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303 MEDIMAGE > 5. Pharmacodynamics: how drugs act > Flashcards

5. Pharmacodynamics: how drugs act Flashcards

1
Q

what are drug targets

A

drugs produce effects by binding to protein molecules

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2
Q

what are the 4 main drug targets

A

receptors, enzymes, carrier proteins and ion channels

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3
Q

do drugs act at non protein targets

A

yes eg DNA

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4
Q

receptors have how many binding sites

A

at least one binding site

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5
Q

what are ligands

A

chemicals which bind to receptors

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6
Q

what does binding require

A

affinity

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7
Q

what does the binding of endogenous and some exogenous ligands result in

A

result in activation of intracellular signaling pathways (signal transduction)

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8
Q

drugs can act by ___ or ____ the process of ____

A

inhibiting/promoting

signal transduction

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9
Q

for a ligand/agonist to have an effect what does there need to be

A

signaling system

binding needs to alter something in the cell

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10
Q

what are the 4 classes of receptors

A

iontropic
metabotropic
kinase linked
nuclear/intracellular

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11
Q

what are ionotropic receptors linked to

A

ion channels

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12
Q

what are metabotropic receptors linked to

A

G proteins (GPCRs)

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13
Q

what are kinase linked receptors linked to

A

certain enzymes

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14
Q

where are receptors found and what is the exception

A

on the membrane of cells unless they are nuclear receptors which are on the inside of the cell

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15
Q

what is an example of ionotropic receptors

A

ligand gated ion channels

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16
Q

what is the response time for ligand gated ion channels ionotropic receptors

A

quick - millisec

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17
Q

what does GPCR do

A

activate G proteins and leads to opening of ion channel/activation of enzyme that leads to cascade in cell and cellular effects

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18
Q

what is the response time for G protein metabotropic receptors

A

quick - within seconds

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19
Q

where are kinase receptor enzymes

and what does it do

A

on transmembrane protein

catalyze phosphorylation of target molecules

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20
Q

what is the response time for kinase linked receptors

A

slower - within hours

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21
Q

what do nuclear receptors do

A

promote gene transcription and synthesis new proteins

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22
Q

what is the response time for nuclear receptors

A

days to hours

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23
Q

what are ligand gated ion channels made up of

A

multi subunit complexes

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24
Q

what are the 3 important properties of ligand gated ion channels

A

activated in response to certain ligands

conduct ions through the otherwise impermeable cell membrane

select among different ions

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25
Q

what happens when an agonist bonds to the subunits of the ligand gated ion channels

A

causes conformational change to receptor and allows ions to flow into cell

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26
Q

what are 3 endogenous ligands for ionotropic receptors

what do they do

A

acetylcholine
GABA
glutamate

regulate flow of ions in and out of cells

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27
Q

what is altered when ligands bind to ionotropic receptors

A

electrical potential across membrane

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28
Q

what happens when an agonist binds to the receptor in a GPCR situation

A

activates signalling protein called G protein

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29
Q

what does the activation of a G protein lead to in the cell

what 2 things are achieved/changed

A

cascade of events activated in the cells

changes the activity of an element usually in an enzyme or ion channel

changes conc of the IC second messenger

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30
Q

how many times does the GPCRs span the membrane

A

7 times

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31
Q

how many subtypes of muscarinic acetylcholine receptors are there

A

5

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32
Q

what does M1 subtype of the muscarinic acetylcholine receptors in control of

A

neural - CNS and peripheral

cns excitation and gastric secretion

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33
Q

what does M2 subtype of the muscarinic acetylcholine receptors in control of

A

cardiac

cardiac inhibition and neural inhibition

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34
Q

what does M3 subtype of the muscarinic acetylcholine receptors in control of

A

glandular/smooth muscle

gastric and salivary secretions, smooth muscle contraction and vasodialtion

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35
Q

what does M4/5 subtype of the muscarinic acetylcholine receptors in control of

A

CNS

m4 = enhanced locomotion
m5 = not well known
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36
Q

what are 2 examples of drugs that act through GPCRs

A

atropine and hyoscine at muscarinic receptors

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37
Q

what does non selective antagonists mean

A

non selective = act on all receptors so effect on drugs have a range of effect

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38
Q

what happens when you have a high conc of atropine and hyoscine

A

toxicity due to their increased effects

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39
Q

what is hyoscine butylbromide

what does it do and what does it allow

A

buscopan

muscarinic receptor antagonist

poorly absorbed and cannot cross the BBB and used to facilitate gastrointestinal radiology as it relaxes the GI smooth msucles

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40
Q

for tyrosine kinase receptors what do they consist of

A

extracellular part that binds the ligand and the intracellular part that functions as a kinase

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41
Q

what does the receptor function as in tyrosine kinase receptors

A

functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues on intracellular target proteins (phosphorylation)

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42
Q

what does phosphorylation do to protein function

A

controls protein function by changing an enzymes activity which then leads on to produce a cellular effect

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43
Q

what does tyrosine kinases mediate the actions of

A

growth factors, cytokines and certain hormones

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44
Q

what is kinase

A

enzyme that transfers phosphate groups

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45
Q

what is vascular endothelial growth factor receptors essential for

A

essential for angiogenesis during development, pregnancy and wound healing

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46
Q

what are the main types of vascular endothelial growth factor

A

VEGFR1
VEGFR2
VEGFR3

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47
Q

what is VEGFR2 overexpressed in

A

cancer

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48
Q

how is VEGFR 2 linked to treating cancers

A

selective antagonists for VEGFR2 can interrupt the signaling pathways involved in tumor angiogenesis

49
Q

where are nuclear receptors located

A

intracellularly in cytoplasm or nucleus

50
Q

what does the activated nuclear receptor do when it is activated

A

function as transcription factor

51
Q

in the absence of ligands where are nuclear receptors located

A

in the cytoplasm

52
Q

when ligands are bound, where are nuclear receptors located

A

travel to nucleus and stimulate transcription of target genes

53
Q

what is affinity

A

attraction of ligand/drug for a receptor

54
Q

what is efficacy

do all drugs that bind to receptor have affinity and effect

what does 0 and 1 mean

A

intrinsic activity

Drugs ability to initiate biological activity as result of binding, some ligands bind to receptor (affinity) and lead to max effect but some will bind and have affinity for receptor but wont have an effect

1 = max effect
0 = no effect
55
Q

what is an agonist

A

have affinity and efficacy - mimics

56
Q

what is an antagonist

A

have affinity but no efficacy - prevents

Binds to receptor and prevents effects or binding of endogenous ligands

57
Q

for a drug conc vs % effect graph as the conc of the drug increases what happens to the effect

A

increases

58
Q

for a drug conc vs % effect graph at low conc increases in drug conc will result in what for the effect

A

proportional increase in effect

59
Q

for a drug conc vs % effect graph at high conc increases in drug conc will result in what for the effect

A

increases in drug conc is no longer proportional and reaches a plateau so the effect is independent of conc

60
Q

for a drug conc vs % effect graph at high conc why is the effect independent of the drug conc

A

limited amount of receptors in tissue, so in high conc, more and more receptors will be occupied/saturated and maximum effect is seen

61
Q

the higher the affinity what happens to the conc at which it produces a given level of receptor occupany

A

lower conc

62
Q

why are conc response curves not good measure of affinity

A

as relationship between receptor occupancy and response is not strictly proportional

63
Q

why are relationship between receptor occupancy and response not strictly proportional

A

amplification may exist so may only take a low level of receptor occupancy to cause a max response in some tissues

many factors downstream of receptor binding may interact to produce the final response

64
Q

the response to a drug can be classified by what 2 parameters

A

EC50 and Emax

65
Q

what is the potency of an agonist measured by

A

EC50

66
Q

what is the EC50

A

effective conc of an agonist that produces 50% of the max response

67
Q

the more potent the agonist, the ___ the EC50

A

lower the EC50

68
Q

antagonist potency is measured by what prinicple

A

IC50 - conc of drug required to produce 50% inhibition

69
Q

what is the relationship with the efficacy and receptor for agonists

A

a drug with positive efficacy will activate a receptor to promote cellular response

70
Q

what is the relationship with the efficacy and receptor for inverse agonist

A

drug with negative efficacy will activate a receptor to promote cellular response

71
Q

what is the relationship with the efficacy and receptor for inverse agonists

A

drug with negative efficacy will bind to receptors to decrease basal receptor activity

72
Q

what is the relationship with the efficacy and receptor for anatagonist

A

a drug with no efficacy will bind to receptors by have no effect on activity

73
Q

what is the Emax

A

point reached beyond which no further increase in response occurs

74
Q

what efficacy do agonists have

A

positive

75
Q

what efficacy do inverse agonists have

A

negative

76
Q

what efficacy do antagonists have

A

no efficacy

77
Q

how do you judge the efficacy of a drug

A

Emax

78
Q

how do you judge the potency of a drug

A

EC50 - how much conc of drug is needed to reach 50% of effects

79
Q

what are full agonists

A

drugs that elicit the max tissues response

80
Q

what are partial agonists

A

drugs that produce less than the max response

81
Q

can partial agonists produce max response even at 100% receptor occupancy

why or why not

A

no never as it binds to receptor it partially activates receptor so produces some effects but competes with full agonists to block some of full agonists to take effect

82
Q

what is the max response of a tissue to a drug determined by

A

efficacy and tissue properties

83
Q

can drugs be a partial agonist in one tissue and a full agonist in another

A

yes

84
Q

what effect do inverse agonists produce

A

opposite effect to full agonists

85
Q

what effect does antagonists have

A

no activity on its own but can block activity of agonists and inverse agonists

86
Q

what are antagonists

A

compound that binds but doesn’t activate/inactivate the receptor

87
Q

do antagonists have affinity and effcacy

A

have affinity but no efficacy

88
Q

what is the type of antagonists defined by

A

how they bind to receptor

89
Q

what are the 3 main types of antagonists

A

competitive reversible antagonists
competitive irreversible antagonists
non competitive antagonists

90
Q

how do competitive reversible antagonists work

A

Competitive antagonist compete for same receptor site and binds so prevents agonist from binding to cause effect

91
Q

how do non competitive reversible antagonists work

A

Non competitive antagonist can prevent effect of agonist without binding to same site as agonist so acts on downstream factors that are needed to produce effect

92
Q

what is irreversible antagonism and how does it work

A

bind covalently to receptor and is nor reversible

reduces the number of receptors avail to agonist so reduces the max response that an agonist can produce

93
Q

for irreversible antagonism can it be reversed by increasing conc

A

Increase in conc cant overcome this blockade as it Is irreversible

94
Q

what does irreversible antagonism do to the max response and shifting of the curve

A

Binding is irreversible so max bio response decreases

Reduce max response and shifts curve downwards

95
Q

what are reversible competitive antagonists and how do they work

A

bind to receptor in a reversible manner to compete directly with agonist binding

96
Q

what effect does increasing the conc of reversible competitive antagonists have on the agonist response curve

A

If you increase the competitive reversible agonist, will shift curve to right, competitive reversible antagonist makes agonist less potent by shifting dose response in right direction

Agonist and antagonist compete for same receptor as increase conc of agonist, increase chance that agonist will bind and produce effect, at a high enough agonist conc the antagonist wont have a change as it is outnumbered

97
Q

since antagonists have no effects on their own, how can you observe it

what effect does it have on the EC50

A

Can only observe by looking at its effect on agonist

EC 50 are increased so same max effect is achieved but higher conc is needed to achieve max response

98
Q

what does a irreversible antagonist look like for a response conc curve at low doses

why does it look like this

A

looks like reversible antagonist

Shows that the number of receptors avail exceeds the number req to produce the max response - oversupply of receptor to begin with but eventually high conc of irreversible antagonist result in downward shift in conc response curve

99
Q

what is selectivity for receptor subtypes

A

preferential binding to a certain subtype leads to greater effect at that subtype than others

100
Q

what does the lack of selectivity for drugs lead to

A

unwanted drug effects

101
Q

what are 3 non receptor protein targets

A

enzymes
carrier proteins
ion channels

102
Q

what are the effects of cyclo-oxygenase inhibition - what does NSAID inhibition of COX1 and 2 lead to

A

decrease in inflammation, pain and fever

reduction in homeostatic pathways involved in kidney function and maintenance of gastric mucosa

103
Q

what is NSAIDS universally inhibited by

A

cyclo-oxygenase

104
Q

what does inhibition of COX 1 do

A

unwanted actions including GI effects

105
Q

what does inhibition of COX 2 do

A

anti inflammatory action

106
Q

what does theophylline do - to phosphodiesterase

A

inhibits phosphodiesterase so stops conversion of cAMP -> AMP

107
Q

what does theophylline do - cAMP

A

increases cAMP levels relax bronchial muscle

108
Q

what does theophylline do - A receptors

A

antagonist at A receptor so blocks effects of adenosine = bronchoconstriction and inflammation

109
Q

what are examples of drugs that interact with carrier proteins

A

drugs that act on monoamine neurotransmitters (serotonin, dopamine and norepinephrine) uptake proteins

110
Q

what do drugs taht act on ion channels do

A

change ability to open and close ion channels

111
Q

what are the 2 voltage gated ion channels

A

Na+ channel blockers

Ca2+ channel blockers

112
Q

what is the dose response relationship

A

dose vs conc

113
Q

what is the relationship of drug conc and dose administered for dose response relationship

A

proportional

114
Q

is there EC50 for a dose response relationship

A

ED50

115
Q

what is the difference between dose response curves and conc effect curves

A

Conc effect curve describe pharmacodynamics, purely dependent on drugs pharmacodynamic characteristics

Dose response curve is function of both pharmacodynamics and pharmacokinetic characteristics

116
Q

for the dose response curve what is the median effective dose

A

ED50

dose at which 50% of individual exhibit specified quantile effect

117
Q

for the dose response curve what is the median toxic dose

A

dose required to produce toxic effect in 505 of subjects

118
Q

for the dose response curve what is the median lethal dose

A

Median lethal dose is dose req to kill 50% of subjects

119
Q

for the dose response curve what are the 2 parameters used to calculate the therapeutic index of drugs

what is the limitation of the therapeutic index

A

LD 50 and ED 50 are used to calculate therapeutic index of drugs

this index has limitation as LD50 cant be measured In humans and were done in humans but animals are not the same as humans so is a poor guide. It has ethical issues

303 MEDIMAGE (14 decks)

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