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Pharmacology 200 > 1-intro > Flashcards

1-intro Flashcards

1
Q

What kind of drugs are antihistamines??

A

Inverse agonists

Suppress activity / make it worse, unlike antagonist that stops it (not Necessarily making it worse)

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2
Q

Why gen 2 antihistamines non sedating

A

P-glycoprotein pumps remove it from the brain while gen 1 cant

Less in brain, less sedation

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3
Q

Pharmacodynamics

A

What drug does to body

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4
Q

Pharmacokinetics

A

what body does to the drug

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5
Q

Prodrug

A

not intrinsically active, activated by a metabolic step

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6
Q

off-target effect

A

influence on other receptors than the one target, they are often related receptors

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7
Q

G-protein coupled receptor

A

ligand bind to extracellular surface, conformational change, activates signalling cascade activated by G proteins

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8
Q

Gs

A

activates adenylate cyclase

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9
Q

what does adenylate cyclase do

A

catalyses ATP to cAMP

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10
Q

Gi

A

inhibits adenylate cyclase

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11
Q

Gq

A

activates phospholipase C

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12
Q

what does phospholipase C do

A

breakdown PIP2 to IP3 and DAG

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13
Q

what does IP3 and DAG do

A

triggers ER to release Ca2+

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14
Q

tyrosine kinase receptors

A

ligand binding causes auto-phosphorylation

dimerization of receptors (ligand binding)

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15
Q

Ion channel

A

fastest
makes electrical signals
ions flowing through proteins
LIGAND BINDING, VOLTAGE GATED

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16
Q

voltage gated ion channel

A

quick, milliseconds, movement of charged a.a. in transmembrane electric field charge position in response to changes in voltage

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17
Q

ligand gated

A

open or close in response to binding of a small molecule

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18
Q

agonism

A

binding of substrate to receptor that generates an effect

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19
Q

EC50

A

conc. of drug that yields 50% of its max effect, same as efficacy

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20
Q

Emax

A

max biological effect observed with the drug

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21
Q

efficacy

A

same as emax

Max biological effect observed with the drug

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22
Q

potency

A

concentration dependence, how much is needed for a certain effect.

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23
Q

what is potency related to

A

EC50

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24
Q

potency EC50 relationship

A

high potency, low EC50

low potency, high EC50

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25
Q

partial agonist

A

can generate a fractional effect

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26
Q

full agonist

A

can generate a max effect

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27
Q

antagonist

A

cannot generate a biological effect, influences receptors response to agonist

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28
Q

inverse agonist

A

suppresses basal activity, opposite effect of agonist

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29
Q

competitive antagonism

A

more agonist required to generate given response

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30
Q

what does competitive antagonism shift

A

potency/EC50

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31
Q

What does non competitive antagoism shift (efficacy and potency

A

reduce efficacy, no change in potency

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32
Q

steroid hormone receptors

what type and mechanism of action

A

intracellular, slow, requires DNA binding

33
Q

cell surface receptor mechanism of action

A

fast, intracellular signalling cascades

34
Q

dose ratio

A

EC50(w/antagonist) / EC50(w/o antagonist)

35
Q

irreversible competitive antagonism

A

cannot be displaced by increased agonist concentration, binds to same site as the agonist

36
Q

allosteric potentiation

A

increase efficacy and/or potency of the agonist

37
Q

mixed antagonist

A

combo of weakened efficacy and potency

38
Q

orthosteric site

A

agonist binding site

39
Q

does COX-1 or 2 have a bigger active site

A

COX-2

40
Q

what do NSAIDS inhibit

A

COX1 and 2

41
Q

what drug is tylenol

A

acetaminophen

42
Q

extraction ratio/factor

A

clearance/blood flow

43
Q

what does low extraction ratio mean

A

organ doesn’t filter much so the drug stays in blood

44
Q

what is high extraction ratio

A

organ clears out most of the blood, like the liver!

45
Q

bioavailability

A

% of unprocessed drug that reaches systemic circulation after being administrated by a particular route

46
Q

receptor reserve

A

when there are more receptors present than are required for a full biological effect

47
Q

Effect formula

A

(Emax)/(1+ EC50/[drug])

48
Q

first pass metabolism

A

drugs pass through hepatic circulation the liver (major metabolism) before entering heptic circulation

49
Q

what is Kd

A

dissociation constant, when 50% receptors are bound

50
Q

why can there be a mismatch between binding and effect?

A

receptor reserve (more receptors needed than required to make effect)

51
Q

what is distribution

A

how drugs are partitioned into different body compartments

52
Q

factors that effect distribution

A
  1. binding to plasma proteins, these are “bound” (not free or pharmacologically active)
  2. drug accumulation in tissues –> favored for lipophilic drugs and purfuse organs
53
Q

are drugs bound to plasma proteins pharmacologically active?

A

NO ! they are not free

54
Q

what does perfuse mean

A

more blood is supplied to the area

55
Q

what kind of drugs collect more in tissues

A

lipophilic

56
Q

volume of distribution formula

A

total amount of drug in body/[drug]

57
Q

high volume of distribution means

and why

A

well distributed

often highly lipophilic

58
Q

low volume of distributed means

A

poorly distributed

often lipophobic and bound to plasma proteins

59
Q

what is biotransformation

A

metabolism in liver

60
Q

phase 1 biotransformation

A

OXIDATION by CYP enzymes

mixed function oxidase system

61
Q

phase 2 biotransformatin

A

add POLAR parts to make it more prone to excretion

62
Q

does phase 1 or 2 biotransformation happen first

A

EITHER OR

63
Q

capacity limited elimination

A

when [drug] is higher than their affinity of the enzyme that breaks it down

64
Q

pharmacogenomics/genetics

A

how drugs affect people because of their genes

ex: CYP enzymes vary a lot

65
Q

therapeutic index

A

TD50/ED50

toxic dose/effective dose

66
Q

is big or small therapeutic index better

A

BIG

67
Q

relative risk reduction

A

1-(event rate in treatment group)/(event rate in control group)

68
Q

is relative risk reduction good?

A

misleading because it does not convey baseline risk and doesn’t capture the diff. b/w large reduction of something frequent vs. infrequent

69
Q

absolute risk reduction formula

A

event rate in control group-event rate in treatment group

70
Q

is absolute risk reduction good?

A

yes, describes # of cases prevented by drug instead of % relative to baseline (RRR)

71
Q

numbers needed to treat formula

A

1/ARR

1/(event rate in control group-event rate in treatment group)

72
Q

is numbers needed to treat good?

A

yes, it shows the population level drug benefit

73
Q

what if you get a negative numbers needed to treat ???

A

it means event is higher in experimental than control group… BAD DRUG–> numbers needed to harm

74
Q

numbers needed to harm

A

when you have a negative numbers needed to treat

75
Q

meta-analysis

A

systematic review, data from multiple trials combined into a forest plot

76
Q

Schild Plot

A

dose ratio vs. log[antagonist]

77
Q

what is IIP3 role

A

bind to ER so calcium is released

78
Q

what is DAG role

A

remains in membrane and activates PKC

Pharmacology 200 (29 decks)

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