Pharmacodynamics II - Darmani

Question 1

Full agonist

Answer 1

Produce a maximal response which a given tissue is capable of producing

Question 2

Partial agonist

Answer 2

• Produce a smaller maximal effect
• Occupy all of the available receptors to produce their effect
• Can antagonize the effects of a full agonist
• Can have a greater affinity for a particular receptor than a full agonist

Question 3

Competitive antagonist

Answer 3

Do not produce any response

Question 4

Efficacy

Answer 4

• The ability or strength of a drug to produce a maximal effect subsequent to binding to its appropriate receptor
• Dependent upon intrinsic efficacy and total receptor concentration
• Varies among tissues because it is dependent on receptor number

Question 5

Efficacy limit for competitive antagonists

Answer 5

0

Question 6

Efficacy limit for full agonist

Answer 6

1

Question 7

Efficacy limit for partial agonist

Answer 7

Between 0 and 1

Question 8

Intrinsic efficacy

Answer 8

• The amount of stimulus a drug molecule applies to the receptor
• Does not vary among tissues, but is a property of the drug molecule itself for any given type of receptor

Question 9

Inverse agonists

Answer 9

Drugs that produce changes opposite to those produced by other agonists

Question 10

Efficacy limit for inverse agonists

Answer 10

From -1 to 0

Question 11

R*

Answer 11

Active form of GPCRs

Question 12

R

Answer 12

Inactive form of GPCRs

Question 13

How do full agonists affect GPCRs?

Answer 13

• Preferentially bind to and maximally enrich R*

* Maximally increase effector activity

Question 14

How do partial agonists effect GPCRs?

Answer 14

• Show a weaker preference for R*

* Shift eq to a smaller extent

Question 15

How do inverse agonists effect GPCRs?

Answer 15

• Bind preferentially to R

* Leads to a reduction in basal effector activity

Question 16

How do silent antagonists effect GPCRs?

Answer 16

• Bind equally well to both R* and R

* Do not alter eq or effector activity

Question 17

Extended Ternary Complex Model

Answer 17

Accounts for allosteric modulators and suggests that GPCRs may spontaneously adopt multiple active and inactive conformational states

Question 18

Functionally selective agonists (aka biased agonists)

Answer 18

A unique drug that recognizes and stabilizes a chimeric conformation of a specific signaling pathway via a GPCR that activates multiple signals

Question 19

Positive Allosteric Modulator

Answer 19

Increases affinity and/or efficacy of an agonist

Question 20

Negative Allosteric Modulator

Answer 20

Decreases affinity and/or efficacy of an agonist

Question 21

Potency

Answer 21

Refers to the dose or concentration of a drug required to produce a given effect

Question 22

Spare Receptor

Answer 22

When the maximal response can be elicited by an agonist at a concentration that does not result in full occupancy of all available receptors

Question 23

Protective Index

Answer 23

• Important measure of safety

* The ratio of ED50 (bad side effect):ED50 (actually doing its job)

Question 24

Chemical Antagonism

Answer 24

Render the agonist pharmacologically inactive

Question 25

Functional Antagonism

Answer 25

Interaction of two drugs whose independent opposing actions in the body tend to cancel each other out

Question 26

Competitive Antagonism

Answer 26

Antagonist competes with the agonist for its binding site on the receptor

Question 27

Noncompetitive Antagonism

Answer 27

Antagonist acts at a site other than the appropriate receptors for the agonist

Question 28

Equilibrium Competitive

Answer 28

* Aka reversible competitive antagonism | * Key feature is surmountability expressed in a rightward parallel shift of the agonist log-dose response curve

Question 29

Non-equilibrium Competitive

Answer 29

* Aka irreversible competitive antagonism * Occurs when the antagonist dissociates very slowly, or not at all, from the receptors * Results: no change in the antagonist occupancy takes place when the agonist is applied