Quote from lifeLONGstudent
Hello biochem smarties......
I have a question for you guys to ponder:
HYPERcalcemia s/sx: fatigue, lethargy, muscle weakness.
HYPOcalcemia s/sx are muscle cramps, paresthesia, tetany (+ trousseau/Chovstek signs).
I know that Ca is necessary for nerve conduction leading to muscle movement/contraction and tone (and it has other functions). If there is too MUCH Ca present, why are the s/sx that of what you would expect of hypocalcemia? I would expect to have muscle movement problems without enough Ca because why is it present with high ca levels?
thanks for any/all explanations, thoughts, theories.
There is more to it than this, but here is a somewhat simplified explanation. (While I will just talk about cardiac muscle, it can also be applied to skeletal muscle, for the most part).
There is a resting membrane potential across plasma membranes of excitable tissues (skeletal muscle, cardiac muscle, nerves). We will use cardiac muscle as an example. Normal resting membrane potential of ventricular cardiac muscle is -90mV, and the normal threshold is -60mV. The threshold is what you have to get to in order for the cell to depolarize. It is an all or nothing principle - you either depolarize or you don't. If you get to the threshold, you depolarize. If you don't get to the threshold, you don't depolarize. Calcium alters the threshold.
Too much calcium will cause the threshold potential to shift away from the resting membrane potential (therefore, the threshold potential becomes less negative). Cells are less excitable
because it is now more difficult for it to get to this threshold. Hypothetically, if the threshold is normally -60mV, but now we have too much calcium on board, our threshold is now -50mv. That is a difference of 40mV that the cell has to account for in order to depolarize. In skeletal muscle, this can cause weakness, fatigue, etc.
Too little calcium will cause the threshold to become more negative (gets closer to the resting membrane potential). Therefore, it requires less to depolarize, and it is more excitable. Hypothetically, the threshold is normally -60mV, but now that we are hypocalcemic, our threshold could now be -70mV. Now there is a difference of only 20mV that the cell has to account for in order to depolarize. The diffusion of calcium into the cell is what maintains
depolarization - and when you don't have as much calcium, it will take longer for the calcium to diffuse in the appropriate amounts, causing a longer depolarization. In skeletal muscle, this can cause tetany, cramps, etc. Hypocalcemia can be particularly of interest to us because of the possibility of airway muscle spasms.
Hope this helped.