Episode 297: Keywords part 29: PE and Parathyroid
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Hello, and welcome back to ACRAC. I'm Jed Wolpaw, and I am thrilled to have back with me the one and only Dr. Tim Kais-Turra. He is, as frequent listeners will know, now doing the keyword podcast with me, and we have another one for you today. So we are going to cover pulmonary embolism and parathyroid disease, and I am thrilled to have him back to do it. Tim, welcome back to the show. Thanks so much for having me again.

All right. So let's jump in. Where should we start? I'd like to knock out pulmonary embolism first, and then we'll do parathyroid disease. And both of these are from the advanced outline for pulmonary embolism. It's under the advanced topics in the organ based advanced clinical sciences section under cardiovascular disease.

And pulmonary embolism. And what I really like about this portion of the outline is that it sort of tells us everything we need to know about pulmonary embolism. So it is 0.7 pulmonary embolism and its subsets are A, etiology, blood, air, fat, amniotic fluid.

B, diagnosis and TE findings. And C, treatment, both acute and preventative. So the nice thing about this topic is in terms of studying for the exams, it tells us exactly what we want to know, unlike some other topics. I feel like we could almost skip the key concepts and knock this entire section out with just that list and some questions. But for the sake of tradition, we'll get some key concepts in.

Key concept one is going to be that pulmonary embolism results from the entry of blood clot, air, fat, and neotic fluid or foreign material into the venous system. The most common cause is blood clot from the lower extremities, and in these cases, venous stasis and or hypercoagulability often contribute.

Risk factors for those things include but aren't limited to long surgical times, immobility, postpartum state, fracture or surgery on the lower extremities, et cetera. I think one of the tricky things with pulmonary embolism is that it's a term that we use both broadly to mean all of these type of embolic events. And then colloquially, at least in medicine, sometimes we just mean specifically thromboembolic events. So we'll just keep that in mind as we do some of the questions.

Key concept two, embolic occlusion of the pulmonary circulation increases dead space, which can cause hypercarbia and hypoxemia. There's an increase in pulmonary vascular resistance from the emboli, which can result in acute pulmonary hypertension and right heart failure in susceptible patients. And if occlusion is large and the bronchial circulation doesn't compensate, pulmonary infarct can result.

Clinical manifestations include sudden typicnea, dyspnea, chest pain, and or hemoptysis, with symptoms usually being nonspecific or mild unless massive embolus has occurred.

And the third key concept in this little section is that the gold standard diagnosis for pulmonary embolism is via CTA or computed tomography angiography. VQ scans can be used if CTA is contraindicated. An echocardiography can be useful to visualize clot in the pulmonary artery or the right heart. This would be if it's thromboembolic disease or to diagnose potential sequelae of massive PEs such as right heart failure.

All right. So that knocks out etiology, diagnosis, and T findings. Any questions about that, Jed? No, I think that's great. I, you know, I would say that the most common thing I think these days that you're going to see is

on exams, and honestly, I think probably both oral and written, is with a PE in terms of echo findings is going to be the right heart failure. And as we get further on, there's more and more specifics, I think, that are fair game about not just saying I would see it, but what are the signs of heart failure you would see on echo findings.

And so I think that's going to be really more and more prominent as Echo and Pocus becomes a bigger piece of our practice. Awesome. So let's do some questions and see if we can come across anything like that.

Question one, a patient in the post-anesthesia care unit with a normal VD-VT ratio of 30% suffers from a pulmonary embolism with an increase of their VD-VT ratio to 60%. So their dead space has increased. To maintain constant alveolar ventilation, the patient will compensate by doing which of the following? A, decrease their tidal volumes. B, increase their respiratory rate. C, maintain their current tidal volume.

Great. So the key here is knowing what a VTV, a VDVT ratio is, right? So if you don't know that, uh, you can probably try to think this through. It's a lot easier if you know it. So what it is is the portion of your tidal volume that is dead space ventilation. And, uh,

Normal-ish is around 30%, right? Because, for example, just to make an obvious example, the air in your trachea obviously does not participate in ventilation. Neither does the air in your main stem bronchi, et cetera. So there's a portion, about 30%, of each tidal volume that is dead space. That's normal. But you have to know that and then know that, therefore, it increased to 60%. If you didn't know that, then you could try to think this out by saying, well, it's a pulmonary embolus.

I don't really know what this VDT, VDVT ratio is, but I do know, hopefully you should know that a pulmonary embolus does increase dead space. And so maybe that helps you figure that out. Or even if you just knew it's a PE, what tends to happen in patients with a PE, they do increase their respiratory rate. And then the reason is what's laid out in this question, which is that they have increased dead space. And so to maintain their CO2, they have to breathe more frequently because the portion of their tidal volume that participates in ventilation has decreased.

Exactly. So the answer is B, increase their respiratory rate. And this is one of the ways that the testers can sort of get at the mechanism or pathophysiology of pulmonary embolism. For question number two, immediately following a sympathetic block for pancreatic cancer pain, the patient is found to be in respiratory distress and hypoxemic.

The most likely causes, A, pulmonary embolism, B, pneumothorax, or C, unilateral diaphragm paralysis. Yeah, so this I think could be a little tricky. Part of it depends on how well you know what block is probably being done for pancreatic cancer pain, which is a celiac plexus block, and then what the potential complications are. That's good to know because that can come up in a lot of different types of questions that they're testing, even if it's directly testing your knowledge of these blocks.

So knowing that that's true and knowing that if the needle is directed too much towards the head, that you can get a pneumothorax is important to know. So that would help you certainly. But if you didn't know that, it can be a little tricky. They give you a patient who has pancreatic cancer. You may be thinking, well, I know patients with cancer have a higher risk of pulmonary embolus. So that might push you that way. You may be thinking about upper, about pancreatic.

neck blocks um like uh i keep wanting to say celiac plexus but what am i trying to say to him uh brachial plexus yeah brachial plexus blocks uh knowing that you can get diaphragmatic paralysis from hitting the phrenic nerve and so you may uh you may go that way but you know if you remember that this or pancreatic cancer the most common blocks is going to be a celiac plexus block and that a potential complication is a pneumothorax then um that would help you here the other thing is that uh

The they really aren't giving you much else, right? You could imagine this question where they might give you some other things that might help eliminate one or the other, but all they're giving you here is respiratory distress and hypoxia. And that could go along with PE or pneumothorax. It'd be unlikely, actually, with a unilateral diaphragmatic paralysis to have that unless the patient was starting off with really poor respiratory status. So that might push you a little bit away from C.

Yeah, I think all of that's perfect. I won't rehash any sort of complications about the celiac plexus block, but you nailed all of those things. But this question is here to point out that the other place that pulmonary embolism shows up on tests over and over and over is as a distracting answer. It's commonly tested, and it's also a great distractor answer. So we'll see in a few places where it's just not the answer as well.

Number three, a patient in the cardiovascular intensive care unit is recovering well two days after an aortic valve replacement. He is extubated and requires no hemodynamic support, but due to poorly controlled pain has not been out of bed.

You are called to resume by a nurse who found the patient tachypneic, hypotensive, tachycardic, hypoxic, with obvious jugular venous distension. Which of the following echocardiography findings is most likely in this patient? A, aortic insufficiency, B, mitral regurgitation, or C, tricuspid regurgitation?

Great. So the one thing that really stands out to me here is jugular venous distension, because left-sided issues like aortic insufficiency or mitral regurgitation really should more cause issues with potentially pulmonary edema, but not with jugular venous distension, which is really a right-sided issue. So if that's all you saw and all you knew, then you should be able to get the right answer here, which is tricuspid regurgitation.

Tim, as a cardiac anesthesia fellow, I'm going to let you explain a little more about what might be happening here and then how all these other symptoms and signs might fit in. Absolutely. So I think what this question is doing is just trying to sell you completely that you should know that this is a pulmonary embolism. You've got all the symptoms.

of a massive PE, the tachypnea, the hypotension, the tachycardia, the hypoxia, and then they give you the obvious jugular venous distension as a way to tell you it's so massive that you have right-hearted failure, which is why you're getting jugular venous distension.

And then what you need to figure out is what might you see on an echo with right-sided heart failure. And if your right heart dilates, you may have dilation of a tricuspid annulus leading to regurgitation. You may see, if they ask you about tricuspid annular plane excursion, you may see that that's decreased dilation.

Or just sort of a hypokinetic, akinetic, or dilated right heart. Those would be sort of the echo findings that they'd look for for a massive PE. Yeah. So I think that's really key is the connection here that it's right heart failure of whatever cause. In this case, probably a PE, but, you know, right heart failure. And again, this is how they get tricky. They don't –

tell you anything that's specific, like an echo finding or a large right heart, they're giving you some symptoms. Then they're giving you what could, they're not asking you to say if it's right heart failure. So you have to take another step. They're asking you what is a result of right heart failure. But then you have to know the tricuspid regurgitation can come from right heart failure. So it's a little bit of a multi-step trickier question, but I think it covers a lot of important stuff. The other thing I would say is that

You know, remember, don't get – I see sometimes people kind of get in their own heads because they might see this and think, oh, it's tamponade, right? And this could be tamponade, but that's not an answer. And so what I see some people do, and this is something you want to work on if you have trouble with test taking, is you say to yourself, oh, it's tamponade. Then you don't see tamponade, and you kind of panic, and you think, oh, my goodness, I don't know what it is because it's not the thing I thought. And that's okay. These questions are not saying that it –

can't be tamponade. It's just they didn't give you that choice. So then you have to think about what else it could be. So don't worry if you think it's something and that isn't a choice. Just then kind of reset and think what else could be going on. Exactly. And we've talked about that before. It's good to sort of try to answer the question before you look at the answer stems, but don't worry if it's not there and just pivot. Try to use the answers to figure out what it could have been if it wasn't what you predicted it was. Yep.

Question four, a 24-year-old male is undergoing craniotomy for tumor resection in a sitting position. While the surgeon is sewing through the calvarium, you notice white, dry bone without bleeding, shortly followed by high-pitched sounds on precordial Doppler and hypotension on the monitors. Which of the following would be expected with venous air embolism? A, an increase in N-tidal nitrogen, B, an increase in N-tidal carbon dioxide, or C, a decrease in central venous pressure?

Great. And here's another good test taking tip. You didn't need any of this except the very last question of the very last sentence of the of the question stem. Right. So it's a good idea, especially with longer questions. And this one wasn't that long, but just as a good point to read the last sentence first, because here they tell you what it is.

It's a Venus air embolism, right? You don't, who cares what the presentation is. You don't want to read this and get caught up on this dry white bone. What's dry white bone. What does that mean? Right? That would be a waste of your time. You already know they're telling you. So that happens. Sometimes they give you this full long stem. Maybe they give you some lab values, all kinds of stuff you can waste your time on and you don't need it. Now, sometimes you do need it, but you might as well figure that out first. Just read the last sentence, see what they're asking. And then you may or may not need to go back and look.

All right. So they tell you it's a Venus air embolism. And then the question is, what would you expect? So,

It is a little, maybe people aren't quite used to thinking about end tidal nitrogen. It's not something we talk about all the time and we'll get to why that's the right answer. But let's look at the other ones first. An increase in end tidal carbon dioxide. So no, right? You're going to have, when you have a venous air embolism, just like a pulmonary embolism, you have a blockage of blood getting back to the, getting out, getting to the, to the alveol, through the alveoli and therefore carbon dioxide getting into the alveoli. And so while you will have an increase in

Pa CO2, you actually have a decrease in end tidal CO2 because it can't get out, right? At least as much as it was. And then central venous pressure, again, will increase because you have now a blockage to blood flow through the lungs. So that blood pressure, that pressure will back up and you'll get an increase in central venous pressure.

Depending on how big the air embolus is, it certainly won't decrease your central venous pressure. Now, why is the correct answer an increase in end tidal nitrogen? The answer here, first of all, is that this only works if you're not ventilating the patient on room air, but we hardly ever ventilate on room air in the operating room. So this question really ideally would say, you know, ventilating a patient on 50% oxygen and, you know, whatever, or they would give you the, or they'd say isonitrous or whatever it is.

But I think here you have to assume that we almost never use room air in the operating room. So the reason that it has to be more oxygen than just room air is that if you are not on room air, you are therefore ventilating on less than the normal amount of nitrogen by definition, right? If you have 21% oxygen, you're

making the numbers just a little easier. And 79% nitrogen is not quite that, but let's just say 20% oxygen, 79% nitrogen is room air. If you're using, let's again, just make it easy, 50% oxygen. Now you only have 50, now you have 50% nitrogen instead of 79% nitrogen.

If you get some air bubbles in the blood and they then get into the alveolus and therefore some of that air will get into the exhaled gas, you now have more nitrogen because those air bubbles are air. They have 79% nitrogen. And so that will increase your end tidal nitrogen from 50% to something higher than 50%.

In the scenario I just laid out. So that's the reasoning. Again, you didn't necessarily even need to know any of that as long as you could think through why B and C were not correct. But that's why an increase in end tidal nitrogen is consistent with a venous air embolism.

Perfect. And I think we can add here that if you are running isonitrous and you're concerned about an air embolism, please turn off the nitrous. Nitrous oxide is contraindicated in the presence of air embolism since it can make the air embolism much worse by expanding it. Absolutely. And in fact, do yourself a favor, Google the graph

of the increase in size of an air embolism in the presence of nitrous, it is amazing. It is an exponential increase. And so if you truly do have an air embolism and you don't turn off your nitrous, it can be fatal very quickly. Question five. A young male is brought to the emergency department following a motor vehicle collision. He has obvious bilateral lower extremity deformities. He is very confused and oxygen saturation is 89%, so the decision is made to intubate.

When listening to breath sounds after intubation, someone notices a particular rash on his chest. The most likely diagnosis for this patient is A, fat embolism, B, air embolism, or C, pulmonary embolism.

Great. So here, right, even though this is a polytrauma, there's lots that could be going on. They're just asking, they're telling you this is an embolism. What kind is it? Or most likely is it? So certainly an air embolism would be very unusual in this situation.

Pulmonary embolism is certainly possible, but they're giving you a petechial rash on the chest and they're giving you what sounds like bilateral femur fractures. They don't specifically say femur. I guess it could be tibia fibia, but it could be femur. And so in the presence of long bone fractures and a petechial rash, that's they're trying to push you to fat embolism. And so that is probably your best answer here.

Agreed. And this is also just a good place to point out again that the nomenclature here is a little bit confusing because C is technically correct as well in that a fat embolism is a type of pulmonary embolism. But generally when you see pulmonary embolism like this, you're talking about thromboembolic embolism.

embolism. And you definitely have a better answer, more specific answer, which is a type of pulmonary embolism, the fat embolism that is probably causing most of those symptoms.

The last thing we need to cover here then for pulmonary embolism is treatment, both preventative and acute. So key concept four, the best treatment for perioperative pulmonary embolism is prevention. The most common approaches include early mobility, DVT prophylaxis with low-dose anticoagulants, and intermittent pneumatic compression stockings.

In key concept five, acute treatment of pulmonary embolism is largely supportive. Additionally, considerations can be made for aspiration of air via central line in the setting of air embolism and cessation of nitrous oxide if in use, like we talked about.

The use of anticoagulation to prevent extension of clots and thromboembolic events, thrombolytic therapy in the setting of massive thromboembolic PE or pulmonary embolactomy, if that's contraindicated, and then AOK therapy in the setting of amniotic fluid embolism, which stands for atropine, undensitron, and ketorolac. And I haven't quite seen that tested yet, but the literature is growing, so that might start showing up. Right.

All right, right into the last set of questions for pulmonary embolism.

Six, a 28-year-old female is undergoing a C-section under spinal with 12 milligrams of bupivacaine, 25 micrograms of fentanyl, and 0.25 milligrams of preservative-free morphine. While the placenta is being separated, the patient states she is short of breath and has numbness in both of her hands. Her oxidation saturation is 100%. The most likely cause of her shortness of breath is A,

A amniotic fluid embolism, B anxiety or C high spinal. Great. Well, one good lesson here is I cannot imagine a situation where the right answer is to describe a laboring patient as too anxious. That is definitely never going to be right. Um,

If they're describing a patient pre-op who is, you know, nervous and they're trying to get at, would you give Versed or something, that's different. But that should, you should immediately say, there's no way they're having this anxiety here. So that really takes you to whether the amniotic fluid embolism or a high spinal. And with an amniotic fluid embolism, you would not be setting 100%. So I think putting those two together,

seems most likely that this is a high spinal. And again, I wouldn't get into thinking to yourself, well, you know, that seems like a reasonable amount of stuff to put in a spinal. You know, again, we don't know how, they don't tell us anything about her size, right? She could be four feet tall. We don't know. And again, different people have different response, different epidural space sizes, and it's under compression because she's pregnant. There's a lot of reasons why

She could have a high spinal, whereas with the same dose, someone else might not. But don't get thrown by that. Just think to yourself what actually makes sense given what they're giving me here. Exactly. And just another great example of embolism being a distracting answer.

Question seven, a 34-year-old, 170-kilogram female presents for elective open gastric bypass surgery given her high risk for development of deep vein thrombosis. Which of the following is most appropriate option to prevent a venous thromboembolism? A, early ambulation after surgery. B, 5,000 units of subcutaneous heparin once prior to surgery. Or C, 17.5 milligrams of subcutaneous enoxaparin prior to surgery and then every 24 hours.

So it's a little bit of a tricky question because you might say, oh, you know, I don't, I think they kind of all are helpful unless you realize that that is a ridiculous dose of enoxaparin. I don't know where they came up with that. But so, but also this is kind of like,

And if they're asking what's the best delirium prevention and they give you a bunch of medications and then they say, you know, non-pharmacologic treatments, right? They are going to want you to recognize that these non-pharmacologic treatments are really important. And so have that in the back of your head. So early ambulation, first of all, is super important and is the best prevention.

Right. That's part of why we don't send patients on subcu heparin when they go home, as long as they can walk and do normal things. So that's definitely the right answer for a lot of reasons. But also just looking at the other ones, it would have been even trickier if they said 5000 units of subcu heparin every eight hours, starting once before surgery and then continuing every eight hours after surgery. That would be tricky because that is helpful.

Probably not quite as much as early ambulation if I had to pick, but that would make this a much harder question. And then similarly, if they had said, well, if they had said 40 milligrams of sub-Q enoxaparin prior to surgery and then daily, that would have been an interesting choice to give it prior to surgery. But if you did it and then continued it post-op, that would be helpful. This 17.5 milligrams is much too low of a dose, and I don't know where they came up with that, but that disqualifies it.

Yeah, I'm not sure about the exact dosing there. They may have just tried to...

Under dose of like, if you were dosing at one milligram per kilogram, this would be one-tenth of the dose at 0.1 milligrams per kilogram instead. And I agree with what you said. It's sort of, they're hard to pick apart. And sometimes it's hard to say that the answer is the easy, obvious thing. But sometimes the easy, obvious thing is clinically the right answer. And it's also the test answer. And here it's just early ambulation. Yeah.

All right. Anything else you'd like to talk about in pulmonary embolism before we move on to parathyroid disease? I think we covered a lot of good stuff. I would just say again that the echo things that you're going to see the most are signs of right heart failure. So think about an enlarged right heart. Think about a poorly squeezing right heart. Think about a D-shaped

left heart, right, with a right heart septum bowing into the left heart. And these are all things that are going to come up more and more as signs of right heart failure or right heart strain. So really, those, I think, are really important to be aware of and then to think it could be a question that has nothing to do with the PE, right? It just could be right heart failure for any reason. But it's really common for them to ask about

P.E. leading to right heart failure. And again, now they're going to ask not just is it right heart failure, but what are the echo signs of it? And so just make sure you're you're comfortable with those. Those are going to come up on potentially oral boards and certainly on your written boards.

All right, let's move on to parathyroid disease. Like we said, also in the advanced topics, it's also in the organ-based advanced clinical sciences section in endocrine and metabolic systems under clinical science.

clinical science parathyroid disease. And here they tell us a lot less specifics than pulmonary embolism and what we need to know. They just say parathyroid disease, and they say one hyperparathyroidism in physiologic effects and two hypoparathyroidism postoperative manifestations in treatment. And this is tucked right away in between thyroid disease and adrenal disease, which we've covered in the past. So we're filling that portion of the content outline nicely, which is pretty satisfying.

I think the best way to approach parathyroid disease is to break it up into three portions, the actual clinical or basic science aspect of it. And then separately, we'll talk about the two common dysfunctions, the hyperparathyroidism and hypoparathyroidism. There's not a lot of variety in what's tested regarding parathyroid hormones. So the questions will overlap the topics a little bit, but that also means we've got some repetition, which is great for learning. Stay with us. We'll be right back.

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All right, and we're back. Okay, so the parathyroids are small glands bilaterally on the thyroid with superior and inferior portions. They secrete parathyroid hormone, which itself has a very short half-life. And when you think of a parathyroid, I just want you to think of calcium. I want that link to be in your head very strongly. That brings us to key concept one,

Parathyroid hormone, or PTH, is the principal regulator of calcium homeostasis. It increases serum calcium directly by promoting resorption of bone and limiting renal excretion of calcium, as well as indirectly by stimulating vitamin D synthesis in the kidney, which enhances gastrointestinal absorption. So more PTH equals more calcium, less PTH equals less calcium.

Then there's also calcitonin, which counters the effect of PTH and decreases serum calcium levels. It also has multiple mechanisms of action. It affects absorption and resorption and osteoblast and clast activity. But we won't see that too much in these questions.

E-concept two, PTH decreases serum phosphate by increasing its renal excretion. And in medical school, someone once called PTH phosphate trashing hormone, and I've never forgotten this association with phosphate before. So anyone's been forgetting that one? Yeah, I was taught the same thing, Tim, and I've never forgot it. Phosphate trashing hormone. Yep.

And then key concept three, 99% of calcium is in the bones. Of the calcium that is in the blood, 40% is bound to proteins and 60% is either ionized or complex to organic ions. And the unbound ionized calcium, which is about 45% of what's in the blood, is physiologically the most important fraction.

Any questions or something to add about those key concepts so far? No, I think that's really key. You're right that this is so tied to calcium. And, you know, that is those questions, as I think we'll see here, the questions about parathyroid hormone, about hypo and hyperparathyroidism are often going to have to do with calcium.

All right, let's dive in. Question one, you see a patient with a hyperfunctional benign parathyroid adenoma in your preoperative clinic prior to a scheduled parathyroidectomy. Which of the following sets of lab results would be most likely in this patient? A, increased serum parathyroid hormone, increased serum calcium, and decreased serum phosphate.

B, decreased serum parathyroid hormone, decreased serum calcium, and increased serum phosphate. Or C, increased serum parathyroid hormone, increased serum calcium, and increased serum phosphate.

Great. So you've got a patient with a hyperfunctional tumor. They're going to be hyperparathyroid. And so you hopefully know that they're going to have increased parathyroid hormone. So you can immediately get rid of B. And then you have to remember to think about calcium. But both of those, both answers A and C have increased serum calcium. So now your comes down to the phosphate. And so it's going to be either B.

decreased or increased. A is decreased and C is increased. And so hopefully you remember phosphate trashing hormone and you will realize it has to be answer choice A because that says decrease serum phosphate. Perfect. Phosphate trashing hormone. You'll never forget.

Question two, a patient with a hyperfunctional benign parathyroid anemoma has undergone a successful parathyroidectomy with no apparent intraoperative complications. Which of the following is standard of care postoperatively for this patient? A, phosphorus infusion for at least 14 hours, B, intermittent monitoring of calcium with repletion as necessary, or C, intermittent monitoring of potassium with repletion as necessary?

Great. So if you're taking care of these patients, you know right off the bat that we monitor calcium and replete and that they often can be hypocalcemic and do need repletion.

If you didn't know that, then phosphorus infusion, you know, you might think, well, let's see. We talked about how parathyroid hormone is phosphate trashing hormone. But remember, they've had the parathyroidectomy. So the issue is no longer having too much trashing. It might be not having enough trashing, but certainly automatically infusing phosphorus for 14 hours is extreme and would not be the right answer. And then potassium, right?

other than routine monitoring we do for all patients, tends to not be an issue in these patients. It really comes down, as we said, to calcium. And so the answer is B, you are going to intermittently monitor calcium and replete as needed. Exactly. And that's just sort of just an example of the question where you have to think just one step further than just naming the electrolyte abnormality that might happen and talk about how you treat it or how you'd monitor for it. Okay.

Question three, which of the following regarding measurement of PTH levels in the setting of parathyroidectomy is most correct? A, postoperative PTH levels do not correlate with postoperative calcium levels. B, measurement of PTH is not required perioperatively. Or C, measurement of PTH is performed intraoperatively to determine whether adequate parathyroid tissue has been excised. Great. So...

One thing that's important to know is you might think to yourself, and they don't give it to you as an answer choice here, but what if they said, in addition, they had a fourth choice that said measurement of calcium is performed intraoperatively to determine whether adequate parathyroid tissue has been excised. You might say, well, that sounds, I mean, we talked about calcium and how they're related.

It's important to realize that parathyroid hormone has a very fast, very rapid half-life, while calcium has a longer half-life. And so we don't monitor calcium intraoperatively because it wouldn't help to check calcium every five minutes. No matter what was happening with the parathyroid hormone or the parathyroid levels, the calcium wouldn't change that quickly. But parathyroid hormone has a very, very fast half-life. And so you can actually check it every five minutes and see declines if they're getting parathyroid tissue out of the body.

And so we do, in fact, measure parathyroid hormone intraoperatively. And that is able to see how much parathyroid tissue they have gotten out. And so that is, again, if you've done these cases, you've done these, you've done this, you've drawn the labs every five minutes, and you've been able to see this. But that's the right answer. They absolutely...

do parathyroid hormone levels do correlate with calcium. So we can get rid of a, and I'm saying measuring parathyroid hormone is not required perioperatively. Again, that's a little tricky. We tend not to necessarily measure it routinely postoperatively because we're doing calcium, but perioperatively includes intraop and we do measure it intraoperatively. Perfect. Yeah. I think the key thing that's being tested here, even if you haven't done these, you can get to the right answer just by knowing that that half-life is really short.

And for the most part, from an exam standpoint, that's what you should expect regarding knowledge of a parathyroid pathway. More PTH is more calcium and less phosphate, and less PTH is less calcium and more phosphate. So let's dive a little more into what else happens clinically with too much PTH.

Key concept four, hyperparathyroidism can be either primary, which is secretion of too much PTH from gland tissue, such as with parathyroid adenomas, hyperplasia of a parathyroid gland, and some carcinomas. Or it can be secondary when it's from a normal parathyroid tissue in response to low levels of calcium. You can see that in end-stage renal disease or malabsorptive states.

I said earlier that when you think about parathyroid hormone, I just want you to think about calcium. And that holds true for dysfunction as well.

E-concept five is that almost all clinical manifestations of hyperparathyroidism are a result of hypercalcemia. They can be remembered by the mnemonic stones, bones, abdominal groans, and psychic moans. The stones refers to nephrolithiasis from increased calcium. The bones refers to osteoporosis and risk of fracture from breakdown of bones by osteoclasts. Abdominal groans refers to nausea, vomiting, constipation, abdominal pain, and the psychic moans refer to depression, confusion, and headaches.

And some of these are pretty nonspecific findings, and some of them in concert together sort of really paint a picture of hypercalcemia.

As a side note, the most common cause of hypercalcemia in hospitalized patients is malignancy, not hyperparathyroidism. Bone invasion with osteolytic hypercalcemia can be seen in multiple myeloma, lymphoma, leukemia, and there are more rare causes of hypercalcemia as well. But this is just to point out that we shouldn't immediately jump to hyperparathyroidism when we see hypercalcemia, even though I did tell you when you see hyperparathyroidism, I do want you to jump to hypercalcemia.

I'll pause there for a second before one other key concept and some questions. Anything from that section we should talk about a little more, Jed? No, I think that's, again, these are just getting in now to what is the result of that process.

hypercalcemia, that's really important to remember. Again, this can come up in a section of the test that's trying to test you on hyperparathyroid, or it can come up in a question about electrolytes, right, where they're just getting at the effects of hyper or hypocalcemia. So this is important stuff to know. Exactly. And then the last key concept for hyperparathyroidism will be that management should aim at decreasing calcium levels. First-line treatment is hydration and or loop diuretic.

You might see numbers for calcium. They can give it to you in different units. You're looking for less than 14 milligrams per deciliter or 7 milliequivalents per liter or 3.5 millimoles per liter. Not that I want you to memorize these, but I thought maybe just saying them would tuck them away somewhere in your head. And then avoid hypoventilations because acidosis increases ionized calcium by decreasing calcium binding to albumin.

And then there are some additional treatments. Use of bisphosphonates, especially in the setting of hypercalcemia of malignancy. They inhibit bone resorption. Dialysis or glucocorticoids, which decrease calcium absorption, and calcitonin, which we talked about, can be given as well.

So let's do some questions on hyperparathyroidism. Question four, which of the following perineoplastic endocrine syndromes is most likely associated with squamous cell carcinoma? A, hypercalcemia, B, Cushing syndrome, or C, syndrome of inappropriate antidiuretic hormone secretion?

And this is really just something you're going to have to know. And it's tricky. It's just a memorization thing. If I think back to medical school, I seem to remember the squamous cell carcinoma can be associated with a parathyroid-like protein that isn't actually parathyroid hormone, but it's similar enough to cause the same effects and that that leads to hypercalcemia. So I think hypercalcemia is the most likely thing here.

It is. A, hypercalcemia is the answer. And this question is tucked in here, not to test that you remember that it's commonly associated with squamous cell carcinoma, but just to point out that the most common mechanism of hypercalcemia is secretion of parathyroid hormone-related protein in these paraneoplastic syndromes.

Question five, which of the following can inhibit neuromuscular blockade produced by non-depolarizing muscle relaxants? A, hypothyroidism, B, hyperparathyroidism, or C, hypoparathyroidism? Yeah. So, you know, the way I remember this is that I think of calcium as

as being related to the strength of muscular contraction. And so I think that hypercalcemia is doing the opposite, right? Calcium is kind of doing the opposite of a neuromuscular blocking drug. In other words, neuromuscular blocking drugs are making you weak where calcium, you know, again, this is not necessarily what it actually does, but I think of it as making you strong so that those are the opposites. And so hyperparathyroidism leading to hypercalcemia is what can inhibit neuromuscular blockade from non-depolarizers.

And as far as I know, those others don't. I actually don't know, Tim, and I don't know if you do, if the hypercalcemia is the mechanism by which this happens.

It is. It is. And actually, in looking this up, I found it fascinating just now that that's how you got to that answer. There's actually some literature I came across promoting the use of calcium with neostigmine to better reverse neuromuscular blockade, which is something that I hadn't heard about before. Interesting. I've never heard of that either. Something you need to try if you run out of Sugamidex. Yeah.

Question six, which of the following is the most common symptom of primary hyperparathyroidism? A, nephrolithiasis, B, extremity fracture, or C, prolonged QTC on ECG? Yeah, tricky because we talked about both A and B as being potential complications of hyperparathyroidism. I think nephrolithiasis is more common. I mean, you have to really have extreme risk

reduction in bone density from hyperparathyroidism to start getting fractures. So not that it couldn't happen, but I think nephrolithiasis just building up from hypercalcemia is probably going to be much more likely. And then prolonged QTC is going to be more from hypocalcemia rather than hypercalcemia. So that they're trying to just trick you a little bit there.

Exactly. So yeah, C, if you get tricked, you might get that wrong. And this is a, is it A or is it B, which is more common? And I stuck this question in here just to give you the stat. Nathrolithiasis is incredibly common in hyperparathyroidism and occurs in about 60 to 70% of patients. So it's not, we're not talking about something that, you know, happens in 25% of patients and the other thing happens in 20% and they want you to know that minutiae

But just really know that nephrolithiasis is one of the most common findings clinically as a symptom of hyperparathyroidism.

Great. Okay. And last, we need to cover hypoparathyroidism, which is usually due to a PTH deficiency secondary to parathyroidectomy. Like with the clinical manifestations of hyperparathyroidism being due to increased calcium levels, the clinical manifestations of hypoparathyroidism are secondary to hypocalcemia.

We talked about how hyperglycemia has other causes as well, and the same is true here for hypocalcemia. So don't get hung up assuming it must be related to the parathyroid. You can see hypocalcemia in end-stage renal disease, in hypomagnesemia, vitamin D deficiency, acute pancreatitis, etc. That being said, key concept six is clinical manifestations of hypocalcemia include prolongation of the QT interval.

And muscular technique, which can be diagnosed by the Chvostek sign, which is the facial twitching after tapping over the facial nerve, or the Tresor sign, which is the carpal spasm after inflation of a non-invasive blood pressure cuff.

And key concept seven is that treatment of symptomatic hypocalcemia involves administration of calcium. Avoid alkalosis from hyperventilation or sodium bicarbonate as they will decrease the ionized calcium. And also be mindful of citrate-containing solutions during resuscitation, such as blood products, FFP, et cetera. Great.

Okay, last set of questions. Question seven, you are called to a rapid response on a post-surgical unit floor patient who has respiratory distress on post-op day one following a thyroidectomy. What is the most likely explanation for her condition? A, she has bilateral recurrent laryngeal nerve injury. B, she has tracheal compression from a hematoma. Or C, she has hypocalcemic tetanychia.

Great. And this could have been a parathyroidectomy too, but important to know that with the thyroidectomy, you sometimes accidentally resect the parathyroid glands too. So that may be what they're getting at here, saying a thyroidectomy. But the key things to know are that

Timing is important. So this is post-op day one. This is, you know, presumably 24 hours or more after the surgery. So bilateral recurrent laryngeal nerve injury, if that had happened during the surgery, you would know right away. You wouldn't find out the next day. So that's not what's going on here because of the timing. Tracheal compression from a hematoma is much more likely to happen in the minutes and hours post-op.

post-surgery. And again, not that it couldn't happen the next day, but it's much less likely. And then hypocalcemia, again, this is key knowing timing. The hypocalcemia that can result from

either removing too much parathyroid tissue or accidentally removing the parathyroids when you remove to the thyroid, that tends to start to take effect. Remember the longer half-life of calcium, so that you tend to see on post-op day one to two. So this is now getting into the time when we would see it, so that hypocalcemia is the most likely answer here.

Exactly. And I can't explain it, but every single one of these questions, like you said, it could be a parathyroidectomy. They're always all thyroidectomies. They just want you to make that leap that you may take some parathyroid tissue inadvertently as well. Maybe it makes it slightly trickier, but yeah, interchangeable for all the stems. But for some reason, you always see thyroidectomy.

Case in point is question eight, a 62-year-old female on post-op day two from a total thyroidectomy. The surgery and her post-operative course has been uncomplicated so far, but she is now developing stridor and oral numbness. What's the most likely cause of her symptoms? A, adverse medication reaction, B, damage to the recurrent laryngeal nerve, or C, hypocalcemia.

And again, we have post-op day two, so much less likely to be damaged to the recurrent laryngeal nerve. Adverse medication reaction certainly can always happen, but to cause oral numbness and stridor seems not like a typical medication reaction. And certainly, again, we're post-op day two. After a thyroidectomy, this is where you are more likely to see that hypocalcemia. So that's going to be much more likely. And they're giving you

Two symptoms that really can go along with it, stridor and oral numbness. So it makes sense to push you towards C. Timing, timing, timing.

Question nine, hypoparathyroidism secondary to the inadvertent excision of a parathyroid glands during a total thyroidectomy typically results in airway symptoms secondary to hypotalcemia at which time point, Jed? A, one to six hours post-surgically, B, 24 to 72 hours post-surgically, or C, six to 24 hours post-surgically? Yeah. And as we've discussed that in that one to three days, so B is the right answer, 24 to 72 hours.

Yeah. And that's hypothyroidism in a nutshell. It leads to less calcium. It's due to excision of the parathyroids. And you'll see the hypocalcemia one to three days after. Fabulous. This is all super high yield, Tim. Thank you. Let's turn to the portion of our show where we make random recommendations.

Do you have something to recommend to the audience? I have. I have been waiting and waiting to record this Akrak episode because I have a really good one. For anyone that likes word games, I found a website. I think it'll be an app soon, but it's still just a website called MinitCryptic.com.

It's one cryptic crossword clue a day. It's scored like golf, so you can get hints to fill in some of the letters if you're struggling. And the fewer hints you use, the more under par you get. Like Wordle, it's just sort of you get to do the one that's available that day and then it goes away.

And I was never a fan of cryptic crossword puzzles. It's just too much effort, but sort of the one clue a day has really hooked me on it. So really recommend it if you like word games. MinuteCryptic.com. MinuteCryptic.com. Okay, I'm going to definitely check that out, and we'll put it in the show notes. Awesome. So we have an audience random recommendation. So Helen Ahn recommends...

the item called a to-go buddy. It's from a company called Frost Buddy. She says she does not work for them, but she really loves it. It's evidently an open-topped insulated tumbler where you can stick any cold beverage cup of any size. So you put your cup inside this thing and it will keep it cold for hours. She says it even keeps ice in the cup intact for hours, even in a cold car, sorry, even in a hot car. So she loves it because she'll get like an ice beverage and

Put it in this thing, and instead of the ice melting and diluting the drink, it'll keep the ice as ice and the drink cold for hours. So sounds very cool. I have not tried it, but thanks, Helen, for that recommendation.

I have two, and the reason I have two is that, Tim, you know, the last time I think we did an episode, you recommended the Lightbringer books, and I said, oh, yes, I love them. They're fabulous. And what I realized is I had actually been thinking of a different series, and I had never read the Lightbringer books. So subsequently, I have now started reading the Lightbringer books, and I think they're fabulous. I'm on the third of, I think, I can't remember, there are five or six total. Five.

Yeah, so I'm getting there, but they're great. And so I stick with my second to your recommendation. But because you just did it last time, I figured I would have something else too. And so I'll add...

that the word game connections from the New York Times, if you don't know it, is fabulous. And the idea is that you have 16 words and you have to figure out the four categories. So there's four words per category and you have to figure out what the categories are and which words go in each category. Some days it's quite straightforward. Some days it's incredibly difficult. But I want to tell you that it's fun to play. So check it out. But also they now have a connections bot that

So much like the Wordlebot, if you know about the Wordlebot, which we'll

break down your wordle answer and tell you how well you did and what you could have guessed to have done better. The Connections bot also will break down your Connections answer and how you approached it. It'll tell you how well you did compared to other New York Times readers and users. And it'll tell you, you know, kind of what common mistakes were and what your mistakes, if you made any, looked like. And it's really kind of fun to see that breakdown. So check it out. Connections, if you don't do it, is a lot of fun to do. And then the Connections bot will give you some insight into your answers.

All right, Tim, thank you so much for coming on the show. All right. Hopefully you got as much out of that as I did. That was really fantastic. Let us know what you thought. Go to the website, akrak.com, where you can leave a comment. Others can learn from what you have to say. If you are a fan of the show, you can follow us. We're on Twitter. We are on Facebook. We are on Reddit. And we are on Instagram. On Twitter, we are on Facebook.

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Even if it's just a dollar or two that you pledge, it makes a big difference and we really appreciate it. You can also make donations anytime by going to paypal.me slash akrak or looking up J. Walpaw on Venmo. Thank you so much to those who have already made donations and become patrons. We really appreciate it. Thanks as always to our fantastic Akrak crew. Sonia Amanat is our tech lead and Sophia Wu is our social media manager. William Mao is our production assistant.

Thank you so much for the great work that you do. Our original ACRAC music is by Dr. Dennis Kuo. You can check out his website at studymusicproject.com. All right. That is it for today. For the ACRAC podcast, I'm Jed Wolpaw. Thanks for listening. Remember, what you're doing out there every day is really important and valued.

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