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Right. Can you guys see the presentation? Oh, it's pil Is that visible? Yes, we're able to see it. Cool and we're live. Right. Yes. Yes. Um So hi, everyone. Uh my name is and do you want my name is? Um and we're going to be um doing our tutorial today on metabolic conditions. So we're looking at sodium potassium and calcium balance. Um quick introduction. Um We are teaching things and we're all clinical medical students and we run tutorials every Thursday at six this time. Um until December, we're focusing on um like core skills and um conditions that we need to know about. And so from next time, we'll be doing Aitor based on co presentations. Um Our slides are reviewed by doctors for accuracy and um we post about ours on social media. So keep an eye out and obviously follow us on me um to see which tutorials we're doing. Um So as I said before, we're going to be covering sodium potassium and calcium balance and I'll be doing sodium balance. So the next 40 minutes or so, um we'll be having some S PA S via poll and I'll also be asking some questions. So please um, respond to those in the chat and also put any questions that you have in the chat and also if you want to, you can. Um, yeah, basically put any questions that you have in the chat and, um, do try and engage and ask as many as possible and let me know if there's anything that isn't completely clear. Um, so we're starting with a case. Um, so we have an 88 year old woman who presents to A&E with a six hour history of vomiting, muscle cramps, lethargy and confusion. She has a past medical history of heart failure and is in RMR Spironolactone and Furosemide and she lives in a care home. So does anyone want to tell me the first thing that we do um for this woman who's presented to A&E is the first thing we do when managing her. Anything in the chart. So far, you guys feel free to add something to the chart. Someone says vitals, vitals, yep, anything else or moving for a specific time? So I'll just move on. Somebody said a nice, yeah, fantastic. So what we really want to do when any patient presents acutely is an a assessment. So we want to assess their airways breathing um circulation disability and um exposure. And so we've quickly examined the patient just to see um assess her kind of state of health acutely. And on examination, she has dry mucous membranes and cold peripheries um with a cap refill of three seconds. Um BP of 98/60 a heart rate of 100 and 20 beats a minute. Um We also do some bloods, never mind. And um these are her bloods. So, can anyone recognize the abnormality here? Please put it in the chart. Anything in the chart? Ok. Great. Hyponatremia. Fantastic. So she has very, very profound hyponatremia. So what actually is hyponatremia? So we know it's no, it's low serum sodium and the normal range is 100 and 35 to 100 and 45 millimoles per liter. So, anything less than that is hyponatremia, um We can classify it into three categories, mild, moderate and profound. So mild is sort of 100 and 30 to 100 and 34 moderate is um 100 and 20 to 100 and 29. And then anything less than 100 and 20 is considered profound hyponatremia. So if your serum sodium is above 100 and 30 you're very unlikely to have symptoms, but less than that, you're more likely to have symptoms. And if someone's having, which will, I'll go onto that in the next slide actually. So, um these are the three categories of hyponatremia. So, on two signs and symptoms. So we can remember them with the pneumonic salt loss. Um And it's important to bear in mind that often hyponatremia is asymptomatic. So it's actually the most common electrolyte abnormality and up to about a third of hospital patients may have hyponatremia. But if it's, if they have a more mild hyponatremia, often they're asymptomatic. And if they are symptomatic, um the symptoms are quite nonspecific. So if someone has um a serum sodium sort of above 100 and 30 they have some of these symptoms, you're more likely to consider other causes because their sodium isn't really so out of balance as to be precipitating these symptoms. But then if you go below sodium of 130 you might start to see symptoms. And if you have a more profound hyponatremia, you might see very, very severe symptoms like seizures, coma, uh cardia, respiratory arrest. Um but basically, there's a grading of severity and sometimes these symptoms can be quite nonspecific. So you have to consider the patient um their history, um uh their drug history, their um their past medical history. Um what their hospital stay has been like um to kind of establish whether the cause of these symptoms is hyponatremia or something else. And you have to look at it in the context of what their serum sodium actually is. So higher serum sodium or closer to normal means that it's unlikely to be causing these symptoms. And you have to consider another cause. If you have a more severe um classification of hyponatremia, then you're more likely to it, that's likely to be pre precipitating some of these symptoms um and it's also important to bear in mind that you have the milder symptoms, like headache, nausea, um lethargy, and then you have the more severe ones. So, vomiting, seizures, coma, cardio, respiratory arrest, uh signs of very um of a severe hyponatremia. And that changes your management basically. Um Any questions so far, so no questions for them to chat at the moment. Um Just feel free to put them there. It's also important to bear in mind that you can develop an acute hyponatremia, which is within less than 48 hours. Or you might have a chronic hyponatremia which develops over more than 48 hours. Unfortunately, lots of patients, um it's unclear when they became hyponatremic. So unless you have evidence to believe that they became hyponatremic acutely, um you assume, and you don't know that they developed hyponatremia within 48 hours, you then assume that it's a chronic hyponatremia and again, acute, how acutely the patients develop hyponatremia is important for management. So let's go on to that. So, first of all, when a patient has low serum sodium, when you have their results, you have to consider how quickly they presented. So if you know, for certain that they've um or you have reason to suspect that they developed hyponatremia within the past 48 hours, regardless of the severity you have to contact ICU so that they can be treated with hypertonic saline. Um The reason for this is that um if hyponatremia develops acutely, the brain doesn't have time to compensate. And because you have this increased um body water like water in the extracellular fluid, water moves into um the neurons and causes cerebral edema which can then cause brainstem death. Um because of pressure on the uh on the um brainstem basically. So it's really, really important to correct this electrolyte abnormality very, very quickly with hypertonic saline. Um However, if um hyponatremia developed more chronically, the brain would have had a chance to compensate um to avoid the development of cerebral edema. So then when you know that a patient has chronic hyponatremia, you um assess the severity of their symptoms. So if they have severe symptoms like um vomiting or they are having seizures or they're in a coma or they're undergoing respiratory arrest, obviously, if they are undergoing respiratory arrest, you have to deal with that. But if they have severe symptoms, again, you want them to be um admitted to ICU and treated with hypertonic saline. However, if they have more mild or moderate symptoms, um like for example, muscle cramps or just a bit of nausea or some lethargy, you then go on to assess, assess them further and determine, and there will be, there are a few stages to that assessment which we'll go through. Um So we'll need to identify the cause and then treat the cause and correct uh sodium and fluid balance. Um Any questions so far. Ok. So how do we actually assess? Um, we, first of all assessed, is it an acute hyponatremia? If it's acute, we had to admit them to ICU to treat them with hypertonic saline. If they have severe symptoms, then we again admit them to ICU to treat them with hypertonic Saline. But now we have a patient in front of us who's got mild or moderate hyponatremia, um, which has developed chronically. So, does anyone know what we have to assess to determine what's causing that hyponatremia and how we can treat that? Any ideas? I said full blood count, full blood count. Not quite. There are other things that we have to look at. It's kind of three main things that we have to look at serum osmolality. Very good. That's the first thing that we look at. So plasma osmolarity, anything. What does anyone know what we look at after that fluid status? Fantastic. And then what's the last thing that you look at to classify the cause of someone's hyponatremia serum sodium, someone? So we've already got, we've already got the serum sodium. That was our first result. But what we need is urine sodium. So the first result that we had was the serum sodium we sent you and we got the serum sodium before. And that's how we assess that they have a hyponatremia. We've established it's not acute and they don't have severe symptoms. So the next things that we look at are plasma osmolarity then fluid balance, then urine sodium and this um we'll go through this diagram in detail to establish um what the cause of this hyponatremia might be. So the first thing we need to look at is plasma osmolarity. So, osmolarity is defined as the number of solute molecules per liter of solvent. And osmolality is the measurement that we more regularly have because you don't routinely go around measuring someone's fluid volume, it's you know what their weight is. And so you can kind of estimate the number of solute molecules um per kilogram. So you can kind of estimate based on a person's body weight, what the weight of water in their body is because that's about 70%. Um So what we have osmolality, we can estimate osmolality. Um And then based on that, we can estimate estimate osmolarity. Um there's a calculation that we do to determine um plasma os molarity and that's uh twice the serum sodium added to the, the um glucose and serum added to the urea. And that sometimes comes up in um b. So it's important to know this formula. Um And we can use this formula based on and um our results and blood glucose to determine plasmas minority. And this allows us to classify um hyponatremia into um hypotonic isotonic or hypotonic hyponatremia. I know that the wrong of it. So, isotonic hyponatremia is where the osmolarity of the plasma is normal between 275 and 295 million osmoles per kilogram. Hypotonic is when the osmolarity of the plasma is lower than it should be. And hypertonic is when it's higher than it should be. And the UCL exams these ranges should be given to you. Um So that's our first stage in assessing hyponatremia. So we've already established persons not acute, hasn't developed an acute hyponatremia. They aren't severely hyponatremic. We don't need to treat them with 3% saline. What we're trying to do is we're trying to get to the cause of their hyponatremia. And the first thing we look at is their plasma osmolarity. And we look at their plasma osmolarity to determine whether they are i their um plasma is isotonic hypotonic or hypertonic. Is it the same concentration that you expect plasma to be? Or is it the normal plasma concentration? Is it more dilute than we expect it to be? Um or is it more concentrated than we expect it to be? And then after that, we'll go on to assess balance and urine sodium. But first of all, let's look at what um it means if um what the different plasma osmolalities might mean for the cause of the hyponatremia. Any questions so far before I move on? No. So we've established, don't worry about this. I'll talk through this in detail. So we've got, we calculated the patient's plasma osmolarity. The first instance is that the first like possibility is that they their plasma osmolarity is lower than the normal range. And this is what we call a hype. And we already know that their serum sodium is low. So they have what we call hypotonic hyponatremia. What this mean? This is basically a true hyponatremia because actually what's happened is that you have low serum sodium and um or increased total body water. So your sodium is actually more dilute than it should be um as opposed to the other um possible cases which we'll look at. So basically, what's happened here is that the sodium irons have been diluted out because you have more water than normal or you have actually lost sodium irons or you've not gained enough or whatever. Basically, there's less sodium compared to water. And this is a true hyponatremia basically. So it's actually low sodium compared to water. You might also calculate a patient's plasma osmolarity and find that it's in the normal range. And this is what we call an isotonic hyponatremia or a pseudo hyponatremia. So the issue here isn't actually that you have low serum sodium compared to total body water. What actually happens is that in these patients um there's high lipidal protein and basically what this does is it makes the plasma volume compartment seem bigger than it is. So your plasma volume seems larger than it is because some of it's been taken up by lipidal protein because your plasma volume looks like it's larger. It seems like you have more body water than you actually do. Um But your sodium levels are proportionate to the level of total body water that's present basically. And because basically, you're dividing the same number of sodium ions by a larger volume or a larger apparent volume, it seems like your sodium's been diluted out. So this is an isotonic hyponatremia, the protein and fat basically inflate the plasma volume compartment artificially and make it seem like the sodium's dilute. Any questions on hypotonic or isotonic hyponatremia. Alternatively, a patient might have higher than normal plasma os minority. In which case, they have hypertonic hyponatremia. What this is called, this is basically called a translocational hyponatremia. So what happens is they have hyperglycemia potentially due to um like obviously you as a complication of diabetes. Um and basically what this does is it increases the plasma osmolarity because um we know from the equation that an increase in glucose or an increase in any of these three electrolytes or substances that you find in the plasma will increase osmolarity. And obviously, this will basically make the plasma more concentrated than it's supposed to be. And so water moves from the intracellular fluid and into the extracellular fluid. And that basically dilutes out the sodium. The issue isn't that you have less sodium um or more water than normal for the plasma compartment. It basically just looks like you have less sodium than your total body water because body water has moved from compartment to compartment. Um and this is what it is meant by translocational hyponatremia that the wa the water is moving out of the intracellular fluid and into the extracellular fluid. So, if we look at osmolarity, these are the and um we know that a patient's hyponatremic. This is how we can classify their hyponatremia and actually only in the first case of hypotonic hyponatremia um is the actual issue to do with sodium Only in hypotonic hyponatremia. Do you actually have less sodium than total body water in isotonic and hypotonic and hypertonic hyponatremia. The issue isn't with sodium. So you don't need to add, you don't need to treat um to correct the sodium balance. You need to treat the cause of the hyperlipidemia, the hyperproteinemia or, and you have to give fluids for if you have um high glucose to allow to dilute out the glucose and allow the translocational hyponatremia to be corrected. Um But the issue isn't with sodium if it's isotonic or hypertonic hyponatremia, the only true hyponatremia. The issue with sodium is hypotonic hyponatremia. Are there any questions so far? So we're continuing to assess this patient and we've determined their plasma molarity and we've determined that they have a hypotonic hyponatremia or a true hyponatremia. So they, it's actually an issue with their sodium. So they've had, they have reduced sodium compared to um their total, their plasma, um the water in their plasma. The next thing we're going to assess is fluid balance. And when we assess their fluid balance, we can either categorize them as hypovolemic. So they have um they're quite dry volemic. So they have a normal um total body water or hypervolemic. So they're fluid overloaded. They have too much um plasma volume and fluid in compartments. It should not be in um or too much, which will obviously, if there's too much plasma volume, it will move up into the extracellular um fluid and cause edema. So my next question for you guys is how do we assess a patient's fluid balance? Which signs do we need to look for when we're doing an examination? What are the stages in examining, what are the stages in fluid balance assessment? So just put anything in the chart. Let me a shot. Oh OK. All right. So cap refill time, edema, mucous membranes. OK. Urine output. Yeah. Any fluid loss via vomiting. Very good skin turgor. Mhm Good. So, yeah, some good, good suggestions though. Some ideas. Um So ki medics has um should have a video and this is their mark scheme um for the fluid balance for how you perform a fluid balance assessment for os. But it's really really important to assess the patient's fluid balance in um clinically. Um And you guys have included many important aspects of fluid balance assessment. It's also really, really important to like we said, we check for peripheral and sacral edema. It's also really important to listen to the lung bases. Um You can also assess the abdomen for ascites. Um also check the JVP. It's sometimes hard to see. So there are other ways of looking um assessing balance that are a little bit more sensitive. You can actually tell, um you also palpate the pulses um for rate and rhythm and then also character and it's important to take the BP, patient's BP as well. Um That's really crucial. Um So you'll have very good ideas, but just make sure take the BP, um listen to the lung bases, check the peripheral and sacral edema. Um And also you can do lying and standing BP, which um obviously, if someone's hypovolemic, then that will drop when they stand up. Um So just take a look at the tics um page and just make sure that, you know, this very, very well because it's really important clinically. And also um it's her when I was in fourth year, one of the doctors mentioned that there was a case of a someone looking at mucous membranes and assessing the patient who's having dry mucous membranes without realizing that they had um crackles on auscultation of the lung bases and they had peripheral edema as well. So, and gave that patient a fluid bolus and they basically had a cardiac arrest. So don't let small signs override the big ones. So try and take into account the entire clinical picture. Really important signs are peripheral and sacral edema crackles. Um raised J BP that patient's fluid overloaded. You not do not wanna give them more fluid. Um Basically. Um So yeah, we've talked through the fluid balance assessment. Um put any more questions that you haven't chat. Um So we're going back to assessing our patient with uh hyponatremia. We've established that they have, they aren't acutely, they haven't developed their hyponatremia acutely. They don't have severe symptoms. Um We, they have uh low plasma osmolality. So we know that actually it's serum sodium, that's low compared to their total body water. Now, we've assess their fluid balance and there are three possible cases. So they could be hypovolemic. So this will be um they don't have any evidence of edema. They probably have sun Chronis reduced skin turgor, um delayed cap refill. Uh probably a low BP. They have a hypovolemic hyponatremia and this is basically where the total body water drops, but total sodium, serum sodium drops even more. Basically, someone might also have a euvolemic hyponatremia. So their, their fluid balance might be normal. There are no signs when you assess their fluid balance, their BP is normal. Um no edema. Um mucous membranes are moist, they look fine. And so this UIC hyponatremia is basically caused by the total body water compartment being slightly larger than usual. So there is some fluid retention, but it's not significant enough to cause edema, but the serum sodium is normal. So this person has a euvolemic hyponatremia. This is the total body water is a little bit inflated. They have normal serum sodium relative, they have normal sodium relative to what a normal total body water would be. But it's the sodium is now slightly dilute because they have more water in their plasma. The third kind of outcome on fluid balance assessment is that you might have someone who's got crackles, who's got peripheral edema, um who has a raised JVP. And this person is clearly hypervolemic. And what's happened here is that there, they have increased total body water. So more um water in the extracellular compartment, more water in their plasma. Um but the water, total body water has increased more than the sodium. And so that's kind of diluted out the sodium a little bit. So they have hyponatremia because they've got more total body water relative to their sodium. So we've assessed a person's os plasma osmolarity and we've used that to identify whether they've actually got a true hyponatremia. And now we've assessed their fluid balance and that's going to help us identify the ultimate cause of hyponatremia. So the next thing we look at any questions there. Um So the next thing we look at you have one question. Yeah. So somebody's asked. So in hypervolemia, both sodium and water are increased. Yeah. Yes. But total body water will increase more than the sodium. So we'll go on, we need to look at the causes of hypervolemic hyponatremia. And we'll see that basically, it's because you have increased fluid volume in most compartments. Um And basically the reasoning for that like or whatever the ultimate cause is for that increased fluid volume, whether that's like heart failure or liver failure or kidney failure, it basically causes you to retain more water than sodium. So there's more water relative to sodium basically. And so that dilutes out the serum sodium Basically. Uh any questions that that doesn't make sense. Ok. Take that yes. Um So the last thing we assessed to establish the cause of hyponatremia is urine sodium. So if someone's urine sodium is high, it means that there is a problem with the kidneys because if you have low plasma sodium or low serum sodium, you should really be reabsorbing more sodium in the, in the in the tubules um to compensate. But if you're not, and you're instead excreting that sodium, it means that the kidneys aren't functioning properly. But if you have low urine sodium, the issue isn't with the kidney because the kidney is performing as expected. And this is probably going to be sodium um loss um due to for example, vomiting or diarrhea, which we'll go into. So now we've finished assessing the cause of a person's. Um Now we've established basically our patient's plasma osmolarity. We've established the fluid balance and now we've established um their urine sodium and that's going to help us classify the course So we've got a patient who's got low plasma osmolarity. So they have a true hyponatremia. They're hypovolemic and their sodium is low. What are the causes of their hyponatremia? So, if they've got a high urine sodium, the issue is with the kidney, you're losing sodium in the kidneys. And that could be because of diuretics. Um or it could be because the kidney itself isn't functioning. And this could be because of adrenal insufficiency or salt wasting properties, which is the actual issue with the kidney adrenal insufficiency is due to hormones not acting properly on the kidney. As we know alternatively, low urine sodium means the issue is not with the kidney. You're not, it's not that you have low sodium because the kidney is not reabsorbing it. It's that you're losing water and sodium because of vomiting and diarrhea, burns dehydration. Basically, anything that causes you to lose fluid is causing you to lose fluid and sodium, but more sodium than fluid. And so um your sodium is getting diluted out basically because you're not or it's not getting diluted up, you're losing more sodium than water. And as a result, your plasma is ending up more dilute. Any questions, sir. So I'll just quickly go over the mechanisms for how some of these um renal issues cause hypernatremia. Um So how do diuretics cause a hypotonic hypovolemic hyponatremia? So we know that diuretics act on different parts of the kidney tubule snake? Ok. They and they act on transporters to inhibit reabsorption of sodium and water. If sodium and water are not being reabsorbed, then you have more sodium and water in the urine and you end up losing more sodium than water in the urine. And then, and you end up with losing w losing water and losing sodium and you end up with hypovolemic hyponatremia. Any questions there? None so far? OK. Um What about adrenal insufficiency? So, adrenal insufficiency means that you can't. Your adrenal glands obviously are being um attacked by um autoantibodies and autoimmune disease. And obviously, your adrenal glands are unable to produce um the hormones they usually produce. So cortisol Aldo our, our cortisol or aldosterone, you aren't going to have as much aldosterone circulating. What does aldosterone do in the kidney? It's a question to everyone. Any ounces. Not yet guys feel free to put it in the chat. If you think back to some preclinical pharmacology, it doesn't even need to be a detailed answer. Generally. What's supposed to do? I don't need transporters or anything, anything. Ok. Regulate BP. Yeah, it does regulate BP and the way it does that is by um causing reabsorption of sodium. And obviously, if you're reabsorbing sodium, you're reabsorbing water. If you have less aldosterone, you're not going to be reabsorbing as much sodium and the transporter that the receptors that aldosterone acts on are in cells that are in the collecting duct. So the the latter part of the Nephron. Um And basically what happens is that if you don't have aldosterone causes excretion of potassium and reabsorption of sodium. If you don't have it, you're not going to reabsorb sodium and actually you'll just keep potassium in the cells. So it's what's called a potassium sparing. Yeah. No, I won't say that. No. Um Basically, no less aldosterone means less sodium reabsorption. If there's less sodium reabsorption, then you aren't going to draw as much water up because obviously there's less of an osmotic effect. And so you have more sodium in the urine and less in the serum. Potassium is the other way around. If you have less, less sodium, you have a hyponatremia, you have more water in the urine and less in the plasma. That's hypokalemic questions. Does it make sense? So, to summarize if you have a hypovolemic hyponatremia, that can be because the kidneys aren't reabsorbing sodium. So you have either diuretics or adrenal insufficiency or nephropathies or it could be because of um a nonrenal issue such as diarrhea, vomiting, burns, blah, blah, blah. Um other ways in which you lose fluid and sodium. So what about euvolemic hyponatremia? So if you have a hypotonic volemic hyponatremia and you have a low urine sodium, that's because of water intoxication. So if someone is drinking too much, basically, and that basically ends up just diluting out the sodium, but you don't, your total body water gets distributed across the different compartments or across the plasma, across the intracellular fluid, across the extracellular um like fluid. So basically, your sodium is getting diluted because you have more water. But you don't really have edema cos it gets distributed. Basically, if we have high urine sodium, again, we establish that's because the kidney isn't working as it should. Um And that's because it's reabsorbing water but not sodium. And this is because of a condition called SI A DH or symptom symptom of inappropriate antidiuretic hormone secretion. So, does anyone know what Si A DH does or how it works? Actually, I'll just do this. Yeah. Any ideas in child, I can just explain it. Um So a DH or vasopressin is released uh from posterior pituitary gland. Um And in si A DH, you have too much a DH. Um And basically what this does is it causes the collecting duct in the kidney to increase its water reabsorption. Basically, what the kidney does is it reabsorbs water but doesn't reabsorb sodium. So you're keeping more water in, but you're not keeping as much sodium in. So, and the water gets redistributed and dilutes out the sodium because if you have more water and not more sodium, you'll just end up with hyponatremia. The way I remember it is A DH is like it's antidiuretic hormone. But I kind of remember it was an anti drying hormone. So it stops you from drying out because it keeps the water in. Basically but it doesn't keep sodium in. Um what are the actual causes of SI A DH as you can remember it as mad chop. So, major operations, ectopic A DH secretions and drugs, um disorders of the CNS. So basically, if that, if you have like head trauma or something like that, um that will cause your pituitary to abnormally produce um A DH um hormone insufficiencies, other causes in pulmonary disease um which can cause ADH production. Um So let's take a look at this. Um SBA. So um would you be able to activate the first pole? Yes. Sure. So I'm just gonna put a pole for this question. So can you guys see them? Just take care for a second? I can't see it. Yeah, they can see it. Great. I stop for a second. Um But have a look at this pole, this question like can anyone see it's what's going on? We can see the poll. Oh, yeah, I can do that. Yeah, I can see the response as well. I'll just wait for a couple more people to answer because you've got three so far people up here. Yeah. Got a few more. We'll wait to like 10 minus just being a bit slow on the uptake. Yeah, I think we've got eight responses so far. OK. Just two more people. Uh Everyone put your answer in. Yeah, it's OK. It's wrong. Got you screen again. I don't think we've got any more but Ok, cool, thanks guys. So, yeah, you guys are right. Um It's s IE DH. So, what we have here is a 45 year old woman who's on the surgical ward, um who's um first exhaustion during the lethargy. So, these nonspecific symptoms which might be indicative of hyponatremia and she does have quite a profound hyponatremia. Um but she seems to be euvolemic. So, um she doesn't have, there's no evidence of hyper or hypovolemia. Um But the key thing is that she's postcolectomy. And so we established that she's got a volemic hyponatremia. Um So adrenal insufficiency is unlikely, dehydration and diarrhea are also unlikely. Um That absorption is just kind of there. So she's got a volemic hyponatremia. So we're thinking si a DH um and that's corroborated by the fact that she's postcolectomy and major surgery is a potential cause of ectopic ADH secretion. Someone's asked, can you go back to this causes slide after didn't have enough. So we'll put the slides up as well. So that's kind of just something you have to memorize, but I'm going to go through it in morning 10 anyway. So basically these are the causes. Um It's just one of those annoying things and I think UCL is a bit, it, it's quite niche. The thing is when it comes to hyponatremia, there are definitely more likely causes. Um Yeah, this is for me, it, it's kind of like people tend to overstate the importance of si DH, it is obviously an important differential to consider, especially if you've got a volemic hypernatremia. But don't consider the other causes. They're more common and they're more likely basically. Um but the causes are major operate are here basically and you'll have the slides. So you can basically memorize um the features. Again, we've said it's caused SAA DH causes a hypotonic u UIC hyponatremia with a high urine sodium because you are reabsorbing water, but you're not reabsorbing sodium. Um And it basically causes urine osmolality to be higher than plasma osmolality because obviously, if you're not reabsorbing sodium, it's just going to be in your urine, which will increase the osmolality of your urine compared to your plasma because it's in the urine and not in the plasma. Um The way you have to treat it is really important. It's fluid restriction. Um And you can also give a DH receptor antagonists, fluid restriction because if you have, if you are, if you're restricting fluid, then you aren't going to lose as much because of the A DH. Um No, basically, if you fluid restrict, then you won't. Um basically the ADH retains water in the kidney, right. So if you're retaining more water than you should be retaining, then you shouldn't be taking in as much. So if you're retaining more, then you compensate for that by restricting intake. So then you won't over dilute your sodium and A DH receptor antagonists because those obviously antagonize the action of A DH and stop it from reabsorbing as much water. Um, there's also a separate Pneumonic for memorize it for, um, drugs that cause it si DH again, probably pretty niche but especially the UCL people. It's one of those things that we should know. Um So si A DH cannot void is the pneumonic. So SSRI is analgesics, antidepressants, diuretics, haloperidol and like carBAMazepine and cyclophosphamide and then, uh, vinCRIStine another chemo therapy. Any questions so far? So somebody, somebody's somebody's asked, can you reexplain the urine? Greater urine osmolality is greater than plasmosis morality. Yeah. So in si A DH, you have more a DH than you should. So it acts on receptors in the collecting duct and causes them to re causes reabsorption of water in the kidney. However, you're not reabsorbing sodium. So the sodium stays in the urine and you have more sodium in the urine compared to in the plasma. And that means that the concentration of your urine is higher, then it is relative to the water in the plasma. Basically. So your osmolality of the urine is higher than the plasma osmolality. It's kind of like you have more sodium relative to water in the urine um than you do in the plasma. Does that make sense? Yeah, great. Thank you. Brilliant. Um I'll try and wrap this up. Um I think we can go back to the SBA at the end. It's also very niche. So, don't worry about that. Um So the last thing we want to, the last kind of main cause of hyponatremia is hypotonic hyponatremia. And this is really, really important. Um The way you can remember it is basically the low urine when your sodium urine is low. Basically, hypotonic hypovolemic hypernatremia is caused by the failures. So heart heart failure, liver failure, um kidney failure and nephrotic syndrome. Basically, what happens is that when you have these failures, um you have more a DH and that causes you to retain more water to compensate for the failure. Basically. So when you have heart failure, basically, you have reduced cardiac output and obviously, like fluids going to become congested in um the vena cover and then it'll get pushed out of the venous system and into the circulation. So you'll have edema anyway, basically. But actually what happens is because you don't have as much cardiac output. Um Your ra system detects that there isn't as much circulating volume and increases your A DH. And as we said, a DH causes your water reabsorption to be greater than your sodium reabsorption. So it actually just triggers you to retain even more water. And that dilutes out your sodium. When you have nephrotic syndrome. Basically, you end up losing protein in the urine. And if you're losing protein in. Mhm Is there a question? Mhm Is there a question? No, there's no, there's no question. There's no questions. OK. Cool. If someone has nephrotic syndrome, then they're excreting the albumin and albumin basically has caused oncotic pressure. So, because you have protein in the plasma, it keeps water in the plasma. If you're losing protein, then you'll lose fluid volume from the plasma. And what this does is it reduces cardiac output. And so again, the body compensates by increasing a DH to retain more water in the kidney. But you retain more water than sodium and you dilute out the sodium that's already there. With liver failure, it's a similar issue. You aren't making albumin. So you don't have as much fluid in the plasma because there's no protein to hold it there. Again, your cardiac output drops, you release more a DH because from posterior pituitary because you, you don't have as much circulating volume. And again, that reabsorbs more water than sodium. And so you end up with the dilution of hyponatremia. So the bottom line is the failures cause hypervolemia basically um because because everything is failing, they just try and keep more fluid in but that dilutes out the sodium. So what are the treatments? We've been through assessing a patient and their plasma osmolarity, their fluid balance and um their urine sodium to establish the cause of hyponatremia. And it's really important that we've gotten to this point because establishing like their fluid status allows us to establish the cause and then to actually treat the cause. That's why we've been through all of this rigor. So the thing. This is kind of a key slide. And I feel like if you are going to remember anything, then it's this slide. Um because this is like summed up everything. If someone's got a hypovolemic hyponatremia, you treat them with naught 0.9% sodium because the issue is they're losing, they've lost water and they've lost more sodium than water. And it will contain like the kind of slightly higher than uh normal plasma, normal serum like concentration of sodium. You also need to treat the underlying course. So for example, you take you base that on the history, you base that on examination. Um they basically base that on the history, right? So if you know that they're taking diuretics, they've recently started, then you start the diuretics. If you know they've got a renal insufficiency, then you give steroid replacement based on history examination investigations. If they've got a euvolemic hyponatremia, you restrict their fluid because it's most likely caused by a SI A DH. And you have to investigate what the cause of SI A DH likely is. So again, based on history and investigations and examinations, if they've got a hypovolemic hyponatremia, you need to fluid restrict and you may want to give diuretics, um fluid restriction and diuretics because obviously it's the dilutional effect that's bad and you need to treat the underlying course. Basically. So hypovolemic, you give fluids u volemic, you fluid restrict because it's most likely si DH hypervolemic, your fluid restrict, you might give diuretics, but obviously that wouldn't be for you to decide it would be the decision of the clinical team, especially if cos we're looking at f one level. Um, and in each case, it's really important to treat the underlying cause. So, could we go through this SBA? Yes. Can we all see this? Yeah, I can't see it but I think I'm just three people answered so far. Oh, is it, is it the 85 year old woman? Yeah, that one. Yeah, I think I'm just again, might be lagging. A little laptop is slow. Got six responses. OK. What are most people saying so far or what is the most? The majority seems to be N 0.9 saline. OK. And some people are saying 3% healing as well. OK. And how many responses do we have? Now? We have eight responses. OK. I think I'm going to go back to presenting now. So what we have here is a, an 85 year old woman who's presenting to a and following a seizure. This is really, really crucial. So she has a seizure and she has quite low sodium. It's probably considered moderate, but you can't establish another cause of her seizure. She's hypovolemic and has very low BP. So she's, she's got dry mucous membranes. No, not visible gene BP but clear. Like crucially, she's got a very low BP. So what we can say probably is based on symptoms, we would classify this as a severe hyponatremia, which means she needs ICU admission with 3% saline. So the thing here is to look out for symptoms of severe hyponatremia basically. Um so she has, she's having a seizure. Other severe symptoms are like coma, respiratory arrest, um vomiting if you have any of those and accompanied by low serum sodium. Obviously, if it, if the serum sodium is sort of like 100 and 30 you have these symptoms, you have to consider an alternative cause. But here, her sodium's moderate and actually very close to 100 and 20. So already quite low, she's had a symptom of hyponatremia, which doesn't seem to have another cause. So you're thinking this is a severe hyponatremia, this is the cause of her symptom. And so she needs to go to ICU, she needs to be admitted to ICU and given hypertonic saline. Um does that I understand why people are giving 1.9% saline? Because she's not clearly like quite, she's hypovolemic, you obviously need to give a fluid bolus. But actually what seems to be the case here is that she has severe hyponatremia and it's really important to be able to check that and also to match that with the results. Any questions there. Ok. So as we said, acute, um or basically, if you have acute hyponatremia, then it's treated with hypertonic saline because again, you don't want to risk basically, if, if hyponatremia develops acutely, the patient is at severe risk of developing cerebral edema. Um Alternatively, if they have severe symptoms, which we went through, um you also treat them with hypertonic saline and you have to monitor the patient. It's also really, really important not to correct hyponatremia too quickly. So you sort of, you, you want, you have to correct it at less than 10, minimal per day. So usually by about 4 to 6 because if you correct hyponatremia too fast, um you risk basically um causing damage to the CNS. Um Basically, what happens is that in a person who's develop, who's got a chronic hyponatremia, they lose um they basically, their brain compensates and they lose osmolyte from the basically neuronal cells. We have one question and also you can't see your screen at the moment. I can't see it. Oh dear. I don't know what happened. Uh Right. So basically, what point, what's the question? First of all? So, yeah, the first question is why is it not naught 0.9% because they are having a severe hyponatremia from symptoms. Um It's a seizure. She has low serum sodium, you can't establish another course of the seizure. And also it kind of matches the serum sodium is quite low. So it's likely to be the cause of her seizure. Basically, if someone has a severe hyponatremia by symptoms, you have to treat them on ICU with 3% saline. And that's why it's not naught 0.9% because you need to increase the, you need to give them hypertonic saline. So you replace more sodium than water because the issue is with their sodium. Great. Thank you. And then the other question is, can you clarify what to do if it's unknown whether the hypernatremia is chronic or acute? Basically, if it's unknown whether it's chronic or acute, then you have to kind of look at the likelihood of it having developed acutely. So for example, if someone has been in a fire and they have a hyponatremia and ba basically, you look at the history and you look at the examination results and you look at the investigations and you see is it likely to have been an acute, is this likely to have developed acutely if it's likely to have developed acutely? So for example, a patient had a vomiting episode like yesterday or like very severe vomiting yesterday or has developed diarrhea yesterday or was in a house fire yesterday and you didn't have the blood results from before. But like now you've got their blood results and they seem to have like a low serum sodium. That kind of history suggests that they've got an acute hyponatremia. So in that case, you treat it as acute if however, you don't have good reason to suspect it's an acute hyponatremia, you assume it's chronic. So kind of like if you just have random U and E results and it looks like hyponatremia has developed. You assume it's chronic unless you have good reason to assume it's acute. Basically. Does that make sense? Great. Thank you. Um So basically, the point was I was making the point that you can't correct hyponatremia too fast and I will not go through this because it's I don't want to delay. But bottom line is, first of all, when you have a patient who you, who has low serum sodium, you assess whether they're severely hyponatremic based on symptoms. And if they are, then you treat them with hypertonic saline. If they're acutely hyponatremic, then you treat them with hypertonic saline. If they have like a chronic, mild to moderate hyponatremia, you assess their plasma os molarity, then you assess their fluid balance and you assess their urine sodium. You look at their history, examination and um investigation results and that allows you to establish the course and then treat um according to that diagram, um any questions. So I'm gonna get over hypernatremia because it's not, it's quite self explanatory. Basically, when it comes to hyponatremia, that's high serum sodium and you treat the cause. Um and the cause could be dehydration and loss of pure water. In which case, you encourage the person to rehydrate or you give them normal saline because actually what's happening is you're losing more water compared to sodium, which causes it to seem like your sodium is more concentrated. Um It could be because someone's got increased sodium intake because they, for example, were being enterally or parenterally fed. In which case you have to dilute out the extra sodium. This is hypernatremia. Um And again, if your sodium is too high, you don't correct it too quickly because then that risks cerebral edema. So I the slides will be there so you can check but hypernatremia is very easy to understand. Um any questions on hyponatremia or its management? I know I stopped sharing it. OK. So just in the interest of time so that I can start on. OK. Are you all right to share the slides with us? Yeah. Yes. Can you can do this? So yeah, I'm going to be taking over for the last few metabolic problems. So I promise I'll try and keep you as aint as possible. So we're going to start with an SBA now. So this SBA here. So we've got a 67 year old woman who started on a new medication. She develops nausea, muscle weakness and this is her CG below. So if we're able to let me put the poll on for this, so if we can quickly vote for this question, OK. OK. So hopefully that's why. OK. So you just get to keep voting on the chart. We have a couple more responses and we move on. All right. So from everybody has voted. Great. So yeah. So now the answer here is spironolactone. So that is the majority of what you guys have said. So we'll go into exactly why this is the case next. So hyperkalemia, this has many causes. And um so here's a, here's a good pneumonic that you guys can look at. So machine. So this covers medications, acidosis, cellular destruction, and you guys can see this new money. But a good way to think about is is to think about potassium in the blood where it potassium, most of the potassium is actually intracellular. So we can think about this as three different ways in which potassium can get too high. Number one is if we take too much potassium. So that's the I in this acronym. So we have intake. So if we're taking in too much potassium, whether this be supplements, this could be through medications that's obviously gonna cause hyperkalemia. Another thing is that as we said, most of potassium is actually intracellular. So that means that when you have things such as things that can cause hemolysis or cellular destruction. So the C and the H hip that's gonna release potassium from inside the cells to outside the cells. And then you've got the other things such as medications, acidosis and nephrons, which is actually due to which is to do with the excretion of the potassium itself. So now let's quickly talk about spironolactone cos this is a really, really important drug that we need to. So it's, it's on this. Yeah, we'll stay on this slide. So it's kind of. So if we think back to what somebody was teaching us with the distal tubules of the kidney. So with aldosterone, so what does aldosterone do? Aldosterone means that potassium is essentially excreted out and sodium is kept in. Now, spironolactone is basically an antagonist of this function. So if you think about if it was an antagonist, what's gonna happen, you're gonna prevent the potassium from leaving and it stays in the bloodstream. So that's why we tend to see this, you know, hyperkalemia build up in, in um spinal lactone. So that's a very, very important example to know. Um So there's other drugs as well. So there's beta blockers. So these are commonly known to, you know, cause hyperkalemia and then other drugs which interfere with kidney mechanisms. So, ace inhibitors, arbs, nsaids as well. These all have impacts with the kidney which can have impact on the excretion of potassium. So I guess if you guys just think of excretion intake and intracellular to extracellular shift, that essentially keeps all of these causes that we've seen in the slide in a, in a good little nutshell. So, yeah, does that make sense? Any, any, any questions on that? Uh Somebody has asked, I can't stay on the recording, I can't stay on. Unfortunately, how do I get access to the recording and the slides? So the recording and slides will be on the middle page. OK. Uh So don't worry about that. OK. So great. So we've got a patient case over here. So we've got a 47 years. So actually. Mm OK. The best thing we can do here is have a rate of this case. So this is a 47 year old female presents to A&E persistent nausea, vomiting. And what we're seeing is feeling tired and some unintentional weight loss, hyperpigmentation in the palms of both hands. And then you've got some observations here which I hope you can see. So if you guys could just think so, first of all, what's the very, very first thing that you're thinking to do if you're in A&E what's the first thing that you'd wanna do here? So if you wanna put that in the chart, so patients presenting like this at A&E what's the first thing we'd want to do? OK. So is that A&E first thing we want to do? So? OK. Great. At, at assessment. Exactly. Exactly. Yeah. Brilliant. So if we can switch slides there? Yeah. Good. OK. So what electrolyte disturbances do you expect to find in this particular circumstance? And a bonus question, I guess is what is, what kind of, what condition is presenting here? So, if you wanna put that in the chart as well, so have a look at some of the keywords in this presentation. Maybe look at the via to drowsiness, hyperpigmentation, unintentional weight loss. It is quite nonspecific but great hyperkalemia and Addison's perfect. Good. So, yeah, along alongside the hyperkalemia. You're also gonna see the hyponatremia. So this has to do with the mineral corticoids, which is not being produced enough since it's insufficiency, it's adrenal insufficiency. Uh So if we go back to thinking about, you know how, you know, mineral corticoids or aldosterone works, you know, it sent the potassium out and kept the sodium in. It's essentially, if that stopped, you're going to get a build up of potassium and you're going to get not enough sodium. So that's why essentially it's, it's a switch of what would happen if you had too much. Um So yeah. OK. Cool. So, hyperkalemia is very important. So we really need to pick it up. So what kind of, so if we just go back one slide, so what kind of clinical features would you expect in hyperkalemia? So that's quite a few and it can be quite nonspecific and that's why it's challenging. So any ideas on what kinds of things to pick up on? So you've got a patient in front of you. What kinds of things are you sort of looking for if it's hyperkalaemia? So if you just wanna put that in the chart as well, just give you a few seconds for that. OK. Arrhythmias. Yes. Very good. So we'll get on to the cardiac side of things. Hyper seconds. Very important. OK. All right, we'll move on. Cool. So we've got a nice uh little Pneumonic here as well. So Murder So I guess it tells us how life threatening hyperkalemia is just to remember, there's something you just can't miss. So, muscle weakness is a very important one just to do with the interactions of these ions in, you know, these myocytes urine output can be low. And we've got respiratory failure as a result of the muscle weakness that you'd have for uh the respiratory muscles, decreased cardiac contractility. And yes, and the main thing is you're gonna see. So, yes, sweating. So that's a very good one. So what that relates to is the sympathetic system and the sympathetic system I believe can actually have an impact on the sodium potassium pump and that can cause hyperkalaemia. So that's, that's a good observation as well. Um Two. So, all right. So now some ECG changes then. So when hyperkalaemia ends up having an impact on the actual ecg the actual cardiac myocyte, that's when you know, you really do need to treat it as soon as possible. Now, the interesting thing is that with, with the E CG, you see different, different waveforms correlating to different severities of the actual um hyperkalemia. So I'll actually, I think there's another slide where it shows you the different yeah. So this one here. So as you can see, it goes all the way down from a potassium level of five, all the way up to eight. And you start with your, you know, your very um classic textbook, tall tented T waves, then you see that you kind of lose your P waves and then you get your wider QR S intervals. So and at, at the very top, you know, when it's life threatening, completely life threatening, you get this sine wave pattern ventricular fibrillation, all these arrhythmias as we talked about, which are essentially life threatening. So this can give us a good idea of how severe it is. But the main thing is if you see ecg changes that in itself should tell you that this hyperkalemia is severe and must be treated as soon as possible. So that leads us on nicely to, that leads us so often. So if you just go back to one slight, yeah, we just talk about the severity. Um Yeah, so we talked about, yeah, this one. Yeah, great. So with the classification of it, we've got, we can, we can call it mild, moderate and severe based on the actual potassium concentration. So you guys can see, you know, from 5 to 5.9 it's mild 6 to 6.4 it's moderate and beyond 6.5 is severe. However, the important thing is if there are ecg changes, arguably if, if at any level that automatically fast tracks it to be a severe sort of hyperkalemia, then that then guides our management of the hyperkalemia as well. So yeah, great, cool. So this is a very important slide because it tells us about the management for hyperkalemia. Now, as we said, this is for all patients with severe hyperkalemia and cardiac monitoring must always be done just to see if you know, we're seeing these ECG changes, which would tell us that it's severe. So there's three main things which we'd consider when it comes to treating the modalities. First of first things, first, we need to take care of the heart itself. So cardiac memory stabilization of the cardiac membrane. So what you need to do for this is you administer something called calcium gluconate. And the way that I used to remember this is the rule of tens. So it's essentially at 10 mL of 10% calcium gluconate over 10 minutes. So this is really important because what we need to see here is that w what essentially happens is it causes an intracellular shift from the extracellular compartment to the intracellular compartment. Now, as we know, most potassium is actually an intracellular compartment. So what this is doing is it's, it's just shifting a bit more of it into the intracellular compartment. So there's less in the blood, less in the serum. So it's, it's essentially just it's it's not changing the amount of sodium in the body. Um So that's for the heart. So that's for the arrhythmias because if we have arrhythmias, you know, there is a chance of death very easy. So the next thing we can do is we can also administer insulin. So insulin also acts on these, you know, transporters and um what you can give is intravenous insulin. So, an very important thing is that this needs to be given with 50% dextrose. So one of the doctors was actually saying that these days what they do is they actually come in preprepared bags with the actual dextrose or the glucose. Because you know, like what can happen is that sometimes if you don't give the round of glucose or if you don't give glucose at all, you can obviously cause some sort of hyperglycemic coma. So that's the kind of risk that we're taking with this here. So it's very important to give the dextrose as well. Uh And then the other thing we can also give is nebulized salbutamol. So the mechanism of this is we don't really know why it actually works, but it kind of makes sense because we remember that beta blockers caused hyperkalemia. So being a beta agonist, it makes sense that this is actually gonna, you know, help us with the hyperkalemia. So again, this is something which helps us with the intra of the shift. So the other other things which we need to look at here is for the removal of the potassium literally from the body. So we've got things such as calcium resonium, we have lokelma, which is sodium zirconium. So both of these are sort of potassium binders, which what they do is they bind the potassium in the gut and they allow for excretion of it. So it essentially just flushes it out and uh loop diuretics as well. So if you remember back to how loop diuretics worked, they blocked the, they blocked the channel, which essentially a lot of sodium potassium. And I think chlorine as well. So if you are blocking potassium from going back into the blood, it is going to go through the Nephron and just get excreted through the collecting dots. So again, it is going to get rid of the sodium. And last thing for refractory hyperkalemia, if you know, nothing has worked, you have given all of these drugs, nothing has worked at all. That's when you'd escalated to dialysis. But you know, at this stage, all of these last few things that you would wanna do, you wanna be with the senior at the level of the F one we are only looking at at least the first two. So this is when you would be liaising with the senior team. So yeah, it's quite a lot. But um hopefully that makes sense. Let me know if you have any questions on that at all. Um Yeah, so yeah, feel free to type in any questions. So we've got another SBA. So I'm just gonna put the call for this. OK. All right. Hopefully he doesn't see that. So you guys just fill in the pole chart. All right, as if you can, I don't know if it's, I can see it in mine. I'm not sure if the others can see the pole, I can see it. OK. So I haven't got any responses yet. Give it a couple more, a few more seconds. OK. Somebody noted. OK, a couple of notes now. OK. All right. We'll move on. Cool. We'll go to the next one. So the correct answer is a, so first of all, just looking at this, at these bloods, see if, if we look at what is actually wrong clearly, we can see that the patient is low on potassium. So it's hypokalemic. Now, you know, I feel like this isn't that talked about as much as hyperkalemia due to how severe hyperkalemia can be. So yeah, the majority of people are saying, you know, yeah, so the main thing is right. So we need to replace this potassium. What we need to think about when, when it comes to replacing this potassium, can you just give potassium by itself? No, this should never be done. So potassium should always be given with, you know, a bolus. So with, so in this case, we are talking about normal saline and it always has to be combined. So b would never be the answer because you could never give um you know, just 40 millimoles of potassium chloride cos it's the huge risk of going straight into hyperkalemia. And you know, we've talked about all the things that can happen, bad things that can happen when it is hyperkalemic, right? So that's why we would never give that. We will see. The thing we see is it doesn't actually address the potassium and D. Well, the thing D is D also gives us the saline and the potassium. But the issue here is we are giving the patient 40 millimeters of potassium within one hour. Now, the recommendation I believe at the moment is you can only give 10 millimeters per hour. Um with the current rec recommendations, I've seen 20 sometimes, but I don't, you can't give more than that. So the issue here is the rate at which you're giving me the potassium again for the risk of hyperkalemia. So yeah, hopefully that makes sense. Let me know if there's any questions. Cool. So just a quick summary on hyperkalemia then. So, you know, with the hyperkalemia again, we tend to have your cardiac effects, you tend to have your muscle effects as well. So, you know, just look out for your sort of nonspecific against very nonspecific symptoms such as muscle weakness, palpitations as you you can in in a sense classify in terms of the different uh actual concentrations. So less than 3.5 and very severe, I believe is something like below 2.5. But the important thing here is here instead of what, what we need to do is we can think about what's happening to the heart. Can we give potassium? Is there anything else we need to do? Before giving the potassium. So if we think about causes, again, we can kind of split this up into renal and extrarenal. So when it comes to renal, it's always gonna be things to do with excretion, right? So are the, is the patient on loop diuretics, for example, or is is there any reason why there's less potassium than there should be? So as we said, like furosemide, that's one of those drugs which can, you know, block the potassium from getting back into the bloodstream. So that could be another reason. So, excretion and then extrarenal is everything apart from that. So that's going to be things to do with intake. Is there less intake than there should be and also potential shift into the extracellular um intracellular fluids. So, you know, as most potassium seems to be in the cells itself, that can also be a very common reason and gut losses as well. So a common cause can be literally, you know, vomiting or diarrhea that can literally flush out the potassium out of the gi system as well. So that's also quite common, it's actually quite a common presentation. Um So, OK, so in terms of investigations, then, so again, potassium has a big impact on the cardiomyocytes. So definitely, definitely, definitely need to check your EC GS. And it's quite interesting because it's essentially almost like the opposite of what you'd see in hyperkalemia. So, you know how we sort of the to 10 T waves. This time, we're looking for more things like your absent or small T waves in a sense. Uh Also U waves, they are quite characteristics and then think about things like long QT as well. And then if there is long qt, you obviously be very wary of the risk that this can bring in terms of arrhythmias, torsades, de pointes, so that we'll talk about a little bit later. And the other thing we need to mention here is also do we check, we need to check the magnesium as well because magnesium is quite interesting because what can happen when you have low magnesium is that that releases in in inhibitory effect on the actual potassium, meaning that that can actually cause hypokalemia as well. Now, if that is the case, you then know to give the pota the magnesium first before replacing with the potassium, since that's internally the underlying cause of why there's hypokalemia. So that's why in terms of management definitely look at the heart as because of the reasons we said before, look at the magnesium if it's, if it's, if it's too low, definitely correct first. And then lastly give the potassium. So one thing that is true is that if it's very, very low, uh one thing you can do is in it, you can give it straight through a central line. So this will be a lot quicker. But you know, this would need to be with senior staff it management and, uh, of course we'd need cardiac monitoring as well. So, yeah. And guys any? Ok. Does Harman's, the question is, does Hartman's have potassium in it? Um, I believe Hartman's may have potassium in it actually, but I don't think it's a huge amount. Um, if you can confirm with me. So I think. Yeah. Yeah. Yeah, it does. It does. It's, it's closer to the physiological quantities, isn't it? Yeah, I think so. I think that, that he doesn't have as much potassium for memory but not. Yeah. Yeah. It wouldn't be enough to correct the hypokalemia. You'd still need to have your, you know, addition to it. So uh yeah, it would act as like a fluid to which you would add the existing potassium to live. So yeah, good question. So OK. So this is the next SBA. So I'm gonna quickly put this on to our pole. OK. All right. Hopefully you guys can see it up. Give you guys a few seconds. I can see that. Yeah. Yep. Just done. OK. Colon response. OK. Get a few more responses. Then we can. OK. Got a couple of responses. All right, we'll move on. So most people have said b have primary hyperparathyroidism is absolutely correct. So if you just look at this question, so we've got this very, very classic, you know, symptoms of, you know, men altered mental status, constipation, abdominal pain. Now, you know, they're very nonspecific but in this case being. So all of these symptoms essentially indicate some sort of electron electrolyte abnormality, which in this case is hypercalcemia. And then the next thing to understand is what is the most common cause. And it is very hyper. So we'll go through this in a little bit more. No. OK. So hypercalcemia is, is, has got quite a few causes and I've summarized on this slide, the most common cause is here. Now, the important thing to understand is the kind of the interplay of hormones that take place in regulating calcium essentially. So, so we're not gonna go too deep into any of this preclinical stuff. But I think the important thing to know is levels of P th calcitonin and also calcium. Now, P th essentially acts in a way to increase the calcium. I think that's the bottom line calcitonin kind of does the opposite. So if you wanna decrease it, it kind of it, it that it acts on, it acts in certain ways to decrease the calcium. Um So the ways in which we can get calcium. So I think we need to understand where is the calcium in our body? So literally 99% of the calcium that's in our body is in solid bone and only about 1% seems to be outside the bone. And within that 1% only a very small amount is actually in the extracellular fluid. So a very small amount is in the fluid but we need to understand. So how do we get increase this, increase this calcium in the bloodstream or in the serum? So, in most of the time, what happens is is that you get this bone resorption and when bone resorption happens, calcium from this bone itself ends up increasing the concentration of calcium in the bloodstream. So that's what usually happens. And the other things that also come into play is Vitamin D Now activated Vitamin D What this can do is it can act on different parts of the body, including the kidneys and also the gut. So it it can increase absorption of calcium from the enterocytes in the gut. So I think you can see that in this diagram here and it can also increase reabsorption in the kidneys as well. So that's another way in which calcium can be increased. So in terms of the most common causes, then, so excess PT release seems to be the most common cause. And within that, I wonder if any of you guys know what is the most common cause of this para hyper para primary hyperparathyroidism. What is the actual, if you guys, if anybody wants to put that in the chart, what is it in particular that causes this primary hyperthyroidism? It's very, it's, it's one of the most common things that can cause it. Ok. Interesting time we'll move on. But if you've heard of a parathyroid adenoma, that is one of the most common causes. OK. So another thing is we need to really be concerned about is malignancy. So, malignancy can cause um you know, hypercalcemia in a different, in three different ways. Essentially. But the two different things that you need to, we need to understand is essentially bones. So a lot of cancers, especially multiple myeloma, they cause these sort of lytic lesions. And what essentially happens is that it breaks down into the bones, it eats into the bones and causes this bone resorption. And this bone resorption is essentially letting go of this calcium from the bone straight into the serum into the blood. And that then manifests as hypercalcemia. There's also another way in which this can happen, you get these paraneoplastic syndromes as well, especially lung cancers. So you can get these cancers which actually secrete P th related proteins. So you, you get these proteins which essentially mimic PTH and act on their receptors and essentially cause the same effect of PTH even though it's not P th. So you get this hypercalcemia and then the last most common thing you see is Vitamin D toxicity. So this is essentially most commonly, you know, if somebody has ingested a bit too much of the supplement tablets or ingest too much of uh foods containing vitamin DS, this can then manifest as hypercalcemia. So we'll move on from here. So what do we want to do for investigations? There's, there's a bunch of things we need to do. Um so in terms of the most important thing, it's the bone profile. So if you remember from, so what it, what it is is that in a bone profile, you need to look for things such as P TH level, Vitamin D So there's AO P levels as well and calcium as well. Now the reason why this is important because this helps us identify which kind of cause we're looking at for a hypercalm. Is it, is it a primary hyperparathyroidism? Is it a tertiary hyperparathyroidism? So we can differentiate these things based on the levels of P TH and uh so based on the bone profile, um another thing you can do is you can also do an EKG because it can affect the QT segment. You can get shortened QT which I guess isn't as you don't think about it as much as a long QT. Another thing of course is a malignancy screen. So this would include so serum protein electrophoresis for multiple myeloma. So there's things such as Ben Jones proteins that you, you'd also look for as well. So it's, it's a very common cause of hypercalcemia. So that's why you can cover that sarcoidosis as well. That's another course of hypercalcemia. So you can look at ace levels. Uh you can also do a 24 hour urine calcium. So this is actually for a familial syndrome, I believe. So it's very rare, but it's something which you can use to differentiate your other causes of hypercalcemia from a familial course. I think it's congenital but it's very, very, very, very rare. Uh You can also do a bone scan in order to look for these lytic lesions. Uh general imaging is also very important because if you want to see if there's been any bone metastasis of any potential tumor from any other part of the body, it's very important as well. Uh T FT S it is very cool actually because what can actually happen is that you can get these thyroid hormones, which thyroid hormone, which can actually act a bit like parathyroid hormone. And that can result in a hypercalcemia in a sort of similar way. Cos I think it acts on similar receptors because it's a similar sort of conformation. So that's why you can also look for uh if there's any, any thy thyrotoxicosis as well. Um Yeah. So management wise. So it's quite simple actually. So you just essentially, you got to think about this as you wanna decrease the concentration of these calcium. So just essentially flush them out with fluid. So you give them IV crystalloid fluid and then the underlying cause needs to also be treated. So for example, if it's a pituitary adenoma, whether whether or not surgery is a viable option, that's something we might wanna think of. Uh there's also another treatment called Sarala. So this I believe is a calcium mimetic. So what it does is it acts on the receptors of calcium pretending to be calcium to kind of get that negative negative feedback loop to kind of decrease it back down again. Um So that's another therapy I think that's used if surgery is not possible. And then finally, we also can use well for refractory hypercalm. So something that's not being treated at all, it's not working at all, nothing's working, then you could go to dialysis bisphosphonate is also an option. But you know, you need to be very careful because of the nephrotoxic side effects of it. Um and also other contraindications. But what it can do it, it can reduce the hypercalcemia because it prevents osteoclast activity, hence prevents bone resorption. As we said, that increases the serum calcium. So bisphosphonate can also help. So I've just attached this other um diagram here. So you can take a look at this in your own time as well. So, Stones Crohn's Bones Crohn's psychiatric all the time. So this is something that you might have heard of many times before. So yeah, that's one of the, that's the symptoms of it. So, yeah, great. So we'll move on. So this is our last SBA. So we'll just get through this as well. So you guys could answer would be great. So let me just put this on. You can see that. Yeah, great. Couple more. All right, we'll move on. Cool. So, all right. So we've got a mixed bag here. So it's actually d um so we've got an interesting few ideas. So PTH levels. Yeah, that's completely understandable. Um Now, what we have here in this presentation is clearly the patient is hypocalcemic. So they've even told us that with the values and the presentation. Now, we, we need to think about what is the thing which can possibly cause the most harm to the patient at this moment in time. Now, we got to think about what does hypercalcemia do. Um So we will go on to this in the next slide and I will explain why it is ECG. So it's all right. So if you stay on that slide and then we'll talk about the ECG stuff. Yeah. All right. So when it comes to OK, somebody else can you repeat what you said about bis? Yeah. Sure. So, bisphosphonates the way they work is it's, it's, it's used in osteoporosis, isn't it? So we essentially wanna prevent osteoclasts from breaking down the bones. So the osteocytes, we don't want them to break them down. So what we know is that when they do break them down, that releases calcium into the serum. So it goes from being in, stored in the bone to the serum. OK. Now, when you stop that from happening, so that's what bisphosphonates do. Osteoclasts don't work like that anymore. So, osteocytes stay there, the bone isn't resorbed anymore. So calcium stops going from the bones store to the serum. So in that sense, we reduce the amount of calcium that's going into the serum and the blood. And as a result, we were able to control the hypercalcemia. Hopefully, that makes sense. Two, let me know if, if you got any more questions on that. Cool. So yeah, we're just talking about the ECG here. So with hypocalcemia, so we'll talk about this in a little bit more depth. Soon. One of the main things that it can cause is that it can cause Long Qt syndrome and Long Qt Syndrome. You may have heard of this in cardio. It's quite a dangerous thing which you need to make sure to treat and manage as soon as possible. The reason being is that this can then progress into things such as torsades, de pointes and you can also get your ventricular arrhythmias as well, which can obviously have the risk of cardiac arrest. So that's why this is something we need to make sure isn't already happening already. So that's why taking the ECG and taking the adequate measures to prevent something from that happening is the most important thing to perform urgently. All right, hopefully, that makes sense. So we move on. So just last couple of slides now, so with hypocalcemia, then now hypocalcemia, I think the way to split this up is to think about low P TH and then high P th. Now, what does it mean if it's low PTH? So P TH is released from the parathyroid gland and that does multiple things around the body. So it acts on the bone, acts on the kidney, acts on the gut in different ways to increase the serum calcium. Right now. If that is low, what's gonna happen is that naturally, you're gonna get low calcium as well. So it's, it's pretty much as simple as that, you know, your parathyroid gland isn't working properly. It may not be secreting enough P TH or the P TH may not be uh it may not be effective. And what can happen as a result is that you just don't get enough calcium. The other thing that can happen is that you can get things like Vitamin D deficiency, you can get chronic kidney disease as well. So that can interfere with the amount of calcium that gets resorbed into your bloodstream and pseudohyperparathyroidism as well. It's an interesting one. what essentially happens is that you have a lot of P TH there but it's just not sensitive. So your receptors just aren't recognizing the fact that there's high P TH and therefore calcium just isn't being increased. So, whatever the problem is there, it's just not communicating. And that's why you have this high P th but calcium is still low, you don't, it doesn't actually act on the calcium at all. So that's what pseudohypothyroidism is. Um And then yeah, Vitamin D deficiency because of, if you don't have enough Vitamin D then that's gonna prevent, you know, your reabsorption of calcium from the gut and the reabsorption of calcium from your renal um from your renal system as well. So, yeah, that's with a high P th um And then finally, you can also get things such as compartmental shifts. Now, this is so in acute pancreatitis. So if you remember in pancreatitis, hypercalcemia is actually one of the components which tell us how severe pancreatitis can be. So this can kind of be thought of if you remember the intracellular and the extracellular shifts with the potassium that we talked about. It is in a similar way. So imagine it is going from the extracellular compartment, which is what we detect in the blood into the intracellular compartment. So there are multiple reasons why that can happen. So acute bronchitis seems to be one of them and I think there is a few more as well. But you know, I think if you just remember if it can shift from the extracellular fluid to the intracellular fluid that can also result in hyperemia. All right, cool. And then uh yeah. So in terms of presenting complaints, then, so I think this is the most commonly seen pneumonic. So cats go numb. So cats kind of covers all the central and important things, you know, which we we hear about quite a lot. So you have convulsions, arrhythmias. So that's you know, with your heart tetany. So things to do with your muscle and also spasms, stridors. If you think about respiratory muscles as well, essentially, it, it acts it, it, it, since calcium is quite important for this muscular contraction, right? If you don't have enough of that, it essentially messes up the whole system. And then that's why you get these spasms tetany and, and then it can affect your respiratory muscles as well. And in terms of peripheral effects, then that's where you get your sort of numbness in your fingers. So this can be quite a really important thing to pick up on as well. So if the patient presents with this always, you know, think hypocalcemia in the back of your mind as well. All right. So in terms of investigations, it's, it follows a similar sort of thing. Um So magnesium actually comes into this as well. So it's, it's again, it has a complex interplay with, you know, calc um calcium and also hyper with the potassium as well. So if that is too low, you'd want to correct a magnesium as well. And then your standard U use E is bone pro for vitamin DPT H and E CG is a lot more important here than in your hypercalcemia. Um So in terms of management, as always treat the underlying cause, so as we talked about before, there can be multiple causes for this, so that needs to be investigated first and that can be treated and then severe hy hypercalcemia. Um So when it's below a certain level. This is when you'd want to think about administering your 10 mL of 10%. So again, it's the same one as we saw before. So the rule of 10 to applies here, so your 10 mL of 10% calcium gluconate over 10 minutes that can be given here. It's another thing to notice here is if you have your ECG changes, that's another sign that it may be severe as well. And if you remember, if you remember the long QT being, the thing that we need to fear the most, always, always, always look for that in your EC GS. And if it is the case definitely act on that. So somebody's asked, so can you explain the super pseudohyperparathyroidism? Of course. Yeah. So it's quite confusing. So the reason why it's called that is because when you look at the results, it looks a bit, it looks like it should be hypoparathyroidism. But in reality, it's not. So what it actually is is that you have your parathyroid gland secreting P th there's a lot of P th in that bloodstream. And usually what happens is is that the PTH goes and binds on the onto these receptors to increase calcium in the bloodstream. Now, that's what usually happens. But in this, in this particular scenario, what's happening is that it's binding onto these receptors, but the receptors aren't actually recognizing what's happening. It's not able to understand what it's asking it to do. So it's not sensitive. So by pth binding to the receptors, it's no longer causing this increase in calcium anymore. So that's why that's why we call it pseudohypoparathyroidism. And in actual case, what happens is that you don't, you get a low calcium sort of a high calcium. Hopefully that makes sense. So, yeah, it was in that pain. OK. OK. So that, that was it guys. Um let me know if you have any other questions and uh we're gonna put our feedback form in the chat. So if you guys could go through that, that would be great. OK. Stop sharing. OK. We've got a question about the lung Q. Yes. So yes, the feedback form is there guys. So it would be amazing if you could fill that in. But yeah, let me just explain about the long QT. So long QT is, I believe it's, I can't remember the exact um you know, ranges of it, but I think it's something like 440 mills. I want, I wanna say that was for males and then 460 milliseconds for females. It, it might be the other way round. Um But that's essentially the limit for what a normal QT should be. And if it's longer than that particular um segment in the E CG, then we'd call it Long QT. And that's when you'd be worried about the risk of these arrhythmias, tosses de pointes. And um you know, that's when you'd be really concerned because there's also the risk of cardiac arrest as a result of that. Um I can double check that for, for you, but I believe that is just, yeah, so if it is greater than 440 in men and 460 in women, not milliseconds on the E CG. So from the Q to the T that's, that's when it would be classed as long QT, hopefully that answers your question. Ok. No questions. Any other questions at all? Um So the feedback forms there, please do finish out. I'll just turn off the recording.