Lect 1 - Pharacodynamics

Question 1

what is the difference between pharmacodynamics and pharmacokinetics

Answer 1

dynamics (what drug do to body) is the effects of the drug on the body, while kinetics (body on drug) has to do with the metabolism, distribution etc of the drug

Question 2

list the 4 protein targets drugs act on

Answer 2

1. enzymes proteins
2. carriers proteins
3. channel proteins
4. receptor proteins

Question 3

what do drugs need to bind to in order to work

Answer 3

it needs to bind to the 4 types of protein

Question 4

what is LR and R0

Answer 4

LR = how much receptor binded to drug
R0 = how much receptors you have

Question 5

what do they mean

Answer 5

• gives proportion of how many receptors are bound vs total number of receptors
• the higher the curve mean the drugs is more effective at binding

Question 6

what does the “near linear” region on the semilogarithmic graph indicate

Answer 6

this is where you see biggest changes relative to drug changes in drug concentration
outside of this, big changes only get small responses

Question 7

potency

efficacy

Answer 7

potency = effective concentration 50% maximal (of it's) effect
efficacy = max effect with that drug

Question 8

agonist vs antagonist

Answer 8

agonist = keeps receptor in active site
antagonist = inhibits action of agonist BUT has NO effect if agonist is not there

Question 9

differentiate between allosteric, competitive, and non-competitive binding sites

Answer 9

allosteric (noncompetitive antagonist) = site other than active site
competitive = bind to active site

Question 10

what are partial agonists, and what are their effects

Answer 10

partial agonists cause a small response on their own
they also reduce the maximum response when paired with full agonist - this is because they act as competitive antagonists by fight for the same binding spots

Question 11

what happens if you have both partial and full

Answer 11

these reduce the efficacy overall

poor partial agonists function as competitive antagonists

Question 12

does reversible and nonreversible antagonism make a difference to the curve

Answer 12

reversible - increasing agonist conc will restore maximal occupancy. there is a shift in the curve

irreversible - does affect anything because antagonist won’t come off. the curve changes shape

Question 13

what happens to curve if antagonist doesn’t come off?

Answer 13

shape changes cause doesnt matter how much shit you add there is no space for it to bind

Question 14

does antagonist affect efficacy?

Answer 14

there is no effect on efficacy because it is still psobbile that 100% receptors can be bound by drugs, you just need more agonist, so potency changes

Question 15

what about irreversible

Answer 15

changes efficacy, there are less things to bind

but there can be no change in potency

Question 16

what’s the 2 state model?

Answer 16

constitutive receptors are slightly activitate even in absence of agonist

agonists and inverse agonists have selective binding affinity, while antagonist have no affinity

agonist -> activated state
inverse agonist -> resting state

Question 17

explain the actions of agonist and inverse agonists in the 2-state model

Answer 17

agonist make the receptor go hard, inverse-agonist makes it go less.
antagonist will try and stop these actions by fighting for binding spots

Question 18

constituitive receptor, agonist, inverse ag, antag

Answer 18

they’re just stealing each others spots…

Question 19

what is the therapeutic window, what happens if you go over it and what happens if you’re under it

Answer 19

optimal range of plasma drug concentration

too high = toxicity
too low = subtheraputic