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.Pharmacology > Lecture 2: Pharmacokinetics > Flashcards

Lecture 2: Pharmacokinetics Flashcards

1
Q

in general, what is a drug?

A

any substance that causes a change in biological effect

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2
Q

epinephrine is an ___ in the heart

A

agonist

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3
Q

administration of epinephrine causes and increase in __ and __

A

heart rate and contractile force

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4
Q

t/f an increase in concentration of epinephrine caused an increase in response

A

true

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5
Q

what is represented by Emax?

A

the max physiologic effect achieved by a drug

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6
Q

Emax is a measure of __

A

efficacy

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7
Q

what is represented by Ed50?

A

the dose needed to reach 50% maximal response

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8
Q

ED50 is a measure of __

A

potency

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9
Q

two drugs can be equally effective, but Ifone drug requires a smaller dose to reach the same response, it is said to be more __

A

potent

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10
Q

a lower ED50 means __

A

the drug is more potent

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11
Q

comparisons of drugs should be made between drugs that produce the same ___ and ideally at the same __

A

response; receptor

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12
Q

graded response curves are useful for comparing parameters in ____

A

controlled experimental system

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13
Q

when comparing two drugs in a cell based assay, what type of dose curve would you use?

A

graded response curve

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14
Q

quantal dose is important to determining ___ and ___

A

range of therapeutic doses and doses where toxicity arises

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15
Q

therapeutic window

A

range of doses with therapeutic effect and minimal toxicity

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16
Q

the therapeutic index is measured as the ration of ___ over __

A

Td50/Ed50

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17
Q

as the therapeutic index (TI) increases, what will happen to the Effective and Toxic curves?

A

they will be further apart

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18
Q

as a therapeutic index increases, what happened to the safety of the drug?

A

increases

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19
Q

t/f the E and T curves can sometimes overlap

A

true

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20
Q

what does it mean when the E and T curves overlap?

A

that in order for the drug to be effective, some patients required a dose that was found to be toxic in some other patients

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21
Q

if a drug has a small therapeutic window, a small increase in dose could be expected to result in

A

more risk of adverse reactions

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22
Q

patients should be closely monitored if the drug has a __ therapeutic window

A

small

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23
Q

give an example of a drug with a small therapeutic window

A

warfarin

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24
Q

drugs with a __ therapeutic index and window can be given in large doses to reach effective dose with little risk of adverse effects

A

large

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25
Q

give an example of a drug with a large therapeutic window

A

penicillin

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26
Q

what is a receptor?

A

protein within a cell that is capable of modulating cellular effects based on the binding of drug or endogenous molecules

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27
Q

activation of a receptor results in __

A

cellular response

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28
Q

agonist binds preferentially to ___ receptors and stabilizes this conformation, resulting in a shift towards more __ and therefore more __

A

active; active conformation and physiologic effect

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29
Q

t/f binding of drug to receptor determines the level of effect

A

true

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30
Q

what is represented by Bmax/

A

max receptor binding

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31
Q

Kd is the __ constant

A

dissociation

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32
Q

what is represented by the Kd?

A

drug concentration required to produce 50% receptor occupancy

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33
Q

the Kd value is a measure of the drug __ for the __

A

Affinity; receptor

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34
Q

if you increase the __ of a drug, you better the chances of receptor binding, even if the affinity is low

A

dose

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35
Q

is there a 1:1 ratio between receptor binding and graded response?

A

not usually

36
Q

explain the concept of spare receptors

A

not all receptors may need to be bound to agonist in order for the full response to be achieved

37
Q

drug’s affinity can be used as a measure of __

A

selectivity

38
Q

t/f it is very rare for a drug to be 100% selective for a specific receptor @ any given dose

A

treu

39
Q

in most cases, a drug is more selective because it has a higher ___ for one receptor than another

A

affinity

40
Q

how can knowledge about affinity be used to better drug therapy? Refer to example of prazosin and tamsulosin

A

prazosin and tamsulosin are drugs used to treat urine retention. praz has a higher affinity for A receptors in the blood vessels, but can cause orthostatic hypertension. Tamsulosin is designed to have higher affinity for B receptors in urinary tract (no dizziness)

41
Q

t/f Kd can provide indication of response, efficacy, and/or potency

A

false

42
Q

what causes off-target drug effect?

A

binding of drug to an unintended receptor

43
Q

what is one of the most common causes of adverse dug effects?

A

unintended and off-target drug effects

44
Q

what are three questions to ask when predicting off-target drug effects?

A
  1. is the target receptor expressed in other tissues?
  2. does the drug easily distribute to other tissues?
  3. does the drug have affinity for other tissue receptors?
45
Q

t/F off-target drug effects are always adverse

A

false

46
Q

explain the example of histamine as an on-target but in wrong tissue

A

blocking histamine receptors in the periphery manages the symptoms of allergies, but blocking the receptors in the CNS results in sedation

47
Q

what are idiosyncratic effects?

A

effects that have origin/cause that is unrelated to known interactions of drug / receptors

48
Q

allergic effects can sometimes be predicted, but are unrelated to the ___ of the drugs and are rather caused by __

A

pharmacological properties; immune system

49
Q

propanolol is an example of a __ blocker

A

beta

50
Q

if propranolol (a beta blocker) is administered before a dose of epinephrine, what is the result on heart rate?

A

no change

51
Q

antagonists are classes by __

A

method used to reach blocking / inhibitory effect

52
Q

non-receptor class antagonists do not __

A

bind to receptor

53
Q

what are chemical non-receptor antagonists?

A

drugs that bind to another to prevent action of agonist

54
Q

provide an example of chemical non-receptor antagonist

A

protamine sulfate to heprin

55
Q

what are physiological non-receptor antagonists?

A

counteract agonist effect by modulating a different target

56
Q

give an example of physiological non-receptor antagosnt

A

diazepam against epinephrine

57
Q

explain the concept of receptor antagonists

A

interact with the receptor in the same way the agonist would

58
Q

what are the 2 types of receptor class antagonists?

A
  1. orthostatic (“active”)

2. allosteric

59
Q

what is the role of orthostatic receptor antagonists?

A

binds to same site as agonist and can be reversible or irreversible

60
Q

reversible orthstatic receptor antagonists are called

A

competitive antagonists

61
Q

irreversible orthostatic antagonists are called

A

non-competitive antagonists

62
Q

allosteric receptor antagonists bind to ___

A

non-active site of receptor

63
Q

t/f allosteric receptor antagonist binding can be either reversible or irreversible

A

true

64
Q

both reversible and irreversible allosteric receptor antagonists are called

A

allosteric antagonist

65
Q

most antagonist binding is __

A

reversible

66
Q

ASA binding is ___ and inhibits ___ (the key enzyme in platelet aggregation

A

irreversible; COX-1

67
Q

why is ASA binding irreversible?

A

platelets cannot make new receptors because they do not have a nucleus and will just die away anyway

68
Q

competitive antagonists can be __ by the agonist

A

bumped out of place

69
Q

you can totally negate the antagosnt by __. However, the agonist will still experience a significant loss in __

A

increasing the concentration of agonist; potency

70
Q

non-competitive antagonists interact __ with the agonist site or bind the ___ site

A

strongly; allosteric

71
Q

why does increasing the concentration of agonist not affect response when in the presence of a non-competitive antagonist?

A

the antagonist binds to a site different than active site the agonist binds to

72
Q

when an allosteric antagonist binds, it makes a ___ to the receptor, which prevents __

A

conformational change; binding of agonist to active site

73
Q

non-ciometive antagonists cause a decrease in __- and possibly ___

A

efficacy and potency

74
Q

if an antagonist binds irreversibly, what must happen to restore full response?

A

new receptor must be made

75
Q

if an antagonist binds reversibly, what must happen to restore full response?

A

wait it out, time course is amount of time taken for antagonist to release from the allosteric site

76
Q

allosteric antagonists may also be called __

A

negative allosteric modulators

77
Q

what is the effect of allosteric antagonists?

A

can decrease or increase the ability of the agonist to bind

78
Q

positive allosteric modulators bind to what site on receptor?

A

non-active site

79
Q

positive allosteric modulators may increase both __ and __

A

efficacy and potency

80
Q

benzodiazepines are PAMs of the __ receptors

A

GABA

81
Q

t/f antagonists are capable of producing a response on their own

A

false

82
Q

t/f antagosnts have no defined Emax for efficacy

A

true

83
Q

role of inverse agonists

A

cause reduction of effect below baseline levels by stabilizing the inactive receptor conformation

84
Q

inverse agonists cause the equilibrium to shift towards __

A

Ri

85
Q

it is very difficult to measure the effect of inverse agonists if the constitutive activity is very __ and in this case, it may be classed as a __ agonist

A

low ; neutral

86
Q

t/f it is not clinically clear if there is a difference between antagonists and inverse agonists

A

true

.Pharmacology (55 decks)

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