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SRNA4TopicsAnesthesia > APEX: VALLEY PHARMACODYNAMICS > Flashcards

APEX: VALLEY PHARMACODYNAMICS Flashcards

1
Q

Pharmacodynacmis is the study of

A

Effect site concentration and CLINICAL EFFECT

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2
Q

Describes the relationship between the DRUG DOSE AND PLASMA CONCENTRATION

A

Pharmacokinetics

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3
Q

Pharmacobiophasics unites

A

Pk and PD by examining the relationship between plasma concentration and effect site concentration

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4
Q

Pharmacokinetics studies primarily 2 things

A

Drug dose

Plasma concentration

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5
Q

Pharmacobiophasics studies primarily 2 things

A

Plasma concentration

Effect site concentration

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6
Q

Pharmacodynamics studies primarly 2 things

A

Effect site concentration

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7
Q

Mnemonic to remember each pharmk,pharmB, PharmD

A

KBD

DPEC

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8
Q

What the body does to the drug

A

Pharmakinetics

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9
Q

Relationship is affected by

A

ADME

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10
Q

The biophase aka

A

Effect site

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11
Q

What the drug does the body

A

Pharmacodynamics

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12
Q

Pharmacodynamics concepts

PEDAPIA LETS

A 
Potency
Efficacy
Dose response curve slope
Agonist
Partial Agonist
Inverst agonist
Antagonist
LD50
ED50
Therapeutic index
Stereochemistry
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13
Q

On the dose response curve, the x-axis correlates with:

A

Potency

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14
Q

Dose requires to achieve a given clinical effect

A

potency

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15
Q

Intrinsic ability of a drug to elicit a given clinical effect.

A

Efficacy

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16
Q

Potency is on ___axis, efficacy on ____axis

A

x; y

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17
Q

What does the slope of the dose response curve tells us?

A

How many receptors must be occupied to elicit a clinical effect.

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18
Q

Dose response curve from multiple patients to learn abou tthe

A

individual variability of each patient.

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19
Q

Measure of potency 2

A

ED 50 and E90

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20
Q

The curve shifts to left meaning as far as affinity , potency , dose

A

Increase affinity for receptor, HIGHER POTENCY, lower dose required

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21
Q

The curve shifts to right meaning as far as affinity , potency , dose

A

Decrease affinity for receptor, LOWER POTENCY, Higher dose required

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22
Q

The height of the plateau on the y-axis represents

A

efficacy

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23
Q

Higher plateau means _____efficacy

A

Greater

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24
Q

Lower plateau means _______ efficacy

A

Lower

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25
Q

A steep slope on the dose-response curve implies

A

Most of the receptors must be occupied before we observe the clinical response.

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26
Q

Once the effect is observed, small increase in the dose can have a

A

Profound clinical effect.

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27
Q

Medications with steep slope

A

NMB and inhaled anesthetics.

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28
Q

A drugs that binds to a receptor follows which law?

A

LAW of mass action

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29
Q

There is rate constant for

A

Drug binding and a rate constant for dissociation from the receptor.

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30
Q

Remember that efficacy is measured by the

A

height of the y-axis on the dose response curve.

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31
Q

Mimics an endogenous ligand

A

agonist

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32
Q

Instructs the receptor to produce its maximal response

A

A full agonist

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33
Q

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

A

potency

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34
Q

Continuous administration of an AGONIST may cause (UP or down)

A

DOWN=REGULATION of the target receptors.

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35
Q

Examples of full agonist at the beta receptor

A

NE

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36
Q

It is less efficacious than a full agonist

A

Partial agonist

37
Q

A partial agonist is also called

A

Agonist-antagonist

38
Q

It can block the effects of an agonist by competing for binding sites

A

Partial agonist.

39
Q

Giving a partial opioid agonist to an opioid addicted patient can

A

Precipitate withdrawal

40
Q

Nalbuphine what you should no?

A

provides pain relief but there is a ceilling to its efficacy.

41
Q

Sits in the receptor and prevents an agonist from binding to it, does not tell the cell to do anything.

A

Antagonists

42
Q

By definition no efficacy

A

Antagonist

43
Q

Continuous ADMINISTRATION of an ANTAGONISTS may cause

A

UPREGULATION Of target receptors.

44
Q

Competitive antagonism is (reversible vs irreversible)

A

reversible

45
Q

If a pt receives a competitive antagonist, the dose response curve for the agonist shifts to

A

shifts to the right.

46
Q

Increasing the concentration of the agonist in a competitive antagonism can

A

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 would reflect a reduction in potency.

47
Q

Example of competitive antagonism: Rocuronium competes with

A

Ach at the NMJ. Increasing the concentration of one susbtance increase its ability to compete for the binding site on the receptors/.

48
Q

NONCompetitive antagonism is (reversible vs irreversible)

A

Not reversible (irreversible)

49
Q

Permanently bind to a receptor through covalent bonds and their effect cannot be overcome by increasing concentration of agonist.

A

Noncompetitive antagonists.

50
Q

Noncompetitive antagonists shifts dose response curve for the agonist

A

down, so that it resembles a partial agonist

51
Q

The effects of noncompetitive antagonists can be only reversed by

A

producing new receptors. This explains why these drugs have long duration of action.

52
Q

Example of noncompetitive antagonists?

A

ASA inhibits the COX-1 enzyme for the entire life of the platelet.

53
Q

Has negative efficacy

A

Inverse Agonist

54
Q

Binds to the receptor and causes an opposite effect to that of a full agonist

A

Inverse agonist.

55
Q

Epinephrine is a

A

Full agonist

56
Q

Epinephrine (Full agonist) binds to beta 1 receptor to _______while propranolol (an inverse agonist) binds to the beta-1 receptor to_____

A

increase cAMP, Decrese cAMP

57
Q

G protein modulates

A

cAMP production

58
Q

G protein: An agonist completely

A

activates the receptor and increase cAMP production

59
Q

G proteins; A partial agonist

A

Partailly activates the receptors, it increases cAMP production, but not as much as a full agonist.

60
Q

G Proteins: An inverse agonist

A

Activates the receptor, but because it causes the opposite effect of the agonist, it decreases cAMP production

61
Q

G proteins: Antagonists

A

blocks the ability of the agonist to bind with the receptor, but it does not increase or decrease cAMP production .

62
Q

A new induction agent has a median effective dose of 125 mg and the median lethal dose of 1500 mg. Calculate the TI of the drug?

A

LED (how to remember)
LD50/ ED50 = TI
1500mg/125mg = 12 mg

63
Q

What is the ED50?

A

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

64
Q

ED50 is a measure of

A

Potency

65
Q

LD 50 is the dose that will

A

produce death in 50% of the population

66
Q

The Therapeutic index is a measure of

A

Drug safety

67
Q

TI is the ratio of

A

TI= LD50/ ED 50

68
Q

A drug with narrow therapeutic index has a

A

narrow margin of safety : Examples VA and chemotherapy

69
Q

A drug with WIDE therapeutic index

A

has a wide margin of safety.

70
Q

Chirality is a division of

A

Stereochemistry

71
Q

Deals with molecules that have a center of

A

3D symmetry

72
Q

A molecule with 1 chiral carbon will exist as

A

2 enantiomers

73
Q

The more chiral carbons in a molecue, the ____enantiomers that are created

A

More

74
Q

A racemic mixture contains

A

2 enantiomers in equal amounts.

75
Q

Study of 3 D structures of molecules

A

Stereochemistry.

76
Q

Enantiomers are

A

chiral molecules that are NON-SUPERIMPOSABLE MIRROR IMAGES of one another.

77
Q

Enantiomers are distinguished from each other by

A

the direction they rotate when exposed to polarized light.

78
Q

The D means

A

Dextrorotary enantiomer

79
Q

The dextrorotary enantiomer (+) rotates

A

Clockwise (think Positive DC)

80
Q

The L means

A

Levorotary enantiomer

81
Q

The Levorotary enantiomer (-) rotates

A

Counterclockwise (Negative Lcount)

82
Q

What is a racemic mixtures

A

Contains 2 enantiomers in equal amount. About 1/3 of the drugs we administer are enantiomers, and just about all of these are prepared as racemic mixtures.

83
Q

Drugs that exists as enantiomers often function as

A

2 different drugs, with different affinities for the target receptors and different side effects.

84
Q

Clinical examples of racemic mixtures: bupivacaine

A

S-bupivacaine (Levobupivacaine) is less cardiotoxic than the R-bupivacine or the racemic mixtures

85
Q

Clinical examples of racemic mixtures: Ketamine

A

S enantiomer of ketamine is less likely to cause emergene delirium than the R form, the S form is also more potent.

86
Q

Examples of racemic mixtures VA

A

Isoflurane

Desflurane

87
Q

Examples of racemic mixtures IV anesthetics

A

Ketamine
Thiopental
Methohexital

88
Q

Examples of racemic mixtures : Amide LAs

A

Mepivacaine
Bupivacaine
Prilocaine

89
Q

Examples of racemic mixtures: Pain meds

A

IBuprofen
Ketorolac
Methadone
Morphine

SRNA4TopicsAnesthesia (47 decks)

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