Also, when there is a deficit of Calcium ions in the ECF, sodium channels become activated. Sodium makes more action potentials (highly excitable) repetitively without provocation, rather than remaining in the resting state. Often causing ‘muscle tetany’.
Thank you for explaining this subject sir, there are not many sources on the internet about this topic. But i have a question and i'd be grateful if you answer it: Why sodium ions rush into the cell during hypocalcemia?
Normally the calcium gets themselves attached to the Na+ channel and makes it stable (Less permeable). When there is extracellular hypocalcemia the calcium ions that are attached to Na+ gets reduced leading to more permeability.
My own lecture says Calcium ions activate the sodium channels. Deficiency of calcium ions lead to decreased activity of Na-channels, which ultimately leads to decrease in membrane potential so that the nerve fiber becomes excited I can't understand :(
@@mobbylca 99% of it is in the cell tho, so it is really hard to find it out only with blood. Make a good hair test and also check your vitamin D. You have pretty much 3 Steps with calcium. 1. Do you get enough calcium intake? If yes, is this calcium absorbed from the body, aka the right ph, stomach acid co factors etc. and step 3. has the body everything it needs to put the calcium into the right places, aka vitamin k2, magnesium, vitamin D deficiencys. Low bone calcium for example has different symptoms then low blood calcium and you can have both at the same time. I would try a little bit of apple cider vinnegar and see if it helps if not try the other things. In my case it was low bone and low blood calcium, after i took Vit k2 my symptoms got worse, i think because the k2 took the little bit i had in the blood and used it. Also careful with high dosage of vit D (if you are low), if you go over kill with it, it can cause both, hypo or hypercal in the blood - even with k2 in the combo. cheers
But when hyper polarization occurs the excitibility of cells decreased (more Na is required to generate Action potential) so how can in this hyper polarisation causes increased in excitibility of cell
That’s a good question. Let’s take 2 examples and let’s consider the RMP as -90. If the threshold is -60 normally it would take more time to reach the threshold and if there is hypocalcemia it gets more negative let’s say -80. From -90 baseline, the threshold of -80 will be reached much faster and earlier. It's not causing hyperpolarisation, it decreases the threshold to be precise.
That’s a good question. Let’s take 2 examples and let’s consider the RMP as -90. If the threshold is -60 normally it would take more time to reach the threshold and if there is hypocalcemia it gets more negative let’s say -80. From -90 baseline, the threshold of -80 will be reached much faster and earlier..
From -90 reaching -80 is easier.. Here we have to understand that the threshold is reduced, meaning the threshold to activate the membrane is reduced, which causes hyper excitability..
Why does calcium stabilize the me m brane? Why not k or na? I mean why this happens when ca goes down? Is it because the resting membrane potential is reduced ?? Why does this not happen in case of hyponatremia or hypokalemia? Please answer
Calcium is a membrane stabilising agent. Whereas the Na stays hydrated so it contributes very little to RMP. Coming to K+, it is the major contributor to RMP so hypokalemia and hyperkalemia affects the RMP by increasing and decreasing the RMP respectively.
Good question.. A) It is called membrane stabilizer because of its property to inhibit the channels. B) Bring the threshold to more negative. Let’s take 2 examples, let’s consider the RMP as -90. If the threshold is -60 normally it would take more time to reach the threshold and if there is hypocalcemia it gets more negative let’s say -80. From -90 baseline, the threshold of -80 will be reached much faster and earlier..
But sir ca ion in synaptic cleft helps to release acetylcholine from the nerve terminal and this this thing helps to carry nerve signal to muscle..if ca ion level is decreased then how nerve impulse will reach to muscle and will cause tetany?? I am realy confused about that and waiting for your kind reply
The calcium levels required for the release of neurotransmitter is very very less. Hence the release of Ach is not impaired. But the calcium requirements for stabilising the membrane is more and even a marginal decrease can increase the activity of Na channel causing hyper excitability.😊
This is basically affecting the excitability. If excitability is increased even a small stimuli will trigger the release of intracellular calcium levels and cause tetany.
@@PhysiologyLearning I so appreciate this video! As a non scientifically educated person I wonder, is there no regulation mechanism that would balance out intra and extra-cellular calcium? Are the cells that excrete calcium muscle cells or just any type of cells ? Is the involuntary stimulus caused by a state of stress? I'm very curious about the type of nervous activity (autonomous, ortho-para - or else) that would cause this. Also, since neurons also fire with calcium, is it a self-maintained condition ?
I've been struggling to understand this concept and you made is so simple. Thanks!
Welcome..😊😊 keep watching and Sharing.. glad u found it helpful
Very clear, well explained and all in 3 mins!! Exactly what I was looking for :D
Thank you Sarah for the compliments..😊
Also, when there is a deficit of Calcium ions in the ECF, sodium channels become activated. Sodium makes more action potentials (highly excitable) repetitively without provocation, rather than remaining in the resting state. Often causing ‘muscle tetany’.
Great explanation, thanks a lot for that!
I wish we had more information regarding how Calcium puts the cell in a hyper-excitable state though.
Thank you! I have Hypoparathyroidism and as a result, Hypocalcemia. It's good to know WHY my muscles spasm & lock up when low.
Take care.
Thank you sir i am searching for this kind of explanation
Welcome shehreen..😊 stay tuned for more videos in the coming weeks. Happy learning. Keep sharing
Thank you for explaining this subject sir, there are not many sources on the internet about this topic. But i have a question and i'd be grateful if you answer it: Why sodium ions rush into the cell during hypocalcemia?
Normally the calcium gets themselves attached to the Na+ channel and makes it stable (Less permeable). When there is extracellular hypocalcemia the calcium ions that are attached to Na+ gets reduced leading to more permeability.
Clear and concise explanation. Thank you
Glad it was helpful! Keep watching and sharing with your friends.
thanks a lot for this explanation
Glad it was helpful! You are most welcome.
You did a great job, Thank you ❤
Glad you enjoyed..😊
Thank you very much for explaining it better!
Stay tuned with the channel for more such videos. Keep sharing. Happy Learning.
Thanks sir I was searching this answer for a while
Hope it helped you. Most welcome.
It's really really helpful.. thank you
Most welcome! Keep watching and sharing..😊
Thank you sir, can you please make a video on why increase in intracranial pressure results in rise in arterial pressure.🙏
Will cover in the coming weeks
tysm! i've been confusing for a while thinking how it causes tetany😂😂
Welcome..😊
Thank you so much ❤🙏
You're welcome 😊
Thank You Sir, it was really helpful😄
Welcome Aakash😊 Happy learning
Thank u that was helpful
Welcome😊 Happy learning
My own lecture says Calcium ions activate the sodium
channels. Deficiency of calcium ions lead to decreased
activity of Na-channels, which ultimately leads to decrease
in membrane potential so that the nerve fiber becomes excited
I can't understand :(
The threshold for activation comes down. With less stimuli itself now it can reach threshold.
@Physiology Learning with Dr. Ram thank you so much
Welcome 😊
Thankyou so much sir
Welcome sid..😊
Thank you!
You're welcome! Keep watching and Sharing..😊
I have tetany. Doctors in Poland only prescribed me magnesium. Magnesium doesn't help. Doctor, tell me, how can I help myself? Thank you very much.
Kindly check your calcium levels once and if needed you can take calcium supplements after consulting your treating physician.
@@PhysiologyLearning calcium level in my blood is in normal... Thx
@@mobbylca 99% of it is in the cell tho, so it is really hard to find it out only with blood. Make a good hair test and also check your vitamin D.
You have pretty much 3 Steps with calcium. 1. Do you get enough calcium intake? If yes, is this calcium absorbed from the body, aka the right ph, stomach acid co factors etc. and step 3. has the body everything it needs to put the calcium into the right places, aka vitamin k2, magnesium, vitamin D deficiencys. Low bone calcium for example has different symptoms then low blood calcium and you can have both at the same time.
I would try a little bit of apple cider vinnegar and see if it helps if not try the other things. In my case it was low bone and low blood calcium, after i took Vit k2 my symptoms got worse, i think because the k2 took the little bit i had in the blood and used it. Also careful with high dosage of vit D (if you are low), if you go over kill with it, it can cause both, hypo or hypercal in the blood - even with k2 in the combo.
cheers
Thank you so much sir😇
😊
But when hyper polarization occurs the excitibility of cells decreased (more Na is required to generate Action potential) so how can in this hyper polarisation causes increased in excitibility of cell
That’s a good question. Let’s take 2 examples and let’s consider the RMP as -90. If the threshold is -60 normally it would take more time to reach the threshold and if there is hypocalcemia it gets more negative let’s say -80. From -90 baseline, the threshold of -80 will be reached much faster and earlier. It's not causing hyperpolarisation, it decreases the threshold to be precise.
Thank you 🙏
You’re most welcome 😊 keep watching and sharing.
Hello, if the threshold becomes more negative, how does that lead to hyperexcitability? Please let me know.
That’s a good question. Let’s take 2 examples and let’s consider the RMP as -90. If the threshold is -60 normally it would take more time to reach the threshold and if there is hypocalcemia it gets more negative let’s say -80. From -90 baseline, the threshold of -80 will be reached much faster and earlier..
@Physiology Learning with Dr. Ram why does thid not happen in hyponatremia, hypokalemia, it's the same principle
@Physiology Learning with Dr. Ram wouldn't it take less time when it's 60 to reach threshold and initiate action potential? Because it gets positive
From -90 reaching -80 is easier..
Here we have to understand that the threshold is reduced, meaning the threshold to activate the membrane is reduced, which causes hyper excitability..
Why does calcium stabilize the me m brane? Why not k or na?
I mean why this happens when ca goes down? Is it because the resting membrane potential is reduced ?? Why does this not happen in case of hyponatremia or hypokalemia?
Please answer
Calcium is a membrane stabilising agent.
Whereas the Na stays hydrated so it contributes very little to RMP.
Coming to K+, it is the major contributor to RMP so hypokalemia and hyperkalemia affects the RMP by increasing and decreasing the RMP respectively.
Few confusions
A) Is calcium a membrane stabalizer or inhibitor of Voltage Gated Na Channels?
B) Does hypocalcemia reduce threshold or increase RMP?
Good question.. A) It is called membrane stabilizer because of its property to inhibit the channels.
B) Bring the threshold to more negative. Let’s take 2 examples, let’s consider the RMP as -90. If the threshold is -60 normally it would take more time to reach the threshold and if there is hypocalcemia it gets more negative let’s say -80. From -90 baseline, the threshold of -80 will be reached much faster and earlier..
Thank you for wonderful explanation sir.
Please make a video on why Dopamine infusion is lifesaving in acute renal failure?
Thank you..Will make a video on it in the coming week Nidhi..
But sir ca ion in synaptic cleft helps to release acetylcholine from the nerve terminal and this this thing helps to carry nerve signal to muscle..if ca ion level is decreased then how nerve impulse will reach to muscle and will cause tetany?? I am realy confused about that and waiting for your kind reply
The calcium levels required for the release of neurotransmitter is very very less. Hence the release of Ach is not impaired.
But the calcium requirements for stabilising the membrane is more and even a marginal decrease can increase the activity of Na channel causing hyper excitability.😊
@@PhysiologyLearning thanks a lot sir
so does this relate to the calcium in the sliding filament theory?
This is basically affecting the excitability. If excitability is increased even a small stimuli will trigger the release of intracellular calcium levels and cause tetany.
@@PhysiologyLearning I so appreciate this video! As a non scientifically educated person I wonder, is there no regulation mechanism that would balance out intra and extra-cellular calcium? Are the cells that excrete calcium muscle cells or just any type of cells ? Is the involuntary stimulus caused by a state of stress? I'm very curious about the type of nervous activity (autonomous, ortho-para - or else) that would cause this. Also, since neurons also fire with calcium, is it a self-maintained condition ?
Is flaccidity the opposite of tetany? Show in Hypercalcemia ?
Yes it can happen in hypercalcemia but the usual incidences of flaccidity usually whenever there is a lower motor neuron damage.
👍
Thank you!
You are most welcome.