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Okay, I think we'll get started. Done. So welcome back, guys. Um, you've been one of the six. Pm serious co founders and, um, the medical curriculum need today we're gonna be covering electrolyte abnormalities. So to start off with just our socials if you haven't already drawing them, it's very post all of our updates, all of our events. And you're supposed to relevant sort of questions based on all the lectures that we teach him or have taught s O if you want, please spread the word drawn, all drawn or social stone on instagram facebook. Twitter. If you haven't already on, you can keep up today with all the latest information about the six PM Siris on just a quick thank you to our sponsors. The end the you the MD has been sponsor. Uh, since sponsoring us since we started the six PM series, and without then, we wouldn't have been able to get this off the ground. Everybody needs medical legal insurance at some point when they're become doctors and they're qualified. So if you're interested and when it happened, it will Look, there's a little QR code on the bottom, right? And if you join. You can also get a freebie, such as some revision cards or a book that you can choose from. Okay, so question number one So 40 year old patient presents to thedy're with acute chest pain that started two hours ago. He's being managed as an end stemi. I'm taking his blood. She noticed it is quite viscous. His bloods were in the table. What is the most likely cause of that is hyponatremia. And let me pop up the pool. Okay, so we're gonna and the pool here. So majority, if you've answered hypovolemia Kaepernick tree, which is the incorrect answer on, will come until I would like to make things a little bit difficult here in the six PM Siris, let me admit. Or so the answer. Pseudo hyponatremia. That's still committed. What about Why? So you know, hyponatremia is the name suggests is a false hyponatremia, and it's related to how the blood is analyzed indirectly in the big machines. When you send a goal top off, which solved the bloods that we you know, just a standard test you that we send out for some of the bloods might be different colors in different hospital. in this city with the way it's analyzed. But if you do on a point of care testing, such is a VBG or anything else, this problem won't a pair, so we'll talk a little bit about sit of hyponatremia. But certain times of the causes of pseudo hyponatremia, which is what sort of the stem alludes do its power. Paraproteinemia can cause there anything, such as multiple myeloma, whether it's excessive proteins. You know, I mean of grumbling to thicken and multiply enormous case or hyper triglyceride. Amy Um, which is what this case time was alert, alluding to in one of this patient's risk factors in that he had a really high triglyceride level of 15 way above the normal for this patient, but also had any systemic steroids probably played a big part as a risk factor in the in. In terms of blood analysis, the way they're a pseudo hyponatremia comes across is that you have a low sodium and you have to look at the plasma well serum osmolality. And if the serum was Manali, osmolarity sorry is normal or high. That suggests a pseudo hyponatremia because normally, with a true hyponatremia, the ceremonies melodic that was minority should be know. So if I just go to the next slide and quickly break it down so again we look at the sodium. It's low sodium of 125 with a high serum was Malala osmolarity and you wouldn't expect that with a true hyponatremia was marital. Keep it very simple, not going to go into the chemistry of it. But think if there's a lot of sort of sort of charged I ions awesome ALS things that are automatically active and attracts water being added together. So if you have a truly have a low sodium, your overall asthma, Larry Tea should be no, because sodium is big contribution to serve osmolarity essentially. So if it's high, it's it's it's most likely a pseudo hyponatremia false, and the triglyceride is one of the risk factors for that Hypertriglycerademia can cause pseudo have been treating you because the way the blood is analyzed and that is the summary for that case I helped. That makes sense, and we can come back towards the end. But we got to move on quickly because we have lots of electrolytes to cover, so move a little bit about some was was minority. So in terms of your total serum osmolarity, your past Malloy serum, your serum was minority is roughly speaking between 275 to 290 minimal Lita on If we're sort of specifically you know, looking at the intravascular space, there's a bit of protein in there, which is albumin, mainly, which contributes to this sort of total serum was March, and you can see how big of a contribution sodium makes. Total samples might need a half of the total amount. So as I said it was, a true hyponatremia would expect the overall serum oh, similarity to be low because of the country. The large contribution of sodium now just a little bit of physiology in terms of sort of fluid shifts with in your interstitial space, there's no protein, so the total samples minority is slightly lower competitive intravascular space. Now the effect that protein has over water in terms of attraction is called the on call tick pressure. So that's why, in patients with a normal albumin horn, hyper up money make or, you know, whatever the case is, water will be sort of attracted back from the interest issue of space into the intravascular space. Now, if you have a really low albumin, um um, you know it's in these patients. They'll have much more peripheral edema saying chronically chronic cancer patients for patients with never dysfunction, whatever the cause of the no albumin is because they've lost that on Kosik pressure that pulls that water back from the interstitial space into intravascular space. So in terms of hyponatremia, it's it's typically a sodium, less than 135. But please look at your hospital ranges because different hospitals have different ranges, bit and standardized population of the area that you're working in. But typically it's less than 135. You should classify according to fluid status on sort of the biochemical markets. Imagine somebody are the biochemistry, and the reason it's important to do that is because the cause of the hyponatremia determines the management of it. The management are very different for different types of hyponatremia, so when a patient has a severe hyponatremia just counted as a sodium less than 100 20 or when there's a very acute change or rapid drop in your sodium, which is also very bad. That rapid change is when the brain can't adjust to that sort of rapid right, the rapid sort of change. And because of that, that's what leads to a spectrum of neurological symptoms. You could be anything from sort of acute confusion away. Two seizures in a coma and death on other symptoms of hyponatremia typically depends on what the cause of it is based on the fluid status. So in terms of castle firing a hyponatremia. So to start off with you have a sodium less than 100 and 35 or whatever your hospital range is. If the remember the serum osmolarity is high or normal, suggested pseudo hyponatremia. In which case have they got high triglyceride, a high sort of protein amount or even high sugar, sometimes conducive as well? And if it's low, that means it's a true hyponatremia. In which case, what's the fluid status, like when you examine them or they fluid overloaded? I you have the, you know, sort of got raised. JVP, peripheral edema. You know, pulmonary edema. Whatever the case may be, Ascites megaly are the you've anemic. In which case, you know, I got normal fluid status or S O r the hypovolemia. In which case, you know, I have to got dry mucous membranes, a hike up in really central committee Really full time. Have they got, uh, low BP tachycardia sort of those sorts of typical things that you're looking at. So in terms of the symptoms of hyponatremia that I've mentioned, remember if there's a low sodium in intravascular space, your brain, which is why there's more sodium in there, will be saltier compared to your blood and naturally aware of a sodium. Wherever there's more sodium, more water will follow because if it's automatic pressure osmotic effect because the sodium in the blood is lower competitive brain, more water shifts into the brain, and that causes a slight bit of cerebral edema, which is what causes those spectrum of neurological symptoms, depending on how severe it is, but sometimes in patients, particularly in the elderly, when this is a chronic process and happening over a period of time, the brain can adjust to these changes, which is why some but most of the time they'll be asymptomatic. But it's Wendy's. Sort of. The sodium is really, really low in the severe levels or when there's an acute or rapid change, then that's typically when you start to see those neurological symptoms that we've talked about. So question number two a central lady, was admitted to the acute medical unit with delirium. She has a history of epilepsy and has recently been diagnosed with gastritis. She has no signs of fluid overload or dehydration and has a on abbreviated a mental test score, for which is how we can look acute confusion, delirium in the UK what is the most likely cause of her hyponatremia? And that's okay. We're gonna move straight on this. Quite a split range of answers, actually. And we'll talk, boys. So majority of you on some vomiting and diarrhea, which is not the correct answer. The correct answer is, um, Epirizole, and we'll talk a little bit about why, specifically in this patient's case. So then you stopped sure, and take that away. Certain correct answers Omeprazole. Let's talk a little bit about life. So from the history she has epilepsy, and that's why she's probably on carbamazepine but sort of alluded to that. She has been sort of an epileptic for quite some time, so the carbamazepine is unlikely to be the sort of cause of it, because she has been on it for quite some time. Um, in terms of what's been newly started, which is in the diet in the diagnosis recent diagnosis of gastritis. That's why she's on the omeprazole. And that's probably what the newly started thing was that might be causing thesaurus hyper the treatment at this specific type of hyponatremia that this patient has. There's nothing in the stem to do to the patient having vomiting or diarrhea. And there's no other symptoms of sort of hypothyroidism, but an acute, confused patient for who you quite don't know what the cause of the Cillium is. I would add on a TSH anyway, because the cheap test to do. But there's nothing suggest that she's Hypo has hyper firing a Zometa, so I hope that makes sense in terms of my little tips box. So this is specifically referring to SIADH as a cause of you've anemic. I put new treatment on in SIADH syndrome of inappropriate anti diuretic hormone secretion so anti drastic on the whole role of it is is it's in the name, it's it's anti genetic. It's supposed to make you stop peeing out water on. That's what concentrates your urine. So if you have a syndrome where you have inappropriate secretion of it, where you have I eat inappropriately high amounts of 88 you're gonna have more reabsorption of water free kidneys. Specifically food collecting that releases are cooperative you to on Because of that you get inappropriately saltier. So you got high urinary sodium of more than 20. So if we break it down and we look at the blood, you've got a low sodium. You've got low sodium with a low samples minority, which suggests a true hyponatremia on you've gone inappropriately high urinary, sodium more than 20 which either suggests that you're concentrating the urine because of SIADH or you're having renal losses of sodium, which would be for a number of reasons to simplest reason. I can think of his Jurat IX and the rest of the Bloods are within normal parameters. So in this patient's case, is it by examination? Probably You've anemic suggests to me, probably SIADH secondary to the new medication that we started the Metoprolol clinicals. Um, I'll come back to that question and I'll come back to that question in a bit. I'll come come back to the management about how to manage drugs and hyponatremia. Specifically. No worries about that should work. Um, so let's talk about euvolemic hyponatremia so commonly caused by a society Ages of mentioned. It's increased anti diuretic on one, the other name of which is vasopressin because it also has the role of causing some basal constriction on. It's important and fluid balance on one of those increases. The amount of aquaporin V two channels in the collecting ducts. And these ducks, specifically only reabsorb water have no business in sort of electrolyte reabsorption month. But it's just specifically water on be a common question that I get about sort of euvolemic hyponatremia in terms of its causes is how does a glucocorticoid insufficiency sort of defer to adrenal insufficiency or Addison's? So where the glucocorticoid insufficiencies it can cause you've anemic cabinetry me because cortisol has an inhibitory. In fact, on 88 less quarters, all, you're not taking a glucocorticoid medication correctly, you're not having enough or, you know you're sick, in which case you need to double your dose in whatever, whatever it may be, it means that you've got more. 80 hates running around, and that's what causes sort of euvolemic hyponatremia, because sort of not really a society hate for more races to quarter saw Les quarters full suppression of 88 an adrenal insufficiency. Remember effects all layers of the adrenal gland, so it also affects the zonegran are below. So which is responsible for releasing or lost urine, which is a mineralocorticoid, which causes sodium re absorption on potassium sort of excretion. That's the course of hyperbole. Make hyponatremia rather, then you've really McAlpin a tree. So that's how the to death for was likely on in terms of the blood, as we've mentioned for, SIADH should expect a low. So most men osmolarity I true hyponatremia and the urine awesome was modality, which is sort of the total amount of sort of sunny or osmos end. But in the urine should be high because the urine is concentrated because you've absorbed all the water and the urinary sodium would naturally be high because it's a specific component of that urine osmolality. So that's the sort of blood that you'd expect with, along with a euvolemic examination, other things to consider severe high profile rate is, um you rarely see it in hyper fired is, um, it would be in a very severe over cases where patients come in very, very, very symptomatic with hypothyroidism so you wouldn't expect to see in mild, moderate psychogenic polyps hear from patients drinking too much water. I have actually recently had a case where patient had a UTI was drinking way too much water to try and try a lot of salt to try and, you know, help sort of flushed in UTI out and as a result, had really no sodium. And that caused confusion afterwards because of the cerebral edema, which was visible on the CT scan. Be able to mania. All that means is Zika, just excessively drinking, dinucleotide out sort of sorts and electrolytes, which again causes the seminal think the dissection. Polyps were diets where you know, having enough salt and glucocorticoid insufficiency for the reason that we mentioned that if you have less quarter so you have less suppression of aviation, there'll be more antibiotic hormone common drugs to think about the the person's anti epileptics, particularly carbamazepine PPI eyes, met Brazil and end sets from time to time a bit more on the rarest side. So that's just a short list for other things, including no malignancies, you know, such as non small cell carcinoma. So it's small cell casts and on carcinoma is or, you know, pancoast tumors or whatever you can think of. There's lots of causes of a T. H. So moving on to the next question. 20 free old gentleman husband admitted TD with severe malaise, fatigue, vomiting and feeling unwell. His observations are swallows heart rate of 110 tachycardia. He's hypertensive. Respect your rate of 21 his SATs 95% 94% on there. And he's a fibro. And he hasn't spiked any temperatures, either. So he's a fibro. What investigation would most likely identified a cause and let me put up the pool? And then I can start on strings of questions. Apologize for that story. TFCC is fired function tests and I left. He's is liver function tests. Lateral flow. Yeah, so liver function tests and fired function tests apologize for that. Okay, we've got quite a mix, that of answers, so let's have a look see, majority of you've answered correctly, So the correct answer is random quarters all on, Let's move onto why so just a little bit about cortisol. Cortisol is released in a positive fashion, and you know there is a diurnal variation with peaks in the morning and the evening. It's why a nine AM test is usually preferred. But that's assuming that the person has a normal circadian rhythm. Because, you know, in modern day populations, we have obviously got shift working and you know, other stresses in life. So and my own necessarily follow that. But that's why nine AM is preferred. But a random cortisol could still be useful in that if a patient has a high cortisol of above 450 roughly speaking, you can confidently, roughly confidently say that they haven't got a gene or insufficiency, and they probably are. Producing cortisol is appropriate now. If it's below that, you can't really say so. There's a range between 104 50 where it's indeterminate, and you'll need to do further testing such a short of that contest or if you suspect it to be an an Addisonion crisis, which is what it is in this case. Anyways, I would just start him on so I would just start him on steroids. I would just give them 100 mg of like the hydrocortisone because the more you dilated treatment and worn, they're basically at risk of dying because of the, you know, hemodynamic instability. That that and there's nothing wrong with having 100 mg of hydrocortisone. Try and take a cortisol test before you do that. If you can. Usually bloods would have take been taken before then on. If it's below 100 I would typically say that suggests that something dodgy is going on. Your cortisol shouldn't typically dipped below 100 no matter sort of what state urine. And that sort of the rough amounts in terms of the Rangers. So let's break it down. So in terms of the blood tests again, you've got a low sodium with a low serum was marital, which is just a true hyponatremia. Got you've got high potassium, so the low potassium in s so high potassium low sodium. It's not always the case that it's the dream or stuff, but I tend to the first thing that pops into my head. Is is there anything that could be related to some of adrenal function. And in a young patient, 24 years old has presented like that, I would typically think of another Syrian crisis. First on, they've got sort of a high urinary sodium. So remember what I said. That could be either because of SIADH or renal loss of sodium. Now in an Addisonion crisis. Remember all layers of thesaurus adrenal blanket affected so well, come on to how that functions in a few minutes. But if you're gonna classify this, it will be a hyper V makai. Podiatry because of sodium in urinary loss is, but also because of the low BP is also related to the fact that he's probably not producing quarters or eat it because it affects all A's and the adrenal cortex on in the hyperglycemic hyponatremia. You want to look at whether the loss of sodium is renal did have a yeah, high urinary sodium, which could also be because you know if they knew of limit. Remember, they also have a concentrated sodium because you re absorbing water, or is it a non renal loss such as, you know, diarrhea and nausea or vomiting, which is three G I losses have they got a high producing stones or have they got a fish enough? Whatever reason and skin, we should get his Well, typically, you know, a marathon. Runners taking all sorts of electrolyte derangements inappropriately sweating on, you know, burns patients is what I lose lots of fluid as well. So that's another thing to consider talking little bit about the adrenal cortex and not the medulla. So remember the medulla releases sort of adrenaline northern and dopamine, your catacholamines. But your cortex, which is the outer layer, has free layers in the way that you can remember is grammar be a lot of the zonegran, um, below says, um, ozone, a flick sick. A lot of his own particular. Remember, that is G f r. And if you remember their remember order of function you remember in in the order, I always say of how you'd spend your evening So you start off with dinner, which would typically be salty and mineralocorticoid, you know, savory. Then you have dessert sugar, critical corticoid. And then, you know, if you like, it ends with sex. So even at that, so that's all what all the layers released the remember, you know, seventies Mineralocorticoid older sister and specifically the physical part of me, says Clinical quarter, quarter, quarter. So at the particulars releases sex hormones. So just DHEA and a bit of testosterone, which is a little bit more important in ladies. Moonman. So you get a lease symptoms, as you mentioned, because, uh, or the steroid or low mineralocorticoid causes Ah, hyponatremia hyperkalemia because of all the store own, causing sodium re absorption in principle, cells in the distal convoluted should be within the kidneys, but it also in return of re absorbing sort of trying to, oh, also trying to re absorb sodium. It releases potassium. So if you have low old Austro, which is what happens in on Addisonion crisis, you'll get the opposite. You get sodium. Urinary loss is, which is why you got high urinary sodium and you'll get hyper clean it because of the Monty potassium. So I already mentioned do cortical thickness. Mineralocorticoid insufficiency already mentioned all those bets, so I'm going to move on. If someone's got low cortisol and you're not sure about it, it's in the in the terminal range or low do shorts. In that contest that's typically done at nine AM. And if there if you think that under Sony in crisis or they haven't taken enough of their glucocorticoid medications. So typically patients on long term steroids, for whatever reason, on the haven't been taking or they've been sick and you need to double the dosage, just give them a dose of IV. Hydrocort will double that dose of whatever they're hydrocort or whatever the steroid is supposed to be. Um, on as we mentioned, Addison's hypovolemia hyponatremia because of sort of the men around corticoid lost weight but also affects cortisol and glucocorticoid insufficiency. You've been in it because it only affects quarters all which suppresses 88 production on the other symptoms of corticoid really mentioned. So if you've got no glucocorticoid, you get non specific symptoms for a long period of time. Hypertension in the hypoglycemia on because of low sort of quarter saw, it causes increased sort of msg eight release an increased sort of a CT hate release, which causes hyperpigmentation which continuously see sort of on the hands and the other sort of sun exposed areas. Okay, okay, I will come back towards our come back towards the end for that No worries or try an answer in the chat for the next question. So a little bit about the rent an angio testicle, Doster and system So you live in release is under 10. Send it in your kidneys of these, Renan, this one converts into angiotensin one. This goes on to your lungs, which produce a six angiotensin converting enzyme which convinced angiotensin two angiotensin two is what stimulates the release of older sister on from the zonegran. Very low. So within the adrenal cortex, it also causes 88 or vasopressin release from the posterior pituitary gland on it also causes a bit of a zoo construction as well. On now, really mentioned all the store inspect it acts in the kidneys and, you know, causes increased sort of expression of these in actual that reabsorb sodium and excrete potassium and 88 again. We've mentioned aquaporin V to insertion within the kidneys. On it causes water reabsorption. So that's the brand angiotensin, although stream system in a nutshell. On if you remember, when you give someone a sin, Hibbitts inhibits the enzymes, and because of that you get increased bradykinins or bradykinins production within the lungs, which is what can cause a cough with ACE inhibitors, which is why sometimes you give them angiotensin receptor blocking enzymes instead of inhibiting eighths, Um, and a little bit about the function of all the stair own. So this is a good a principal cell looks like, and that typically found a distal convoluted sugar within the within the nephron of the kidney on what the steroid does is as we've mentioned, it's it's it's it's a steroid hormone. So it enters the cell, and Interest said it really causes increased expression of these epithelial sodium channels that reabsorb sodium and excrete potassium. So if you know all the star Oh, for whatever reason, that can cause increased sodium excretion and more attention of potassium. Which is why nascent habits is. You can get hyper convenient, so moving straight on to the next case. So you've got first year old lady who presents your GP practice because she's concerned her urine is becoming increasingly foamy and she's got new ankle swelling. You have the bloods below what investigation would be most useful, and that's really watch the pool. Oh, thank you for that. Anything Always his message. Me bench, Netflix, these, um Okay, so let's see the majority answer The urine dip, which is the correct on certain will come on to why and a second select Tradjenta results. So, um, that's the correct answer, because this thing gets the leading to a frantic syndrome. So, uh, ignore ignore these boxes. Apologize. Ignore the books on the left politics for that. But let's talk a little bit about a hypoalbuminemia on a few other things. So in terms of the summary of this, you've got low. Silien were hyper very me on examination i e they've got peripheral the much dust of that fluid overloaded. It's not the only sign, of course, because you know, you be looking to see if the hypertensive if they've got a raise JVP if it's really bad, you know, pattern megaly Sometimes you know, Ascites is lots of other things that could suggest, you know, hyperbole. Me but perfor Dema hypovolemia so and they've got a low albumin which is likely secondary to protein urea, which is where the foamy urine comes into place. So when you're on this typically foamy, it consisted of something in it that isn't supposed to be such a proteins and they've got a low albumin, which is just they're peeing out there protein for whatever reason. So hypovolemia is chemically determined and usually cries diuresis. As I've mentioned, If there's, you know, there's lots of causes for it. So you know, typically the organ failure. So that could be liver failure, heart failure, kidney failure on nephrotic syndrome. So all the organ failure is do it on the for trick syndrome, including enough for a different reason. So if you have left sided heart failure, you can get pulmonary edema. If you've got right sided heart failure, you can get, you know, a raised JVP, hypertension, peripheral edema, which can go all the way up to the belly. You know, ascites reason if you've got liver failure, those sorts of things and so with the thought Extendryl, um, in terms of how you would explain it. So for whatever reason, there's lots of causes of nephrotic nephrotic syndrome. But what happens is you get this loss of protein in the urine because your your kidney shouldn't be excreting more protein typically within a day. Your your excrete about 150 mg of protein within a day, but shouldn't be more than that, and the dipstick shin picked it up. A dipstick is the most sensitive test for protein urea, but it doesn't really tell you how much. Which is why you need to know creatinine racial protein, creatinine ratio. But we're coming through later. If you have a nephrotic range protein urine, you're excreting about 3.5 g of protein production. It's almost 1 20 times the normal amount of a person because, as I said, your glamorous enough room shouldn't be letting if the membranes in tact. It shouldn't be letting a lot of protein fruits to get loss of this protein, which causes protein urea. But you also get loss of anti from Been free, which is, the name suggests is very important for stopping you from forming too many clots inappropriately, which is why one of the treatments can sometimes involves anti coagulation. You get hypoalbuminemia because you'll get your releasing your proteins within your urea, and that causes ah, loss of oncotic pressure so more fluid seeps from the intravascular space into the interstitial space and see peripheral edema as the next symptom. And because you got a loss of those proteins, your body tries to make up for it by making low density lipoproteins. That's where you get hyperlipidemia because you get increased production of LDL low density lipoproteins from the liver on. That's why sometimes statins are included in the treatment eight, and habits are to help protect your kidneys in. I'm not gonna go too much into the mechanism of that, but it can help protect your kidneys further and further damage on what you get following. That is an appropriate anti genetic hormone response because you get a loss of that interest vascular of one day, Um, and that releases 88 also leads to hyponatremia. So that's the security of Nephrotic syndrome explain and all the symptoms that you need to know for On the typical triad of protein urea hypoalbuminemia on a Dema, you see Nephrotic syndrome. But there's lots of different causes over. I won't be going into that Okay, 30 seconds or one minute break, and then I can answer any questions that anybody has. There's an extent so far, guys I might talk to fast from time to time, Pollen Jai's for that. But you know, the video be uploaded and your heart of slides. Rogard this. You know, you can try and slow my voice down like a soft. It's if you want to do that. Thank you. Sorry. Brilliant. Let's move on for the sake of sign. But we'll get on time, actually, about halfway there. That's good. I'm usually never on time. So a 25 year old lady has been brought to et having had multiple seizures. She has a background of bipolar depression on gastroesophageal reflux disease. That's what going to stands for. Her bloods were in the table. What is the likely cause of her hyper true? Me also increased sodium. Let's put up the pool. Uh huh. Yeah. Okay. For the sake of time, we're gonna move straight on. So majority of you've answered correctly. The correct answer is lithium s o lifting toxicity or, you know, newly started lithium in particular, particularly when you're in that sort of titration period of it can cause nephrogenic diabetes insipidus. And the reason why it's nephrogenic is because it causes resistance to anti genetic hormone response from the kidneys. So if your kidneys aren't responding to anti drastic hormone, as you can imagine, that means you're excreting morp your water from your kidneys, and that can cause hyponatremia because of pure water loss. If that makes sense. And this this vineyard religious about the some lithium toxicity going on, you know other symptoms and the CD changes with lithium toxicity as well, because because you're toxic and a few other things. But we won't be doubling into that because that's not the focus of this topic. So weird. Hyper Nutri meal, uh, terms of causes, wise thinking. Let's eat assault game. There's either more salt than water loss or there's pure water loss or pure water. And take that the simplest way I can explain it. So salt gain. It could be something for whatever reasons, having to wait too much salt. You have to have a lot of salt to get yourself in that level. But good examples of this I can think of this, for instance, also is, you know, fluids. So yeah, Tradjenta in terms of food twice So, you know, saving giving someone saying you can get them into hyperkalemic acidosis, but also increases the sodium amount n G feeding. If it's not properly adjusted, what else could do it? So the human albumin solution has has lots of has that we give to. You know, patients would really bad sort of cirrhosis who were typically tapping to get some fluid off a scientist and to send it off to see if you've got, you know, continuous bacterial peritonitis and stuff like that has has a lot of salt sodium in it on hyperaldosteronism, which is typically Ray, remember what I said? All those strong doesn't reabsorb sodium excrete potassium. So that's why I can cause a high protein. But that's very, very rare. I have no ever seen that before. Um, you can get more salt than water loss because remember your body can use Also do all sorts of things in terms of the proportionate news is electrolytes and water, So kidneys diuresis. Sometimes in some patients you can have more water than salt loss, which can cause the imbalance again. G I losses and vomiting and diarrhea. You can sometimes have more water than G water than you know in salt lost, depending on how your body, you know, re absorbs everything or whatever happens. And skin as well with sweating, can sometimes get more pure water lost in salt loss. All sorts of arrangements can happen. With these, Aside said on the last course is pure water loss. So patient are hyper dipsy a with pour water or or intake, which could be for a number of reasons. The most common reason. It could make it to the frail elderly person that's confused and not drinking enough, essentially, and diabetes and separatists, which can be off for neurogenic cause which is related to, you know, posterior pituitary gland not functioning properly where 88 was released from or nephrogenic diabetes insipidus Where your kidneys being resistant to antigenic Holman on That's hyponatremia, cause in a nutshell. But the most common cause, the most common cause that I see is dehydration. For whatever reason, dehydration from poor or and take or, you know, sort of loss is from skin Gee I tracked or the kidneys. Dehydration is the most common cause that I see of hyponatremia were in the hospital setting of people coming in. Marathon runners were a good example of that as well. So diabetes insipidus is the opposite of S I s I a th. So it's either a lack of 88 production, as I've mentioned from posterior pituitary gland or resistance to a T H nephrogenic diabetes. Insipidus causes can include sort of corn, a car, acute nephew ingestion, particularly on that titration period off the end of being in their toxic level. For whatever reason, ah, hyper hyper calcemia because again it can cause increased resistance to 88 in in in the kidneys. On you can also be hereditary is what which is a lot rarer and again needs the pure water excretion you treat with a D H analog, which is an anti diuretic hormone unlocks itches, doesn't present, which basically just axis a normal function of it on a B H. And looks can also be used to differentiate between a nephrogenic diabetes insipidus on a neurogenic diabetes insipidus in that if you give them an ADH analog and you know respond to it, that probably means it's nephrogenic because the kidneys are, I think, resistant to it. Or if it's neurogenic, it means you're not producing enough of the heat they should have a response to. They should have a response to 88 unlocks for hyponatremia, which food is better to use. Treatment wise will be dextrose. I wouldn't use sort of only time you would use what it's a bit difficult. So in terms of treatment for hyponatremia, I would go with dextrose 5%. 1st, you can also use the bags with a lower amount of sodium. In them, the no 50.18% sodium, with dextrose in them. Saving. Technically speaking, no pain under sensing. If you're hyponatremia, severely hyponatremia. Technically speaking, if you're thinking about it, it's It's it's It's has less tenacity than your than your blood and that the soul you know my eyes. Lower concentrations lower in the bag compared to your blood, which is even if you give it will lower it, but I won't lower as much. But 5% dextrous is typically will use or the lower amount of sodium banks. And you have to monitor the sodium multiple times throughout the day because if you rapidly correct, it will come in two hours later. You get complications on you can't correct it more than 10 million miles, 8 to 10 minimal in 24 hours, and I would recheck the sodium immediately in the first hour after you start treatment. So that was a private question that was asked apologize guys on. So next question during the night shift your call to see the same patient. GCS is five and she snoring, her blood seen below What complication may she have experienced? And that's real orange. Uh, a lot of questions. So let's pull. So yes, the majority of guys that correcting you've been listening or did you just Smarties eso? The correct answer is cerebral A Dema. So this patient was a patient with hyponatremia. It would have been corrected with, you know, 5% dextrose of whatever it is. But as I said, it was way too over correct. And you can see how, how big of a drop. It wasn't a venue and she had a So you have 100 100 and 20. So what was the sudden it was 150 something above. And then that stopped 220. That's more than 30 Change. That's a massive massive change in very, very dangerous 10. Minimal within 24 hours is dangerous already s o over exaggeration, and they wouldn't typically happen. But it's extreme example of it. So with hyponatremia as I mentioned, the brain assaulted in the blood so you get cerebral edema and for the same reason, if you overcorrect hyponatremia way too quickly before the brain can adjust to it, which is why we do it slowly. You get cerebral edema as well, because she's gone from hyponatremia to a very quick hyponatremia brain. That's enough time to adjust. Water's going to seep into the brain because the brain is salty than the blood. Now, uh, again, the opposite is also true in hyper s and hyponatremia. If left uncorrected or it's very severe, you get automatic demyelination, which is the brain stem essentially cleaning. The best significant is the brainstem, sort of peeling away, which was all sorts of neurological symptoms from it, or a cerebral bleed a swell, as with our high risk up. And if you have an over corrected hyponatremia that can also lead to more on demand, urination or cerebral bleed because you've gone from hyponatremia to an over corrected hyponatremia. In other words, hyponatremia for that patient, if you correct it more than 10 million walls within 24 hours and a person at significant risk of that as well. So that would be your number 8 to 10 minimal within 24 hours. Repeat the sodium blood often when you're correcting them on. If it's very, very severe, they may need to go to intensive care for appropriate where they can monitor the blood regularly with, you know, on online, where they do regular a beegees and stuff like that. And in case they, you know, have neurological. So Queenie, where they might need to be introduced. It'd so again, just a picture to say in cerebral edema. The reason it happens is when the blood is much more salt in the brain, and you haven't had time to adjust its eat a severe or acute change. You get cerebral edema because water seeps from the blood into the brain. Wherever sodium goes, water follows, and the opposite is true is well. If the blood is salt here, then the brain water will go wherever sodium goes. So water will go from the brain into into the back into intravascular space that dries the brain out. And the way that I find myself, I think of like crack sort of desert ground. The brain stem, which is sort of peels and drives and cracks and deem I know later is the way that I think about it that way and cause all sorts of neurological symptoms on also because your brain is dry. Think of your blood vessels is cracking and being able to sort of crack because they're dry and it can cause a cerebral bleed. That's the easiest way that I used to remember. Okay, Uh, so moving on to the next question. So 62 year old lady presents to her GP with uncontrolled hypertension current. Take the Senna product. I'm not Dippin. She's been started on another medication. This is very UK based guidance guys are pollens rise for the any chest guidance. Based a week later, her renal function was checked. What is the mechanism of the newly started medication? You have to know your nice guidance for this one. Unfortunately, let's restart the pool and they have a little look at the chart. Okay? For the sake of time, I'm gonna move on, share the results. The majority answered angiotensin receptor blocker, which is the incorrect answer because she's already on an ace inhibitor. In which case, as long as she's tolerating it, we wouldn't need to change to an ARB. So the correct answer is NCC inhibition sodium chloride cold transporter inhibition in this complex issue, but we'll talk about why in a second, so in terms of let's go to in terms of hypertension guidance would in the UK This is based on my skied in. If a patient's less than 55 years old and they've got a confirmed hypertension, either fruit sort of ambulatory monitoring or from sort of two different tests showing hypertension within a GP setting, you would start them on a sentimental on ARB is appropriate on. Then, if they're more than 55 result or Afro Caribbean, you start them on the calcium channel blockers such as, um, not typically. So she's already on the Cinopril on a centimeter and a radio on. I'm not a peanut costume channel blocker. So the next thing the guidance is the fires I genetic such a bendroflumethiazide or the other one, which I always forget. There's always one more that I always forget. We'll come back to that later, but 506 inhibit sodium. All right, that's it. And that might thank you sodium chloride code transporters within the distal convoluted achieve use now, the quickly of that is that when there's more sodium within the nephron cheap, you remember what I mentioned about the sort of principle cells are cells that reabsorb sodium and release potassium. When is more potassium sense within the within the cheap? You'll those principle cells are going to try and absorb and retain more sodium on. Because of that, they're going to excrete more potassium. Now this lady has an exaggerated response to that. But it's meant that she's released. Released What's What's was released more potassium or potassium because of this drug. And that's why she's hyperkalemic. Apologize s also, if you're diabetic, that is correct. A. Send him. It is our preferred because they have a nephew. A protective effect. Thank you sure, because with diabetic patients you can have diabetic nephropathy, which leads the protein urea. It's the same reason why it considered a sin and Byetta in a patient with no photic syndrome. I thank you for that show. What? So coming back that, uh, a z I said eight and habit is typically increase. Potassium of this lady has a low potassium and she was started on fire sign genetic, which decreases protesting for increased sodium courage to do the CT stimulating principal cells to be absorbed, sodium on. Release more potassium in response. Very quick nephron picture. So I got to remember this. The proximal convoluted TV or the descending and ascending you have handy, the distal, convoluted cheap you and the collecting dot. So in the ascending loop of Indian ascending group of handy, that's where you have the encasings. See the sodium potassium chloride Code transporter, which is also known as a simple water. All of Cymbalta Means is a channel that brings two things in the same direction. On Manti Porter is two. Things are brought in opposite. Opposite directions can give you examples later, but we can come back towards the end of it. Lucrative. Such a ruse, mind bumetanide actor. And that's when it can cause low electrolytes. And, because they're released sodium, they can help with diaries and excretion of fluid in the distal computer sheet. Or that's where you have the neck sort of on your principal cells. The back channels that we talked about that swelled Austro necks and your potassium sparing diuretic. So act on that. But I do inhibiting all those strong or causing decreased synthesis of in Actonel's you also have your NCC, a sodium crawl right code transporter, which is type of Cymbalta, which where fires I genetics act and then in the collecting ducts to simplify things. That's where 88 88 look act Teo cause increased expression of these aquaporin be two channels that reabsorb water. That's the nephron and diarrhetics and 88 in a nutshell. So 24 year old, uh, I'm going to say, lady supposed to say that is five days POSTOP for Pam Pocket for Prime Proctor Colectomy for severe crone's her. The ostomy is producing a high I put with output, which is more than 1500 mL per day. Usually, you notice she is hyperkalemic, but with adequate intravenous replacement, it does not improve. What other blood test would you like to carry out? I'll come back to your question towards the end, Andrew. Uh, yes s Oh, it's It's a new idea. Ostomy. So POSTOP and proctor colectomy they removed all of the gut on. They've had to produce 90. Awesome, because you've got no code on left. So moving on. So yeah, the majority of the answers correctly. Magnesium, magnesium, magnesium, magnesium seems to play a part in so many things in the hospital times testing, including people presenting with a F four, weird of redness and lots of other things that plays a hand and of all into. But what you need to check is is theme acne Z um, getting pulling in surgical patients, especially if you're gonna end up on a colorectal surgeon called drop or any sort of cardio or any sort of, you know, cardiology job or acute medicine Drug. Magnesium is gonna play such important, you know, to use Nasonex using different me as it's used. It's checked in hypocalcemia. Hypokalemia has a hand everywhere, Really, weirdly enough, Um, so in terms of magnesium, when it's a decreased amount of magnesium, it means your kidneys excrete more potassium in return. That's a simple it's simplest way to think about it. So low magnesium was increased renal potassium excretion. So if you've got potassium that's not really responding to treatment or improving, we'll check the magnesium. And if it's a post surgical patient, check the magnesium anyway. They often do refleeting blood on these colorectal patients because they're slowly trying to get their feeding regime up. You know, they start with sort of water and then, you know, soup diets, super sweet and then, you know, soft I and then a normal diet because you know the risk. I liest on some of the other nutritional risks and stuff like that so often you know it will be part of the feeding screen. In these patients. Check magnesium with the potassium's low and make sure to replace it along with the potassium at the same time. Now you can either replace or Leo intravenously, depending on how low it is. If they've got diarrhea as the cause of their hypokalemia and it got low magnesium, don't replace it or really replace it intravenously, because magnesium and all these other electrolytes, if you replace them already all have a small tick effect. So someone stay within the gut and pour more water in with it, so they'll make the patient more dehydrated and make their diarrhea conversely, worse and actually paradoxically, lower their electrolytes more on return again. So in the in, a patient with severe diarrhea, I would replace intravenously regardless of hard Noda, magnesium or potassium is so in terms of the causes of, uh, hypokalemia. It's a decreased intake because post up and your local he cheese, uh, so, uh, shift. So I need a decreased intake. Um, is can be a common cause of it. I've seen patients, you know, for patients not eating enough. And if patients are eating for a number of days or potassium could drop quite quickly. You're interested in potassium is much higher. Combative intravascular potassium by intravascular. Potassium is a good reflection of how much potassium you have within your within yourselves as interested in the store. And it can drop quite quickly if you don't. If you're not eating essentially or if you're not eating enough, you know, make them have a banana, I guess, or whatever I'll spinach. There's lots of things I see. Um, they can be shifting typically because of drugs. Or, you know it can happen in DKA or, you know, hyperglycemia. Whatever other cause. So insulin typically call, which is why it's part the hyperkalemic. A treatment shifts potassium into intersolv. Eso can cause interested in the shifting of someone's on higher months of instrument, taking the DKA protocol or, you know, in a patient with hyperglycemia or patient Who's diabetic POSTOP. You need to not eating and drinking. You need for them on a sliding scale. Monitor potassium very closely because you may need to replace it, which is why it's part of the guidance and they're beat. Adrenergic also typically cause shifting of potassium interest. Senator. A zoo. Well, that's why it's also again Part uses part of hyperkalemia guidelines sometimes with, you know, nebulized so beautiful, sometimes used as well. Now increased excretion is the most common cause. So the way I remember is grand G I losses, diarrhea, vomiting I'd ostomies fish, nose, whatever you can think about renal, which could be because of diuretics or, you know, whatever other cause there is a diuretic. So most common thing, I could think of adrenal causes. So, you know, if you've got hyperaldosteronism, i e. Something like cons yoga. You'll get more sodium reabsorption and more potassium excretion on D again. Conversely, if you've got cushings that a similar thing can happen a Z well, in that you get more sodium reabsorption and more potassium execution. I won't go into why. But cortisol also has some mineralocorticoid effects. That's why magnesium as I've mentioned. If you have low magnesium going to excrete more potassium renally on, that's all the course that you need to think about. For someone with hyperkalemic, check the magnesium tract imaging using, injecting, make museum and replace appropriately or early or intravenously. We're on the last few questions just before I start, The next question I'm actually going to do is post the link up in case anybody wanted to leave. You only got about two more questions left, guys, but opposed to link up. Now, in case anybody wanted to leave is the feedback link s so moving on to the next question. So you've got 25 gentlemen was taking a heroin overdose and had a long life on the floor for several hours before paramedics got him. Let's say about 10 hours or something like that. Something ridiculous. He's currently stable, needing his bloods on the table. What is the cause of his hyper continue? And that's reset. Pull. Um, I have my you guys are coming over to all the jokes today. I don't think there is a hair Adidas. Sorry, guys. Check movie. Good. So the correct answer is, uh, is rubbed of my anus is so on. So the reason it's rhabdo is because he's patient has been lying, called up for a few hours, probably in the same position on the same muscle. Puts a lot of pressure on it, and not moving can cause the muscle to destruct, essentially because it's putting pressure on it on. That causes release of the interest and the contents of the muscle, including potassium and myoglobin. Now the potassium increase is because of the interest sending the destruction of the cells. But also myoglobin causes kidney damage and blocks, which evils up so it causes a K I, which again causes the hyperkalemia because of the A k I E s. Oh, that's what the mechanism, if that was so, anybody would hyperkalemic if they've got a bad kidneys, take a. I would ever stop the neck from nephrotoxic drugs or any drugs that increase the potassium amount mix to give them IV fluids on, uh, if they've got severe hyperkalemic, which can depend on your trust guidance. So in my trust, it's either a potassium of above 6.2 or potassium of 5.5, with the typical each CT changes of a broadening QRS complex flat and P waves tall 10 2 t waves, Um, or, if it's very severe, sinusoidal waves, and you would typically treat with calcium gluconate. Now what custom duking it does? It's called a membrane stable stabilizer in that what it does is in hyperkalemic. A. You have increased my myocardial excitability, which is what pushes you into arrhythmia, and it very serious condition to V. F and VT, which is why we want to make sure it doesn't happen, because remember, kinda caressed four pages. Forties. One of the waitresses hyperkalemic. So you've got this mild cardio increase. Excitability because it's a lower, fresh hold of excitability for the myocardium is increase potassium. Now what given calcium gluconate does is it makes that fresh hold higher so it makes it more difficult to stimulate myocardial cells. And it's less hyper excitability, which means that's less likely for you to go into V F and VT, which is where the most important thing and potassium That's very high, say, above 6.2 or with the C G, uh, changes gift calcium gluconate, because that stops them that protects them from going into a written me a such a V f and VT and you know, subsequently a cardiac arrest. That's what we have. Carson do connect first. You can also get casting chloride, but custom chloride contains three times a much as cast in gluconate, and it's very irritated veins. So you have to you to give it through a big proximal Uh, let's give it for a big proximal can, you know, basically is just unless of it, Compatic calcium gluconate and it typically say, 10% 10 mills. What followed the be enough guidance, whatever it is for your trust, because in mind, it's 15 mills. Whatever reason, um, relax need to do. Is that potassium still within? So you're myocardium is protected because you've given calcium gluconate, but you still go higher months for task in within, within an intravascular space. So eventually, when the calcium gluconate stop protecting your heart, that potassium still there to cause my cardio excitability, so you need to shift that fasting and packet elsewhere. That's when you give them insulin dextrose interest in packs of passing into the cells. Dextrose protects them from coming hypoglycemic when you give them insulin, and you can also give them nebulizers are beautiful. And that's the temporarily Schefter passing intra similarly so that eventually, um, make sure to put a catheter in or make sure you monitor your own upper very closely. They need to journey the potassium out. So it's time buying measures to help try and get the kidney started up, depending on whatever the cause of it was to try and get them to pee it out. Now, if they're not peeing it out, it's it's and it's not responding to treatment. You can also give new things, which is you can look it up yourself. There's a particular new drug called McCalman, which is called sodium sodium zirconium. Funny enough, sounds like something from a marble movie that the neck shields off like almond is something that you can give. Or really, it's a key native agent for potassium. Remember what I said. If you're not eating and drinking, your potassium stores will go down very slowly, so it stops you from Reabsorbing protesting from your gut and it can be very helpful is the time buying measure as well. And then my trust you give the inpatient for the potassium of 6.5 or very severe potassium doesn't respond to the initial amount of treatment with multiple doses of insulin. Dextrose, uh, you get backed up to 5 to 10 units, something of that time. Now again, if you've got refractory hyperkalemic, it's not responding to treatment, and they're not peeing they, if appropriate on. You know, I see you allows they're appropriate for I see you if it's not down or if the renal units open during the day don't need to go for hemodialysis. Think that's one of the indications for him with Allis refractory hyperkalemia on That's the nutshell for hyperkalemia in terms of management treatment, then you have to find the cause, of course. So it's a shifting or selling a destruction, which come because of tumor lysis syndrome, rhabdomyolysis had mentioned or mass blood transfusion can even lose patients. I have given lots of blood because the cells you know, or being sort of because the blood is being rapidly given it consort of, you know, cause damage and destruction of those red blood cells when, as it's being transfused very quickly and that can cause an increase potassium now it can also be because of decreased excretion. AKI being the most common reason. Hypo Doctor. Oh, no, no. Is, um, because that because of multiple things. But I think of Addison's or adrenal insufficiency for whatever cause DKA can also that can also do it a sin hip. It is again for the reason that we mentioned it's effects on the stern on potassium, sparing diuretic again for its effects on August run or in actuals. In a nutshell. On Yes, sir, this content will be uploaded to meddle, so yesterday's content will be uploaded to meddle today, and today's Contin will be uploaded tomorrow, doing the video and the slight last two questions on our post the link up one more time in case somebody wanted to fill out the feedback and go, uh, pump pump Army air. On the last set, eso a 70 or drunk moon. Longstanding, poorly controlled diabetes comes in for his annual diabetes checkup. He has his bloods taking and the results of table What is most likely what is the likely cause of his hypocalcemia? Let's put the pull up. Oh, okay. For the sake of time movements in a majority of you've answer to correctly. So the correct answer is diabetic correct answer is diabetic nephropathy, and I'll explain why in just a moment have, uh, put that picture in our put that picture and but the picture and someone will come back to doctor about it. So correct answers. Diabetic nephropathy reason Why is your kidneys or very important in the last stage of vitamin D synthesis? So when you're synthesizing vitamin D does free steps, either you can get it for your diet or freestyle lite. Your skin reacts the sunlight Every a UVB on produces sort of the initial sort of vitamin D metabolites, then subsequent. Your liver is the next step in vitamin D synthesis, where it gets turns into one hydroxy vitamin D as a hydroxy group. And then the last stage that's involved is your kidneys, where it turns into a 1 25 dihydroxy Vitamin D, a k a. Calcitriol, a k a. Factive vitamin D. And as you guys know, vitamin D is very important for re absorption casting from your gut, but also causes some release of calcium from your from your bones. And it's also important for re absorption of calcium from your kidneys, kidneys acting on themselves. If you got very severe kidney disease. Kidneys simplistic, important, you know, to produce PPO. So you know, I should have made it. Probably made this patient anemic, actually. So you know, if you can get very bad kidney function, it can become anemic because they're not producing the PA up converse. It can also very low vitamin D because the kidneys are off the last stage of vitamin D synthesis and that can cause they're hypocalcemia as well as a hyper hyper force 30 me A. Well, for the same reason. Um so, uh, either give a little IV calcium and also consider a place in vitamin D. If know, consider a phosphate binder. Agent such a Savella. Assemble it kind of lancets Salamah. I don't have the proper several a more hide. I don't pronounce it, but it's a phosphonate binding agent and I'll explain to you why a bit late for unlike any to give those and definitely place the magnesium if you know again, magnesium also plays an important part in parathyroid hormone production. And simple thing is, you guys now para fired home. One is important for the release of it's born in calcium sort of physiology and that causes a release of calcium from the bone when your calcium stores are low, but also increase your ejection from the gut and also acts on your kidneys. Very similar. Walter Payton, Indy and then that If you have a low vitamin D a month, you will be producing a recent as much parathyroid hormone on, uh, again that cause hypercalcemia again. So make sure to check the magnesium again. Low, low calcium, low potassium Check. Magnesium, magnesium, Magnesium IV. Custom can be given as casting broken your calcium chloride. Some anemia guidelines on its concentrated form Again, Just remember the side. Calcium chloride is three times more concentrated than calcium gluconate, so give it for a large vein as it's very irritating. Symptoms of Hypocalcemia Remember spots more Dixie Get spasms. Power Part ST Parasthesia and shares you get seizures. Increased muscle tone. Imperatori Ent. A shin dermatitis In pet, I go herpetiformis, which is a type of posture. Psoriasis. It's not impetigo, it's a push. This rises a specific type of it sometimes associate with pregnant ladies. Vast X, which is the slime where if you tap the facial nerve, this hyper excitability of the neurons you get sort of touching of the nerve. You know, cardiomyopathies cataract on the most sensitive sign for hypocalcemia is true. So signed competitive of sex time, which is where you get that sort of that sort of hand position when you put a BP. That's sort of weird flex in hand position. When you put a BP cuff and on the patient's arm and inflated for 2 to 3 minutes, it's more sense of than Boston Exline. Okay, uh, lost question. Pump a bum. So 43 year old African American lady presents the GP with painful modules. All notions she crossed. Say, check you. You cross a chest X ray shows abnormal changes. Have blood indicate happy consuming. What is the most likely cause almost question, guys. Okay, Britt, we're gonna move on for the sake of time because the last one shows results. So that, um, your teeth you've answered correctly. It is sarcoidosis. So, uh, come on. What cycle Basis is in a second. So I pick all senior management is fluids, fluids, fluids, fluids, fluids, settle, ization you to get them. Saving saline is the preferred choice of fluid and hypocalcemia, and you can also consider this force minutes and calcitonin, depending on the course to pack that calcium away from the blood and treat and find the underlying causes the most important thing. Symptoms wise. Just remember renal stones because calcium conform stones with lots of things. Pissing phones because calcium has an osmotic effect when it's really excreted. So you'd be dehydrated with paying for bones because sometimes you can get depending on the cause of it. Bone breakdown being the cause of the hypocalcemia in some cases, which can cause painful bones because the bone integrity is affected because of less calcium and phosphate within the bone. Abdominal moans because calcium is a stabilizer, so it remember what I said. It's a membrane stabilizer in the same way that it can stabilize the heart. It stabilizes your gut, so there's less gut motility, so that's working, cause constipation is very simplistic way of thinking about it. Low energy levels and can cause some of the become delirious psychiatric overtones is in terms of causes. So if you remember, hyper parathyroidism is the most common cause of hypocalcemia malignancy following closely second multiple by in my low march, where you know you get these possible side time was affecting the bone on you get that typical sort of crab signs and symptoms. I e. Hypocalcemia renal failure wouldn't acute a k I. Because the calcium causing stones and blocking of the cheap pills and causing dehydration on anemia on also, what was the last word crabs be be, be bumping. That was it vitamin D toxicity. I won't come on to that. That's very rare. And milk alkalize syndrome, which used to happen to patients that were given a milk of magnesia with different. I forgot what it was on assets to essentially help with reflux, and it's basically higher. It's a trial of high bicarbonate amount. So you get a metabolic alkalosis, you get an A k I. But you also get a bump up on a K I metabolic alkalosis, and I forgot what the other part the Triad was. But we'll come back on towards the end. Sarcoidosis, a Z mentioned fire toxicosis in rare cases, and pseudohypoparathyroidism, which is, uh, quite a mouthful. But essentially, you paradoxically got high power fibroid hormone levels. But your organs, your gut, your kidneys and your bones are resistant to the effects of the parathyroid hormone similar to, you know, nephrogenic diabetes and separate it where the kidneys are resistant to 88 effects. So because it's resistant, power fired hormone, you know, going to get much reabsorption, or absorption of calcium so it gets not absorbed from the gut, and it gets more released in the kidneys. Simplest way to explain it. Oh, that was to try and hypocalcemia, because your metabolic alkalosis under any K I, um so sarcoidosis. Very briefly multi system, monkey seat and granuloma. This disease most commonly affects an underbite confected any or consistent really cause a rough. You manage those in a while, which is these painful fat nodule on your shins? Usually chest X rays compare with by natural height and lymphadenopathy, which is a stage one. Chest X ray shin just on hypocalcemia on acutely presents with all free could be something called laughter and syndrome. There's lots of syndromes for sarcoidosis, depending on the weight presents, but just start on the back of your head. Chest X ray changes of sarcoidosis have four different stages, so stage one presence of bilateral hilum adenopathy Stage two is that, plus particular rapacity is stage three is Reticular passes by shrinking of the highly nodes were infiltrates on Stage four is Reticular Pasties with fibrotic changes sicroidosis in the nuptial. Who that is a very quick whistles off of all the electrolytes, haven't covered everything. I will probably do a separate teach for calcium because I think calcium is important to teach because calcium is important because I don't like the use of adjust the calcium. I actually prefer a casting from the VBG, where it's an ionized calcium because I nice calcium is the active form of calcium. Because calcium can be 50% ionize with in the blood, 40% is bound to albumin, which is why they look at the adjusted calcium and and 10% is floating around in different ways, about in different things such as force mate and other things and the majority of your blood. And the home only active as a non bloody, physiologically active calcium is ionized calcium, which is why I prefer VBG. So I think calcium probably needs a known session, which I will cover it some point. Has anybody got any questions? Seeing a very quiet chat? I really explain things very well have you talked to far. So you're overwhelmed? Uh, nobody has any questions. Oh, I can, um you're like, there's some things like that because it's such a broad. It is such a broad topic is a very big somebody named or already already enough. So, uh, let me see. There's anything else that's worth talking about very briefly for anybody that wants to stay opposed to the link up again. You go. Uh, let me have a little look. Uh, that's a little look around. Seen anything else? Like an overload? You guys with, um oh, I think probably worth mentioned. The treatment forces. Somebody asked me to treatment for SIADH verses. So in terms of hyponatremia, the treatment versus euvolemic hyper really make and hypervenom it or keep it very simple. It still depends on the cause within, within the within the classification of it. But if it's hypovolemia, it's treatment fluids. You need to get salty fluids to replace the sodium that's been lost in to give him some fluid. If it's hyperbole, make either fluid overloaded. It's typically, Diary says, and if it is euvolemic, it's typically stop the cause. Find a cause and fluid district I typically say, by about 500 mils of whatever they take within a day, but sometimes is very difficult because patients don't know the total amount of fluid take within a day. So often, I say, restrict a 1500 mL on, then see what happens the next day. But just remember, if someone's really small 1500 millimeters might be their normal fluid intake. In which case, if you've restricted under that you've not made any difference, such is better in mind. So is that just yet? All it is related is excessive water, water, excessive water intake without salts. If you excessively taken water without salts, you're gonna just dilute all of your electrolytes. And that would basically cause hyponatremia, the psychogenic caught being for whatever reason, you know forever reason they feel the need that they're constantly first C and a half to drink without any organic cause being in place. That's what's known a psychogenic polyps. Here. Let's see. Just meaning first, hope that make sense. Um, okay. Done. Uh, how fast can you replace potassium? Good question. In another, I see you setting 10 minimal you can give it would influence at a rate of 10 IV 10 Minimal uh, power. So typically a flu regime is you give them no 0.9% saving where one liter bag with 40 minimal of potassium given can only be given as fast as over four hours because of the rate of 10 minimal. A power of potassium is how fast you can place and again recheck the bloods. Now, um, I see you setting you can actually go assassins 20 minimal power, but only in in in a very monitored hate to use setting where they you know you central lines and concentrated a month's of potassium instead of giving them lots of fluid to replace it and they can see, really monitor monitor it Would you know our lines where you can constantly take a BeeGees? How can distinguish a b a k i from CKD from electrolytes. So ckd commonly you know again you'll get your gut sort of other siquiera the long term effects of the CKD, which is anemia because it began the e p o that I've mentioned a low vitamin D amount, which is where you get the low calcium and the high phosphate amount The problem with high phosphate in CKD also is the fact that phosphate binds to activate it or free calcium. So the only two you're below casting because because the low vitamin D um, you also have a lower calcium because you have high phosphate, typically within the five or four range on faucets, typically around one or less than one. It's not, so you sometimes get forced a binding agent, so that's I say, electrolytes wise. That would be a pretty good starting point. You can sometimes get renew excretion of sodium because skinny, they're damaged. All sorts of electrolyte changes can appear, but I think the most important part with CKD in terms of distinguishing it from an a k i one looking back at previous Bloods so critical contacts so compare their renal function compared to six months ago. Is it similar if know it might be in a k I and if it is similar than it probably has a CKD. Another thing of looking at if there's kind of kidney damage, particularly in diabetics, is an album and creatinine ratio. See if it's more races of chronic chronic changes typically in diabetics on, uh, what else would I say? I think that we just did an a k I you'll get, you know, a very rapid rice. And, you know, the creatinine creatinine wouldn't know Egypt far because of the higher creatinine, but it will be very acute compared to previous blood. Comparative previous blood is the most important thing that I will say. Um I hope that helps on K. What would you recommend? The staff studying for electrolytes So good. I've just had an interesting that writes for years. So I started as a medical student, which is why I kind of know, like the back of my hand now. But I think the most important things that you can use the good resource is our up today. I always use up to date for the latest guidance and evidence for managing things. You get up today account when you have a, uh, any chest open Athens account or when you join your trust when you're enough. One. You can also get open Athens. I count through them or the trust will also have access to up to date by the trust Internet updates a good place in terms of management stuff or anything. Whenever I need to look for the latest evidence, it's all on there. Another good website that I recommend is Ono Book. Actually, Where's the book? Another good book. All of your clinical Come sheets. This's a pretty good book I use. This book still commonly has chemical. I would get test specifically for clinical chemistry and hematology if you're interested in not because I want to be hematologist or a biochemist, but because you can see this sort of sensitivity in specificity of different tests. And you can work out when the test for something when it's appropriate and we're not to. And I think this has lots of things about electrolytes and testing in general as well. So clinical chemistry nine. Finishing is another good resource, I think, just for the generic looks like the Oxford Handbook and just, you know, reading online and your village your knowledge of the time with sort of experience and seeing these things over and over again, you know you'll get so bored of sodium eventually unless the sodium's like really know, like 100 25 in which case I started doing all the investigations. Typically in my trust, what I do is if I see a sodium below 125 and I'm not sure of the cause. I will do a T. I will do Sarah most minutes, so I typically only do a serum. Osmond Osmolarity urine was Milan itty and plan on urinary sodium as well as a TSH and a quarter. So if the sodium is below 125 and I'm not quite sure of what's going on, just exclude all the other cause is because sometimes what you find is examination is very difficult. I find that sometimes they distinguish you've really me or from Hypovolemia sometimes, yeah. Oh, sorry. That's the other thing, for I would function tests as well. But again, I think for a function, tests might be a little bit of a waste of money. But we added on anyways, because, as I said, you typically don't see hyponatremia fire function tests unless they have overt, itchy over severe hypothyroidism. Basically very severe end of the hypothyroidism scale of things basically. But I added on anyway, so far, oId cortisol, urinary sodium, plasma ceremonies, morals, minority and urinary ALS minority would be my my test. Like typically do to try and distinguished all quarters, along with my examination findings and a good review of the drugs, medications and their kidney function and whatever else I think might be appropriate in the clinical context and a urine dip if I think it's appropriate. Eso stuff like that is what I'd say. Uh, I hope that makes sense. Uh, any other questions? And he takes us. Okay, Britt Fine. I think I will leave it at that. Opposed to feed back one more time, and I'll leave it up for a minute. Yeah, no worries at all Now or is it a pleasure? Good. Anybody who's in peninsula or you know, you know, Truro, if you're on feel free to say hi. I don't mind teaching on the wards and I have no problem saying high whatever it is on. Please spread the word. Please join again. Spread the word. Please join the Facebook page instagram page. Because again, the more people we can get, the more sponsorship we can get it because we want to keep everything free. 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