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ESA 2 > M+R > Flashcards

M+R Flashcards

0
Q

What is a plasmalogen and give an example?

A

A non classical phospholipid

Sphingomyelin - doesn’t have a glycerol

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1
Q

What makes up a cell membrane including percentages?

A

Dry weight
Lipid 40%
Protein 60%
Carbohydrate 1-10%

Water 20%

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2
Q

What are the two main types of glycolipid and what is the difference between them?

A

Cerebroside - head group is a monomer

Ganglioside - head group is an oligosaccharide

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3
Q

What are the possible lipid motions?

A

Flexion
Lateral diffusion/drift
Rotation
Flip flop

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4
Q

What are the possible protein movements?

A

Rotation
Lateral diffusion/drift
Conformational change

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5
Q

Why can’t proteins “flip flop”?

A

It requires too much energy

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6
Q

What is the evidence for membrane proteins?

A

Freeze fracture
Specificity of function
SD page

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7
Q

What determines what movement proteins are capable of?

A

Size
Association with extra-membranous proteins
Move toward fluid areas and cholesterol poor areas

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8
Q

What are the differences between integral and peripheral membrane proteins?

A

Peripheral - bound to surface by electrostatic and hydrogen bonds. Removed by change in pH or ionic strength
Integral - strongly bound to hydrophobic areas. Removed by detergents or organic solvents

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9
Q

Outline the protein secretion pathway

A

A free ribosome initiates protein synthesis from mRNA molecule. A signal sequence is produced at the N-terminal. SRP binds to the signal sequence and stops protein synthesis. Ribosome goes to ER due to GTP on SRP. SRP dissociates and protein synthesis restarts with the polypeptide feeding into the ER via a pore. Signal sequence removed and ribosome dissociates

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10
Q

How does a membrane protein remain in the membrane? How can you get proteins with multiple trans membranous regions?

A

A stop transfer signal is in the polypeptide and this stops the protein feeding into the pore.
Multiple start and stop transfer sequences

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11
Q

What does cholesterol do in a membrane?

A

Increases stability by increasing fluidity when it is cold by pushing phospholipids apart and decreasing fluidity when it is too hot by forming hydrogen bonds

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12
Q

Why is the membrane referred to as a fluid mosaic?

A

Fluid - integral components move around

Mosaic - many different components

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13
Q

What makes up an erythrocytes cytoskeleton?

A

Spectrin and actin molecules attached to the membrane by adaptor proteins - ankyrin and glycophorin - which attach to band 3 and 4.1 respectively

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14
Q

What types of molecule can pass through the cell membrane? And therefore cannot?

A

Hydrophobic
Small, uncharged, polar molecules

Large, uncharged, polar molecules
Ions

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15
Q

What are the differences between passive diffusion, facilitated diffusion and active transport?

A

Passive - dependent on permeability and gradients
Facilitated - membrane permeability increased by incorporation of a protein
Active transport - uses energy from ATP hydrolysis to move molecules against an unfavourable gradient

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16
Q

What are the 3 types of transporter?

A

Uniport
Symport
Antiport

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17
Q

Name two proteins that move K+ ions and explain how

A

Na pump - 3Na+ out 2K+ in using ATP

K+ channels - K+ diffuses out

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18
Q

Name 4 proteins that move calcium and explain how

A

Ca2+ATPase - use ATP to pump Ca2+ out
PMCA - H+ in and Ca2+ out. Uses ATP. High affinity, low capacity
SERCA - move Ca2+ into the SR/ER for H+ using ATP. High affinity, low capacity
NCX - move Ca2+ out and 3Na+ in. Low affinity, high capacity

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19
Q

What happens to NCX in the case of ischaemia?

A

Less ATP produced so Na+ can’t be pumped out and accumulates in the cell, depolarising it and reversing the direction. Ca2+ accumulate inside and causes cell death

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20
Q

Name two proteins that affect pH and explain how

A

NHE - 1Na+ in, 1H+ out using Na+ gradient. Raises pH

AE - Cl- in HCO3- out. Lowers pH

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21
Q

How is cell volume controlled?

A

If cell is swelling - move K+ and Cl- out and water will follow out
If cell is shrinking - move Na+ and Ca2+ in and water will follow inside

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22
Q

Explain how renal anti hypertensive therapy works

A

Reduce renal Na+ reuptake which reduces the reuptake of other molecules and therefore reduce how much water is reabsorbed by osmosis. His lowers blood volume and therefore blood pressure

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23
Q

What does aquaporin do and how is it placed in a membrane?

A

Increase membrane permeability to water. Anti diuretic hormone increases its inclusion in the membrane

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24
Q

What do loop diuretics do and give specific examples

A

Block Na+ in thick ascending limb.
Amiloride prevents Na+ reuptake.
Aldosterone would increase reuptake so spironolactone is used to counter the aldosterone

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25
Q

How can a CFTR molecule cause diarrhoea?

A

It becomes overly active if it is phosphorylated by protein kinase A. This means excess Cl- moves into the lumen and water will follow

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26
Q

How can a faulty CFTR gene cause cystic fibrosis?

A

Doesn’t work so Cl- accumulates in cell and water follows in. This means the mucus has less water so is very thick

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27
Q

Define the resting membrane potential

A

The potential inside the cell relative to the extra cellular solution

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28
Q

Give the approximate membrane potential ranges of:
Nerve cells
Smooth muscle cells
Cardiac and skeletal muscle cells

A

-50 to -75
Approximately -50
-80 to -90

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29
Q

How is the resting membrane potential established?

A

Predominantly from the open K+ channels

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30
Q

What is the equilibrium potential and how can it be calculated?

A

The membrane potential at which there is no next movement of the ion across the membrane. Calculated using the Nernst equation

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31
Q

Define depolarisation and what ions movements can cause it?

A

Membrane potential decreases in size (gets less negative)

Na+ or Ca2+ ions

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32
Q

Define hyperpolarisation and what ions would move to cause it?

A

Membrane potential increases in size (becomes more negative)

Cl- or K+ ions

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33
Q

What is the difference between fast and slow synaptic transmission?

A

Fast - the receptor protein is also the ion channel

Slow - the receptor is coupled to the ion channel e.g. by G proteins

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34
Q

What channels would open in excitatory synapses and what are the neurotransmitters?

A

Na+ and Ca2+ channels

Glutamate and acetylcholine

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35
Q

What channels would open in inhibitory synapses and what are the neurotransmitters?

A

K+ or Cl- channels

Glycine or GABA

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36
Q

What is an action potential? What are some features of it?

A

A change in the voltage across a membrane. Dependent on ionic gradients and relative permeability of the membrane. All or nothing response. Propagated without loss of amplitude

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37
Q

What is the sodium hypothesis?

A

The cell is depolarised to the threshold potential and voltage gated Na+ channels open allowing Na+ influx due to the concentration gradient. This causes further depolarisation and the opening of more channels

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38
Q

How does repolarisation occur?

A

During prolonged depolarisation the Na+ channels start to close by inactivation and K+ channels open causing the Na+ influx to stop and K+ effluent to start.

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39
Q

Why is an action potential an all or nothing response?

A

Because positive feedback will open enough Na+ to send an impulse but has to be reached in the first place

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40
Q

What are the refractory periods?

A

Absolute refractory period - nearly all Na+ channels are inactivated so excitability is 0
Relative refractory period - some Na+ channels are recovering so excitability slowly returns to normal

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41
Q

Explain accommodation

A

A slower stimulus will require a larger depolarisation to reach the threshold potential as Na+ channels are becoming inactivated

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42
Q

What is the structure of a voltage gated Na+ and Ca2+ channel?

A 
1 peptide
4 homologous repeats
6 transmembrane domains
1 voltage sensitive domain
Functionality requires 1 subunit
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43
Q

What is the structure of a voltage gated K+ channel?

A

4 peptides
6 transmembrane domains
1 domain = voltage sensitive
Functionality requires 4 subunits

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44
Q

How might an anaesthetic like procaine work?

A

By blocking Na+ channels stopping action potential generation

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45
Q

What is the order that anaesthetics block Na+ channels and what is the significance of this?

A

Small myelinated
Non myelinated
Large myelinated
Sensory neurones are affected before motor neurones

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46
Q

How could you measure conduction velocity?

A

Electrode raises membrane potential to threshold generating an action potential. Then measure the change in potential between stimulating cathode and recording anode. Calculate velocity by distance/time

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47
Q

What is local circuit theory?

A

Depolarising a small region produces transmembrane currents in neighbouring regions which open their Na+ channels, propagating the action potential. The larger the local current, the faster the transmission

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48
Q

What 3 factors will increase the conduction velocity?

A

High resistance
High axon diameter
Low capacitance

49
Q

What is the effect of myelination?

A

Reduce capacitance and increase resistance

50
Q

Explain saltatory conduction

A

The action potential jumps between nodes of ranvier which are gaps between the myelin sheath with a high concentration of Na+ channels. The myelin acts as an insulator

51
Q

What myelinated the peripheral nervous system? And the central nervous system?

A

Schwann cells

Oligodendrocytes

52
Q

Explain multiple sclerosis

A

Autoimmune destruction if the myelin which decreases the velocity of action potential transmission and can completely block it

53
Q

How do action potentials open Ca2+ channels?

A

The action potential arrives at the pre synaptic membrane and opens voltage gated Ca2+ channels so Ca2+ can flow in down the concentration gradient

54
Q

What is the significance of the diversity of calcium channels?

A

A blocker that blocks one channel won’t block another and different channels have different primary locations so can get localised blocking

55
Q

How is a neurotransmitter released?

A

Ca2+ enters via channels and binds to Synaptotagmin. This brings the vesicle containing the neurotransmitter close to the membrane and combines it with a snare complex making a fusion pore. Neurotransmitter released through the pore and binds to post junctional membrane to produce end plate potential

56
Q

What are the two types of blocker, how do they differ and give an example of each?

A

Competitive blocker - bind to same site as acetylcholine. Tubocurarine
Depolarising blocker - cause maintained depolarisation at membrane so Na+ channels won’t activate due to accommodation. Succinylcholine

57
Q

Explain myasthenia gravis

A

Autoimmune destruction of NAchR. Causes drooping eyelids and profound weakness which increases with exercise. Treat with acetylcholinesterase inhibitor

58
Q

What are the advantages and disadvantages of a large calcium gradient?

A

Advantages - change in concentration occurs very rapidly with little movement
Disadvantages - overload can easily occur which causes cell death. Epsetting up gradient is energy expensive

59
Q

What 4 things are required to set up a calcium concentration gradient?

A

Relatively impermeable membrane
Ability to expel Ca2+ - Ca2+ ATPase and NCX
Ca2+ buffers
Intracellular stores

60
Q

How does Ca2+ ATPase work?

A

Ca2+ binds to calmodulin. Calmodulin-Ca2+ complex binds to Ca2+ ATPase and is removed

61
Q

How do you increase [Ca2+]i?

A

Increase membrane permeability - voltage gated calcium channels
Release from rapidly releasable stores - GPCRs and CICR
Release from non-rapidly releasable stores- mitochondria

62
Q

How do you lower [Ca2+]i?

A

Terminate signal
Remove Ca2+ by same mechanisms that set up gradient
Refill stores

63
Q

What is a receptor?

A

A molecule that recognises specifically a second molecule or family of molecules and in response to binding brings about regulation of a cellular process

64
Q

How do you classify receptors?

A

Primarily by specificity of a signalling molecule

Sub divided on basis of affinity to a series of antagonists

65
Q

What is the difference between a receptor and acceptor?

A

Receptors are silent at rest. If it operates without the ligand it is an acceptor

66
Q

What is a ligand?

A

Any molecule that binds to a receptor site. If it activates receptor it’s an agonist if not it’s an antagonist

67
Q

Why do we need signal transduction?

A

Hydrophilic signalling molecules cannot cross the cell membrane

68
Q

What are the three main methods of of signal transduction?

A

Integral ion channels
Integral enzyme activity - tyrosine kinase
Coupling to effectors by transducing proteins

69
Q

How do intracellular receptors work?

A

Hydrophobic ligands bind to receptors inside the cell, dissociating the receptor from heat shock or chaperone proteins and translocating to the nucleus where it binds to DNA and regulates gene expression. This is a slow response

70
Q

How are cardiac pacemaker cells controlled?

A

Noradrenaline binds to B1 adrenoceptors and increases heart rate
Acetylcholine binds to M2 muscarinic receptors and decreases heart rate

71
Q

What is phagocytosis?

A

A particle binds to a receptor in the membrane. The cell extends pseudopods that allow membrane invagination or particle internalisation

72
Q

What is pinocytosis for?

A

Retrieve membrane and uptake extra cellular impermeable solutes

73
Q

What happens to the receptor and the ligand for the following ligands: LDL
Transferrin
Insulin
IgA

A

Recycled/degraded
Recycled/recycled
Degraded/degraded
Transported/transported

74
Q

What are G-protein coupled receptors? What are G-proteins?

A

A family of receptors that act by altering the activity of an effector via G-proteins.
Guanine nucleotide binding proteins - made up of an alpha, beta and gamma subunit with a GDP bound to the alpha subunit in its resting state

75
Q

Outline the mechanism of G-protein action

A

Agonist binds to GPCR
Protein-protein interaction releases GDP and binds GTP instead
Alpha-GTP and beta-gamma split and interact with effectors
GTP hydrolysed to GDP by GTPase
Alpha-GDP and beta-gamma reform heterotrimer

76
Q

What are the cellular targets of Gs, Gi and Gq?

A

Gi - inhibit adenylyl cyclase
Gs - stimulate adenylyl cyclase
Gq- stimulate phospholipase C

77
Q

How do the cholera toxin and pertussis toxin work?

A

Cholera toxin eliminates GTPase activity do the G-protein becomes irreversibly activated
Pertussis toxin stops GTP/GDP exchange so the G-protein is irreversibly inactivated

78
Q

List 3 disorders due to G-protein mutations

A

Retinitis pigmentosa
Nephrogenic diabetes insipidus
Familial precocious puberty

79
Q

How does adenylyl cyclase cause an effect? Use the heart as an example

A

Adrenaline/noradrenaline binds to the GPCR which causes the activation of adenylyl cyclase. When activated, it converts ATP into cAMP which in turn activates PKA. PKA phosphorylates the voltage operated calcium channels, opening them leading to Ca2+ influx which has a positive ionotropic effect

80
Q

What other cellular reactions are stimulated by adenylyl cyclase?

A

Glycogenolysis and gluconeogenesis in liver
Lipolysis in adipose tissue
Positive chronotropy in the heart

81
Q

How does phospholipase C cause a cellular reaction? Use vasoconstriction as an example

A

Phospholipase C catalyses the cleavage of PIP2 into IP3 and DAG. IP3 allows Ca2+ to leave the ER lumen. More calcium causes more contraction. DAG and Ca2+ combine to activate PKC

82
Q

What is the effect of cyclic GMP phosphodiesterase?

A

Found in photo receptive cells in the retina and breaks down the cGMP

83
Q

What factors help towards G-protein deactivation?

A

After the GPCR interacts with a G-protein the agonist dissociates
Protein kinases phosphorylate the GPCR and stop it activating further G-proteins
GTPase deactivates alpha-GTP
Enzymes rapidly break down the secondary messengers

84
Q

How do M2 receptors affect chronotropy?

A

Open more K+ channels causing hyper polarisation and therefore slowing pacemaker cells fire rate

85
Q

How does morphine affect neurotransmitter release?

A

Morphine binds to mu-opioid receptors and reduce Ca2+ influx by inhibiting voltage operated calcium channels

86
Q

What are some targets for drugs?

A

Mainly proteins - enzymes or GPCRs

Can bind to DNA

87
Q

Define affinity and effinity

A

Affinity - likelihood of a ligand binding to a target

Effinity - likelihood of activation

88
Q

What is the difference between agonists and antagonists in terms of affinity and effinity?

A

Agonists have both, antagonists just have affinity

89
Q

What is Bmax? What is Kd?

A

Bmax - maximum binding capacity - number of receptors

Kd - dissociation constant - concentration needed to reach half Bmax - lower = higher affinity

90
Q

What is the difference between a concentration and dose response curve?

A

Concentration - response in tissues/cells measured

Dose - response in a whole animal

91
Q

What is EC50?

A

Effective concentration that gives 50% of the maximal response - a measure of potency (affinity and effinity combined)

92
Q

What is the significance of spare receptors and how do you know if a cell has them?

A

Less than 100% receptor occupancy still gives 100% response (EC50<Kd)

93
Q

What is a partial agonist?

A

Cannot produce maximal effect despite full receptor occupancy. EC50=Kd.
As potency is dependent of affinity and effinity partial agonists may still be more potent than full agonists. Partial agonists may not be partial agonists in all tissues

94
Q

Give a clinical example of the use of a partial agonist

A

Morphine is a full agonist. Buprenorphine is a partial agonist with a higher affinity so if less of a response is needed it is used instead as there is less respiratory depression

95
Q

What are the 3 types of antagonist, give an example and explain briefly how they differ

A

Reversible competitive antagonist - shift curve to right. Can be overcome by high concentration of agonists. Naxolone competes with opioids
Irreversible competitive antagonists - slow or no dissociation. Shift curve to right and lower maximal response at higher concentrations due to running out of receptors. Phenoxybenzamine - alpha 1 adrenoceptors
Non competitive antagonism - allosterically bind. Similar to irreversible competitive antagonists. Ketamine

96
Q

Define pharmacokinetics

A

What the body does to the drug

97
Q

How are drugs delivered?

A

Solid
Liquid
Locally
Systemic - parental/enteral

98
Q

What is the therapeutic ratio?

A

Maximum tolerated dose/minimum effective dose
Lethal dose to 50% of people/effective dose in 50% of people
Bigger=better

99
Q

What is the first pass effect?

A

When drugs are given orally they pass from the ileum to venous blood to the hepatic portal vein to the liver where they are extensively metabolised
Avoided if drug is given by rectal, parental or sublingual routes

100
Q

What is drug distribution?

A

The theoretical volume into which a drug has distributed assuming it occurred instantly
Amount given/plasma concentration

101
Q

Why does it matter that drugs bind to plasma proteins

A

Drugs bind here but it is only the level of free drug that exerts an effect
Important if highly bound to albumin or has a low therapeutic index like warfarin

102
Q

What are the 2 different classes of drug and the significance of this?

A 
Object drug (class I) - a dose that is much lower than number of albumin binding sites
Precipitate drug (class II) - a dose that is greater than the number of available sites
If both drugs are administered simultaneously class I drugs are displaced from albumin by class II drugs raising free levels
E.g. Aspirin/sulphonamides displace warfarin and tolbutamide
103
Q

What are is the difference between first and zero order kinetics

A

First order - metabolism is proportional to drug concentration. Straight line on a log scale. Half life proportional to drug level
Zero order - enzyme is saturated to rate of metabolism stays the same despite changing the drug concentration. Straight line when not log scale. An example is alcohol
Whilst first order gives predictable therapeutic response to dose increase a zero order drug can escalate suddenly

104
Q

How long does it take for a steady state to be achieved? What is the significance of this?

A

5 half lives

If an immediate effect is needed a loading dose needs to be given

105
Q

Outline how drugs are metabolised in the liver

A

Phase 1 - reactive group exposed usually by an oxidation, reduction or hydrolysis reaction. CYP and NADPH needed
Phase 2 - conjugate to make water soluble. Requires NADPH and UDPGA
Enzymes are inducible and inhibitable

106
Q

Outline metabolism of drugs in the kidney

A

Free unbound drugs are filtered by the glomerular tuft or can be actively secreted. Urine pH can be measured to determine excretion level. Weak acids - aspirin - make urine alkaline to ionise drug and reabsorb less, therefore excreting more. Opposite is true for weak bases like amphetamine

107
Q

Outline the main differences between the sympathetic and parasympathetic nervous system

A

Sympathetic - thoracolumbar, short preganglionic, long postganglionic, most post ganglionic release noradrenaline, fight or flight
Parasympathetic - craniosacral, long pre ganglionic, short post ganglionic, all postganglionic release acetylcholine, rest and digest

108
Q

What is the reaction and enzyme for the formation of acetylcholine?

A

Acetyl CoA + choline –> acetylcholine + CoA
Choline acetyltransferase
Occurs in cytoplasm

109
Q

What can happen to acetylcholine after it’s production?

A

Degraded into acetate and choline

Put into vesicle by active transport and then released by Ca2+ mediated exocytosis

110
Q

What happens to acetylcholine after it has reacted a choline receptor?

A

Degraded by cholinesterase and then the choline is recaptured by a choline transporter

111
Q

What is the reaction sequence for the synthesis of noradrenaline including enzymes

A

Tyrosine –> DOPA –> Dopamine –> Noradrenaline

Tyrosine hydroxylase, DOPA decarboxylase, Dopamine beta-hydroxylase

112
Q

How is noradrenaline reabsorbed?

A

Mainly uptake 1 (high affinity)

Some uptake 2 (low affinity)

113
Q

Name an NAChR antagonist and what it does

A

Tubocurarine

Muscle paralysis

114
Q

Name a muscarinic AChR agonist and what it does

A

Pilocarpine.

Treat glaucoma. Can suppress tachycardia

115
Q

What would you use a muscarinic AChR antagonist for?

A

Treat bronchoconstriction, as an anaesthetic premedication and to dilate pupils

116
Q

What would you use acetylcholinesterase inhibitors for?

A

Treating glaucoma, myasthenia gravies and Alzheimer’s.

117
Q

Name a selective beta 1 agonist and what it does. Do the same for a selective beta 2 agonist

A

Dobutamine - positive chronotropic and ionotropic effects

Salbutamol - bronchodilator

118
Q

Name a selective alpha 1 agonist and what it does. Do the same for an alpha 2 agonist.

A

Adrenaline - vasoconstrict to slow anaesthetic loss

Clonidine - anti hypertension. Reduce noradrenaline release

119
Q

Name an alpha antagonist and what it does. Do the same for a beta antagonist (blocker)

A

Phentolamine - a peripheral vasodilator used to treat peripheral vascular disease
Propranolol - treat hypertension, MI and angina. Can cause unwanted bronchoconstriction

120
Q

What does alpha methyl tyrosine do?

A

Inhibit tyrosine hydroxylase thereby stopping noradrenaline synthesis. Used to treat pheochromocytoma

121
Q

What are uptake 1 inhibitors for? What does an IASA do?

A

Antidepressant

Leak NA

ESA 2 (4 decks)

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