Physiology: Shelf Review: #1: Cell

Front 1

connections between cells (junctions) - what kind are there and what are they like?

Back 1

tight junctions = zone occludens, like between epithelial cells. there are tight and leaky (tight in the distal tubule, leaky in the prox) - some sollutes get across this way.

gap junctions - this is how adjacent cells talk to each other. this is how current gets between cardiac cells, for example.

Front 2

what's an equation we can use for simple diffusion?

Back 2

flux = PA (C1-C2)

where P is the permeability
A is the surface area
c1 and c2 are the concentrations. note that the higher concentration is C1.

simple diffusion is the only transport mechanism that doesn't use a carrier.

Front 3

what's an example of facilitated diffusion? why?

Back 3

glucose transport.

uses a transport carrier, goes downhill, exhibits competative inhibition (galactose can out compete it), is MORE RAPID THAN SIMPLE DIFFUSION

Front 4

what's an example of a counter current transport/exchange? how does digoxin work?

Back 4

The super common Ca++/Na++ exchanger.

Salt is pumped into the cell with its gradient (set up by the NaK pump somewhere else) while Ca++ is pumped AGAINST its gradient out of the cell.

DIGOXIN: works by inhibiting the Na/K pump, so salt builds up in the cell.

This prevents the Na/Ca++ exchanger from working (depends on low intracellular sodium to pump out Ca++) - so Ca++ accumulates in the cell. This allows the pump to pump HARDER with each contraction.

but ALSO decreases the heart rate! all that extra Ca++ floating around increases the length of phase 4 and phase 0

Front 5

how do you calculate osmolarity?

Back 5

number of particles X concentration.

so: 1 mMol NaCL solution would have an osmlarity of 2 osm/L, because there are two particles.

Front 6

what's our osmoltic pressure calcuoation? what does having higher pressure mean? what about effective oxmotic pressure?

what's colloid osmotic pressure?

Back 6

osmotic pressure = (# of particles) X (concentration) X (RT)

note that RT is the gas constant and T is temperature in K

note: the higher the osmotic pressure, the more water will flow into it.

colloid osmotic pressure = oncocitic pressure = created by protein. no big difference.

effective osmotic pressure is the above calculation multiplied by the relfection coefficient.

Front 7

what's a reflection coefficient?

Back 7

if it's 1, then a solute doesn't cross the membrane: this allows it to exert a high osmotic pressure.

if it's 0, the solute moves freely back and forth and no water will flow. urea's an example of something with a relfection of 0

Front 8

sodium gates: inactivation and activation. what makes them open or close?

Back 8

the activation gate is turned on by depolarization.

the inactivation gate is closed by depolarization, allowing the cell to repolarize.

so both gates are activated by by depolarization - difference is that one closes and one opens.

Front 9

what's a major ligand gated channel we know about and what happens?

Back 9

binding of Ach to its ligand gated channel causes the cell to become premeable to both Na+ and K+, so the cell depolarizes (goes up to zero, between their two nernst potentials).

this causes the motor end plate to depolarize.

Front 10

what's equilibrium potential?

Back 10

same things as the nernst potential. it's the potential generated by a solute flowing through a permeable membrane at which no more solute flows (the electrical gradient made by the ion leaving counteracts its osmotic pressure trying to make it leave).

it's equal to;

E = -2.3 [-60/charge] log10 [Ci/Ce]

so, 60 divided by charge (Na is +1, Ca++ is +2, Cl is -1).

concentration in the cell divided by concentration outside the cell.

Front 11

what are some common nernst potentials?

Back 11

Na+ = +65
Ca++ = +120

Cl- = -85
K+ = -85

Front 12

at rest, compare the cellular permeabilities of Na+ and K+

Back 12

The cell is far more permeable to K+

we know this because the resting potential is far closer to K+

Front 13

what does tetrodotoxin block?

Back 13

it blocks voltage sensitive Na+ channels, so you completely stop action potentials.

Front 14

action potentials : after reaching its peak, how does the cell re-polarize again?

Back 14

depolarization closes Na+ INACTIVATION gates, stopping the influx of Na+

depoalrization also causes the opening of K+ channels and increases K+ efflux of the cell. This increase in permeability drives the cell back towards the nernst potential for K+

note that the closed Na+ and super-open K+ channels make the cell undershoot (hyperpolarizing afterpotential) for a little while.

Front 15

what are the relative and absolute refractory period?

Back 15

absolute refractory period means that no stimuls can cause a new action potential because the Na+ channels are not yet re-set (their inactivation gates are still closed).

the relative refractory period beings when the absolute ends and happens because the cell is still in UNDERSHOOT due to opened K+ channels allowing K+ to leave.

because you're further below threshold than when resting, it takes a larger than normal stimulus to get to threshold.

Front 16

what's accomidation and what pathological state causes it?

Back 16

it's when the cell potential is kept de-polarized for a long time, so when a signal comes in, action potentials aren't generated.

even though the signal gets the cell to threshold potential, no action potential happens.

this can be due to the fact that sodium inactivation channels are closed by depolarization, so staying depolarized keeps Na+ channels closed and you don't get action potentials.

this happens with HYPERKALEMIA - the cell stays depolarized all the time and action potentials don't happen.

Front 17

what increases the speed of action potentials down nerves?

Back 17

large nerves go faster.

mylenated nerves go faster (they have saltatory conduction meaning that action potentials are generated only at the nodes of ravnier)

Front 18

describe the conduction of action potentials across a synapse:

Back 18

at the nerve terminal, depoalrization wave causes influx of Ca++. This makes neurotransmitters leave into the cleft.

neurotransmitters bind receptors on the post synaptic nerve and change permeabilities to ions.

excitatory neurotransmitters cause the post synaptic cell to depolarize, inhibitory cause hyperpolarization.

Front 19

talk about the neuromuscular junction: how is neurotransmitter made? how is it degraded?

Back 19

the neuron releases Ach.

the post-synaptic tissue has NICOTINIC receptors.

presynaptic nerve has CHOLINE ACETYLTRANSFERASE, which turns acetyl CoA and a choleine in to Ach.

Depolarization wave causes Ca++ influx and release of vessicles into the space.

Ach binds nicotinic receptors on the muscle end plate, increasing permeability to both Na+ and K+ (so you reach a potential between the two, namely about 0 mEV).

Ach is degraded by acetycholine esterase on the muscle end plate.

Front 20

what's myasthenia gravis? what is it treated with?

Back 20

autoimmune disease attacking the Ach receptors on the muscle end plate, so you end up with serious muscle weakness.

treatment is acetycholine esterase inhibitors, so Ach hangs out in the synapse longer allowing the few receptors to work more. Drug name is neostigmine.

Front 21

after the influx of Na+ and K+ into the endplate, what happens? what's a MEPP?

Back 21

NOT AN ACTION POTENTIAL - simply end plate potential goes up to zero.

this gets transmited locally and action potentials happen in the adjacent tissues.

MEPP is a miniature end plate potential caused by one quantum (one vessicle) worth of ACh binding and doing its thing.

lots of MEPP end up summing to an EPP

Front 22

what kind of synapse is at neuromuscular junctions?

Back 22

one to one.

Front 23

neuron/neuron junctions - which cell 'decides' to fire or not fire? how is this determined? what neurotransmitters are excitatory or inhibitory?

Back 23

This is the EPSP vs. IPSP. Excititory post synaptic potential vs. inhibitory.

The post synaptic cell is affected by excitatory and inhibitory neurotransmiters.

excitatory neurotransmitters depolarize the cell closer to threshold, inhibitory hyperpolarize.

excitatory work through increasing permeability to both Na+ and K+. Inhibitory work through increasing permeability to Cl- (driivng it down to close to -95).

inhibitory neurotransmitters are GABA and glycine.

everything else is excitatory.

Front 24

what kind of summation happens at synapses?

Back 24

spacial - this means two input nerves end on one ontput. when they fire together, it adds.

temporal - when one fires signals rapidly.

Front 25

what kind of nerve releases norepi?

Back 25

post-ganglionic sympathetics

Front 26

norepi- what does it bind? how is it removed from the synapse?

how is norepi and epi made?

Back 26

alpha or beta receptors.

removed by reuptake

also by monoamine oxidase (MAO) and COMT

start with tyrosine, go to L-dopa, then to dopamine, then to norepi, then to epi.

Front 27

what kind receptors does dopamine use? what's parkinsons disease?

Back 27

dopamine uses D1 and D2 receptors.

D1 receptors activate Gs
D2 activate Gi.

parkinsons disease is when Gi receptors don't work, so get inappropriate stimulation of nerves.

note that schizophrenia involves too many D2 receptors.

Front 28

what amino acid makes serotonin?

Back 28

tryptophan.

Front 29

organization of muscles: bands, etc.

Back 29

each fiber represents multinucleated cells linked up together.

each fiber has lots of myofibrils

an A band is all the thick filament, including that which overlaps with the thin.

the H band is just the thick portion.

the M line runs through the middle of the A and H band.

The I band represents only the thin filaments

there's a Z band going through the middle of the I band.

Front 30

what's in a thick filament? what does it look like?

what's in a thin filament>

Back 30

thick filament: myosin! has two heads that can bind actin and ATP.


thin filament: made of ACTIN. Anchored at Z lines.

Front 31

how does a muscle fiber move?

Back 31

excitation contraction coupling. T tubles (which go down the intersection of A and I bands and are connected to the extracellular space) carry depolarization down themselves.

the depolarization causes Ca++ channels in the SR to open releasing Ca++.

Ca++ binds Troponin C on the actin (thin filaments)

troponin changes shape and makes TROPOMYOSIN get out of the way (it's a blocker).

first, there's no ATP bound so the myosin heads are firmly attached to the actin.

ATP binds MYOSIN and myosin lets go of the actin. One of the myosin heads jumps up one step (this is POWER STROKE).

ADP gets released, so get back to rigor.

Front 32

where does tetanus come from?

Back 32

Non-relaxation of muscle from repeated stimulus, preventing the re-uptake of Ca++. No relaxation because tropomyosin never goes back and gets in the way.

Note that the SR has a continuously pumping Ca++ ATP ase that pumps Ca++ out of the intracellular fluid into the SR.

Front 33

what are our types of smooth muscle?

Back 33

multi-unit - these don't have a lot of connections between cells and so have a LOT OF NERVES GOING TO THEM. think of the eye and vas deferans.

unitary - the cells are connected to one another to a high degree. they enable organs to contract together (bladder, uterus, GI, ureter). note that they have some PACE MAKING ABILITY.

vascular SM - has properties of both unitary and multi-unit.

Front 34

what's different about SM contraction?

Back 34

the excitation coupling is different.

there's NO TROPONIN: so the presence of Ca++ is through the direct action on myosin, rather than through tropomyosin.

depolarization opens Ca++ channels. More Ca++ from the T-tubules causes more release of Ca++ from the SR (Ca/Ca positive feedback).

Ca++ here binds to CALMODULIN. Ca/Calmodulin complex binds MYOSIN LITE CHAIN KINASE, which phosphorylates myosin and then it binds actin and shortens.

so, with smooth muscle, you have a Ca++/Calmodulin mediated phosphorylation of the myosin fiber, driven by Ca++ concentrations that go up.

can be driven by hormones that activate IP3 and let Ca++ in.

Front 35

what does a substance with a high oil/water partition do?

Back 35

this means a fat soluble solute will get through a lipid membrane more easily.

note that changing the concentration of the solute can make it move faster too, but it won't affect permeability (that's an inherent property of the membrane itself, not dependent on anything else)