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ESA 2 -Rhianna > Membranes And Receptors > Flashcards

Membranes And Receptors Flashcards

0
Q

Name four ways phospholipids can move within the cell membrane.

A

Lateral
Rotation
Kink formation within fatty acid chains
Flip flop

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1
Q

On the cell membrane, how does a peripheral protein differ from an integral protein?

A

Peripheral - removed by simple change in pH or charge

Integral - only removed by strong solvents

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2
Q

Name three ways proteins can move within a cell membrane

A

Lateral
Rotation
Conformational change

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3
Q

Why can’t proteins flip flop in a cell membrane?

A

It would take too much energy for the hydrophilic sections to cross the hydrophobic bilayer.

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4
Q

What is membrane fluidity?

A

The ability of the molecules within the cell membrane to move around.

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5
Q

How does cholesterol affect membrane fluidity?

A

It stabilises it by 1. inhibiting movement of the membrane and 2. increasing fluidity of proteins within the membrane. It is more effective at higher temperatures.

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6
Q

What is the cytoskeleton of an erythrocyte composed of?

A

Spectrin and actin fibres form a lattice which is tethered to adapter proteins on the membrane by ankyrin.

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7
Q

What is the purpose of the cytoskeleton in an erythrocyte?

A

Provides strength and prevents membrane proteins from being sheared off when the cell pushes through tight capillaries.

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8
Q

What disorder is caused by DEFECTIVE spectrin which makes up the rbc cytoskeleton?

A

Hereditary elliptocytosis - rugby ball shaped cells

It is a form of haemolytic anaemia caused by a weak cytoskeleton that leaves the cell vulnerable to lysis.

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9
Q

What disorder is caused by a DECREASE in spectrin which makes up the cytoskeleton of rbcs?

A

Hereditary spherocytosis - ball shaped cells

A type of haemolytic anaemia caused by a weak cytoskeleton that leaves the cell vulnerable to lysis.

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10
Q

What is the mechanism of a transporter protein?

A

Ion attaches and causes conformational change. Ping pong to the other side.

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11
Q

Name three types of transporter protein and give an example of each.

A

Uniporter - GLUT 1
Symporter - Na/K/2Cl in the ascending limb of loop of Henle
Antiporter - Na/K ATPase; Na/Ca exchange; Na/H exchange

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12
Q

What is the difference between active and passive transport?

A

Passive follows the combined electric and concentration. Active uses energy to move against it.

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13
Q

What is the difference between primary and secondary active transport? And what are their functions?

A

Primary directly uses ATP
Secondary indirectly uses ATP

Primary mostly just generates the gradient to drive secondary.

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14
Q

Which transporters might be used to maintain levels of resting calcium?

A

Primary transport using H+:
PMCA ATPase pumps calcium out of cell
SERCA ATPase pumps calcium into the ER

Secondary transport:
Na/Ca exchange

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15
Q

Which transporters might be used to control cell pH?

A

Acid extrusion:
Na/H exchange
Na/ bicarbonate cotransporter

Base extrusion:
Anion exchange

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16
Q

Which ions cross the membrane at an anion exchange transporter?

A

HCO3 goes out

Cl goes in

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17
Q

How do some diuretics work?

A

Block the Na/K/Cl cotransporter in the ascending limb of the loop of henle. This stops Na, K and Cl being reuptaken into the blood so there is also a decrease in reuptake of water. This increases the amount of urine.

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18
Q

Describe the action of the Na/K ATPase pump in detail.

A

Uses ATP which is converted to ADP + Pi.
Pumps out 3Na
Pumps in 2K

Keeps the concentration of Na relatively high outside and K relatively high inside.
Maintains the electric potential across the membrane.

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19
Q

What sets up the uneven distribution of ions across the cell membrane?

A

The Na/K ATPase pump

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20
Q

What sets up the resting membrane potential?

A

Potassium channels which are open at rest allow potassium to flow out of the cell which initiates a potential difference.

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21
Q

What is the equilibrium value EK?

A

The is the value in mV when the electric potential across the membrane is enough to prevent any more potassium leaving the cell through the open ion channels. The uneven distribution of ions is maintained so the charge is also retained but there is no movement.
Ek = -85mV

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22
Q

What effect will increasing the permeability to sodium and calcium have on the resting membrane potential?

A

Shift towards ENa (65mV) and ECa (120mV) which is less negative. This is depolarisation.

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23
Q

What effect will increasing the permeability to Chloride have on the resting membrane potential?

A

Shift towards ECl (-90mV) which is more negative than the Ek so hyperpolarises.

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24
Q

Why is the real resting potential in the cell not equal to Ek?

A

Ek assumes the membrane is only selectively permeable to potassium but in reality there are also some sodium and calcium channels transiently open and closed at rest. This means the real resting potential is slightly less negative than Ek.

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25
Q

What is the value of EK?

A

-90mV

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26
Q

What is the value of ENa?

A

60mV

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27
Q

What is the value of ECa?

A

120mV

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28
Q

What is the value of ECl?

A

-70mV

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29
Q

What is the value of the resting membrane potential?

A

-70mV

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30
Q

What is the average length of an action potential in ms?

A

5 ms

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31
Q

What processes occur during the first ms of the action potential?

A

Synaptic potentials excite the dendrites. The excitation is summated at the axon hillock and voltage gated Na channels open. If enough open to reach threshold, they enter a positive feedback loop and there is a rapid depolarisation of the cell membrane as it shifts towards ENa.

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32
Q

What is meant by the threshold of an action potential?

A

The amount of membrane depolarisation required before the membrane enters a positive feedback loop and an action potential can be triggered.

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33
Q

Name 2 factors which determine whether the action potential threshold will be reached.

A
  1. Rate of Na channels opening
    because after some time they deactivate. Enough channels must be activated at once for threshold to be reached.
  2. Total excitation from the synaptic potentials
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34
Q

What processes occur during the second ms of the action potential?

A

Membrane potential reaches peak at 30mv causing voltage gated k channels to open. Voltage gated Na channels also began to inactivate. Membrane therefore repolarises towards EK.

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35
Q

What processes occur during the final 3ms of the action potential?

A

Cell membrane hyperpolarises (beyond resting potential) because both the leak and voltage gated K channels are open. Potential heads closer to EK than at rest. Potential slowly returns to rest as voltage gated k channels inactivate.

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36
Q

What is meant by accommodation of an action potential?

A

The longer the potential takes to reach threshold, the more total stimulus is needed to trigger the AP. This is because Na channels start to inactivate and can no longer contribute to the potential. Extra channels must be activated.

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37
Q

What is meant by the absolute and relative recovery periods of an action potential?

A

ARP is when another action potential cannot be triggered because too many Na channels are either already open or inactive.

RRP is when another action potential is difficult to trigger for this reason but with enough stimulus it is possible.

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38
Q

Why does the action potential only travel in one direction?

A

Local currents pull the ions in both directions. But only the Na channels in front can be triggered to threshold because the ones behind are inactive. Therefore the ARP causes directionality.

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39
Q

What is a myelin sheath?

A

The lipid bilayer surrounding neurons

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40
Q

What effect does myelin have on resistance and capacitance of the neuron?

A

Increases resistance

Decreases capacitance

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41
Q

If myelin decreases capacitance of the neuron, what effect does this have on the action potential?

A

Decreases the amount the neuron needs to be charged before propagation of the action potential because there is less storage of charge.

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42
Q

Why does myelin aid the propagation of action potentials?

A

Increase in resistance encourages the action potential to jump between the nodes of ranvier. Decreased capacitance allows this to happen with less excitation.

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43
Q

Why is myelination of no benefit to small fibres?

A

In small fibres the myelin would squash the axon last too much and increase the resistance within the nerve too much. The action potential would struggle to travel at all.

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44
Q

Why can’t an action potential be propagated along a neuron immediately after removal of the myelin sheath?

A
  1. Decrease in resistance means no jumping between nodes of ranvier. But it can’t travel along because the Na channels are all concentrated at the nodes. In time they will spread out and there can be slow propagation.
  2. But the increase in capacitance means it must also charge for longer so there will be accommodation and propagation will never return fully to normal.
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45
Q

What is the pathophysiology of multiple sclerosis?

A

Autoimmune destruction of myelin sheath. Propagation fails because

  1. resistance decreases so can’t jump between nodes
  2. Capacitance increases so accommodation occurs and can’t reach threshold
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46
Q

How can multiple sclerosis be treated?

A

Diaminopyridine increases the length of the action potential so that the neuron has extra time to reach threshold.
It does this by blocking voltage gated k channels. Hyper polarisation is slowed.
However eventually capacitance will get so high that threshold can’t be reached regardless of how much time is allowed because there are a limited number of Na channels to activate.

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47
Q

How is Ach released into the synapse? (5 steps)

A
  1. Action potential reaches the axon terminal and triggers opening of voltage gated ca channels
  2. Ca enters the neuron
  3. Ca activates synaptotagmin which binds to Ach vesicle
  4. Ach vesicle taken to the snare complex
  5. Snare complex opens and Ach is released
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48
Q

How does Ach propagate the action potential beyond the synapse to the next neuron?

A

Binds at nicotinic receptor causing a conformational change. Na enters cell which causes depolarisation. At threshold the action potential is triggered and propagates further.

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49
Q

How does Ach propagate the action potential beyond the synapse to a myocyte at the neuromuscular junction.

A

Binds at nicotinic receptor causing a conformational change. Ca enters cell which binds to troponin. This moves the tropomyosin out of the way so that myosin can bind to actin.

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50
Q

What is the difference between a receptor and an acceptor?

A

A receptor is silent at rest but an acceptor may operate without a ligand.

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51
Q

What is a ligand gated receptor and give an example.

A

A receptor with an integral ion channel.

Eg. A nicotinic receptor

52
Q

How does an integral enzyme receptor work? and give an example.

A

Ligand binds
Dimerisation
Auto phosphorylation
Enzyme activation

Eg growth factor receptors with tyrosine kinase

53
Q

Describe the process of receptor mediated endocytosis.

A

Spontaneous formation of clathrin coated pits
Receptor and ligand enter pit
Clathrin triskelions allow vesicle to bud off
ATP dependent uncoating
Leftover is called an endosome and has a low ph
Uncoupling of receptor and ligand
Recycled or degraded

54
Q

What is useful about the fact that both receptor and ligand are recycled after receptor mediated endocytosis of insulin?

A

Receptor number is modulated so when the sugar level is high the receptors are destroyed.
But can lead to insulin resistance if high sugar level prolonged because no new receptors are produced

55
Q

Which viruses take advantage of receptor mediated endocytosis to enter the cells?

A

Enveloped only eg cholera, diphtheria

56
Q

How do enveloped viruses take advantage of receptor mediated endocytosis to enter the cells?

A

Enter inside envelope which looks friendly. The low ph in the endosome causes fusion proteins to unfold and poke through the membrane of the endosome. It enters the cytosol….

57
Q

How many transmembrane domains are there in G protein coupled receptors?

A

7

58
Q

How is a signal transduced across a G protein coupled receptor?

A 
Ligand binds outside the membrane causing a conformational change inside
G protein attaches inside
GDP - GTP on the G protein (activation)
Subunits dissociate into 
1. Alpha GTP
2. Beta gamma
59
Q

What two subunits does a G protein dissociate into after activation?

A

Alpha gtp

Beta gamma

60
Q

Describe the cAMP pathway. (3 steps)

A
  1. Alpha GTP causes conformational change in adenyl cyclase
  2. Adenyl cyclase catalyses ATP to cAMP
  3. cAMP activates pka so it is ready to phosphorylate
61
Q

Describe the IP3 pathway. (3 steps)

A
  1. Alpha GTP causes conformational change in phospholipase c
  2. Phospholipase c catalyses PIP2 to IP3 and DAG
  3. Ip3 releases Ca from ER and DAG activates pkc
62
Q

What modulates the effect of G protein subunits?

A

GTPase inactivates back to GDP.

63
Q

What is the beta gamma subunit useful for?

A

Modulation of neurotransmitters by closing v-gated Ca channels and decreasing number of vesicles that reach the snare complex.

64
Q

Give the G protein, pathway, action and location of

M1 muscarinic receptors

A

Gq
IP3
Constrict bronchioles smooth muscle

65
Q

Give the G protein, pathway, action and location of

M2 muscarinic receptors

A

Gi
cAMP
Inhibits SA node - negative chronotropy

66
Q

Give the G protein, pathway, action and location of

M3 muscarinic receptors

A

Gq
IP3
Activates endocrine and exocrine glands
Micturition

67
Q

Give the G protein, pathway, action and location of

Alpha 1 adrenoceptors

A

Gq
IP3
Activates smooth muscle - eg vasoconstriction

68
Q

Give the G protein, pathway, action and location of

Alpha 2 adrenoceptors

A

Gi
cAMP
Inhibits presynaptic nerves - negative feedback

69
Q

Give the G protein, pathway, action and location of

Beta 1 adrenoceptors

A

Gs
cAMP
Activates AV node - positive ionotropy

70
Q

Give the G protein, pathway, action and location of

Beta 2 adrenoceptors

A

Gs
cAMP
Relaxes smooth muscle eg bronchioles

71
Q

How is the acetyl choline signal in the synapse terminated?

A

Acetyl choline esterase

72
Q

How is the noradrenalin signal in the synapse terminated?

A

Reuptake by 1. NET then 2. VMAT

Any not recycled into vesicles is degraded by monoamine oxidase in the cytoplasm

73
Q

How is noradrenalin synthesised?

A

Tyrosine - (tyrosine hydroxylase) - DOPA - dopamine - noradrenalin - adrenalin

74
Q

Which symptom do alpha blockers treat? Which receptors do alpha blockers target?
What is the problem side effect?

A

Alpha 1 adrenoceptors to decrease vasoconstriction and relieve hypertension.
Side effect is postural hypotension because baroreceptors have decreased sensitivity.

75
Q

What symptom do beta blockers target? Which receptors do they target?
Which patients cannot therefore be given beta blockers?

A

Target hypertension by blocking beta 1 adrenoceptors to decrease force of contraction at the av node. Therefore decrease cardiac output.

Can’t be given to asthmatics because beta 1 adrenoceptors also effect smooth muscle of bronchioles.

76
Q

What symptom does salbutamol target? Which receptors does it target?

A

Agonist for Beta 2 adrenoceptors to relax the bronchioles during asthma attack.

77
Q

Define kd of a drug.

A

Concentration of the drug when 50% of receptors are occupied.
It is a measure of drug affinity. Decrease in kd is increase in affinity.

78
Q

What equation would you use to calculate molarity of a solution?

A

M= g/L

Molecular weight

79
Q

Define the affinity of a drug

A

How readily the drug binds to the receptor. It can be measured by kd

80
Q

Define the efficacy of a drug

A

How readily it elicits a response from the receptor.

High efficacy = can elicit response without using all receptors = full agonist
low efficacy = needs all receptors, still may not have a full response =partial agonist.

81
Q

Define EC50

A

Concentration of drug at which 50% of full response is elicited. Measure of potency - decrease in ec50 is increase in potency.

82
Q

Define drug potency

A

A combination of affinity plus efficacy. So how readily the drug binds to and elicits a response from the receptor. Measured by EC50.

83
Q

If you increase affinity which way does the response curve shift?

A

Left

84
Q

If you increase efficacy which way does the response curve shift?

A

Up

85
Q

If you increase potency which way does the response curve move?

A

Left (and up if spare receptors can be released)

86
Q

Define affinity, efficacy and potency for an antagonist

A

Antagonists do not elicit a response from the receptor by definition. So there is no efficacy.

Affinity is readiness to bind = potency in this case.

87
Q

What is the difference between an agonist and an antagonist?

A

An agonist activates a receptor response

An antagonist does not activate a receptor response

88
Q

Name 4 ways an antagonist can have its effect

A
  1. Competitive reversible antagonism
  2. Competitive irreversible antagonism
  3. Non competitive antagonism
  4. Physiological antagonism
89
Q

Describe competitive reversible drug antagonism, including how it appears on a graph. And give an example.

A

Blocks receptors so agonist cannot have its effect.
Decreases affinity of agonist - shift left, maximum remains the same
But can be overcome by adding enough agonist.
Eg atropine on muscarinic receptors

90
Q

Describe competitive irreversible drug antagonism including how it appears on a graph. And give an example.

A

Blocks receptors so agonist cannot have its effect and decreases the total number of receptors because it is irreversible.
Decreases efficacy of agonist - shift down, maximum is reduced.
Eg phenoxybenzamine on alpha adrenoceptors

91
Q

Describe non competitive drug antagonism including how it appears on graph.

A

Acts at a distal site to change the receptor in some way.

Decreases efficacy of the agonist - shifts down

92
Q

Describe physiological drug antagonism. And give an example.

A

Does not act on the agonist at all but has opposite physiological effects through a different pathway.
Eg adrenalin acts via alpha 1 adrenoceptors to vasoconstrict but histamine acts through a different pathway to vasodilate.

93
Q

Define first pass metabolism

A

The process that any ingested substance must follow before reaching the blood stream. Goes from gut to liver to circulation.

94
Q

Give 3 examples of methods of drug delivery that avoid first pass metabolism.

A

IM
IV
Rectal
Sublingual

95
Q

What is meant by volume of distribution of a drug and how is it calculated?

A

The theoretical volume of the body reached by the drug if it spread out instantly to the concentration it reaches in the blood, where time =0

Amount given
[in plasma] at t=0

If it is high it shows is relatively dilute in the plasma (and lots is in the tissue).

96
Q

Drugs will be constantly swapping between two states while traveling in the circulation. What are they?

A

Free drug
Or
Bound to protein - albumin

97
Q

In which form does a drug have its therapeutic effect?

A

Free drug

98
Q

What is meant by therapeutic ratio and how is it calculated?

A

Refers to the size of the therapeutic window which lies between the minimum effective dose and the maximum safe dose of a drug.

Lethal dose 50
Effective dose 50

99
Q

Give an example of a drug with a high therapeutic ratio.

A

Omeprazole

100
Q

Give an example of a drug with a low therapeutic ratio

A

Warfarin, diogoxin

101
Q

What are protein binding interactions? Give an example

A

A second drug can displace the first from albumin - leaving a higher and potentially toxic dose of the first.
Eg aspirin added to existing warfarin

102
Q

How does the body cope with protein binding interactions?

A

They even themselves out quickly because although free drug levels rise, elimination rate also rises.

103
Q

Which 4 properties of a drug increase its risk of protein binding interactions?

A

Being a class 1 drug with a class 2 added
Highly bound to albumin
Low volume of distribution
Low therapeutic ratio

104
Q

What are drug elimination interactions? Give one example of inhibition and one example of induction

A

The enzymes (eg cytochrome p450) which break down and eliminate drugs can be inhibited or induced by other drugs, affecting how long they are in the system.

Eg warfarin and cimetidine inhibits c p450
Warfarin and phenobarbitone induces c p450

105
Q

What is the difference between Class 1 vs class 2 drugs?

A 
Class 1 is used at a dose lower than the number of binding sites. 
Class 2 is used at a dose higher than the number of binding sites so can overpower class 1 more often.
106
Q

During repeat drug administration, how long will it any drug to reach a steady state?

A

5 half lives

107
Q

Why are zero order kinetic drugs more dangerous? Give an example.

A

Even with a constant dose, the elimination enzymes can become saturated. After some time there can be a sudden increase in plasma levels of the drug as the liver struggles to break down the back log. It only moves at a set rate.
Eg alcohol, phenytoin

108
Q

What is meant by zero order kinetics?

A

1st order: Constant fraction of drug eliminated in unit time. Increase drug, increase rate of elimination.

Zero order: rate of elimination is constant. Increase drug, still same rate of elimination.

109
Q

What is meant by linear and non linear kinetics?

A

Linear = 1st order
Non linear = zero order

Seems counter intuitive but describes elimination pattern on a log scale.

110
Q

What properties of a drug leave it vulnerable to elimination interactions?

A

Used at min effective dose
Low therapeutic ratio
Zero order kinetics

111
Q

What order of drug elimination tends to occur in the liver?

A

Zero order kinetics

112
Q

What order of drug elimination tends to occur in the kidneys?

A

First order kinetics

113
Q

What 2 processes modulate drug elimination via the kidneys?

A

Active elimination in the proximal tubule

Passive reabsorption in the distal tubule

114
Q

Explain how an aspirin (weak acidic drug) OD can be treated.

Hint: it takes advantage of passive reabsorption in the distal kidney tubule.

A

Passive reabsorption only occurs when the drug is in the protonated, lipid soluble form.
Forced alkaline diuresis: force urine pH to increase so the aspirin will be in the deprotonated form and less will be reabsorbed. The aspirin is therefore forced out through the urine.

115
Q

What is the mechanism of action of tubocurarine?

A

Competitive antagonist of nicotinic acetylcholine receptors.

Therefore antagonises neuro muscular junction and causes paralysis.

116
Q

What is the mechanism of action of succinylcholine?

A

Competitive partial agonist of nicotinic receptors at neuro muscular junction.
Blocks action because not broken down by acetyl choline esterase so the receptor cannot be hyperpolarised to accept another action potential.
Ca mopped up by a different process, leading to prolonged muscle relaxation.
Used to treat malignant hyperthermia

117
Q

What is the mechanism of action of atropine?

A

Competitive antagonist of muscarinic receptors in the parasympathetic nervous system.
Leads to pupil dilation, increased heart rate and reduced salivation

119
Q

How is acetylcholine synthesised?

A

Acetyl CoA + choline

using cholineacetyl transferase

120
Q

Name 4 neurotransmitters other than acetylcholine and noradrenaline.

A

Nitric oxide - used in erection
ATP
Serotonin - 5HT
Dopamine

121
Q

What is the name of the cells in the adrenal medulla which release adrenaline onto the blood stream?

A

Chromaffin cells - similar to post ganglionic sympathetic neurons but release into the blood

122
Q

Why do beta blockers cause hypERtension in patients with pheochromocytoma?

A

Adrenalin secreting tumour of the adrenal gland.

Adrenalin has alpha and beta effects on blood pressure. If beta effect of AV node is blocked, there is unopposed alpha 1 vasoconstriction.

123
Q

What is the role of calcium at the neuromuscular junction?

A

Activates synaptotagmin, to open snare complex and release Ach.
Ach activates nicotinic receptors which depolarise the membrane and allow ca in through vocc
This binds to troponin which allows myosin to bind to actin heads

124
Q

How does PTH increase plasma calcium?

A

Bone - increase osteoclasts action
Kidney - increase reabsorption
Small intestine - stimulates vit d absorption, activated to calcitriol in liver, this improves kidney reabsorption

125
Q

How does lidocaine work?

A

2 pathways
Either “hydrophobic” active straight away in the pore
Or “use dependent block” crosses the membrane and goes into the pore after.

Blocks sodium channel so that action potential can’t be propagated.

126
Q

Which nerves are affected first by lidocaine? What is the implication?

A

Small myelinated
Non myelinated
Large myelinated

Means it affects sensory before motor

127
Q

What is the difference between phagocytosis and pinocytosis?

A

Phagocytosis internalises a particle into phagolysosome (for destruction)

Pinocytosis internalises into vesicles eg receptor mediated endocytosis

128
Q

Name a high affinity, low capacity calcium transporter(s)

And name a low affinity, high capacity calcium transporter(s)

A

High affinity = PMCA and SERCA

High capacity = Na Ca exchange

ESA 2 -Rhianna (7 decks)

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