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Discussion Starter · #1 ·
The s/s of hypercalcemia: muscle weakness
hypocalcemia: muscle convulsion or tetancy

But in pysiology, calcium cuases muscular contraction, isn't it?
Isn't there any opposite between theory and clinnical manifestation? Why?

Thx a lot!
 

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More likely to Depolarize- Low Ca - thus you get muscle spasm, tetany, cramps

Less likely to depolarize- high Ca thus you get weakness

All muscles contract because of INTRAcellular Ca.

I think your getting confused on Intracellular and Extracellular calcium.
 

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Plasma Calcium affecting Neuronal Excitibility

Low plasma calcium increases the permeability of neuronal membranes to sodium ions, causing a progressive depolarization. This increases the ease with which action potentials can be initiated. If the plasma Ca2+ decreases to less than 50% of the normal value action potentials may be spontaneously generated, causing contraction of peripheral skeletal muscle.

The reverse is true in hypercalcemia. High Calcium causing decreased permeability and thence muscle weakness.

So in essence it's about neuronal excitation rather than the muscle itself. That's why you have signs such as the Chvostek's sign (tapping of the inferior portion of the zygoma will produce facial spasms) it's because you are tapping on the nerve (not the muscle) further exaggerating the neuronal excitation.
 

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many thanks

many thanks to you ,, I had the same confusion previously but now it's all clear to me ,, :)
 

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hypocalcemic tetany

1. increased neuronal exitibility--- when extracelluler ca level dec this inc neuronal memb permeability to sodium ions allowing easy initiation of action potential in other words dec threshold for exitation.

2. ca req for relaxation---ca ATPase( ca activated) p/in memb of SR pumps ca back into SR. so in this condition ca will still be released but not pumped back at the same rate and thus contr will persist....tetany

hope this helps

 

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Discussion Starter · #6 ·
Thank you a lot!!

Clinically, there is a Trousseau sign of latent tetany, which means hand convulsion while using tourequit.

We also find that pregnant women in 3rd trimester often complain calf muscle convulsion, esp in supination.

We highly suspect hypoperfusion exacerbates tetancy in hypocalcemia pt.

But I can't explain.


Besides, if the plasma Ca++ is low, intracellular Ca++ should be suspected at low level, too. Since Ca++ would shift out initially at hypocalcemia, isn't it?

THX a lot.
 

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The answer

This is a good question.

It actually has very little to do with the RMP or intracellular Ca. Remember membrane potential is determined by electrochemical (electrical and concentration) gradients and conductance. K and Cl are really the only ions that have a high conductance at RMP (Na conductance is small until threshold). Equilibration potentials for ions are:

K ~ -90 mV
Cl ~ - 70 mV
Na ~ +60 mv
Ca ~ +125 mV

RMP is about -70 to -80 mV, close to the only two ions (K and Cl) that have high conductances. Both the Na/K ATPase and leaky K channels help maintain RMP until the cell is depolarized.

Because Ca has essentially zero conductance at RMP, hyper-/hypocalcemia will not alter the resting membrane potential in any significant manner. However, Ca does have the important role of modulating the behavior of Na channels. :D

Divalent cations (E.g. Ca) have a small affinity for the Na channel and can essentially "plug" it up during the influx of Na. At normal Ca levels, this acts as an important modulator of excitability. Hyper-/hypocalcemia can alter that modulating activity as follows:

Hypercalcemia: there are more Ca ions to "plug" the Na channel, thus Na influx will be reduced in neurons transmitting impulses resulting in muscle weakness, constipation, etc.

Hypocalcemia: there are less Ca ions to "plug" the Na channel, thus Na influx will be increased in the neurons transmitting impulses resulting in muscle twitching, tetany, etc.

The literature states that changing extracellular Ca is like changing the threshold potential. For example hypercalcemia would increase (make less negative) threshold potential, while hypocalcemia would decrease (make more negative) threshold potential. Thus at RMP, each scenario would required wither more or less input to reach threshold and thus and action potential. However, in reality, RMP does not change.
 

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Really good explanation, just the last statement...I think that hypocalcemia should INCREASE (make less negative) RMP, because it decreases positive charge of ECF, therefore it decreases the difference between inside and outside and makes it less negative, or?
 

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Found an interesting article.

Reference attached. Here's the summary

The inverse relationship between extracellular calcium and neuronal excitability could be explained by several complementary molecular events (summarized in Table 1 and Figure 2). External calcium inhibits NALCNs, shifts the voltage dependency of voltage-gated Na+ channels, stabilizes CNG channels, reduces inward current through AMPA channels, and depresses the release of excitatory neurotransmitters. Conversely, it enhances transient K+ current and KCa channels and perhaps potentiates GABA sensitivity. Some of these modulatory effects may depend on CaSR while others may require calcium influx. It is these processes that we theorize may help shed light on the calcium paradox and lead to further understanding of the mechanisms behind production of seizures through hypocalcemia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4374060/#!po=19.5652
 

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Why does supplemental calcium cause cramps/spasms

If I ingest any amount of supplemental calcium I get painful cramps/spasms throughout my body. If I don't take magnesium(800m) daily I get the same cramping.
If calcium relaxes muscles why am I getting cramping?
 
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