Cram The Pance - S1E4 Hyperparathyroidism vs. Hypoparathyroidism

Episode Date: January 7, 2021

All of the high yield info you need to know about Hyperparathyroidism and Hypoparathyroidism in less then 10 minutes!►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

All right. So we're going to do, it's going to be a little bit short of a podcast today. We're going to do hyperparathyroidism versus hypoparithyridism. Still two pretty high yield topics. So let's start with primary hyperparathyroidism. So this is going to be caused from an excess pthiroid hormone. So we know pthage regulates the serum calcium in the body by acting on the bones, the kidneys, the intestines to control the amount of calcium released into the body. So in this case, it's, it's an excess. And the most common cause by far is going to be a parathyroid adenoma. That's going to be about 80 to 85% of all of the cases of primary hyperparathyroidism. So that should be your first thought if you see this in a vignette. That's really important to remember. Another important one as well that I remember seeing on a lot of exams throughout school is lithium. That's another big one that can cause this. And then it's also seen in Men 1 and Men 2A in the multiple endocrineoplasia syndrome.

So remember that as well, not as important. but definitely remember the parathyroid adenoma. That's the big one. That's almost all of the cases of this. So what are we going to see in a patient presenting with hypercalcemia? So most patients are honestly asymptomatic. A lot of times it's just an incidental lab finding. But if they do have symptoms, what you should remember, and a lot of times what you'll be tested

on is stones, bones, abdominal groans, psychic moans, and those are the ones you should remember. So stones is going to be kidney stones. Obviously, you have an increased calcium. of kidney stones, painful bones because the PTH is pulling the calcium from the bones. So you can actually have weakened bones. You can have bone and muscle pain. So that's something you'll see as well.

Abdominal groans. Again, PTH is pulling from the intestines as well. So you can have some abdominal pains and different GI problems. Psychic moans is actually because increased calcium changes the monoimmune metabolism and the CNS, which can actually alter the mood and cognition. So sometimes you'll have some. altered mental status in these patients in real severe cases. And then also don't forget, they're also going to have decreased deep tendon reflexes. That's a big one too. So as far as the

diagnosis, what you're going to see is going to be a triad of hypercalcemia, increased ptch and a decreased phosphate. So the increased ptchitis we know is going to lead to hypercalcemia. So that makes sense. Anytime the ptch is going up, you're going to see an increase in the calcium. But why the decrease in phosphate. So phosphate is actually absorbed in the kidneys. And when the PTH goes up, the phosphate actually is excreted that has more, it's excreted more frequently in the urine and through the kidneys. So anytime you see an increase to pt, you're normally going to see a decreased phosphate because PTH is signaling to have it excreted out through the kidney. So if you can remember that, you can remember the triad, the increased PTH and increased calcium makes sense. And then the phosphate is

because the extra clearance. As far as another way you can diagnose it as well besides seeing these things in lab findings, you can also do a 24-hour urine calcium to see the increased calcium in the urine. As far as treatment, in a lot of cases, again, this is going to be from the parathyroid adenoma. So all you're going to do is cut it out. It's just going to be a surgery, a parathyroidectomy. and then also after they have the parathyroid ectum, you need to correct what's going to be deficient now because of actually removing the parathyroid.

So you're going to have to make sure you treat them with vitamin D and calcium. If the patient isn't a surgical candidate, if they're older, if they have a lot of comorbidities, you can use something called synchalcit, which actually inhibits PTH. So synachalcit, it increases, actually tricks the body. So it increases the sensitivity of the calcium. sensing receptors to calcium. So it tricks the body into thinking it has more calcium and thus decreases the PTH. So basically it takes the same amount of calcium you have in the body, makes the body think there's more by increasing the sensitivity and, you know, thereby your

body decreases the PTA because it thinks you're sufficient with your calcium or, you know, even in excess. In real severe cases, somebody coming in with a very, you know, very symptomatic patient, you're going to go ahead and tree with IV fluids and then furoosomide. And if you're Remember, furocimide actually flushes calcium out through the urine through the kidneys. So you'd give them IV fluids and furocimide. So there is secondary hyperparathyroidism. This is going to be associated with renal osteodistrophy. This isn't as important, but you should know it as well.

This is caused from the kidneys failing, for whatever reason it is, chronic kidney failure. But they're not eliminating phosphate. and the increased phosphate can actually is one of the things you'll see. You're going to see an increased phosphate. And then the kidneys also are poorly synthesizing vitamin D. So this is all going to lead to hypalcemia because you're not having vitamin D to convert the calcium. And then you're going to have a compensatory increase in PTA because you have low calcium. How does the body respond by increasing the PTH?

And then, of course, like I talked about before, the body. is not eliminating the kidneys are eliminating the phosphates you're going to have an increased phosphate. So what you'll see in secondary is going to be a decreased calcium because of the poor vitamins, the vitamin D synthesis in the kidneys, a compensatory increased PTH, and then an increased phosphate because the kidneys aren't clearing that. This can lead to osteoporosis. It can lead to bone weakening because the body is trying to increase the PTAH and pull all of the calcium from the bones, trying to compensate. And a lot of times you'll see patients with very frail and weakened bones.

As far as treatment, the way you're going to treat this, it's going to be with phosphate binders to decrease some of the phosphate in the body. And then also you're going to give them vitamin D and calcium supplementation. Moving on to the last topic, you know, not as much to know here, but hypoparthiroidism. The most common cause is going to be secondary to either a parathyroidectomy, some kind of neck surgery. The thyroidectomy is obviously one of the most common causes of this. And then there's also some causes from autoimmune destructions like Hashimoto.

You can see this as well. But the most common cause is going to be post-neck surgery. So something that just had their thyroid removed and then all of a sudden they're deficient in calcium, you need to suspect that it was secondary. It was iatrogenic causes from the next surgery. So as far as the patient presentation, one of the, some of the key things that you should remember is there's a couple physical exam findings that you can see. One is Vostek sign. I don't know if I'm pronouncing that right, but it's C-H-V-O-S-E-S-E.

T-E-K sign. And this is when somebody has a decreased calcium and you tap the cheek, you're actually going to see a spasm in the cheek. Another one is Cotrasso sign. It's when you pump a blood pressure cuff up on their arm and they have a carpopetal spasm with a blood pressure cuff. So when you pump it up above the systolic limit of what their blood pressure is, you're actually going to see the hand spasming. A couple of the things that you can see as well as tetany in severe cases and then some peri-oral numbness around the lips around the mouth. They may have some numbness and tingling around that area. So the increased muscle contraction that we see in hypoparathyroidism from the decreased calcium,

the actual pathophysiology behind this is because when you have decreased calcium levels in the extracellular fluid, you have increased permeability of sodium ions. So this increases the depolarization, increases the action potential. And so this decreased calcium level in the body is causing all of these. these things, the tetany, the Vostec sign, the Trousseau sign, all of these things because of the increased permeability of sodium ions leading to increased action potential. So that's kind of the reasoning behind it. And it may help you to remember that. As far as the diagnosis, again, you're going to look at your triad like you did in hyperparathyroidism. You're going to have a triad

of hypocalsemia, decreased calcium, decreased PTH, again, because remember some of your causes, so if it's a post-neck surgery and the parathyroid area was injured and it's not functioning properly. It's not going to be able to pump out the PTH. And then therefore, your calcium is going to decrease. So hypocalcemia makes sense. Decrease pt makes sense. And then, of course, your increased phosphate in response to that. In your EKG, you may see a prolonged QT interval. And then as far as treatment, it's pretty straightforward. You're going to give them calcium and vitamin D supplements. And then if they're really severe and symptomatic, you can give them IV calcium gluconate. And that's pretty much it for these two topics. I think those are the main things you should know.

pretty cut and dry and straight to the point, but it's one of those things that has some high yield topics and things to remember within there. So make sure you know those and study those and good luck on your exams.