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ESA 4 revision > M&R > Flashcards

M&R Flashcards

1
Q

What does amphipathic mean?

A

Containing both hydrophilic and hydrophobic moieties

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2
Q

Describe a phospholipid:

A

Polar head group with large FA chains - C16-18

Unsaturated C=C chains in cis formation with kink reducing phospholipid packing

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3
Q

Which phospholipid is the only one not based on glycerol?

A

Sphingomyelin

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4
Q

What is a glycolipid?

A

Sugar containing lipids

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5
Q

What is cholesterol?

A

a plasma membrane lipid that adds structure to the lipid bilayer

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6
Q

How do bilayers form in water?

A

Spontaneous due to the van der walls forces between the hydrophobic tails

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7
Q

What forces aid the bilayer formation?

A

Electrostatic and H-bond between hydrophobic moieties, interactions been hydrophilic groups and water

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8
Q

What movements can lipid molecules do in the bilayer?

A

Intra-chain motion
Fast axial rotation
Fast lateral diffusion
Flip-flop exchange

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9
Q

Examples of membrane proteins?

A

Enzymes, transporters, pumps, ion channels, receptors

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10
Q

What movements can membrane proteins do?

A

Conformational change
Rotational
Lateral

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11
Q

What movement do proteins not do in membranes?

A

flip-flop because of their large hydrophilic groups - it would take too much energy to pass through hydrophobic regions

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12
Q

Forces in peripheral membrane proteins?

A

Electrostatic and H-bonds

Removed by changes in pH and ionic strength

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13
Q

Forces in integral membrane proteins?

A

Hydrophobic regions in lipid bilayer.

Can’t be removed by changes to pH or ionic strength, - requires detergent to compete for non-polar interactions

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14
Q

What function do unsaturated fatty acids do?

A

kink in chain > reduces phospholipid packing > increasing membrane fluidity

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15
Q

What does cholesterol do?

A

H-bond to the FA chains
Reduces phospholipid packing > increasing membrane fluidity

Also reduces phospholipid chain motions > decrease membrane fluidity

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16
Q

Function of erythrocyte cytoskeleton?

A 
Hold the shape of RBCs
Peripheral proteins (low ionic strength wash) = spectrin & actin - network attached to membrane by Ankyrin & Glycophorin binding to Band 3 & 4.1
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17
Q

What happens when there is a general deficiency of cytoskeleton?

A

RBC round up to become more spherical which rupture in capillary beds and cleared by spleen

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18
Q

What is Hereditary Spherocytosis

A

Depleted Spectrin levels by 40-50% > haemolytic anaemia

RBC lysis > BM production

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19
Q

What is Hereditary Elliptocytosis?

A

Spectrin molecule unable to form heterotetramers > fragile RBCs > haemolytic aneamia

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20
Q

What types of molecules can pass through membranes?

A

Hydrophobic

Small, uncharged polar molecules

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21
Q

What type of molecules can’t pass through membranes?

A

Large, charged polar molecules

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22
Q

Function of Na/K-ATPase?

A

Electrical excitability

2ndary Active transport for:
pH, cell volume, Ca conc, Na absorption in epithelium, nutrient reabsorption in gut

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23
Q

How are calcium levels controlled?

A

Na/K-ATPase pump generates Na+ gradient for:

Active Transport - using ATP
PMCA - Expel Ca from cell in antiport with with H+, using ATP

SERCA - antiport with H+

2ndary AT:
NCX - low affinity, high capacity - removing most of Ca

Ca uriporters into mitochondria

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24
Q

What type of operations are PMCA and SERCA?

A

High affinity & low capacity

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25
Q

NCX in ischemia?

A

ATP is depleted of X Na pump > Na accumulates in the cell causing depolarisation - reversing the NCX causing Ca entry - high Ca = toxic

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26
Q

Ions responsible for raising pH?

A

2nd AT - NHE = Na/H exchanger - inhibited by amiloride (K-sparing diuretic)

Sodium-Bicarb Co-transporter (NBC) with Cl/HCO3 exchanger - raising pH

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27
Q

Ions responsible for lowering pH?

A

Amion exchanger - Cl/HCO3 exchanger - removal of base

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28
Q

What happens if cells swell?

A

Extrude ions (K, Cl) to lose water

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29
Q

What happens if cells shrink?

A

Influx of ions (Na, Ca) to gain water

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30
Q

Describe Cystic Fibrosis?

A

Faulty CFTR > unable to transfer Cl out cells (normally 2ndary AT symport of Cl-) so Cl accumulates in cell > water movies into cell via osmosis > viscous, thick mucous in lumen

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31
Q

What causes diarrhoea?

A

Over active CFTR by phophorylation by Protein Kinase A - excess Cl- in lumen drawing water

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32
Q

What is resting membrane potential?

A

The potential inside the cell relative to extracellular

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33
Q

RMP of nerve cells?

A

-50 to -75 mV

34
Q

RMP of cardiac/skeletal muscles?

A

-80 to -90 mV

35
Q

How is the RMP created?

A

selective permeability to K+

36
Q

What is the equilibrium potential?

A

The membrane potential where there is no net movement of ions across the membrane

37
Q

What is the Nernst Equation?

A

Calculation to work out equilibrium potential:

Elon = 61?z log10 [ion]out/[ion]in

38
Q

What is depolarisation?

A

membrane potential decreasing in size so that the interior is less negative - causes by opening Na or Ca channels

39
Q

What is repolarisation?

A

Increasing membrane potential size so inside is more negative - opening K and Cl channels

40
Q

difference between fast and slow synaptic transmission?

A

Fast - receptor = ion channel

Slow - receptor & ion channel = separate requiring G-protein or intracellular messengers to open

41
Q

The binding of Ach on post-synaptic membrane triggers?

A

Excitatory post-synaptic potential

42
Q

Explain sodium’s affect on APs?

A

depolarised threshold > voltage-gates Na channels open > influx of Na as move to reach their ion equilibrium>influx causes further depolarisation & opens more channels> inactivation > v-gated K channels open > K efflux > depolarisation

Na inactivation = accommodation

43
Q

What is the Absolute Refractory period?

A

All Na channels are inactivated, unable to generate an AP

44
Q

What is the Relative Refractory Period?

A

recovering Na channels -need large stimulus to generate ab AP

45
Q

Describe the Na and Ca channels?

A

similare - 1 peptide of 4 homologous repeat. Each repeat = 6 transmembrane domains with one sensing voltage of the membrane

46
Q

Describe the K channel?

A

4 peptides - Each repeat is in fact a subunit with 6 transmembrane domains

47
Q

List an example of a local anaesthetic?

A

Procaine - blocks Na channels

48
Q

Order of block in nerve fibres?

A
  1. Small myelinated
  2. Non-myelinated
  3. Large myelinated
    Sensory before motor
49
Q

What properties about axons lead to high conduction velocity?

A

high resistance
high diameter
low capacitance - ability to store charge

50
Q

What does myelination do?

A

Increases conduction velocity by reducing capacitance and increasing membrane resistance

51
Q

Features of propagation?

A

Saltatory conduction
Nodes of Ranvier
One direction

52
Q

What is the difference between Schwann cells & oligodendrocytes?

A

Schwann cells = peripheral axons

Oligodendrocytes = CNS

53
Q

What is Multiple Sclerosis?

A

Auto-immune destruction of myelin > decreased conduction velocity / block/ only few APs pass

54
Q

Describe transmitter release at synapses?

A
  1. Ca enters via channels
  2. Ca binds to synaptotagmin
  3. vesicle brought closer to membrane
  4. snare complex makes a fusion pore
  5. transmitter released via pore
55
Q

What is a competitive blocker?

A

Bings at recon. site for Ach

Eg, Tubocurarine

56
Q

What is a depolarising blocker?

A

Binds to cause constant depolarisation –> accommodation

Eg, Succinylcholine

57
Q

What is Myasthenia Gravis?

A

Autoimmune destruction of nicotinic Ach receptors
Present with drooping eyes, weakness

Tx with Ach-esterase inhibitors (ice on eye lid)

58
Q

How is Ca gradient maintained?

A

Impermeability
Ability to expel Ca
Ca buffers
Intracellular Ca stores

59
Q

What are Ca buffers?

A

Limit diffusion by binding to Ca, e.g. Calsequestrin and calmodulin

60
Q

What are the calcium channels found at synapses?

A

Voltage gated Ca channels triggering Ca influx by depolarisation

61
Q

Describe the rapidly-releasing Ca stores?

A

Ca stored in SR & ER by SERCA.

Ligand binds to GPCR> activates G alpha Q > binds to PIP2 releasing IP3 > binding to receptor on SR> triggers Ca release down gradient

62
Q

Ca induced Ca release (CICR)?

A

Ca binds to Ryanodine respecters on SR> trigger release of Ca down gradient

Important in cardiac myocyte where initial Ca entry by VOCCs triggered by depolarisation

After release, signal terminated, Ca removed and stores refilled.

63
Q

Non-rapidly releasable Ca stores?

A

Ca taken up by mitochondria due to microdomains (regions of high conc) to buffer. Ca uriporters

Mit. Ca used to replenish SR stores via store-operated Ca channels

64
Q

Describe G-proteins:

A

& transmembrane domain receptors coupled with a transducing molecule - GTP-binding regulator protein (g-protein) that triggers enzyme or channel activation

65
Q

Which type of receptors are GPCRs?

A

Muscarinic - seen with parasymp.

66
Q

Discuss steroid hormones:

A

Able to pass through membrane to bind to intracellular receptors which at resting state are bound to heat shock/chaperone proteins which dissociate and translocate to nucleus to alter DNA genre expression.

Slow rate of action as requires changes to transcriptions and translation

67
Q

What is pinocytosis?

A

Invaginations of membrane to form lipid vesicles for uptake.
Fluid phase is as it is,
Receptor Mediated Endocytosis = specific binding to receptors for selective uptake

68
Q

Describe the uptake of cholesterol?

A

Example of RME:
LDLs in the liver, surrounded by apoproteins. Ldl receptors recognises Apoprotein B > receptors clustered in Catherine Coated Pits > LDL bind > pits invaginated to form coated vesicles.

Vesicles uncut with ATP > fuse with larger smooth vesicles = endosomes > pH of endosomes = lower so LDL and receptor dissociate > endosomes = Compartment for Uncoupling of Receptor & Ligand (CURL)

LDL receptor recycles to membrane.

LDL ruse with lysosomes where cholesterol is hydrolysed into esters > released into cell

69
Q

Mutations of LDL receptors?

A
  • Non-functioning receptor > X uptake
  • Receptor binding normal, but X interaction between clathrin coat & receptor so not concentrated
  • Receptor deficiency as X expression
70
Q

Describe Fe3+ uptake:

A

Apoptransferrin + 2 Fe = Transferrin > receptor binding > acidic endosome = releases Fe, but receptor & apoptransferrin bound > complex into CURL to recycle to membrane > dissociates

71
Q

Insulin uptake?

A

Clathrin pit - insulin binding = conformational change > endosome - insulin still bound > complex goes to lysosomes for degradation = reduces insulin receptors to protect cell

72
Q

What is transcytosis?

A

Transfer of IgA from circa to bile in liver.

73
Q

What is Oral Bioavailability?

A

Proportion of dose given orally that reaches systemic circulation in unchanged form

74
Q

What is Therapeutic ratio?

A

Max. tolerated dose/minimum effective dose

LD50 (lethal dose for 50% people) / ED50 effective dose for 50% people

75
Q

What is Drug Distribution?

A

Theoretical volume into which a drug is distributed into

Amount give / plasma conc at time 0

76
Q

What is an object drug?

A

Dose is lower than the number of albumin binding sites

77
Q

What is a precipitant drug?

A

Dose is greater than number of available binding sites

78
Q

Class 1 & 2 together makes..?

A

object drug level is higher due to displacement by class 2 drugs, so can be toxic

Eg, aspirin is precipitant for warfarin

79
Q

What is 1st order kinetics?

A

metab. proportional to drug conc. - straight line with log-scale against time, half-life can be determined.

predictable response

80
Q

What is zero order kinetics?

A

drug conc higher than Km - enzyme = saturated so rate of decline is constant despite conc.
straight-line when normal conc vs time

81
Q

What is the loading dose?

A

When drug admin is steady - reached within 5 half-lives

82
Q

Describe drug excretion?

A

free unbound filtered at glom.
actively secreted
urine pH = determinant.

weak acid, like aspirin, attracted by alkaline urine so less reabsorption

vice versa

ESA 4 revision (4 decks)

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