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Pharmacology > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

What is a receptor?

A

component of a cell to which drug binds to initiate the chain of events that leads to a biological response

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2
Q

what is the duration of action for most drugs directly related to?

A

time the drug is bound to the receptor

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3
Q

what happens once the drug is cleared from the bloodstream?

A

actions will be terminated

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4
Q

what type of drug will persist for several weeks even after the drug has been cleared from the body?

A

corticosteroids

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5
Q

what happens when drugs irreversibly bind to an inhibit enzyme?

A

their effects persist much longer than the free drug in the plasma

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6
Q

what drug-receptor interactions are reversible?

A

electrostatic interactions, hydrogen bonds, van der waals forces, and hydrophobic interactions

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7
Q

what drug-receptor interactions are irreversible?

A

covalent binding

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8
Q

what is a intracellular receptor?

A

hormone or drug that crosses the plasma membrane that stimulates intracellular receptor

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9
Q

what hormones and drugs bind to intracellular receptors?

A

corticosteroids, mineralocorticoids, sex steroids, vitamin D, thyroid hormone

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10
Q

what binds to protein tyrosine kinase?

A

insulin, epidermal growth factor, platelet derived growth factor

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11
Q

which ligand-gated channels excites and which inhibits?

A

Nicotinic acetylcholine receptor - excitatory, depolarizes
GABA receptor - inhibitory, hyperpolarizes

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12
Q

what binds to the ligand-gated ion channels (specific for nicotinic vs GABA)?

A

Nicotinic - acetylcholine
GABA - GABA, benzodiazepines
Ca++/Na+ - glutamate

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13
Q

what happens when a drug binds a G-coupled receptor?

A

G-protein activates hydrolysis of GTP->GDP

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14
Q

What does receptors linked to Gs do to the formation of cAMP?

A

stimulate formation of cAMP

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15
Q

what does receptors linked to Gi do to the formation of cAMP?

A

inhibit formation of cAMP

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16
Q

what hormones and drugs bind to Gs to stimulate cAMP formation?

A

epinephrine (B1 and B2)
norepinephrine (B1)
isoproterenol (B1 and B2)
dobutamine (B1)
histamine (H2)
FSH
ACTH

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17
Q

what hormones and drugs bind to Gi to decrease cAMP formation?

A

norepinephrine (a2)
epinephrine (a2)
dexmedetomidine (a2)
acetylcholine (M2)
morphine (u,k,d)
serotonin (5-HT1)

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18
Q

what drugs and hormones bind to GQ to stimulate formation of IP3/DAG?

A

acetylcholine (M1 and M3)
norepinephrine, epinephrine (a1)
phenylephrine (a1)
serotonin (5-HT1c)

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19
Q

what are some non-receptor mediated effects?

A

simple chemical interactions with body components, other drugs, and infective agents

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20
Q

what does IP3 and DAG do?

A

IP3 stimulates Ca++ release from intracellular store
DAG stimulates protein kinase C -> Ca++ pumped out

second messenger, influx of Ca2+ into ER

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21
Q

how many drugs can combine with one receptor?

A

one drug

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22
Q

How is the amount of drug bound compared to the amount of free drug available?

A

negligible

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23
Q

what type of curve is this?

A

dose-response curve

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24
Q

what is EC50?

A

dose required for half maximal effect

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25
Q

what type of curve is this?

A

Quantal dose-response curve

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26
Q

which curve is in relation to a single animal and which is in relation to a population?

A

single animal - graded dose-response curve
population - quantal dose-response curve

27
Q

which curve has a response of all or none?

A

quantal dose-response curve

28
Q

How is the quantal dose-response curve obtained?

A

transformation of data used for frequency distribution plot

29
Q

which curves can you use to calculate ED50?

A

quantal dose-response curve and dose-response curve

30
Q

what is the equation for therapeutic ratio?

A

LD50/ED50

31
Q

define affinity

A

measures binding of drug to receptor

32
Q

what is Kd

A

concentration needed to produce half maximal binding

33
Q

define potency

A

dose required to produce a given effect

34
Q

define efficacy

A

degree of biological response produced by binding of a particular drug to the receptor

35
Q

what is the relationship between potency and efficacy?

A

not related

36
Q

define intrinsic aftivity

A

ability of a drug to initiate a response
synonymous with efficacy

37
Q

what type of activity do agonists have?

A

affinity and intrinsic activity

38
Q

what type of activity do antagonists have?

A

affinity and no intrinsic activity

39
Q

what type of activity do partial agonists have?

A

affinity and lower intrinsic activity

40
Q

what is drug X and Y in the top graph and then the bottom graph?

A

top
X and Y - full agonists

bottom
X and Y - partial agonists

41
Q

what causes a maximum shift of receptors to the activated state?

A

agonist

42
Q

what blocks a response to an agonist?

A

antagonist and partial antagonist to full agonist

43
Q

what are the types of antagonists?

A

competitive
non-competitive
functional
chemical

44
Q

what type of antagonist takes receptors out of play?

A

non-competitive

45
Q

what type of antagonists bind to receptor and compete with agonist?

A

competitive

46
Q

what type of antagonist produces opposing physiological effect?

A

functional (physiological)

47
Q

what type of antagonist neutralizes chemically?

A

chemical

48
Q

how much intrinsic activity to competitive antagonists have?

A

0

49
Q

how does a competitive antagonist shift a dose response cuve?

A

to the right

50
Q

which antagonist binds irreversibly to the receptor? what does this do to the agonist?

A

bind irreversibly to receptor so agonist cannot bind

51
Q

How is EC50 affected by non-competitive antagonists?

A

might or might not change
maximum response is decreased

52
Q

what produces a response but with lower efficacy?

A

partial agonists

53
Q

How is tolerance seen in pharmacokinetics?

A

drug induces its own metabolism
drug may increase metabolism of another drug
dec plasma conc, dec biologic effect

54
Q

How is tolerance seen in pharmacodynamics?

A

usually due to receptor down or up regulation
ex beta receptor agonists or antagonists (opioids)

55
Q

How can increased drug activity be induced?

A

chemically induced, surgically induced, antagonist induced, deficiency in degrading enzymes, competition for binding sites, physiologic synergism

56
Q

when do we see adverse effects?

A

when there are multiple responses to a drug due to the presence of multiple receptors being activated at different dose levels

57
Q

what are drug examples that several dose-dependent responses can be obtained with one drug?

A

phenothiazines, antihistamines, CNS depressants

58
Q

are drugs more selective or specific?

A

at most selective rarely specific

59
Q

what are the two responses drug selectivity can have?

A

therapeutic and adverse

60
Q

Define dose dependent toxicity

A

if an adverse reaction is mediated by the same receptor-effector mechanism

61
Q

what is an overextensions of the therapeutic effect?

A

dose-dependent toxicity

62
Q

what type of drug is added after the control?

A

competitive antagonist

63
Q

what type of drug is added to epi in this curve?

A

non-competitive antagonist

64
Q

what type of drug is each line?

A

Pharmacology (8 decks)

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