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Can anybody explain to me how hypocalcemic tetany works?
I'm a veterinary technology student, but I'm at a complete loss here. I've spent an unholy amount of time trying to figure this one out, and I just plain have not found a direct, precise answer.
Isn't tetany a non-stop contraction of the muscle? If the patient in-question is severely hypocalcemic, how does the contraction occur in the first place? Correct me if I'm wrong, but it seems to me that hypercalcemia would cause tetany, not hypocalcemia.
The case is that hypocalcemia occurs secondary to metabolic bone disease (in green iguanas, Iguana iguana in particular, however their muscles work the same as mammals, and this apparently occurs in other animals as well). If the MBD is allowed to progress to a stage where the Ca deposits in the bones are no longer enough to sustain the animal, hypocalcemia sets in, tetany occurs, the animal is paralyzed, and death soon follows after (apparently) heart failure.
I was also under the impression that the physiology of cardiac muscle contraction is different than that of skeletal muscle?
If anyone could give me a little insight into this topic, I will be incredibly grateful!
Thank you for your time,
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| mdwannabe
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Ca is necessary for the actin dissociation from myosin, if not enough Ca, sarcomere contract, but fail to relax.
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| mani
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decreased Ca is associated with incresed nueral excitability
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| mdwannabe
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that has to do with stabilization of charges across membrane that is done by Ca ang Mg. Thats why we give Ca gluconate in cases of V-tech or hypo K, and can give Ca in case of Mg def or vice versa.
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| MLF
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Also decrease calcium decreases the threshold of the action potential.
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| Kazem
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I agree with the above answers, but would like to give more explanations as to how a decrease in plasma calsium can cause tetany.
when the extracellular conc. of calcium ions falls below normal, the nervous system becomes progressively more excitable, because this causes neuronal membrane permeability to Sodium ions, allowing easy initiation of action potentials.
At plasma calsium ion concentrations about 50 percent below normal, the peripheral nerve fibers become so excitable that they begin to discharge spontaneously, initiating trains of nerve impulses that pass to the peripheral skeletal muscles to elicittetanic muscle contraction. consequently, hypocalcemia causes tetany.it also occasionally causes seizures because of its action of increasing excitability in the brain.
I hope the above helps 
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| Herptiles.net
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Thank you very much for the detailed explanation, Kazem Thanks to everyone else who replied, too.
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| Kazem
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you are most welcom!
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| vrach
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I agree with all the above explinations. I would just like to correct mdwannade's first post.
As far as I know, calcium is only involved in the formation of cross bridges between actin and myosin (contraction is a passive process!!). It is ATP and its hydolysis that is involved in the dissassociation of the cross bridge (Relaxation is an active process and involves two types of ATPases-1.ATPase on the myosin cross bridges, 2.Ca ATPase in the membrane of the sarcoplasmic reticulum, which pumps Ca back into the SR!!). So it is due to a deficit of ATP, that the sarcomere fails to contract (e.g:riger mortis).
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| mdwannabe
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if you read again...a bit more attentively...it says...Ca needed for dissociation of actin and myosin...which is relaxation. I just did not want to get in to biochem of the contr and relax. Which was successfully done by others. So what are you correcting?
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| mdwannabe
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To add to the ATP-ase story, the sarcolapsmic retic has Ca pump, that is Ca activated, that is if at some point Ca level falls, and Ca is still released to cause contraction, Ca will not be pumped back at same rate and cotraction will persisit. Which is tetany.
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| vrach
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Hey mdwannabe, no need to be sarcastic dude. I really do respect your command over the subjects, as I have seen several of your other posts and have gained a lot from them. I was just trying to point out what I thought was a mistake.
I did read your post attentively and it says "Ca is necessary for the actin dissociation from myosin, if not enough Ca, sarcomere contract, but fail to relax".
My point is that:
1. Ca is needed for the association of actin and myosin. Ca is not necessary/responsible for the dissociation of actin from Myosin. It is the attachment of ATP to the myosin and its subsequent hydrolysis, which causes the dissociation of actin from myosin.
2. If there isn't enough Ca in the cytoplasm, crossbridges fail to form and the sarcomere 'fails to contract', not "fail to relax", as stated in our post.
Please correct me if I'm still misreading/misunderstanding your post. Or if what I said is wrong.
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| mdwannabe
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you still are misreading. No sarcasm..only serious question, of where am I wrong. Thats the only reason for the question. If I am ever sarcastic or wishing for some humor I attach smilicons.
Anyway... As I understand it...relaxation is dependent upon removal of Ca. And Ca removal is dependent upon Ca-ATP-ase, which is Ca activated/dependent. The higher the concentration of Ca in cytoplasm, the more pumps are active and the faster the Ca is removed. So...if there is not enough Ca, the activation of the pumps will not be as complete as needed for timed relaxation...hence tetany is achieved, which is by definition caused by repeated stimulation to the muscle with out appropriate time or faculty to relax. ...
Anyway...
Such simple question...brings out such deep discussion. Exellent excersise.
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| vrach
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My bad....for misreading. Anyway this is such a minor point, and is highly unlikely to be tested!!!
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| mdwannabe
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Not at all...thank you again.. I have also corrected Vit D q in Anatomy section...take a look.
I trully think that even very small point that brings out discussion and manipulation of learned material, is just as important as general cocepts learned and glued to our minds.
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| adeelmd
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what if the ca-atpase reuptake mech is blocked? i remeber reading something somewhere about that....dantrolene would inhbit the release of ca from sr, but is there anything that would inhibit the reuptake of ca?
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