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Today, we'll be talking about parathyroid calcium disorders. Uh I'll be going to the aims and objectives uh shortly. But um realistically what I want is I, I'm not really trying to, you know, drill home every single concept of parathyroid calcium disorder. It's obviously quite a vast subject uh to discuss, especially in just one hour. What I really want to do is give everyone here a strong foundation of, of how to really think about things and to really understand what's going on, right? I'm not here to um you know, build, build the nitty gritty and the niche things and, but at the end of today, when you do read a textbook or you do read a question, you should be able to visualize and understand what it's asking of you and the physiology of what you should be knowing. So that's really what I want to really drill the basics uh down really well uh for you guys. So as for the aims, it's mainly uh talking about parathyroid physiology, uh identification and management of parathyroid cancer disorders and for you to apply this knowledge to clinical scenarios, scenarios. Um We've got quite a few objectives here. But realistically, all we're talking about is hypoparathyroidism, hypoparathyroidism, um and hypercalm of malignancy and pretty much everything you need to know about it as a medical student and very soon uh as well as a doctor, right. So I, I've, I've tried to make things a lot more clinical based for you guys um because you are, are going to be doctors very soon and this is really how you, where your learning is going to be uh put to use. Can I get anyone to interact and potentially read um the, the first uh clinical vignette. So it is, this whole thing is gonna be quite interactive. I'd really appreciate if, oh, is that gone? He's back? Oh, it's not back, da da da da. Is it back for you guys? There you go. It's, it's gonna be quite interactive. I really appreciate if someone could uh unmute themselves and read it out, you're not gonna have to answer anything. I promise we get to that at the very end after I finish teaching. But is there any anyone brave enough to unmute um over here today? Ok. Can you, are you not or can you not? All right, never mind then? Oh. Oh, that's OK. Then I'll just read, I'll just read through it. Um You should be able to see this now. So the F and so you are clock in the AM U is on the acute tech and you've got two patients waiting uh for you to see. Uh The first patient is a 47 year old woman. She recently underwent a thyroidectomy due to thyroid cancer and she complains of cramps and muscle spasms. Uh You, do you come, you do you take a history from the patient? You do a clinical exam. The patient has a positive chopstick sign and the nurse reports spasms of the patient's hand while you're checking the vitals. That's your first patient. Um And at the end of the teaching, we, we want to basically answer the three questions below which is the suspected diagnosis, the tests that we'd like to order and our primary management. So this is the first patient that we've seen. The second one is a 55 year old woman complaining of generalized weakness and bone pain. She's got a history of frequent stools, uh frequent kidney stones and depression. She's also recently started taking Micol and Senna, which are both laxatives, which means that she's also recently got some constipation going on. So let's talk about parathyroid physiology. So this is a very sus succinct succinct uh image but really is a very, very good image to take home with you. At the end of today, it has pretty much everything you need to know about parathyroid physiology and can really explain everything about hyper and hypoparathyroidism uh for you. So let's change this to a laser pointer. Yeah. So you should see a laser pointer now. Um So these four small things here are your rice grain sized parathyroid glands. And these are pretty much the topic of the lecture today. Um And they secrete parathyroid hormone, right. So that's pth that these small four glands are secreting. So these act in three main ways. Uh but they mainly effect two, they have two areas that they mainly affect. So you can see it goes down into your bones, increase the osteoclast activity. And because of that, you have increased calcium absorption from your bones. That's one way, parathyroid hormone makes your calcium go up. The second way is it makes your kidney reabsorbed. The calcium is going to secrete right. So your no, your, your kidney normally secretes your calcium out by urine and it parathyroid hormone acts in your kidneys and increase the reabsorption of that calcium. So that's your second way. And then the third way is via the kidneys. It actually leads to a Vitamin D to be activated. And the Vitamin D then goes and acts on increasing your intestinal absorption of calcium. So that's the third way in which you, it increases your calcium. So you can see all three of these um mechanisms really of parathyroid hormone lead to increase serum calcium. This provides negative feedback and reduces the amount of P TH being secreted. Now, just speaking about this way, the exact opposite thing. So, decreased serum calcium here is what's going to se uh stimulate the parathyroid glands to secrete parathyroid hormone. And that really increases the cycle all over again. So you can see this is a feedback loop which really ensures calcium home he homeostasis um in the body. And a very easy way to remember what they do is a parathyroid hormone increases cal more parathyroid hormone, more calcium, less parathyroid hormone, less calcium. And that's a very easy way way for you to remember what does what and wherever your parathyroid hormone and calcium is that your phosphate does the opposite thing. So, if you have high parathyroid hormone, you then you've got high calcium, you'll get low phosphate uh as a result of it, obviously, I'm, I'm really simplifying it, but it's an easy way for you to remember what really goes on uh physiology wise. So, in a now, in a very, very simple manner, what is hypoparathyroidism? It's pretty much self exp expanded, it's hypoparathyroidism. So, hypersecretion of parathyroid by the parathyroid parathyroid hormone by the parathyroid gland. Um and the most common cause as was in our first patient. Um If you recall is the removal of the parathyroid glands, uh which is commonly happening during third or parathyroid surgeries. And you can also have hypoparathyroidism from autoimmune conditions or genetic conditions. But the vast majority, all your questions and main, most of your patients are also gonna be due to removal of the parathyroid glands. So, let's talk about the pathophysiology, right. So you have any cause um that causes it. But you're gonna have a in hypoparathyroidism, decreased gland function, decreased parathyroid hormone levels, decreased calcium. Due to all three of the mechanisms we just spoke about your blood calcium goes down and now you have muscular hyperirritability. How do we get hyperactivity of your muscles is because calcium essentially acts as um it, it, it stabilizes the resting membrane potential um in your cells. So it's, it's sort of like having a class of, of say second graders and the, if there's no one there looking after them, if there's no teacher in the class, for example, um things really do go haywire. I think that that's how it was for me and every everything just hypert you get someone in to look after them, someone there to stay in the, in the class and it sets a better tone or order um in the classroom. And that's pretty much what happens in your body when your calcium levels go down, everything goes haywire. Every everything is hyper, irritable, hyper excitability. Uh And it's hyper excitability of your muscles. Uh But why is that a bad thing? Can anyone tell me? Why do we care? Why are we having this talk? Why does it matter? Um If you have muscular hyperirritability, you can drop it in uh and chat um Since you can't uh actually speak. So what, what's something bad that can happen? W what do we not want? What are we looking out for anything? Uh of that sort. Yeah. What, what can be a bad thing due to low calcium arrhythmias. Yes. So, the muscular hyperfil can happen in, in, in many, um many ways. Right. So, your brain, you can have seizures because of uh muscular hypertil, you can have arrhythmias because of uh myocardium having hypertil um everything is just working too fast. So your, your, your neurons are firing too much. You start having a seizure, your heart's contracting too fast and it goes into an arrhythmia and uh something that a lot of people forget about. And I would urge you to remember because it's gonna have real world consequences is you can also have airway spasms, right? And that's very important cause the, your, the A of your A two E is your airway. If you have an airway spasm, that is an emergency, you need it there. So here you go. So airway spasms, cardiac arrhythmias and seizures. Um So if a very easy and good take home message is if you have a patient with hypocalcemia or suspected hypocalcemia and they, they start to struggle with their breathing, you need to be worried, you need to go, go, you know, to get your c you need to get it, you need to get things going. Uh because that would be obviously something to really w uh worry about. So let's talk about the, the signss and symptoms of uh hypocalcemia. So we've spoken about that, we've spoken about that. Now, what most of your patients going to come in and say is that they've got tingling of extremities, tingling of their fingers, they've got muscle cramps, which they are all quite nonspecific uh symptoms. But something that can be some signs that are quite specific are chopstick sign and TRS sign and of the, of the two truss sign is more specific for hypercalcemia. So keep in mind, these aren't always elicited. These are only in severe hypercalcemia, but none of those are very important signs to keep in mind. So the first one is positive chopstick sign. Um also keep in mind these signs are quite subtle. They can be quite, you, you have to be really concentrating to elicit them and tell that you're able to elicit them. Um So I'll just give you guys a quick um almost a demonstration of, of, can you guys see my picture? Yeah, demonstration of, of how to elicit it. So, for a patient, you're gonna be looking at the Zygomatic process of cheek bone right here. You're gonna go just below it and you should be able to feel your, your uh parotid gland, which is underneath, which is your, where your facial nerve is, is running. And that's what you're trying to tap uh to, to show the hyperirritability that you will see in hypocalcemia. So you essentially tap like. So uh for your patient and as you can tell you tell the patients to relax when you do this for me, nothing's happening because I don't have hypocalcemia. But this is what you tend to see, which is like a very subtle sign. You see, you see a twitch of the facial muscles to where you are tapping, which is when you'd have a positive chopstick. And just as so in the uh the slide. So facial muscle twitch after the facial nerve is slightly tapped once a little bit of the Zygomatic process, which is right here. And then you've got the positive to sign, which is, it's unlikely for you to see. Uh usually it would be the nurses checking it, but you can see it if you're at a GP practice. Uh regardless this is the more um specific sign, something to keep a to be aware of. Again, this is also a very subtle sign. So as the BP cuff tightens um tightens you're gonna see flexion of the wrist joint and the metacarpophalangeal joints. So it's gonna be something like this, ok? It's gonna be a quite subtle. It's not gonna be like a focal seizure. You're gonna see an arrhythmic jerking movement, it's gonna be a very subtle movement just like that. But if you know what you're looking for, you'll be able to see it. Or the nurse might tell you that this is what they saw. But again, this is in severe hypercalcemia. So you might not always see it. So, again, here, the BP cuff applies pressure on the brachial nerve causing it to fire. It's again, hyperirritability, uh, and it causes flexion of the wrist and metacarpophalangeal joints. So, investigations and treatment the, these are rather straightforward. You're gonna check your parathyroid hormone, you're gonna check your calcium, you're gonna check your phosphate, you're gonna check magnesium as well. Uh, because hypo uh, magnesemia can cause hypoparathyroidism. You check T FS and ACTH uh to look for other causes. So, adrenal and thyroid causes E CG for QT interval. You can have a prolonged QT interval and hypocalcemia, that's something to keep in mind. Hypocalcemia will prolong your QT interval. Hypercalcemia will shorten your QT interval and then you can have imaging test for localization, uh developing bone density and risk of fractures. But that's something you really do undertake. Um I mean you start up as a doctor. Um So the management for hypercalm as one would quite easy to tell is to replace the calcium initially. So if the calcium levels are below 1.88 millimoles per liter, you'll give IV calcium gluconate. Um and something well, as I said earlier, to really keep in mind is me, uh mechanical ventilation can become necessary in a patient uh who is developing respiratory distress. So please please please take this message home and keep that in mind. Um You will need to escalate a patient with a resp respiratory distress when they have hypocalcemia as well. So that would be our entire first patient that we saw that's hypocal, that's hypoparathyroidism and hypocalcemia that comes with it. Do we have any questions so far? Uh, about hyper hyper or hypercalcemia? I'll just give you guys a couple of seconds. Um, just try to pass everything we spoke about. So, the etiology, the path of the physiology, pathophysiology, um, and then the investigations and management and things to keep in mind, anything at all, anything that wasn't clear, just drop in the chart and then we're gonna move on to hyperparathyroidism. All right, I'll take that as. Yes. All right, wonderful. I'll hear. So I appreciate that. Um, I think it should have come back. It has come back. There you go. So we're gonna move on to hyperparathyroidism, which again is very self-explanatory, pretty much from the name hyperparathyroidism, hypersecretion of parathyroid hormone by the parathyroid glands. Um, I mean, I, II wish you guys could. Uh, I mean, but that's ok. Um, it's good there. And so there's three main types of hyperparasitism. So you have primary, secondary and tertiary. Um, it's quite important that you really understand and are able to differentiate between the main types. Once you've got the blood results back and once you have a good history from the patient. So once again, any questions whatsoever over here, just drop in the, in the chart and I'll be happy to clarify, but this is an important concept. I want you to take home with you. So in primary hyperparathyroidism, the parathyroid gland itself is just making the parathyroid hormone and this is now causing the effects further downstream. So it's primary, it's from the parathyroid gland itself in the parathyroid gland. This normally happens because of parathyroid adenoma and that's just having autonomous. Uh It means it's pretty much just having its own function. It's not listening to the feedback it gets from the increased or decreased calcium levels and just really sending things all the way up. It's almost always a parathyroid adenoma. Uh that's primary hyperparathyroidism. So it's from the parathyroid gland itself. Then you, you then obviously, you've got secondary hyperparathyroidism and this is when there is hypocalcemia further downstream, that's always stimulating the parathyroid hormones to secrete to pa glands to secret parathyroid hormone. This can happen in the kidneys. So once again, going back to our physiology that, that we went by, we, we said that there's three main mechanisms through which the parathyroid hormone acts and increases calcium levels. And if you remember only one of those were bones, the other two were essentially kidney. So the kidney gave the, the, the Vitamin D to act on the intestine and cause dietary absorption of calcium. And the kidney also um reabsorbed the calcium instead of secreting it. So if, if your kidneys aren't working that well, and you, you take away two of these three mechanisms, it quite obviously is going to uh cause hypercalcemia. You can't just keep degrading your, your bones and taking all the calcium from there and not taking any of the calcium you eat while simultaneously the calcium that you take from the bones. You are urinating that uh away as well. So you're gonna end up in this chronic state of hypocalcemia. You end up in this chronic state of hypocalcemia. You keep stimulating the parathyroid glands who can't really do much because whatever it's trying to do downstream isn't working right. And you'll see what this means for the body in a longer term picture. But I hope that overall makes sense with the, with the physiology and part of the physiology side of things, something else that makes things worse is we've always, we've also said earlier that your calcium and phosphate kind of stayed at opposite levels. And this chronic hypocalcemia and hyperphosphatemia causes further hypocalcemia because the these high levels of phosphate bind to the free calcium levels, uh reducing the calcium that your, your body can, can use as well. So with the long term secondary um hyperparasitism, your your your parathyroid glands have just been continuously been stimulated and stimulated by these low calcium levels that you sort of have this autonomous parathyroid secretion. Now, your body just says, you know, forget about that. The, the low calcium, high calcium doesn't matter. At the end of the day, we have just been producing so much parathyroid hormone, we're just gonna keep doing it and your body just produces a ridiculous amount of parathyroid hormone, which is usually due to parathyroid hyperplasia from continuously producing the hormone over so many, so many years. And this now starts hyper calcium because you've just got ridiculous levels of parathyroid hormone. And from this chronic bone degradation, you start getting your calcium levels high in tertiary parathyroid in tertiary and tertiary uh hyperparathyroidism. Um we get, we'll get to this side in just a second. So if you look at the blood results that you would see in these three types of hyperparathyroidism. So, and primary, it's very straightforward. You, you, you've got this adenoma making parathyroid hormone, it pushes the calcium up, pushes the phosphate down or keeps it normal. And you have a high ap from obviously the uh uh from a on the bone, it's gonna be high throughout secondary. You get this high parathyroid hormone, but that's secondary because of the low calcium. Um if it's normal, it would be inappropriately normal because you've got a high parathyroid hormone and your phosphate uh levels are going to go down because it goes opposite of however your parathyroid hormone is. Now, you see in tertiary hyperparathyroid, you hyperparasitism, you've, you've got really, really high parathyroid hormone because uh of chronic stimulation from the secondary hyperparathyroid and you've got low phosphate here as well in a high AO P. So I hope this kind of makes sense from the physiology and we'll get to this in a second. Any questions so far, just keep dropping them in the chat. I'm just taking a look now. Um I assume everything's clear so far, but feel free to drop anything in the chart even from previous um topics. Um at any point. So now we're talking about familar hypocalciuric hypercalcemia. Once again, the name pretty much says everything that we need to know. Uh familial. So genetic hypocalciuric, so low calcium in urine, hypercalcemia, high calcium in blood. So, it's a genetic condition in which you have low calcium in your urine and high calcium in your blood. And this is something you always look out for. When you have hyperparathyroidism, you want, you just wanna make sure it's not this that you're looking at. Uh So how do you really make a difference is because in hyperparathyroidism, you're gonna have um usually normal to high calcium um output in your urine. Whereas this is obviously hypocalciuric. So you have low calcium output um in your urine and this condition is pretty much al always benign. Uh the patient that's usually asymptomatic. So it'd be a a coincident finding that you do blood. So you find high calcium. Then the first thing you do is parathyroid, you find hyperthyroid and, and you take things from there, but this is a benign condition. No treatment is required and you really, this is why you're always going to do a urine calcium level when you've got a patient with suspected hyper so, signs and symptoms. I'm sure we've all heard. Um the center has been thrown around for hypercalcemia. It is a very good way to remember. So it's stones, Thrones bones grows and psychiatric overtones. It really covers all of these nonspecific symptoms. Uh We get for hypercalcemia, which is what you will see in hyperparathyroid. So frequent urination and constipation, these patients can frequently also be quite dry. So you, so you have dry mucous membranes, you'll have poor radial pulse volume while assessing such patients. Uh bones is they can have bone pain, nonspecific, muscle pain as well and they can just a general fatigue, uh groins as well. So Groh's will be the constipation that they get. They just generally feel unwell, they feel weak um from having these high calcium uh levels and psychiatric overtones that can complain of the symptoms of depression of confusion. You can really tell that this is quite stark, stark difference to uh hypopara muscular hyperirritability. And you've, you've got all these heightened symptoms of things really just being hyperirritable. Um with the low calcium levels, you can see with the with these high calcium levels and the really increasing the rest of number and potential. It's really hard to actually get any sort of neuronal activation, which is why you've got these symptoms like depression, confusion, constipation, weakness, fatigue, and you can really quite easily draw these star differences even though both. Um I can appreciate both of these conditions have really vague um presenting symptoms. So we're talking about management. Uh We're gonna get all pretty much the same tests and we're gonna throw in our 24 hour urinary calcium as well. Um not mentioned here, but you also need to be getting the ECG as we discussed. So, QT prolongation and calcium levels are inversely proportional. So you're gonna see a high QT prolongation, hypocalcemia, uh A decreased QT prolongation and hyper uh calcemia. So, the management for the types of hyperparathyroidism are different, which is why it's important to be able to differentiate between them. Uh primary hyperparathyroidism. The first line is a total parathyroidectomy, uh especially for all symptomatic patients. There are a few guidelines which aren't really that important on patients who don't really require a total parathyr toy. It's about patients that are above the age of 45. Uh The CCIS are less than 0.25 above the limit. Uh up above the upper limit of normal. They aren't symptomatic as well, but anyone who is symptomatic requires surgery, um very, very, very important. You might see this in the ward as well. When you start, when you start working, you need to ensure all the patients uh who are going to have a parathyr have their Vitamin D replaced uh prior to um the procedure. Why is this? It's, it's very interesting. It's called hungry bone syndrome. So, essentially what happens is once you've, you've taken out the these parathyroid gland, this overproduction of parathyroid hormone. You need to remember that. What had been happening was this chronic bone demineralization. Once you stop causing this bone deer, your body is quite happy, its affect healthy again. And it tries to immediately remineralize and fix up all this bone that has been lost over the last few weeks, months, et cetera. And what happens is just that starts using all the calcium that you have available to fix all of all of your bones. And that's what's called hungry bone syndrome. You start getting hypocalcemia which can be symptomatic and can be quite severe. So how does it all kind of the Vitamin D As long as you have Vitamin D available, you can always reabsorb that calcium from your diet. So again, it all ties back to the first picture we saw of um parathormone acting on your kidney and that acting on your intestine and allowing dietary calcium to be absorbed. And as long as you've got enough Vitamin D you can almo your body can sort of counteract or fight with the hungry bone syndrome and replace the calcium that's being absorbed by the bones. Whereas if your Vitamin D is low, you now need to replace the Vitamin D at the point where your body is already suffering for calcium. So it's kind of like fighting an uphill battle. Best practice is replace the Vitamin D preoperatively and you minimize complications in your patients. So that's something to keep in mind that's hungry bone syndrome. It's like, again, a very practical real world use. Um, on this topic, then that's just for primary hepar. Then you've got secondary and tertiary. Um, so as we've established, most, most of these patients will have known chronic kidney disease. You, you're gonna, uh, restrict the amount of dietary phosphorus they can have. Again, keep in mind that the dietary phosphorus can worsen the hypocalcemia, the high because it binds to the free calcium ions. And if despite dietary restriction, you're not able to, to get um everything within control, you can start prescribing phosphate binders. But really your, your management would be ideal if you could just manage the underlying cause, which is the chronic kidney disease, which is obviously uh difficult to manage. So the going back to our clinical vignette. So we've got the first patient again who had a thyroidectomy, do thyroid cancer, muscle, uh cramps and spasms, positive chopstick sign and positive to sign. Now, we can tell uh because the nurse reported spasms of her hand while checking her vitals suspected diagnosis. I hope everyone's aware this one would be hypopara would order PTH calcium um excuse me, uh parathyroid hormone, calcium phosphate, magnesium, you can order a good set of using these, you can do an ECG uh as well. Keep in mind um if the patient has uh any other symptoms of respiratory distress, depending on her calcium levels, you also make your CS aware you'd replace the calcium if it's less than 1.88. Um I really take, take something there further during her inpatient journey, you could do imaging tests uh as well. The second, uh that's a test and um, yeah, that's primary management as well. Um Then the sec second patient is a 55 year old woman complaining of generalized weakness and bone pain, frequent uh kidney stones and depression started taking what we call in senna. So we think she may have uh calcium and if this patient is symptomatic and she's got primary uh, management would usually be surgical and we'll make sure to replace the Vitamin D prior to surgery. Any questions so far, it'd be very surprising if you ever understood everything, any question I'm happy to answer. Um So I'm gonna give you guys a few seconds again to see if you, you've understood everything, um, understandably hyperparasitism, I'd say is, is more complex than hyperparasitism. Um So just take a moment, see if you've understood everything, primary, secondary, tertiary uh investigations, the signs, symptoms, uh the management, how are we doing for time? Very good. And keep in mind the familial hypocalciuric hyper calcemia as well, um, that just occur while you'll be thrown and uh hyperparathyroid. So I take the s as everyone's uh understood everything and really following on really well. Uh Now we're not done yet. So as you were on a um acute take, you're almost done you're ready to go home. You've just got like 20 minutes to shift left and the consultant just comes and asks you to see one more patient before you leave. Um So we're gonna quickly run for this patient so we can go home at the end of the day. So this patient is a 62 year old man. He's got prostate cancer and he complains of severe fatigue when you take the history. he sounds confused. The son says he is confused and on examination, he's also got dry mucous membranes. So similarly, we're gonna be running through it. Uh see what our suspected diagnosis is, what test we'll order and what the primary management is. So something else to keep in mind would be hypercalcemia of malignancy. So the three major mechanisms through which you get hypercalcemia malignancy. The first one would be tumor secretion of parathyroid hormone related peptide. This is something that would obviously parathyroid hormone related peptide. Again from the name, it's gonna increase your calcium levels, decrease your phosphate levels. But something to please, please, please keep in mind is this is not biochemically the same as parathyroid hormone on your lab tests. When you order parathyroid hormone, it will come up as low. It is not the same as parathyroid hormone related peptide. This is a separate test. It needs to be ordered separately for your test for this. The second one is ostro metastases with localytics, which really is basically bone degradation causing hypercalcemia. And the third one is tumor production of calcitriol, which again cause hypercalcemia because it increased uh intestinal absorption. So you can see in hypercalcemia, malignancy, we sort of mimic the physiological manner in which we increase um calcium levels. However, the the main difference would be that um this is not uh adherent to feedback mechanism, which is why it is causing the hypercalcemia. So the main cancer, you see this with uh breast cancer, lung cancer, bladder cancer, multiple myeloma, um renal cell carcinoma. But you, but you can see this with pretty much any cancer that's really, but I've seen with colorectal cancer as well, you can see the prostate cancer as well. So patients do come with severe symptoms that present quite acutely as well. Um You can see in patients with increased urination, increased thirst, which is why you'd have a patient that's quite dry. Patients who have constipation, patients would have confusion. And it's quite important to keep us in the back of your mind, heals malignancy as a differential for patients who have known cancer cancer and uh present with such symptoms also depending on the clinical sc and the history you take and the exam you do, uh patients might even present with uh hypercalcemia malignancy um as the first sign of cancer, but it's it that that would obviously be quite low down your differential. Um It's not as likely as other diagnoses. So, as for your investigation you do pretty much the same thing as you would for hyper hyper. Uh except you, here is the big one, parathyroid hormone related peptide is something you'd also be testing for uh as with hypercalcemia, your main treatment is going to be IV fluids. So I it can be up to a bag every 4 to 6 hours and you keep giving them bags of fluids uh and checking their uh calcium levels following that, you would get bisphosphonate to reduce calcium levels. Uh Depending on your trust, you may need to, to speak to other teams to organize this and again, for severe resistant cases, you, you definitely have to ask to speak to other teams. The absolute treatment is uh to treat the underlying cause, which over here would be the malignancy, which again can prove uh to be quite challenging. So it usually ends up being IV fluids and bisphosphonates and that's for hyper cancer malignancy. So that runs us past uh the clinical vignette as well. So there's a man who's got prostate cancer, severe fatigue, sign of hypercalcemia confusion that come in the psychiatric overtones and he's got dry mucous membranes. It because you get increased urine output as well with high calcium. So that's our suspected diagnosis. We've run through our tests and the primary management would be IV fluids hope that makes sense.