ICPP MMF overview Flashcards
list 3 endocrine signalling molecules
hydrophilic:
catecholamines
peptides and proteins
Lipophilic:
steroids
what is paracrine signalling
signalling from cell to cell e.g. NT
what happens to cholesterol in a cold vs warm env?
cold env- pack closer together
warm- more fluid
which molecules can’t pass through the bilayer directly?
large, polar, hydrophilic molecules
which mode of transport through the bilayer can proteins NOT do
flip flop
there integral, go from top to bottom of bilayer
which structural feature of cholesterol makes it rigid?
carbon rings > steroid
hydroxyl groups
which structural feature of cholesterol makes it fluid
non polar, hydrophobic tail
modes of movement for phospholipids
flip flop
rotation
lateral diffusion
modes of movement for proteins
conformational change
rotation
lateral diffusion
difference between uniport, symport and antiport
uni- one molecule transported
symp- more than one
anti- more than one in diff directions
what are the relative extra/ intracellular ion concs (Na, K, Cl, Ca, A-)
more Na+ and Cl- and Ca2+ outside (low intracellular, high extra)
more K+, A- inside (high intracellular, low extra)
compare the affinity and capacity of Na Ca exchanger (NCX) and plasma membrane Ca ATPase (PMCA)
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
what is the role of SERCA
pump Ca into cell. using H conc gradient.
calcium store in ER.
calcium stores?
in ER (SERCA) in mitochondria (ca uniporter)
which ion transporters are used in pH regulation- acid extrusion
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
which ion transporters are used in pH regulation- alkali influx
sodium bicarbonate co transporter (NBC)
- alkalinises cell by bringing bicarbonate IN.
can be coupled with Na H exchange
which ion transporters are used in pH regulation- alkali extrusion
acidifies the cell
anion exchanger
- one Cl- in for HCO3- out
compare hypo/iso/hypertonic
hyper-water moves out cell. shrink/ shrivel
iso-water movement balanced
hypo- water moves into cell. lyse/burst
what is resting potential
-70mV
what is the Ek (equilibrium potential for potassium)
-95
depolarisation, repolarisation, hyperpolarisation terms.
which channels open / close?
De- LESS negative Na open
Re- LESS positive. Na close K open
Hy- MORE negative. K channels are slow to close
threshold reached at what mV, which channels open?
-55mV, Na open
describe how AP is fired
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
Describe the sequence of events at neuromuscular junction
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.
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
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.
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.
features of myasthenia gravis
autoimmune disease targeting nACh receptors.
end plate potential fails to reach threshold. reduced in amplitude.
- muscle weakness/ fatigue
- droopy eyelids.
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.
how does organophosphate poisoning occur?
acetylcholinesterase inhibitors form a stable irreversible covalent bond to the enzyme. > need synthesis of new enzymes to overcome
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.
what is the QISS QIQ mnemonic?
see photo
when NA binds to B1 adrenoreceptors, HR?
HR inc
when ACh binds to M2 receptors, HR?
HR dec
structure of GPCR
binding domain on N terminus (extra cellular)
coupling domain
role of adenyl cyclase
adenyl cyclase converts ATP to cAMP > can activate PKA.
what are the 3 components of signalling cascade?
-G protein
-effector molecule e.g. -enzyme/adenyl cyclase/ phospholipase C
ion channel
autocrine
cell producing own signalling molecule acting on its own receptor
general structure of G proteins
heterotrimeric
alpha, beta, gamma subunit
