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ESA 2 > M&R > Flashcards

M&R Flashcards

0
Q

What 4 molecules can make the head of phospholipids?

A

Choline, Amines, Amino Acids and Sugars

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1
Q

Where are phospholipids synthesised?

A

Endo plasmic reticulum

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2
Q

Normal length of fatty acids in phospholipids?

A

C16 C18

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3
Q

Name 2 proteins that are integral eyrthrocyte proteins and 2 that are peripheral. How are peripheral proteins attached?

A

Integral: Ban 3 -anion exchanger and Glycophorin A

Peripheral: spectrin, actin (make actin-spectrin network) and adducin, ankyrin, band 4.1 ( adapter proteins which bind to ban)

Spectrin formed from a2 and b2 subunits (rods) and bound via an adaptor called ankyrin.

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4
Q

How long are membrane spanning domains

A

18-22 amino acids

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5
Q

What is the role of ribophoryns?

A

Anchor ribosome to ER

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6
Q

How may the energy for active transport be found?

A

ATP hydrolysis

Concentration gradient of transported substance/ the electrical potential across the membrane (secondary)

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7
Q

What is he difference between carrier and channel proteins?

A

Channel proteins allow specific ions to pass through them.

Carrier proteins usually move molecules by binding to them, changing shape and releasing it the other side of a membrane.

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8
Q

What does NCX exchange?

A

3Na for 1Ca

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9
Q

What protein can mediate alkali extrusion

A

Anion exchanger.

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10
Q

Cell shirking/ swelling questions

A

J

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11
Q

Why do phospholipids form a bilayer instead of micelles?

A

Due to 2 FA chains.

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12
Q

4 types of motion of a phospholipid

A

Flexion (vibration) and intra chain motion e.g. Kink formation.
Flip-flop
Rotation
Lateral diffusion

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13
Q

What are the functions of cholesterol in a cell membrane?

A

Reduces endothermic phase transition (prevents changes of state)
Bonds via OH to hydrophilic heads (C=O)
Increases fluidity - reducing phospholipid packing.
Decreases fluidity - reduces phospholipid chain motion.

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14
Q

What is freeze fracture.

A 
Lipid bilayer frozen in ice.
Split.
E fracture extracellular.
P fracture is in cytosol.
Shows membrane proteins either side.
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15
Q

How can membrane proteins move?

A 
Conformational change.
Rotation
Lateral diffusion
NO FLIP FLOP
** Tend to spread out into cholesterol poor areas (called lipid mediated effects)
**may be restrained by associations
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16
Q

What is the purpose of a hydropathy plot?

A

Shows the charges of amino acids of a protein e.g. Transmembrane domains.

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17
Q

Briefly how are membrane proteins orientated?

A

If no signal peptidase. Hydrophilic NH3 terminus stays on outside (often accompanied by hydrophobic domain) and COOH terminus is synthesised through ER and into the lumen.

If signal peptidase then NH3 is created on the luminal side and COOH is in the cytosol (split in two).

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18
Q

What is a molecule called which has both hydrophobic and hydrophilic regions?

A

Amphipathic

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19
Q

What is a plasmalogen?

A

A non classical phospholipid

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20
Q

What is Sphingomyelin?

A

A plasmalogen.
Only phospholipid not based on glycerol.
Resembles other phospholipids in a membrane.

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21
Q

What is the difference between cerebrosides and gangliosides?

A

Both are glycolipids.
Cerebrosides contain a monomer head.
Gangliosides contain a oligosaccharides head.

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22
Q

What can be the result in a deficiency of erythrocyte cytoskeleton?

A

Haemolytic anaemia.

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23
Q

What protein is most important in allowing ionic movement to establish the resting membrane potential?

A

Voltage insensitive K+ channels

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24
Q

The nicotinic acetylcholine receptors are permeable to which main ions?

A

Na, K, Ca

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25
Q

The glycine channel is permeable to which ions?

A

Cl

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26
Q

Which can permeate a lipid membrane? H20, urea, glycerol?

A

All because they are small molecules

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27
Q

What is a P-type ATPase?

A

ATP phosphorylates an aspartate to produce energy for active transport e.g. Na/K ATPase

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28
Q

Intra and extracellular Na?

A

I:12mM
E:145mM

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29
Q

Intra and extracellular K?

A

I:155mM
E:4mM

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30
Q

Intra and extracellular Cl:

A

I: 4.2mM
E: 123mM

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31
Q

Intra and extracellular ca?

A

I: 10(-7)M
E:1.5mM

32
Q

What does the Na pump do? (Nakatpase)

A 
2k out
3na in
ATP->ADP
Restores gradients
Monitors pH with Na (with NHE)
Allows nutrient uptake with Na/glucose symporter
33
Q

What does pmca/serca do (Ca-mg ATP ase)?

A 
Ca out
H+ in
ATP-> adp 
Controls resting ca.
High affinity low capacity
34
Q

What does NCX do?

A 
3na in
1ca out
Low affinity, high capacity
Controls ca
Electrogenic.
35
Q

What does NHE do?

A

Na in
H out
Controls pH
Acid exchanger

36
Q

What does Hco3 co transporter do?

A 
HCO3 in
H out
Na in
Cl out
Acid exchanger
37
Q

What does ae do?

A

Swaps anions
Cl in
Hco3 out
Base extrusion

38
Q

How is the pH controlled in a cell? (What channels?)

A

NHE
HCO3 cotransporter
Anion exchanger
Na/HCO3 symporter

39
Q

How is cell shirk age avoided?

A

Na in with Cl
H out
Ca in

40
Q

How is cell swelling avoided?

A

Different in all cells.
K and Cl out
E.g. Cl out, hco3 in (one transporter) with h in and k out (another transporter) forming h2co3 -> co2 and h20 in the cell. (Co2 and h20 leave)

41
Q

How is bicarbonate absorbed in the proximal tubule?

A

NHE pumps h into lumen and Na into cell.
Na pumped into capillary.
H makes h2co3 in lumen.
Co2 and h20 from h2co3(carbonic anhydrase)
H20 absorbed and reacts with co2 from metabolism to make h2co3-> hco3(carbonic anhydrase)
Anion exchanger puts hcl3 into capillary

42
Q

How is Na reuptaken in the thick ascending limb?

A

Lumen side:
Nakcc2: Na k 2cl in
Romk: k out

Capillary side:
Na/k ATPase
Clc kb: Cl out
Kclct: k and Cl out

Mg and ca diffuse between cells.

Loop diuretics inhibit nakcc2

43
Q

How can the membrane potential be measured?

A

Micropipette (microelectrode) with KCL, one placed intracellularly, another extracellularly.

44
Q

What is an equilibrium potential?

A

The potential difference at the equilibrium reached if the membrane was only permeable to a specific ion e.g. Ek. This occurs when charge and concentration gradients are matched.

45
Q

What’s the difference between fast synaptic potentials and slow synaptic potentials in terms of receptors?

A

Fast synaptic potentials use ligand gated ion channels as a receptor.

Slow synaptic potentials use g-protein receptors to open other channels via an enzyme cascade.

46
Q

What channels may cause an excitatory post synaptic potential (epsp) and which channels may cause an inhibitory post synaptic potential (ipsp)?

A

Excitatory = ligand gated ion channels Na or Ca or several other cations.

Inhibitory= ligand gated ion channels k or Cl.

55
Q

How does the myelin sheath affect velocity of an ap?

A

Increases membrane resistance and decreases capacitance and increases diameter so increases speed.

Below a certain point un myelinated axons give faster impulses (1um diameter) and this is because the diameter includes the MS so there is a larger surface area to volume ratio so the cytosolic resistance increases and this is significant enough to make myelinated axons slower.

Myelinated = linear.
Unmyelinated = speed is proportional to square root of diameter.
56
Q

What are the problems associated with multiple sclerosis?

A

Muscle weakness due to loss of myelin sheath- channels spread throughout axon so decreased membrane resistance and increased capacitance leading to slower/ non existent impulses due to losses of local current.

57
Q

What is the structure of the VOCC channels

A

4 subunits in one chain with multiple phosphorylation sites (allowing subtlety of control).

58
Q

Describe myasthenia gravis.

A

Autoimmune destruction of nAChR.
Widening of synaptic cleft
Profound weakness.

72
Q

What is hereditary sphereocytosis?

A

40-50% spectrin deficiency.

Round erythrocytes more prone to lysis.

73
Q

What is hereditary elliptocytosis?

A

Spectrin abnormal

Fragile elliptoid cells

74
Q

What is accommodation and why does it occur?

A

Constant stimulus means that AP will decrease in amplitude and eventually threshold won’t be reached. This is because with the constant stimulus (slight depolarisation) more and more Na channels become inactive. This is also added to be the fact the cell does not hyper-polarise properly. This results in the threshold level increasing until the depolarisation caused by the stimulus never reaches the threshold level.

Accommodation means a larger stimulus is needed for an action potential.

75
Q

What is the length constant and what factors affect it?

A

The distance at which the ap amplitude decreases by 37% (before it can no longer cause an ap)

Membrane Resistance- higher the resistance (e.g. Myelin sheath) the faster the conductance. (How many Na channels available). At a high membrane resistance, channels are closed so the spread of the local current effect is limited (effectively capacitance).

Diameter - velocity increases as there are more channels with a larger surface area. Cytosolic resistance is decreased.

Capacitance (ability to store charge) - the lower (e.g. Myelin sheath) the better as depolarisation needed for ap is lost.

76
Q

How is Ca expelled from the membrane?

A

Ca ATPase- binds to calmodulin. High affinity, low capacity

NCX. Low affinity, high capacity.

77
Q

Name a protein that binds ca in stores

A

Calsequestrin

78
Q

How does ca increase?

A

GPCR e.g. Q and s

CiCR as a result of VOCC e.g. RyR

79
Q

What is the role of the mitochondria in ca regulation

A

When ca is high… E.g. In microdomains.
Low affinity, high capacity.
Uni porter uses pmf.
Role in apoptosis and in matching mitochondrial metabolism supply with demand.

80
Q

How are stores refilled with ca?

A 
Depleted signal (e.g. Stim on ER membrane)
Opens SOC (store operated channel) e.g. ORAI. Uptake by serca.
81
Q

Describe the structure of a voltage gated Na channel.

A

4 subunits like Na channel.

82
Q

Which type of channel is blocked by dihydropyridine DHPs? (E.g. Nifedipine)

A

L type found in muscles and neurones and lung.

83
Q

Describe the events underlying fast synaptic transmission

A

Depolarisation due to AP causes Ca influx.
Binds to a group of proteins associated with vesicle e.g. Symaptotagmin.
Vesicles bind to snare complex to make a fusion pore.
Exocytosis of neurotransmitter
2Ach binds to one receptor
Fast because bound to a channel not G protein.

84
Q

Describe the effect of a depolarising blocker.

A

If depolarising blocker is bound and the channel is opened then it will remain open and adjacent channels will not become open due to accommodation/ inactivation of Na.

85
Q

Give an example of depolarising blocker of a nicotinic receptor

A

Succinylcholine

86
Q

Give an example of a competitive nicotinic blocker

A

Tubocurarine

87
Q

What causes miniature end plate potentials

A

Random release of vesicles

88
Q

Why are muscurinic slower than nicotinic?

A

G proteins.

89
Q

What is the purpose of a voltage clamp?

A

Set the MP to see which channels are open

90
Q

What’s the difference between Na and k channels

A 
Na = 4 subunits/ repeats on one protein each with 6 transmembrane domains, one of which is positive.
K= each subunit is separate
91
Q

describe ARP and RRP

A 
ARP= Na inactivated 
RRP= Na recovering from inactivation.
92
Q

How does procaine act?

A 
Blocks Na channels to prevent an AP
Blocks in order:
Small myelinated
Non myelinated
Large myelinated
93
Q

What is the difference between hydrophilic and hydrophobic Na channel blockers?

A

Hydrophilic work better when channel is open and have a higher affinity to inactive Na.- use dependent. Hydrophobic work any time.

94
Q

Describe diphasic, monophasic and compound readings of action potentials.

A

Diphasic- two probes A and B along axon. S wave produces as A-B.

Monophasic - two probes but B is on damaged section. A-B = half S shape.

Compound - many ‘A’ probes at different distances but one B probe in damaged section. Can measure speed of impulse.

95
Q

Explain local current theory of propagation.

A

An AP/ depolarised membrane causes depolarisation in adjacent membrane basically spreading the depolarisation which propagates the action potential. The speed of an AP depends on how far these local currents spread. This depends on capacitances (lower better), membrane resistance (higher better) and a large axon diameter (due to low cytoplasmic resistance).

96
Q

How is conduction velocity linked to fibre diameter?

A

Myelination: linear increase

I myelinated: proportional to root of diameter.

97
Q

How does myelinated increase conduction

A

Increases membrane resistance (less channels and only at NOR) and decreases capacitance. Note sheath is included in fibre diameter.

98
Q

How do cholera and diphtheria toxins enter the cell?

A

Endocytosis- GM1 ganglioside

ESA 2 (9 decks)

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