Q

Aspirin forms covalent (irreversible) bond with this

A

Cyclooxygenase

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14
Q

Type of drug-target binding that is the primary electrostatic attractor

A

Ionic bond

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15
Q

Type of drug-target binding that is the secondary attractor; increased influence with better “fit”

A

Hydrogen and/or Van der Waals bonds

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16
Q

Opiate stereoisomers that are analgesic

A

L opiates
(D opiates are not)

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17
Q

Opiate stereoisomers that are antitussive

A

Both L and D opiates

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18
Q

Do stereoisomers require a symmetric or asymmetric center?

A

Asymmetric

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19
Q

proteins that bind with specificity and selectivity but are not receptors
No activity change with binding

A

Acceptors

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20
Q

Is there activity change with binding of acceptors?

A

No

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21
Q

Acceptors can affect pharmacodynamics by binding the drug and preventing:

A

Prevent drug interaction with the receptor

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22
Q

Drugs binding to acceptors is also referred to as this

A

Nonspecific protein binding

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23
Q

Nonspecific protein binding refers to this

A

Drugs binding to acceptors

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24
Q

Part of the dose response curve that is a measure of drug effectiveness or efficacy

A

Emax or the ceiling

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25
Q

Part of the dose response curve that is an indicator of binding affinity (strength) for the drug

A

Steepness of curve

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26
Q

Part of the dose response curve that is a measure of drug potency

A

Dose at 50% = effective dose 50% (ED50)

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27
Q

Emax or the ceiling of the dose response curve is a measure of this

A

Drug effectiveness / efficacy

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28
Q

Steepness of the dose response curve is an indicator of this

A

Binding affinity (strength) for the drug

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29
Q

Effective dose 50% (ED50; dose at 50% response) is a measure of this

A

Drug potency

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30
Q

Comparison of dose at a single level of effect
Does not allow comparison of effectiveness, merely dose at each drug’s half maximal response

A

Potency

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31
Q

Potency is this

A

Comparison of dose at a single level of effect
(dose at each drug’s half maximal response)

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32
Q

Does potency increase or decrease as the dose response curve shifts left?

A

Increases

33
Q

Measure of maximal response effect
Does not compare dose at maximal effect
NOT a dose

A

Efficacy (aka intrinsic activity)

34
Q

Efficacy (intrinsic activity) measures this

A

Maximal response effect

35
Q

Does efficacy increase or decrease as dose response curve shifts down?

A

Decreases

36
Q

Does potency or efficacy measure dose?

A

Potency

37
Q

Intrinsic activity is also referred to as this

A

Efficacy

38
Q

Efficacy is also referred to as this

A

Intrinsic activity

39
Q

Describes when fewer than the total number of receptors are required to be occupied to achieve a maximal response

A

Receptor reserve (“spare receptors”)

40
Q

Receptor reserve (“spare receptors”) describes when:

A

Fewer than the total number of receptors are required to be occupied to achieve a maximal response
Maximal effect may not require maximal binding

41
Q

Type of antagonism that binds the receptor but does not activate
Prevents other molecules from binding the receptor

A

Receptor antagonism

42
Q

Type of antagonism that is a direct chemical interaction between agonist and antagonist, that renders agonist inactive

A

Chemical antagonism

43
Q

Type of antagonism that involves two agonists with opposing effects

A

Functional antagonism

44
Q

A receptor antagonist does this

A

Binds receptor but does not activate
Prevents other molecules from binding the receptor

45
Q

A chemical antagonist does this

A

Directly chemically interacts with agonist and renders it inactive

46
Q

Functional antagonism involves this

A

2 agonists with opposing effects

47
Q

Type of antagonism where the agonist and inhibitor compete for access to binding site
Maximal effect maintained; potency reduced

A

Competitive

48
Q

Type of antagonism with two major types: irreversible (covalent binding) and allosteric antagonists
Reduces efficacy

A

Noncompetitive antagonism

49
Q

Competitive antagonism reduces this

A

Potency

50
Q

Competitive antagonism has no effect on this

A

Maximal effect / efficacy

51
Q

Noncompetitive antagonism reduces this

A

Efficacy

52
Q

Allosteric antagonists mimic the dose response curve of this

A

Noncompetitive antagonism

53
Q

Allosteric ______ enhance effect of primary receptor activation

A

Allosteric agonists

54
Q

Allosteric _____ reduce the effect of primary receptor activation

A

Allosteric antagonists

55
Q

Allosteric agonists has this affect on dose response curve

A

Opposite of competitive = increase potency, shift left

56
Q

Allosteric antagonist has this affect on dose response curve

A

Mimic non-competitive = lower curve

57
Q

Type of agonists that when added to a full agonist, may reduce the maximal activity achieved with only the full agonist by blocking the full agonist’s access to the active receptor

A

Partial agonists

58
Q

_________ by partial agonist has less effect than full agonist

A

Maximal activity

59
Q

Type of agonists that have intrinsic activity opposing agonist activity
Some receptors are normally ‘active’ and require an agonist to turm them “off”

A

Inverse agonists

60
Q

Type of agonist that lowers the activity from that of full agonist, but still remains more active that constitutive activity

A

Partial agonist

61
Q

Type of agonist that decrease activity below that of the constitutive activity level

A

Inverse agonist

62
Q

state of decreased responsiveness to a drug (describes loss of response to drugs)

A

Desensitization

63
Q

rapid desensitization due to repeated exposure to the same drug concentration

A

Tachyphylaxis

64
Q

Desensitization that is rapid and receptors are usually retained

A

Tachyphylaxis

65
Q

Type of desensitization that is not dose dependent

A

Tachyphylaxis

66
Q

Tachyphylaxis describes this

A

rapid desensitization due to repeated exposure to the same drug concentration

67
Q

reduced response to drug exposure over a long time frame, usually involving reduced receptor numbers

A

Tolerance

68
Q

Type of desensitization involving changes in receptor number and/or function due to drug exposure

A

Tolerance

69
Q

4 mechanisms of desensitization

A

Uncoupling of the receptor from downstream signaling
Endocytosis
Degradation
Down regulation

70
Q

Uncoupling of the receptor, endocytosis, degradation, and down regulation are mechanisms of this

A

Desensitization

71
Q

processes that reduce the number of receptor in a cell membrane
Occurs following continuous exposure to agonist or endogenous ligand, dictated at least in part by negative feedback
Mechanisms may include decreased gene transcription or increased mRNA degradation

A

Down regulation

72
Q

2 mechanisms of down regulation

A

Decreased gene transcription
Increase mRNA degradation

73
Q

Occurs when:
The cell is continuously exposed to an antagonist, decreasing exposure to agonist, Disease reduces concentration or availability of endogenous ligand
Genetic amplification

A

Up regulation

74
Q

Up regulation may occurs due to these 3 things

A

Continuous exposure to antagonist, decreasing exposure to agonist
Disease reduces concentration/availability of endogenous ligand
Genetic amplification

75
Q

Drug that induces up-regulation of opioid receptors

A

Naloxone

76
Q

Stroke or spinal cord injury induces upregulation of these

A

Cholinergic receptors

77
Q

Receptor that is upregulated in non-small cell lung cancer

A

EGFR (epidermal growth factor receptor)

78
Q

exaggerated receptor response resulting from chronic reduction of receptor stimulation
Usually due to prolonged lack of exposure

A

Supersensitivity

79
Q

Supersensitivity describes this:

A

Exaggerated receptor response resulting from chronic reduction of receptor stimulation