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Extra ESA 1 flashcards > ICPP MMF overview > Flashcards

ICPP MMF overview Flashcards

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

A

-70mV

20
Q

what is the Ek (equilibrium potential for potassium)

A

-95

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
Q

how does myelin sheath improve conduction

A
  • 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
Q

how does curare work?

A
  • causes paralysis.

D- tubocurarine acts as competitive blocker. binds to Ach binding site BUT effects can be overcome if you inch Ach conc.

27
Q

how does succinylcholine work?

A

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
Q

features of myasthenia gravis

A

autoimmune disease targeting nACh receptors.
end plate potential fails to reach threshold. reduced in amplitude.

  • muscle weakness/ fatigue
  • droopy eyelids.
29
Q

diagnosis of myasthenia gravis

A

give patient a short acting anti cholinesterase- blocks enzyme > build up of ACh > overcome weakness by inc end plate potential.

eyelid control regained.

30
Q

how does organophosphate poisoning occur?

A

acetylcholinesterase inhibitors form a stable irreversible covalent bond to the enzyme. > need synthesis of new enzymes to overcome

31
Q

how do nicotinic and muscarinic receptors operate differently?

A

nAChR- fast depolarisation. ligand gated.

mAChR- slower response. GPCR. G proteins trigger a cascade of events within the cell.

32
Q

what is the QISS QIQ mnemonic?

A

see photo

33
Q

when NA binds to B1 adrenoreceptors, HR?

A

HR inc

34
Q

when ACh binds to M2 receptors, HR?

A

HR dec

35
Q

structure of GPCR

A

binding domain on N terminus (extra cellular)

coupling domain

36
Q

role of adenyl cyclase

A

adenyl cyclase converts ATP to cAMP > can activate PKA.

37
Q

what are the 3 components of signalling cascade?

A

-G protein
-effector molecule e.g. -enzyme/adenyl cyclase/ phospholipase C
ion channel

38
Q

autocrine

A

cell producing own signalling molecule acting on its own receptor

39
Q

general structure of G proteins

A

heterotrimeric

alpha, beta, gamma subunit

Extra ESA 1 flashcards (17 decks)

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