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23 spring: pharm > Test 1: lecture 7-8 > Flashcards

Test 1: lecture 7-8 Flashcards

1
Q

what does agonist do?

A

binds and causes cellular response

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2
Q

what does antagonist cause?

A

binds to receptor and has NO effect

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3
Q

4 criteria for being receptor

A
  1. Saturability
  2. Specificity
  3. Reversibility- ligand can attach and detach
  4. Bifunctional Role
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4
Q

4 classes of receptors

A
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5
Q

example of ion channel receptor

A

many neurotransmitter receptors, e.g. acetylcholine (nicotinic), GABA, aspartate, glycine.

neurotransmitter binds: ion channels open, ions flow through down concentration gradiant (immediate)

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6
Q

how does ion channel receptor work

A

neurotransmitter binds: ion channels open, ions flow through down concentration gradiant (immediate)

very fast, milliseconds

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7
Q

examples of G-protein coupled receptors

A

neurotransmitters, most peptide hormones, some biogenic amines (e.g. catecholamines, serotonin).

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8
Q

Nearly 1000 genes in the human genome encodes for proteins in — class of receptors 40 - 50% of pharmaceuticals in the market today act on these receptors

A

G-protein coupled receptors

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9
Q

how does G-protein coupled receptor work

A

ligand binds
causes change in structure
GTP comes in and bumps off GDP
alpha(GTP) and gamma(beta) uncouple and cause down stream effects

fast,100s of ms to seconds

  • Transducing agent that couples the activated receptor to the cellular response
  • Trimeric protein
  • Binds GTP and then uncouples from receptor upon receptor activation
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10
Q
A
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11
Q

AT1 receptors can —

A

have several intracellular responses (both + and -)

G-protein coupled receptors can link to more than one G-protein.

G-protein coupled receptors may be able to initiate cell signaling not traditionally associated with G-proteins.

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12
Q

how does tyrosine kinase receptor work?

A

ligand bins
dimerizes
autophosphorylation
cause chain reaction of adding phosphate to targets in cells

cause intracellular signals (seriers of kinases)

Receptors for insulin, growth factors (growth hormone)

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13
Q

examples of tyrosine kinase receptors

A

Receptors for insulin, growth factors (growth hormone)

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14
Q

how long does tyrosine kinase receptor take?

A

minutes

Receptors for insulin, growth factors (growth hormone)

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15
Q

what are some transcription factor receptors?

A

Receptors for steroids, thyroid hormone, vitamin D, retinoids

hydrophobic (can move through membrane)

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16
Q

how do transcription factor receptors work

A

ligand moves into cell, binds in cytoplasm, moves to nucleus, change genes made

Receptors for steroids, thyroid hormone, vitamin D, retinoids

very slow, hours to days

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17
Q

how fast are transcription factor receptors

A

very slow, hours to days

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18
Q

fastest to slowest receptor classes

A
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19
Q

many receptors systems have — which are distributed in the body in specific areas

A

subtypes

can make drug target specific receptor in specific tissue

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20
Q

Kd

A

dissociation constant= (Koff)/(Kon)

free/bound
how tightly ligand is bound to the receptor

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21
Q

two types of binding analyses

A

saturation isotherm
competition bind analysis

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22
Q

how to make saturation isotherm graph

A

tubes of same amount of tissue and increasing amount of radiolabeled drugs

washed through filter

count radioactibity associated with tissue on the filter: can have bound and unwashed unbound drug

23
Q

this is a total binding curve which means Binding experiment done with — amount of tissue in each tube but with — concentrations of radioligand

A

same

increasing

24
Q

how to measure nonspecific binding of radioligand binding?

A

combine tissue, radioligand and excessive amounts of nonradioactive competing ligand

filter

the competing ligand will bind to tissue, any radioactivity on the filter is from unbound drug stuck to filter (not important) can be used to subtract from total to get actual radioacivity of the sample→ specific

25
NON-SPECIFIC BINDING CURVE: Binding experiment is same as for Total Binding Curve but in the presence of high dose of --- ligand
COMPETING NONRADIOACTIVE
26
how to get specific saturation isotherm curve
total- nonspecific **total**: all radioactivity on filter, bound and free radioligand **nonspecific**: noncompetive bound to tissue, all radioligand attached to filter
27
what is Bmax?
maximal number of binding site= y axis (top of curve)
28
what is KD?
concentration of radioligand where half maximal binding is obtained x axis equal to 1/2 Bmax
29
lower KD = --- receptor affinity
higher Kd= (Koff/Kon) Kd= concentration of radioligand where half maximal binding (1/2Bmax) is obatined
30
higher Kd = --- receptor affinity
lower high Kd means takes longer for ligand to bind to receptor
31
how does competition binding analysis curve created?
measure radioactivity of a drug and then slowly increase competiting non radioactivity until there is only competing ligand attached to the receptors
32
Competition binding analysis measures the ability of the --- ligand to compete off the radioligand in the binding to the same receptors.
NON-radioactive
33
what is IC50?
concentration of competitor which inhibits binding by 50%. rank order of potency should correspond with their biological potency lower IC50= higher receptor affinity in comparing competitors decreased radioactivity= more competiting ligand pink curve has no affinity for receptor= does not kickoff radioactivty ligand
34
explain pink vs red
this graph is showing the same ligand and receptor with **different** competition ligands **pink** competition ligand does not bind/ has no affinity for the receptor orange: competition ligand binds to receptor IC50 is where 50% of radioactive ligand has been kicked off receptor lower IC50= higher receptor affinity in comparing competitors
35
dose response curve shows Effect of drug was thought to be proportional to the fraction of receptors occupied by the drug. Maximal effect when all receptors are ---
occupied. more drug= more recptors bound has max effect when receptors are saturated
36
which curve is the antagonist?
red= flat either antagonist= binds but nothing happens or drug does not bind at all
37
which curve has the lowest EC50? what does that mean?
EC50= amount of drug needed to fill 50% of receptors (to create half max response) lower EC50 means a more potent agonist
38
which drug has the lower Kd
Kd for black is lower then Kd for orange lower EC50= more potent agonist
39
which curve is agonist, partial agonist, antagonist?
40
The ability of ligands to activate receptors is not an all or none property, but is actually a graded property.
intrinsic efficacy FULL AGONISTS * Get maximal response * Intrinsic Efficacy = 1 PARTIAL AGONIST * Less than maximal response * Intrinsic Efficacy between 0 and 1 ANTAGONIST * No response * Intrinsic Efficacy = 0
41
what kind of receptor has intrinsic efficacy of 0
antagonist= no reponse ## Footnote **intrinsic efficacy**= The ability of ligands to activate receptors is not an all or none property, but is actually a graded property.
42
what type of receptor has intrinsic efficacy of 1
full agonist gets maximal response ## Footnote **intrinsic efficacy**= The ability of ligands to activate receptors is not an all or none property, but is actually a graded property.
43
what type of receptor has intrinsic efficacy of 0-1
partial agonist less than maximal response ## Footnote **intrinsic efficacy**= The ability of ligands to activate receptors is not an all or none property, but is actually a graded property.
44
the effect/potency of a ligand is determined by --- and ---
**fractional occupancy** (how many receptors bound) **intrinisic efficacy** (how well the ligand activates the receptor)
45
what happens to does response curve with competitive antagonist?
still gets to max, but needs more of original drug to get there parallel shift of dose response curve to right without affecting maximal response
46
what is red curve?
non competitive antagonists
47
how does non competitive antagonist effect the dose response curve?
**takes more drug, but never gets to max** * Antagonist causes **reduced efficacy** of agonist, maximum response no longer achieved. * Covalent modification of receptor or interacting regulatory site is possible. May involve destruction of receptors * Shift of dose-response curve to right WITH **REDUCTION OF MAXIMAL RESPONSE.**
48
An --- induces a biological response upon binding to the receptor, BUT in OPPOSITE direction compared to an agonist.
inverse agonist if normal agonist causes increased cAMP, then inverse agonist does the opposite → would cause decreased cAMP
49
what will spare receptors cause
hypersensitive reaction would reach max, much faster then normal binding Because of a surplus of receptors, can get a GREATER level of response despite an EQUIVALENT concentration of agonist Because of a surplus of receptors, can get an EQUIVALENT level of response from a LOWER concentration of agonist
50
Because of a surplus of receptors, can get a GREATER level of response despite an --- concentration of agonist
EQUIVALENT
51
Because of a surplus of receptors, can get an EQUIVALENT level of response from a --- concentration of agonist
LOWER decreased amount of drug would cause same reaction cause there are more receptors to start intercellular reaction
52
what is receptor desensitization
over time same amount of drug will have decreased effect if you take away drug, give body time to recover, you can restart drug to get original response levels
53
what is receptor downregulation
cell will move receptor off of cell wall in response to long term drug if you take away drug, receptors will move back to cell wall can then give drug again
54
explain receptor supersensitivity after denervation
cell is used to getting drug from nerve nerve damaged= no drug cell tries to find drug by increasing amount of receptors on its wall if nerve repaired and impulse comes back, there are now too many receptors and will cause very **large response/supersensitive**

23 spring: pharm (46 decks)

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