Tetany Question

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InHoc

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Forgive if this is an ignorant question...

Can someone explain to me how hypOcalcemia causes tetany?

I've read somewhere that Ca plays a role in 'stabilizing' nerve transmission, and a lack of Ca subsequently results in over stimulation and tetany. If this is true or not, does anyone have any better or more detailed explaination of this?

Further, if Ca levels are high in a given muscle cell, relaxation is inhibited via binding Troponin C, correct? If relaxation is inhibited - wouldn't that be tetany. For completeness... wouldn't those two points yield that hypercalemia also causes tetany?
 
I believe it lowers the threshold for nerve firing. I know it's a little counterintuitive, but I think that's the mechamisn.
 
InHoc said:
Forgive if this is an ignorant question...

Can someone explain to me how hypOcalcemia causes tetany?

I've read somewhere that Ca plays a role in 'stabilizing' nerve transmission, and a lack of Ca subsequently results in over stimulation and tetany. If this is true or not, does anyone have any better or more detailed explaination of this?

Further, if Ca levels are high in a given muscle cell, relaxation is inhibited via binding Troponin C, correct? If relaxation is inhibited - wouldn't that be tetany. For completeness... wouldn't those two points yield that hypercalemia also causes tetany?

Hypocalcemia results in a partial depolarization of nerves and muscle, so less stimulus is need to get an AP. This probably has something to do with Nernst Equilibrium potentials, but not 100% sure.
 
Spontaneous action potentials occur in peripheral nerves when the ionized (not total) calcium falls below 4.5 or thereabouts. This possibly demonstrates calcium's role in establishing the membrane potential, and anything that raises that membrane potential closer to threshold increases the irritability (just my take on it), or possibly calcium's role in propogating the refractory period. Im not sure if the physiology is spelled out clearly. Alkalosis can cause a normal total calcium to have a decreased serum ionized calcium also, remember.
 
Idiopathic said:
Alkalosis can cause a normal total calcium to have a decreased serum ionized calcium also, remember.
Yea, I didn't quite get that. Like alkalosis can increase the negative charges on Albumin to bind more calcium---> leading to hypocalcemia, rite? So, how come there's no immediate feedback to compensate the blood Ca levels. I mean, when you increase the albumin levels, the total Ca increases, but the free levels remain normal, therefore you don't get tetany. I see both of these to have similar mechanisms, in that you are binding more Ca, but only in alkalosis do u increase the binding at the expense of the free levels. Any thoughts?
 
Idiopathic said:
Spontaneous action potentials occur in peripheral nerves when the ionized (not total) calcium falls below 4.5 or thereabouts. This possibly demonstrates calcium's role in establishing the membrane potential, and anything that raises that membrane potential closer to threshold increases the irritability (just my take on it), or possibly calcium's role in propogating the refractory period. Im not sure if the physiology is spelled out clearly. Alkalosis can cause a normal total calcium to have a decreased serum ionized calcium also, remember.

I can live with that - thanks.

If I may pose another...

Is there a point at which tetany progresses to flaccid state? (ie. using succinylcholine - theoretically it causes continued Na channel depolarization via Ach agnonist action, and after a certain point, the Na channels are inactivated - unable to be continually depolarized - leading to flaccid state). Approaching this concept from the point of tetany - would continued spontaneous action potentials ellicited from hypocalcemia lead to tetany and then on to flaccidity?

Are there different mechanisms here (between 1. the action of continued deopol of succ and 2. the continued nervous stimulation via hypocalcemia) that I'm not seeing??

these may be moot points, but it seems like some basic phys questions could be gleaned from them.
 
InHoc said:
I can live with that - thanks.

If I may pose another...

Is there a point at which tetany progresses to flaccid state? (ie. using succinylcholine - theoretically it causes continued Na channel depolarization via Ach agnonist action, and after a certain point, the Na channels are inactivated - unable to be continually depolarized - leading to flaccid state). Approaching this concept from the point of tetany - would continued spontaneous action potentials ellicited from hypocalcemia lead to tetany and then on to flaccidity?

Are there different mechanisms here (between 1. the action of continued deopol of succ and 2. the continued nervous stimulation via hypocalcemia) that I'm not seeing??

these may be moot points, but it seems like some basic phys questions could be gleaned from them.

Of course this could potentially happen, either when the resting membrane potential effectively equals the threshold potential or the cell deplets all sources of ATP.

As far as the mechanisms, they are obviously different, but could effectively have the same endpoint.
 
HiddenTruth said:
Yea, I didn't quite get that. Like alkalosis can increase the negative charges on Albumin to bind more calcium---> leading to hypocalcemia, rite? So, how come there's no immediate feedback to compensate the blood Ca levels. I mean, when you increase the albumin levels, the total Ca increases, but the free levels remain normal, therefore you don't get tetany. I see both of these to have similar mechanisms, in that you are binding more Ca, but only in alkalosis do u increase the binding at the expense of the free levels. Any thoughts?

This is an interesting observation. There is obviously a system in place to maintain serum ionized calcium, and I believe that PTH is directly related to ionized calcium, not total calcium. The badness comes when an internal derangement of the A/B equilibrium (i.e. alkalosis) causes the environment to be out of whack acutely. Simple increase or decrease in albumin would give you a transient delta in ionized calcium, but this would be compensated for by absolute loss or gain of total calcium. There might be a measureable change initially, but nothing akin to what an A/B disturbance will cause, especially when total calcium is not altered.
 
Idiopathic said:
This is an interesting observation. There is obviously a system in place to maintain serum ionized calcium, and I believe that PTH is directly related to ionized calcium, not total calcium. The badness comes when an internal derangement of the A/B equilibrium (i.e. alkalosis) causes the environment to be out of whack acutely. Simple increase or decrease in albumin would give you a transient delta in ionized calcium, but this would be compensated for by absolute loss or gain of total calcium. There might be a measureable change initially, but nothing akin to what an A/B disturbance will cause, especially when total calcium is not altered.
Yea, I understand what you are saying. But, what I don't get is how come PTH does not compensate, or attempt to maintain the ionized levels in alkalosis. Unless, ofcourse, it is jjust acutely or transiently that you see the hypocalcemia, but I don't think that's the case. Someone living in the mountains will be hypocalcemic. But, someone on steroids will have normal ionized Ca, but increased total Ca; I can see that transiently the increased albumin will bind more at the expense of ionized Ca, but eventually, or shortly after, PTH or whatever mech will compensate. I just don't understand why it's not compensating in alk.

Also, as a side note, like in cirrhosis and stuff, when there is decrs albumin, you have to adjust for the albumin. So, the point of the calculation is to just rule in that the decreased total Ca is secondary to decreased albumin?
 
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