In this lecture we will review calcium homeostasis disorders
such as hypocalcemia and hypercalcemia.
So in order to think about this let's try and remember
the basic fundamental control mechanism
of our calcium levels in our blood.
Parathyroid hormone is controlling this
and the parathyroid hormone receptor.
We have vitamin D controlling this
and we have a calcium-sensing receptor
and these are all things that are helping us to control our levels.
On this slide you can see a general overview
of how we control calcium levels.
Let's go through this bit by bit.
Remember vitamin D in general is absorb from the skin
through light exposure or in the diets.
In patients with darker skin there is less effective absorption of light
and conversion of vitamin D in our blood.
Generally, this vitamin D level is then travels to the liver
where this metabolize into 25-hydroxy vitamin D.
It then goes from the liver to the kidney
and the kidney turns this in to 1,25-Dihydroxy vitamin D
which is the active metabolite of vitamin D.
The kidney can dispose of 1,25-hydroxy vitamin D.
So it's a bit difficult to overdose on that particular formulation.
The 1,25-hydroxy vitamin D then goes to the bone
where it promotes the resorption of calcium and phosphate
from the bone and into the blood.
Likewise, the 1,25-hydroxy vitamin D, proceeds to the intestine
where it promotes absorption of calcium and phosphate from ingested contents.
Also, remember that PTH has an effect
of increasing 1,25-hydroxy vitamin D conversion in the kidney
and promotes resorption via the osteoclast.
And remember there is a negative feedback loop
where 1,25-hydroxy vitamin D is actually
inhibiting the activity of parathyroid hormone.
Basically all of these activities promote the production
of calcium and phosphorus in the blood
and those two metabolites go on to be important
in both bone mineralization, a variety of metabolic functions
and neuromuscular functions, especially the calcium.
There are a few things that can inhibit calcium
in the blood outside of the system, one is high phosphate levels.
High phosphate levels reduce serum calcium
through simple binding of the two elements together
and deposition in tissues.
Likewise, a low magnesium will inhibit the production of calcium
because magnesium is a cofactor for the function of the parathyroid hormone.
So ionized calcium can be measured,
probably we should stop getting calcium levels
because that will go up and down depending on binding to albumin.
But ionized calcium can be measured
and this is the true amount of calcium in the blood.
Total calcium needs to be corrected if there is low albumin,
because some albumin is binding some of that calcium
and thus the calcium levels maybe off.
In fact we're going to adjust that using a formula.
For every gram that your albumin is low
you should actually correct your calcium up by 0.8.