Calcium Disorders UPDATED | Clinical Medicine

what's up Ninja nerds in this video today we're going to be talking about calcium disorders again this so part of our clinical medicine section if you guys like these videos they make sense they help you please support us you can do that by hitting the like button commenting down in the comment section or subscribing also check out the link down our our description box below that'll take you to our website on our website we have a lot of amazing sources that we can help you out with such as notes illustration quiz questions go check that

out and I think you're going to learn a lot all right let's talk a little bit about calcium disorders beginning our discussion with hypocalcemia all right so let's begin our discussion with hypocalcemia discussing the pathophysiology the reason why this is super crucial is because it helps to build a foundation to understand the causes but not just that I thoroughly believe that the understanding of the pathophysiology plays a massive massive role and the diagnosis of different types of causes of hypocalcemia so it's really dig into this a little bit it's important to remember that hypocalcemia is

controlled via what's called pth that's parathyroid hormone right we know that the parathyroid hormone is released right from these little glands on the back of the thyroid gland called your parathyroid glands so they're responsible for making this hormone referred to as pth now let's say for whatever reason and we'll discuss those reasons in a second the parathyroid gland is not producing an adequate amount of pth if it doesn't produce an adequate amount of pth what's going to happen that's a great question well one of the things that's going to happen is it's not going to

work on the Osteo class you know in the bone tissue if we were to zoom in the bone tissue you have these bone cells in these bone cells there's different types osteoblast osteoclast osteocytes Osteo class are going to be the big one now osteoclast what's important with these is that they have different receptors for pth when pth is actually low what actually happens is it affects the osteoblast and those osteoblast then communicate with the Osteo class if there's low pth what it does is it tells the Osteo class hey don't do anything don't resorb any

bone don't break down any bone so that's officially what's going to happen is it's going to shut down or inhibit the osteoclast if you inhibit the Osteo class they won't chew away the actual bone tissue and liberate calcium into the bloodstream so as an effect here what's going to happen to the amount of calcium that gets into the bloodstream it's going to be lower so there's going to be decreased calcium due to less liberation of calcium from the bone so there's going to be a decrease and what we refer to as bone resorption so if

there is a decrease in bone resorption that means that we're going to break down less bone this process will not occur and we won't liberate calcium into the bloodstream that's one of the reasons for hypocalcemia the other concept is what if pth also is low there'll be less ability to interact with the kidneys now you know in the kidneys there's different receptors for pth especially on the distal conut tubular cells as well as on the proximal conut tubular cells on the distal convoluted tubular cells pth is really really important because what it helps to do

is is it helps to increase the expression of channels that help to reabsorb calcium and excrete phosphate if there's less pth will you be able to and this is actually should be a blue arrow here a dark blue arrow here so if you have less pth will you be able to increase the expression of the calcium channels and the phosphate channels no so what happens is less calcium gets reabsorbed and less phosphates get excreted so now as a result here look what happens you're going to have less calcium and less phosphate if I inhibit this

process what happens is that calcium gets lost into the urine and not it doesn't get reabsorbed the end result here is that I'm going to lose the calcium from being reabsorbed and I'm also not going to excrete my phosphates and so another little side result here if you want to is a little kind of like side off effect here is that this can slightly increase the phosphates in the bloodstream but the profound effect here is that you're not going to be reabsorbing calcium so there is a what we say a decrease in calcium reabsorption at

the kidney all right so that's one really big effect there as well so decreased calcium reabsorption at the kidneys leads to hypocalcemia decreased bone resorption leads to hypocalcemia the next component here is that pth also acts on another part of kidney but I just I don't want to clutter the diagram here so it acts at the DCT it also acts at the PCT so for Simplicity sake let's come over here and look what happens P you know the pth comes over here to the kidneys right acts on the proximal con tubul which would be right

here what it does is it's supposed to increase the expression of an enzyme inside the cell you know what it's called it's called alpha 1 hydroxy now that alpha1 hydroxylase is actually a really important hormone I mean um enzyme and the reason why that's an important enzyme is it helps in a very specific biochemical process you know there's a vitamin it's called vitamin D and it comes in different forms but the one that we ingest often times can be 25 or the form the form that comes from the skin eventually gets converted into what's called

25 hydroxy vitamin D and what we what we want the effective the active form of vitamin D we want to be what's called one comma 25 I'm going to bring you that dihydroxy vitamin D now in order for this process to occur I need to add a hydroxy group on the one carbon guess who does that this guy now he's supposed to help this process if I have less of him I am I going to express as much of him no and so if I don't express as much of this enzyme is this process going

to occur this process will not occur I will not convert him into him so I'll get less of this guy why is that a problem reason why that's a problem is he comes down here to the good old git and increases the expression of the good old calcium channels and if you're supposed to express calcium channels and you don't have them guess what you're not going to do my friends you're not going to absorb calcium and so in that process you're going to have inhibition and you're going to have decreased calcium and what's the reason

why you're going to have a decreased calcium because of decreased calcium absorption this would because of decrease calcium absorption at the git so decreased calcium absorption at the git is the reason for this process now here's what I want you to see if the body is not making pth this is how we end up with hypocalcemia the same effect occurs because guess what pth it goes and acts on specific receptors on the bones on the distal convoluted tubules on the proximal convoluted tubules and so if pth is normal but it binds onto the receptors and

The receptors are dysfunctional it's going to precipitate the same effect we'll talk later about what diseases cause low pth and a receptor resistance at the receptor site all right what's another reason for patients developing hypocalcemia well one is low vitamin D now vitamin D is important because we ingest vitamin D right in different types of food sources and supplements and so that should be absorbed across your git also in normal sun exposure we should be able to absorb vitamin D into the bloodstream either way usually that form of vitamin D is what we refer to

as like a inactive sometimes we call it cold calciferol right so we're going to represent that as CCF that kol calciferol which is kind of like a very very inactive form of vitamin D should then move through the bloodstream where it reaches the liver the liver is then supposed to say okay I'm going to then convert this K calciferol into what's called 25 hydroxy vitamin D oh that sounds familiar this is the one who does that so he's going to then convert this into what's called 25 hydroxy vitamin D now from here the 25 hydroxy

vitamin D is supposed to go to the kidneys what's the reason why I already told you why because it has an enzyme the one alpha hydroxy that the pth controls and so from here it should then be easily converted into what's called 1 comma 25 dihydroxy vitamin D now if we have decreased vitamin D and we'll talk about the reasons why maybe because there is a problem here at this site with the intake or with this the sun exposure or there's a problem with the liver where it can't convert that into the 25 hydroxy vitamin

D or there's a problem with the kidneys not being able to activate the vitamin D either way if it's a absorption problem a skin uh sunlight exposure problem a liver disease problem or a kidney disease problem all of these can result in this what's the issue with this well let's just kind of save some space decrease calcium absorption in the git that's going to lead to hypocalcemia so we see this we understand this now that's not too bad let's come down to the last reason the last reason is kind of interesting and this is often

times we can kind of break this into acute and chronic and we'll talk about that there's different types of let's say molecules in the bloodstream that we have present that are negatively charged all right often times the big ones that I want you to remember are going to be what's called phosphates right we'll represent it with this one this one we can say sometimes what's called citrate and we'll make this one fatty acids now naturally these have negative charges on them now what is calcium it's positively charged if you have negative charges what if for

some reason right you develop a disease process and in that disease disas process you end up with an increase in all of these right so now I have an increase in phosphate I have an increase in citrate and I have an increase in the fatty acids if I increase all of these for whatever reason we'll talk about those reasons why is that a big big deal well calcium exists in two forms in our bloodstream it exists in a free form and a bound form the problem with hypocalcemia is disease processes occur when you lower the

free or ionized calcium well guess what if I have a lot of these maybe I only have a couple of these and so they only bind a little bit of the calcium all of a sudden I end up with a ton of these with a bunch of negative charges this is like this is like you know trying to be able to see oh baby I this calcium is be like oh I see lots of negative charges over here I'm going to go over here and bind one of these and that calcium will do that so

what will happen is you have so many negative charges and what they're going to do is they're going to bind the calcium and when they bind up the calcium they lower the free calcium and that is what's going to lead to hypocalcemia now we'll talk about this a little bit more and the reason why is some diseases and most of them I should say acutely cause this rise and so often times phosphates can be built up in acute processes citrate acute processes and fatty acids in acute processes there's only one disease that chronically causes rises

in phosphate levels and we'll talk about that often times it's CKD so we' seen all of these Concepts how we actually cause hypocalcemia what I want you to do now is take a second and say okay what causes low pth what causes the low pth effect or the no pth effect what causes low vitamin D and what causes High phosphates high citrates and high fatty acids and we can answer our questions let's do that now all right so let's talk about the causes here so we have to then take each one of those pathophysiological Concepts

and really build on it so low pth and low pth effect right this is very very straightforward now what causes low pth which leads to low calcium well one is you cut the parathyroids out these are the source of your parathyroid hormone production so often times this is a you know we can see this as a iatrogenic effect so this could be after a parathyroid ectomy which could be an actual process that they're going for but you can also see it in thyroid ectomies and this could be accidental so in other words they were going

out to take some of the thyroid tissue and they accidentally took one of the parathyroid or two of the parathyroid glands so parathyroidectomy or a thyroidectomy so you can also see this in thyroid ectomies which lead to kind of an accidental taking or remov removal I would say of the actual parathyroid gland if that happens there boom you just lost some sources of pth these are supposed to be able to produce pth now you only have maybe one or two glands that are producing the pth so that could be one potential reason and we know

that pth leads to less osteoclast activity less vitamin D activation and less calcium reabsorption all right cool here's another thing if you look in the patient's history in this and you'll often times see this in the vignette oh they were just had a thyro rectomy that some type of neck surgery of sorts if they had anything like that often times that's going to be the answer there could be autoimmune diseases there is like an autoimmune polyg glandular syndrome type one it's very very rare and usually it presents with adrenal insufficiency and mucocutaneous candidasis and hypothyroidism

but it's a really really rare thing and I don't think that you'll see it too often on the boards what I would be thinking about in true clinical reality might be more likely is when a patient has no underlying neck surgery or anything that was near the PA of thyroids think about magnesium so hypomagnesemia can also be a pretty like common cause here and that's because calcium and magnesium often kind of go hand in hand now with hypomagnesemia whenever there's low magnesium magnesium is actually essential for the development the synthesis and the release of parathyroid

hormone so whenever a patient has low magnesium levels this actually will kind of inhibit the parathyroid gland and the parathyroid gland as a result won't be able to produce pth and so that's another really big one now the question comes up what leads to hypomagnesemia why would patients have hypomagnesemia because that's what you have to look for in the vignette it's not going to be super obvious they're not going to probably give you the magnesium level they're going to say some of the diseases that make them predisposed what could be some of those things well

I would think about patients who have some type of bowel disease so small bowel disease of sorts what do I mean by that well do they have any history of celiac disease do they have any history of um Crohn's disease do they have any history of like a small bow reection or some type of B bypass surgery that's what I would be thinking about or a malabsorptive syndrome of sort the other one I'd be thinking about is patients who drink a lot of alcohol this can definitely them not getting enough of their nutrients um you

know in their actual diet so alcohol abuse would be a really really big one as well and then chronic diuretics so diuretic use can also definitely lead to hypomagnesemia so these are some of the things there's even sometimes you may see this on the board but ppis also cause this as well but this is what I would really be looking for that is a dead giveaway on the exam is small bow disease alcohol abuse and diuretics that lead to hypomagnesemia shut down pth production and lead to hypocalcemia the last one's really interesting and this one

is called uh pseudo hypoparathyroidism and I'll explain this one one um here in a second but before I do that I want you guys to notice something really interesting now when patients have this pth right low pth we know that their effect is going to be they're going to go here and they're supposed to bind to this receptor on the bones bind to the receptor on the proximal tubal and the distal tubu and then hopefully as a result it's supposed to reabsorb calcium here lead to the activation of vitamin D chew up the bones via

the osteoclast but what if there's a disease process that this isn't the problem so this is one of them but what if when pth goes and binds here I don't get this effect then what this is an issue now let's actually talk about this because pseudo hypoparathyroidism is kind of an interesting disease it's kind of rare it's a genetic condition and the concept here is that there is some type of pth receptor resistance often times these patients have like weird metacarpal disorders um and sometimes very common there's some degree of mental retardation of effect there

but what happens is is pth is supposed to bind to these receptors now when pth binds to these receptors it should then do what trigger the effects that we talked about with bth but if there's some type of receptor resistance you're not going to get that effect so this is due to pth receptor resistance so it's like pth is not even present essentially what happens then well if I don't stimulate osteoclast I won't reabsorb resorb calcium if I don't tell my DCT to reabsorb calcium I won't get calcium into the bloodstream and if I don't

activate vitamin D I won't absorb calcium across the gut all of these things lead to what effect hypocalcemia well hypocalcemia is a very very very strong stimulus for the hormone that's supposed to control him and guess what that tissue is it's the parathyroid glands calcium should then say hey para thyroids calcium's low here buddy I need you to go ahead and pump that pth up and that's what we is really really weird about this disorder is that now they're going to go ahead and say okay I got it I'll pump up the pth and I'm

going to do this in hopes that I'll be able to go back to the bones back to the kidneys and help us to get calcium but it will have to no avail it won't be able to do that that's what's really important this is where diagnostically this is super helpful what do you notice with pseudo hypoparathyroidism with the pth levels it's high what do you notice with a parathyroidectomy thyroidectomy or hypomagnesemia it's low that's the difference here that's what I want you to remember again remember pth yes it is supposed to go here to these

actual sites and work on the bones and go and work on the DCT and the PCT and hopefully help to increase calcium but in all of these scenarios it won't it's the exact act same situation except the receptors aren't responding the parathyroids fine it's the receptors that aren't working that's the difference between these two and you can actually differentiate this by getting a pth level all right now that's the low pth or pth effect what about low vitamin D well I kind of introduced this to you already it's not too bad but what if same

thing what if I have a disorder of my git yeah it could be a lot of things right let's say that you have some type of like malab absorption of sort so this could be due to malabsorption that can definitely cause this type of problem what's another one well what if there's decreased sun exposure we see this a lot and people who are kind of around the different parts of the Equator maybe people have jobs or they're working inside they're techies they're not outside a lot this could definitely be a very very common one so

you see this a lot on the exams either way if you're not getting in the proper nutrients because you have a malabsorptive disorder or you're not being exposed to the Sun what happens in both of these they're supposed to help us to take in some degree of vitamin D in that K calciferol form right will they be able to do that no so now you're not going to get that kic calciferol and that's where we kind of left off if I can't get that kic calciferol well eventually I won't lead to the formation of vitamin

D the active form here's another point this is why I like to build on this right what's he supposed to do take and convert this into what he's supposed to convert that kic calciferol into what's called 25 hydroxy vitamin D now if he's supposed to do that what if a patient has underlying disease of the liver what could this be therosis right so if a patient has underlying therosis this will impair their conversion of that kic calciferol into the 25 hydroxy vitamin D now I have less vitamin D here oh son of a gun now

next concept your kidneys the proximal convoluted tubular cells are supposed to express what particular enzyme the alpha 1 hydroxylase now if it's supposed to express that enzyme that should then do what convert this puppy into 25 hydroxy baby to one comma 25 dihydroxy vitamin D and this is that active form of vitamin D right now if I have some type of disease of my kidneys where the tubular cells are dying or the nephrons are dying then will I be able to perform this process no so in the same way I can't perform this process I

can't perform this process and so I won't be able to form him and so in this situation what could we see this where there's lots of death of the nephrons and disease of the nephrons and chronic kidney disease so CKD is a really really big one out of all of these I really really want you to remember this one and I also want want you to remember decreased sun exposure these are oftentimes really big ones for the exam for a diminished vitamin D level now the concept here is also really interesting because there's really one

disease two diseases I would say that cause low pth parathyroidectomy thyroidectomy and magnesium levels that are low can cause hypoparathyroidism pseudo was high pth what do you think is going to happen with low vitamin D what does it eventually lead to supposed to go to the git right and absorb calcium if I don't have that will I absorb calcium no if I can't absorb calcium what will happen to my calcium levels in the blood they'll drop what's calcium a very very very very strong stimulator of pth and if it's going to be a strong stimulator

of pth what will happen to the pth levels in the bloodstream they'll be high so if pth levels come back high you got to think about pseudo hypoparathyroidism and vitamin D deficiency that's really important if it's comes back low you think about hypoparathyroidism or hypomagnesemia either way they're both a hypoparathyroidism all right the last scenario here calcium sequestration in calcium sequestration it's important to remember that there is acute causes and chronic causes the most important one for The Chronic causes is going to be CKD so I want you to remember this is the only example

of like a chronic calcium sequestration if a patient has disease of their kidneys usually for example it's chronic kidney disease is kind of a perfect example here they lose the ability to excrete phosphates because you know your GFR is low right you're supposed to be able to excrete phosphates now if I can't excrete those phosphates they're going to build up in the bloodstream so that's the problem here is that what happens is they can't filter it out and that phosphate builds up in the bloodstream right so what am I going to end up with a

lot of lots of phosphates remember I told you with the high phosphates what do they do they bind the calcium what do they do to the free calcium they decrease the free calcium so that's kind of interesting right that's the problem with this one here right now we'll come back to this all the rest of these so this is the only chronic cases CKD all of the rest of these are acute now what that is important for is when it comes to the pth levels and I'll explain in a second acute diseases include rabdo myisis

rabdo myisis what is this you break open you destroy those skeletal muscle cells this can happen when you have seizures this can happen when you have Crush injuries like trauma what does it do it pops open releases a bunch of different things right CK is the big one myoglobin's the big one but what's the other thing that's a problem for us that phosphate that phosphate bro and when it pops that phosphate out there guess that's what the phosphate does it binds with the actual calcium so now calcium is going to bind with this and it's

going to do what to my actual free calcium this should be a red arrow sorry guys free calcium is going to decrease but this is acute right so I want you guys to please remember this this is chronic this is acute and I know that sounds kind of dumb but I promise it's important now the next example is another disease and this is acute as well and this is called tumor liis syndrome we've seen this before remember in hyperemia we saw this same thing tumor liis syndrome is in patients we see who have like what's

called um non- hodkin lymphoma or acute um myogenous leukemia and they get get chemotherapy and all of a sudden that chemo kills all of those cells they bust open they bust open to release potassium ITA causes hyperemia they release uric acid causes hyperemia they release LDH but what else do they release they release phosphates if they release phosphates what's that phosphate going to do baby it's going to bind up the calcium so you're going to get that acute rise in the phosphate again acute rise now let me explain this for a second why is this

so important if it's an acute rise whether it be rabdo or tumor liis this will not cause the calcium levels to drop consistently enough enough to stimulate pth production if it's chronic and only if it's chronic this has the capacity to tell the parathyroid glands hey calcium is low I need you to go ahead and start pumping out the pth all right this is only if it is chronic this will do this if it's acute we don't really know it's super variable and so you can get variable levels of pth for Simplicity sake we're just

going to put the pth as being somewhat between the normal range so it's super variable I'll put that here in the parenthesis in the sense that we can't have a consistent determination of what their pth level is going to be but when it's chronic we can and so that's actually helpful because this can be useful in determining diagnostically if it's CKD versus some other process but we can also just base it on on the it of their presentation of hypocalcemia so rabdo tumor liis you're going to see more in that acute phase but if I

have a patient with hypocalcemia and I check their pth is low it's hypoparathyroidism if it's high it could be vitamin D deficiency pseudo hypoparathyroidism or CKD I can't really make a definitive answer with the rabdo or the tumor lasis the last ones are pretty much similar in the sense that they're acute but they release different things you know when a patient gets tons and tons of blood transfusions so I usually I've seen this a lot in the ICU where a patient gets a ton of blood transfusions and when they get lots and lots of blood

transfusions we're actually supposed to very very closely monitor their calcium and the reason why is like during for example a massive transfusion protocol what happens is you give them so much blood and that blood releases a very specific molecule um that you give them and it's called citrate that citrate we talked about before guess what super negatively charged guess what it's going to do it's going to bind up the calcium and when it binds up the calcium is going to drop the calcium super acutely and so that's why in these patients who actually get massive

blood transfusions we tend to see their serum calcium levels drop acutely and so that's a perfect clinical vignette where you would see this the last one don't it's not worth the squeeze to really really remember this but you can think about it hypocalcemia is funny because it can it can actually lead to um in some of these patients you may see some type of issue particularly is a result of pancreatitis and why I laugh is because hypercalcemia can cause pancreatitis so hypercalcemia can cause pancreatitis and hypocalcemia can be the result of pancreatitis it's just funny

I don't know why but anyway when we talk about pancreatitis guess what happens in some situations of pancreatitis you'll release out the enzymes like your lip paces and those Li Paces get oh son of a gun what are those light Paces supposed to do those light Paces they end up unfortunately breaking down the fat tissue and the pancreas all the peripancreatic fat fat tissue when they break down the fat tissue it breaks it into what's called fatty acids and if we have lots of these fatty acids guess what that's going to do so if I

get lots of lipases it's going to help to convert the fat into fatty acids and those fatty acids are going to build up in the bloodstream if they build up in the bloodstream what are they going to do they're going to bind to the calcium ions and if they bind up to the calcium ions what's that going to do to your whole serum calcium it's going to drop your serum calcium and so sometimes we actually give this a very interesting term we call it saponification and so we can see this in patients who have what's

called acute pancreatitis so please don't forget these things now we've talked about hypocalcemia what I want to do is is go through hypercalcemia so now let's talk about hypercalcemia which is the other spectrum of uh calcium disorders so this is when the calcium is too high so calcium too low less than 8.5 calcium too high greater than 10.5 now when we talk about when the calcium is too high we have to think about again the pathophysiological concepts what are the reasons why well one of them is that the pth is just too dang ha right

you're making too much of that parathyroid hormone now when we talk about this we kind of are going to be repeating what we talked about in hypocalcemia So I won't waterboard you with all of this stuff but pth if you're making a lot of this again parathyroid glands are usually the primary source now if you're making a lot of this poppy what is it going to do let's just have a quick quick reminder it's going to act on the what the bone right particularly what the Osteo class when it works on the osto class it

does it technically indirectly by working on the osteoblast which then help to activate the Osteo class in this case we're going to stimulate the Osteo class who are then going to start breaking down the bone tissue when they break down the bone tissue they'll liberate and release the calcium from the bone tissue and this is going to be the mechanism what we call increased bone resorption so you're actually resorbing some of the calcium from the bone so this is increased bone resorption and this will when you liberate that calcium into the bloodstream lead to high

calcium in the blood so that's one mechanism eth also likes to act here on the kidneys and particularly as the distal convoluted tubal and again we know that this acts via these different types of receptors The pth receptors same thing there's pth receptors here in the distal convoluted tubal now when ax here the distal convoluted tubal what it's supposed to do is is increase oh son of a gun that went far what it does is is it actually increases the expression of a channel that plays a role in calcium re absorption and phosphate excretion now

when it binds to this receptor it's going to stimulate this receptor who then helps to activate the expression and the opening of these channels which will then allow for calcium to be reabsorbed and phosphate to be secreted as a result as we do this you will reabsorb calcium into the bloodstream because you're going to be pulling it from the kidneys into the bloodstream so there's going to be increased what's called calcium reabsorption via the kidneys but as a byproduct whenever you actually are going to stimulate pth you remember pth also known as what called the

phosphate trashing hormone so it will actually excrete the phosphate into the urine so what will happen to the phosphate levels in the bloodstream it should theoretically drop and so that's one thing that we see whenever parathyroid is actually the issue is that calcium will go up and phosphate will go down now that's one mechanism right so we got one two what's the third again I don't want to clutter the diagram here but it acts on the proximal convol tubal so when it comes here it acts on the proximal convoluted tubular cells in the kidney and

increases the expression yeah you guessed it of the alpha 1 hydroxy now if we increase the expression of this enzyme what's going to happen I will then convert 25 hydroxy vitamin D which is made by the liver into 1 comma 25 dihydroxy vitamin D which is then going to be the active form who helps to facilitate this pth by increasing the expression of this enzyme who then will stimulate the rapid conversion into this if I have more of this what's going to happen he'll then go to the git he'll plug some calcium channels into the

luminal membrane if you plug calcium channels here what's going to happen the more calcium channels the more calcium can move across the git and if you have more calcium coming across via the git what's going to happen it's going to increase the calcium in the bloodstream and this is going to be via increase calcium absorption across via the git W baby we good right so it's going to stimulate this process you're going to express these more now the next concept is what if pth isn't really the problem what if it's due to vitamin D excess

vitamin D now it is possible to develop a vitamin D intoxication it's just not as common as some of the other diseases that we can talk about here but again you have to remember that that K calciferol which is the super inactive form of the vitamin D can come from the gut and it does come from the skin right now if patients do take in they ingest way too much vitamin D it is a possibility that they could develop hypercalcemia as a result but we'll see down here a little bit later that there's another interesting

process now colly calciferol goes to the liver and when it goes to the liver again what we know is that the liver will help to convert that into what's called 25 hydroxy vitamin D 25 hydroxy vitamin D now you're probably like oh probably something wrong with the liver right the liver is probably the reason why and it's hyperactivating not necessarily so you're like okay all right well where's the issue actually occurring here well the next thing is that you know that the kidneys Express this enzyme called one alpha hydroxy right and that one alpha hydroxy

or the alpha 1 hydroxy what we know about this enzyme is that he helps in being able to convert 25 hydroxy vitamin D into 1 comma 25 hydroxy vitamin and so what we know is is that with the presence of this enzyme what we will see here is so whenever you have the expression of this enzyme this helps to stimulate the formation of 1 comma 25 dihydroxy vitamin D this is usually where the problem exists now you're probably like oh it's the kidneys right there's something going on with the kidneys not necessarily and that's what

we'll talk about later but often times the problem with excess vitamin D is usually and increase in this enzyme and we'll talk about how certain tumor cells have the capacity to overexpress this enzyme or granulomatous cells have the capacity to increase the expression of these enzymes there is the possibility of us taking in way too much vitamin D across the diet that also can cause this but more particularly through the pills itself either way when you get too much vitamin D in the body what happens if there's too much of this active form of the

vitamin D he'll go to the git when he goes to the git he will increase the expression of these calcium channels absorption of calcium leads to hypercalcemia the next one is pthrp and pthrp is what's called parathyroid hormone related peptide meaning it's not parathyroid hormone it can act like it this is released by very specific types of cells and again I want you guys to start getting yourself ready of trying to ask yourself what kind of cells is pthrp released to aadin what type of cells are releasing increased Alpha 1 hydroxy but regardless of that

if we make lots of pthrp and we're going to kind of keep these cells somewhat of a mystery for right now when that pthrp is released guess what it does it kind of Acts just like parathyroid hormone except it does one less thing so what it's going to do is O this should be the blue arrow here guys it's going to act on the bone tissue and it's also going to act on the kidney tissue but only on the distal convoluted tubular cells so so what it's going to do is it's going to stimulate these

osteoclast right you know the osteoclast it's going to increase the osteoclastic activity when you increase osteoclast activity you're going to resorb the Bone tissue when you resorb bone tissue what's that going to do to the calcium levels it's going to increase the calcium levels because you're going to liberate calcium from the bone right the other thing that it's going to do is is it's going to increase the expression of the channels in the distal convoluted tubal to reabsorb calcium and excrete phosphate so in this process you'll reabsorb calcium and you'll excrete phosphate it'll stimulate this

process and if this occurs what's going to happen this will lead to increased calcium reabsorption which will then lead to increase calcium the only thing that pthrp does not do is it doesn't play a role in activating the vitamin D via the one alpha hydroxy that's the only difference between these two all right that's very important as well this is the concept for pthrp so all right we know now high pth high vitamin D high pthrp is the reasons why patients would develop hypercalcemia there's one last one this last one can exist whenever you have

lots and lots and lots of bone turnover so imagine here we have a bone tissue and in the bone tissue again we always have these cells the bone eating cells called Osteo clap and these osteoclast it's important to remember that they have receptors on them right they have lots of different receptors that can respond to cyto kindes and ligans of all kinds of sorts if someone has diseases all right particularly malignancies that super activate these osteoclasts what can they then go and do they can then say all right baby I'm going to chew through this

bone like a son of a gun and they are going to massively massively increase bone resorption and if you increase your bone resorption you're going to as a result liberate calcium from the bone so here you can see bone resorption here you're going to see tons and tons of bone resorption to the point and which we'll talk about this later it starts to eat through the bone tissue and these start to cause a lot of problems here to the bones and cause a lot of bone disease so looking at all of this is the framework

that I want you to form in your head when you think about a patient having hypercalcemia is it high pth high vitamin D high pthrp or lots of bone turnover let's now go through each one of these and think about the causes of those scenarios all right so now we formulated our kind of overall understanding right now let's go through each one talk about what's causing these particular Concepts so high pth we know that because it's acting on the osteoclast it's acting on the proximal convoluted tubal distal convol tub we got that all down we

just got to ask ourselves the question why is pth high there's two reasons one is what we call primary hyper parathyroidism hyper parathyroidism and again if you guys are having any confusion we talk more about parathyroid disorders in the endocrine section so go watch that if you need a little bit more help but primary hyper parathyroidism is often times due to an adenoma so often times the patient will have like an adenoma that is causing this there is other reasons but I would say you know often more than not it's an adenoma that's usually present

80% of the time that is pumping out it's gaining the capacity an autonomous capacity to produce pth in large amounts so this thing is just straight pumping out the pth now we know what we just talked about here that if you're pumping out lots of pth here we know that this is going to work because it goes down to the bone tissue the Osteo class and it goes down to the kidneys via the proximal tubal and the distal tubal and what does it do at these particular areas it works by stimulating osteoclast increase bone reabsorption

of resorption increases the distal convoluted tubular cells to cause calcium reabsorption and increases the expression of alpha 1 hydroxy to form more vitamin D lead to more calcium so either way in all of the scenarios here we lead to a patient developing what high calcium as a result now here's where it's really really important pth is the reason the calcium is high there's another disease and this is called tertiary hyper parathyroidism now you're probably like okay Zach you skipped one of them because does a go primary secondary tertiary yes secondary hyper parathyroidism is often times

defined as patients who have CKD or vitamin D deficiencies when they have those they produce hypocalcemia and that hypocalcemia as we talked about in hypocalcemia P portion stimulates pth production and that pth will go up and up and up but it's not gaining the capacity to cause the calcium to go up what happens is chronic kidney disease is one of the really prominent secondary hyperthyroid states that if continuously occurs and progresses over time that can lead to tertiary hyperparathyroidism let me let me explain let's say here I have a patient who has CKD and this

is often times usually the most common cause and patients who have CKD they lose two things one is they lose the ability to excrete phosphates we talked about that in the hypocalcemia portion right so phosphates go up the other thing is they lose the capacity to express lots of alpha 1 hydroxy what does that lead to less conver version of 25 hydroxy vitamin D to 1 comma 25 hydroxy vitamin D now I'll have a decreased vitamin D now here's what I want you to remember if I have high amounts of phosphates and I have low

amounts of vitamin D they just work through different mechanisms but both of them end up with the same result which is what they end up with a patient developing what hypocalcemia now you're probably like okay Zack wait a second we're talking about hypercalcemia bro what's going on here hang on hang on we know that high phosphates will bind up the calcium and reduce the free calcium we also know that low vitamin D won't absorb calcium across the git this is what leads to low calcium now here's what's cool this low calcium will then just peack

away at the parathyroid gland constantly continuously continuously this part here this is secondary hyperare thyroidism what happens is is once these parathyroid glands start to undergo hyperplasia they gain what's called autonomous hyp secretion what the heck does that even mean all that means is that I tell these parathyroid glands to replicate replicate replicate and then they gain the capacity on their own like an adenoma to start pumping out pth when that conversion occurs that is when we we've reached the state of tertiary hyperparathyroidism NOW Watch What Happens here once that occurs we're going to pump

out so much pth it's absolutely insane when this pth is pumped out in super high amounts guess what happens it then goes over here same thing it's going to go to the kidneys and it's going to go to the Bone but it prefers because the kidneys are damaged to really Target this one very very heavily and what it's going to do is it's going to massively stimulate osteoclastic activity to break down the bone tissue and lead to massive bone resorption this is the difference so when you look at these two here they both have high

pth levels they both have high calcium levels but what's the difference what do you notice here this one's going to have high phosphate what happens if you have high pth and good kidneys you dump phosphate so often times in patients who have primary hyperparathyroidism they have hypophosphatemia patients with tertiary hyperparathyroidism have hyperphosphatemia that's a big difference also low vitamin D if you have high pth you'll have high vitamin D that's an important thing to remember for these all right so we talked about these pretty good I think we have a good idea the differences between

these two high pth high tph pth high calcium both have high calcium this one has high phosphate low vitamin D this one has low phosphate and high vitamin D all right let's now move into to The Next Step vitamin D too high now if the vitamin D is too high what's the reason oh bro you're just popping vitamin D pills every day yeah it's got to be the reason right no that's not the reason often times often times it's due to rare granulomatous disorders what the heck does that even mean exactly what you're talking about

often times there's a disease it's called U sarcoidosis and another one called Hodgkins lymphoma so let's say that a patient has lymphoma particularly we see it more commonly in Hodgkins lymphoma or you have sarcoidosis these are often times what we Define as like granulous diseases now these granulous diseases all right have the capacity to increase the expression of a very special enzyme that I talked about to you what is that enzyme this is the alpha one hydroxylase now you're like okay all right Big Daddy in I got it I know now what he's talking about

if I increase the expression of this enzyme if these tumor cells or granulomas increase the expression of this enzyme why is that important if you remember the liver helps to convert what's called kic calciferol into what's called 25 hydroxy vitamin D and then what ises this enzyme do he takes and converts this bad boy into 1 comma 25 dihydroxy vitamin D now if I have this guy present and he's stimulating this like like a son of a gun oh baby we G to have a lot of this and if we have a lot of this

what are you going to do it's going to go to the git it's going to stimulate the expression of these luminal calcium channels if I have lots of luminal calcium channels that are present guess who's going to come flowing across this calcium so I'm going to get increased calcium absorption across the git into the bloodstream now here's where it's important diagnostically pth is high in hyperparathyroidism primary and tertiary but pth should theoretically be low in these states now I'll explain why because if calcium's coming up what should that do to the parathyroid it should suppress

him so now this calcium is going to go to the parathyroid shut him down say hey shut her down boy and that's going to drop the pth levels so if you check a patient's pth levels and you find that they're low you should suspect high vitamin D if you check it and it's high you should suspect high perpare thyroidism primary versus tertiary all right so the next situation is what if the pthrp is the problem so all right so it's not high pth and if it's not high high pth then it's probably a low pth

state if it's low pth you think about oh okay it could it be high vitamin D if it's not high vitamin D you think about the high pthrp now with this particular scenario we often times see this in lung cancer I'd say it's the most common type of malignancy that you can see this in all right and it's usually seen in What's called the squamous cell type all right so squamous cell cancer or carcinoma so you can often times abbreviate that SEC right so we can see it a but you also can sometimes see it

in breast cancer all right and again what type is it again Squam cell carcinoma and sometimes you can even see it in renal Cancers and again that's going to often times be swam cell carcinoma now the big thing with this is that these cells have what's called A paraneoplastic syndrome in other words they gain the capacity to secrete these types of peptides so to pump out pthrp if I'm going to pump out lots of this pthrp because it is produc a normal amounts by certain types of tissue cells but it shouldn't be produced in large

amounts if I'm producing it in large amounts what's the end result well it's the same thing I told you guys it goes to the Osteo class and it stimulates the osteoclast to do what increase bone resorption it goes to the kidneys but it only does one thing at the kidneys it increases calcium reabsorption it does not it does not lead to the formation of active vitamin D so vitamin D levels would be What What In this one it would be low right the vitamin D levels would be low in this one because it doesn't lead

to the activation of vitamin D as much this one would have high vitamin D this one wouldn't have as much of a high vitamin D it should usually be normal or low in this situation now what's going to happen I'm going to liberate sorry wrong color I'm going to liberate calcium from the bone and I'm going to reabsorb calcium across the distal convoluted tubule that's going to increase the calcium in the bloodstream what does increase calcium do to the parathyroid gland suppresses the parathyroid gland what will the parathyroid gland do as a result shut down

its pth production so we can see here how if you have low pth levels think think about vitamin D and pthrp being elevated okay my friends we come to the last particular cause and scenario here if patients having hypercalcemia what if it's lots of bone turnover okay I told you before that it had something to do with the Osteo class they were going absolutely ham bone and if these osteoclast if you're having massive massive osteoclast activity what's the issue with this well again I told you have the receptors right they have these receptors all over

them they can be very very heavily influenced byy cyto kindes and other ligans uh in patients who have what's called liic lesions so you see this it's it's a kind of you're destroying the bone so we have liic lesions there's two differentials that I'd want you guys to consider one is multiple Myoma so multiple Myoma is definitely going to be a big one so it's when those plasma cells are pumping out lots of those imunoglobulin and sometimes the plasma cells can infiltrate into the bone tissue right that's one big one the other reason is bone

metastasis I had to be quiet because I had to think about how to spell these dang things but in patients who have liic lesions it's usually due to multiple Myoma or bone metastasis now often times in multiple Myoma it can release like a molecule I don't want to get too crazy but it can release these different types of lians like what we call Rank liand and this may directly activate the Osteo class bone Matas es they may also release certain cyto kindes like inter lucans and tumor necrotic Factor Alpha that may stimulate these osteoclasts what

I want you to remember is when you have this effect these tissues and these liic lesions they are going to massively stimulate these osteoclastic to to go haywire when they go Haywire they are just going to start causing massive massive bone resorption they're going to chew through this bone look at this it's just wearing away now when they do that what's the obvious effect we already kind of talked about it we're going to liberate calcium from the bone and this is going to cause hypercalcemia now that hyper calcemia when we get lots and lots of

calcium into the bloodstream what can that do to your parathyroid glands again it should suppress the parathyroid glands and should say hey bro the calcium is too high you got to shut down your pth so that this thing isn't pumping it out as much and if I shut down the pth production this hopefully theoretically will cause less calcium to be formed in other words from the bone from the kidneys and from the vitamin D activation big thing to remember though with this is we talked about a lot of these things right how would I know

multiply Lomo from bone matastes we'll talk about this later sometimes it can come down to what's called alkaline phosphatase and also for this one you would check what's called an spep we'll get into the diagnostic measures what I want you to think is often times in patients who come into the hospital who have hypercalcemia the most common cause 50% of the time is hypercalcemia of malignancy and what are things here that you see as a result of malignancy litic lesions so if a patient has litic lesions like Mula bone metastases this can cause hypercalcemia malignancy

anything that causes an increase in pthrp this can cause hypercalcemia malignancy and even in these particular situations maybe like having hodkin lymphoma this can even potentially cause hypercalcemia malignancy so I don't want you to forget that in the sense that hypercalcemia malignancy is the most common cause of inpatient hypercalcemia whereas hyper parathyroidism is the most common cause of outpatient hypercalcemia all right all right my friends we have talked a ton and dedicated a lot of time into understanding the patho fiz the causes let's dig right into the complications of why calcium can be so detrimental

if it's too high or too low all right my friends so now we've talked about the reasons as to why the calcium is too low in hypocalcemia and the calcium's too high in hypercalcemia we now need to understand how would a patient who has hypocalcemia and hypercalcemia present because that's often times the most important thing often times more than not they're asymptomatic you may get lucky and find a couple different manifestations but often times this is an incidental finding that you you obtain during a workup of something else or you get routine labs and you

find that their calcium's high or low but let's talk talk about this pertinent to the exam because that's how they're going to try to trigger you to think about this in the vignette so hypocalcemia one of the biggest findings is neuromuscular irritability on the exam concept behind this is actually pretty simple let's say you have too much calcium right I mean too little calcium the reason why that's a problem is calcium naturally sits to some degree around these voltage gated sodium channels on neurons right and so let's say that you have less calcium that means

that you'll have less positive charges around these voltage gated sodium channels right so again essentially if you have a decrease in your calcium such as a hypocalcemia there'll be less uh let's say blockage of the sodium channels now if you have less blockage of the sodium channels that means that if sodium is present in an adequate amount and you have less of this calcium to block this when these these channels are open oh baby are they open and they will flood with sodium and so what will happen is is in this particular scenario you'll increase

the sodium influx more than usual if a patient has low calcium because again they have less positive ions around the edge because you know sodium is positively charged if I have calcium ions here they're also positively charged what would the positively charged ions do to each other they would repel so that kind of when you think about it it prevents sodium from rushing into the cell if I have less calcium I'll have less repulsion it'll be less repulsed right so it'll rush into this neuron if it rushes into the neuron all the sodium what's going

to happen is it's going to cause the inside of the cell to become super positive and what this will do is it'll generate an action potential and if I generate a lot of action potential down this neuron what's going to happen this can then present with kind of excitability of the nerves but it can release cyto kindes I'm sorry uh neurotransmitters such as acetylcholine and that acetylcholine May stimulate these muscles to contract as well and so that's the concept is that this nerve is super excitable and then it'll also stimulate the muscle and if the

muscle becomes hyper stimulated it will trigger and increase and contraction of the muscle if this does happen here's what we need to think about if a patient has excitable neurons and excitable muscles how could they present one way in the worst case scenario actually could be seizures now these seizures is usually the worst case scenario and I would say it would actually be the least likely but it is possible now the concept behind this is that you're causing neurons in particular areas of the brain to become super irritable and you're creat this cortical irritability and

that cortical irritability is enough to be able to trigger seizures to form often times this could be tonic clonic this could be focal but I'd say if you have some kind of metabolic process more common than not you'll generate some type of generalized seizure another one that they love to put on the exams is tetney findings so one of them you can see here is called peroral Paris athas and this is basically when the patient develops numbness and tingling around this area of the mouth that's pretty straightforward right I think that's pretty self-explanatory here's the

one that's interesting if I come over to the side of the face and I tap tap tap right here is my nerve called the facial nerve so if I tap on the facial nerve so let's say I tap on the facial nerve this is cranial nerve 7 that should cause if it's super excitable it should cause contraction of the facial muscles so you'll activate the facial nerve so you'll stimulate cranial nerve 7 and this will cause facial contraction what is this called what is this you know what this is called This is called chave St

sign and so we can see this in patients who have hypocalcemia it's called chave St sign now these are the big things to think about all right the last type of presentation here and this is interesting is let's say that you take a blood pressure cuff right and what you do is you inflate the blood pressure cuff and when you inflate the blood pressure cuff you kind of activate some of the nerves that are running through the arm maybe it's the median nerve of sorts but you'll stimulate a peripheral nerve when you stimulate that peripheral

nerve it'll cause especially if it's like the median nerve it can cause some contraction and what happens is if you can cause carpopedal spasms and so this may create a carpopedal spasm the most common example that we can potentially see with this is the carpal spasms and we see this when we inflate the blood pressure cuff in the arm and it causes intense flexion at the wrist and this is usually when you inflate the blood pressure cuff to a couple millimeters of mercury usually 20 30 above what their systolic is when we see this kind

of like flexion 3 minutes afterwards this is called trose sign okay so tro sign is going to be when you inflate the blood pressure cough they have carpal spasm maybe a couple minutes after you inflate above their systolic and then if you tap the facial nerve and it causes contraction Ipsy laterally that's chave sign these are the big things to remember but I want to add one more thing to it because this is actually kind of a high old fact if you have a patient what notice is all of these can be exacerbated we can

literally exacerbate all of these what could exacerbate this so you can increase the let's called neuromuscular excitability via hyperventilation you're probably like what the heck how would I do such a thing it's actually quite interesting I'm not going to go crazy into detail but what I want you to know is is when a patient hyperventilates what they do is is they blow off their CO2 when you blow off your CO2 you decrease your partial pressure of CO2 when you decrease the partial pressure of CO2 you do what to the pH you cause the pH to

rise when the pH Rises guess what that does it actually causes more sights on albumin to open up because albumin's negatively charged and it likes to bind to protons if your proton if your pH is going up you have less protons if you have less protons you have more you have increased free albumin and guess who loves to bind to albumin if he can calcium and if you can do that it'll bind the actual calcium and decrease it even more so if you have hypocalcemia you hyperventilate blow off your CO2 increase your pH you can

have more free ALU human which will bind the calcium and if you bind the calcium that'll decrease your free calcium and worsen the hypocalcemia and worsen these signs or precipitate these signs okay so the next thing here that's really important is with you know hypocalcemia you can develop arrhythmias but I would say it's more particularly ECG changes that increase the risk of you developing a scary arhythmia now calcium's interesting because it's involved kind of within the plateau phase of the action potential within the contract myocardial cells so it's supposed to be moving into the cells

during the plateau phase right so what happens is is calcium's movement is obviously dependent upon you know its concentration gradient to a degree right and so what we want to have is we want calcium to be able to move into these cells but if there is less calcium present out here it will interfere with that normal gradient and what actually ends up happening is something kind of odd which is that when you look at the duration of the plateau phase it's now kind of prolonged and their entire repolarization phase is then prolonged right so if

you notice that you'll notice kind of a delay or a prolongation in that kind of like entire repolarization period in the plateau phase and so what that ends up kind of doing is is it leads to changes in their ECGs and so what we notice is is we start to notice that their QT interval begins to become significantly prolonged and so we'll notice an increase in their QT interval now why is that a problem the reason why this is a problem is when the QT interval begins to prolong it increases the risk of a patient

developing a very disastrous arhythmia and that AR arhythmia is called torsades dep points so that's what you want to be kind of fearful of here in this scenario is it does increase the risk of what's called torsades dip points and the problem with tors sadda points is is that this can obviously break down into ventricular fibrillation and lead to Cardiac Arrest often times in patients who have uh what we refer to is the three lows so if you have hypocalcemia hypomagnesemia and hypokalemia these are the three particular electrolyte derangements forgive me that can then lead

to this prolong KT interval and increase risk of torsades to points all right so that's the big thing is watch out for the prolongation of the QT interval I like to think about these as inversely proportional and that the sense that this more specifically the calcium will lead to a increase a inverse proportional relationship with the QT interval and so that's kind of helpful when you look at this and that's why whenever we get into hyper calcemia what do you think it'll do if it's high then it's going to decrease the QT interval all right

let's now move into our next component here which is hypercalcemia complications all right so now we're going to move on to the complications of hypercalcemia so what's completely fearful with this one well often times same thing a patient with hypercalcemia is often times asymptomatic we usually don't see symptoms or clinical manifestations of hypercalcemia until the calcium gets to greater than 12 generally as we get closer to 14 we start seeing some severe symptoms a lot of the times in school you can remember the pneumonic Stones bones Thrones groans psychiatric overtones and I like to add

in the last one M A prone but that's a pneumonic that may help you in remembering the clinical manifestations and complications of hypercalcemia let's go through these so stones nephrolithiasis or kidney stones is a very high-risk complication usually from chronic hypercalcemia the concept here is that if patients have hypercalcemia especially hypercalcemia malignancy or hypercalcemia due to high pth States they're going to have a lot of calcium in their bloodstream when you have high calcium present within the bloodstream that's not actually the specific issue the issue really exists when that calcium then gets filtered into the

urine and when it gets filtered into the urine we call that calciuria so when patients have what's called increase calcium in the urine or hypercalciuria that is really the issue because this can now bind with things like oxalate and phosphate and increase the risk of kidney stones all right and so if combined this increases the risk of kidney stones now again I think the biggest concept here is when you form kidney stones in these patients with hypercalcemia you're going to have to think about the common complication that they'll have which is or the presentation that

they'll have they'll usually have that flank pain they can also have nausea vomiting and they may even have hemera if it's kind of stuck within the urer it's causing a little bit of damage to the epithelial tissue so again hypercalcemia leading to hypercalcuria and if that calcium binds with you know you know oxalate or citrate oxalate or phosphate it can lead to calcium I'd say the most common one is going to be oxalate Stones these are the most common type of U nephias there or type of stone now that's one thing so Stones the next

one's bones now this one's actually kind of interesting in the sense that if you think about every type of reason that a patient develops hyper calcemia um except for like maybe the vitamin D excess if you have high pth if you have pth RP that's elevated or if you have liic lesions what does this start to do to the Bone it's one of the ways that we generate high calcium right so you're liberating calcium from this area and that's how the patient is developing hypercalcemia right so this is often times the result um of what

happens when you try to resorb Bone all right so things like High pth high pthrp or liic lesions when you activate those osteoclasts if you have any of these particular things they're going to really lay down this Wasteland of liic lesions and they do that by helping to activate these particular cells which are the Osteo class if you stimulate these Osteo class these will tear away the bone right so they'll increase your bone resorption now when you start chewing through the bone obviously the end result is that you can lead to hypercalcemia but what happens

is after you continue to lead to this you start to chew through the bone enough that it increases the risk of lots of complications one of them is you can get these moth eaten holes into the bone when you look at an x-ray you see all these like moth eaten holes appearance this is called insy osteitis OST IUS cystica fibrosa and this is kind of like what we call moth eaten hole appearance and cyst appearance on x-rays another one is you make the bone super porous right so you can literally lead to osteoporosis this can

be accelerated osteoporosis and the last thing is if you chew through this bone you make this bone super brittle and you definitely increase the risk of pathological fractures so in other words pathological fractures there's a lot of different areas that these can occur long bones like the femur the humorous but the spine is also a big one so you can get kind of compression fractures there as well so all of these are the potential complications that can result from a lot of bone disease particularly due to hypercalcemia right now big thing is how will these

patients present well if they present with Osteo toysical fibrosa they may present with some degree of pain pain in the particular bone that's being eaten away osteoporosis they may present with that pain as well but if they come in what's the biggest way that they could potentially present pathological fractures all right so you may find this based upon the presentation of pain in a fracture or you may find it via some type of dexa scan scanning bone density or getting an x-ray and seeing these cyst and moth and whole appearance on x-rays so that's the

big thing with a bone disease the next one is nephrogenic diabetes and cidus this actually tends to be I'd say one of the more common presentations I've seen in patients who have hypercalcemia greater than 12 concept here is actually kind of interesting and it's one of the biggest reasons why hypercalcemia severe needs to be treated with IV fluids is based upon this concept ADH is a hormone that binds on to What's called the V2 receptor in the distal uh the collecting duct and when it binds on here ADH is supposed to stimulate this receptor and

hopefully tell this receptor an intracellular signaling mechanism to increase the expression of aquaporn units and aquaporn units are supposed to help to bring water across the luminum membrane across the cell and into the bloodstream that's the job of ADH to reabsorb water when you have a patient who has super high calcium right what happens is and this is actually kind of interesting here the calcium will then kind of send some signals here that will shut down this interaction so what it's going to do is it's actually going to shut down this interaction so ADH won't

be able to precipitate this effect here on the receptor it won't be able to stimulate this process here so you won't be able to reabsorb water there'll be less reabsorption of water so there'll be decrease in water reabsorption and as a result where is that water going to go my friends right into the urine and as a result these patients will lose tons of water into the urine we call this polyurea and that polyurea can lead to hypo Valia it can lead to dehydration but also it can lead to so much water loss that the

patient could develop hyper nmia because you lead to so much water loss especially if they're not keeping up with their water intake and so this is a big thing to remember is it can cause dehydration and hypernatremia so often times when a patient comes in they'll say stones kidney stones bones bone pain Thrones they're peeing all the time that's the concept there all right so often times these patients will come in with polyurea polydipsia often times dehydration and maybe even some hyperia due to water loss this is a very common presentation all right we come

to the next one which I'd say is a less common presentation and that is pancreatitis now this one's slightly a little bit of a stretch when we say Stones bones Thrones groans we do know that hypercalcemia can do a couple things I'm just going to quickly annotate because this is not the only reason for the groans but high calcium can also induce what's called constipation which can definitely cause abdominal pain and it also may increase the risk of peptic ulcer disease so if you have this this can also cause abdominal pain but I'd say these

are the less common of the situation here what I would want you guys to remember is that it can increase the risk of pancreatitis when a patient has super high calcium what we notice here and this is actually kind of perfect it worked out here when we look at the pancreas we have the asinar cells and the pancreatic duct right the asinar cells are responsible for making these enzymes these inactive um kind of molecules which we refer to as zymogens uh these are kind of just inactive pancreatic enzymes like pancreatic proteases and lipases Etc that's

what these things are the zymogens if calcium is present calcium actually may be able to convert these into active enzymes and so now I could have active enzymes here who now inadvertently I activated because of my high calcium guess what these puppies can go and do these active enzymes can now start causing unfortunate destruction of my pancreatic tissue and that's what they'll do they'll actually start causing inadvertent destruction of the pancreatic tisue is an inflammation of the pancreatic tissue so that's the effect that this high calcium can have is it could stimulate the inadvertent activation

of pancreatic enzymes and lead to digestion of the pancreas leading to pancreatitis increasing the pr presentation of abdominal pain so that's another thing to think about okay so there's Stones bones Thrones groans psychiatric overtones this one's interesting as well in the sense that when a patient has again too high of calcium what does the calcium do you got lots and lots of calcium blocking these voltage gated sodium channels if you have lots of calcium all right and what are they going to do they're going to block the sodium channels what is that going to do

to the sodium influx well I think you just answered it you're going to block it the calcium is is not going to be able to move into these cells as easily why because they have positive charges that are repelling them around that entry site and if that happens we won't be able to stimulate these cells you'll have less Action potentials and if I have less Action potentials moving down this membrane I'll have less signals those less Action potentials that we release from these neurons what is that going to do well think about this if the

neurons aren't firing your neurons going to be like yo bro we're super chilling just you know hanging bro you and so this can slow everything down and so often times this can present in a spectrum we may see this as lethargy it may progress to confusion right and sometimes it can even lead to severe depression so it's definitely a kind of a degree or Spectrum I would say of how these patients could potentially present so this is one potential thing that I would think about with these patients all right the last one is they are

arhythmia prone so Stones bones Thrones groans psychiatric overtones and arhythmia prone the concept behind this one is that when patients have arhythmia again it's calcium is moving into these myocytes during the plateau phase so if you have lots of calcium if you got lots of calcium out here in the extrasellar space it's going to easily flush into these cells super quick right when it flushes into these myocytes super quick what's it going to do to the plateau phase it's going to shorten it because it's going to be flushing in and so what you'll notice here

is that these patients tend to have a very shortened kind of like repolarization period and that will do what it'll change the QT interval so again I wanted you to remember here that as you do what as you increase the calcium you de decrease the QT interval which is again from here to here so again high calcium will lead to a decrease in the QT interval now as you decrease the QT interval is there any specific arrhythmias that you are at risk for not necessarily and so that's why it's more of just an ECG finding

that you want to be aware of my friends we went pretty hard on calcium talking about the path of is and the causes and the complications and I think it's important because it's now going to set us up for an immediate success and understanding of the Diagnostics in the treatment so let's move into that the next thing is how do we really approach it so if I get a patient who has a you know a calcium less than 8.5 what do I do well the first thing to do is make sure it's real so we

like to check what's called an ionized calcium all that's essentially saying is calcium can come in two forms a free form which is the ionized form it's bound to nothing and then the bound form it's usually bound to things like albumin most of the time and so if I check and ionized I'm only checking that free form all right so that's one thing the second thing is I can check what's called corrected calcium so another words I can take into consideration what it's bound to most often which is albumin and if I take into consideration

maybe a patient has an albumin abnormality and I when I correct for it if the calcium comes back normal okay then this is not even real so if I check an ionized calcium and a corrected calcium and they come back normal all right in other words between the 8.5 to 10.5 this is not real hypocalcemia this is pseudo there's probably something wrong with the albumin what do I mean well again calcium comes in a free form in a bound form which is calcium and albumin so when you think about this formula per se it's looking

at the total calcium which is both of these all right and so whenever you have a patient who has you're looking at their total calcium you're trying to say okay it's a free and bound form well really if it's pseudo hypocalcemia it's not going to affect the free form it's really going to affect the bound form and so when a patient has a decreased total calcium there should be a decreased bound form that's what causes pseudo hypocalcemia well what will cause a decrease in the bound form a decrease albumin like hypoalbuminemia which we can see

in sorosis where they don't produce albumin or nephrotic syndrome where they secrete or they lose albumin into the urine either way if I have less of the albumin I have less of the bound form which drops my total calcium so if I throw this into the equation what they total calcium is what their alumen is this will figure it into say okay the corrected calcium is actually normal or it is actually low and that's the purpose of this so if we do these things and if we correct or we obtain the ionize question is how

do I know which one to do ionize is better for inpatient corrected calcium is better for outpatient um but either way if it comes back low then this is real all right and then I got to get a pth level because then I need to know is it pth dependent or pth independent so if I get the pth level and it's low it's pth dependent now and so what I know is is that this is driving the hypocalcemia and this is usually hypoparathyroidism if it comes back high then it's none of those things that's something

to do with low vitamin D or calcium sequestration or that pseudo hypoparathyroidism and so for those I would get something like a phosphate and i' get some vitamin D levels right let me explain a little bit more again if I look at the pth and I'm really trying to get this the low pth what it's telling me is I've cut out a chunk of of the parathyroid like a surgical reason of some sort right and or I had let low magnesium and I'm not producing the pth that's driving the hypocalcemia if the pth is high

this isn't what's driving the hypocalcemia something else is so it's because the pth receptors aren't responding on the bones and on the kidneys and the calcium staying low or because I have low vitamin D and I'm not absorbing enough calcium across the gut or I have CKD and I'm not activating vitamin D or I'm having lots of phosphate that's sequestering the calcium and dropping the calcium either way these things are leading to low calcium which is telling the parathyroid gland hey man help me compensate and pump up the pth so in these diseases it's a

compensation not the cause of the calcium and this disease it is the cause of the low calcium so if we go back to this side of this limb of the algorithm we say okay they have low pth levels it's hypoparathyroid I just need to know do they have neck surgery or some kind of parathyroidectomy thyroidectomy if they did it's that if they didn't then I should check a magnesium level and see if it's low if it's low it's likely hypomagnesemia give them back magnesium in this scenario I got to figure out if it's CKD vitamin

D deficiency or pseudo hypoparathyroidism how the heck do I do that well all right if I check all of these things here I know that the phosphat is going to help me in some way shape or form with CKD and then this is going to help me in some way shape or form with the vitamin D deficiency all right let's check it well if I get a high phosphate a low of one 25 dihydroxy vitamin D this is less active vitamin D oh this well if I don't have any effect of the PT so let's

say thing pseudo hypo parathyroidism and pseudohypoparathyroidism they're making pth but the pth isn't hitting the receptor well pth for phosphate what is it supposed to do reabsorb calcium excrete phosphate it can't do it phosphate goes up okay CKD we know the phosphate goes up and we know it can't activate vitamin D the other thing is was with Su hypoparathyroidism it can't it it can't act on the proximal to other cells so it can't lead to the expression of alpha 1 hydroxy and it can't activate vitamin D oh well then pseudohypoparathyroidism and CKD should both have

this all right well then how do I differentiate them look at the renal function right look at the renal function this thing is going to be jacked up so if you get a renal function panel and they're all jacked up at CKD if it's normal it's likely the pseudo hypoparathyroidism right and in the other s situation here I really want to know that uh vitamin D deficiency often times due to decreased sun exposure or malabsorptive syres or things like that nature it's really only this guy that's the problem not this guy so they'll have a

low 25 hydroxy vitamin D and that'll cause their vitamin D deficiency so that's the difference here and after you've done this let's say that you've done all this and you're like man the pth levels I can't even depend on them or there was an acute drop in the patient's calcium think about calcium sequestration right so think about did they have seizures Crush injury did they have an acute kidney injury elevated CK it's rabdo do they have non- Hoten lyoma AML they got chemo they got elevated LDH elevated uric acid um they got elevated phosphates and

then all they hypocalcemia it's tumor liis do they have uh epigastric pain lipas three times the upper limit of normal it's pancreatitis did they get massive blood transfusions it's citrate excess those are the ways that I want you to think about this When approaching hypocalcemia what about hypercalcemia again same thing is it greater than 10.5 okay it is let's make sure let's check the ioniz make sure that the ioniz actually is elevated let's check the corrected calcium for abum why well if hypocalcemia I was looking for them having low bound form and hyper calcium they

would have to have high bound form that means they would have to have high alumin I should check this even though that's less likely all right well if I do that and the calcium and the ionized and the corrected calcium comes back normal okay then it could be pseudo hypercalcemia and I got an issue with the albumin right in that case think about this again it's free and there's bound the bound is calcium and abuin so when you look look at the total calcium you're looking at the bound form and the free form and again

it can't affect the free form for it to be real all right for for it to be uh for it to be pseudo you can't affect the free form you have to affect the bound form so if I have an increase in the total calcium I have to have an increase in the bound form for it to be pseudo what's increase in the bound form albumin so hyper albuminemia there's not many things that do this dehydration maybe pregnancy potentially but again this is the only reason the patient would have this High abant the only way

you can figure this out is to plug it into this equation all right often times we kind of look at this as every kind of one drop in alumin you just multiply um you add 08 so usually for every kind of like one drop in this you can just add 08 to whatever the calcium is and determine if it's high or if it's low all right in this s situation if I check the ionize of the corrected calcium for abum and it comes back elevated then I know okay this is real and I got to

check a pth I need to know if it's pth dependent or pth independent if I check it and the pth comes back high that's hyperparathyroidism but if it comes back low it's anything with the vitamin D that's elevated the pthrp that's elevated the litic lesions or the increased bone turnover and I got to get a bunch of tests to think about this again let's talk about this you have to remember that when you're talking about high pth this is driving their hypercalcemia because their parathyroid in primary is pumping out pth or in they have CKD

that's leading to high phosphates low active vitamin D less calcium over time the parathyroids gain the capacity to overproduce the pth and eventually that drives up the calcium as compared to the low pth States it's something else that's causing their hypercalcemia and the pth is a reflection of that hypercalcemia in other words if they have high vitamin D high pthrp or high bone turnover all of these things lead to high calcium and that high calcium shuts down the parathyroid from producing pth now if we look at the hyper parathyroidism your job is to decide is

it primary or is it tertiary and we'll add in a small little caveat there for this I like to look at the urine calcium and the phosphate now in patients who have primary hyper parathyroidism what we'll find is that they'll have a very high urine calcium and their phosphate in the bloodstream will be low think about that if pth is high and primary it's going to reabsorb calcium and excrete phosphate it's going to trash the phosphates the phosphate trashing hormone so this right here suggests that a patient has what's called primary hyper parathyroidism now if

I check the urine calcium and it comes back low and they have a low phosphate this means something very very interesting so if a patient has high pth but they have a low urine calcium always think about this disease on your boards it's called familial hypocalciuric hyper calcemia it's a weird defect in their calcium sensitive receptor and the last scenario here is tertiary so their urine calcium will be high but their phosphate is what's really high because again in this scenario the kidneys are working and responding to the bth to trash the phosphate in this

one the kidneys are diseased they can't respond to the pth to trash the phosphate and the high phosphate is actually what dries IES these patients to have high pth levels right and so this is tertiary hyper parathyroidism for these we have to look at all of these okay let's think about this if I have high pthrp oh boom that's those was those Squam cell carcinomas of the lungs the kidney the breast done that's the type of hypercalcemia malignancy boom if I check the 1 comma 25 dihydroxy vitamin D and it's super elevated boom that's the

uh granulomatous diseases like sarcoidosis or potentially Hodgkins lymphoma but if those are relatively normal um or they're not super concerning that's when I got to think about potentially liic lesions or have elevated a bone turnover so that's when we get like a Skeletor survey we may do a bunch of different x-rays we may do potentially uh CT scans whatever it may be and you'll find all of these liic lesions when you see these liic lesions that's when you want to check this thing called the alkaline phosphatase it kind of determines a lot of bone turnover

uh per se and we see this a lot in cancers so when there's lots of cancers they can really chew up the bone and we'll see their ALK phosphate levels Elevate not so much a multiple Myoma so if the AL fos is relatively normal it's probably multiple Myoma but if the ALK fos is super elevated you should definitely be on the lookout for a bone metastasis all right this is the way that I want you to think about the bone turnover the elevated vitamin D the elevated pthrp and the elevated pth which could be primary

tertiary and I threw in this little nugget here that you may see on the exam whenever see low urine calcium high pth and high calcium think about fhh now what about the calcium uh other other reasons why hypercalcemia these can sometimes be on the board exams I would think about some miscellaneous causes like milk Alkali syndrome oftentimes these patients present with u metabolic alkalosis hypercalcemia and Aki thide diuretics can also cause hypercalcemia because they help to actually play a role in reabsorbing calcium across the distal tubal and lastly immobilization can also be considered if a

patient's history fits that scenario but I think this gives you everything you need to know for hypercalcemia let's now move on to how do we treat this stuff when a patient's got low calcium you just give them calcium right pretty much in the in the sense you can give them oral or IV it's just the indications depend on which one you give for example if the calcium is not like super scary low you know for example it's like greater than 7.5 but less than 8.5 I would feel comfortable not rapidly having to increase their calcium

I give them oral calcium right and the whole point is I don't want to get get these neuromuscular irritability I don't want them to get arhythmia that's the reason why if I have to give them IV calcium I'm giving it because their calcium is less than 7.5 or they're having symptoms like neuromuscular irritability or their QT interval is getting super prolonged that's when I'll give IV calcium gluconate or chloride all right the other scenarios I can give vitamin D now vitamin D is also known as calcat trial but this is the active form this is

this right here is 125 dihydroxy vitamin D the indications to give this is pretty pretty much any scenario where the patient has decreased active vitamin D watch this secondary hyperparathyroidism hypoparathyroidism and pseudo hypop pariis that's a lot of stuff let's explain this for a little bit because the purpose of this is to again prevent them from developing recurrent hypocalcemia because if you give them vitamin D you're treating their deficiency in vitamin D and you'll prevent them from developing recurrent hypocalcemia over time so watch this in patients who you're giving the oral calcium and vitamin D

to prevent recurrent hypocalcemia and hypoparathyroidism they have low pth they directly drop the calcium via the bone and reabsorption across the kidney but they also lead to less active vitamin D if I give them vitamin D and I give them calcium I fix these two it issues some would say why don't you just give them pth we don't necessarily give patients pth who have hypoparathyroidism the other thing here is what if they have secondary hyperparathyroidism or pseudo hypoparathyroidism well again in these particular scenarios where they have CKD vitamin D deficiency which is the secondary type

they have low vitamin D that again is going to lead to low calcium so if I give them vitamin D I will also give them calcium I'm going to fix the issues that they have and reduce recurrent hypocalcemia and then lastly if they have pseudo hypop parismodesen responding and they're not reabsorbing the calci resorbing the calcium you're not getting an effect at the kidney so you're not activating the vitamin D and you're getting less active vitamin D as well as less calcium reabsorption so if I give them calcium and I give them vitamin D I'm

fixing their problem all right if you could come up with a way to reduce the receptor resistance cool so again you may think oh in this scenario give pth no we actually give them vitamin D and calcium in this scenario vitamin D calcium in the scenario of vitamin D calcium now the only time where I'll give another drug like magnesium is if they truly have hypomagnesemia because if you give them magnesium it'll restore their pth production and they'll be able to you know prevent from developing recurrent hypocalcemia the next situation is phosphate binders this is

really good in situations where patients are having significant elevated levels of phosphate chronically not so much acutely so I wouldn't really say that this is the best in scenarios of high acute phosphate levels like rabdo or tumor liis syndrome things like that I say this is best in CKD so in CKD the reason why we do this is because they have high phosphate levels their GFR is dropping they're having high phosphates and that's binding to the calcium and it's sequestering and dropping the free calcium so if I give them a phosphate binder and they absorb

they they ingest this anything that they eat in their diet that has phosphates this puppy is going to bind to that phosphate and it's going to cause less phosphate to get absorbed if less phosphat is absorbed less phosphate is going to bind to the calcium and cause the calcium levels over time the free calcium to go up and again the whole point of that is that the phosphates will get lost into the stool so this is a really good indication in patients who have CKD which is that secondary hyperparathyroidism all right so hypoparathyroidism calcium vitamin

D pseudo hypoparathyroidism calcium vitamin D vitamin D deficiency calcium vitamin D CKD vitamin D calcium and phosphate binders if they have hyperphosphatemia lastly we can consider thide diuretics we only really do this in patients who have really significant issues with their pth such as hypoparathyroidism or pseudo hypoparathyroidism that is not respond to calcium and vitamin D the concept behind this is that if we're giving this what it does is is when you give thotics you're inhibiting the sodium chloride reabsorption of the distal tubule and so what happens is when you inhibit this you get less

sodium that's actually going to be present inside of the cell when you have less sodium present inside the cell now these sodium calcium exchangers become activated because sodium easily rushes into the cell because if it's lower here it can go down its concentration gradient when sodium comes in guess who comes out calcium and calcium will flush out if if calcium flushes out here what happens to the calcium inside the cell now that is going to drop and if calcium drops guess what then calcium in the tubular Lumen is going to say oh calcium in here

is really low I'm going to start flushing into this cell and eventually that calcium will get reabsorbed so you get lots of calcium reabsorption with thide diuretics which leads to hypercalcemia and so it may help to prevent that recurrent hypercalcemia and patients who aren't responding to the traditional therapies of calcium and vitamin D now this may seem like a lot let's do in an approach kind of algorithmic manner if a patient has a calcium greater than 7.5 that's safe I'm not too worried I'll go oral if it's less than 7.5 or they're developing neuromuscular irritability

QT changes IV regardless of which one I'm giving them I then need to treat the underlying cause if it is secondary hyperparathyroidism if it is hypoparathyroidism or pseudo hypoparathyroidism all of these situations respond well to giving them oral calcium and vitamin D if they do have refractory pseudo hypoparathyroidism and hypoparathyroidism and they're not responding to the calcium and vitamin D that's when I would consider thide diuretics especially if the calcium and the urine is high if a patient has hypomagnesemia give them magnesium and lastly if they have high phosphate levels and CKD add on a

phosphate binder like sevir calcium carbonate or calcium acetate all right what about hyper calcemia believe it or not the most common manifestation of hypercalcemia is often times dehydration due to excessive polyura when the patient has excessive polyera they get super volume depleted guess what we want to give them acutely so in a patient who has acute hypercalcemia and it's severe how do I Define severe less I would say in this situation the patient has to have a calcium greater than 14 and if they're symptomatic that's even worse in this situation they're likely severely volume depleted

I need to give them heavy amounts of IV fluids so I'm going to give them normal saline the purpose of this is to rapidly decrease their calcium and also improve their volume status so think about this in a patient who has hypercalcemia causes nephrogenic di which leads to polyera I then can see that these patients would lose a lot of blood volume become significantly dehydrated I'm going to give them the IV fluids to replace their vasculature and pump up their blood volume that's the design of giving the ivy fluids but it also will in the

process rapidly decrease their calcium the only time we used to back in the day but this is no longer recommended is they used to use Loop Diuretics and IV fluids like normal salum we don't recommend that anymore the only time that you'll use diuretics if the patient is getting IV fluids and because of the excessive amounts of IV fluids because you have to give these patients sometimes 3 to six liters of IV fluids to rapidly replace their volume losses and help drop their calcium if they start to develop pulmonary edema uh and as well as

excessive like a volume overload with respect to their legs they're developing a lot of swelling and hypertension then I would consider giving the patient diuretics only then after you've given them a good amount of fluids to replace their volume losses and help to drop their calcium the next drug that you want to give is calcitonin the reason why you want to give calcitonin is this has a very quick and acute onset and what it's going to do is it's going to go at the bone and it's going to shut down these Osteo class if it

inhibits the Osteo class it's going to shut down the bone breakdown if I shut down the bone breakdown I'm going to reduce the liic lesions and all the bone disease processes and I'm going to help to decrease the calcium because if they're not breaking down bone they're not liberating calcium again calcitonin is the first line agent because it has the quickest onset but its duration is not as long so then after I've given them IV fluids and I've given them the calcitonin if I need a drug because I suspect that they have hypercalcemia of malignancy

which is often times the most common cause of severe hypercalcemia that's when I would make a decision to give one of the two drugs next a bis phosphinate or a denap bis phosphinates are good to give in the acute management especially when the calcium is greater than 14 they're symptomatic but more specifically you want long-term control because you think that they have hypercalcemia malignancy the purpose of this is to also help to decrease the calcium but it's not going to be rapid it's more of preventing bone disease and preventing recurrence of hypercalcemia and hypercalcemia malignancy

again bis phosphinates and nsab just through different mechanisms are going to shut down the osteoclast decreased bone breakdown decrease bone disease like osteitic fibrosa osteoporosis uh pathological fractures as well as they'll decrease the calcium the only difference between these and calcitonin is that bis phosphinates have a longer onset so they're going to have a longer onset you're going to use these more likely continuously in the patient but you have to be careful because they're somewhat contraindicated in severe kidney disease so if the patient has severe kidney disease you may want to go the route of

dsap who also has a long onset but it's a little bit more safe in patients who have underlying kidney disease so this is what you're going to throw on ivu fluids calcitonin and then one of the other drugs can be added on for long-term control not as much acute control and that's the bis phosphinates and denap if you've done all of these things you started a patient on IV fluids you've given them calcitonin started them on a bis phosphinate and their calcium remains elevated despite these measures that's when I would go the route of putting

a patient on hemodialysis all right the next thing is after youve treated the acute problem which is the severe hypercalcemia then you need to treat the underlying cause and so sometimes we'll then move to the next thing which is okay what was really driving this if a patient has what's called hyper parathyroidism whether it's primary AR or tertiary and they're not a good surgical candidate all right in other words if they have parathyroids that are really big because of primary problem so an an adenoma or they have parathyroids that are enlarged because of the uh

CKD that's cause them to hyperplasia undergo hyperplasia we would want to cut that out but if we can't cut that out let's suppress those cells from releasing pth the best that we can so that's when we use calcium edics like cic calet what's really interesting about this is that this can help to prever prevent re urrent hypercalcemia in hyper parathyroidism how these work is really interesting calcium binds to a calcium sensitive receptor and that's supposed to say hey if calcium's High shut down pth well if I give a drug that acts like calcium it can

do the same thing and it'll bind to the calcium sensitive receptor and say hey calcium's kind of high shut down the pth synthesis and this can potentially help in patients with hyperthyroidism it can prevent hypercalcemia if the patient is a good candidate for surgery and they have lots of bone disease lots of kidney disease this is where I would potentially say we should do a parathyroidectomy we should cut out the parathyroid glands and after we cut them out we want to in case they need to have uh the parathyroid at least some degree of it

having a basil release or if we have to go back in and cut something out let's not keep it in the neck often times what they'll do is they'll implant that par thyroid gland into the forearm so it's an easier side of access if they have to remove it later all right lastly if a patient has hypercalcemia due to uh some type of lymphoma or sarcoidosis cortical steroids are actually preferred and it's because these help to suppress this alpha 1 hydroxy which leads to less active vitamin D and then less calcium so again giving steroids

will suppress this alpha 1 hydroxylase and that's the concept here to remember now I know this is a lot how do we do this how do am I supposed to remember this here's the way I want you to remember if it's high and they're symptomatic this is not good you got to get acute management ongoing now get them some fluids get them calcitonin and get bis phosphinates or denosumab on board if the calcium is less than 12 so they're likely to be less severe they're asymptomatic in this situation you can take your time and treat

the underlying cause if the patient has been treated with IV fluids calcitonin bis phosphinates and they're not getting any better that's when you go to hemodialysis but if they are experiencing Improvement then we fix the acute issue now we got to prevent them from developing recurrent hypercalcemia how do we do that we ask ourselves the question is it hypercalcemia malignancy oh it is keep going with these is it some type of primary tertiary can we cut out the parathyroid or can we suppress the parathyroid cal cal mics like calet or parathyroidectomy depending on their surgical

candidacy and then lastly is it um in this scenario IO sarcoidosis or lymphoma corticosteroids so this is the way that we acutely treat them determine if they need rigorous hemodialysis or if we can just go straight to treating the underlying cause ninja Nur I lo I know this was a lot but I really hope it made sense I hope that you guys enjoyed it and I love you I thank you guys and as always until next time [Music]