Section 1

Question 1

Pharmacodynamics

Answer 1

drug on the body

Question 2

Pharmacokinetics

Answer 2

body on the drug

Question 3

Tachyphylaxis

Answer 3

reduced effect of the drug over time after repeated administration of the same dose of a drug (effect)

Question 4

Desensitization

Answer 4

reduced ability of a receptor to respond to stimulation by a drug or ligand (cause), like PKA, GRK (Arrestin), receptor internalization and can be homo or hetero

Question 5

Inactivation

Answer 5

loss of ability of a receptor to respond to stimulation by a drug

Question 6

Refractoriness

Answer 6

inability of receptor to respond to a drug for a period of time after the first drug-receptor interaction (example in the heart pumps)

Question 7

Down-regulation

Answer 7

reduction in the number of receptors after chronic stimulation by agonists (lysosomal degredation)

Question 8

Up-regulation

Answer 8

increase in the number of receptors after chronic inhibition by antagonists (Beta blockers)

Question 9

An increase in Kd means what for affinity?

Answer 9

decrease in affinity

Question 10

A decrease in EC50 means what for potency?

Answer 10

increase in potency

Question 11

When you increase the concentration of agonist at Emax or greater what could happen?

Answer 11

toxic effects

Question 12

What does Intrinsic Efficacy compare (hint- it’s on the dose response curve)

Answer 12

Emax

Question 13

What is the Emax (Intrinsic activity) of a full agonist, a partial agonist, and an antagonist?

Answer 13

full agonist (a=1)
partial agonist (0<a><1)
agonist (a=0)

Question 14

When EC50 < Kd for a full agonist, what does this mean?

Answer 14

spare receptors

Question 15

Can a partial agonist have spare receptors?

Answer 15

no

Question 16

How could a non-comp antag decrease potencyof a full agonist?

Answer 16

increase concentration of non-comp antag, but still having a small concentration, and the agonist has spare receptors

Question 17

Does a non-comp antag effect efficacy or potency?

Answer 17

efficacy

Question 18

Does a comp. antag effect efficacy or potency?

Answer 18

potency

Question 19

When there is an increase of antag with constant agonist what happens to the affinity?

Answer 19

it decreases

Question 20

How is potency of antagonists determined?

Answer 20

IC50

Question 21

If there is a decrease in IC50, what happens to potency?

Answer 21

increased potency

Question 22

Are competitive or non-competitive antagonists surmountable?

Answer 22

competitive

Question 23

What do agonists with spare receptors keep constant with a low concentration of non-comp antag?

Answer 23

effect

Question 24

What are other ways of non-receptor antagonism that decrease efficacy but not potency?

Answer 24

1. down stream signaling
2. opposite physiological effects (2 diff receptors)
3. chemical antag?

Question 25

What do inverse agonists do?

Answer 25

inactivate receptors via their conformation, doesn't need full agonist to see reverse products

Question 26

What is ED50 and slope of quantal responses?

Answer 26

``` ED50 = median effective dose slope = PD variation of population ```

Question 27

Is a narrow therapeutic index good or bad?

Answer 27

bad

Question 28

a TI <2 is also known as what?

Answer 28

a narrow therapeutic index

Question 29

The range btwn ED50 and the start of toxic curve is known as...

Answer 29

therapeutic window

Question 30

What does a smaller/flatter slope of the toxic effects mean?

Answer 30

greater likelihood of undesirable effects

Question 31

Is CSF (margin of safety) <1% good or bad?

Answer 31

bad

Question 32

What is the therapeutic effectiveness of the drug in humans? (determined by % population responding)

Answer 32

clinical efficacy

Question 33

What is the capacity of agonist to activate a receptor?

Answer 33

Intrinsic efficacy

Question 34

What is the difference btwn on-target and off-target effects?

Answer 34

``` on-target = drug hits intended receptor off-target = unintended receptor ```

Question 35

difference btwn deleterious and non-deleterious? (Usually due to off-target receptor binding)

Answer 35

``` deleterious = toxic effects non-deleterious = side effects ```

Question 36

Dose-related, extension of desired response, on-target effects due to different tissue receptor dist. are examples of what kind of ADR?

Answer 36

Predictable ADR

Question 37

What is it called when there is no cause found to drug toxicity?

Answer 37

idosyncratic responses

Question 38

What is Acetaminophen's antidote?

Answer 38

N-acetylcysteine

Question 39

What do you call something that chemically, physically, or biologically insults that cause DNA damage (initiators) OR facilitate in proliferation of mutated cells (promoters)?

Answer 39

carcinogens

Question 40

What is the inductions of structural defects in the fetus (usually w/in 3rd trimester)?

Answer 40

teratogenesis

Question 41

What are 3 examples of Teratorgens?

Answer 41

retinoic acid isotretinoin ACE inhibitors

Question 42

What are the 4 types of hypersensitivity immune responses that are drug-induced?

Answer 42

``` I = Immediate anaphylaxis (IgE) = wheel and flare II = Ab-dep cytotoxic hyper. = hemolysis III = Immune complex-mediated hyp, = serum sickness IV = Delayed-type hyp. = cytokine storm, contact dermititis ```

Question 43

What is a Hapten?

Answer 43

small molecule drug

Question 44

What are 3 types of PD DDIs? (Effects of the body)

Answer 44

1. Additive (1+1=2) 2. Synergistic (1+1>2) 3. Antagonism (Agonist + Antag)

Question 45

3 types fo PK DDIs?

Answer 45

1. Metabolism (P450) 2. Transportation 3. Protein binding

Question 46

What 2 hypersensitivity drug reactions use haptens?

Answer 46

``` Immediate anaphylaxis (Type 1) and Delayed-type hyp. (Type 4) ```

Question 47

What 2 hypersensitivity drug reactions consider drug the Antigen?

Answer 47

Type 2 - Antibody-dep cytotoxic hyp. and | Type 3 - Immune complex-mediated hyp.