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L2 pharmacology > Receptors > Flashcards

Receptors Flashcards

1
Q

What is the active ingredient of opium?

A

Morphine

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2
Q

How many types of opiate receptors are there?

A

3

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3
Q

Which drugs bind to the mu (μ) opiate receptor? (4)

A
  • Morphine
  • Heroin
  • Codeine
  • Fentanyl
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4
Q

What are the endogenous ligands for opiate receptors? (2)

A
  • Endorphins
  • Enkephalins
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5
Q

What is a drug?

A

A chemical of known structure which produces a biological effect when administered to a living organism

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6
Q

What is a biopharmaceutical?

A

A drug made from DNA (proteins, oligonucleotides, antibodies)

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7
Q

What is a medicine?

A

A chemical preparation that contains a drug(s) which is administered to produce a therapeutic effect

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8
Q

What are the 2 types of biologics?

A
  • First generation
  • Second generation
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9
Q

What are first generation biologics?

A

Copies of endogenous proteins produced by recombinant DNA technology

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10
Q

What are second generation biologics?

A

Engineered proteins to improve their performance e.g. humanised monoclonal antibodies

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11
Q

What are the 4 main classes of proteins targeted by drugs?

A
  • Receptors
  • Enzymes
  • Transporters
  • Ion channels
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12
Q

What happens if you increase the dose of drug too much?

A

Starts to have off-target side effects, toxicity etc.

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13
Q

What is an agonist?

A

A drug which switches on a receptor when it binds and brings about change in a cell

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14
Q

What is an inverse agonist?

A
  • A drug which binds to the same site as an agonist but reduces receptor activity (opposite response to the agonist)
  • Reduces its basal, constitutive activity
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15
Q

What is an antagonist?

A
  • Blocks the activity of the receptor when it binds
  • Stops the effect of an agonist/inverse agonist
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16
Q

What kind of receptors are opiate receptors?

A

G protein coupled

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17
Q

How does lidocaine work?

A

Blocks voltage gated Na+ channels for analgesia

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18
Q

What is a prodrug?

A

A drug which is processed by an enzyme to produce an active version of the drug e.g. L-dopa

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19
Q

What is the treatment for opioid overdose?

A

Naloxone

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20
Q

What are the 4 classes of receptors?

A
  • Ligand gated ion channels (ionotropic)
  • G-protein coupled receptors (metabotropic)
  • Kinase-linked receptors
  • Nuclear receptors
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21
Q

What is the structure of ionotropic receptors? (2)

A
  • Subunits have a few transmembrane domains
  • Multiple subunits come together to form the channel
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22
Q

What is the structure of metabotropic receptors? (2)

A
  • 7 transmembrane domains
  • Coupled to a G protein
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23
Q

What do kinases do?

A

Phosphorylate other proteins

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24
Q

Where are nuclear receptors found in a cell?

A

Cytosol or nucleus

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25
Q

What is the function of nuclear receptors?

A

Regulate transcription in cells

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26
Q

What are the 3 subunits of G proteins?

A

Alpha, beta and gamma

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27
Q

What happens when a G protein coupled receptor is activated? (4)

A
  • G protein activated
  • Alpha subunit has GDP in its resting state, once activated binds to GTP instead and dissociates from beta-gamma subunit
  • Alpha and beta-gamma subunits interact with downstream target proteins
  • Alpha breaks down GTP into GDP and binds with the beta-gamma subunit again
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28
Q

What are the 3 main G proteins?

A

Gs, Gi, Gq

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29
Q

Which receptors do cytokines act on?

A

Kinase-linked receptors

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30
Q

What are the 2 types of nuclear receptors?

A
  • Class 1
  • Class 2
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31
Q

What is the difference between class 1 and 2 nuclear receptors?

A

Class 1 are outside the nucleus and move in once activated whereas class 2 are already inside the nucleus

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32
Q

What is the structure of class 1 nuclear receptors?

A

Homodimeric

33
Q

What is the structure of class 2 nuclear receptors?

A

Heterodimeric

34
Q

Which receptors do steroids bind to?

A

Class 1 nuclear receptors

35
Q

What is myasthenia gravis?

A

Autoimmune disease which targets nicotinic receptors

36
Q

What kind of receptor is the insulin receptor?

A

Kinase-linked receptor

37
Q

What is the efficacy of an antagonist?

A

0

38
Q

What is the difference between affinity and efficacy?

A

Affinity is how well the ligand binds to the receptor whereas efficacy is how well the ligand elicits a response

39
Q

What is Kd? (3)

A
  • Dissociation constant, measure of affinity
  • Concentration of drug which occupies 50% of receptors
  • Low Kd = high affinity (lower concentration needed to fill 50% of receptors)
40
Q

What is Kd for a drug with a high affinity for its receptor?

A
  • Very small
  • Reverse reaction (dissociation) is very slow compared to the forward reaction (binding)
41
Q

How is Kd calculated?

A

Rate of the reverse reaction divided by the rate of the forward reaction

42
Q

What is Kd for a drug with a low affinity for its receptor?

A
  • Large
  • Reverse reaction (dissociation) is fast compared to the forward reaction (binding)
43
Q

How is occupancy calculated?

A

Number of receptors occupied /
Total number of receptors

44
Q

What is occupancy determined by?

A

Affinity

45
Q

What is the scale of occupancy?

A

Between 0 (no receptors occupied) and 1 (all receptors occupied)

46
Q

What method is used to determine occupancy and therefore affinity?

A

Radioligand binding assays

47
Q

How does a radioligand binding assay work?

A
  • Apply radioactive ligand to the tissue containing the receptors and incubate at an appropriate temperature to prevent protein degradation
  • Wash off unbound ligand and look at level of radioactivity in the tissue
48
Q

What is the most common radioactive label used?

A

Iodine

49
Q

How is non-specific binding accounted for in radioligand binding assays?

A
  • One sample has the radioactive ligand which is bound to receptors and also non-specific binding sites (plastic etc)
  • Unlabelled ligand is added in excess to the other sample, outcompetes the radioligand for the receptors so the radioligand is only bound non-specifically
  • Specific binding i.e. occupancy = total radioligand binding in first sample - non-specific radioligand binding in other sample
50
Q

What is EC50?

A

The concentration of drug that gives 50% of the maximum response for that tissue

51
Q

What does ‘receptor reserve’/spare receptors mean?

A
  • Not 100% of receptors need to be occupied to give 100% response i.e. EC50 is lower than Kd
  • Spare receptors shift the response curve to the left of the binding curve
52
Q

How does EC50 relate to potency?

A

Drugs with a lower EC50 are more potent because a lower concentration of the drug is needed to produce 50% of the max response

53
Q

What is a partial agonist?

A
  • An agonist that can’t produce the same maximum response as a full agonist
  • Efficacy is always lower than the full agonist
54
Q

What happens to the concentration-response curve if you mix an agonist with a partial agonist?

A
  • Partial agonist behaves like an antagonist
  • Causes a shift to the right
55
Q

What occupancy does a partial agonist need to achieve in order to produce 100% of the max response? (2)

A
  • 100%
  • Kd = EC50
56
Q

What kind of drug has an efficacy of 1?

A

Full agonist

57
Q

What 3 properties determine the effect of a drug in a living system?

A
  • Specificity
  • Affinity
  • Efficacy
58
Q

How do you determine potency of a drug? (2)

A
  • Potency is relative
  • Need to compare full dose-response curves
59
Q

What are the 5 classes of antagonists?

A
  • Chemical antagonism
  • Pharmacokinetic antagonism
  • Physiological antagonism
  • Non-competitive antagonism
  • Competitive antagonism
60
Q

What is chemical antagonism?

A
  • Where an antagonist binds to the active drug and ‘mops it up’ to prevent its action
  • Chemically alters the agonist
  • E.g. monoclonal antibodies
61
Q

What is pharmacokinetic antagonism?

A
  • Where an antagonist reduces the amount of drug absorbed/metabolised/causes excretion
  • E.g. opiates inhibit gut motility so reduce absorption of other drugs from the gut, antibiotics can stimulate enzymes involved in warfarin metabolism, diuretics cause increased urine flow
62
Q

What is physiological antagonism?

A
  • Interaction of 2 drugs with opposing actions, different receptors but same system
  • E.g. noradrenaline raises arterial pressure but histamine lowers arterial pressure
63
Q

What is warfarin?

A

Anti-coagulant given to reduce the risk of stroke and heart attack

64
Q

What is non-competitive antagonism?

A
  • Non-competitive antagonists block the effect of an agonist indirectly
  • Binds to a different site on the receptor/interferes with a signalling molecule
65
Q

What is competitive antagonism?

A

Competes with the agonist for occupancy of the same binding site, blocks the receptor activity

66
Q

How do you overcome the effects of a competitive antagonist?

A

Increase the concentration of agonist

67
Q

What is the effect of adding competitive antagonist on a concentration-response curve for an agonist? (3)

A
  • Parallel shift to the right
  • Maximum and slope stays the same
  • EC50 increases with increasing antagonist concentration
68
Q

What is the dose ratio?

A
  • Quantification of the rightward shift in the curve when adding competitive antagonist to an agonist
  • How many more times agonist is needed to reach the same response
69
Q

How is dose ratio calculated?

A

[Conc. agonist in PRESENCE of antagonist] /
[Conc. agonist in ABSENCE of antagonist]
- Concentrations for the same response e.g. at the EC50 values

70
Q

What is Schild analysis?

A

Measure of the affinity of a competitive antagonist

71
Q

What are the features of Schild plot? (3)

A
  • log(DR - 1) on the y axis
  • log[antagonist] on the x axis
  • Both linear scales, values are logged
72
Q

What is the pA2 value?

A

Measure of affinity

73
Q

What does a large pA2 value indicate?

A

High affinity

74
Q

What does a small pA2 value indicate?

A

Low affinity

75
Q

How do you calculate pA2?

A

x intercept of the Schild plot x -1

76
Q

How do you calculate Kd from pA2?

A

Kd = 10^(- pA2)
pA2 = -1 x log(Kd)

77
Q

What happens to the concentration-response curve for an agonist when you add a partial agonist?

A
  • Partial agonist behaves like a competitive antagonist in the presence of an agonist
  • Causes a shift to the right
  • Difference is that the partial agonist can cause some signalling on its own but a competitive antagonist never induces signalling
78
Q

What are irreversible competitive antagonists?

A

Antagonists which bind permanently to the agonist binding site and can’t be removed by washing the tissue

79
Q

What happens to the concentration-response curve for an agonist when an irreversible competitive antagonist is added? (3)

A
  • Initial shift to the right and max response can still be reached by adding more agonist due to spare receptors
  • Over time max response decreases because all receptors used
  • Can’t use Schild analysis

L2 pharmacology (9 decks)

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