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ICPP Flashcards

1
Q

What is the difference between exogenous and endogenous signalling molecules?

A

Exogenous = from outside the body

Endogenous = made within the body

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2
Q

Outline the main features of AMINE signalling molecules

Solubility, Plasma 1/2 life, Time of action, Receptor location, mechanism

A 
Hydrophillic
Plasma half life = seconds
Time of action = milliseconds to seconds
Receptors in the plasma membrane
Mechanism = changes membrane potential + triggers synthesis of cytosolic 2nd messengers
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3
Q

Outline the main features of PEPTIDE and PROTEIN signalling molecules
(Solubility, Plasma 1/2 life, Time of action, Receptor location, mechanism

A 
Hydrophillic 
Plasma half life = minutes
Time of action = minutes to hours
Receptors located on the plasma membrane
Mechanism - triggers protein kinase activity + the synthesis of cytosolic 2nd messengers
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4
Q

Outline the main features of STEROID signalling molecules

(Solubility, Plasma 1/2 life, Time of action, Receptor location, mechanism

A 
Lipophillic
Plasma half life = hours
Time of action = hours to days
Receptors in they cytoplasm or nucleus
Mechanism is the receptor-hormone complex controls transcription and mRNA stability
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5
Q

What are the three main types of signalling molecules used in the endocrine system?

A

Amines
Peptides (+proteins)
Steroids

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6
Q

What are some examples of local chemical mediators?

A

Cytokines (eg. Interleukins, chemokines, interferons, histamine)
Eicosanoids (eg. prostaglandins + leukotrines)
Neuropeptides

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7
Q

What type of signalling molecules does paracrine signalling use?

A

Neurotransmitters (amino acids, mono amines, peptides + ACh)

Local chemical mediators (cytokines + eicosanoids)

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8
Q

What are the types of signalling molecule targets?

A

Receptors
Ion channels
Transporters
Enzymes

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9
Q

What are the main types of receptor?

A

Kinase linked
Ion channels (ligand gated) - ionotropic
Nuclear (intracellular)
GPCRs - metabatropic

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10
Q

By what mechanism do kinase linked receptors work?

A

Phosphorylation of groups to start a signalling cascade

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11
Q

What neurotransmitters are taken up using cotransport of Na+?

A

Noradrenaline
Serotonin
Glutamate

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12
Q

What is an agonist?

A

Signalling molecule which binds to a receptor and activates it - causes a measurable response

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13
Q

What is an antagonist?

A

Signalling molecule that binds to a receptor but doesn’t activate it - blocks the actions of agonists

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14
Q

Outline the main features of GPCR structure

A

Single polypeptide chain
7 Transmembrane domains
N terminal is extracellular
C terminal is intracellular

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15
Q

What is a G protein?

A

Guanine nucleotide binding protein

Heterotrimeric - has alpha, beta and gamma subunits

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16
Q

How are G proteins activated?

A

Replacement of GDP with GTP

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17
Q

What happens when GTP binds to the alpha subunit of a G protein?

A

The beta/gamma subunit dissociates and now both can go on to interact with effector proteins

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18
Q

When does the activity of G protein subunits stop?

A

When GTP on the alpha subunit is hydrolysed back to GDP (carried out by GTPase)
Alpha subunit has a high affinity for the beta/gamma subunit so the G protein is easily reformed

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19
Q

What ligands bind to Beta-adrenoreceptors?

What is their effect?

What is the effector molecule?

A

Adrenaline and noradrenaline

Stimulatory

Adenylyl cyclase

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20
Q

What are the types of alpha-adrenoreceptors?

Give their effect and what their effector molecules are.

A

Alpha 1 = Stimulatory - phospholipase C

Alpha 2 = Inhibitory - adenylyl cyclase

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21
Q

What GPCRs does ACh act on?

What is its effect on these? Give the effectors the G proteins act on

A

M1+M3 muscarinic receptors - Stimulatory (Gq protein) - acts on phospholipase C

M2+M4 muscarinic receptors - inhibitory (Gi protein) - acts on adenylyl cyclase

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22
Q

How does Cholera toxin (CTx) interfere with G protein function?

A

Prevents termination of signalling - stops Gs proteins hydrolysing GTP to GDP by systematic modification
G proteins continue to activate adenylyl cyclase to activate cAMP

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23
Q

How does Pertussis toxin (PTx) interfere with G protein function?

A

Covalently modifies GPCRs what prefer Gi proteins so they can no longer be stimulated - uncoupling

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24
Q

What does phospholipase C do to PIP2?

A

Convert it to IP3 and DAG

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25
Q

What is needed to convert PIP2 to PIP3?

A

PI3K

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26
Q

How many subunits does PKA have and what do they do?

A

4 Subunits

2 R - regulatory, binding of cAMP to these causes them to release the C subunits
2 C - catalytic, carry out phosphorylation of target proteins

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27
Q

What concentration is cytoplasmic Ca2+?

A

1 x10-7M (100nM)

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28
Q

What concentration is extracellular Ca2+?

A

1 x10-3M (1mM)

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29
Q

How is cytoplasmic Ca2+ increased?

A

VOCCs (voltage gated calcium channels)
LGICs (ligand gated ion channels)
CICR (Calcium induced calcium release)

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30
Q

How is cytoplasmic Ca2+ decreased?

A

PMCA (plasma membrane Ca2+ ATPase)
NCX (Na+/Ca2+ exchanger)
SERCA (Smooth/sarco endoplasmic reticulum ATPase)

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31
Q

How do VOCCs work?

A

Open in response to depolarisation

Once open Ca2+ will move down its concentration gradient into the cell

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32
Q

How do LGICs work?

A

Activated by the binding of an excitatory neurotransmitter

These bind and open the channel so Ca2+ can enter

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33
Q

How do SOCs work to increase Ca2+?

A

Activated by a Ca2+ sensing protein in the ER which detects low levels and so stimulates to SOC to move extracellular Ca2+ into the store

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34
Q

How does PMCA work?

A

Primary active transporter - Uses one ATP molecule per Ca2+ ion that is moved out

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35
Q

How does the NCX work?

A

Moves 3Na+ in for every Ca2+ moved out
Reverses if the cell is depolarised
Has low affinity for Ca2+ but high expression

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36
Q

How is Ca2+ released from the ER (using IP3)?

A

A suitable ligand brings to the Gq receptor on the membrane which triggers production of IP3 by membrane phospholipids
IP3 diffuses through the cytoplasm to bind with IP3 receptors on the ER - these are LGICs
The IP3R opens on binding of IP3 and allows the efflux of Ca2+ into the cytosol from the ER

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37
Q

How does CICR work?

A 
Ryanodine receptors (RyR) on the ER membrane are LGICs that are activated upon binding of Ca2+
When Ca2+ binds to the RyR Ca2+ will efflux from the ER into the cytoplasm
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38
Q

Explain what happens in agonist stimulated regulation of phospholipase C

A

Activation of the Gq protein stimulates release of the alpha subunit - this binds to phospholipase C
The complex binds with PIP2 and causes its cleavage into IP3 and DAG
IP3 binds to an IP3 receptor causing it to open and let Ca2+ out of the store
DAG has its own protein kinase C - increase in DAG and Ca2+ will activate the PKC and cause it to phosphorylate it’s substrates in the cells

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39
Q

How is ionotropy increased using signalling pathways?

A

Adrenaline/noradrenaline binds to beta1-adrenoreceptors in the ventricles
These receptors then activate Gs proteins which activate adenylyl cyclase
This will increase activity of cAMP and cause activation of PKA
PKA phosphorylates a VOCC to allow Ca2+ to enter the cardiac muscle cells
By increasing Ca2+ the contraction of the heart is increased

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40
Q

What receptor does sympathetically released noradrenaline interact with to cause vasoconstriction?

A

Alpha1-adrenoreceptors

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41
Q

What binds with M3-muscarinic receptors to stimulate bronchoconstriction?

A

Parasympathetically released acetyl choline

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42
Q

What type of transporter do all human cells have?

A

Na+/K+ATPase pump

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43
Q

What types of molecules can pass through the membrane easily?

A

Hydrophobic

Small + uncharged

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44
Q

What information does the permeability coefficient give you?

A

The likelihood of substances passing across a membrane

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45
Q

How do voltage gated ion channels work?

A

They have positively charged amino acids in the centre of their structure
Upon depolarisation of the membrane these are repealed and so move up and cause a structural change in the protein - causing it to open

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46
Q

What sort of ΔG value does active transport have

A

Positive

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47
Q

What sort of ΔG value does passive transport have?

A

Negative

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48
Q

What is the intracellular concentration of Na+?

A

12mM

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49
Q

What is the extracellular concentration of Na+?

A

145mM

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50
Q

What is the intracellular concentration of Cl-?

A

4.2mM

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51
Q

What is the extracellular concentration of Cl-?

A

123mM

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52
Q

What is the intracellular concentration of K+?

A

115mM

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53
Q

What is the extracellular concentration of K+?

A

4mM

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54
Q

Where is ATP synthase found?

How does it make ATP?

A

Found in the mitochondria

When protons from the intermembrane space move back into the matrix they move through ATP synthase and it makes ATP

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55
Q

What is the difference between uniport and cotransport?

A 
Uniport = movement of one molecule/ion at a time
Cotransport = movement of more than one molecule/ion at a time
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56
Q

What are the main functions of the Na+/K+ pump?

A

To maintain a high intracellular K+ (moves 2K+ in for every 3Na+ out)
And maintain the concentration gradient of Na+
Drive secondary active transport

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57
Q

What are the two types of cotransport?

A 
Antiport = movement of the molecules in opposite directions
Symport = movement of the molecules in the same direction
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58
Q

What are the NCX and Na+/H+ transporter examples of?

A

Secondary antiport transport molecules

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59
Q

How does Prozac (Fluoxetine) work?

A

Inhibits the serotonin reuptake transporter (SERT) so increases the action of serotonin

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60
Q

What protein is affected in Cystic Fibrosis and what does it lead to?

A

A mutation in the CFTR protein
This leads to it not being able to pump Cl- out of the cells, and causes the water potential in the cells is lower than that in the mucus and so less water moves out of the cells and the mucus becomes thick and sticky

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61
Q

How does cholera affect the CFTR protein to cause diarrhoea?

A

It produces a toxin which activates PKA
PKA then phosphorylates CFTR and cause it to pump lots of Cl- out of the cell into the lumen of the gut, taking water with it to give watery stools

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62
Q

What does the Na+/H+ exchanger do?

A

Exchanges extracellular Na+ for intracellular H+

Regulates cell volume

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63
Q

Give two examples of bicarbonate transporters

A 
NBC - alkalinises the cell by moving H+ out and HCO3- in 
Anion exchanger (AE1)/Band 3 - acidifies the cell by moving Cl- out and HCO3- out (present in erythrocytes)
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64
Q

What is the range of normal cell pH?

A

7.2-7.5

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65
Q

How many molecules of water do Na+, K+ and Cl- move with them?

A

Six

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66
Q

How can movement of ions oppose cell swelling/shrinking?

A

Cell swelling - extrude ions

Cell shrinking - influx of ions

67
Q

Give an example of how a conductive system helps to resist cell swelling

A

K+ and Cl- are moved out by facilitated diffusion and water follows
With this there is no net change in membrane potential

68
Q

Give two examples of cotransport systems that resist cell swelling and explain how they work

A

Use anion exchangers to move Cl- and HCO3- in and K+ out and H+ in. The H+ and HCO3- will make carbonic acid which carbonic acid will act on to make water and CO2 which move out of the cell

Symporter moving K+ and Cl- out/amino acids out. Water will follow their movement

69
Q

Give an example of how a conductive system will resist cell shrinking

A

Influx of osmotically active ions (eg. Na+, K+ or Cl-)

70
Q

Give two ways in which a cotransport system will resist cell shrinking

A

A Na+/K+/dichloride transporter moves all these osmolytes into the cell and so lots of water moves in (there is no net change in membrane potential as the charges cancel)

Use AE1 and NHE to make carbonic acid, the water will follow the influx of osmolytes

71
Q

What are thiazidines used for and what do they do?

A

Used treat type 2 diabetes

Stop symport of Na+ and Cl-

72
Q

What is spironolactone?

A

A mineralocorticoid receptor agonist

Used for people with high levels of hypertension

73
Q

What does an aquaporin do?

A

Moves water across a membrane five times faster than it would move alone

74
Q

How can we measure membrane potentials?

A

Using a microelectrode (very fine micropipette) to penetrate the cell membrane
This has a tip filled with conducting solution (eg.KCl)

75
Q

What range does cardiac and skeletal muscles resting membrane potential have?

A

-80mV to -90mV

76
Q

What is the resting membrane potential for red blood cells?

A

-9mV

77
Q

How is an electrical gradient created across a membrane?

A

Selective ion channels

Asymmetric distribution of ions across the membrane

78
Q

What is the value of Ek?

A

-95mV

79
Q

What is the value of ECl?

A

-95mV

80
Q

What is the value of ECa?

A

+122mV

81
Q

What is the value of ENa?

A

+70mV

82
Q

What is depolarisation?

A

A decrease in the size of the membrane potential from its normal value - cell interior becomes less negative

83
Q

What is hyperpolarisation?

A

An increase in the size of the membrane potential from its normal value - the cell interior becomes more negative

84
Q

Opening of which channels will cause hyperpolarisation?

A

K+ and Cl-

85
Q

Opening of which channels will cause depolarisation?

A

Na+ and Ca2+

86
Q

What effect does increasing membrane permeability to a particular ion have on membrane potential?

A

Moves the membrane potential towards the equilibrium potential for that ion

87
Q

What causes mechanical gated ion channels to open?

Give an example of one

A

Membrane deformation

Hair cells in the inner ear

88
Q

What are three excitatory neurotransmitters?

A

ACh
Glutamate
Dopamine

89
Q

How do inhibitory synapses work?

A

Binding of the neurotransmitter causes opening of K+ or Cl- channels which cause hyperpolarisation- larger stimulus is needed to reach threshold

90
Q

What is the difference between slow and fast synaptic transmission?

A

Slow - receptor and ion channel are separate

Fast - receptor protein is also an ion channel

91
Q

How are cardiac ion channels more selective than other ion channels?

A

Only permeable to one ion

Specific membrane potential is required for the opening of specific channels

92
Q

How is excessive influx of ions controlled by ion channels?

A

Some are configured to close a fraction of a second after opening

93
Q

What is an action potential?

A

A rapid change in the membrane potential

94
Q

What is the value for depolarisation for axons, the sino-atrial node and ventricular myocytes?

A

+30mV

95
Q

What does skeletal muscle depolarise to?

A

+40mV

96
Q

What is the driving force for the movement of ions?

A

The difference between the membrane potential and the equilibrium potential

97
Q

What is the conductance of a membrane to an ion?

A

The degree of permeability of the membrane to that ion

98
Q

What does conductance of the membrane depend on?

A

The number of open ion channels

Increases with the number of ion channels

99
Q

What is the capacitance of a membrane?

A

It’s ability to store charge

100
Q

Which channels lead to an undershoot after repolarisation and why?

A

K+ channels - they open and close more slowly

101
Q

What happens after depolarisation to repolarise the membrane?

A

Voltage gated Na+ channels open - influx of Na+

Voltage gated K+ channels open - efflux of K+

102
Q

What happens when Na+ channels are inactivated?

A

They cannot open or recover until hyperpolarisation occurs

103
Q

Why can no action potentials occur in the absolute refractory period?

A

Nearly all Na+ channels are inactivated so no Na+ can move in and so depolarisation cannot occur

104
Q

What is happening in the relative refractory period?

A

The Na+ channels are recovering from inactivation

An action potential may be activated if the stimulus is large enough (as time goes on excitability will increase)

105
Q

Describe the structure of a voltage gated Na+ channel

A

Made of one polypeptide chain
4 domains (6 alpha helix cylinders in each)
Inactivation particle which acts as a ‘plug’
4th region of each domain made of many positive amino acid residues - allows sensitivity to volatage

106
Q

Describe the basic structure of a voltage gated K+ channel

A

Four subunits
Each made of 6 alpha helical cylinders
4th region has many positive amino acid residues - contributes to voltage sensitivity

107
Q

How does the change in voltage field cause voltage gated ion channels to open?

A

It changes the forces on the positive amino acids in the fourth region of the channel causing a conformational change

108
Q

How does procaine work?

A

Stops the firing of action potentials by blocking Na+ channels
Blocks it in a use dependent way - blocker gets into the channel when it opens

109
Q

What is a A-alpha peripheral axon?

A

Sensory fibres from muscle spindles

Motor neurones to skeletal muscle

110
Q

What is an A-delta axon?

A

Sensory fibres from pain and temperature receptors (detect sharp and localised pain)

111
Q

What are B axons?

A

Preganglionic neurones of the ANS

112
Q

What are C axons?

A

Sensory fibres from pain, temperature and itch receptors (detect diffuse pain)

113
Q

What is the local current theory?

Why does it occur?

A

Injection of current into an axon will cause the resulting change of charge to spread along the adjacent sections of the axon, causing an immediate local change to membrane potential

Occurs due to influx of positive Na+ ions repealing the surrounding negative ions

114
Q

What is λ?

A

The length constant - the distance it takes for the action potential to fall to 37% of its original value

115
Q

What does membrane resistance depend on?

A

The number of open ion channels - the lower the membrane resistance the more ion channels that are open

116
Q

What effect does having a high capacitance have on the change in voltage?

A

Slower changes in voltage in response to current injection

117
Q

What does high resistance mean about the spread of change in voltage?

A

It will spread further along the axon

118
Q

What does a wider diameter of an axon mean?

A

Higher conduction velocity - spread of depolarisation will move further along the axon

119
Q

What is the myelin sheath and what does it do?

A

Made of tightly packed layers of Schwann cells (+oligodendrocytes in the CNS)
Insulates the axon

120
Q

What are the gaps in the myelin sheath called?

What is here?

A

Nodes of Ranvier

High density of ion channels

121
Q

Why does saltatory conduction occur?

A

The action potential will have to jump from node to node as it cannot occur in regions which are myelinated

122
Q

What are four diseases which results from the breakdown of the myelin sheath?

A

Multiple sclerosis
Devic’s diseases
Landry-Guillon-Barre syndrome
Charcot-Marie-tooth diesease

123
Q

How does damage to the myelin sheath reduce local current spread?

A

The next node may not reach threshold and so an action potential cannot be fired

124
Q

What is a neuromuscular junction?

A

The synapse between a nerve and a skeletal muscle fibre

125
Q

What is the ion channel that opens upon depolarisation of the nerve terminal in a neuromuscular junction?

A

Voltage gated Ca2+ ion channels

126
Q

Describe the structure of a voltage gated Ca2+ channel

A

Made of one peptide
Has 4 domains
6 alpha helical cylinders in each domain
4th region of each domain is a voltage sensing domain

127
Q

What sort of receptors are present on the muscle in a neuromuscular junction?

A

Nicotinic acetyl choline receptors

128
Q

Describe how Ca2+ causes exocytosis of neurotransmitter from vesicles in the presynaptic membrane

A

Ca2+ binds to synaptotagmin
Synaptotagmin brings the vesicles close to the membrane
The vesicles interact with a snare complex to form a fusion pore at the membrane
The neurotransmitter is released into the synaptic cleft through the fusion pore

129
Q

Describe how nicotinic ACh receptors work

A

They are activated upon binding of two ACh molecules
Binding causes a conformational change
It is a cation selective pore so let’s Na+ and K+ through (difference in speeds is due to equilibrium potentials)

130
Q

What is the reversal potential?

A

Where there is no net flow of charge when an ion channel is open

131
Q

How does a depolarising blocker work?

A

Binds to nACh receptors and activates them
Cannot be broken down due to there being no enzyme - the membrane remains depolarised
The Na+ channels become inactivated so can’t stimulate any more action potentials

132
Q

What is mayasthenia gravis?

How does it affect neuromuscular junctions?

A

An autoimmune disease targeting nACh receptors - patient has weakness which increases with exercise

Antibodies are produced against nACH receptors
Leads to loss of receptors by complement lysis and receptor degradation
End plate potentials have a reduced amplitude - threshold not reached

133
Q

What is the intrinsic efficacy of a drug?

A

The ability of a drug to switch a receptor on

134
Q

What is a ligands efficacy?

A

The ability of a ligand to cause a response

135
Q

Why do antagonists have affinity only?

A

They bind to a receptor but do not activate it

136
Q

What is Kd and what does it show?

A

Dissociation constant - the concentration of drug required to occupy 50% of all available receptors

137
Q

What is the intrinsic efficacy of a drug?

A

The ability of a drug to switch a receptor on

138
Q

What is a ligands efficacy?

A

The ability of a ligand to cause a response

139
Q

Why do antagonists have affinity only?

A

They bind to a receptor but do not activate it

140
Q

What is Kd and what does it show?

A

Dissociation constant - the concentration of drug required to occupy 50% of all available receptors

141
Q

What sort of graph will using a logarithmic scale for drug concentration give?

A

Sigmoidal

142
Q

What is EC50?

A

The effective concentration of drug giving 50% of the maximal response
Measure of potency

143
Q

What is the difference between dose and concentration?

A

For dose the concentration at the site of action is unknown, the concentration gives the known concentration of drug at the site of action

144
Q

What does the value of EC50 depend on?

A

Affinity and intrinsic efficacy

145
Q

Why may salbutamol have adverse effects on heart rate?

A

It has poor selectivity (so low affinity) for Beta-2-adrenoreceptors (in lungs) so may affect Beta-1-adrenoreceptors (in heart) and cause relaxation here too

146
Q

What is the difference between salmeterol and salbutamol in terms of their effects on Beta-adrenoreceptors?

A

Salmeterol - high selectivity but low efficacy (No selective efficacy - will turn on beta 1 and beta 2)

Salbutamol - poor selectivity but high efficacy (for beta 2)

147
Q

What shift will spare receptors cause of a binding curve?

A

Left

148
Q

What positive effect do spare receptors have on drug response? How do they do this?

A

They increase sensitivity - smaller proportion of receptors have to be occupied for a dull response

149
Q

How will the body change number of receptors on cells with low activity?

A

Increase to increase sensitivity - upregulation

150
Q

What can downregulation lead to?

A

Tolerance to a drug - don’t have sufficient receptor number to generate a full response

151
Q

What direction will a partial agonist cause the binding curve to shift in?

A

To the right

152
Q

Why will partial agonists not generate a full response even if all receptors are occupied?

A

They do not have sufficient intrinsic efficacy for a maximal response

153
Q

What is an example of a partial agonist alternative to morphine?
How is it different to morphine?

A

Bupernorphine

Higher affinity but lower efficacy

154
Q

Can a partial agonist be converted to a full agonist? If yes, how?

A

Yes - increasing receptor number

155
Q

What are the three ways that antagonists block the effects of agonists?

A
  • reversible competitive antagonism
  • irreversible competitive antagonism
  • non competitive antagonism
156
Q

What does IC50 give?

A

An index of agonist potency - it’s the concentration of antagnoist that gives 50% inhibition

157
Q

How will reversible competitive antagonists cause a shift of the agonist concentration-response curve?

A

Parallel sift to the right

158
Q

What is a good reversible competitive antagonist used at μ-opioid receptors? Why is it a food competitor?

A

Naloxone - has high affinity

159
Q

When does irreversible competitive antagonism occur?

A

When the antagonist dissociates slowly or not at all

160
Q

What does it mean when it is said that irreversible competitive antagonists are non-surmountable?

A

Increased agonist concentration cannot overcome their effect

161
Q

What direction do irreversible competitive antagonists cause the agonist concentration-response curve to shift?

A

Parallel shift to the right

162
Q

What is pheochromocytoma?

A

Tumour of the adrenal chromaffin cells

163
Q

How does non competitive antagonism work?

A

The antagonist binds to an allosteric site causing a change in the conformation of the of the orthosteric site (where the natural ligand would bind) so the agonist can no longer bind

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