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Mine ESA 2 > Membranes & Receptors > Flashcards

Membranes & Receptors Flashcards

0
Q

Membrane composition

A

40% lipid
60% protein
1-10% carbohydrates
20% water if hydrated

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1
Q

Main functions of a biological membrane?

A

Continuous highly selective permeability Barrie’s
Communication
Control of enclosed chemical environment
Signal generation in response to stimuli
Different regions of different membranes have different properties

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2
Q

Membrane phospholipids consist of…

A

Phospholipid -> glycerol, phosphate head, 2 fatty acids

Polar head groups: choline, amines, aa, sugars

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3
Q

What are glycolipids?

A

Sugar containing lipids

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4
Q

What are cerebrosides in glycolipids?

A

Head group is a sugar monomer

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5
Q

What are gangliosides in glycolipids?

A

Head groups is an oligosaccride

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6
Q

What is the ratio of cholesterol to phospholipase in the membrane?

A

1:1

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7
Q

Amphipathic molecules form….

A

Micelles and bilayers

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8
Q

What are the modes of mobility of membrane lipids?

A
  • intra chain motion
  • fast axial rotation
  • fast lateral diffusion
  • flip flop
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9
Q

How cholesterol contributes to membrane stability?

A
  1. Reduces phospholipid packing -> increased fluidity, low temp
    By interaction of TSH rigid planar conjugated ring
  2. Reduces phospholipid chain motion -> decreases fluidity, high temp
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10
Q

What is the functional evidence for membrane proteins?

A

Facilitated diffusion, ion gradients, specificity of cell membrane

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11
Q

What is the biochemical evidence for membrane proteins?

A

Membrane fractionation, gel electrophoresis, free fracture

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12
Q

Mobility of proteins in bilayers?

A

Conformational change
Rotational
Lateral diffusion

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13
Q

Why does flip flop not occur in proteins in membrane?

A

Due to having to move large hydrophilic moieties through hydrophobic region requires lots of energy and it would be too destructive.

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14
Q

What re the constraints of proteins in bilayers?

A

Aggregates, tethering, interaction with other cells, membrane protein associations, lipid mediated effects: separate into fluid phase and cholesterol poor regions, associated with extra membranous proteins e.g. Cytoskeleton

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15
Q

How to peripheral proteins associated with lipid bilayer?

A

Electrostatic and hydrogen bond interactions

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16
Q

How do integral membrane proteins associate with the lipid bilayer?

A

Ine at with hydrophobic regions

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17
Q

What is needed to remove integral membrane proteins from the bilayer?

A

Detergents and organic solvents

-> agents that competed for non polar interactions

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18
Q

What is needed to remover peripheral proteins from the bilayer?

A

Changes in pH or ionic strength

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19
Q

How do membrane proteins contribute to the (erythrocyte) cytoskeleton?

A 
There is a network of spectrin and actin attached to the membrane via adaptor proteins. 
10 major proteins 
Bands 3 + 7 are transmembrane  
Anhydride band 4.9 + 4.1 link spectrin 
Band 3 protein and glycoprotein A
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20
Q

What are the two possible causes of haemolytic anaemias?

A

Hereditary spherocytosis

Hereditary elliptocutosis

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21
Q

What is hereditary spherocytosis?

A

Autosomal dominant

Your spectrin levels are depleted, so RBC round and are lysed by the spleen prematurely so have shortened lifespan

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22
Q

What is hereditary elliptocytosis?

A

Mutation in spectrin prevents end to end association so unable, to from stand hereotertramers resulting in fragile elliptoid cells

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23
Q

Transport proteins have important roles such as….

A

Regulation of cell volume
Maintenance of intracellular pH
Extrusion of waste products of metabolism and toxic substances
Generation of ionic gradients necessary for electrical activity
Concentrated metabolic fuel and a building blocks

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24
Q

What are the ways in which facilitated diffusion occurs?

A

Carrier molecules/ping pong
Protein flip flop
Protein pores -> ligand, voltages gated
Remember is saturable!

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25
Q

Describe the two types of active transport?

A

Directly -> primary active transport

Indirectly -> secondary active transport

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26
Q

What are the main differences between passive and active transport?

A

Activate transport is against the concentration gradient of the transported species and free energy is used

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27
Q

What is a co transport system?

A

More than 1 type of ion or molecule is transported per reaction cycle

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28
Q

What are the three types of transport?

A

Uni port
Symport
Anti port

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29
Q

Describe uniport

A

1 solute molecules is transported from 1 side of the membrane to another

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30
Q

Describe symport

A

Transfer of 1 solute molecule depends on the simultaneous sequential transfer of a 2nd solute in the same direction

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31
Q

Describe anti port

A

Transfer of 1 solute molecule depends in the simultaneous transport of a 2nd solute molecule in the opposite direction

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32
Q

What transporters are involved in the control of the resting intracellular calcium concentration?

A

PMCA
SERCA
NCX
Mitochondrial Ca2+ uniporters

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33
Q

What transporters are involved in opposing the acidification of a cell?

A

So expel H+ and more HCO3- inwards
NBC, NHE, Na+/HCO3- co transporter
Then Na+/K+ ATPase creates the Na+ gradient.

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34
Q

What transporters are used in opposing alkalinisation of the cell?

A

Alkali extrusion

AE, HCO3- out and Cl- in

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35
Q

How is cell volume regulated?

A

Cells with extrude and influx certain ions in responses to cell swelling and shrinking such as Na+, Cl- and K+
NBC, AE, NHE

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36
Q

Why can we not use buffers to regulate cell pH?

A

Because they would be quickly overwhelmed

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37
Q

Why does the kidney reabsorb the bicarbonate a filtered into the PCT?

A

To retain the bases for buffers

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38
Q

Explain renal bicarbonate reabsorption

A

So use NHE to collect Na and the this goes back into the blood using sodium potassium ATPase then the H+ in the lumen combines with the HCO3- to form H2CO3 which forms H20 and CO2 (carbonic anhydrase) which is reabsorbed then forms H2CO3 which goes to H+ and HCO3- then using AE HCO3 absorbed into the blood then the H+ is reused in NHE

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39
Q

Explain the action of 1 diuretic

A

In the DCT, amiloride blocks the sodium transporter ENaC hence preventing sodium reabsorption and therefore water

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40
Q

What is the intracellular and extracellular concentration of calcium?

A

Intracellular: 10^-7 M
Extracellular: 1.5 mM

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41
Q

What is the intracellular and extracellular concentration of chloride?

A

Intracellular: 4.2 mM
Extracellular: 123 mM

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42
Q

What is the intracellular and extracellular concentration of potassium?

A

Intracellular: 155mM
Extracellular: 4mM

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43
Q

What is the intracellular and extracellular concentration of calcium?

A

Intracellular: 12 mM
Extracellular: 145mM

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44
Q

Why is the membrane selectively permeable to certain ions and molecules?

A

Channel proteins and membrane spanning proteins

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45
Q

Properties of ion channels?

A

Selectively
Gating
High rate of flow that is always down the ions concentration gradient

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46
Q

How is the resting membrane potential set up?

A
  1. Membrane has open K+ channels so it is selectively permeable to K+, which diffuse out of the cell down its concentration gradient
  2. Since anions cannot follow the cell becomes negatively charged on the inside
  3. The membrane potential will oppose the outward movement of potassium until an equilibrium is reached, Ek which is the point as which the electrical and diffusion all forces balance another and there is no net movement of an ion
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47
Q

Define equilibrium potential

A

is the point as which the electrical and diffusion all forces balance another and there is no net movement of an ion

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48
Q

Define depolarisation

A

A decrease in the membrane potential from its normal value so that the inside of the cell becomes less negative
Opening of potassium and sodium channels

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49
Q

Define Hyperpolarisation

A

An increase in the membrane potential so that the inside of the cell becomes more negative
Opening of potassium and chloride channels

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50
Q

What is fast synaptic transmission?

A

Were the receptor is an ligand gated ion channel

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51
Q

What is an EPSP/excitatory post synaptic potential?

A

Is caused but depolarising transmitters opening channels, Ca2+, Na+, cations leading to an excitation of cells/depolarisation.
Longer time cause than and AP
Grade with amount of transmitter, ACh and glutamate

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52
Q

What is an IPSP/inhibitory post synaptic potential?

A

Hyper polarising transmitters, glycine and GABA open K+ or Cl- channels.
Leads to inhibition,

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53
Q

What is slow synaptic transmission?

A

Receptor itself is not an ion channel but signal in 1/2 ways both involving GTP-binding proteins.
Direct G-protein gating or via an intracellular messenger

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54
Q

What is the formulae for conduction velocity?

A

Distance between stimulatory and regarding electrode/ tie gap between stimulus and AP registered by recording electrode

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55
Q

What is the difference between diphasis and monophasic recording?

A

Diphasic, neurone is not damaged at end
Monophasic, neurone is damaged
See notes for pictures

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56
Q

How are axons artificially raised to threshold?

A

Excitability will be reduced under a anode so excitation occurs under a cathode directly stimulating an axon to threshold

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57
Q

What are the things that effect conduction velocity?

A

Capacitance, ability to store charge
Membrane resistance, more ion channels open = low resistance
Diameter of axon

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58
Q

What does a high capacitance mean?

A

Decrease in the spread of local current

59
Q

What does a low membrane resistance mean?

A

More ion channels are open limiting the spread of local current

60
Q

What does a small axon diameter mean?

A

Higher cytoplasmic resistance, smaller spread of action potentials.

61
Q

What do we have to to have to achieve a high conduction velocity?

A

High membrane resistance
Low membrane capacitance
Large axon diameter

62
Q

In myelination–>

A

Velocity is proportional to diameter

63
Q

In demyelination –>

A

Conduction velocity is inversely proportional to diameter

And there is an even distribution of sodium channels

64
Q

What is the name given to the type of conduction in myelinated nerve fibres?

A

Saltatory conduction

65
Q

Describe the action potential?

A
  1. Open potassium channels
  2. Stimulus causes the opening of voltage gated sodium channels
  3. Depolarisation to threshold causes the opening of voltage gated sodium channels so sodium enters the cells, causing further depolarisation causing more channels to open
  4. Voltage gated sodium channels are inactivated and voltage gated potassium channels open resulting in potassium influx and reopolarisation
  5. Cells become hyperpolarised and this allows inactive voltage gated sodium channels to recover
    Absolute refractory period -> voltage gated sodium channels are inactivated and no matter how strong the stimulus an AP cannot be generated
    Relative refractory period -> some voltage gated sodium channels are now in their closed state and an AP can be generated.
66
Q

Describe how local anaesthetics work?

A

Injection causes pain so ap to signal this so sodium channels are open and then aesthetic can bind blocking them only hence why can still wall. Block when open and have a higher affinity for them in inactive state.

67
Q

What order will local aesthetics block in?

A

Small myelinated axons
un myelinated axons
Large myelinated axons

68
Q

Describe accommodation

A

Principle by which you can make a longer slower gradual depolarisation go last try threshold potential but not cause an AP Threshold rises a bit,
1. Whilst in recovery period refractory if stimulating again will not have full population of channels available, if keep going in in recovery phase then it will accommodate as taking more channels out of game and back to absoukte refer story period

  1. Hyperkaelimia is, membrane potential is less negative if near threshold potentials, if membrane then hyperpolarised and opens then keeps activated. But if potential not siuffcientky negative then may not be enough to, as channels spontaneous opening can to be reactive from this.
    So when stimulus gets an ap of reduced amplitude

So threshold does rise a little bit, sad have to bring a certain number if channels to activation so slightly increases threshold.
All clinically if a bit accommodated then is simply less excitable

69
Q

What are the three ways I which we can control channel activity?

A
  1. Ligand gating
  2. Voltage gating
  3. Mechanical gating
70
Q

Describe the diversity of calcium channels

A

Have lots of different types in different locations e.g. l types in lungs, can exist with other sub unit such as beta, alpha and gamma, are similar to sodium, have glycosylation and phosphorylation sites

71
Q

Describe the events underlying fast synaptic transmission

A
  1. Calcium entry through voltage gated calcium channels located close to vesicle releases sites
  2. Calcium binds to synaptotagmin
  3. Vesicles containing neurotransmitters brought closer to the membrane
  4. Snare complex makes a fusion pore
  5. Neurotransmitters are released through this pore via Exocytosis
72
Q

Properties of Nicotinic ACh receptors?

A

Channel has 5 sub units: 2 alpha each with ACh binding site, B, gamma and delta
Pore is either oeln or closed
Requires two molecules of ACh to bind and open the channel
Does not distinguish between cations
Open results in depolarisation of the cell membrane

73
Q

Molecular properties of voltage gated sodium channels?

A

1 peptide consisting of 4 homologous repeats
Each peptide consists of 6 transmembrane domains
1 domain can sense the voltage field across the membrane

74
Q

What is a competitive blocker of Nicotinic receptors?

A

Tubocarine

Binds at recognition site for ACh causing channels to close as ACh cannot bind

75
Q

What is a depolarising blocked of Nicotinic ACh channels?

A

Binds to Nicotinic ACh receptors causing a media gained depolarisation as less susceptible to Acetylcholine esterase so adjacent sodium channels will be inactivated and can to be activated
Succinylcholine, used as a muscle relaxant

76
Q

Name some of the functions intracellular calcium regulates

A

Fertilisation, secretion, metabolism, proliferation, neurotransmitters, contraction, learning, memory, apoptosis, necrosis

77
Q

What are the four ways in which a low resting basal intracellular calcium concentration is maintained?

A
  1. Relative impermeability of the plasma membrane
  2. Dependant upon cells ablity to expel Ca2+
  3. Calcium bugged e.g. Calsequestrin
  4. Intracellular calcium stored
78
Q

Increasing intra cellular calcium at a signalling event

A
  1. Calcium influx across the plasma membrane
    -> voltage gated calcium channels
    -> receptor operated calcium channels
  2. Calcium released from rapidly releasable intracellular stores
    -> G-protein coupled receptors
    phospholipase C and IP3 receptors on ER
    Adenyl cylase
    -> calcium induced calcium release by ryanodine receptors
  3. Non rapidly releasable intracellular calcium stores
    Low affinity but high capacity
79
Q

How are intracellular calcium levels restored to normal?

A
  1. Taken back into readily releasable stores -> SERCA
  2. Binging proteins/calcium buggers
  3. Back into non readily releasable stores -> mitochondrial uni porter
  4. Revers back of NCX, PMCA
80
Q

What does return to basal levels of calcium require?

A

Termination of signal
Calcium removal
Calcium store refilling

81
Q

What prolongs the cardiac action potential?

A

As voltage gated calcium channels show voltage sensitive activation and inactivation but this is slower than sodium and a lower potassium conductance results in a prolonged AP in cardiac myocytes

82
Q

What are the roles of receptors in cellular physiology?

A 
Neurotransmission 
Control of gene expression 
Sorting of intracellular protein 
Releasing of intracellular calcium stores
Cell adhesion
83
Q

Name the four types of signal transduction and receptor sub type families

A
  1. Membrane bound receptors with integral ion channels
  2. Membrane bound receptors with integral enzyme activity
  3. Membrane bound receptors that signal through transducing proteins
  4. Intracellular receptors
84
Q

Describe signalling via tyrosine kinase linked receptor

A
  1. Binding of agonist/hormone to Extracellular binding site activates protein kinase activity in the cytoplasmic domain in the receptor protein
  2. Protein kinase auto phosphorylated tyrosine residues on the cytoplasmic domain of the receptor
  3. a) phosphorylated tyrosine residues are reconciled by transducing proteins
    b) or by enzymes containing phosphotyrosine recognition sites
  4. Get transduction of message into a cellular event
85
Q

Define receptors mediated endocytosis

A

The selective internalisation of molecules into the cell by binding to a specific cell surface receptors

86
Q

Receptor mediated endocytosis -> LDL, contribution to uptake of metabolites

A
  1. Cells that require LDL synthesis receptors that specifically recognise apoprotein B
  2. Clatherin coated pits are where there receptors are located
  3. On binding of ligand the receptor and coated pit invaginate and pinch off from the membrane forming coated vesicles
  4. Coated vesicles are then uncoated
  5. Uncoated vesicles fuse with endosomes, CURL
  6. Due to the pH 6.0 the LDL receptor now has a a low affinity for the LDL particle and they dissociate.
  7. Receptors returns to cell membrane or Golgi
  8. LDL goes to lysosome where is degraded to give cholesterol esters and is released into cell
87
Q

What can cause hypercholestranemia

A

Receptor deficient
Non functional receptor
Receptor binding normal but no internalisation as not located in coated pits.

88
Q

Describe the passage of iron into the cell

A

Iron binds to apotrasnferrin forming transferrin which then binds to receptor at neural pH, internalised, in acidic endosome the Fe3+ ions are released from transferrin but apotrasnferrin is still bound to the receptor. Then sorted by curl so receptor and apotrasnferrin are returned to plasma membrane where at neutral pH they have low affinity for each other and apotrasnferrin dissociates from the receptor

89
Q

What is the example for control of receptor number at the cell surface?

A

Insulin and type II diabetes

90
Q

What do virus do when they enter the cell?

A

Bind to cell by factors associated with cell receptors and enter the cell via Clatherin pits, then unfolding hydrophobic domains in membrane fusion proteins in response to pH of endosome. Then insert membrane fusion proteins into endosome membrane allowing the release of genomic RNA into the cell cytoplasm then uses cell machinery to replicate RNA and capsid proteins to bud new vesicles at the cell membrane

91
Q

What are the viruses that take example of receptor mediated endocytosis

A

Cholera toxin

Diptheria toxin

92
Q

What does cholera toxin do to g-proteins

A

Specifically modifies Gs type proteins evading to irreversible activation, as eliminates GTPase activity

93
Q

What does pertussis toxin do to g-proteins?

A

Involves Gi type proteins and uncouples the receptors effector linkage
interferes with GTP/GDP exchange of G alpha

94
Q

What does DAG interact with?

A

Protein kinase C

95
Q

Where is cyclic GMP phosphodiesterase activity and what is the g-protein?

A

Found in photoreceptors cells in the retina (rods and cones)
G T

96
Q

What does GT cause?

A

Cyclic GMP breakdown so channels close and there is membrane hyperpolarisation which signal to the CNS
followed by the excitation of rhodopsin by a photon of light

97
Q

Describe the two mechanisms of neurotransmitter release?

A
  1. In CNS and PNS by pre-synaptic g-protein coupled receptors
  2. Pre synaptic u-opioid receptors block neurotransmitter release by reducing calcium entry into the presynaptic knob.
98
Q

What does an agonist have that an antagonist doesn’t?

A

Has intrinsic activity and efficacy

99
Q

What is Kd

A

Concentration of ligand required to occupy 50% of the aa I label receptors

100
Q

What is Bmax?

A

Maximum binding capacity, gives us information about receptor number

101
Q

What is EC50?

A

Measure of the amount of drug necessary to produce an effect of a given magnitude

  • > measure of agonist potency
  • > depends on affinity, intrinsic activity and potency
102
Q

Define Potency

A

Measure of the amount of drug neccessary to produce an effect of a given magnitude

103
Q

Efficacy

A

The ability of a drug to illicit a responses when it interacts with a receptor.

104
Q

What do spare receptors do?

A

They increase the sensitivity and allow responses at lower concentrations of agonists

105
Q

What is tachyphylaxis?

A

A sudden decrease in drug effectiveness after admits ration can be caused by down regulation of receptors so sensitivity is reduced

106
Q

What is a partial agonist?

A

Is a ligand that even when all the receptors are occupied if cannot illicit and maximum response
Can be an anatognist for a full agonist if it has a higher affinity
Can also be a full agonist if there is a great enough número of spare receptors
And can also have a greater potency
Example clinically is buphenomorphine has a higher affinity but lower efficacy.

107
Q

What is IC50

A

Concentration of agonist giving 50% inhibition

108
Q

What does an agonist do to the agonist concentration response curve?

A

It causes a shift to the right

109
Q

What are the three types of antagonists and describe them

A

Reversible competitive antagonist
Reversible non competitive antagonists
Irreversible competitive antagonists

110
Q

What is LD50

A

Lethal dose in 50% of the population

111
Q

Define affinity

A

Measure of the ability of a drug to form a drug receptor complex, degree in which a ligand binds to a receptor

112
Q

Efficacy on a graph?

A

How far up it goes

113
Q

Potency on a graph

A

How close it is to the y axis

114
Q

Intrinsic efficacy

A

Ability of a ligand to turn a receptor on

115
Q

Intrinsic activity

A

The magnitudes of a response in a system

116
Q

What are the two types of drug formulation?

A

Liquid

Solid

117
Q

What are the ways in which you can administer a drug?

A

FOCAL: eyes, skin, inhalation
SYSTEMIC:
-> enteral: sublingual, oral, rectal
-> parental: subcutaneous, intramuscular, intravenous, transdermal

118
Q

What are the advantages to focal?

A

Concentrated drug at site of action
Less systemic absorption
Less of target effects

119
Q

Define oral bioavailability

A

Is the proportion of term dose given orally (not IV) that reaches the systemic circulation in an unchanged form.
Can be expressed as amount (depends on GI absorption, first pass)
Or rate of availability (depends on pharmaceutical and rate of gut absorption)

120
Q

What general factors effect oral bioavailability?

A

Obesity
Oh
Protein binding
Administration of more than 1 drug

121
Q

What is amount measure by?

A

Measured by area under curve of blood drug level vs time plot

122
Q

What is rate of availability measured by?

A

By peak height and rate of rise of drug level in blood

123
Q

What is therapeutic ratio?

A

LD50/ED50

124
Q

Define volume of distribution?

A

The theoretical value into which a drug has distrusted assuming that this has occurred spontaneously.

125
Q

Wen are protein binding interactions important?

A
  1. When drug is highly bound to albumin
  2. Drug had a small volume of distribution so a concentration change has a greater effect
  3. Drug has a low therapeutic window
126
Q

Describe object and precipitate drugs and how they relate to each other

A 
Object drug/class 1: used at a dose which is much lever that the number of albumin binging sites e.g. warfarin -> low free drug concentration 
Precipitate drug/class 2: used a a dose which is greater than the no of availed binding sites -> high free drug concentration e.g. Aspirin 
Class 2 drug will displace the class 1 drug giving temporary high levels do it before the elimination rate rises
127
Q

Define first order kinetics

A

Rate of developed do plasm drug is proportional to drug level
Has half lives

128
Q

Zero order kinetics

A

Rate of decline is plasma drug level is constant

Elimination mechanisms can be saturated quickly.

129
Q

What happens in renal disease?

A

Half life is prolonged so need lever maintance dose
Takes longer to reach a steady state
Protein binding of drug is altered

130
Q

In liver disease we have to be carful with drugs with a low therapeutic ratio, why?

A

Cellular dysfunction, warfarin
Parasystemic shunts, propranolol
Reduced blood flow, propranolol
Reduced albumin, affects drugs binding to plasma proteins

131
Q

What is the enzyme that catalyses the conversion of acetyl CoA and choline to ACh?

A

Choline acetyl transferase

132
Q

What happens to the acetate and choline broken down by acetylcholinesterase?

A

Actetae and CoA -> acetyl CoA, acetyl CoA synthetase and absorbed by glial cells
Then choline is recaptured by choline tars ported present in the synaptic terminal

133
Q

Tyrosine to DOPA? Enzyme?

A

Tyrosine Hydroxylase

134
Q

DOPA to dopamine, enzyme?

A

DOPA decarboxylase

135
Q

Dopamine to NA, enzyme

A

Dopamine B Hydroxylase

136
Q

NA to adrenalin, enzyme?

A

Phenylthanolsnine N-methyl transferase

137
Q

What is the name of the two enzymes that breakdown NA?

A

Monamine oxidase and catechol-o-methyl transferase

138
Q

What do presynaptic receptors do?

A

Feedback loop regulating release

139
Q

What does alpha methyl tyrosine do?

A

Competitively inhibits tyrosine Hydroxylase blocking de novo synthesis of NA

140
Q

What does alpha methyl dopa do?

A

Is a competitive inhibitor as it is converted to alpha methyl NA by dopa carboxylase and dopamine B Hydroxylase, it accumulates in NA vesicles and is released with them but preferentially acts on the pre synaptic receptors inhibiting further release of NA, use at alpha 1 adrencoeptors in boldly vessels in hypertension

141
Q

What does carpi DOPA do?

A

Inhibits dopa carboxylase in periphery not CNS due to blood brain barrier, Parkinson’s

142
Q

What does adrengic blocking drugs do?

A

Reduce impulse conduction as block action of re uptake of neurotransmitter so NA depleted form vesicles but side effects are too great such a hypotension, renal failure,

143
Q

Indirectly acting sympathamimatic agents, IASAs do what?

A

Cause NA to leak form synaptic vesicles into the synaptic cleft
Action can be enhance by inhibiting action of MAO

144
Q

Uptake 1 Inhibitors are?,

A

Tricylic antidepressants

But can cause tachycardia and dysrhytmias but these can abide by drug and dose

Mine ESA 2 (3 decks)

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