ICPP MMF overview Flashcards

(39 cards)

1
Q

list 3 endocrine signalling molecules

A

hydrophilic:
catecholamines
peptides and proteins

Lipophilic:
steroids

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2
Q

what is paracrine signalling

A

signalling from cell to cell e.g. NT

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3
Q

what happens to cholesterol in a cold vs warm env?

A

cold env- pack closer together

warm- more fluid

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4
Q

which molecules can’t pass through the bilayer directly?

A

large, polar, hydrophilic molecules

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5
Q

which mode of transport through the bilayer can proteins NOT do

A

flip flop

there integral, go from top to bottom of bilayer

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6
Q

which structural feature of cholesterol makes it rigid?

A

carbon rings > steroid

hydroxyl groups

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7
Q

which structural feature of cholesterol makes it fluid

A

non polar, hydrophobic tail

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8
Q

modes of movement for phospholipids

A

flip flop
rotation
lateral diffusion

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9
Q

modes of movement for proteins

A

conformational change
rotation
lateral diffusion

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10
Q

difference between uniport, symport and antiport

A

uni- one molecule transported
symp- more than one
anti- more than one in diff directions

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11
Q

what are the relative extra/ intracellular ion concs (Na, K, Cl, Ca, A-)

A

more Na+ and Cl- and Ca2+ outside (low intracellular, high extra)

more K+, A- inside (high intracellular, low extra)

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12
Q

compare the affinity and capacity of Na Ca exchanger (NCX) and plasma membrane Ca ATPase (PMCA)

A

NCX-low affinity. high capacity. gets the bulk of Ca out of the cell. 3Na in.

PMCA- high affinity. low capacity. gets the last trickle of Ca out of the cell

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13
Q

what is the role of SERCA

A

pump Ca into cell. using H conc gradient.

calcium store in ER.

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14
Q

calcium stores?

A
in ER (SERCA)
in mitochondria (ca uniporter)
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15
Q

which ion transporters are used in pH regulation- acid extrusion

A
Na H exchanger (NHE)
Na in (uses Na gradient)

sodium bicarbonate co transporter (NBC, coupled Na H exchange)

  • alkalinises cell by bringing bicarbonate IN.
  • one Na and one HCO3- in
  • cl- out

> H+ out cell

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16
Q

which ion transporters are used in pH regulation- alkali influx

A

sodium bicarbonate co transporter (NBC)
- alkalinises cell by bringing bicarbonate IN.

can be coupled with Na H exchange

17
Q

which ion transporters are used in pH regulation- alkali extrusion

A

acidifies the cell

anion exchanger
- one Cl- in for HCO3- out

18
Q

compare hypo/iso/hypertonic

A

hyper-water moves out cell. shrink/ shrivel
iso-water movement balanced
hypo- water moves into cell. lyse/burst

19
Q

what is resting potential

20
Q

what is the Ek (equilibrium potential for potassium)

21
Q

depolarisation, repolarisation, hyperpolarisation terms.

which channels open / close?

A

De- LESS negative Na open
Re- LESS positive. Na close K open
Hy- MORE negative. K channels are slow to close

22
Q

threshold reached at what mV, which channels open?

A

-55mV, Na open

23
Q

describe how AP is fired

A

1) threshold reached
2) voltage gated sodium channel open
3) Na influx
4) depolarisation
5) Na channels deactivate
6) K channels open
7) efflux of K
8) repolarisation
9) hyperpolarizarion
10) relative refractory period

24
Q

Describe the sequence of events at neuromuscular junction

A

1)AP arrives at presynaptic membrane
2) Ca enters via channels
binds to synaptotagmin
3) vesicles containing Ach move towards membrane
4) snare complex makes a fusion pore
5) exocytosis of Ach
> binds to nicotinic Ach receptor > ligand gated ion channel opens
6) depolarisation spreads down T tubule in muscle> Ca release. muscle contraction.

25
how does myelin sheath improve conduction
- inc membrane resistance (change in voltage spreads further along the axon) - dec membrane capacitance (voltage changes quicker) - inc length constant - slight dec in time constant
26
how does curare work?
- causes paralysis. D- tubocurarine acts as competitive blocker. binds to Ach binding site BUT effects can be overcome if you inch Ach conc.
27
how does succinylcholine work?
depolarisation blocker. bind to nicotinic ach receptors. but not broken down by acetylcholinesterase. Na+ influxing. maintained depolarisation will fail to activate adjacent Na+ channels because they have become inactivated.
28
features of myasthenia gravis
autoimmune disease targeting nACh receptors. end plate potential fails to reach threshold. reduced in amplitude. - muscle weakness/ fatigue - droopy eyelids.
29
diagnosis of myasthenia gravis
give patient a short acting anti cholinesterase- blocks enzyme > build up of ACh > overcome weakness by inc end plate potential. eyelid control regained.
30
how does organophosphate poisoning occur?
acetylcholinesterase inhibitors form a stable irreversible covalent bond to the enzyme. > need synthesis of new enzymes to overcome
31
how do nicotinic and muscarinic receptors operate differently?
nAChR- fast depolarisation. ligand gated. mAChR- slower response. GPCR. G proteins trigger a cascade of events within the cell.
32
what is the QISS QIQ mnemonic?
see photo
33
when NA binds to B1 adrenoreceptors, HR?
HR inc
34
when ACh binds to M2 receptors, HR?
HR dec
35
structure of GPCR
binding domain on N terminus (extra cellular) | coupling domain
36
role of adenyl cyclase
adenyl cyclase converts ATP to cAMP > can activate PKA.
37
what are the 3 components of signalling cascade?
-G protein -effector molecule e.g. -enzyme/adenyl cyclase/ phospholipase C ion channel
38
autocrine
cell producing own signalling molecule acting on its own receptor
39
general structure of G proteins
heterotrimeric | alpha, beta, gamma subunit