B4.074 Prework 2: Systemic Hyperkalemia vs Local Hyperkalemia Flashcards

1
Q

what is the resting Na+ channel

A

activation gate closed
inactivation gate opened
normal resting potential -70 to -80 mV

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2
Q

discuss the logistics pf the voltage gated sodium channel

A

both gates must be open for Na+ ions to flow
when both gates are open gNa is increased, so INa will increase
this causes V to move toward ENa
this is the basis for the upstroke in action potential

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3
Q

inactivation gates open and close

A

slowly

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4
Q

activations gates open and close

A

rapidly

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5
Q

sequence of gates during action potential

A

activation gates open at threshold potential
inactivation gates begin to close when activation gates open
at +60 mV, inactivation gates are all closed and activation gates begin to close
as V declines back to normal resting, activation gates stay closed and inactivation gates all reopen to prepare for next impulse

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6
Q

what is the consequence of moving resting potential more positive?

A

closer to original threshold BUT excitability will decrease
number of resting Na+ channels will be decreased because there will be an incomplete repolarization
decreased number of channels will decrease current
threshold will move more positive and amplitude and rate of AP and conduction will be reduced

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7
Q

what is meant by incomplete repolariazation

A

repolarization stops at “new” resting potential before all inactivation gates have a chance to open back up

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8
Q

what happens when Na+ current is decreased

A
  1. threshold potential more positive (decreased excitability)
  2. rate of rise of AP decreased
  3. amplitude of AP decreased (diminished height of QRS)
  4. decreased conduction velocity (wide P wave, wide QRS)
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9
Q

what is the effect of hyperkalemia on resting membrane potential

A

resting membrane potential must be more positive than potassium Nernst and more negative than sodium Nernst
hyperkalemia shifts potassium Nernst more positive
shifts resting membrane potential more positive

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10
Q

normal Ki conc

A

150 mM

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11
Q

what is the effect of extracellular K on Nernst

A

as Ko increases, becomes more similar to Ki
reduces electrical driving force
Ek becomes less negative and moves toward 0

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12
Q

normal Ko conc

A

5 mM

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13
Q

what happens if you double Ko

A

Ek goes up 18 mV

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14
Q

normal Ek

A

-80ish

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15
Q

normal resting potential

A

-70 mV

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16
Q

what is flaccid paralysis

A

reduced voltage gated Na+ current in nerve and skeletal muscle will result in difficulty in a person contracting their limbs

17
Q

what can cause flaccid paralysis

A

hyper or hypokalemia

18
Q

hyperkalemia effects on K current

A

increased gK > increased IK > shorter AP duration

increased amplitude, short duration T wave, spiked T wave

19
Q

hypokalemia effects on K current

A

decreased gK > decreased IK > longer AP duration

low amplitude, long duration flat T wave

20
Q

methods to reverse hyperkalemia

A

calcium gluconate
NaHCO3
glucose & insulin
lasix

21
Q

mechanism of calcium

A

recovers resting sodium channels by shifting sodium channel inactivation curve toward more positive potentials
doesn’t actually get rid of K

22
Q

mechanism of sodium bicarb

A

indirectly enhanced Na-K pump by increasing Na influx via Na-H exchanger

23
Q

mechanism of insulin

A

stimulated Na-K pump, which moves extracellular K into cell

24
Q

mechanism of lasix

A

diuretic

enhanced K excretion by the kidney

25
Q

effect of hypercalcemia

A

depolarizing shift of Na+ inactivation curve
depolarizing shift in the Na+ activation gate curve, makes threshold more positive
benefit of increasing # of resting sodium channels outweighs the more positive threshold

26
Q

overall benefit of calcium

A

recovers more resting Na+ channels to increase Na+ current towards normal in nerves and muscles

27
Q

treatment plan of hyperkalemia

A

recover excitability w calcium
THEN
correct underlying hyperkalemia

28
Q

what is a U wave

A

follows a T wave

becomes more prominent as hypokalemia becomes more severe

29
Q

treatment of hypokalemia

A

slow IV infusion of K

30
Q

how does myocardial ischemia shift the ST segment

A

away from isoelectric line

due to hyperkalemia

31
Q

why does the ST elevation arise?

A

insufficient blood flow to area causes extracellular K+ to rise
resting membrane potential in this area is more positive than in rest of ventricle
different in resting potentials results in current flow even before depol
shifts apparent isoelectric point
“injury current”