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Pharmacology > Pharmacodynamics 2 > Flashcards

Pharmacodynamics 2 Flashcards

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1
Q

DR complex causes ..

A

biological effect

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2
Q

drug binding to the receptor is governed by

A

affinity for the receptor

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3
Q

how does the drug create the biological effect

A

by causing a conformational change - efficacy or intrinsic activity

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4
Q

partial agonist

A

– no matter how much drug – cannot achieve full response in tissue

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5
Q

what can a log conc. curve tell you

A

what drug is more potent

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6
Q

what would you use to compare potencies from a conc response curve?

A

EC50 values

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7
Q

Antagonists have

A

affinity for a receptor - but they have zero efficacy

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8
Q

Antagonists - zero efficacy

A

do not activate a receptor they just block

- con observe an effect but there is no response

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9
Q

beta blocker

A

antagonist which stops the endogenous ligands binding - lowers HR

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10
Q

agonist potency only involves

A

affinity

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11
Q

antagonists

A

block the action of agonists

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12
Q

agonist and increasing agonist cone-response curve

A

shifts the curve rights
drug - receptor interaction is reduced
alters the effective association - changing the apparent affinity of the drug

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13
Q

concentration ratio (r)

A

EC50 Antagonist /EC50 agonist

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14
Q

r - 1

A

[B] /Kb

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15
Q

what should the axis for the Schild plot be?

A

X - Log [B] M

Y - Log (r-1)

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16
Q

what is the X intercept on the Schild plot

A

Kb

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17
Q

Log (r-1) =

A

Log [B] - LogKb

Think that B is the conc of the antagonist

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18
Q

what is the gradient of the schild plot slope for a competitive antagonist?

A

gradient 1

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19
Q

pA2 =

A
  • Log KB
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20
Q

what measures of affinity do we use for agonist or antagonist

A

agonist - Kd

antagonist - pA2

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21
Q

what would the child plot slope being less than 1 suggest?

A

negative cooperativity - something happening to deplete it - overestimated the affinity of the agonist to start
- agonist acting on a second receptor type

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22
Q

what would schild slope being greater than 1 suggest?

A

cooperativity between the agonist and the antagonist - r the antagonist is being inhibited by being bound to somewhere else
- non specific binding, depletion of agonist

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23
Q

what must hold true for the child plot to work?

A

one molecule binding to one receptor (agonist or antagonist)

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24
Q

what wold you see in a IRREVERSIBLE competitive antagonist graph?

A

the graphs shift down - get less response with higher conc of antagonist

(could also see some parallel shift but draw above in exam)

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25
what happened to Kd with a irreversible competitive antagonist?
KD stays the same as the amount required to occupy receptors stays same – reducing amount of receptors (not changing the affinity)
26
what allows irreversible antagonism?
a covalent bond being formed
27
what is non-competitive antagonism?
Preventing receptor activation or significantly reducing the receptor activation – reduced
28
what is chemical antagonism?
Two substances combine in solution | Result effect of active drug is lost
29
what are 2 examples of chemical antagonists?
- Dimercaprol - | - infliximab
30
what do collating agents do?
mop up the excess - for excretion
31
what does Dimercaprol do?
use to to treat heavy metal poisoning – lead – makes lead excretal by the body
32
what does Infliximab do?
– anitinflamatory drug that targets tumor nercrosis factor – mops up TNF – less inflamation – antibody concept
33
what receptors in the heart does noradrenaline act on? Effect?
B2 receptors | increase HR
34
what receptors in the heart does Acetylcholine act on? Effect?
mAchR | decrease HR
35
explain biased agonism
1 receptor type - 2 different agonists - would produce both responses equally or favour making more of one response than the other - but creates more of one response than the other - select which pathway becomes activated on binding
36
what is pharmacokinetic antagonism?
injected somethnig – another drug affects something making the first drug less effective (one drug affecting another metabolism - dangerous)
37
what is allosteric modulation?
a substance which indirectly influences (modulates) the effects of a receptor agonist or inverse agonist at its receptor protein target.
38
how would a positive modulator affect the conc. response curve?
curve would shift left – positive effect on affinity
39
what would happen to the conc response curve if there was an allosteric modulator which has a negative affect on efficacy?
would become more squished down
40
what is efficacy? (Emax)
maximum response achievable from an applied or dosed agent, for instance, a small molecule drug. Intrinsic activity is a relative term that describes a drug's efficacy relative to a drug with the highest observed efficacy.
41
what is the therapeutic index equation?
TD50 / ED50 TD - toxic dose ED - effective dose
42
what is the therapeutic window between?
MED and MTD | minimum effective dose and maximum tolerated dose
43
what would a therapeutic index of 2 or less be
very risky
44
what do the allosteric modulators valium/diazapan do?
positively modulate and calm down inhibitory neurones GABA receptor
45
Ion-Channel Linked Receptors: Location/effector
membrane channel
46
Ion-Channel Linked Receptors: coupling
direct
47
Ion-Channel Linked Receptors: time
milliseconds
48
Ion-Channel Linked Receptors: Structure
Many different sub-units, generally 4-5 f
49
Ion-Channel Linked Receptors: Examples
Nicotinic ACh | GABAA
50
G-protein Coupled Receptor: location and effector
membrane, enzyme or channel
51
G-protein Coupled Receptor: coupling
G - protein
52
G-protein Coupled Receptor: time
seconds
53
G-protein Coupled Receptor: structure
A single protein with no subunit. Has 7 transmembrane α-helices as the binding domain with an intra-cellular G-protein coupling domain
54
G-protein Coupled Receptor: examples
Muscaranic Ach | adrenorerceptors
55
Tyrosine-Kinase Linked Receptors: location and effector
membrane, enzyme
56
Tyrosine-Kinase Linked Receptors: coupling
direct or indirect
57
Tyrosine-Kinase Linked Receptors: time
mins - hours
58
Tyrosine-Kinase Linked Receptors: structure
A single α-helix which passes through the membrane. The catalytic domain contains the tyrosine kinase which phosphorylates tyrosine
59
Tyrosine-Kinase Linked Receptors: examples
insulin and cytokine receptors
60
Receptors Linked to Gene Transcription (nuclear receptors : locations and effector
intracellular and geen transcription
61
Receptors Linked to Gene Transcription (nuclear receptors: coupling
via the DNA
62
Receptors Linked to Gene Transcription (nuclear receptors time
hours
63
Receptors Linked to Gene Transcription (nuclear receptors - structure
Close to nucleus and causes changes in DNA transcription. Has a binding domain and a DNA-binding domain (“zinc fingers”)
64
RTK examples
Steroid receptors | Thyroid Hormone receptors
65
ligand gated ion channels - where does the drug bind
N terminus tail outside the cell | C terminus is also outside the cell
66
where is the N terminus on the RTK
on the top - where the drug binds - C terminus inside the cell
67
Gas
coupled to adenylate cyclase which converts ATP --> cAMP cAMP acts as a second messenger to phosphate kinase
68
Gai
inhibitory inhibits cAMP formation - less PK action
69
Gaq
coupled to phospholipase C (membrane bound) PLC activates and cleaves PIP2 to form DAG and IP3 DAG activates PKC and IP3 regulates [Ca} intracellularly
70
which G protein dos the cholera toxin activate?
Gas - which blocks GTPase activity preventing inactivation
71
GPCRs how much genome
1% of the human genome huge diversity
72
in GPRCs which ion channels activated how
Betagamma subunit principly activates K channels and inactivate voltage-gated calcium channels
73
what is pharmacogenomics?
Genetic variability in the way drugs behave in the body
74
Pharmacodynamic:
receptor variants

Pharmacology (18 decks)

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