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Okay. Hi there, guys. Men use the coupon. One of the co founders of the six PM Siris. Unfortunately, today we were supposed to have the acute medicine to talk by Kitty. But that's been there. Books boned, too, next week. So instead, I'm going to replace Saturday and be covering electron manatees, which I've come in previously in the first series this year. Um, so without further ado, let's get started and we'll come back to questions about other slides and videos towards the end and as well as feedback guys, I can consider the feedback stuff towards the end. So let's get started. So in terms of you really know, if you haven't really joined are sort of social, please join our social because that's how we keep you up to date on the latest information about six PM Siris, including sort of what Syriza's running what weapons were running on a day to day basis is when it's questions to consolidate your learning on. It's also where we post other bits information. So please join our instagram Facebook and Twitter on a quick thank you to our sponsors thie nd you without the end the you we wouldn't have been able to get the six PM Siris off the ground. So once you finish medical school, every day is going to need some sort of legal advice and eminently insurance and some sort of support and the MD use able to provide that one should go into sort of judge formal training as an F one f two. So if you're interested in joining, there's a QR code at the bottom. Right on. If you drawing, you could get a freebie, such a pocket prescriber book, some flash cards that you can use for your vision, which I've used previously. You can also get a foundation program booklet. Okay, so first question a 14 or patient presents the E. D with acute chest pain that started two hours ago. He's being managed as an end stemi on taking his blood. You notice that it is quite viscous on his bloods are in the table. What is the most likely cause of his hyponatremia? And that's been the pool okay, really forced into the same pitfalls with this question every time when I do it. So the majority of you answered hypovolemia keep putting a treatment, which is the incorrect answer that the correct answer is pseudo hyponatremia. We'll talk a little bit about why so soon and tree me A is a type of false hyponatremia, which is just how the but indirectly analyzed. So when it's center and lab, it's the it's the type of testing they do on it. But when you analyze the point of care testing, you won't get this sort of mistake and what causes a pseudo hyponatremia? Typically, it's something like a paraproteinemia or hypertriglycerademia, and in this case, if we go back to the vignette, this patient when you look fruit blood results. When you look at the triglyceride is they're stalking Lehi and had viscous blood, which is another clue that the hyponatremia maybe force. But if you're wondering in terms of other Bioko chemical markets that indicate a seat up in the tree, me, let's actually go through the blood and talk through the table. So we're looking at the sodium first season. We look at the sodium range to 135 131 145 which means it's low, so that counts as a hypo. Nutri Mia Now the raised. There's a race troponin with normal renal function. When you look at the Bloods, which suggests some sort of myocardial damage in a ski mia, which is why it points more toward the end. Stemi is he doesn't have ST Elevation on his C G. And he's got chest pain on the high triglyceride, which is likely causing a pseudo hyponatremia. Now, when you are going through sort of a list of sort of what your causes of hyponatremia is, which we're going to do later on the thing that you want to look at, whether something is a true hyponatremia, where you know you're just a fluid status and look to see what the cause is. A pseudo or fourth type of treatment is when you look at the serum or similarity. So for true hyponatremia, the ceremony similarity or the total amount of sort of osmosis ions together, which mainly includes sodium potassium bicarbonate in chloride should be below it should be. It should be a low serum was malarkey. If you have a true hyping a treatment, you should be below 275. The fact that it's normal or high points that it points to something and you've gotta hyponatremia means that it's likely pseudo hyponatremia and the likely cause of that are paraproteinemia, which can happen in things like multiple myeloma. Or, you know, anything that causes sort of increase proteins in the blood on hypertriglycerademia, which is in this patient's case, which is the one from this case. So just a little bit about sort of similarity and on cultic pressure. So you've got intravascular space, which have chosen for similarity about roughly about 275 to 290 on In the interstitial space. You have a similar sort of similarity on or similarities rated ability of sort of the most attractive water to the area. I think of a zoo, that stability to attract water. That's the simplified version of it. But within the intravascular space, the similarities a little bit higher in that it contains albumin and albumin and other proteins, or provide something called on cottage pressure, which is the Pacific type of similarity, which gives it the edge over the interstitial space, which means it holds fluid morning intravascular space, competitive interstitial space. Now, why is that clinically relevant? An important So say you've got a patient with a low albumin or whatever. For whatever reason, I say. And cirrhotic patients, because the liver produces argument, will say in a 40 patients where oh, on the Forteo syndrome patients where they news protein in the urine. When you get lost of that protein, you get lost. Or that oncotic pressure, which means less of a forced pulling water to intravascular space. And that means water seeps out more into the interstitial space, causing the eczema. So that's the relevant of sort of proteins and albumin. Other things in terms of causing pressure. Now again, hyponatremia have. It has to be less than 100 35. It's classified according to fluid status and biochemistry, and it's important in terminal cause as the management deficits, depending on what the cause of the hyponatremia years and a severe hoping the treatment cancers anything less than 1 20. And the kill hyponatremia means a rapid change where the brain is unable to adjust to it. Because you're sometimes seeing clinical practice is these Albany patients with a sodium level of about 115. But they're not having seizures, and they're relatively okay, and it's because the change has happened over a period of time that allowed their brain to adjust that sodium level. But when there's an acute change that can lead to neurological symptoms, which can be a spectrum of things from anything to sort of confusion, aggression, irritation all the way to seizures, coma and potentially death and that's all related to cerebral edema, in the case of hyponatremia and other symptoms can depend on the course where it's hypothalamic, hyperglycemic or you've anemic. So this is just diagrammatically representing what a I planetary making calls in terms of the spectrum of symptoms. So when you get a hyponatremia, there's less sodium in the blood, compared to the tissues in the interstitial sort of indecision space on other sort of interesting the spaces. That means that because of sodium's lower, that water goes where it has more sodium. So if there's more sodium, say within tissues such as the brain, which is most sensitive, the same two changes more water will seep into the brain, causing cerebral edema, which causes that spectrum of neurological symptoms that you can see in hyponatremia, the Pentagon, hallak you and rapid the changes and sort of how young and physiologic in coping. The person is a swell on then, as mentioned when you've got a hyponatremia First the workout, whether it's a true hyponatremia, it has to be a low serum was married E or if it's a pseudo hyponatremia with a high or normal serum, was minority. So moving onto D. Next question. So a 70 year old lady was a military acute medical unit with delirium. She has a history of epilepsy and has recently been diagnosed with gastritis. He has no signs of fluid overload or dehydration and has an a M. T s, a acute mental sort of test score of four. What is the most likely cause of her hyponatremia? And that's pretty cool. Okay, so the majority on carbamazepine, which is a little bit of a trick, So yes, it can cause hyponatremia. But this lady, the vignettes suggests that she's had epilepsy for some time and probably would have been on carbamazepine for quite some time. The clue is that she's been newly diagnosed with gastritis, so the correct answer is a map. Brazil. So, as mentioned from the history she's probably been taking carbamazepine Oh, about the faxing for a long period of time, so it's unlikely to be the cost of agent because she's epilepsy for quite some time. But I do agree carbamazepine, which is what it was in the previous slide, can be a cause of agent. Or my personal, however, was newly started because she has new gastritis. Sort of the most likely cause it'd agent on in this case is specifically rated toe s I 88 took a little bit of alcohol. SIADH SIADH stands for syndrome of inappropriate anti Giaretta common sort of excretion, or secretion on weapons. When you have antigenic all men as it suggests, it stops you from peeing, So concentrate your urine by purely causing water. Reabsorption within the collecting ducts of the nephron would indicate within the glamorous of the kidneys on within the class conduct. You've got these channels called aquaporin, specifically our cup or inversion to, and there's increased expression when you have antigenic hormone release. So when you have more energetic or memory, she got more. These are cup or V two channels in the collecting doctor. They absorb more pure water by concentrate your sodium and causes a salty you're in. Hence, a high urinary sodium so if we break it down in terms of the Bloods and have a look at the table. So once again, when you look at the sodium, it's low because it's below the reference range of 135. So it's a hyponatremia now. What makes it a true hyponatremia is when we look at the serum or similarity. Remember what I said? The ceremonies large. He has to be low below the reference for to be true hyponatremia if it's normal or above. That suggests a pseudo hyponatremia, in which case you need to look for other causes. So it's a true hyponatremia, and when you look at the urinary sodium, it's inappropriately concentrated. So think of it this way. If someone's hypovolemia or you know they've got low, the kidneys would want to try and preserve as much sodium. It's possible because wherever sodium goes, water follows, so he would see a low urinary sodium in someone. That's hyperbole make now in this lady who's euvolemic because she's got SIADH. What it means is that because there's Mawr, 88 secretion get pure water absorption from the kidneys, and that concentrates the urine, and that means a high urinary sodium and the rest of the bloods are within normal parameters again points all towards SIADH. So how does represent effect into traffic? A woman so imeprazole causes. So I can't tell you the exact mechanism. But a meprazole, as I said it can cause increased release of anti drastically. It can cause it can be a sickly be a cause of SIADH. That's the answer, that question. So as mentioned, let's talk a little bit about you very much hyponatremia. So the important part in any hyponatremia assessment is fluid status, fluid status, fluid status. So one should work out on a patient has a true hyponatremia. You need to know if the hyperkalemic i e. R. They overload it so you know things like heart failure, never failure in the front like syndrome kidney failure. You know those sorts of things that you need to be looking up you to see if the hypovolemia, in which case, if the hypovolemia why they losing water and fluid is it from the gastro in the gastrointestinal tract? So is a vomiting and diarrhea. Is it from a lack of intake or the use of the losing it through the kidneys? Or are they using it from skin such as sweating, burns or the things if that makes sense, So this patient examines as a normal fluid status, which is commonly caused by a sayedee age has mentioned. So it's increased anti diuretic hormone, which is also known as a suppressant, and I've already mentioned it's increased expression of these are cup or on V two channels within the glamorous within the nephron of the kidneys. Specifically in the connecting duct, you get a think sort of decreased water excretion because more water gets absorbed on there's Morson, um, excretion. Comparatively so again, things that concern of cause it are cortically insufficiency. And this is because your tonsil has an inhibitory effect on ADH. So less cortisol or less glucocorticoids equals more radiation, which you need to SIADH and will come onto why adrenal insufficiency is a little bit different. So when you look at SIADH in terms of the Bloods, you have to have a low ceremonies mill. Air it as I mentioned to be a true hyponatremia. Three urinals. Malala tea is high because the urine's been concentrated, so it's gonna be more sort of electrolyte contents when it compared to a water concentration is gonna be high. And again there's gonna be a comparatively high urinary sodium because he really warm or from the kidneys. And in terms of euvolemic sort of causes of hyponatremia, SIDH is in their severe hyper fire. It is, um, with hyperthyroidism. It's very rare. It has to be severe in terms of the cause. You won't see it with sort of moderate or sort of borderline high profile. It isn't psychogenic politics. He has another cause because of you, sort of. They lived in everything and the peeing everything. Now we're diets or excess beer, which is called bare bottom, any excessively drinking amounts of and which contains lots of water again and glucocorticoid insufficiency and drugs to remember for SIADH, including antidepressants, anti epileptics, PP, eyes and inserts. But it's probably more, but those would be a good set of drunks for you to remember in terms of SIADH. So a question number free A. Uh, let's see. 23 old gentleman has been admitted TD with severe malaise, fatigue, vomiting and feeling on. While his observations are as follows, he's got a heart rate of 100 time he's got a low BP of 80/50. He's got radius respiratory rate of 21 it sucks, or 94% on with a temperature of 37.6. What investigation is most likely to identify the cause of MS issues based on the table blood results? And that's but the pull up. Okay, so let's see the majority of Johnson Random Cortisol, which is the correct answer whenever I see somebody young or anybody who has a high, a low sodium and a high potassium, even if it's a girl, my first, the first thing that ever pops into my head is cortisol is sort of an Addisonion crisis or anything Addison's for. So let's have a little look. Eso random cortisol. So cortisol is released in a port. It'll fashion, and there's journal Variation peaks in the morning and evening. That's why they like to do you know a nine AM cortisol? So not why lots of people ask is what? Why, why we're not doing the 90 mg dose instead of a random cortisol. The answer. That question is practically what's easy? It's just, I don't know. Quarter so on the blood that already done. And if the quarter sores high in in those circumstances that that tells you that you don't need to repeat the course with that, so say, if you do around them, quarter. So when it's above 4 50 that tells you that the adrenal off our most likely functional and they're very, very, very unlikely to have adrenal insufficiency is or, you know, specific. In this case, you know, Addisonion crisis is what we were looking at specifically for this patient. So that's why I pick a random quarter. So and then if the random cortisol is low, then I choose to do either or nine AM cortisol or I'm going to do a short term that contests. So if we break down the Bloods in terms of the table results, so you've got a low sodium, which there's just hyponatremia. You've got a low ceremonies mill air itty again below the reference range, which is just a true hyponatremia. Instead of a pseudo hyponatremia, you've got high potassium with no with normal reflux in plus a normal person, so sodium and again that always makes me think that always makes you think, or does strong adrenal function because of Austronesian. What's implicated in this? And we'll talk a little bit about why later you've got a high, you know, sodium that's so with a high urinary. So you already mentioned it's one of two things. So either you're inappropriately concentrating your urine because of SIADH or you're having a renal loss of sodium. Your kidneys are not holding onto sodium on. Do you have to ask yourself, What reason is that? So again, we've mentioned so in this patient. He's got a hypothalamic hyponatremia. So he's got high heart rate. No BP. Looks like he's under filled. So you wondering why So? And he's got a true hyponatremia, sometimes of fluid status status. He's hyper filament. So when you've got a hype of anemic hyponatremia patient, you gotta ask yourself, they're losing fluid. They losing sodium. Where are they losing it from and why? So the organs that I look at is the kidneys. So again you can have a higher researching for two reasons. One is SIADH, but this patient isn't usually make everything suggested the hype of anemic, and if it isn't euvolemia and SIDH, then they're probably losing sodium from their kidneys. in which case why and then if it's a non renal awesome, then common things are vomiting and diarrhea. If they've gone in the ostomy, they can sometimes of high upper. If they have a fish, you know that can also need to if they've got sort of skin causes. So that would be sweating marathon runners or, you know, burns patients. Or, you know, any issues with skin that could also be the course of. These are things that you should be looking at, and then other things we could sort of, you know, poor or and take on. Do you know those sort of things is what you want to be looking at. So let's talk a little bit about the, uh, always like talking about adrenal physiology because it just makes sense. So let's talk about the layers of the adrenal gland so you're on the outside of the renal grand. You've got the adrenal cortex, which let's into flu, Renata's and then on the inside, you've got the medulla. The medulla is more related to sort of the release of catacholamines And what I mean, what Catacholamines is adrenaline or German and a tiny bit of dopamine. Now the cortex is what's what's implicated in and sort of adrenal insufficiency or, in this case, another Sony in crisis. So you split the layers, and the way you can remember them is zona g F. R. So the first thing is that remember, the low side, which is the out a bit, then, is the physical Arte. And then there's the ridiculous. And then, if you want to remember what each layer releases, it's the way I remember is how you'd spend your evening. So you know, you start with dinner, in which case it's salt, and that's been around a quarter quarter. Then you're going to have dessert glucocorticoids, and then, if you're lucky, you're going to have sex. For whatever reason, leave it at that. So then you from the last day of reached D H E A or testosterone. So that's the way that I like to remember the layers of the adrenal cortex and and what Intron releases. So the glomerulosa release assault mineralocorticoid. It's sold for elated, and that's all that's there. Own that was specifically talking about the Fasciculus releases is raise the sugar. It releases glucocorticoids, specifically cortisol, and as I've mentioned a particular risk. Is great sex hormones particular more important than ladies? Because it's where they least a small amount of testosterone from his dihydrote epiandrosterone, which is a precursor to hold onto things that's talk a little bit about renal insufficiency. So in adrenal insufficiency, all the layers are affected, so that's why it's called adrenal insufficiency. So it means that the later releases Mineralocorticoid hasn't affected, which causes mineralocorticoid insufficiency and array that Reese's quarter source affected, which causes glucocorticoid insufficiency. So, as I've mentioned, if you've got a quarter quarter so above 4 50 there's no insufficiency. But if there's free 50 there or anything below, unlikely to be deficient. But you need to go on to do further testing, which could either mean a nine AM cortisol or more easily, just go do a short Senexon test. So if you've got low cortisol, do a short snack run test on a Z. I mentioned with sort of the difference between adrenal and sufficiency and glucocorticoid insufficiency. So if you've specifically grow glucocorticoid insufficiency alone, which is typically related to patients who take steroids, glucocorticoid insufficiency is related to sort of 80 hate production, so if you're insufficient and cortisol, that means there's less suppression of 88 which means there's more release of 88 on. That's why it can sort of lead to sort of SIADH in that method, which caused the you've anemic hyponatremia. Now what difference in Addison's or complete adrenal insufficiency is that the mineralocorticoid releasing layer is also affected and that mineralocorticoid insufficiency leads decreased, although stroke, which needs to sort of decreased sodium reabsorption or more sodium excretion from the kidneys. Because what all the estrone does is it causes reabsorption of sodium from the kidneys, and it releases the past. Seems you've got a low amount, you excrete more sodium, and you all want to more potassium. Hence you've got a no sodium hyponatremia on ah, high potassium and dory know sort of urinary sodium is high because you're increasing the excreting it because you're not reabsorbing it, and that's why it causes a hypovolemia Kaepernick trivia instead of a jubilee. Make hyponatremia with glucocorticoid insufficiency around. So that's the difference between the two, and I'm happy to go from that towards the end. It's well, it sometimes takes a while to click, so the symptoms weird adrenal insufficiency. When you've got no glucocorticoids, you've gotten these non specific symptoms of fatigue, malaise generally feeling on well, which can happen in understanding crisis on you also get hypertension and hypoglycemia, and with mineralocorticoid you insufficiency, you get hyponatremia and hyperkalemic a. But it doesn't happen. Always 7, 25 sort of percent of patients. You'll have no more electrolytes, so you won't always see it on because of sort of increased a CT hate excretion because of low uh, all the steroid excretions. You get this hyper pigmentation in sort of sun exposed areas such as the hands, neck face, where you can think of particular Palmer creases. So why does courts insufficiency Doesn't cause hyperbole. Um, company I'll come towards that was the end fat in life. That's okay just for the sake of time. But we will definitely cover this again. So let's have a little look on very quickly. The rennin angiotensin aldosterone system. So again a bit of good physiology, so liver releases angiotensin urgent. The kidneys release running from the drugstore very apparatus in response to either low BP picked up by the granular cells or low sodium picked up by the macula denser but causes Renan Release, which releases, which causes deep a sort of conversion of angiotensin agent. Under Tencent, 100 tens and one goes to the lungs. A second verts it to angiotensin two. An angiotensin two calls All these dance from effects of azo construction. Release of all the stair own from these owner Glomerulosa, specifically recent 88 will raise oppressing from the posterior pituitary gland and these again act on the kidneys again, causing sort of increased water retention and increased sodium retention to help increase your BP again s so that's how it works. So eight inhibitors inhibit a six and the common side effect is a cough because when you inhale it, the enzyme you cause increased buildup bradykinins, which is why they can cause coughs. Which is why when someone gets a cough with ace inhibitors, you could give them angiotensin receptor blockers instead, because it doesn't inhibit a specifically it's. It stops angiotensin two from binding to it's receptor sites and hence doesn't cause the coughing on again about the function of all the estrone. So August really acts on the principle cells within the distal convoluted tribunal of the nephron of the kidney, and they caused increase expression of these epithelial sodium channels that cause sodium reabsorption is a mass and potassium excretion. So when you have low old Austro because of either the effect of a thing habit is all because of, you know, men around corticoadrenal and sufficiency. You get increased excretion of sodium and increased retention of potassium. So, uh, quite a mouthful. Question Number four a 30 year old lady presents to your GP practice because she's concerned her urine is becoming increasingly foamy and she has new ankle swelling. You have the bloods below. What investigation will be most useful in this case? And let's re launch to call. So the majority you answered this question correctly. The correct answer is a year and because what we're concerned about in this patient is the thought xon drum, and they seem to have a hyper feeling make hyponatremia. So, uh, let's talk a little bit about so ignore. The box is below guys, but let's talk a little bit about sort of hyper vilamit hyponatremia. So let's first break this, uh, break this table down so you've got low sodium as mentioned, so you've got hyponatremia again because below the reference range and you've got hyper very me A on examination. So it's likely a hyper Viliami hyponatremia, and you you've got a low albumin, likely secondary to protein urea. The reason, because we're worried about protein urea is because the urines for me and has a little bit of a K I. And the kidneys are office well for someone which you wouldn't expect for someone their age when they normally fit and well. So let's talk a little bit about Nephrotic syndrome, which is one of it is in this patient's case. So with Nephrotic syndrome, who, whatever reason, the basement remember, my brain of the sort of grammar Bulus of nephrons within the kidneys is not fully intact. It's not sort of functioning properly because it shouldn't be letting proteins leak now when it gets protein leak. That means there's protein in the urine, since this protein urea, which could be clinically sort of seen as a phone me a type of urine, which is what what's what looted to intervene yet, and you also get lost of anti from been free and we'll talk about it. We'll talk about downstream why that's important. So because you get loss of protein in the urine inappropriately from the bloodstream, you get hyper up. Money me A. Because albumin is being lost because you lose albumin from the intravascular space, you get the loss of this on contact pressure. Remember, I said about a coated pressure. That's the tiny amount of force competitive interstitial space that helps keep fluid in the intravascular space. If you get loss of that one, contact pressure because of loss of proteins. You get a demon because water moves from the intravascular space into the interstitial space, hands causing interstitial demon, which in this lady's case, clinically present this ankle edema. Now what the liver does to compensate for these loss of proteins is they cause, sort of try to up regulate the production of proteins. But at the same time, it up regulates the production of cholesterol. So you get increased production of LDL, low lipo density protein, sort of cholesterol, and that's where you can get a hyperlipidemia or hypercholesterolemia. Now, because you get loss of this water from the intravascular space, you get this sort of low volume status of that mix. And so whilst you're technically speaking, not losing volume fluid. Overall, you're losing it to the interstitial space you're using Intravascular. This course is sort of inappropriate release of Anti Dramatical Month, which causes hyponatremia, hyponatremia. So that's when a forensics syndrome is a little bit different, and also because you get the loss of this anti from been free, which is to stop you from forming lots of clots. You get increased risk of clot formation, which is why I sort of anti coagulation is important to consider in these patients. A Sinemet has helped with sort of reducing protein. Urea and statins help reduce sort of the hypercholesteremia as well. And you've got to figure out what the cause of the Nephrotic syndrome. It's and potentially think about giving steroids as well. So that's the sort of pathophysiology of Nephrotic syndrome. In a nutshell, I guess the other sort of important thing worth mentioning, which I haven't mentioned here, which might be information overload, is that, but we talk about nephrotic range proteinuria. So within the 24 hour period, you shouldn't be released and more than 150 mg of protein within a day within your German if your recent more than that, that suggests that you've got protein urea for abnormal reasons and that needs to be investigated. And that will probably on the dipstick as pretty a dip sticks very sensitive for protein urea. Now, if you get anything in the range of Morgan Freak rams of protein lost in 24 hours within the urine, that is no photic range protein, urea and another way of sort of working out, which is the easier way of doing it because they used to collect 24 hours sort of urine, which is a lot more difficult to do, is to look at thesaurus of album in sort of the urine protein creatinine ratio, which is sort of the amount of protein loss competitor out of craft me and A. Your protein creatinine ratio of about 303 100 is the equivalent of a 40 range protein urea in a nutshell. So 30 seconds or one minute to ask me all the questions that you want, which I will cover again at the end, because I know that we're covering a lot and we're going at a fast pace. I apologize for that guy's, um so somebody asked, Why does quarter insufficiency doesn't cause Hypo anemic happy new treatment? So the important distinguishing factor and I always forget wise and SIADH it's It's not really that type of anemia. It's related to sort of. You've really makes you remain within a normal fluid. Six. I couldn't tell you why. Because I always forget every single time. But we need to remember it. Cortical insufficiency is quarters all inhibits to release release of 88. So you've got less quarters all Oh, geez, A lot of questions. If you've got less quarters, all that means you've got less inhibition of 88. So you get more 88 trees. And hence if you get this effective, um, or increased the fact that answered your attic or more like SIADH intensive course is the euvolemic hyponatremia and a difference. Being with adrenal insufficiency is that affect all the layers and it's racism in a cap mineralocorticoid insufficiency. Let's go back up to to to to do all the slides for the stock available anywhere is the mailing this? I'll come back to that question towards the end. Yes, Ben Sweeney. When you complete the feedback on, we always always post all the talks and videos on metal. Sorry. Could you explain the step from edema type? Really? Medium ear doesn't get how hard the electric bass goes. Okay, I can do that in just a second. And sorry. Could you go over? Why it is I pavilion it. I've been a tree me one last time. Yes, I can. And why does listen Course. Hopefully it will go back for it again. So let's go back. Food or steps of Nephrotic syndrome. So remember what I said with Nephrotic syndrome. For whatever reason, you're not friends who sort of the membranes is no able to hold onto protein. Is it because you shouldn't be releasing lots of protein in your urine? So you get protein urea because you get the loss of protein in your urine from the vascular space you get hypo up a sort of hyper abdomen, email, hyper hyper protein, protein sort of anemia. So you get lost. A protein from the intravascular space, which manifests hypoalbuminemia albumin, is important for that one. Contact pressure to hold on to fluid into the intra intravenous color space. If you get the loss of protein from the intravascular space. You have less oncotic pressure, so fluid seeps from the intravascular space into the interest issue space, which causes edema. The liver tries to compensate for that loss of protein, but because it's trying to increase the regulation of production of proteins that also produces more cholesterol on more LDL's, why it causes hyperlipidemia and because so on examination your hyper believe it because hyper remember the examination is what the time is, what we say in terms of the fluid status so clinically she's hyper, really make because she has ankle edema. But intravascularly, she's deplete and dry because the fluids moving from the intravascular space two D sort of interstitial space. And because there's loss of fluid from the intravascular space, that's what that's what causes a D hate release and 88 release causes, the sort of because the morgue, lots of age being released, it causes more sort of water to be be held on in general, and that's why it causes hyponatremia. So that's the sort of order of things. And why does Addison cause hypovolemia? So it's related to quarter sore and sort of the sympathetic nervous system in that if you've got decreased recent quarters or you get loss of that sort of sympathetic effect and that causes the low BP. But also you also get loss of mineralocorticoid. So remember, wherever sodium goes, water follows. So in Addison's, you get loss of sodium. And because you've got lots of sodium in the urine, sort of you'll get the release of more water as well. So there's more water excretion as well. So because of that, you could get hypovolemia for two reasons. That's where you get Hypovolemia and Addison's. I hope that make sense, guys, uh, cover again towards the end. No worries. No, but I'm going to move on for the sake of time. Oh, sorry about that. Certain other guys. Eso next question will hopefully haven't seen a 25 year old lady has been brought TD. Having had multiple seizures as a background of bipolar depression and gastroesophageal reflux disease, her bloods are in the table. What is the likely cause of the hyponatremia? Okay, I'm just going to move on from this question. Note about that s Oh, yes, the majority. You have answered it correctly. There correct answers lift you were concerned about with this with this sort of being yet is lifting toxicity, which can lead to nephrogenic diabetes and separatists and think of diabetes and some of this as the opposite in 88. And it needs the pure water loss and hence equals is sort of lots of lots of urine, and we'll talk a little bit about why. So let's talk first about hyper sort of hyponatremia and courses of hyponatremia. So most common cause of hyponatremia is sort of reduced fluid intake or fluid loss because you know all sorts of electron, the mountain fruit. But it's typically when when you've had decreased fluid intake, for whatever reason or sort of increased fluid losses. That's the most common cause of hyponatremia, high piper nutrients of increased sodium. Um, on in terms of hospital stuff. Yeah, Tradjenta is a common cause because what lots of people like to prescribe is saline, and when you overdo it on the same, you cause hyponatremia. That way is what is the hyper Corinna or increased chlorine amount? Hyperaldosteronism the opposite of hyper sort of. The opposite of low mineralocorticoid can also do, but that's very rare, so you can either have salt gain you can have more water loss compared to sort loss, which could be because of renal reasons or loss of water from the GI tract or skin. And you can have pure water loss or poor intake, which is rated diabetes. And instead of this, or high production which is poor first mechanism. So diabetes in separatists opposite of SIADH. So it's either due to a lack of a D H production, which comes from the posterior pituitary gland within the brain, which is known as a neurogenic diabetes insipidus. Or it's because of resistance to anti drastic hormone as well, was in this case because of lithium toxicity. Nephrogenic diabetes insipidus on with nephrogenic diabetes and services courses can include chronic acute nephew may ingestion hypocalcemia, and it can also be hereditary, which tends to be more. And because you get a low amount of 88 because of resistance or the effects of a th are less because his resistance from the kidney to defects of a th remember anti dreaded common means your Penis, if there's less effect from 88 means you excrete more water because there's less alcohol poor in the V two channels to re absorb water in the kidney, and that is the pure water excretion and hands sort of that sort of polyuria. In this case, the treatment is typically 88 analog. But if there's nephrogenic diabetes insipidus, they won't have as much of effect and 88 locks can also help to differentiate between the two. And then, if there's a response to an anti diuretic hormone analog such as desmopressin, or whatever you can think of, that probably means that the kidneys off are functioning normally. And that means probably Petrucci. God isn't releasing a teaches it should. Now, if there's no sort of or lack of response to 88 analog, that likely means that they've got nephrogenic diabetes Insipidus um, which is you got to try and find a course and reverse it if it's something that is reversible, such as lifting toxicity. So a question number six uh, during the night shift you a call to see the same patient and her GCSF five and she snoring big, big trouble are blood have seen below? What complication may she have makes you have experienced, and that's been up the pool. Okay, let's have a little look at what the majority, if you have answered. So the correct answer is cerebral, a demon, and it's talking little bit about why. So this patient was initially hyper in the treat that a high amount of sodium on when you get over correction or too quick, and the correction, which is very dangerous, Which is why we have to be so careful with correcting sodium much. You have to carefully monitor these patients with multiple bloods over today. It can cause a very rapid hyponatremia when we over correct it. And when we do that, we can call cerebral edema because remember what I mentioned. If you've got a low amount of sodium within the blood, that means compared to the tissues, the tissues are salty, a competitive intravascular space. The water moves from intravascular space into the tissues, the brain of which being the most sensitive, so over correction of hyponatremia needs to cerebral edema. For that reason now, conversely, if you have hyponatremia or if you have hyponatremia low, assume that's correct too quickly. You can lead to automotive D minor relation or cerebral bleed, and the reason for guys is because the blood with the intravascular space is salty up competitive issues. Water moves from the tissues into intramascular space. And when you dry out the issues such as the brain, I think it's sort of like a crack desert or crack ground. So don't so the brain stem will sort of kind of peel and get damaged, which is why it will cause the my elation and you more like it's real bleeds because the blood vessels are dried and because of that sort of shrinking, they can. Maury's The crack is what I think about it because they're dried out. So that's what the risk factors with those are in terms of complications of trying to treat these. And, as I said and, um, overcorrected hyponatremia can also lead to all started the my elation or cerebral bleeds because you've caused the hyponatremia too quickly. So the important point to remember it is whenever you're collect, correcting a low sodium or high sodium do not correct the sodium more than 8 to 10 minimal within a 24 hour period, and you have to repeat the sodium blood. Often there's not really a railroad answer in terms of how often you should be doing it. But the point is, you should be doing it multiple times within the day and again as I as I mentioned. So if the tissues are salty, a competitive blood, if that's hyponatremia, water moves from the intravascular space into the tissues and that causes cerebral edema and that spectrum neurological symptoms that we talked about. And conversely, if you've got hyponatremia or if the intravascular space is salty, a competitive shoes water moves from the issues into the intravascular space and that causes. This is drying, which causes the brain stem to peel, which is what leads to a small to be mine elation syndrome, which is very dangerous on as well as that needs to increase risk of cerebral bleeds because the brain's shrinking and drying and the blood vessels cracking. So moving on to the next question, a 62 year old lady presents to her GP with uncontrolled hypertension. She currently takes lisinopril and Amlodipine. She's been started on another BP medication. A week later, her renal functions checked. What is the mechanism of this newly started medication and let's bring up the pool? So that's the majority answered inhibition of in actuals who support this. This is sort of a two to step question. You need to sort of know the UK guidance for which drug is further lined to prescribe when they already taking the first two, which is a a centimeter as well as a calcium channel blocker. So actually the correct answer should be. See then that stopped sharing, and that's move on subsides sodium chloride channel and a Bishan in the d. C. T. And that's still committed about why so a centimeters can increase potassium and in this case, a fires I genetic was given because that's further line in terms of anti hypertensive guidance. And it can decrease potassium from increased sodium carriage to the distal, convoluted she bill, which stimulates the principal cells to reabsorb sodium and release potassium a little bit about the hypertensive guidelines with in the UK So first line for anybody less than 55 years old is an ace inhibitor or angiotensin receptor blocker on sort of. Or if they're over 55 years old or if the Africa or B, you tend to pick out some channel blockers. One caveat. Sinuses. If they've got diabetes and I got protein urea, regardless of whether they're sort of Africa are being, you know, a sin hypnotist tends to be better because they reduce protein. Yes, that's the one caveat that in in sort of diabetes, then second line is you add them together. If they're not working third line, you can add, um, the fires I diarrhetic and a four flying you can add in another such a drug, such as an alpha blocker up, such as doxazosin. So a little bit about where genetics in sort of the's all these drugs work. So you've got the grow at the nephron of the kidney. You've got the grammar venous, the proximal convoluted Cipro. You've got the death so convoluted she blow and then you've got sort of so the loop of Henle down here and then you've got the collecting ducts. So in the distal convoluted, she goes when you get every feel your sodium channel expression which is related to all those strong, which increases expression of these channels on where that's where potassium sparing diuretic act now where fires are genetics act is also this to convert your sugar, but the activities sodium chloride, sort of cold transported channels or they're also known a simpleton. So if you ever confused about what a code transporter, a simpleton and tea party mean, so court transporter means a sort of channel that uses Theo the grading or transfer energy of one electrolyte to transfer another a simple water. What it does is, is a type of co transported that transports two things in the same direction. Which is why I called the Cymbalta and an anti porter is something that that use the energy or grading from one electrode to transport another one within the opposite direction. Handsome anti Porter. So that's what a cold transporter, simple zehren anti port in is Loop diuretics Act on the loop of Henle E S o Remember Loop loop of Henle E. That's where they act, and they act on the ascending loop of handy. Really, NK CC is the sodium potassium chloride, cold transporter or Cymbalta, which is type of simpleton. So that's where you get generally low electrolytes with Lupus, your ethics and lastly, where a th unlocks an antidiuretic hormone and looks act is on the collecting ducts because it caused the act like a D H course, increased expression of these aquaporin be two channels that reabsorb water wouldn't be collecting ducts. What I think I'll do is because there's this is about half way through the lecture, What we're going to cover his next time I will do potassium, calcium and magnesium on its own, covering the second half this lecture because it's quite a lot to be honest. So what I'm probably going to do is end. It's here just for the sake of time, because I don't want to go over. Does anybody have any questions about what I've covered so far? Because I'm happy to go over everything else that we've come so far and honestly, we've got 10 minutes. So I'm happy to go for anything that confused you at all. Because this is half way through and this is a big is a really big topic in terms of electrolytes. I'll make sure to apart, too, which covers potassium, calcium, magnesium as well. Okay, Uh, what I'll do is first or post of the feedback. And I'm happy to go for any questions that anybody has. How does the NCCN. Cause you have course, I could go back for that. Let me posted the feedback first, and then I'll answer that question. I always love talking about electrolyte abnormalities because it's such a big talk back, and it's It's so useful to know, because every patient, for whatever reason, comes in with, um, electrolyte abnormalities. It wouldn't also with such a common topic, and it's such a big topic. And I think it's a useful want to think about for exams finals on being a foundation doctor as well. So let me just postop the feedback first, and then we can talk about if you nails just a second, guys. Okay, that's POSTOP feedback. Thank So just pop the feedback liquid in the chat on our postop other feedback links as well. Yeah, also, I can. So let me bring the slides back up in them are post of any other feedback. Thanks. That you guys want in in minute. Let me just just screen. Okay, Let's have a little look of the questions. Yeah, I I think what I'll do Nico is a separate one from the ones advertise. Just because this is an extra electric. So you're still gonna have acute medicine too, which is being moved to next week and I just decided to do instead of canceling everything I feel would be nice to just do a teacher I've already done. So that's why. And, uh, I sent the feedback like privately apologies for that. Here we go on, let's go back through questions, so I'll go back to the first question. So how does the how does the NC cause potassium loss again? Let's go backwards. So when you give someone a fires, I diarrhetic What you're doing is is you inhibit this sodium chloride. Simple to channel. That means that as well as the loss off chloride, you cause the loss of sodium. Now remember, there are other cells within the distal, convoluted, cheaper or I eat. These channels called the inactions, the epithelial cell in sodium channels. So because fireside your attics cause an increased amount of sodium within the tubule of the nephron, this is sensed or picked up by these in actuals. On what these in actuals will do to compensate for this is they will increase the absorption of sodium because they sensing more of it because these channels have been inhibited and because of that it causes the loss of potassium. Conversely, if that makes sense. So it's an indirect effect if that makes sense in the reclast of potassium, because these channels cause increased sodium amount within the cheap pills. This is picked up by the's in actuals, which means they'll try and reabsorbed more sodium to compensate. And in return they excrete more potassium. And I can show you the picture of what the channels do again. When I go back, Where is it? Here we go. So again, as I mentioned, So when you inhibit those NCC's channels because of fires are genetics. There's increased sort of sensing of sodium by the in actuals. They'll try and compensate for the sodium lost by re absorbing more. And that causes a potassium loss. Because when these are more active, they excrete potassium. I hope that makes sense. Er, I phone possible. Okay, Britain, Let's move on to the next question. So can you go over how correcting hyponatremia cause the of course that can do that. So let's go back to that little picture that I talked about because I always like talking about pictures so on. Can I draw on this board because that will make it a lot easier. Let's do a pen. So let's say someone is hyper to the tree Make for whatever reason. So they've got a solium of, let's say, 155 initially when they come in, but they're okay with it now. You want to be correcting it, but you want to be correcting it slowly. So what you need to do is you need to give them. Dextrose is the choice of flu flu, typically because it's just sugary water, and that helps dilute. So that's typically the choice of off or if they've got an N G in situ. What's even better is if you if they've got a nasogastric tube in situations typically, you know, on surgery and more, and I see you. To be honest, you can just give them free water for your stomach, which is the safest thing to do. So you could also give free water fly an N g free water mg. Now the issue lies, and when you overcorrect hyponatremia, remember what I said. You don't want to correct it more than 10 minimal police so that that's just the reference range. Within a 24 hour period or a day Now, uh, let's admit that person so say you've overcorrected it way too quickly. So say, within a 24 hour period you've brought down the sodium to 135 which, which whilst wouldn't it is within the normal reference range you've corrected way too much compared to the reference range of what we're supposed to do. No, because that's happened so quickly. The brain hasn't had time to adjust. So when you get a overcorrected hyponatremia that's the same as causing an acute hyponatremia, if that makes sense, even though it's within the normal reference range because your brain hasn't had time to adjust. So now, all of a sudden, because your blood sodium is so low, it means the tissues are a lot saltier compared to what's in your intravascular space. And because you've done it so quickly, that means it's going to be a rapid sort of movement off what er from the less saltier intravascular space into the salty A tissues. And because of that rapid movement of water you call cerebral edema, which causes those severe neurological effects that we talked about in a spectrum and because you're over corrected hyponatremia, too quickly, and it's become hyponatremia or and overcorrected hyponatremia. That means you're gonna get cerebral edema and potentially seizures and coma. And that's why it's so dangerous. I hope that makes sense for the person answers that question. Who asked that question? It was. See who answered. Ask that question. Does that make sense? See? Okay, fine. So could you explain the mechanism of water movement? So you have a low you need to know is Sodium is, um, is an osmotic agents. It attracts water, so wherever sodium goes or ever, there's more sodium water will follow. So if the tissues are more salty, combative intravascular space is going to be water movement from intravascular space into the tissues. And conversely, if if if the intravascular space is salty, a competitive issues, water is going to go where there's more sodium, so water will move from the tissue into intravascular space. And that's fluid dynamics and sort of automatic pressure related. Because sodium is an automatic agent attracts water wherever sodium goes, water follows. I hope that makes sense. 100 um, with the correction of so just imagine. So I've got a sentence for If it doesn't make sense, So when you have liver corrected hyponatremia, that's the same as causing an acute hyponatremia. So these two things are practically the same thing, and they both lead to severe boa Dema. Does that make sense? Humbler. It's again because of those fluid dynamics that we talked about. So when you overcorrect a yeah, so they both cause cerebral. So why didn't call pseudo so again in hyponatremia When we go back to the picture, The little vignette that we talked about the intravascular space contains less sodium compared to the tissues such as the brain. Remember what I said? Wherever there is more sodium, comparatively or relatively more water will go towards that area. So because the tissues or the brain assault here, competitive blood water's going to move from that intravascular space into the tissues such as the brain. And when there's more water going into the tissue, such a a brain that causes swelling of the brain and hence cerebral edema and overcorrected hyponatremia. As we've mentioned, that causes a effect. You're lowering the sodium too, too low levels, so that's similar to having an acute hyponatremia. And again, that's why it leads to a cerebral edema because those fluid mechanics does that make sense. Maybe, maybe not. It's a bit of a difficult concept. I hope that this bridge. So even if you forget the fluid mechanics or whatever it is just to remember from the slides that I post that DCed to are practically the same thing. If you've got an acute hyponatremia that can lead to severe anemia, which is why you get too confused patients or even seizures and other things or overcorrected hyponatremia, we'll we'll we'll lead to the same thing. Cerebral demon, because you're in effect, causing an acute hyponatremia. Same thing. So even if you don't remember the mechanism, just remember, put these two sentences together. Um, do do do does anybody else have any other questions otherwise about anything else? Okay, Britt in So as usual, instead, because this was a lecture that was supposed that wasn't supposed to happen, or post stopped electric slides today because already available up halfway of what we've covered and also post of the video today on, there's going to be so a little break so no nothing on Friday, Saturday, Sunday, but join us again next week, where we'll be going for endocrine acute medicine as well. On the date, Specify, specify the day of the acute medicine lecture tomorrow. Yes, Lola. Both can cause confusion and patients because they're swelling and there's a swelling of the brain or shrinking of the brain. So anything that messes with the brain can can lead to confusion, basically, if that makes sense. But typically the most common thing that you see in hospital is hyponatremia, Uh, but both can cause confusion because they swell or shrink the brain. And anything that messes with the brain can be to spectrum neurological symptoms, which includes confusion. And that's why sodium you got to remember is the neurological electrolyte potassium as the cardiac electrolyte as well as the muscle electrolyte. But we'll talk about potassium in the next lecture a bit more, and and calcium magnesium is, well, brilliant. Fine. I think we'll leave it that Ah, thanks a lot. Guys are just postop the feedback and for more time, please do please complete the feedback. Make sure to drawing mad at, because that's where we post up. Like I said, all of our content on or leave it for one more minute, and I hope to see you guys again soon. Next week. I hope you guys have enjoyed it. And I'm sorry that it was an impromptu lecture. But I hope you still manage to learn things from it. And I will definitely be doing a part to of this during the Siris or will rearrange that, guys, um, take her on SSI soon.