Pharmacology 02: Drug Receptors And Pharmacodynamics

Front 1

What are orphan receptors?

Back 1

receptors whose function is not yet determined

Front 2

What is the EC50?

Back 2

dose at that provides 50% of maximal effect

Front 3

What is the Kd?

Back 3

equilibrium dissociation constant; concentration of a drug where 50% is bound to receptors and 50% is free

Front 4

What is "coupling" when discussing receptors?

Back 4

the process of converting the binding of a receptor into an actual response

Front 5

What happens to the EC50 of a drug if an antagonist is also administered?

Back 5

the EC50 must rise to compensate for the additional antagonist. more drug is needed to provide 50% maximal effect since there is an antagonist working also. but there is a point where if the [antagonist] is too high, it is impossible for the agonist drug to even produce 50% effectiveness since it is out competed by the antagonist

Front 6

What are spare receptors?

Back 6

excess receptors that a cell may have; if we give an antagonist + agonist, we can still have a maximal effect (but it will require more agonist) since there are spare receptors to accommodate the antagonist

Front 7

What is a temporal spare receptor?

Back 7

only a few receptors are needed because binding of a drug/hormone to that receptor elicits a long response. therefore there are extra receptors that are not needed, since only a few can elicit a strong long term response

Front 8

What is meant when receptors are spare in number?

Back 8

there are physically more receptors than needed

Front 9

Which will have a greater effect on diminishing a hormone's actions? Competitive inhibitor or non-competitive inhibitor?

Back 9

non-competitive inhibitor has more inhibition. a competitive inhibitor still has to compete, a non-competitive inhibitor can just bind anywhere on the receptor prevent the drug from binding. With a competitive inhibitor, higher [drug] can overcome the inhibition. not true with a non-competitive inhibitor

Front 10

Which is more likely of an irreversible antagonist? Covalent binding or electrostatic binding?

Back 10

covalent binding typically = irreversible binding

Front 11

What are allosteric modulators?

Back 11

bind the receptor (not in drug's active site) and change the receptor's function (not necessarily inhibiting it though)

Front 12

If the concentration of a full agonist is kept constant and concentration of a partial agonist is constantly increased, what will eventually happen?

Back 12

the partial agonist will exert more of an effect compared to the full agonist. this will lead to the total overall response being lowered

Front 13

How do lipid soluble drugs bind to their receptors and elicit a response?

Back 13

they can diffuse into the cell and bind to their receptors in the cell/nucleus. this complex then binds to hormone responsive elements on the DNA that regulate transcription

Front 14

How do tyrosine kinase receptors work to elicit a response?

Back 14

hormone binds, tyrosine kinase on receptor initiates a kinase cascade.

Front 15

What is "down-regulation" regarding the tyrosine kinase receptors?

Back 15

after a hormone binds, the receptor is endocytosed and removed. if this process outpaces receptor synthesis, there is a decrease in # of receptors available = down regulation

Front 16

How do the cytokine receptors work?

Back 16

quick acting JAK/STAT pathway. JAK phosphorylates STAT, STAT dimerizes and enters the nucleus to regulate transcription

Front 17

What happens when acetylcholine binds to nicotininc receptors?

Back 17

opening of a voltage gated channel allowing Na to enter the neurons to cause depolarization

Front 18

How do G protein receptors initiate a response in a cell?

Back 18

hormone binds, G protein dissociates subunits, activate adenylyl cyclase or PLC, cAMP or DAG or IP3 initiate cascades

Front 19

In a G protein receptor, dissociation of a Gq subunit has what direct effect in the cells?

Back 19

activates phospholipase C which cleaves PIP2 into IP3 and DAG that will increase Ca++ levels

Front 20

In a G protein receptor, dissociation of a Gs subunit has what direct effect in the cells?

Back 20

activate adenylyl cyclase = more cAMP

Front 21

In a G protein receptor, dissociation of a Gi subunit has what direct effect in the cells?

Back 21

inhibit adenylyl cyclase = less cAMP

Front 22

The B-adrenoreceptor is what type of receptor?

Back 22

heptahelical G-protein receptor

Front 23

How is cAMP degraded?

Back 23

phosphodiesterases

Front 24

cAMP has what effect on smooth muscle tone?

Back 24

cAMP = smooth muscle relaxation

Front 25

Function of phospholipase C

Back 25

cleave PIP2 into DAG and IP3

Front 26

Function of IP3

Back 26

release intracellular Ca from sarcoplasmic reticulum

Front 27

Function of DAG

Back 27

activates protein kinase C

Front 28

When discussing potency of a drug, what are we referring to?

Back 28

the dosage (EC50) needed to provide an effect. a more potent drug will have a lower EC50, since less is needed to create an effect

Front 29

When discussing efficacy of a drug, what are we referring to?

Back 29

the potential maximal effect of a drug

Front 30

What is LD50?

Back 30

the dosage of a drug that will kill 50% of patients

Front 31

What is ED50?

Back 31

the dosage of a drug that creates a desired therapeutic effect in 50% of patients

Front 32

What is TD50?

Back 32

the dosage of a drug that will give toxic effects in 50% of patients

Front 33

What is the therapeutic index?

Back 33

ratio of TD50:ED50 to related the doses therapeutic and toxic capabilities

Front 34

Which piece of data would tell us variability of drug effects in patients? Graded dose curve of Quantal dose curve?

Back 34

Quantal dose curve

Front 35

What is an idiosynchratic response?

Back 35

response to a drug that is not commonly seen

Front 36

If a patient is hyporeactive to a drug, what would we need to do to adjust the dosage?

Back 36

increase dosage since the patient is less responsive to the medication