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POM Exam 2 > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

drug targets that are proteins

A
  • receptors
  • ion channels
  • enzymes
  • carriers
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2
Q

ion channels

A
  • when activated will open and form pores in cells and allow ions in and out
  • blockers
  • modulators
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3
Q

blockers

A
  • permeation blocked
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4
Q

modulators

A
  • increased or decreases opening probability
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5
Q

enzymes

A
  • inhibitors
  • false substrate
  • pro-drug
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6
Q

inhibitors

A
  • normal reaction inhibited
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7
Q

false substrate

A
  • abnormal metabolite produced
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8
Q

pro-drug

A
  • active drug produced
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9
Q

carriers

A
  • molecules that transport molecules from one side of a membrane to another
  • normal transport
  • inhibitor
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10
Q

agonist drugs

A
  • mimic the effects of the endogenous agonists
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11
Q

antagonist drugs

A
  • block the effects of endogenous agonists
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12
Q

Kd

A
  • the concentration of the drug at which 50% of receptors are occupied
  • direct reflection of the affinity of the drug for the receptor
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13
Q

low Kd means

A
  • greater affinity
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14
Q

all reactions between agonist and receptor

A
  • reversible
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15
Q

dependence of agonist binding to receptors

A
  • concentration dependent
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16
Q

Hill Langmiur equation

A

Y = [D]
Kd + [D}

[D] = dose of drug
Kd = dissociation constant
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17
Q

the lower the Kd

A
  • the more potent the drug

- further to the left

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18
Q

efficacy

A
  • how much effect the drug can produce

- looking for 100% therapeutic effect

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19
Q

what determines potency

A
  • how tightly the drug binds to the receptor
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20
Q

what determines effectiveness

A
  • what that drug does to the receptor after it is bound to it
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21
Q

which y axis tells you the Kd

A
  • has to say receptor occupancy
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22
Q

relationship between receptor occupancy and therapeutic effect

A
  • no relationship

- possible to achieve a full therapeutic effect while only occupying a certain percent of receptors

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23
Q

signal amplification

A
  • maximal cellular response at less-than-maximal receptor occupancy
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24
Q

receptor reserve

A
  • receptors that are available for agonist binding but are not necessary for maximal effect
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25
Q

competitive antagonist

A
  • binds for same binding site as the endogenous agonist
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26
Q

non-competitive agonist

A
  • endogenous agonist and antagonist bind at different sites

- can be reversible or irreversible

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27
Q

how competitive agonist affects dose curve

A
  • decrease in potency
  • Kd shifts right
  • need more substrate to outcompete the antagonist
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28
Q

how non-competitive agonist affects dose curve

A
  • decrease in efficacy

- you have knocked out receptors so you can’t get the same effect

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29
Q

full agonist

A
  • elicits maximal response from its receptor

- may be an endogenous molecule or a drug

30
Q

how is maximal response defined

A
  • defined based on natural agonist that exists in your body
31
Q

partial agonist

A
  • elicits a submaximal response from its receptor
  • doesn’t elicit response to the same level
  • you may not want a drug to be a full agonist
32
Q

neutral antagonist

A
  • reduces effect of an agonist but has no effect itself

- inhibits normal agonist from producing any response

33
Q

inverse agonist

A
  • receptors have a low level of signaling even when there is nothing bound to them
  • inhibits basal activity of a receptor in the absence of the normal agonist
  • may be competitive antagonists if they bind to the same receptor site as the endogenous agonist
34
Q

why don’t we consider inverse agonists to be antagonists?

A
  • they aren’t competing with the endogenous agent
35
Q

clinically relevant inverse agonists/antagonists

A
  • metoprolol
  • losartan
  • famotidine
  • risperidone
  • naloxone
  • MFLRN
  • mutha fuckas lit right now
36
Q

full agonist example

A
  • endorphins
  • morphine
  • heroin
37
Q

partial agonist example

A
  • bupenorphine

- Nalbuphine

38
Q

neutral antagonist example

A
  • naltrexone
39
Q

inverse agonist example

A
  • naloxone
40
Q

what are drug response curves useful for

A
  • describing effects that are continuous
41
Q

example of continuous effects

A
  • reduction of pain
  • reduction of BP
  • reduction of BP
42
Q

what do you do with dose response curves when the variable isn’t quantal

A
  • you describe a population of people instead of an individual
43
Q

ED50

A
  • effective dose at which 50% of patients are benefitting
44
Q

TD50

A
  • toxic dose at which 50% of patients are suffering toxicity
45
Q

LD50

A
  • concentration at which 50% of patients die
46
Q

therapeutic window

A
  • the range of drug concentration between the minimum effective dose and the minimum toxic dose
  • TD-ED
47
Q

minimum effective dose

A
  • dose at which drug is minimally effective
48
Q

minimum toxic dose

A
  • dose at which toxicity starts in the patients
49
Q

big therapeutic window

A
  • far apart curves

- you want therapeutic dose to have good benefit with little to no toxicity

50
Q

therapeutic index

A
  • measure of the safety of a drug

- not always the best measurement

51
Q

therapeutic index formula

A
  • TILE

TD50/ED50 OR LD/50

52
Q

do you want therapeutic index to be high or low?

A
  • high
  • you want toxic dose to be extremely high
  • and effective dose to be low
53
Q

why might dose response curves look different?

A
  • dependent on drug binding to the same receptor or not to exert its effects
54
Q

what does the curve look like on a drug binding to different receptors

A
  • share a point of origin and then spread apart
55
Q

off-target toxicity

A
  • produce toxic effects by binding to a different receptor
56
Q

mechanism based toxicity

A
  • drug binds to the same receptor for therapeutic and toxic/lethal effects
57
Q

certain safety factor

A
  • LD1/ED99
58
Q

what value do you want for the certain safety factor?

A
  • HIGH
  • you want the lethal dose that kills 1% of people to be high
  • you want the effective dose that helps 99% of people to be low
59
Q

drug antagonistic relationship

A
  • two drugs together produce less than additive effect
60
Q

drug additive relationship

A
  • two drugs together produce additive effect
61
Q

drug synergistic relationship

A
  • two drugs together produce more than additive effect
62
Q

potentiation

A
  • when one drug has therapeutic effect and a second drug helps it
63
Q

potentiation example

A
  • cephalosporins and probenecid
64
Q

cephalosporins and probenecid

A
  • probenecid has no effect of its own
  • potentiates the effect of antibiotics
  • increased serum concentration of drug and prolonged therapeutic effect
65
Q

tolerance/desensitization

A
  • reduced effect with continued use of a drug
66
Q

short term tolerance/desensitization

A
  • tachyphylaxis
67
Q

receptor inactivation

A
  • after a receptor has been bound to an agonist for a period of time or after multiple times
  • it can become inactivated
  • will turn off and no longer produce effect
68
Q

receptor internalization

A
  • once it binds to the agonist,
  • it get internalized into the cell
  • and then becomes recycled
69
Q

receptor down regulation

A
  • receptor binds to agonist
  • becomes internalized
  • then degraded
  • cell has to resynthesize a new receptor
70
Q

fewer active receptors but still enough to give 100% of a response

A
  • shifts right on dose response curve
71
Q

fewer active receptors but NOT enough to give 100% response

A
  • decrease % effect
  • may shift left
  • you have deactivated some of the receptors to help you get that effect

POM Exam 2 (21 decks)

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