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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
Q

NON-SPECIFIC BINDING CURVE: Binding experiment is same as for Total Binding Curve but in the presence of high dose of — ligand

A

COMPETING NONRADIOACTIVE

26
Q

how to get specific saturation isotherm curve

A

total- nonspecific

total: all radioactivity on filter, bound and free radioligand

nonspecific: noncompetive bound to tissue, all radioligand attached to filter

27
Q

what is Bmax?

A

maximal number of binding site= y axis (top of curve)

28
Q

what is KD?

A

concentration of radioligand where half maximal binding is obtained

x axis equal to 1/2 Bmax

29
Q

lower KD = — receptor affinity

A

higher

Kd= (Koff/Kon)
Kd= concentration of radioligand where half maximal binding (1/2Bmax) is obatined

30
Q

higher Kd = — receptor affinity

A

lower

high Kd means takes longer for ligand to bind to receptor

31
Q

how does competition binding analysis curve created?

A

measure radioactivity of a drug
and then slowly increase competiting non radioactivity until there is only competing ligand attached to the receptors

32
Q

Competition binding analysis measures the ability of the — ligand to compete off the radioligand in the binding to the same receptors.

A

NON-radioactive

33
Q

what is IC50?

A

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
Q

explain pink vs red

A

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
Q

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 —

A

occupied.

more drug= more recptors bound

has max effect when receptors are saturated

36
Q

which curve is the antagonist?

A

red= flat

either antagonist= binds but nothing happens
or
drug does not bind at all

37
Q

which curve has the lowest EC50?
what does that mean?

A

EC50= amount of drug needed to fill 50% of receptors (to create half max response)

lower EC50 means a more potent agonist

38
Q

which drug has the lower Kd

A

Kd for black is lower then Kd for orange

lower EC50= more potent agonist

39
Q

which curve is agonist, partial agonist, antagonist?

A
40
Q

The ability of ligands to activate receptors is not an all or none property, but is actually a graded property.

A

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
Q

what kind of receptor has intrinsic efficacy of 0

A

antagonist= no reponse

intrinsic efficacy= The ability of ligands to activate receptors is not an all or none property, but is actually a graded property.

42
Q

what type of receptor has intrinsic efficacy of 1

A

full agonist

gets maximal response

intrinsic efficacy= The ability of ligands to activate receptors is not an all or none property, but is actually a graded property.

43
Q

what type of receptor has intrinsic efficacy of 0-1

A

partial agonist

less than maximal response

intrinsic efficacy= The ability of ligands to activate receptors is not an all or none property, but is actually a graded property.

44
Q

the effect/potency of a ligand is determined by — and —

A

fractional occupancy (how many receptors bound)

intrinisic efficacy (how well the ligand activates the receptor)

45
Q

what happens to does response curve with competitive antagonist?

A

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
Q

what is red curve?

A

non competitive antagonists

47
Q

how does non competitive antagonist effect the dose response curve?

A

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
Q

An — induces a biological response upon binding to the receptor, BUT in OPPOSITE direction compared to an agonist.

A

inverse agonist

if normal agonist causes increased cAMP, then inverse agonist does the opposite → would cause decreased cAMP

49
Q

what will spare receptors cause

A

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
Q

Because of a surplus of receptors, can get a GREATER level of response despite an — concentration of agonist

A

EQUIVALENT

51
Q

Because of a surplus of receptors, can get an EQUIVALENT level of response from a — concentration of agonist

A

LOWER

decreased amount of drug would cause same reaction cause there are more receptors to start intercellular reaction

52
Q

what is receptor desensitization

A

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
Q

what is receptor downregulation

A

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
Q

explain receptor supersensitivity after denervation

A

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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