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Pharmacology 1A > Receptors and enzymes, transporters and ion channels > Flashcards

Receptors and enzymes, transporters and ion channels Flashcards

1
Q

how many main types of receptors are there?

A

4

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2
Q

where are receptors found and what is the exception to this?

A

in the cell membrane
except nuclear receptors

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3
Q

4 main types of receptors

A

ligand-gated ion channels
GPCRs
enzyme/kinase linked receptors
nuclear receptors

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4
Q

most common type of enzyme linked receptor

A

Receptor tyrosine-kinases (RTKs)

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5
Q

what are RTKs?

A

the most common type of enzyme linked receptor

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6
Q

how do kinase linked receptors exist and until when?

A

in an inactive state until they bind to signalling molecules

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7
Q

when do kinase linked receptors stop existing in an inactive state?

A

when bound to signalling molecules

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8
Q

what happens to inactive RTKs?

A

the tyrosine residues become phosphorylated by activated kinase domains

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9
Q

what happens as phosphorylation of tyrosine residues in RTKs happens?

A

monomers come together to form a dimer

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10
Q

why is it important that kinase residues in RTKs become phosphorylated?

A

phosphorylation of kinase residues provides a point of binding for extracellular signalling proteins

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11
Q

what provides a point of binding for extracellular signalling proteins?

A

phosphorylation of kinase residues

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12
Q

what happens when RTKs bind to proteins?

A

it produces downstream signalling pathways

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13
Q

stages before an RTK can cause downstream signalling

A

tyrosine residues phosphorylated –> docking sites for intracellular signalling proteins –> downstream signalling

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14
Q

examples of RTKs

A

insulin receptor
EGF receptor
VEGF receptor
IGF receptor

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15
Q

what do RTKs tend to regulate?

A

transcription and translation

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16
Q

due to RTKs regulating transcription and translation what does this effect?

A

DNA synthesis and cell survival, growth and proliferation

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17
Q

which RTK signalling pathways are frequently mutated in cancer?

A

MAPkinase and PI3 kinase

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18
Q

what happens in terms of RTKs when cancer cells become mutated?

A

can effect the level of expression of kinase signalling pathways

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19
Q

biologics

A

antibody based drugs

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20
Q

what do biologics bind to?

A

surface molecules like RTKs

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21
Q

what is breast cancer caused by and what is done about this?

A

a rise in one type of RTK and so there’s an antibody in a drug to block this receptor

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22
Q

what do RTKs have synergy with?

A

G-protein coupled receptors

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23
Q

what’s the only type of receptor that isn’t membrane bound?

A

nuclear receptors

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24
Q

stages that take place with nuclear receptors

A

hormone/agonist enters cell

interacts with IC nuclear receptor in cytosol or nucleus

NR/drug complex (drug-receptor complex) moves to nucleus

drug-receptor complex interacts with DNA to alter gene transciption

altered protein synthesis

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25
Q

what enters the cell to interact with an intracellular receptor protein (nuclear receptors)?

A

small hydrophobic signal molecule

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26
Q

what does a signal molecule bind to in the nucleus or cytosol (nuclear receptors)?

A

intracellular receptor protein

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27
Q

what are nuclear receptors in cytosol called?

A

cytosolic

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28
Q

what are the two types of nuclear receptors?

A

cytosolic
nuclear

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29
Q

example of cytosolic nuclear receptors

A

steroid receptors

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30
Q

example of nuclear receptors

A

thyroid receptors

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31
Q

examples of things that bind to nuclear receptors

A

endogenous hormones (e.g - corticosterone, aldosterone)
synthetic analogues (e.g - dexamethasone (steroid anti-inflammatory), anabolic steroids

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32
Q

where do nuclear receptors exist?

A

some in the nucleus, some in cytosol

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33
Q

what are anabolic steroids used for?

A

muscle growth

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34
Q

how do nuclear receptors work?

A

small hydrophobic signal molecule gets across the cell membrane by attaching to carrier proteins that deposit them where target cells are

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35
Q

are there a wide variety of nuclear receptors for drugs to bind to?

A

yes

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36
Q

type of drug targets

A

GPCRs
channel-linked receptors
enzymes
transport protein drug targets

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37
Q

what are enzymes?

A

proteins that catalyse chemical reactions, the conversion of substrate(s) to product(s)

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38
Q

what do enzymes catalyse?

A

chemical reactions where substrates are converted into products

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39
Q

are enzymes destroyed in chemical reactions? what does this mean?

A

no, they can be used over and over again

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40
Q

what do enzymes take us from and to?

A

substrates to products

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41
Q

modes of drugs inhibiting enzymes

A

competitive
false substrate
non-competitive (allosteric)

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42
Q

explain how competitive drugs inhibit enzymes

A

mimics the substrate, but not converted

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43
Q

explain how false substrate drugs inhibit enzymes

A

mimics the substrate, converted to abnormal product

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44
Q

explain how non competitive drugs inhibit enzymes

A

binds to allosteric site to alter activity of enzyme towards substrate

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45
Q

how can drugs reduce the amount of substrates enzymes convert into product?

A

by chemically resembling substrates and competitively inhibiting the substrate

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46
Q

which drugs mimic substrates for enzymes and are not converted and which which are converted to abnormal product?

A

competitive - not converted
false substrate - converted to abnormal product

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47
Q

what happens when non-competitive drugs bind to allosteric sites in enzymes?

A

alter the activity of enzyme towards substrate

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47
Q

where do non-competitive drugs bind to an enzyme?

A

to allosteric site

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48
Q

what are the two possible scenarios following a drug inhibiting an enzyme?

A

reversible
irreversible

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49
Q

explain reversable changes caused by drugs inhibiting enzymes

A

high levels of substrate overcome inhibition, if competitive (Km increases, Vmax is unaltered)

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50
Q

explain irreversible changes caused by drugs inhibiting enzymes

A

binds very tightly or covalently modifies the enzyme, long lasting clinical effect

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51
Q

what will happen eventually in a reversable inhibition of an enzyme with a drug?

A

eventually substrate will overcome the inhibition of a reversible enzyme inhibitor

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52
Q

what do all modes of inhibition by a drug on an enzyme lead to?

A

normal reaction blocked

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53
Q

well known examples of enzyme inhibitors

A

acetyl salicylic acid (aspirin)
ibuprofen

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54
Q

aspirin

A

acetyl salicylic acid

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55
Q

acetyl salicylic acid

A

aspirin

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56
Q

what does aspirin do at low doses?

A

anti thrombotic drug

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57
Q

what does aspirin do at high doses?

A

pain killer

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58
Q

when is aspirin an anti thrombotic drug?

A

at low doses

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59
Q

when is aspirin a pain killer?

A

at high doses

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60
Q

mechanism of action of aspirin

A

irreversible (covalent) inactivation of COX-1 and COX-2 by acetylation of enzyme

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61
Q

how does aspirin inactive COX 1 and 2?

A

by acetylation of the enzyme

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62
Q

what type of inactivation is irreversible?

A

covalent

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63
Q

what is aspirin an inhibitor of?

A

COX

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64
Q

how does aspirin inhibit COX 1 and 2 enzymes?

A

covalently

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65
Q

what is COX 1 involved in?

A

TxA2 synthesis in platelets, which amplifies platelet function

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66
Q

what are platelets involved in?

A

blood clotting

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67
Q

explain how aspirin behaves as an anti-thrombotic drug

A

thromboxane A2 (TxA2) is involved in the synthesis of platelets - aspirin is an anti-thrombotic drug and so at low levels, aspirin reduces the levels of TxA2

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68
Q

what is involved in the synthesis of platelets?

A

thromboxane A2 (TxA2)

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69
Q

what produces mediators that cause pain and fever and inflammation?

A

arachidonic acid

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70
Q

what does arachidonic acid do?

A

produces mediators that cause pain and fever and inflammation (what aspirin is used against)

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71
Q

how does aspirin act as a pain killer at high concentrations?

A

aspirin inhibits all of the inhibitors produces by arachidonic acid at high concentrations

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72
Q

what does COX 2 do?

A

involved in the synthesis of prostanoids which induce inflammation, pain and fever

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73
Q

what synthesises prostanoids which induce inflammation, pain and fever?

A

COX 2

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74
Q

what do prostanoids do?

A

induce inflammation, pain and fever (synthesised by COX 2)

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75
Q

difference between aspirin and ibuprofen

A

aspirin –> irreversible
ibuprofen –> reversible

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76
Q

what does ibuprofen do?

A

pain killer
reduces inflammation and temperature

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77
Q

mechanism of action of ibuprofen

A

competitive reversible inhibitor of COX 1 and COX 2

78
Q

how does ibuprofen act as a pain killer?

A

by covalently inhibiting COX 2 which is involved in the synthesis of prostanoids which induce inflammation, pain and fever

79
Q

what are enzymes important for in terms of drugs?

A

important as drug targets but also in producing drugs

80
Q

pro drugs

A

drugs that require metabolism to work

81
Q

drugs that require metabolism to work

A

pro drugs

82
Q

up to which point do pro-drugs not work?

A

until they’re metabolised by an enzyme, they don’t work

83
Q

how do pro-drugs start to work?

A

enzymes product an active metabolite which acts as a drug

84
Q

what are enzymes also involves in apart from being drug targets?

A

also involved in the conversion of pro drugs from an inactive to an active form

85
Q

examples of enzymes being involved in the conversion of pro drugs from an inactive to an active form

A

cortisone –> hydrocortisone (anti-inflammatory)

clopidogrel –> active metabolite (inhibits platelet aggregation)

86
Q

what do concentration gradients result from?

A

the unequal distribution of ions between intracellular fluid and extracellular fluid

87
Q

what are concentration gradients maintained by in cell biology?

A

the cell membrane

88
Q

what does the cell membrane form around cells?

A

an impermeable barrier around all cells

89
Q

what does the cell membrane allow to happen and why?

A

allows concentration gradients to exist between the inside and outside of cells since it forms an impermeable barrier around all cells

90
Q

how come ionic concentration gradients can be maintained within a cell?

A

by having a lipophilic membrane that won’t let charged molecules through, it allows cells to maintain their ionic concentration gradients

91
Q

what does the lipophilic membrane around cells not let through?

A

charged molecules

92
Q

what does the phospholipid bilayer not allow the passive transport (diffusion) of across the membrane?

A

charged particles or large polar molecules across the membrane

93
Q

what does the phospholipid bilayer allow the passive transport (diffusion) of across the membrane?

A

gases (O2, CO2)
small polar molecules (H2O, EtOH)
lipid-soluble molecules (e.g - cortisol, benzene)

94
Q

why do cells maintain different concentration gradients of ions?

A

osmosis
cell signalling

95
Q

what do cells use to maintain concentration gradients?

A

transporters and ion channels

96
Q

do transporters use passive or active transport?

A

both

97
Q

passive transport

A

doesn’t require energy - going down concentration gradients

98
Q

active transport

A

requires energy (ATP) - ging against concentration gradients

99
Q

what do transporters and ion channels allow cells to do?

A

to control their intracellular environment

100
Q

two types of passive transport

A

channel-mediated
transporter-mediated

101
Q

what needs to happen when transport with transporters occurs?

A

the molecule needs to bind first

102
Q

what do molecules need to bind to first before transport can occur?

A

transporters

103
Q

what happens during transporter mediated passive transport?

A

the transporter actually binds the molecule even though there’s still a concentration gradient

104
Q

types of passive transport

A

channel or transporter mediated

105
Q

what happens when a molecule binds to a transporter?

A

it causes conformational changes in the transporter in order for it to transport the moleule

106
Q

explain channel-mediated passive transport

A

ion channels that allow molecules to easily pass down through concentration gradient

107
Q

what does active transport use?

A

a transporter

108
Q

what are steroids an example of?

A

lipophilic molecules

109
Q

properties of transporters

A

multipass transmembrane proteins
bind transported molecules
wide variety of molecules transported by transporters
undergo a series of conformational changes to transfer bound molecule
involved in passive or active transport
slower than ion channels
movement of ions can occur down or against their concentration gradients

110
Q

how do transporters transfer bound molecules?

A

by undergoing a series of conformational changes

111
Q

what type of transport are transporters involved in?

A

passive or active

112
Q

are transporters or ion channels faster at transporting?

A

ion channels are faster

113
Q

how do ions move using transporters?

A

down or against their concentration gradients

114
Q

explain how glucose is transported across a cell

A

glucose gets across the cell by binding to a glucose transporter and when it binds, there’s a conformational change in the transporter, which allows glucose to flip from the outside to the inside of the cell and then be released into the cell

115
Q

types of transporter

A

uniport
symport
antiport

116
Q

what type of transporter is a glucose transporter?

A

glucose transporter

117
Q

uniport transporter

A

moves one type of molecule across the cell membrane

118
Q

moves one type of molecule across the cell membrane

A

uniport transporter

119
Q

symport transporter

A

moves two types of molecule across the cell
membrane in the same direction
uses the energy provided by the molecule moving down the concentration gradient to power the other molecule to move against its concentration gradient

120
Q

moves two types of molecule across the cell
membrane in the same direction
uses the energy provided by the molecule moving down the concentration gradient to power the other molecule to move against its concentration gradient

A

symport transporter

121
Q

antiport transporter

A

one molecule moves one way and the other molecule moves the other way at the same time
(the other may be moving against its concentration gradient or with)

122
Q

one molecule moves one way and the other molecule moves the other way at the same time
(the other may be moving against its concentration gradient or with)

A

antiport transporter

123
Q

what are transporters important for?

A

maintaining membrane potential and electrochemical gradients

124
Q

what are important for maintaining membrane potentials and electrochemical gradients?

A

transporters

125
Q

how are cells charged compared to the outside of the cell?

A

relatively negatively charged

126
Q

how do cells maintain their negative charges?

A

by using transporters that maintain ion gradients

127
Q

what can cells maintain by using transporters that maintain ion gradients?

A

negative charges

128
Q

what is essential to maintaining ion gradients?

A

active transport

129
Q

what is active transport essential for?

A

maintaining ion gradients

130
Q

name two transporters that are essential in maintaining ion gradients

A

Na+/K+ ATPase
Na+/Ca2+ exchanger

131
Q

what type of transporter is Na+/K+ ATPase? explain

A

antiport (K+ in, Na+ out)

132
Q

what type of transporter is a Na+/Ca2+ exchanger? explain

A

antiport, but this time is passive since molecules are moving down their concentration gradients

133
Q

explain the importance of a Na+/Ca2+ exchanger

A

Ca2+ is an important regulator and is essential for cells to work properly

134
Q

give two examples of things that maintaining ion gradients is important for

A

muscle contraction
synaptic neurochemical release

135
Q

what is important for muscle contraction and synaptic neurochemical release?

A

maintaining ion gradients

136
Q

what is proof that maintaining ion gradients is importnat?

A

it accounts for 1/3 of total energy expenditure

137
Q

what accounts for 1/3 of total energy expendicture?

A

maintaining ion gradients

138
Q

name an active ingredient found in fox gloves

A

digoxin

139
Q

what is digoxin?

A

an active ingredient found in fox gloves

140
Q

what was digoxin used for?

A

an 18th century cure for dropsy (congestive heart failure)

141
Q

what was used as an 18th century cure for dropsy?

A

digoxin

142
Q

why isn’t digoxin used to treat dropsy anymore?

A

it’s been superceded by newer more selective drugs since there’s lots of side effects to using digoxin

143
Q

explain how digoxin works

A

digoxin blocks Na+/K+ ATPase transporter

increase in intracellular Na+

decrease in electrochemical gradient Na+

decrease in Ca2+ extrusion from cell (since the second transporter doesn’t work as effectively)

increased Ca2+ in cell (less exiting via transporter)

increased concentration of Ca2+ in cardiac cells allows cells to contract more frequently

= digoxin is good in treating cardiac insufficiency

144
Q

what is digoxin used to treat?

A

cardiac insufficiency/fibrillation/congestive heart failure

145
Q

what do serotonin transporters do?

A

bring serotonin back into the cell

146
Q

what type of transporter is a serotonin transporter? explain

A

symport that takes sodium and serotonin at the same time

147
Q

explain how antidepressant drugs work

A

serotonin transporters are blocked by classes of antidepressant drugs to increase serotonin levels to improve mood

148
Q

what are antidepressant drugs essentially?

A

drugs that stop serotonin transporters from working (block them) to increase serotonin levels to improve mood

149
Q

what do antidepressant drugs cause a rise in and how?

A

synaptic serotonin levels by blocking transporters for therapeutic benefit

150
Q

what rises when antidepressant drugs are used?

A

synaptic serotonin levels

151
Q

what do ion channels do?

A

rush molecules across the concentration gradients at high speed

152
Q

what do ion channels and transporters allow cells to do?

A

control their intracellular environment

153
Q

properties of ion channels

A

small pores in the cell membrane formed by proteins
do not bind transported molecules
specificity determined by size and charge
open/closed conformations
voltage or ligand gated
very fast
movement of ions only occurs down their concentration gradients

154
Q

do ion channels bind transported molecules like transporters do?

A

no

155
Q

what is the specificity of ion channels determined by?

A

size and charge

156
Q

two types of ion channels

A

voltage or ligand gated

157
Q

how is a voltage gated ion channel opened?

A

change in electrochemical gradient to open

158
Q

how is a ligand gated ion channel opened?

A

ligand/chemical binds to the channel to open them

159
Q

how fast are ion channels?

A

very fast in terms of how quickly ions come through
>10^7 ions/sec cf transporters 10^2-3 molecules/sec

160
Q

why is it important to maintain concentration gradients inside and outside of a cell?

A

since the movement of ions through ion channels only occurs down their concentration gradients

161
Q

since the movement of ions only occurs down their concentration gradients, what’s it important to happen?

A

that concentration gradients inside and outside of the cell are maintained

162
Q

example of a voltage-gated ion channel

A

voltage-gated Na+ and Ca2+ channels

163
Q

what are Na+ and Ca2+ channels examples of?

A

voltage gated channels

164
Q

example of a ligand gated ion channel

A

nicotinic AChR
(Na+ channel)

165
Q

what is a nicotininc AChR (Na+ channel) an example of?

A

a ligand gated ion channel

166
Q

explain how nicotinic (Na+) ion channels work

A

acetylcholine binds to ligand gated channel to allow Na+ through
change in voltage (depolarisation of cell) to open Na+ and Ca2+ channels
Na+ required for muscle contraction

167
Q

other way of describing change in voltage

A

depolarisation of cell

168
Q

depolarisation of cell

A

change in voltage

169
Q

what is Na+ required for?

A

muscle contraction

170
Q

what is required for muscle contraction?

A

Na+

171
Q

what type of voltage gated channels are there in the neuromuscular junction?

A

Na+ and Ca2+

172
Q

what do the vesicles contain at the neuromuscular junction?

A

acetylcholine

173
Q

give an example of where ion channels are important

A

neuromuscular junction

174
Q

what is maintained along the axon membrane when no nerve impulse is being transported along the axon?

A

resting potential

175
Q

potential difference across the axon membrane during a resting potential

A

-70mV

176
Q

explain how a resting potential is maintained

A

by active transport: sodium-potassium pump pumps 3Na+ out of the axoplasm and only 2 k+ in. Also the axon membrane is highly permeable to K+ and they leak out by fascilitated diffusion through open channels. the outward movement of positive ions means the outside of the axon membrane is positive relative to the inside. the membrane is polarised. the atp needed to maintain a resting potential is produced by the numerous mitochondria presnent in the axoplasm of the axon.

177
Q

what does the sodium-potassium pump do in order to maintain a resting potential?

A

pumps 3 Na+ sodium ions out of the axon for every 2 potassium ions that is pumps in. this is active transport which requires energy in the form of atp.

178
Q

explain the action potential

A

nerve impulses are caused by a rapid change in the permeability of the neurone membrane to K+ and Na+
sodium ion channels in the membrane open; Na+ flood into the axon down their concentration gradient
potential across the membrane changes from -70mV (resting potential) to +40mV (action potential) - the membrane is said to be depolarised
around a millisecond after the sodium ion channels close, the potassium ion channels are open and K+ flood out of the axon. this repolarises the membrane.
an excess of K+ leave the axon before the Na+/k+ pump restores the resting potential. this is known as the refractory period during which no further action potentials can occur.

179
Q

describe synaptic transmission

A

down nerves, there are a series of voltage-gated Na+ channels
change in voltage = channels will open
electrical signal down neurones
each sodium channel open in turn to get an electrical current running down the nerve cells = propagation of action potential
when a nerve impulse (Action potential) arrives at a synaptic end bulb, voltage-dependent calcium channels in the membrane open and calcium ions diffuse rapidly into the end bulb down their concentration gradient
synaptic vesicles, containing neurotransmitter (e.g - acetylcholine) move towards and fuse with the pre-synaptic membrane. the contents of the vesicles are released into the synaptic cleft by exocytosis.
the neurotransmitter diffuses across the synaptic cleft and binds to a receptor (ligand gated ion channel - a transmembrane protein) in the post-synaptic membrane
sodium ion channels in the post synaptic membrane open and sodium ions diffuse into the post-synaptic neurone causing depolarisation
if the threshold potential is reached, an action potential is initiated in the post synaptic neurone = sodium rushed in, which is required for muscle contraction

180
Q

what does tubocurarine chloride interfere with?

A

the neuromuscular junction

181
Q

give an example of something that intereferes with the neuromuscular junction

A

tubocurarine chloride

182
Q

where does Tubocurarine chloride naturally occur?

A

from the bark of the S. American plant Chondrodendron tomentosum

183
Q

what is Tubocurarine chloride used for?

A

source of arrow poison by S. American Natives to hunt animals

first skeletal muscle relaxant (stops muscle contraction)
used in surgery/reduces muscle damage
blocks the nicotinic acetylcholine receptor

184
Q

what type of cells recognise changes in glucose levels?

A

beta cells in pancreas

185
Q

where are beta cells found?

A

pancreas

186
Q

what happens when beta cells in pancreas recognise changes in glucose levels?

A

pancreas can release insulin so that glucose can be taken up by cells

187
Q

what can happen once the pancreas has released insulin?

A

glucose can be taken up by cells

188
Q

what type of cells do people with type 1 diabetes not have?

A

beta cells in pancreas

189
Q

what does insulin release involve?

A

transporters or ion channels

190
Q

explain the stages of insulin release

A
  1. glucose moves down its concentration gradient and enters the cell
  2. glucose used in glycolysis and respiration = increase in ATP in beta cells in pancreas
  3. ATP binds to an ATP-sensitive K+ channel
  4. this closes the channel which causes the beta pancreatic cell to have a rise in intracellular potassium
  5. this rise causes the voltage-gated Ca2+ channels to fire off = influx in Ca2+
  6. rise in intracellular Ca2+ needed for the release of insulin
191
Q

explain how drugs can be used to treat type 2 diabetes

A

can block the processes involved in insulin release with drugs. block ATP-sensitive K+ channels to cause an increase in insulin release

192
Q

treatment for type 1 vs type 2 diabetes

A

1 = inject insulin
2 = drugs to cause more insulin release

193
Q

why do we treat type 1 and 2 of diabetes differently?

A

type 1 = don’t have beta cells at all (=inject insulin)
type 2 = have the cells, they just don’t work properly so can use drugs to cause more insulin release

Pharmacology 1A (5 decks)

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