The Pre Paces Podcast is brought to you by two fantastic sponsors. Firstly, Quest Med is a brilliant online Paces Revision Resource over at quesmed.com. They've got tons of videos which will help you revise from the comfort of your own home and you can use the discount code Pre Paces 15. That's Pre Paces, All-in Capitals and the number 15 at the checkout to get 15 percent off this essential tool to maximise your chances of success in Paces and the only other essential tool you need is a market leading Paces course. Speaking of which, Paces ahead is run out of Central London. They bring you a whole host of patients with fascinating stories and reliable clinical signs all of whom are absolutely delighted to allow you to hone your examination skills prior to exam day. And so the dates for your diary are the next course is running the 28th of September to the first of October 2026 and the following week which is the 5th to the 8th of October. All you need to do to sign up is go to pacesahead.com and I advertise for these two sponsors because I genuinely believe that combined they essentially guarantee you'll get that all important parts in Paces. So use the discount code Pre Paces 15 at quesmed.com and sign up today. Welcome listeners, Sam Williams here and welcome to 2026 and we kick things off with a bang and another listener requested episode from our quesmed giveaway with Dr. Layla Thurston, consultant in endocrinology and diabetes from Imperial College London as we considered all aspects of hyponatremia in context of a clinical consultation station covering off history taking, key examination findings and investigations and management but before we get into the show proper it's time for me to pay tribute to the legends on the Bimeo Coffee page. Thank you to Sir Rika, thank you to Han who both donated, thank you to Ben who bit the bullet and sat his exam and jokingly remarks he was going to start producing a postpaces podcast, don't get any ideas Ben. Thanks to Sophie who passed second time round to Hannah who listened on her commute and passed first time and finally thank you to everyone who let me know about their Spotify wrapped Amy Birch enough with over 3000 minutes to Keana who racked up 4571 minutes but the golden medal goes to Shreya who clocked in a ridiculous 5,589 minutes may god have mercy on you Shreya but enough on that for now let's get into this week's episode Welcome back listeners to the pre paces podcast I'm your host Dr Sam Williams and it's happy new year and it's high-boned naturally okay it doesn't really work but anyway we absolutely have had to start off this year with a bang and we are absolutely doing that with a brand new guest on the podcast who is most definitely worth their salt I'm delighted to welcome Dr Layla Thurston who is a consultant in endocrinology and diabetes at Imperial College London who's kindly giving up some of her valuable time to provide some expert insights on managing hyponatremia and our approach to hyponatremia in paces so Layla welcome to the podcast thank you thank you Sam it's good to be here and I should say also that this was a request from one of our listeners who entered one of our giveaways towards the back end of last year and just to remind ourselves of the request hi Sam thank you for your reply it's a pleasure contributing to your show my name is M&E and I'm a speciality doctor I'm preparing for bases the upcoming few weeks so I suggested hyponatremia because of its complexity you know the clinical consultation it has numerous differential diagnoses and that means that it just a single historical detail from patient history can completely change the diagnosis approach and one more point is beyond diagnosis you know the management of hyponatremia itself is for me it's particularly challenging and to know when to admit the patient versus letting them go home for just an outpatient fall-up so these for me are very crucial aspects in non-consultation stations so I believe that comprehensive review from one of your high-valued and featured guests would be very very incredibly helpful for listeners thank you for your help so Layla with hyponatremia in mind I wonder I wonder if you could just give us a little bit of an overview why is hyponatremia so important for our listeners to know about comprehensively not just for paces but also in their day-to-day clinical practice yes of course so and hyponatremia is really really important to know about ultimately because it is the most common electrolyte abnormality it's super common on the medical take as well as in impatience and I'd say it's one of the most common endocrine referrals that we receive it also covers a range of specialities from gastroenterology to nephrology and then the are in endocrine causes and it's really important to to work through the correct algorithms when distinguishing the diagnosis as incorrect management can end up with severe consequences for the patient importantly we're going to be looking into SIEDH and the reason why this is so important is because of the underlying causes for SIEDH and the importance of investigating thoroughly for those yeah absolutely and one interesting little tidbit that I came across Laila in my research for the episode is that whatever the cause regardless of the cause hyponatremia is a poor prognostic marker among all hospital impatience so I think really that underlines for the listeners just how important our approach to managing these types of patients is so I'm convinced this is a super crucial topic as I said not only in our paces but also in our day-to-day clinical practice so without further ado I think let's get into hyponatremia so Laila we are going to approach hyponatremia from the perspective of our trainees entering a clinical consultation station so they will have 15 minutes of contact with a patient and five minutes of discussion with the examiner and with that in mind I wonder if you can maybe talk us through some possible vignettes which might flag to the candidates that a patient has an abnormality with their sodium levels yes of course so symptoms of hyponatremia can be quite vague and non-specific such as fatigue and nausea vomiting but then progressing to headaches and drowsiness and falls in the elderly or cognitive deficit and alternatively hyponatremia can be picked up incidentally if it's mild or even sometimes moderate depending on the cremacity of the hyponatremia so in paces this could be a vignette whether the GP has taken some routine bloods and noted the low sodium or it could be that they are presenting with with one of those symptoms that I listed and it's it's picked up that way yeah and again an interesting tidbit that I came across in the nice guidance on hyponatremia was that the severity of symptoms may not match the degree of hyponatremia in the patient you're assessing so again we need to be conscious that different levels of sodium may affect patients differently compared to some other groups so I guess that's important to bear in mind the other thing that was mentioned in the nice guidance is that severe symptoms are unlikely to be found at levels greater than 130 which I think is probably fair to say but later there were three main features which basically as I found in my research three features which will ascertain which will guide our approach to managing hyponatremia and I wonder if you could just talk us through those and how important they are in managing our patients. Oh yes so it all boils down to fluid balance and a really accurate assessment of fluid balance is crucial in making the diagnosis so we can split the causes of hyponatremia into patients who are fluid overload so hypervalemic those who are uvalemic and those who are hypotherlemic. There are various ways of assessing this both on clinical examination but also biochemistry and the history will give us a clue too. Yeah absolutely so just before we get to talking about hyperhypo and uvalemia I wonder would it be possible for you to just talk through a brief explanation of the sort of basic pathophysiology involved in hyponatremia? Yes so I mean it's all a question of free water balance and there's
dilutional effect of the salts in the body. So hyponatremia is relative excess of body water compared to total body sodium when the serum water increases with oral intake and reduces with insensible losses. So vice sweating, vomiting and urinary dilution. And urinary dilutions regulated by ADH which is produced in the hypothalamus but sored and secreted in the posterior pituitary gland in response to reduced effective arterial blood volume. So a low blood pressure acts to increase the absorption of water from the collecting dust of the nephrons. Therefore urine becomes more concentrated hence the word antidiuretic and retains water to the body. So hyponatremia may be physiological in hypolimia, pathological in fluid overloadued heart failure or ionogenic as a result of diuretics. Yeah and I think that's absolutely crucial to understand the no where you are in your assessment of the patient and will come onto the assessment of fluid balance of the patient a little bit later. I think the other thing just to have a brief reality check is that this is paces and it's probably quite unlikely that the examiners will manage to find a patient who is truly overloaded with decopensated heart failure or severe nephrotox syndrome, severe enough to be clinically fluid overloaded. So I think the chances of finding a hypervalemic or severely hypervalemic patient is unlikely and so we'll be focusing most of our discussion on um uvalemia and SIADH but with that in mind we're just going to sort of rattle through hypervalemia and hypervalemia just because we feel those might be slightly less common in paces and of course the benefits of the examiners is if they have a uvalemic patient they can have an actor or a surrogate in the exam who can just provide a history and no physical signs are required. So um lately if first of all we come to hypervalemia what are the sort of top causes of hypervalemic hyponatremia? So you need to remember these as the three failures so heart failure kidney failure or liver failure. So in heart failure a low cardiac output stimulates sodium and water retention via increased A/ZH secretion. In liver disease so cirrhosis there's reduced effective arterial blood volume from reduced vascular resistance which activates bar receptor mediated A/DH secretion leading to water retention and then in kidney disease when you have a reduction in EDFR or cases of tubular injury the ability to dilute urine and excrete water reduces. So for example in the frotic syndrome blood volume may be reduced due to low serum on cotic pressure resulting in stimulation of A/DH secretion. So the the fix for these is to treat the underlying cause so it might seem counterinsuitive to give a diuretic to someone who is overloaded when we know that diuretics can of course cause hyponatremia but if the cause for the hyponatremia is the fluid overload and heart failure then diarysis is necessary and there are other ways that we can top up the the sodium levels. In liver disease again it's treating the underlying cause and kidney disease similarly. Yeah interesting lovely stuff so as Laila has gone through the three failures of hypervelemia obviously crucial but we're going to move on to hypoverlemia because as we said at the top it's very unlikely to find a profusely overloaded patient who's going to be happy to have a caracel of candidates come round to take their history and examine them for three or four hours. So moving to hypoverlemia this is probably arguably the commonest cause that we see in clinical practice. So Laila what are the more common causes that we see of hypoverlemic hyponatremia? Yes so as you said some this I mean it's very unlikely to come up as a clinical case in cases but importantly on the medical tape we see this a lot so patients coming in with gastroenteritis with severe diureum vomiting will have dropped their sodium. Also severe burns or sweating is going to increase the insensible sodium losses through the skin and the case of medication so overdioresis in cases of heart failure and then very rare is cerebral salt wasting so which is an intracranial pathology so from a subrachnotemorrhage or head trauma where there's increased level of AMP and BMP which can increase renal sodium loss but that's right down the bottom of your list. There's also sodium losing nephropathies so polycystic kidney disease, chronic pylonofritis and then third space losses from severe illness so bowel obstruction or pancreatitis. Yeah really really important and I guess the thing is as similarly to hypervelemia the chances of the examiner is finding a patient who is clinically so dry from any causes is unlikely so we're just going to touch very briefly on adicence disease because this is something which I have I don't actually think I've ever diagnosed it de novo in my clinical practice I asked you before we hit the record button layler where this would fit whether or not it would be in a hypervelemia or a uvelemic hyponatremic picture but I wonder can you just give us sort of a brief overview of adicence disease and we can talk about the investigations maybe a little bit later but maybe just an overview of the condition and anything you'd like to say as an expert in endocrinology. Of course yeah so adicence disease is the one that we really don't want to miss we want to be recognising it at the front door when a patient comes in patient presenting with hypotension, hyponatremic perhaps vomiting alongside that. Now in cases of adicence disease so that's your primary adrenal insufficiency you've got destruction of all the layers of the adrenal cortex so you'll have mineral corticoid deficiency in addition to hypercortisolism and so with that mineral corticoid deficiency you will have a hyperclemia associated to so that's an important distinction between primary adrenal insufficiency adicence and secondary adrenal insufficiency so in secondary adrenal insufficiency the mechanism is slightly different in that you have a reduction in cortisol which will then you have lack of negative feedback so you've got increased CRH production from the hypothalamus which then stimulates adh production from the poduratory and then with that excess adh more waters reabsorbed and hyponatremia develops that way but you won't get the associated hyperclemia that you will have with your primary adrenal insufficiency so any suspicion of adrenal insufficiency either primary or secondary we're going to be going straight in with our intravenous hydro corticone at a dose of 100 milligrams and getting that in alongside my big bonus of IV fluids ensuring that the cortisol is sent on that first set of bloods ideally before the hydro corticone has gone in but not delaying administration. Thank you so much for that, Leyla so really nice overview of adhison's disease and I'm sure we'll come to talk about the investigations and management a little bit later for that as well but now to move on to uvalemic hyponatremia and as I said this is arguably the most likely to get in paces and so the examiners will be able to get actors and surrogates to provide a history with no clinical signs required and so in terms of our history taking of a patient with uvalemic hyponatremia we've talked about the symptoms which they may be describing but I guess the most important thing is establishing the severity which will be provided to you so hopefully in the vignette they will tell you what the sodium level is but I guess it's establishing the timescale and the fluid status of the patient as we've talked about is going to be really important followed of course by the symptoms. I guess establishing something as S.I.A.D.H. is going to cover all a whole range of differential diagnoses so what Leyla are the most common causes of an S.I.A.D.H. Sure so just to mention that alongside checking a cortisol level, ideally a 9M cortisol level we also want to be checking thyroid function before we can make a diagnosis of S.I.D.H. we need to have ruled out hypothyroidism because we know that reduced levels of circulating free thyroid hormones can cause a bradycardia which is going to reduce cardiac output and then increase A.D.H. production. Similarly the reduced reduction in cardiac outputs is going to reduce the GFR, activate the RAS system and lead to increase retention of free water and hyponatrymyivirac mechanism.
So do not forget TFTs. Then moving on to SIDH in terms of the different causes, drugs very commonly. So your SSRIs, tricyclic antidepressants, opioids, ACE inhibitors, ARBs, thysi, diuretics, PPI's, anti-psychotics, pamiodaron, NSAIDs, long list of drugs that can cause hyponatremia. Now, if the patient isn't on any medications that can cause hyponatremia, we really want to be thinking about malignancy and walling that out and making sure we've done sufficient investigations to do so. - I guess the main thing to talk about with the, obviously it's making sure you're not just asking a blanket drug history saying, "What do you take?" But it's then asking specifically for the culprits is probably what the examiner's gonna be looking for. They're going to be expecting you to know a list of drugs that can precipitate a hyponatremia off the top of your head rather than expecting the patient to tell you. I guess the other thing is they might give you a list of drugs and you'd be expected to identify the culprits from that list going further with the malignancy. I guess in terms of a history taking, it's gonna be a case of asking about constitutional symptoms. And I guess one of the most common culprits being small cell lung cancer, your history taking is gonna be focused on the risk factors for that. So things like smoking, obviously the symptoms of it, breathlessness, productive cough, hemoptosis, recurrent infections and the like. And similarly with gastrointestinal cancers, things like abdominal pain and masses in the abdomen, for example. So I guess those are probably the most important things from a history taking perspective, which is probably more likely, or probably most likely in paces. (drone music) So we've talked about S.I.A.D.H. and we've talked about adrenal insufficiency and hypothyroidism, but one of the other things is high water or low solute intake. And one of those is Laila is primary polydipsia. Now, in the vignette, that might be presented to you. So I think it's quite unlikely for paces, but possibly something for listeners to consider in their clinical practice maybe. Is that something you see commonly in your line of work? - I do see this commonly as an endocrinologist. Certainly, so water intoxication, secretor, psychogenic polydipsia, but also we see it in exocetion, marathon runners drinking far too much, once they've crossed the finish line and dropping their sodiums to 120. I've seen that coming in very unwell. And then of course, we've got our alcohol misused disorder. You've got the so-called B-apotomania which will also dilute the blood and typically have reduced solute intake there. So those are important causes to look at, but it should become apparent within the history and then our urinary testing, urinary sodium urinary arzmalarity is gonna give us answers there. So these patients typically have a urinary arzmalarity of less than 100 mls per kilogram with a urinary sodium of over 20. - I guess the last thing to mention as well is pseudo-hypone-tremia. I guess I don't know about with modern lab assays whether or not this is particularly relevant, but I guess something to bear in mind. So Leila, can you just explain to a pseudo-hypone-tremia? - Yes, so this can be a lab artifact when the sodium appears low, but this can be due to either high protein, high triglycerides or even very high glucose, which will interfere with the measurement of sodium and give you an artificially low result. And so the obviously by treating the actual sodium will become apparent. - Yeah, absolutely. So I think we've talked through most of the components of a history and how we should think about our approach to the patient, but now part of your clinical consultation is obviously going to be your examination of the patient. And it's gonna be important to perform a diligent examination looking for signs of hyponeipervileemia, despite the fact we've talked about the fact they probably won't have any clinical signs, but I guess Leila, it's important to demonstrate to the examiners that you know how to assess for this. So what sort of features would be most important for our candidates to look for in an examination of their patient? - Yes, sure. So really important that you can perform a comprehensive fluid balance assessment and the examiners will be looking for some key things. So starting with the hands, as you always would, you can assess skin turga, moving on to the pulse, hypoverlemic patients are gonna be typically tacky cardic. You would want to blood pressure at this point, then moving up to the face and mouth, you're gonna have dry meekest membranes, have a look at the JVP at 45 degrees. You might not see the JVP in hypoverlemia. Of course in hypervelemia, it's going to be raised. And then I'm gonna have a listen to heart sounds and listen to the chest in hypervelemia. You might hear some fine bivasal crapetations. I'm supposed to be some cardiac wheeze. You want to be looking at the abdomen for any ascites and you want to be looking at the lower limbs for any peripheral edema. In addition to getting blood pressure, we'd be good to ask for a lying and standing blood pressure as a postural job is a good indicator of over fluid status. So those are your key features when assessing fluid balance status on a patient. Now in terms of the underlying cause of the hyponatremia, we talked about at low cortisol, so adrenal insufficiency, so when performing an examination for that, if we're talking about primary adrenal insufficiency, we're gonna be looking for hyperpigmentation, typically found in the parma creases and the all-new COSA associated with that increased ACTH production. We're gonna be looking for any features of hypothyroidism, so that's gonna be a bradycardia. You might parpeid a goiter. You might notice proximal myopathy, hypobreflexia, pre-tibial mixidema. And then also we mentioned malignancy as an important underlying cause of SIDH. So there we might do perform a breast examination on a woman or we would parpeid the abdomen for any abdominal masses in the chest examination, parpeid for cervical infadal neuropathy and specifically, burcos node. So all of these things to think about when you're approaching a patient who has hyponatremia and you're unsure of what the cause is. - Yeah, absolutely fantastic. So there's two aspects of the examination. One is looking at the fluid status of the patient and then the other is going to be looking for features related to an underlying cause, brilliant. Once you've established the fluid status of your patient, you'll be in a much better position to narrow down your differential diagnosis. It's almost always going to be made with the relevant blood tests and further investigation. So why don't we talk through those? It's a distinct possibility that some of these may be provided to you in your station and you might be expected to interpret it. So I'm sure in their various trusts, our candidates may well have some form of flow chart for the management or approach to hypolimia, but Leylev, they won't have access to the flow chart in the exam. So what are the crucial bedside tests that they're going to need to ask for and hopefully be proficient at interpreting as well? - So it's all about doing your bedside test. So that's going to be your urinalysis, which straightaway is going to tell us if there's blood or protein in the urine, which may reflect a urinal disease. As I mentioned, we want to blood pressure and then we want to be focusing in on our biochemistry. So urine, urine, urine is absolutely crucial in making that diagnosis of SIDH and it's commonly not sent on time. It's sent after we've given several liters of fluid or diuretic or whatever, and it just muddies the water. So get that urine off early and it's both the urinary osmolality and urinary sodium that are essential to make the diagnosis. So looking at the urinary sodium first, the magic number is 30. So if the urinary sodium is less than 30, you've got less solute in your urine and it's being lost somewhere. So either from diureum vomiting, insensible losses as described earlier with burns, sweating, bowel obstruction, pancreatitis. But if the urinary sodium is over 30, then you're losing sodium in your urine. So that's either diuretics forcing sodium into the tubules from an AKI or real disease affecting the kidney's ability to conserve sodium. You've got your adicence, so lack of mineral corticoid. The urinary sodium is really going to give you
your lot of information. You're in osmolality as well, will help you differentiate between primary polydipsia that we talked about and then SIDH and the cut off there is 100 and then moving on to blood tests. We want to be sending off our serum osmolality and in SIDH we're looking for a serum osmolality of less than 275 mAh per kilogram because the ADHD is overactive because your serum is dilute and your urine osmolality is high because sodium is being excreted. Now in addition to the osmolate pared osmolalities and urine resodium and the cortisol and thyroid function that we've already talked about we've course what to be looking at the other using ESO kidney function, liver function and then glucose as you know, congrucus typically causes a high osmolality. So serum osmolality should be checked but then also can be a course of pseudohypo nutrimia. BMP is really helpful when diagnosing heart failure. What a fantastic run through. So I guess the main things which are going to be crucial for our listeners are all the things which often tripped me up when I was revising for this exam is the mostly the pared urine and serum osmolalities and sodium that those were often the things which tripped me up. I guess the thing we haven't really mentioned throughout the record is that we're probably talking really about a chronic hypo nutrimia something which has either been happening for a long time that the GP has maybe kept an eye on and now it's coming to a more severe end of measurement. If we come towards the management end of hypo nutrimia there's a whole section of the nice guidelines to do with managing chronic hypo nutrimia and this is mostly done within primary care but again this might be something which is fair game in which our candidates may see in their clinical consultation as potentially an estic patient. So the nice guidelines suggest that asymptomatic moderate hypo nutrimia and they define moderate hypo nutrimia as anything between 125 to 129 with severe being defined as less than 120 millimoles. They say anything within that range can be managed in primary care but they suggest discussion with an endocrinologist presumably via some sort of advice and guidance pathway. I guess if it's towards the severe end or if they are symptomatic that's the sort of patient where they should be admitting the patient for these tests. Would that be fair to say? Yes so obviously anything symptomatic needs to come in. I mean my clinical practice I tend to use a cut off of 125 so I think lower than 125 would require a mission. There are caveats to that with patients with chronic SIDH where the underlying cause has been thoroughly investigated and they're known to have idiopathic SIDH and they tolerate a much lower sodium than your eye would then those would be the exceptions but otherwise get 125. If it's over 125 this can definitely be managed in SEDEC and yeah we would work through the different investigations and then start a management plan before referring back to the GP to continue management. Yeah absolutely and I guess the other thing to bear in mind is that or one question which the candidates might have is when should they be seeking an endocrinology referral rather than just trying to work blindly through a protocol of sorts from their trust. When would you expect to be called about these types of patients? An endocrine referral is warranted if there's any question about the diagnosis if it's unclear or if it's unexplained SIDH so idiopathic without malignancy or another endocrine cause obviously if there is an underlying endocrine cause such as adrenal insufficiency or hypothyroidism you're going to be discussing with an endocrinologist and then if so standard management of SIDH would be a fluid restriction starting off at 1.5 litres and reducing to 1 litre a day if tolerated and if required and if the patient's not tolerating that or if it's not working then at that point an endocrine referral would be warranted to explore pharmacotherapy options namely toll-vaptan which is a vasopressin 2 receptor antagonist but that prescription would need to come from an endocrinologist. Yeah exactly and the thing we said before we hit record was that you probably wouldn't be expected as a paces candidate to consider a patient suitable for toll-vaptan but it might be worth saying something like that would be the question you'd pose to the endocrine team. Exactly yeah so you'd be calling them to ask them if toll-vaptan treatment would be indicated. I know this is probably less related to a paces layer but I have in my time come across probably a handful of patients presenting with acute hyponatremia so this is potentially a slightly tricky presentation to manage especially for the more junior medical registers who won't have come across it before but what are the cornerstones of managing a patient presenting acutely with a newly found hyponatremia? Yeah so I mean acute hyponatremia something acute symptomatic hyponatremia is a medical emergency and so you definitely want to be involving your seniors possibly ITU depending on the severity. So the cornerstones of management really come down to slow correction so you don't want to be increasing the sodium by more than 10 millimoles per liter in the first 24 hours and then 8 millimoles per liter every 24 hours thereafter and this is because of the risk of cerebral pontine malinalysis associated with those rapid changes in wall should salt balance. This can present a few days after the rapid correction with paralysis, dysphazure, dysarthria and the patients who are particularly susceptible to this are those who have alcohol misuse disorder who are malnourished and so in those patients they might also have had hyponatremia for a longer period and so we really don't want to be rapidly correcting sodium and in those patients their brains will be more susceptible to that damage. So the aim is to correct the symptoms rather than normalising the levels. Like saline you might have encountered is only really reserved for those who are fitting as a result of hyponatremia. You can actually be more harm than good giving hypotonic saline certainly if it's not adequately monitored and if it is given it needs to be given either in any recess or in an H2U ITU level setting and you be giving aliquots of either 150 mills of 3% sodium chloride or alternatively 300 mills of 1.8% sodium chloride if the 3% isn't available in your trust and you want to be doing a VBG after that aliquot and you want to be stopping once you've achieved what the patient is no longer fitting and certainly want to go above and increase in 5 millimoles per liter in that short period of time. Yeah absolutely so I think that's really valuable just brief overview of acute hyponatremia. I've only come across it a couple of times in my career but when it comes to it I always have to remember that really importantly it's about slow correction you're not looking to immediately normalize the level like you might do for something like a very low potassium it's got to be dealt with in a slow fashion go low and slow. That's correct yeah low and slow and if you do over correct and the sodium comes up too quickly then you would want to be discussing with an endocrinologist about managing over correction possibly bringing the sodium back down and we can do this by giving dextrose but this requires further discussion and as I mentioned it's just really important to try and ascertain how quickly the sodium has fallen so is this a patient who has had a really insidious onset
set of hyponotreme, it's developed over weeks to months, the underlying the lignancy, or is this a marathon runner who has drunk five liters of water on completing the London marathon? In those cases, a rapid correction is going to be more appropriate than correcting somebody who's had a sodium for weeks to months. So that's a really important part of the history. - Wow, well, fantastic. And that pretty much draws us to a close on this episode covering all aspects of hyponotreme. And that only leaves us to say a huge thank you to Dr. Laylet Thurston Consultant in Endocrinology and Diabetes at Imperial College London. Laylet, it's been an absolute pleasure having you on the podcast. Thank you so much. - Thank you for having me, Sam. And good luck to all the candidates. - That's very kindly, Laylet. I'm sure they will take your luck and run with it. But listeners, that is just about all the time we've got for this week's show. Please don't forget, you can like, follow, and subscribe to the show. Leave a five-star review wherever you get your podcasts. We always love to hear from you. So please do give us a shout on our website. You can do that at prepacespodcast.com or you can email
[email protected]. And if you really want to go above and beyond and support the show, you can do that at bimicoffee.com/prepacespodcast. But for now, we're just about out of time. Thank you so much for listening. That's my dog. (laughs) I'm Sam Williams and we'll see you next time on the prepacespodcast. (upbeat music) [MUSIC PLAYING]
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