Drug Receptors

Question 1

B adrenergic =

Answer 1

GPCR

Question 2

NAchR

Answer 2

ligand gated

Question 3

NMDA

Answer 3

dual ligand gated (needs gly and glu)

Question 4

DAT

Answer 4

dopamine transmembrane transport protein

Question 5

acetylcholinesterase

Answer 5

enzyme

Question 6

vitamin d and retinoid receptor dimer

Answer 6

nuclear receptor

Question 7

MU opioid receptor

Answer 7

GPCR

Question 8

affinity

Answer 8

the ability of a drug to bind its biological target (once its in the compartment how does it bind the receptor)

Question 9

kd =

Answer 9

[k-1]/[k+1]= [L][R]/[LR]

Question 10

ka =

Answer 10

1/kd

Question 11

high affinitry drug has

Answer 11

a low kd and it will bind more receptors at a low concentration than a low affinity drug

Question 12

affinity is more highly influenced by

Answer 12

off rate than on rate because of the ka formula and the kd formula

Question 13

buprenorphine affinity compared to morphine, fentanyl, and methadone

Answer 13

higher affinity; can bind receptor at sub nanomolar concentrations

Question 14

potency

Answer 14

drugs that are more potent take less concentration to have the same effect than less potent drugs

Question 15

clinical example for potency

Answer 15

fentanyl was more potent than alfentanil for patients that needed to be intubated

Question 16

term for what happens when we bind the receptor…then this can be determined

Answer 16

efficacy….but efficacy does not equal binding

Question 17

EC50

Answer 17

median effective concentration; the concentration at which you get 50% of the maximal drug effect

Question 18

full agonist

Answer 18

a drug that can provide the maximal effect at a given receptor so morphine is a full agonist at the Mu opioid receptor

Question 19

partial agonist

Answer 19

cannot get 100% efficacy

Question 20

neutral antagonist

Answer 20

sits on the receptor and does nothing

Question 21

inverse agonist

Answer 21

inverse agonist is a drug which when I place it on the receptor it does the opposite- so this curve shows a partial inverse agonist (if I went all the way down to 0 on the bottom it would be a full inverse agonist)

Question 22

clinical example of opioids @ receptor (agonists vs. partial agonists)

Answer 22

morphine (full agonist) > thienorphine > buprenorphine

Question 23

reversible inhibition

Answer 23

noncovalent binding example would be ibuprophen for cox 1

Question 24

irreversible inhibition

Answer 24

permanent alteration- aspirin is a permanent cox 1 inhibiotr; organophosphates lead to acetylcholinesterase inhibition

Question 25

competitive inhibition

Answer 25

tends to be at the same site; In order to get the same EC50 effect in the presence of the antagonist I have to give you more of my agonist- you will see a shift right
parallel shift but no change in maximum

Question 26

noncompetitive inhibitor

Answer 26

site other than the active site; the inhbitior has irreversibly destroyed the enzyme
So it doesn’t matter if I give you more and more and more of the drug, but I will keep getting decrease in the efficacy axis

decrease in maximum and no change in EC50

Question 27

agonist + neutral competitive antagonist

Answer 27

compared to full agonist, you have the same efficacy and you can reach that 100%, but you have a shift to the right because you need to add more agonist

Question 28

agonist + noncompetitive antagonist

Answer 28

you will have the same curve but it will be lower- theres no shift right but there is a change in the maximum because you can no longer hit that 100% due to the noncompetitive inhibition

Question 29

experimental example of agonists/antagonists

Answer 29

i have a patient whos breathing, i give them morphine and their ventilation depresses, and then i give them naloxone which is an opioid antagonist and their ventilation increases again. what happened? naloxone is a neutral receptor antagonist that did nothing except block the morphine from binding to the Mu receptor

Question 30

naloxone and morphine show you…

Answer 30

the action of a neutral antagonist with an agonist already on board