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A. Apex Review > Pharmacology: Pharmacodynamics > Flashcards

Pharmacology: Pharmacodynamics Flashcards

1
Q

what the body does to the drug is known as?

A

Pharmacokinetics

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2
Q

Explanation of the relationship between the dose you administer and the drugs plasma concentration over time is known as?

A

pharmacokinetics

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3
Q

Pharmacokinetics relationship is affected by what four variables?

A

absorption
distribution
metabolism
elimination

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4
Q

Does plasma concentration always correlate to clinical effect?

A

No

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5
Q

Biophase is also known as?

A

effect site

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6
Q

What determines the clinical effect of a drug?

A

The drug concentration in biophase (not plasma)

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7
Q

What the drug does to the body represents what?

A

Pharmacodynamics

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8
Q

Pharmacodynamics describes the relationship between what two things?

A

effect site concentration and the clinical effect

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9
Q

Units PK and PD by examining the relationship between plasma concentration and effect site concentration, is known as?

A

Pharmacobiophasics

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10
Q

What does the dose response curve illustrate?

A

relationship between the drug dose and its clinical effects.

It tells us about potency, efficacy, and slope

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11
Q

Where is potency represented on the dose response curve?

A

x-axis

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12
Q

dose required to achieve a given clinical effect is known as?

A

Potency

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13
Q

What affects potency?

A 
absorption 
distribution
metabolism
elimination 
receptor affinity
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14
Q

What are measures of potency? (2)

A

ED50

ED90

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15
Q

What causes a left shift on the dose response curve?

A

increased affinity for the receptor
higher potency
lower dose required

increased affinity for the receptor leading to a higher potency and ultimately a lower dose required

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16
Q

What cause a right shift on the dose response curve?

A

decreased affinity for the receptor
lower potency
higher dose required

decreased affinity for the receptor leads to a lower potency and a higher dose is then required

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17
Q

explain efficacy, what does it measure?

A

efficacy is a measure of the intrinsic ability of a drug to elicit a given clinical effect

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18
Q

Where is efficacy represented on the dose response curve?

A

The y axis represents efficacy, it is the height of the plateau

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19
Q

Once the plateau phase is reached (max efficacy) for a given drug, what will giving more drug do?

A

More drug administration once plateau phase is reached (efficacy) will increase the risk of toxicity.
It will NOT produce additional effect.

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20
Q

What does the slope of a drug on the dose response curve tell you?

A

The slope tells us how many of the receptors must be occupied to elicit a clinical effect

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21
Q

What does a steep slope on the dose response curve tell you?

A

A steep slope implies that most of the receptors must be occupied before we observe the clinical response.

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22
Q

Name two types of drugs that have steep slopes?

A

NMB and inhaled anesthetics

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23
Q

How would you learn about individual variability of each patient?

A

compare the dose response curves from multiple patients

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24
Q

On graph of agonists, partial agonists, antagonists and inverse agonist. (looks like a head scratcher)

Which curve represents each drug classification?

A

A (Top curve) - Full Agonist
B (Second curve) - Partial Agonist
C (middle/straight line from 0 on y-axis) - Antagonist
D (bottom curve) - Inverse Agonist

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25
Q

a drug that binds to a receptor follows what law?

A

law of mass action

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26
Q

There is a rate constant for drug ___.

A

binding.

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27
Q

There is a rate constant for drug dissociation from ____.

A

the receptor

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28
Q

Drugs may be classified based on their degree of

A

efficacy.

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29
Q

On the dose response curve. the Y-Axis represents?

A

Efficacy — it is measured by the height of the y-axis

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30
Q

Full agonist binds to a receptor and turns on a specific cellular

A

response

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31
Q

Full agonist mimic what?

A

endogenous lignads

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32
Q

Full agonist instructs the receptor to produce its

A

maximal response

33
Q

Full agonist:

Different drugs may produce the same clinical effect, but each may require a different dose to do so. This is a difference in

A

Potency

34
Q

Continuous administration of an agonist may cause what to happen to the target receptors?

A

down -regulation

35
Q

an example of a full agonist at the beta receptor is:

A

Norepinephrine

36
Q

examples of Full agonist:

A

dopamine
propofol
alfentanil

37
Q

Partial agonist bind to a receptor but is only capable of….

A

partially turning on a cellular response

38
Q

it is less efficacious than a full agonist:

A

a Partial agonist

39
Q

Partial agonist can block the effects of an agonist by

A

competing for binding sites

*example - giving a partial opioid agonist to an opioid addicted pt can precipitate withdrawl

40
Q

an example of a partial agonist that provides pain relief:

A

nalbuphine – provides pain relief but there is a ceiling to its efficacy.

41
Q

the antagonist does what to the receptor?

A

sits in the receptor

prevents an agonist from binding to it.

42
Q

what does an antagonist tell the cell?

A

it does not tell the cell to do anything.

43
Q

what is the efficacy of an antagonist?

A

by definition, it does not have efficacy

44
Q

continuous administration of an antagonist may cause what to happen of target receptors?

A

up-regulation

45
Q

is competitive antagonism reversible?

A

yes

46
Q

if a pt receives a competitive antagonist, the dose response curve for the agonist shifts right or left?

A

to the right

47
Q

Increasing the concentration of the agonist can overcome competitive antagonism (the agonist can achieve the same efficacy), but since it requires more drug molecules to achieve the desired clinical effect, the dose response curve would reflect…

A

a reduction in potency

48
Q

give an example (scenario) of competitive antagonism:

A

Rocuronium competes with Ach at the NMJ.

Increasing the concentration of one substance increases its ability to compete for the binding site on the receptor.

other examples - atropine, NMBDs

49
Q

is noncompetitive antagonism reversible?

A

not reversible

50
Q

Noncompetitive antagonists bind to a receptor how?

A

Permanently

usually through covalent bonds

51
Q

the effects of this drug class cannot be overcome by increasing concentration of agonist:

A

noncompetitive anatgonists

52
Q

What does a NC Antagonist do to the dose response curve?

A

shifts the dose response curve for the agonist DOWN

so that it resembles a partial agonist

53
Q

The effects of a NC antagonist can only be revered by:

A

producing new receptors.

54
Q

explain the DOA of NC antagonist

A

they have long DOA due to their permanent binding to the receptor. new receptors must be produced.

55
Q

common example of a noncompetitive antagonist:

A

Aspirin – it inhibits the COX-1 enzyme for the entire life of the PLT

56
Q

Inverse agonist bind to the receptor and cause…

A

an opposite effect to that of a full agonist.

57
Q

inverse agonist effect on efficacy

A

Negative efficacy

58
Q

example of an inverse agonist:

A

propranolol - binds to the beta-1 receptor to decrease cAMP

59
Q

looking at a hypothetical receptor. it is a G-protein that modulates cAMP production.

an agonist completely activates the….

A

receptor and increase cAMP production

60
Q

looking at a hypothetical receptor. it is a G-protein that modulates cAMP production.

a partial agonist would….

A

partially activate the receptor.

Increase cAMP production but not as much as the full agonist would

61
Q

looking at a hypothetical receptor. it is a G-protein that modulates cAMP production.

an inverse agonist activates the receptor, but …

A

b/c it causes the opposite effect of the agonist, it decreases cAMP production.

62
Q

looking at a hypothetical receptor. it is a G-protein that modulates cAMP production.

an antagonist blocks the ability of the….

A

agonist to bind to the receptor

does not increase or decrease cAMP production.

63
Q

the effect of two drugs given at the same time are added to each other (1+1 =2)

this is known as

A

addition

64
Q

the effect of two drugs given at the same time is greater than the sum of their individual effects (1+1 = 3)

this is called

A

synergism

65
Q

the effect of one drug is enhanced by a drug that has no effect of its own (1+0 = 3)

this is known as

A

potentiation

66
Q

simultaneous administration of one drug cancels out the effect of a second drug (1+1 = 0 )

this is called

A

antagonism

67
Q

1 + 1 = 0

A

antagonism

68
Q

1 + 0 = 3

A

potentiation

69
Q

1 + 1 = 3

A

Synergism

70
Q

1 + 1 = 2

A

addition

71
Q

formula for therapeutic index (TI) =

A

LD50 / ED50

72
Q

median effective dose = 125mg
median Lethal dose = 1500mg

what’s the TI?

A

1500mg/ 125mg

TI = 12

73
Q

this is the dose that produces the expected clinical response in 50%. of the population

A

ED50

74
Q

ED50 is a measure of

A

potency

75
Q

the dose that will produce death in 50% of The population

A

LD50

76
Q

how do we determine the median therapeutic safety margin for a desired clinical effect?

A

LD50- ED50

77
Q

the measure of drug safety is?

A

Therapeutic Index
the ratio of the LD50 and ED50

TI = LD50 / ED50

78
Q

a drug with a narrow therapeutic index has a narrow ….

A

margin of safety

79
Q

a drug with a wide therapeutic index has a ….

A

wide margin of safety

A. Apex Review (4 decks)

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