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Week 2 Flashcards

Pharmacodynamics (77 cards)

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1
Q

pharmacodynamics

A

the study of the effects of a drug on the body

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2
Q

receptor

A

a macromolecule (protein) or macromolecular complex (protein complex) which a ligand (drug) acts on to elicit a physiological effect

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3
Q

ligand

A

an endogenous (endorphins) or exogenous (drug) molecule that acts on a receptor to elicit a physiological effect
-fits like a lock and key in receptor

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4
Q

what are the two states receptors exist in during equilibrium and what do they produce?

A

On-producing a physiological effect
off- not producing a physiological effect

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5
Q

what causes the equilibrium to shift

A

ligands binding (endogenous or drugs)
-can be reversible and fast

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6
Q

how do ligands shift the equilbrium

A

endogenous ligands bind>change receptors shape> cause downstream effects in cell

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7
Q

what is the dose response curve

A

also known as the concentration response curve…shows the physiological effects of a given amount of agonist

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8
Q

EC50 is

A

the concentration necessary for an agonist to elicit 50% of a maximal response

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9
Q

what does an agonist do

A

binds to receptor and turns it on (mimic the natural ligands)

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10
Q

what is the endogenous ligand of opioid receptors

A

endorphins (produced in the body)

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11
Q

what are the agonist of opioid receptors

A

opiates like morphine
(some are full agonist, some are partials)

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12
Q

what is a partial agonist

A

bind to receptors and turns it on but not fully like fill agonist

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13
Q

example of a partial agonist

A

methadone which is why its a good treatment for prevention of withdrawal symptoms in patients with opioid use disorder(they dont get high but helps with the withdrawal because it binding the same receptors)

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14
Q

how do you know when a drug is a partial agonist reading a graph

A

it only reaches 50%/half way while the full agonist reaches 100%

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15
Q

efficacy

A

is the capacity of a drug to activate a receptor and generate a cellular response

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16
Q

Emax

A

the maximum effect a given drug can produce

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17
Q

100Emax means

A

full agonist

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18
Q

lower Emax under 100 means

A

partial agonist

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19
Q

potency

A

measure the amount of drug needed to produce an effect of a given magnitude

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20
Q

EC50

A

concentration necessary to elicit 50% maximal response
lower the EC50 the more potent
(amount of drug needed to cause a response)

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21
Q

when reading a graph how do you know which drug is the most potent

A

it reaches 100 quicker at a lessor dose than the others

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22
Q

positive allosteric modulators

A

-stabilize the protein to allow the site to work more effectively
-increases the activity of another ligand at a receptor

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23
Q

how do you recognize positive allosteric modulator on a graph

A

they have no intrinsic activity
therefore on a graph by themselves they produce a flat line at zero(dont activate the receptor directly)

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24
Q

what does a positive allosteric modulator do

A

makes an agonist more potent
-increases efficacy

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25
what does positive allosteric modulators do the the EC50
it goes down because it is more potent (closer to 0) because it makes the agonist more important increasing potency
26
why are PAMs( positive allosteric modulators) important as it relates to analgesia
PAMS bind seperate site on opioid receptor> increasing the receptors sensitivity to the bodys natural opioid peptides>lower risk of addiction, respiratory depression -allow for lower doses of opioids because of the increase of potency due to PAMs
27
antagonist
prevents a receptor from being activated by binding to receptor -no intrinsic factor as well by itself it will be zero on a graph
28
ex of antagonist
Naloxone (Narcan) is an opioid receptor antagonist. -prevents endorphins or opiates from activating the receptor (reversing overdose)
29
Competitive Antagonist
competes with agonist to prevent activation however can be outcompeted by agonist by increasing doses(of agonist)
30
do competitive antagonist effect efficacy
no, but the do decrease affinity(desire to bind to receptor) and potency
31
noncompetitive antagonist
CANNOT be outcompeted by increasing amounts of agonist
32
what are the two types of noncompetitive antagonist
allosteric and irreversible
33
allosteric (noncompetitive antagonist)
binds to a site on the receptor other than the agonist binding site> changes the shape of the receptor> making it less responsive to the agonist
34
irreversible (noncompetitive antagonists)
binds to the receptor and doesn't leave> permanently blocking the receptors response to the agonist (decrease EC50)
35
how does the graph looks of an irreversible vs allosteric noncompetitive antagonist
Irreversible= flat lines Emax Allosteric= decreases Emax but not to 0 and can be reversed
36
Example of irreversible antagonist
Aspirin=permanently blocks COX> prevents prostaglandins and thromboxanes> cannot form clots(can cause excessive bleeding)
37
example of allosteric antagonist
Ibuprofen=can inhibit multiple targets (ion channels, enzymes, and proteins pops on and off can cause a little bit of bleeding but increase bleeding if takin with aspirin
38
how can partial agonist act like an antagonist
can act as an competitive antagonist against full agonist -too much partial agonist inhibits fully agonist from binding
39
inverse agonist
bind and turn receptor off
40
example of inverse agonist
Atropine>turns of baseline activity of the receptor(in SA and AV node)>blocking acetylcholine> treats bradycardia -acetylcholine slows the SA and AV nodes down (PSNS)
41
drug specificity
extent to which a drug acts on a single receptor -extent in which a drug produces therapeutic effect without causing any other physiological changes
42
what is a dirty drug
a drug that acts on multiple receptors causing adverse affects -dose dictates the amount of binding to different receptors
43
example of dirty drug
Olanzapine (Zyprexa) binds on many receptors
44
drug affinity
measure how much a drug loves the receptor -probability of a drug occupying a receptor at a given concentration(how attracted to the receptor the drug is)
45
Kd
how tightly a ligand binds to a receptor (how strong the binding affinity is) is the conc. at which 50% of receptors are occupied=conc. of ligands when half are bound(how many receptors are needed for the conc.) (lower Kd=Higher Affinity=less ligands are needed to occupy significant portion of the receptors)
46
how can partial agonist become full agonist
by binding to more receptors (spare receptors) to get a better Emax
47
can Full agonist increase efficacy by binding more
no because they have high affinity >binds strongly=high efficacy> able to produce maximal response when bound to receptors
48
IC50
conc. of antagonist necessary to inhibit 50% maximal response
49
how does IC50 graphs looks
start at 100 and decline(going away from maximum)
50
what does competitive antagonist do to EC50
increase dose needed to reach max therefore shifting chart to the right.
51
types of receptors
1.Intracellular 2. Receptor Tyrosine Kinases 3.cytokine Receptors 4. Ion channels 5.Ligand gated ion channels 6. G Protein couples receptors (GPCRs)
52
intracellular receptor
nuclear receptors=stimulate gene transcription by binding intracellular response elements -slow acting(require gene transcription) -long lasting effect>cause cancer *extremely lipophilic (allows their ligands to easily diffuse through cell membrane)
53
example of ligands that bind to intracellular receptors
endogenous ligands: Sex hormones(steroids), Corticosteroids (aldosterone, cortisol), Vitamin D, and Thyroid hormone
54
Drugs that target Intracellular receptors
estrogen replacement therapy, synthetic thyroid hormone, tamoxifen(breast cancer), prednisone (allergies, blood disorders, etc)
55
Receptor tyrosine kinases (RTKs)
without a ligand=monomers with ligands> dimerize)bind each other> phosphorylation>activate kinase domain> activate other proteins
56
examples of endogenous ligands bind to RTKs
Growth (trophic factors)= VEGF (angiogenesis), hGH (gene expression), EGF(promote cell proliferation), cytokines ANP(vasodilation), hormones insulin(glucose uptake)
57
drugs that target RTKs
tyrosine kinase inhibitors for the treatment of cancer
58
Cytokine receptors
cytokines from immune cells act on cytokine receptors (JAK-STAT receptors) -triggered by infection, inflammation, trauma, sepsis, cancer, reproduction
59
what is an endogenous ligand that bind cytokine receptors
cytokines
60
Drugs that target cytokine receptor
monoclonal antibodies for the treatment of autoimmune disease (immune disease)
61
ligand gated ion channel
ligands open and close gate to allow for ions to travel
62
Examples of endogenous ligands
Acetylcholine, GABA, glutamate, serotonin
63
Drugs that target ion channels
Many anticonvulsants(treat seizures), anti-arrhythmic (treat irregular heartbeats), analgesics(pain reliever), anesthetics (insensitivity to pain)
64
GPCRs
binding of a ligand causes G protein activation (GDP>GTP)< dissociation, and interaction w.secondary messengers
65
how many percentage of drugs are G-protein coupled receptors
30%
66
What do GPCRs drug regulate
-sensation -behavior and mood -immunity and inflammation -ANS -cellular density -tumor growth
67
Secondary messengers (GPCRs)
extracellular agonist>activate GPCR > trigger intracellular signaling molecules
68
GaS
Stimulatory (increase production of cAMP) =turn on
69
GaI
inhibitory (decrease production of cAMP)=turn off
70
GaQ
increase cytosolic Ca2+
71
therapeutic index
measures drug safety
72
LD50
median lethal dose=dose which kills 50% of the subjects
73
ED 50
median effective dose= dose at which 50% of the population have the desired therapeutic effect
74
Sensitization
: increased response to the same dose with repeated exposure i. Due to receptors being off for so long> when reintroduced super sensitive
75
desensitization
reduction in signaling in response to continuous stimulation
76
tachyphylaxis
acute desensitization. Decrease in response to a given dose after repetitive administraton.
77
tolerance
decreased responsiveness to a drug following repeated administration. i. Higher doses are needed to produce the same effect ii. Can cause tolerance of other related drugs
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