3 Parathyroid Final Edit
[00:00:00] Okay, here we go behind the knife ab site review topic today is parathyroid. So let's jump right into it with some anatomy and physiology. So John parathyroid client, let's talk about their relationship to the recurrent laryngeal nerve as well as the embryologic origin. Talking about the superior as well as the inferior.
Yep. So clinically relevant as well as for the ab site, the superior parathyroid glands are posterior and lateral to the recurrent laryngeal nerve. And from an embryology standpoint, they originate from the fourth pharyngeal pouch. The inferior parathyroid glands are anterior and medial to the recurrent laryngeal nerve.
They originate from the third pharyngeal pouch. The inferior glands can also be more variable in location. And just to note, as we're talking about the third pharyngeal pouch, the thymus also migrates with the third pharyngeal pouch. Yeah, I think what's clinically significant there is, [00:01:00] is, you know, it's a little bit backwards, like the superior parathyroids are from the fourth pharyngeal pouch and the inferior from the third.
But the thing to remember is the inferiors have to migrate farther. So that's why they have a more variable location. And again, that relationship to the recurrent laryngeal nerve is very important to know as well. So Kevin blood supply to the parathyroid glands. Okay. So, this is the inferior thyroid artery, which if you remember comes off the thyrocervical trunk and this is the blood supply to all four glands and 80 percent of cases.
Okay. John, what cells release parathyroid hormone and what is the stimulus to do so? The parathyroid hormone is released from chief cells in the parathyroid. In response to low calcium levels. Yeah. So again, with any of these endocrine chapters, it's really important to understand the physiology.
I mean, what the organs actually do as well as a feedback mechanism. So that feeds into the pathology and having an understanding that is going to help you answer some questions. So [00:02:00] let's talk a little bit about that. So Kevin actions of the parathyroid hormone. Let's, you know, they act primarily on the bone and on the kidney.
So what do they do? So for the bone, it indirectly stimulates osteoclasts for resorption of calcium and phosphate. And in the kidneys, it stimulates resorption of calcium and inhibits the resorption of phosphate and bicarbonate. Always remember that PTH is the phosphate trashing hormone. Yeah, great. So, Trash is phosphate, but it is all also stimulated to be released in low calcium.
You know, its overall goal is to increase calcium levels in the bloodstream. And in addition to the mechanisms that you mentioned it also stimulates the conversion of vitamin D to its active form. Through one alpha hydroxylase and this stimulates absorption of calcium and phosphates in the gut.
So that's also important. It does a lot of things, but understanding those feedback mechanisms are going to be key to answering questions on the outside. So John, how about calcitonin? What is calcitonin's [00:03:00] effect on calcium homeostasis? Yeah. Calcitonin is released from periphallicular C cells in the thyroid.
into response to high calcium. Think calcitonin tones down calcium. In the bone, it indirectly inhibits osteoclast bone resorption. And the kidney inhibits resorption of calcium and phosphate. Okay, great. So let's talk about that's the physiology. So let's move into a little pathophysiology. And again understanding how these work is going to help you understand how things go wrong.
And we do have a good figure in the book that, that explains. Explains some of the things we just talked about, about parathyroid hormone and calcium effect on, on, or I'm sorry, parathyroid hormone and calcitonin effect on, on calcium homeostasis. And a lot of times it's better to visualize those things and to talk through because it can become quite confusing.
But moving on to a pathophysiology. So hyperparathyroidism so what's the most common cause of hypercalcemia [00:04:00] in the outpatient and inpatient settings, Kevin? So in the outpatient setting, it's primary hyperparathyroidism and in the inpatient setting, it's malignancy. Great. Outpatient, primary hyperparathyroidism.
Inpatient, think malignancy. John, what's the mechanism of hypercalcemia due to malignancy? Yeah, you need to think about the production of PTH related protein. And this is common in squamous cell lung cancer as well as breast cancer. And less commonly hypercalcemia and malignancy can can be from lytic bone lesions.
Yeah, that's, that's important to remember that again, that parathyroid hormone related protein a lot of times you would, you would think it's due to calcium or to bone reabsorption or, or lytic bone lesions, but it's really that, that, that parathyroid like protein. protein and thinks way muscle lung cancer and breast cancer.
When you see that John, what is the presentation and management of a hypercalcemic crisis then? Yeah. So the presentation of this is nausea, [00:05:00] vomiting, abdominal pain, constipation, weight loss, bone pain, fatigue, weakness, and neurologic changes. The management of this all stems around fluid resuscitation such as normal saline around 300 milliliters an hour and once you're euvolemic, you consider Lasix.
Okay, so you said normal saline, yeah, I agree, 300 an hour, so a high rate. For Hypercalcemic crisis, but why not? Lactated ringers it's controversial, but LR contains calcium. Yeah. Okay. So, best to avoid lactated ringers, especially on exams for hypercalcemic crisis, normal saline, three oh an hour.
And then diuretics once Euvolemic or Kevin. What are the three different types of hyper hyperparathyroidism? Okay. So this is one of those things that you just kind of have to review every once in a while. So the primary hyperparathyroidism is the most common, and this is related to abnormal gland function or excess PTH.
Then you have your secondary hyperparathyroidism. And this is a excess PTH secretion [00:06:00] due to hypocalcemia, usually related to renal failure. And then you have your tertiary hyperparathyroidism in post renal transplant patients. And so they've had longstanding parathyroid stimulation from preoperative hypocalcemia results in autonomous PTH secretion once they have that new kidney.
Okay, great. Yeah. Good description. Primary, secondary, tertiary, hyperparathyroidism. How about the most common cause of say primary hyperparathyroidism ketamine? The most common cause is from an adenoma 80 to 90 percent will be a single adenoma versus 2 to 5 percent will be a multiglandular adenoma.
Yeah, exactly. So most commonly an adenoma most commonly a single adenoma but certainly there can be also hyperplasia about 10 to 15 percent of the time. Parathyroid cancer can result in primary hyperparathyroidism and there's a much higher prevalence in MEN1 and MEN2A as well. So John, laboratory test, what do we [00:07:00] use to work up and diagnose hyperparathyroidism?
So obviously you're going to check a serum calcium level, which will be elevated in hyperparathyroidism. You also want to check a serum phosphate, which will be decreased, except for patients who have renal failure and they can't waste that phosphate. You want to check a serum PTH, which will be elevated.
The normal level is between 5 and 40. Serum chloride to phosphate ratio will be greater than 33. And also you want to check a 24 hour urine calcium and that would also be elevated. If it's, if that 24 hour urine calcium is less than 100, you want to consider familial hypocalceric. hypercalcemia.
Yeah, of course. Never forget about familiar hypocalceric hypercalcemia. And of that, what is the most reliable way to diagnose hyperthyroidism? And which test is most frequently used? Great question, Jason, that would be your chloride phosphate ratio. Okay, great. And so, you know, we're dealing with patients that most commonly are incidentally found to be hypercalcemia.
And [00:08:00] we're trying to figure out why, again, like Kevin said, most likely we're dealing with an adenoma. So now we're trying to work that up. So let's say, you know, we're thinking that maybe there's an adenoma. So what studies can we be used to localize this adenoma, Kevin? So, yeah, there's a few imaging modalities, ultrasound system, maybe scans and a 40 CT scan, but generally you're going to start with a system, maybe scan plus an ultrasound, which allows for evaluation of concurrent thyroid disease.
Okay. Is there anything else? Anything say more invasive? Yeah. So, you can do angiography with venous sampling for PTH gradients. This is typically reserved for reoperative or otherwise complex patients. Great. Yeah. So for most people are going to start with a cestamib scan and an ultrasound. There are institutions that are going to that for DCT, but I still think probably the best answer on the outside would be cestamib and ultrasound.
What's the management of hyperparathyroidism and who should undergo a parathyroidectomy? John. Yeah, so parathyroidectomy is the only long term [00:09:00] treatment for hyperparathyroidism. You can consider a minimally invasive or single gland parathyroidectomy for localized disease on your preoperative workup, or you may need to do a three and a half or four gland expiration for non localized disease.
Yeah. So I think what you're saying there is we're dealing with symptomatic patients. So all of these symptomatic patients should undergo some form of parathyroidectomy, whether that's a single adenoma you do your localization and you can confirm that interoperatively and get your drop. And then you're done for, for multiple adenomas or.
Hyperplasia, then you can talk about doing a, you know, a subtotal or three and a half and four gland with re implantation. It's getting a little bit into the weeds there, but yeah, I think a good general rule there is definitely symptomatic patients should undergo a parathyroidectomy. And it gets obviously more complicated from there.
So, Kevin let's talk about asymptomatic patients. Are there any criteria for When asymptomatic patients with just an incidentally noted to be hyperparathyroid when they should undergo a parathyroidectomy. [00:10:00] So yeah, if they're serum calcium is greater than one milligram per deciliter above normal, that would be an indication.
Also, if they have any renal disease such as nephrolithiasis or hypercalciuria, or if they have a decrease creatine clearance GFR less than 60. Also, if they have any bone loss, if they're. I have evidence of osteoporosis with a T score less than 2. 5, negative 2. 5. or if they're really young, so if their age is less than 50 or they have poor access to care follow up, these would all be reasons to do a parathyroidectomy.
Yeah. So basically any sequela of having a high parathyroid hormone it seems like you're just looking for an excuse to do it. But yeah, those are, those are the well established criteria that would make asymptomatic patients meet the criteria for prepare a thyroidectomy. Intraoperatively we mentioned it briefly, but John, how would you.
Confirm that you had resection, you had adequate intraoperative resection of a parathyroid adenoma. How do you confirm that? Intraoperatively? Yeah, you do an intraoperative PTH so you use a dual [00:11:00] criteria, which is the most sensitive, so you need to draw APTH prior to the start of the operat. But what you're looking for after you move the adenoma, you get a 50 percent drop from the pre incision value at 10 minutes after the resection.
And that, and that 10 minute value should be close to normal. Okay. Excellent. Yep. You're looking for that 50 percent drop in 10 minutes intraoperatively. Kevin, how do you treat multi gland parathyroid disease? So briefly mentioned this, but you can do a three and a half or four gland parathyroidectomy with re implantation into the SCM or brachioradialysis.
Okay. I can stay in with Kevin there. So you talked earlier about secondary hyperparathyroidism. Remind us quickly what that is and what the management is. So that's when you have hypocalcemia from your renal failure. And so you're having excess PTH secretion. And so really you can treat this just with calcium and vitamin D supplements.
You know, a quote unquote renal diet and phosphate binders. Okay. John tertiary hyperparathyroidism. So this is once you, you have that longstanding [00:12:00] kidney disease, you know, maybe you get a kidney transplant and, and now you're repair thyroids are all amped up and they start you, they're producing excess PTH.
So what's the management for tertiary hyperparathyroidism? Yeah, you would go to a three and a half or a four gland parathyroidectomy with auto transplantation. Okay, great. Okay. Kevin parathyroid carcinoma. So in what patients would you be concerned for parathyroid cancer? And how do you approach that?
Yeah. So this is a very rare form of a primary hyperparathyroidism. They're going to have very high levels of calcium, like greater than 14 milligrams per deciliter. They may have a palpable neck mass. You're going to evaluate them the same way with a neck ultrasound and a system ED scan. And the management of this is an in block resection and may require resection of ipsilateral thyroid.
And then if you have evidence of lymph node involvement, you wanna do a ipsilateral neck dissection. Okay. What about you know, bad situation, you have recurrence or, or [00:13:00] metastasis of of an aggressive parathyroid carcinoma? Yes, you can do palliative surgery and use some calcium lowering drugs such as bisphosphonates or calcium emetics and then chemo and radiation therapy.
Unfortunately, are rarely effective. Yeah, you're in a bad situation there. Okay, so let's move on to our quick tips for the day. So john, a patient with a high normal range serum, calcium and elevated parathyroid hormone with evidence of bone loss. What's the diagnosis? Yeah, so this is normal calcemic hyperparathyroidism.
It's early primary hyperparathyroidism. And you would do surgery if it's symptomatic. Okay, Kevin? Electrolyte disturbances found with hyperparathyroidism. You can see hyperchloremic metabolic acidosis. PTH results in bicarb excretion from the kidney. And you'll also see hypophosphatemia with significant renal impairment.
Phosphate may be elevated. Okay, John, so you have a patient with an elevated parathyroid hormone, elevated calcium and low urinary calcium. What's the diagnosis and management? Yeah, this [00:14:00] is the benign familial hypercalceric hypercalcemia. And the treatment for this is observation. Okay Kevin.
Surgical treatment of primary hyperparathyroidism in a patient with MEN1 or MEN2A. So this would be the three and a half or four gland resection of autotransplant and the thymectomy. Okay. And what's important to remember there and you have to watch for is there's a frequently with the ectopic and extranumerary glands so you have to watch for those with that as well.
John, doing a neck exploration for hyperparathyroidism, you find three normal glands and cannot identify a superior gland. Where should you look next? Yeah. The next spot you should look is the retro esophageal space, and then you want to go to the carotid sheath if you can't find it. Okay, great. So again, we're thinking about where is a superior gland if we can't find it, and that's most commonly, as you say, the retro esophageal space or the carotid sheath.
Now, Kevin, alternatively, you're doing your neck exploration, find three normal glands, but this time you can't identify that inferior gland. So where [00:15:00] should you look for that? You can look in the ipsilateral side of the mediastinal thymus, and you should also consider intrathyroid gland. Yeah. So remember that that inferior thyroid gland had to travel further during embryology, so it has a more variable location, but those are absolutely the right places to look, most commonly the thymus.
And consideration of an intrathyroid gland, which intraoperative ultrasound can be helpful there. So, let's see, John you identify, this time you identify four normal appearing glands but your intraoperative PTH remains elevated. Yeah, you need to consider a hypersecreting supernumerary parathyroid gland.
Once again, this is most commonly located in the thymus, and you would, if you, Our concern that it isn't a thymus, you perform a thymectomy. Yeah. These can be very frustrating and challenging. And sometimes it even requires you to close and do more localizing tests and coming back and fighting another day.
So that can be very challenging. Kevin, what's the most common location of a missed gland? That would be the [00:16:00] normal anatomic position, right? It's a little bit of a trick question But sometimes they ask that if you can't find it the most common places, it's in the right place. You're just missing it John what's the most common location of an ectopic gland?
Yep. So once again the thymus Okay. Yep. Thymus is the most common location, which is the reason for that recommendation to perform a thymectomy sometimes if you can't find it. Okay. That does it for our quick hits and that does it for our review of parathyroid for the ab site. Thanks again for listening.