Lecture 4/5 - Pharmacodynamics Flashcards Preview

Pharmacology I > Lecture 4/5 - Pharmacodynamics > Flashcards

Flashcards in Lecture 4/5 - Pharmacodynamics Deck (65):
1

What is different about how corticosteroids interact with the cell?

Act on nuclear receptors, altering genes expressed. this causes its effects to be expressed for several weeks even with the drugs gone

2

What is an electrostatic interaction?

Attraction between functional groups w/ opposite charges
Can be either strong or weak depending on the charge strength

3

Describe hydrogen bonds.

Hydrogen covalently bonded to an electronegative atom
Weak

4

What tends to act on intracellular receptors?

Hormone/drug crosses plasma membrane

5

What is commonly the effect of intracellular receptor activation?

As a complex, stimulates gene transcription OR removes an inhibtion

6

What is the typical characteristics of intracellular receptor reaction time?

Normally has a lag period but will persist over time

7

What five examples given in lecture activate intracellular receptors?

Corticosteriods
Mineralcorticoids
Sex steroids
Vitamin D
Thyroid hormone

8

What is the structure of a transmembrane protein?

Polypeptides w/ extracellular hormone binding domain + cytoplasmic enzyme domain

9

What are the three kinds of enzymes involved with the transmembrane proteins?

Tyrosine kinase + Serine kinase + Guanylyl cyclase

10

What happens to the transmembrane protein receptors once stimulated?

They are down regulated

11

What are three examples given in lecture of protein tyrosine kinase receptors?

Insulin + Epidermal GF + PDGF

12

Describe ligand-gated channels.

Receptor is linked to an ion channel, when ligand binds channel is opened and ions rush in or out of the cell

13

What ion is paired with acetylcholine/nicotinic receptors?

Na

14

What ion is paired with GABA receptors?

Cl-

15

What ion is paired with benzodiazepine receptors?

Cl

16

What ion is paired with the glutamate receptor?

Ca or Na

17

Describe a G-protein coupled receptor.

Coupled with G-protein to intracellular second messengers, spans the whole membrane

18

What do G proteins interact with?

GTP, stimulate binding + hydrolysis = GDP

19

What do Gs receptors do?

Stimulation the formation of cAMP

20

What do Gi receptors do?

Inhibit the formation of cAMP

21

What does cAMP do if it is activated?

PDE breaks down cAMP
cAMP also binds to intracellular protein kinases = phosphorylation of PKA + CREB

22

What is a major Gs receptor?

Beta1

23

What is a major Gi receptor?

Alpha 2

24

What compounds stimulate Gs?

EPI - NE - Isoproterenol - Dobutamine - Histamine - FSH - ACTH

25

What compounds stimulate Gi?

NE - EPI - Dexmedetomidine - Acetylcholine - Morphine - Serotonin

26

What does Gq activate?

Phospholipase C

27

What does PLC do?

Hyrolyze PIP2 into
IP3
DAG

28

What does IP3 do?

release calcium stores

29

What does DAG do?

Stimulate PKC

30

What compounds stimulate Gq?

Acetylcholine - NE/EPI - Phenylephrine - Serotonin

31

How does the amount of drugs bound to receptors compare to the amount of free drug?

Negligible

32

What is response directly related to?

Number of receptors occupied

33

When do you get a maximal response?

When all receptors are being used, at this point no matter how much drug you introduce into the system it will do nothing

34

What does a sigmoid dose response curve allow you to do?

Determine EC50 (effective concentration)

35

What direction are more potent drugs on dose-response curves?

Left

36

What does the slope tell you on a dose-response curve?

How fast response changes with dose

37

What does the quantal dose-response curve show you?

Frequency of desired effect with each dose (a yes or no response)
use frequency distribution plot

38

What are the two components to therapeutic ratio?

ED50 + LD50

39

What is Kd?

Concentration needed to produce half the maximal binding

40

What is affinity ?

Measures the binding of drug to receptor

41

What is Potency?

Dose require to produce a given effect

42

What tells you potency?

EC50

43

What is efficacy?

Degree of biological response via the binding of the drug to the receptor. NOT POTENCY

44

What is intrinsic activity?

= efficacy, ability of the drug to initiate response
Number btwn 1 and 0

45

What type of activity do agonist have?

Affinity + Intrinsic

46

What type of activity do antagonists have?

Affinity + no intrinsic

47

What type of activity do partial agonist have?

Affinity + lower intrinsic

48

What is an agonist?

Bind to receptor and cause a response

49

What is an antagonist?

Binds to receptor but does not cause a response, blocking the agonist from doing it's job

50

What is a partial agonist?

Binds to receptor and causes response but not as good on one, will block the max effect of the agonist

51

What are the four types of antagonists?

Competitive
Non-competitive
Functional
Chemical

52

What is a competitive antagonist?

Compete for binding site w/ agonist but with zero activity

53

What effects does the competitive antagonist have?

Decrease affinity
NO EFFECT on maximal dose response
Shift curve to the right

54

Can the agonist overcome the competitive antagonist?

Yes, in high enough doses

55

What are non-competitive antagonist?

Bind irreversibly to receptor so agonist cannot bind, can also bind to a secondary site preventing the agonist from acting

56

What are the effects of a non-competitive antagonist?

Max response is decreased
EC50 may or may not change

57

What is a functional antagonist?

Acts through different receptor mechanisms to alter response, less specific and harder to control

58

What is a chemical antagonist?

Neutralizes drug or compound

59

What is a partial agonist?

Partial agonist produce response but w/ lower efficacy than full agonist

60

For most drugs, what is the duration of activity linked to?

Time that drug is bound to receptor, meaning once drug is cleared from the blood stream action is terminated

61

What happens when a partial agonist combines with a full agonist?

Competition for the receptor will occur causing a decrease in the response, causing them to look like antagonists

62

What is an inverse agonist?

Does the opposite, physiologically, of what the Agonist does
Example: if the agonist increases heart rate the inverse will decrease it

63

What causes tolerance?

Chronic administration of drugs

64

How is pharmacokinetic tolerance?

Drug induces its own metabolism
Drug increase metabolism of another drug

65

What is pharmacodynamic tolerance?

Up or Down regulation of receptor