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Old 05-25-2013
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Star Physiology question.

A 56 year old woman with severe muscular weakness is hospitalised. The only abnormality in her lab values is an elevated serum potassium. The raised serum potassium causes muscle weakness because

A. The resting membrane potential is hyperpolarised
B. The K+ equilibrium potential is hyperpolarised
C. The Na+ equilibrium potential is hyperpolarised
D. K+ channels are closed by depolarization
E. K+ channels are opened by depolarization
F. Na+ channels are closed by depolarization
G. Na+ channels are opened by depolarization

Please offer an explanation for your answer.
Thanks.
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Old 05-25-2013
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Quote:
Originally Posted by asioqua View Post
A 56 year old woman with severe muscular weakness is hospitalised. The only abnormality in her lab values is an elevated serum potassium. The raised serum potassium causes muscle weakness because

A. The resting membrane potential is hyperpolarised
B. The K+ equilibrium potential is hyperpolarised
C. The Na+ equilibrium potential is hyperpolarised
D. K+ channels are closed by depolarization
E. K+ channels are opened by depolarization
F. Na+ channels are closed by depolarization
G. Na+ channels are opened by depolarization

Please offer an explanation for your answer.
Thanks.
I will go for A.
Explanation not so forthcoming.
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Old 05-25-2013
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K+ efflux is responsible for the RMP coz of leaky K+ channels which throws K+ to outside and making the membrane potential to more negative.
In -90mv ... -85mv is due to K+ and -5mv is due to NA-K ATPase.

In hyperkalemia , no efflux of K+ , the intracellular K+ makes the resting membrane potential very near to threshold.
If RMP is near to threshold chronically , it gives wrong signal to de-activation gate of Na channel , and as a result the Na channel is closed most of the time or permanently closed. Now suppose if the RMP touches the threshold , Na activation gate opens but the de activation gate is still closed , so no or less action potential will be there. Results in decreased contractility in case of less action potential and paralysis in case of no action potential. ( hyperkalemic periodic paralysis )
In case of Myocardial cells .......Mild hyperkalemia causes arryhthmias in cardiac cells and severe hyperkalemia causes asystole. ( FLAT LINE )

I will go with ''F''. Na+ channels are closed by depolarization.
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Quote:
Originally Posted by mohdkhan View Post
K+ efflux is responsible for the RMP coz of leaky K+ channels which throws K+ to outside and making the membrane potential to more negative.
In -90mv ... -85mv is due to K+ and -5mv is due to NA-K ATPase.

In hyperkalemia , no efflux of K+ , the intracellular K+ makes the resting membrane potential very near to threshold.
If RMP is near to threshold chronically , it gives wrong signal to de-activation gate of Na channel , and as a result the Na channel is closed most of the time or permanently closed. Now suppose if the RMP touches the threshold , Na activation gate opens but the de activation gate is still closed , so no or less action potential will be there. Results in decreased contractility in case of less action potential and paralysis in case of no action potential. ( hyperkalemic periodic paralysis )
In case of Myocardial cells .......Mild hyperkalemia causes arryhthmias in cardiac cells and severe hyperkalemia causes asystole. ( FLAT LINE )

I will go with ''F''. Na+ channels are closed by depolarization.
You're right, the answer is F.
I wanted to understand the mechanism by which hyperkalemia caused closure of the inactivation gate of sodium channels. Your explanation is sufficiently cconvincing.
Thanks a bunch.
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