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ESA 2 > Membranes > Flashcards

Membranes Flashcards

1
Q

What are the 5 main functions of biological membranes?

A

Provide a continuous, selectively permeable barrier.
Control internal chemical environment
Communication between cells and environment
Recognition of other cells/substances
Signal generation in response to stimuli

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2
Q

What’s the rough compostion of biological membranes?

A

60% Protein, 35% lipid and 5% carbohydrate

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3
Q

What kind of phospholipid can cause a kink in the phospholipid chain of biological membranes?

A

Phospholipid with unsaturated fatty acid side chains that are in cis formation.

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4
Q

What effect does kinks in lipid chains of biological membranes have?

A

Reduces packing so increases fluidity

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5
Q

What is sphingomyelin?

A

A fatty acid that isn’t based on glycerol

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6
Q

What provides evidence for the presence of proteins in biological membranes?

A

Functional such as ion gradients, cell response specifictiy and facilitated diffusion. Also biochemical evidence derived from freeze fracturing and gel electrophoresis

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7
Q

Which main bands found by osmotic haemolysis are found to be integral proteins and why?

A

Bands 3 and 7 as they can only be removed by treatment with detergents

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8
Q

How is the spectrin-actin network of erythrocyte cytoskeletons, attached to the membrane?

A

Through adapter proteins. Ankyrin attaches network to band 3 integral protein and band 4.1 links network to glycophorin A (7) intergral protein

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9
Q

What is the difference between hereditary spherocytosis and hereditary elliptocytosis?

A

Spherocytosis is a depletion in spectrin in RBC cytoskeleton. Cells are more rounded and prone to lysis.
Elliptocytosis is a defect in spectrin so can’t bind with actin so cells become elliptoid.
Both cause haemolytic anaemia

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10
Q

What gives rise to membrane potential?

A

Selective permeability of membrane to ions

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11
Q

What are the normal extra- and intracellular levels of Na+ and K+?

A

Extracellular Na+ = 145mM K+ = 4.5mM

Intracellular Na+ = 10mM K+ = 160mM

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12
Q

What is equilibrium potential?

A

When electrical and chemical movements of an ion are equal and there’s no net movement of an ion across the membrane

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13
Q

How does increasing ion permeability affect membrane potential?

A

Increasing the permeability to an ion, brings the membrane potential closer to the equilibrium potential of that ion.

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14
Q

What are the equilibrium potentials of K+, Na+, Ca2+, Cl-?

A 
Na+ = +70mV
K+ = -95mV
Ca2+ = +122mV
Cl- = -96mV
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15
Q

What is fast synaptic transmission?

A

When receptor protein is an ion channel so transmitter binding opens channel causing depolarisation if excitatory (eg Na+, Ca2+, cations) or causes hyperpolarisation if inhibitory (K+, Cl-)

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16
Q

What are 2 inhibitory neurotransmitters?

A

Glycine and GABA

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17
Q

What are 2 excitatory neurotransmitters?

A

ACh and Glutamate

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18
Q

What is slow synaptic transmission?

A

Where receptor and ion channel are different proteins. Uses intracellular messenger or direct G protein gating

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19
Q

What’s the difference between the absolute and relative refractory periods?

A

ARP means most sodium channels are inactive so another action potential can’t be initiated, regardless of stimulus.
RRP means sodium channels are recovering from action potential and their excitability are returning to normal but are still closed

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20
Q

What’s the voltage change involved in action potential at axon, skeletal muscle, sinoatrial node and cardiac muscle?

A

Axon is -70 to +30
Skeletal muscle -90 to +40
Sinoatrial node -60 to +30
Cardiac muscle is -90 to +30

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21
Q

What is the length constant?

A

Distance taken for membrane potential to fall to 37% of it’s original value

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22
Q

What is the main symptom in Guillain Barre syndrome?

A

Ascending paralysis due to autoimmune destruction of myelin

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23
Q

What is the role of calcium in neurotransmitter release?

A

Depolarisation opens calcium channels allowing entry into. Bind to synaptotagmin on internal surface, this brings neurotransmitter-containing vesicle close to membrane. Snare complex makes a fusion pore and transmitter is released into synapse

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24
Q

What is myasthenia gravis?

A

Autoimmune disease where Nicotine ACh receptors are targeted on postsynaptic skeletal muscle. There’s therefore a loss of fucntional nAChR and so there’s decreased amplitude of endplate potentials and there’s profound muscle weakness and fatigue

25
Q

What does the calcium gradient depend on?

A

Variable permeability of membrane to calcium
Ability to expel calcium across the membrane using NCX/Ca2+ATPase
Intracellular Ca2+ stores
Calcium buffers

26
Q

What are calcium buffers?

A

Proteins that bind to calcium to limit its diffusion

27
Q

What’s the process involved in calcium release from the SER?

A

Stimulus binds to GPCR. Alpha q subunit activates phospholipase C which converts PIP2 into IP3+DAG
IP3 binds to IP3 receptors on SER, stimulating calcium release

28
Q

What is capacitative calcium entry?

A

Occurs when SER calcium stores are low after signalling. SER sends a depleted signal to calcium channels on cell membrane to stimulate calcium entry into the cell and then into the SER

29
Q

What’s the difference between a receptor and an acceptor?

A

Receptors are silent at rest

Acceptors are operational without a ligand present. Binding modulates and regulates response

30
Q

What are the 4 main types of receptor?

A

Membrane bound receptor with integral ion channel
Membrane bound receptor with integral enzyme activity
Membrane bound receptors signalling via transducing proteins
Intracellular receptors

31
Q

How is immunoglobulin transcytosed?

A

Binds to cell surface receptor and is internalised. Vesicle is uncoated and enters endosome where it pinches off as part of transfer vesicle, in which it’s transported to the bile. Ig and receptor then dissociate

32
Q

How is cholesterol endocytosed?

A

LDL binds to receptor in clathrin coated pit and is internalised. Vesicle’s uncoated and enters endosome where it dissociates from receptor. Receptor is recycled back to cell surface and LDL is transported to lysosome where it’s degraded

33
Q

How is Fe3+ endocytosed?

A

2 Fe3+ bind to apotransferrin which makes transferrin. This binds to receptor and is internalised. Vesicle is uncoated and complex enters endosome. Once there, Fe3+ dissociates and enters cytosol and apotransferrin and receptor are recycled back to surface, where they dissociate

34
Q

What is pinocytosis?

A

The invagination of plasma membrane to form a vesicle to allow uptake of extracellular solutes

35
Q

How does parasympathetic innervation at M2 decrease heart rate and contractility?

A

M2 is a GPCR using Gi. Gi inhibits adenylyl cyclase so inhibits cAMP. This therefore inhibits protein kinase A so there’s decreased calcium influx so contractility reduces.
Also increases K+ conductance so decreases heart rate

36
Q

What effect does the Botulinum toxin have?

A

It’s taken into nerve terminus through endocytosis and degrades proteins on the inner membrane surface. This prohibits ACh containing vesicles from being brought close to the surface so ACh can’t be released. There’s no contraction.

37
Q

What are the 2 types of glaucoma?

A

Closed angle where there’s an abnormally shallow anterior chamber so intraocular pressure increases more easily
open angle which occurs secondary to trauma or inflammation

38
Q

How can glaucoma be treated?

A

Muscarinic agonists eg pilocarpine which act on M3 to contract sphincter pupillae and ciliary body so aqueous humour outflow is increased and pressure decreases
Beta antagonists eg timolol or betaxolol which decrease aqueous humour production
Physostigmine which is an AChE inhibitor to increase parasympathetic effect

39
Q

What is the parasympathetic innervation of the eye?

A

Acts on alpha 1 to contract the dilator pupillae muscle so pupil dilates

40
Q

How is noradrenaline synthesised?

A

Tyrosine converted to DOPA using tyrosine hydroxylase.
DOPA converted to Dopamine using DOPA decarboxylase
Dopamine converted to noradrenaline

41
Q

What does G protein alpha s do?

A

Stimulates adenylyl cyclase which converts ATP into cAMP. cAMP activates protein kinase A which goes onto phosphorylate target proteins

42
Q

What does G protein alpha q do?

A

Stimulates phospholipase C which stimulates conversion of PIP2 into IP3 and DAG and these activate protein kinase C

43
Q

How is GPCR signalling terminated?

A

While the receptor’s activated, it’s vulnerable to phosphorylation by protein kinases which would prevent activation of any more G proteins
After G protein receptor interaction, agonist binding is weakend
Cellular enzymes favour basal state and metabolise second messengers into their inactive form
Alpha GTP has a limited lifespan due to cellular processes stimulating GTPase activity
Enzyme cascades further down oppose protein kinase activation

44
Q

How does amplification of GPCR signalling occur?

A

GPCR can cause GTP/GDP exchange on more than one G protein
G protein subunits can activate more than 1 effector molecule
Effector molecules act catalytically. eg adenylyl cyclase can convert thousands of ATP into cAMP

45
Q

What are Kd and Bmax?

A

Kd is concentration of drug needed to occupy 50% of receptors
Bmax is maximum binding capacity

46
Q

What’s EC50 and Emax?

A

EC50 is concentration of drug that gives 50% of maximum response
Emax is maximum effect

47
Q

What is IC50?

A

Concentration of antagonist that gives 50% inhibition

48
Q

using a drug concentration/response curve, how can you tell the difference between a full and a partial agonist?

A

Full agonist exerts a full response with EC50 being less than or equal to Kd. May not be any spare receptors
Partial agonist doesn’t have sufficient efficacy to exert a full response. EC50 is roughly equal to Kd (or less) There are no spare receptors

49
Q

How are partial agonists used clinically?

A

Safer than full agonists as they have higher affinity but lower efficacy. Can be used to antagonise full agonists, eg heroin but without causing withdrawal

50
Q

What is oral bioavailability?

A

Proportion of drug given (not by IV) that reaches the systemic circulation, unchanged
Calculated by AUC oral/AUC injected x 100

51
Q

What is the therapeutic ratio?

A

Maximum tolerated dose/Minimum effective dose

A low therapeutic ratio indicates a narrow therapeutic window

52
Q

What is volume of distribution?

A

Therapeutical volume into which drug has distributed, assuming it takes place instantaneously
= amount given/ conc when time = 0

53
Q

What is first order kinetics?

A

When rate of drug metabolism is proportional to drug concentration. There’s a defined half life and elimination occurs at a constant fraction per unit time. There’s also a predictable therapeutic response to dose changes

54
Q

What is zero order kinetics?

A

When drug is metabolised at the same rate, regardless of dose, frequency or route of administration.

55
Q

Why are lipid soluble drugs particularly vulnerable to drug interactions?

A

As the enzymes in liver used for phase 1 metabolism have low affinity and specificity so enzymes are inducible and inhibitable

56
Q

How does urine pH affect drug excretion?

A

Only lipid soluble, non-ionised drugs can be reabsorbed in kidney from urine.
If urine is acid, it will decrease reabsorption of drugs that are weak bases - increased elimination and increases reabsorption of weak acid drugs
If urine is alkaline, it will increase reabsorption of drugs that are weak bases and decrease reabsorption of weak acid drugs (increased elimination)

57
Q

Roughly, what are the stages of neurotransmission from precursors?

A

Uptake of precursors and synthesis of neurotransmitter. THis can either then be degraded or packaged into vesicles. When in vesicles, depolarisation and calcium influx bring vesicles close to the surface and they’re released by exocytosis into synaptic cleft. Then, they’re either taken up by post-synaptic receptors, interact with pre-synaptic receptors and and taken back up or are inactivated. This then forms precursors which are taken back up into neurone

58
Q

What are the 2 methods of Noradrenaline removal and inactivation?

A

Uptake 1 where NA is rapidly removed back into pre-synaptic terminal
Uptake 2 where NA is taken up by non-neuronal substance and either repackaged or metabolised

ESA 2 (4 decks)

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