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Y2S1 - Drug Action > Drug Action 1 > Flashcards

Drug Action 1 Flashcards

1
Q

What are drug targets?

A

Proteins

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2
Q

What proportion of drugs interfere with membrane receptors?

A

30-50%

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3
Q

What is the primary site of drug interference?

A

Membrane receptors

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4
Q

How many categories of drug receptors are there?

A

Four

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5
Q

What are the four broad categories of receptor?

A

Ligand gated ion channels, GPCR receptors, kinase-linked and nuclear receptors

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6
Q

What is the fastest receptor?

A

Ligand gated ion channels

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7
Q

What is the one common feature to all receptors?

A

Binding domain

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8
Q

Approximately how many asthma sufferers are there in the UK?

A

5.4 million

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9
Q

Describe the early phase of an asthma attack.

A

Mast cells in lungs secrete histmines; these signal other immune cells (causes late phase; shortness of breath, especially when breathing out; cough

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10
Q

Describe the late phase of an asthma attack.

A

Secondary inflammatory immune response; inflammation of the airways

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11
Q

Describe bronchial hyper-reactivity.

A

Long term changes in the lungs - mast cells migrate to smooth muscle layer which increases long term sensitivity

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12
Q

What is the effect of mast cell migration to the smooth muscle layer of the lungs?

A

Increased long term sensitivity

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13
Q

What is the term given to the situation where mast cells have migrated to the smooth muscle layer of the lungs?

A

Bronchial hyper-reactivity

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14
Q

What are the two main anti-asthmatic drug groups?

A

Bronchodilators and anti-inflammatory agents

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15
Q

Give one example of a bronchodilator.

A

Salbutamol

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16
Q

Give two examples of anti-inflammatory agents.

A

Pednisolone & omalizumab

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17
Q

How does omalizumab work?

A

A humanised antibody, it stops mast cells from responding

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18
Q

What reduces the efficacy of bronchodilators?

A

Polymorphisms in ß2-adrenoceptors

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19
Q

What do polymorphisms in ß2-adrenoceptors cause?

A

Reduced efficacy of bronchodilators

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20
Q

What kind of disease is myathenia gravis?

A

Autoimmune disease

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21
Q

How common is myasthenia gravis?

A

1 in 2000

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22
Q

What is the main symptom of myasthenia gravis?

A

Muscle weakness

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23
Q

What is the main cause of myasthenia gravis?

A

Decreased nAChR in neuromuscular junctions

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24
Q

What does NMJ stand for?

A

Neuromuscular junction

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25
Q

What is the primary treatment for myasthenia gravis?

A

Anti-cholinesterase and immunosuppressants

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26
Q

What are the two steps involved in agonist function?

A

Bind to the receptor, cause a response

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27
Q

Define affinity.

A

The strength of interaction between agonist/antagonist and receptor

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28
Q

What value defines how well an agonist/antagonist bind a receptor?

A

K+1

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29
Q

What is the value K+1?

A

How well an agonist/antagonist BINDS a receptor

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30
Q

What value defines how well an agonist/antagonist UN-binds a receptor?

A

K-1

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31
Q

What is the value K-1?

A

How well an agonist/antagonist UNBINDS a receptor

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32
Q

How is K-A calculated?

A

(K+1) / (K-1)

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33
Q

What does a K-A value indicate?

A

Strength of interaction between a drug and its receptor, i.e. constant

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34
Q

What is the strength of interaction between a drug and its receptor often referred to as?

A

K-D

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35
Q

How is K-D calculated?

A

1 / K-A

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36
Q

What does a high K-D value indicate?

A

Low affinity

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37
Q

What does a low K-D value indicate?

A

High affinity

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38
Q

Would a drug with low affinity have a high or low K-D value?

A

High

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39
Q

Would a drug with high affinity have a high or low K-D value?

A

Low

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40
Q

Define occupancy.

A

How many receptors are occupied at any one point

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41
Q

How is occupancy calculated?

A

[Receptor/Drug-Complex] / [Receptor]

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42
Q

What two ions are used in the radio ligand binding assay?

A

H-3 or I-125

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43
Q

What are the five steps in the radio ligand binding assay?

A

Prepare cells; place cells on filters; add radioligand and leave to equilibrate; remove excess radioligand; count radioactivity on filter - directly proportional to radioactive ligand

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44
Q

What are the two main problems with radio ligand binding assays?

A

Non-specific binding, radioligand must be pure and specific

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45
Q

How is non-specific binding in radio ligand assays overcome?

A

Add anti-adsorbants; use two tubes - one with RL and one with RL + L - L displaces RL from receptors, leaving only adsorbed RL - subtract this from first tube to give only bound RL

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46
Q

What must a radioligand be?

A

Pure and specific

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47
Q

What is the main issue with radioligands, and how is it overcome?

A

Degradation - overcome by including free-radical scavenger in the drug solution, storing it at cold temp, avoiding light or the incorporation of an antioxident

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48
Q

Why must a radioligand be specific?

A

To be able to use very low concentrations to avoid excessive adsorbance to other sufraces

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49
Q

What are the advantages to using H-3 as a radioligand?

A

Labelled product indistinguishable from natural compound, high specificity, good stability, long half life

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50
Q

What is the half life of H-3?

A

12.5 years

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51
Q

what are the disadvantages to using H-3 as a radioligand?

A

Specialised labs required, labelling is expensive and difficult

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52
Q

What are the advantages to using I-125 as a radioligand?

A

Iodination is easy in most labs, its cheap, high specificity, easy to attach to aromatic compounds

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53
Q

What are the disadvantages to using I-125 as a radioligand?

A

More readily degraded, activity can easily be reduced, short half life

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54
Q

What methods are employed to separate bound radioligands from free?

A

Filtration, centrifugation, dialysis, column chromatography, precipitation, absorption

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55
Q

What is the major problem with bound/free radioligand separation?

A

Rate of dissociation of ligand-receptor complex

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56
Q

What shape is the radioligand assay curve?

A

Sigmoid

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57
Q

Why does the specific binding curve in a radioligand assay level off?

A

Only a fixed number of receptors

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58
Q

How is K-D deriven from a graph?

A

50% occupency

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59
Q

What is a scatchard plot?

A

Straight line on a bound/free against bound graph

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60
Q

What does the slope on a scatchard plot represent?

A

minus 1 / K-d

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61
Q

What does the x-axis intercept on a scatchard plot represent?

A

B-max

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62
Q

Define the equation of the scatchard line.

A

SEE PAD 6

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63
Q

Is 50% occupancy required for 50% response?

A

No

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64
Q

Why is % occupancy not always the same as % response?

A

Secondary messengers amplify the response

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65
Q

What determines the response of a drug?

A

Downstream activation

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66
Q

What is the receptor ‘reserve’ and what purpose does it serve?

A

Extra receptors that are no necessarily needed - means that they can be lost without losing function, and more chance of a vew low [agonist] will cause a response

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67
Q

What is X-a?

A

[agonist]

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68
Q

Define response as an equation.

A

SEE PAD 9

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69
Q

Define bound receptors as an equation.

A

SEE PAD 8

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70
Q

What does the phrase ‘higher affinity’ mean?

A

Better at binding receptor

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71
Q

What does the hprase ‘higher efficacy’ mean?

A

Better at causing change

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72
Q

What is a partial agonist?

A

Agonist that cannot cause 100% response of the tissue

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73
Q

What does a partial agonist need to get its full response?

A

100% occupancy

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74
Q

Define what an antagonist is.

A

Drug that prevents the agonist response

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75
Q

What are the 6 different classes of antagonism?

A

Chemical, biological, pharmacokinetic, physiological, non-competitive, competitive antagonism

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76
Q

What is chemical antagonism?

A

Combination of antagonist and agonist in solution so the effects of the active drug are lost, i.e. agonist is chemically altered

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77
Q

What is a chelation agent?

A

Drug that combines with heavy metals in the body to inactivate their pharmacoogical effects

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78
Q

What is biological antagonism?

A

Antagonism of endogenous mechanisms in the body

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79
Q

What does omalizumab bind to?

A

IgE

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80
Q

What is pharmacokinetic antagonism?

A

Increased clearing of the drug from the system

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81
Q

What are the three main pharmacokinetic antagonistic pathways?

A

Reduction of absorption, reduction of renal excretion, change in drug metabolism

82
Q

What is physiological antagonism?

A

Interaction of two drugs with the body causing opposing actions

83
Q

Give an example of physiological antagonism.

A

Noradrenaline and histamine on BP

84
Q

How do opiates act as general pharmacokinetic antagonists?

A

They reduce drug absorption

85
Q

How does aspirin generally interact pharmacokinetically with other drugs in the body?

A

Reduces the rate of renal excretion, thus increases drug half life

86
Q

Give an example of a drug interaction that increases an agonist’s metabolism.

A

Antibiotics can trigger Warfarin metabolism

87
Q

What is non-competitive antagonism?

A

Blocking a step in the process between receptor activation and response - does not compete with the agonist for the receptor site

88
Q

What is competitive antagonism?

A

Competition with the agonist for a receptor, which can be reverse by increasing [agonist]

89
Q

What does an increase of competitive agonist concentration cause?

A

Shift to the right on concentration/response curve, effectively increasing K-d

90
Q

What is a dose ratio?

A

Comparison of the EC-50 with and without antagonist

91
Q

Define the dose ratio equation.

A

SEE PAD 10

92
Q

What is pA2?

A

The negative logarithm to the base 10 of the molar concentration of antagonist that makes it necessary to double the concentration of agonist needed to elicit the original submaximal response.

93
Q

Define the pA2 equation.

A

SEE PAD 11

94
Q

How is [antagonist] required to create a DR of 2 deriven?

A

SEE PAD 12

95
Q

What is irreversible competitive antagonism?

A

Time-dependent antagonism that cannot be washed out or effected by [agonist]

96
Q

What is the only way to counter irreversible competitive antagonism?

A

Re-synthesis receptors

97
Q

What is tachyphylaxis?

A

Acute down turn in drug response

98
Q

What is tachyphylaxis also known as?

A

Densensitisation

99
Q

What causes tachyphylaxis?

A

Loss of receptors by internalisation/recycling/degradation; altered receptors through phosphorylation/decreased effector coupling; exhausted mediators; increased degradation of drug; physiological adaptation

100
Q

What does drug effect depend on?

A

Mechanism of action, physicochemical properties, concentration

101
Q

What are physicochemical properites?

A

Affinity, efficacy and potency

102
Q

What two methods do drugs distribute themselves through the body?

A

Bulk flow transfer through the bloodstream and diffusion through lipids, channels and carriers

103
Q

What is lipid solubility defined as?

A

Partition coefficient

104
Q

What is the partition coefficient?

A

Lipid solubility of a drug

105
Q

What is diffusivity defined as?

A

Diffusion coefficient

106
Q

What is the diffusion coefficient?

A

Diffusivity of a drug

107
Q

What is the most important property of a drug?

A

Partition coefficient - how soluble in lipids they are

108
Q

What three characteristics mean non-polar molecules are the best drugs?

A

Increased rate of absorption form the gut, increased penetration into the brain and other tissues, increased renal elimination

109
Q

What is the BBB?

A

Blood brain barrier - endothelial cells lining blood vessels in the CNS forming tight junctions that are impermeable to water molecules

110
Q

What substances does the BBB restrict and allow?

A

Restricts water soluble molecules, allows lipid soluble molecules

111
Q

What happens to the BBB during inflammation? Give an example.

A

Tight junctions can become leaky, such as during meningitis, hence why it can be treated by IV penicillin

112
Q

What three major factors affect drug distribution?

A

BBB, binding to plasma proteins, partition into specific tissues

113
Q

How does albumin interact with drug affinity?

A

Binds to mainly acidic drugs, restricting their binding to receptors

114
Q

What are the six methods of drug delivery?

A

Oral/rectal, percutaneous, intravenous, intramuscular, intrathecal, inhalation

115
Q

What does intrathecal mean?

A

Through the CNS (i.e. CSF)

116
Q

What is CSF?

A

Cerebrospinal fluid

117
Q

What are the four methods of drug excretion?

A

Urine, faeces, milk/sweat, expired air

118
Q

What are the two main biochemical reactions in drug metabolism?

A

Phase 1 - catabolic (which can produce more reactive compounds); phase 2 - synthetic (conjugation to produce inactive product)

119
Q

What are pro-drugs?

A

Must cross the hepatic plasma membrane and be metabolised to activate

120
Q

What role does metabolism of a drug have in its life span?

A

End, alter or prolong pharmacological actions

121
Q

What does the molecular weight of a drug affect?

A

Rate of diffusion

122
Q

Why does pH and ionisation affect many drugs?

A

Many drugs are weak acids or bases, and only uncharged species can cross the lipid barrier; only during the correct pH are these drugs un-ionised and able to diffuse and activate

123
Q

What three systems comprise the ANS?

A

Sympathetic, parasympathetic and enteric

124
Q

What does ANS stand for?

A

Autonomic nervous system

125
Q

What does SS stand for?

A

Sympathetic nervous system

126
Q

In what three systems do the SS and PSS oppose each other?

A

GI smooth muscle, heart rate and bladder control

127
Q

What system controls sweat glands and most blood vessels?

A

SS

128
Q

What system controls sweat glands?

A

SS

129
Q

What nervous system controls most blood vessels?

A

SS

130
Q

What nervous system controls the ciliary muscle of the eye?

A

PSS

131
Q

What nervous system controls the salivary gland?

A

PSS + SS

132
Q

What effects do the PSS and SS have on the salivary gland?

A

Exactly the same - stimulate release

133
Q

What is the neuronic pathway from CNS to blood vessels?

A

To cholinergic ganglion then on to adrenergic end point

134
Q

What is the neuronic pathway from CNS to sweat glands?

A

To cholinergic ganglion then on to cholinergic (muscarinic) end point

135
Q

What is the neuronic pathway from CNS to adrenal medulla?

A

To cholinergic (nicotinic) end point

136
Q

What is the neuronic pathway from CNS to salivary glands?

A

To cholinergic (nicotinic) ganglion then on to cholinergic (muscarinic) end point

137
Q

What is Dale’s criteria?

A

That a neuron releases the same NT at every terminal branch

138
Q

What does NT stand for?

A

Neurotransmitter

139
Q

What are the 5 steps in synaptic transmission?

A

NT synthesis, storage in synaptic vesicles, release upon neuronal activation, post-synaptic receptor activation, breakdown and/or reuptake

140
Q

What are the 5 principal targets for drugs?

A

Receptors, transmitter synthesis, transmitter breakdown, transmitter reuptake/packaging, exocytosis

141
Q

What two types receptors are used in the ANS?

A

Ligand gated ion channels (ionotropic) and GPCRs (metabotropic)

142
Q

What flavour of ligand gated ion channels are in the ANS?

A

Nicotinic cholinergic receptors

143
Q

What flavours of GPCRs are in the ANS?

A

Alpha 1, 2; beta 1, 2; muscarinic receptors 1-5

144
Q

What does nAChr mean?

A

Nicotinic cholinergic receptor

145
Q

What does mAChr mean?

A

Muscarinic cholinergic receptor

146
Q

How many distinct GPCR receptors exist?

A

> 1000

147
Q

What does GPCR stand for?

A

G-protein coupled receptor

148
Q

What are GPCRs often referred to as?

A

Metabotropic

149
Q

What are ligand gated ion channels often referred to as?

A

Ionotropic

150
Q

Describe the structure of GPCRs.

A

Mono or dimeric, 7TM alpha-helices with a ligan binding domain in extracellular loop or buried within TM2&3

151
Q

What does the 3rd intracellular loop and C-terminal tail of a GPCR do?

A

Highly variable in length and sequence, responsible for G protein interaction and are sites of phosphorylation

152
Q

How many classes of GPCR are there?

A

Four

153
Q

What are the four general classes of GPCR?

A

Class 1 - rhodopsin like; class 2 - secretin related; class 3 - metabotropic glutamate like; class 4 - frizzled

154
Q

What signalling function do GPCRs serve?

A

Transducers

155
Q

How many subunits comprise a GPCR, and term defines this?

A

3 - heterotrimeric

156
Q

Which subunit defines a GPCR, and why?

A

Alpha - it binds the GDP/GTP

157
Q

What do beta/gamma subunits do in GPCRs?

A

Anchor GPCR to inner surface of PM

158
Q

Which two GPCR subunits form a tight complex?

A

Beta/gamma

159
Q

What kind of control does adenylyl cyclase GPCRs have?

A

Bidirectional control

160
Q

What terms are given to GPCRs for both sides of the bidirectional adenylyl cyclase control?

A

G-i - inhibitory; G-s - stimulatory

161
Q

What terms are given to both alpha subunits of the bidirectional adenylyl cyclase control?

A

Alpha-s - stimulatory; alpha-i - inhibitory

162
Q

What kind of control does phospholipase C GPCRs have?

A

Unidirectional

163
Q

What term is given to the phospholipase C GPCR?

A

G-q - stimulatory

164
Q

What term is given to the phospholipase C GPCR alpha subunits?

A

Alpha-q - stimulatory

165
Q

What is PIP2?

A

Phosphatidyl inositol 4,5 bisphosphate

166
Q

What is IP3?

A

Inositol 1,4,5 trisphosphate

167
Q

What is DAG?

A

Diaglycerol

168
Q

Describe the phospholipase C unidirectional GPCR pathway.

A

GPCR activation leads to PIP2 hydolysis, which generates two more messengers - DAG and IP3

169
Q

How do you terminate GPCR signalling?

A

Remove agonist, GTPase activity of alpha subunit, desensitisation of receptor

170
Q

How is GTPase activity in G-alpha initiated?

A

RGS-proteins

171
Q

What are RGS-proteins?

A

Regulators of G-protein signalling

172
Q

How are GPCRs desensitised?

A

Phosphoralysed or internalised

173
Q

Which GPCRs are adrenergic?

A

Alpha 1, 2; beta 1, 2

174
Q

Which GPCRs are muscarinic?

A

M1-5

175
Q

Which receptors associate with G-s?

A

Alpha 1; beta 1, 2

176
Q

Which receptors associate with G-i/o?

A

Alpha 2

177
Q

Which receptors associate with G-i alone?

A

M2 + M4

178
Q

Which receptors associate with G-q?

A

M1, M3 and M5

179
Q

What are NSAIDs?

A

Non-steroidal anti-inflammatory drugs

180
Q

What do NSAIDs do?

A

Anti-inflammatory - modify inflammatory reaction; analgaesic - reduce certain sorts of pain; anti-pyretic - lower raised temperature

181
Q

How are NSAIDs anti-inflammatory?

A

Decrease vasodilation, and in turn oedema

182
Q

What are NSAIDs ineffective against?

A

Mediators that contribute to tissue damage associated with chronic inflammatory conditions

183
Q

How are NSAIDs analgaesic?

A

Decrease PG production in damaged and inflamed tissue which would otherwise sensitises nociceptors to inflammatory mediators

184
Q

Name two inflammatory mediators.

A

Bradykinin, serotonin (5-HT)

185
Q

How are NSAIDs antipyretic?

A

Thermostat in hypothalamus activated via IL-1 induced COX2 production of PGE

186
Q

What is COX?

A

Cyclooxygenase

187
Q

What occurs in the COX active site?

A

Oxidation of arachidonic acid

188
Q

Describe the structure of COX.

A

Made up of two identical subunits, each with two catalytic sites

189
Q

What are the two kinds of catalytic site found on COX?

A

Peroxidase and cyclooxygenase sites

190
Q

Where is COX active?

A

ER membrane

191
Q

How does aspirin interact with COX?

A

Binds covalently to Ser residue, preventing arachadonic acid from reaching cyclooxygenase site

192
Q

What are the five main side effects of NSAIDs?

A

GIT problems, renal failure, liver damage, bronchospasm, skin rashes

193
Q

What doe GIT stand for?

A

Gastrointestinal tract

194
Q

What GIT problems occur as side effects of NSAIDs?

A

Dyspepsia, diarrhoea, nausea, vomiting, gastric bleeding, ulceration

195
Q

What can be co-administered with NSAIDs to protect the GIT?

A

Misoprostol

196
Q

What is misoprostol co-administered with, and why?

A

NSAIDs to protect the GIT

197
Q

What is dyspepsia?

A

Indigestion

198
Q

What is misoprostol and analogue for?

A

PGs

199
Q

What does PG stand for?

A

Prostaglandin

200
Q

What pathway does COX contribute to?

A

Inflammatory

Y2S1 - Drug Action (4 decks)

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