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Final year series Medicine. Session 7: Endocrinology

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Summary

This medical education session focuses on endocrinology for medical professionals taking final exams. Led by Dr. Glenn Davies, the session will cover differentiations between primary and secondary endocrine gland disorders, initiating investigation of high calcium, and how to work through hyponatremia and adrenal insufficiency. Dr. Davies will also provide exam style questions related to hormones and the hypothalamus and pituitary gland, discussing lytic bone lesions and multiple myelomas, and share the four question method for understanding the underlying process that leads to hyponatremia. The session will also be sponsored by Wesley and Next Step - providers of guidance and resources to help you transition into F One.
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Description

This is our 7th session in the final year medicine series. This webinar will be lead by Dr Glen Davies, an AFP F2 currently working in endocrine. He will cover key topics which are examined in final year medical student exams and will end with some SBA questions to assess your knowledge

Make sure you register for the event to attend on the night!

20th March 2023

7pm-8pm

Learning objectives

Learning Objectives: 1. Understand the differences between swing and seesaw endocrine glands 2. Explain the causes of primary and secondary hyperparathyroidism 3. Describe the investigation and management of hypercalcemia 4. Distinguish between true and false hyponatremia 5. Apply a 4-question approach to the diagnosis of hyponatremia
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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hi, everyone. Um Everyone's tuned in so far. We're having 1/7 session tonight and that's an endocrinology. We've got to Doctor Glenn Davies is doing the presentation tonight covering all things under crying and they'll be really useful for your finals. There will be a QR code for his feedback at the end. So please make sure you give both good and any improvement feedback because it's all useful for the future. Um So I'll hand over to you now, Glenn. Thank you. Thanks very much live. Thank you for joining us, everybody. Um As I've said today, we'll be running through the basics of endocrinology for finals. I would assume that that most if not all of you are finally medical students coming up to your finals later on this year. So I hope this is useful for you folks. So before we start properly, I'd like to say that we are sponsored by Wesley and next step who offer guidance and resources for helping you transition into F one and there's a QR code there if you would like to access any of their support. So after discussing with some of my colleagues in the endocrinology department some of the consultants and having a quick perusal of what my uh finals curriculum looked like. I thought that this would be a particular reasonably useful set of topics together. So I thought I'd offer a brief overview, perhaps a do conceptualization as to how to differentiate primary and secondary and Oakland disorder endocrine gland disorders will also cover the basics of initiating investigation of high calcium. And we'll spend probably the majority of our time this evening working through hyponatremia as it's continuously flagged up as, as an area of difficulty for most people. And it certainly was for me until I've started to get my hand around it. Not that I've completely gotten my head around it yet. And we'll work through the two main types of hypoglycemia that's H H S and D K A and we'll finish off with a brief discussion of adrenal insufficiency before working through some exam style questions. If at any point, I'm talking too quickly, please just flag up on the chat and live. Can let me know to slow down. Um I'll request that if anybody has any major questions or any particular sticking points, there should be time at the end to discuss these things. There's quite a lot to get through. So we'll, we'll work through this without too much uh dialogue back and forth, but that we will make sure that if you have any burning issues, we will cover them at the end. So without further a do um the most useful way that anybody ever explained to me. Um Endocrinology was to start thinking about swings and seesaws. That is how a specific gland works. That is endocrinology is all about the input and output mechanisms by which are hormonal processes work. Now, the first broad category of organ is one that works by stimulation. That is the input, gives a big push and that causes a bigger output much like a swing. If the input drops and you give a smaller push, then that gland will end up giving a smaller output. Now, conversely, some other glands work through inhibition and that's more like a see saw rather than a swing as the input rises. That inhibitory effect causes a drop in gland output and vice versa. When that inhibitory input level drops, that actually results in a net increase in hormonal output from that gland. Broadly speaking, the main hormonal axes that you will encounter for your finals and through F one. And I think majority of your, your doctoral life, if you don't become an endocrinologist will be uh the hormonal pathways that involve the hypothalamus and pituitary gland. So the main three of the thyroid, the adrenal glands and the gonads. And you can see here that all three of those glands work through direct stimulation. That is they're supposed to swing glands and they, they're output has a negative impact as an inhibitory impact on the hypothalamus, um interior pituitary that work as a single unit. So that's where the negative feedback works and that's inhibitory and that results in a homeostatic, a negative feedback loop within the body. The important exception here is the parathyroid gland. And I think for finals, this is the only one that works really differently that you're likely to encounter broadly speaking, the hypothalamus and pituitary aren't really involved here. And the simple loop is that the parathyroid works through inhibition. That is the input here is calcium and when calcium levels rise, it causes P T H levels to drop. And when calcium levels drop, it causes P T H levels too. Right? I think that's conceptually is probably the most useful thing when it comes to thinking about hyper or hyperparathyroidism. It's that we often relate it closely to calcium levels, but calcium is actually the input for the parathyroid gland, not the output. And this leads me onto a discussion of hyper and hypo calcemia. So there are a few different mechanisms by which the body's calcium levels can rise. And so where relevant to us can rise to dangerous or damaging levels. But it's mainly the bones that provide the main output here. Calcium is released by the bones, not by the parathyroid gland itself. And so bones can release more calcium, but through excessive stimulatory input. Now, this can be through rising levels of P T H from the parathyroid gland itself or from ectopic parathyroid hormone secretion through paraneoplastic syndrome. So there's a tumor somewhere in the body that is secreted this hormone that acts very much like parathyroid hormone and stimulates the bones to produce calcium in the same way that the parathyroid gland would. Now, you can see in the case of primary hyperparathyroidism that both calcium levels are high and P T H. Now, calcium here is the input and so if it's high, if the parathyroid gland is working properly, P TH should drop, but both are high. So you know that it's a problem with the parathyroid gland itself that's causing this state, the bones are working through stimulation. And so actually, they're working just as they're supposed to, the bones are just receiving the wrong signal. Here, there is another means by which a person can develop hypercalcemia. And that is when there's a problem in the bones itself, that is despite low levels of P TH calcium levels continue to rise. And those are most commonly caused by neoplastic or malignant process is that is lytic bone lesions or multiple myeloma. And it's for this reason that I would suggest that for where final exams are relevant. Whenever it comes to a work up for hypercalcemia, you need to be thinking about the possibility of malignancy. So I would at least be sending off a myeloma screen. That is urinary Ben's Jones proteins and serum electrophoresis to look at all those proteins. And just a quick aside there when it comes to your foundation practice. When it comes to hypercalcemia. A lot of people don't prescribe enough fluid. We could be very tentative and hesitant. We're worried about sending somebody into pulmonary edema fluid overload with fluids. If you want to get somebody's calcium levels down, you really need to be quite assertive with your fluid management. And quite a lot of people, especially over the weekend when there's less staffing levels really don't get their calcium levels down because nobody's really prescribed the right amount of fluid. I'm talking 34 liters even potentially. But once you've graduated, you can look at your trust protocols moving on to hyponatremia, which certainly for me when revising for finals was, was the biggest stiff sticking point. Um Some of you may well have your own methods and that's absolutely fine. I think it's something that's generally speaking is talk quite poorly, especially when it comes to interpreting tests. So I'm going to propose and we'll work step by step through a four question methods that I think certainly works well for me. And I hope what, what works well for you today before we do. So I think it's important to remember to key things that is firstly that hyponatremia is a sign, it's almost a symptom or a stigmata. Um not a diagnosis in of itself. If somebody is hyponatremia, if somebody has low sodium, that is consequent to a process that is happening within them and it is your job to work out what that process is out of the multitude of possible pathophysiology is that could be occurring here. The second thing is that hyponatremia is a low concentration. It is not necessarily a low absolute level of sodium. You could well have a low amount of sodium and be hyponatremic. But if you have a normal amount of sodium in your body, but your fluid overloaded or you have too much fluid there, then the concentration will be diluted. And that will also present as a hyponatremia. Now, this is the graph that hopefully in about 10, 15 minutes, we will be understanding quite well. It's an awful lot to take in. But this is what hopefully by the end of this lecture, you'll be able to understand and it starts with these four main questions. They are. Firstly, is this a true hyponatremia? And we'll discuss how you can assess that. Secondly, is water being retained? We talked about hyponatremia being an issue with concentration. So if you can work out what the water's doing, it will help you work out whether or not you're being concentrated or diluted. Thirdly, is this state of water attention? If there is one an appropriate response and finally, if salt is being lost from the body, where is it being lost? So let's look at this first question. Is it true hyponatremia? Now, sodium is the I'd say predominant osmotically active substance within your blood. There are other substances and we'll go on to discuss those. But since sodium is the main one, I would expect that if you are truly hype on a tree, Mick, then the tonic city, the osmolality of your blood and by osmolality, I mean, it's a relative proxy. It's a relatively good measure that you can use in most cases, interchangeably with, with concentration. If you are hyponatremic, you should be hypotonic. Now, there are instances in which you can get a falsely low sodium reading. And that is when the blood is not truly hypotonic, that can be norm a tonic or hypertonic hyponatremia. And this can be caused for instance by a high glucose. So if somebody's got a rip roaring hyperglycemia, then that glucose might be dragging a lot of water out of the intracellular space into the blood and causing a false dilution of that sodium. In other instances, you might have a really high cholesterol or high protein or high paraprotein level. And this tricks the machine put in simplistic terms, the machine that tells you what your sodium level is, effectively counts the amount of sodium and then everything else that is not sodium, it assumes is water and therefore uses that to calculate the concentration. If you have a really, really high cholesterol level or really, really high protein level in your blood, then the machine will read a higher level of not sodium in your blood. And therefore, we'll assume that there is a lot more water in your blood than there actually is. And so it will falsely interpret this is a diluted sample. So you can work this out by looking at the serum osmolality. If serum osmolality is low, that is the blood is hypotonic, then it is a true hyponatremia. If serum osmolality is normal or raised, then it's worth checking your glucose, your cholesterol and your protein to work out whether or not this might be a pseudo hyponatremia. That's step one. We're off to a flying start. Now, once you've confirmed that this definitely is a true hyponatremia. A low osmolality, hypotonic hyponatremia. The question is, is water being retained? That is in the first instance, is this being caused by water being retained in the body causing the sodium to become diluted. Now, you can look at the activity of anti diuretic hormone here because A D H as hopefully, we're all already aware is the primary hormonal means by which we regulate our water retention within the kidneys. And so if A D H is high, our urine osmolality should also be high. So if you're in osmolality is low, we know that water isn't being retained. And in fact, if water is not being retained and 88 is being inactivated, then we know the body is trying to jettison water, you're trying to lose water to correct this low sodium. So if you have a low urine osmolality, you know that A D H is being inactivated, it's being suppressed and therefore, the body has too much water on board and is trying to get rid of it. And logically speaking, why might a person be trying to get rid of water to create the sodium? They might be taking in too much water caused by polydipsia and excessive first or a PPO tomainia, excessive alcohol or water intake caused by any number of psychogenic or physiological reasons. Okay. That's effectively diluting their sodium by taking in too much. Of course, we have to consider iatrogenic causes as well. Perhaps a patient's was fine when they arrived on the ward. But we've given them far too much normal saline, we've given them far too much fluid intravenously and that has caused them to dilute their sodium. Now, thirdly, they might just have poor sodium intake, they might have not gone anywhere near efficient chips for the last 20 years, never taken in any salt. And they've got really low dietary sodium. Now, the only way that the body can correct that concentration is by jettisoning water to try and bring that water level back in line so that the amount of sodium you do have sits at the correct concentration. So that's step one, if it's a true hypernatremia, if you look at the urine osmolality to assess ADH function and it's low, that gives you your first possible set of cattle. Well, your first category of possible causes. Now, what if A D H is being active activated, that is the body is trying to retain water. And there are a few instances in which this is inappropriate. So the next question is, is this an appropriate response? And the way you assess whether or not this is an appropriate response is to see, should the body be retaining water? And logically speaking, the instance in which a body should be retaining water is if it's dehydrated or hypothalamic. So if the patient is not hypothalamic, then this would be an inappropriate retention of water. So the urine osmolality is raised. A D H is being activated, but it shouldn't be. And broadly speaking, there are two main categories in which of physiological process in which this could occur. Going through the bottom category, there could be some hormonal imbalance within the body that's causing this. So, low cortisol or low thyroid hormones, hypothyroidism and the one that we all know about and that drummed into his in lectures syndrome of inappropriate anti diuretic hormone secretion. All of these processes could accidentally cause the body to, to retain water through activation of A D H inappropriately. But what if the body is trying to retain water for the right reasons? What if your fluid overloaded? Yes, but none of that fluid is in your veins or your arteries and you're trying to maintain your BP. So really, whilst it's an inappropriate activation of A D H because you do have fluid in you you've got poor circulating volume and you can't maintain your BP. So things like heart failure, liver cirrhosis and nephrotic syndrome could also cause activation of A D H in a, in a futile attempt to maintain your BP even if you are nonetheless fluid overloaded. So those are the two broad categories in which a euvolemic or hyperbole Mick patient might have inappropriate activation of A D H. I hope that makes sense. So far after this, after this discussion of hyponatremia, we will have a two minute break and I'll leave this diagram up on the board so that you can copy it down and you can go and get a cup of tea and have a bit of a lie down if it's still too much. What if this is an appropriate activation of A D H that is the patient is dehydrated. They are hypothalamic and there is a really great way of assessing hypovolemia and that's looking at their postural drop. If the patient stands up and the BP drops, that's a really good indication of hypochelemia. And indeed mind the bleep, the there is an article about assessing fluid balance which I worked on the if I may say so myself also gives a really good overview how to comprehensively excess fluid balance. If you establish that a patient is hypovolemic, then you've established this is a true hyponatremia, water is being retained. You can see that through the raised or normal urine osmolality and it is indeed appropriate. But here's the next question, if a person's dehydrated, then surely there sodium should go up. That is the concentration should rise. And indeed, hypernatremia is, is most commonly caused by dehydration. The only way that you can lose water or be dehydrated and also be hype on a tree. Mick is if you also lose sodium at the same time, that is your concentration drops despite also losing water. And so the next question is if you're losing salt in this hypovolemic state, where are you losing it from? And I'd say that that can be split into two categories. It's either being lost through the kidneys or it's being lost somewhere else. So you can look at the sodium content of the urine to figure that out. If you have a high urinary sodium, then you can establish that it's being caused by renal losses. So it could be renal disease or use of diuretics and even recent use of diuretics, it's may well be worth looking at patient's past medical history. They might have not been taking the diuretics for a couple of days or it might not have been prescribed on admission. But if they've been taking it, you may well see the effects on the hyper nitrogen atretic state within a few days, maybe even up to a week after their admission. If they're urinary sodium is low, then you know, they're dehydrated and they're losing the salt somewhere else. And this could be through vomiting or diarrhea, through burns through sweat. And I'd say also it could be through pretty, pretty large surgical wounds, abdominal surgery, big enough surgical sites through which you'll be losing a lot of, I'd say I so worried, maybe even hypertonic fluid. So we've now worked through this entire diagram and I hope this looks a lot less scary now, but I hope you can see that through asking these four questions in order and understanding why you're asking them and also how to answer them. You can start breaking down this clinical syndrome into its potential pathophysiology. ICAL causes once you've ruled out that it is a false hyponatremia. Super hyper hyponatremia. Look if water is being retained to dilute that sodium. If not, then you can start thinking about the pota mania is the polydipsia is the low sodium intake. The estrogenic uh fluid prescriptions, if it is appropriate, then you can start thinking about uh salt losses, fluid losses through the kidneys or through somewhere else. And if it's inappropriate, you can start looking at the other clinical syndromes that might be causing perhaps a low circulating volume or a low reflective BP or some other hormonal causes. And this is why we send off a cortisol level, a thyroid function test before we start thinking about SIADH, right. We're going to have a quick two minute break there. Before we start, we're moving on to the next topics. So I'm just gonna have a drink of water. I turn my camera off for a couple of seconds. If anybody's got any burning questions, you're welcome to ask them. But I will leave this up for a couple of minutes, uh, for you to copy that down if you'd like to. I'm more so, more than happy for my slides to be shared after this presentation. Right. I'll be back with you in two minutes. So at 25 past seven will rejoin to work through the rest of our topics. I hope this has been useful so far. Thanks. Okay, then folks hope this hasn't been too much so far. We'll move on. What I will say about hyponatremia is that if you can at least ask these questions as a foundation doctor, you're probably doing much better than, than most of your colleagues and at least starting to begin this work up before referring to an endocrinologist. They will probably love you because a lot of patient's refer to endocrinology without even having their osmolality is taken if you can begin this work and you may well be able to come to an answer yourself before referring or you will at least save your endocrinologist a lot of time by having ruled out a few possibilities. So without further a do, let's move on to the hyperglycemic states and what you may be faced with in a finals exam. So there are two main hyperglycemic emergencies and they are diabetic ketoacidosis and hyperglycemic hyperosmolar states or what used to be called Honk. Um and in medical school, it may well have been taught to you that D K is seen in type one diabetics and HHS is seen in type two diabetics. It's actually more of a Venn diagram with significant overlap. I wouldn't never assume that somebody who has a diagnosis of type two can't have DKA. DKA can occur in type two diabetics. And frequently people who are actually type one who present later in life may incorrectly be diagnosed as type two and therefore, are much more likely to, to come in with DKA. So always have a broad mind I think would be very cruel for an exam question to try and lead you down the wrong path by saying somebody's type two and then giving you a D K a question, but it could happen because it is possible. Now the criteria for DK A uh A raised blood glucose, a keto anemia or the result of of Quetta genesis within the body and an acid emmick state diabetic keto acidosis. The three clues are in the name diabetes, glucose, keto, the ketos and acidosis. Remember that ketones are produced when the body is starving. It's an attempt at producing an alternative energy source for the brain and that's exactly what's going on in people with type one in some type two diabetics. There is a lot of sugar in the blood, but the body doesn't know it's there, the insulin isn't there to signal that. And so the body is in starvation mode and an insult infection or excessive stress could tip the body into full on catastrophize ing starvation mode. That's what D K A is now slightly differently in people with who have HHS, they will have some residual insulin sensitivity. So the body doesn't think it's completely starved. And so therefore, there shouldn't be a significant amount of Quetta genesis as a result. The predominant pathological issue here is one of dehydration through osmotic diuresis. As the sugar levels rise, the person ends up extremely dehydrated and crucially, there may well be some ketones but there is no significant ketoacidosis in H H S and that informs how we treat these things in DKA. The treatments is were predominantly with insulin and of course, also aggressive fluid resuscitation. Remember it is fixed rate insulin. I've seen a few students accidentally say maybe just by force of habit that they would prescribe a variable rate insulin regime in DKA. A variable rate is for nice nuanced, little touches to control and already normal blood sugar level. You want to get this sugar level down in somebody with D K A variable rate ain't going to do it. You want a fixed rate, rapid ongoing insulin infusion to bring it down alongside that food resuscitation. A quick comment on using these uh specifically potassium. Um Generally speaking aside, emmick states tend to cause your potassium to rise. Um And then as you treat it with insulin that can drive the potassium into the cells, which can cause a hypokalemia X state. So I would never automatically give anybody in DKA potassium because they may well have a high potassium. All protocols should say that you should monitor the potassium and then treat it and supplement it accordingly. You should never automatically initiate potassium supplementation in somebody with DKA. It may well be low but only after you've gotten that result, should you supplement it? If it is low? And as with all things, endocrinological or otherwise, you want to treat the underlying cause. Remember as I said, the bodies tinkling along in starvation mode and then something's tips it over. That could be infection could be bodily insult to stress trauma. Figure out what's going on and fix that to stop the person from tipping back into DKA. Now, as we said in HHS dehydration is the main issue here. And so it's aggressive fluid resuscitation and just like with hypercalcemia, you give more than you think frequently in recess and on, on some high dependency wards. I've seen people with HHS who just aren't improving and people start wondering, oh, we've got the right diagnosis. We need to step up treatment. They're just not getting the right amount of fluid. My local trust policy says you want them in as soon as possible and you want three liters, positive fluid balance, you want to be achieving that really quickly. So I I would not be hesitant, all tentative in prescribing fluid in these patient's. This is what's going to save their life. Just as with DKA, you want to treat the underlying cause and something that's not commonly raised. Certainly in medical school when it comes to HHS when they are that dehydrated, their blood is going to be an awful lot more clotty. So considerations of venous thromboembolism, prophylaxis, Delta power in fragment enoxaparin, whatever you have in your local trust is something that you should be thinking about. So I think that's enough for DKA and HHS. I think any greater understanding or any greater nuanced interpretation of results would probably require something greater than the level of knowledge you should have for finals. And indeed beyond those basic principles, I I would say that you should be referring to trust guidelines which of course a final exam can't be assessing your knowledge of because it will vary from trust to trust. So, moving on to our final topic, which is adrenal sufficiency. And I don't think we need to go into tremendous depth here because there's loads of things that can cause it, there's loads of ways it can present and there's a multitude of hormonal pathways that I don't particularly understand myself. But for the purposes of a finals exam, you need to be able to recognize it and you need to be able to initiate the life saving treatment when that person comes through recess, maybe not recess, they might just be sat in ambulatory majors because nobody's realized what's going on. So, hypercortisolism is what we're talking about predominantly when we say adrenal insufficiency. So, low levels of cortisol is what's causing the body to be unable to mount that acute stress response. Of course, in Addison's disease, it's not just hypercortisolism, it's all the other hormones that are produced by the adrenal glands, your sex hormones, your adrenaline, I think your growth hormones as well. But when we talk about adrenal insufficiency in this context, we're specifically talking about hypercortisolism that could well be caused by long term steroid use that suppresses production uh of the bodily body, body's own cortisol through those negative feedback loops that we've already talked about on the hypothalamus pituitary. In this case, adrenal axis. So this person is not going to be able to, to mount a stress response to bodily insult. So they may well be fatigued, they'll be very weak. They may well be confused. Lethargic may well even have dropped their G C S. They will be hypertensive and may well even be in hypertensive shock without any obvious cause. As you start working through your difference causes of shock, they will likely be high pod glycemic and maybe even hyponatremic in people with Addison's disease. They are also more likely to be hyperkalemic as the aldosterone levels, the mineralocorticoid levels are also reduced. And in a patient who presents like this, you should consider the like the possibility of adrenal insufficiency if they have known Addison's disease or the possibility of Addison's disease, significant autoimmune history, perhaps, or if there's anything to suggest that they might have recently used long term or high dose steroids of people on with hard to treat asthma COPD, rheumatological disease. In rare instances, people perhaps you have had COVID and have been on steroids for an overly long time to help control that inflammation. So how do we treat it? It ain't difficult. We've got to replace that life saving steroid. So in the first instance, step one wax, some steroid in them 100 mg. IVR I am hydrocortisone stat. And the great thing is that if you are wrong and this isn't adrenal insufficiency, the hydrocortisone won't do any great harm. So it's, I would say that on balance, if there's a risk, there's a chance this could save somebody's life without any great consequence if you're wrong. Secondly, get that BP back up. It's the shock that in this, in the next instance, mechanically speaking is what's going to kill them. So aggressive fluid resuscitation and then once you've saved their life, you want to give them 200 mg of hydrocortisone over the next 24 hours could be split into 4 50 mg dose is now the society for Endocrinology advises I am intramuscular administration because it lasts longer rather than going through the veins. But you could do IV or I am really. And then longer term, this will be your, I suppose your longer term management. Maybe when you're thinking about primary care, you'll be thinking about people on long term steroids, not because they need it to control any disease, but to supplement their bodily supply of cortisol. And of course, hopefully we're all aware of sick day rules. Different trust will have different policies. There's a fantastic website, I think it's the adrenal insufficiency website that can give you some advice on sick day rules. Generally speaking, if a person is unwell or they are about to have a high stress procedure, then they may, well, I need to double their usual dose of steroid within a day for some weird reason. Exam questions really like to talk about dental appointments when it comes to some form of bodily insult that initiates a an adrenal crisis. For some reason, it tends to be root canal surgery if an exam question comes up. And I, and I see it says, um, a woman has, uh, you know, she's asthmatic or she's got COPD. And then three days ago, she had dental surgery and then now she's presenting acutely hypertensive. The first thing on my mind because of the nature of the question is to start thinking about adrenal insufficiency in this instance. So, dental surgery, very common red flag when you, when it comes to exam questions. So we've run through all those topics and I think in good time we have, I've offered you thinking about the analogy of, of swings and seesaws to think about differentiating primary and secondary endocrine gland dysfunction. Thinking about whether or not they're stimulatory or inhibitory lee driven. We've talked about the initial investigations of high calcium with regards to assessing whether or not there might be primary hyperparathyroidism going on here and crucially that all important screen for malignancy. We've worked through a full question method to consider the potential categories of process that are driving a hyponatremic state. We've talked about the two broad types of hypoglycemic emergency and how you manage those and differentiate those. And we've also talked about the bare bones recognition presentation and acute management of adrenal insufficiency. So I think the next topic is questions. I think I saw a question flag up. What if patient has heart failure or has CKD? Do we still give three liters? Oh, no, I, I can see that lives already answered this. Yeah. Yeah, completely agree. Um I would say that it would be that the, the, the the topic of our talk today is is being able to answer exam style questions for your finals. These issues shouldn't really be raised in an exam question for finals. Um because it's a very difficult thing to ask because it's so much dependent on the clinical state of the patient and it's often a trial and error, try a bit of fluid, try a bit of diaries is when it comes to heart failure. Um I don't, I would say that it would be very unfair for, for them to throw a fluid resuscitation question in any, in any patient at risk of overload. Um But it's great that you're thinking about this because it's these considerations that you, that will make you a better doctor once you've gone through the rigmarole of getting that certificate, because of course, as we're all aware by now, passing your finals and being a good doctor aren't necessarily the same thing. But hopefully, the topics that we've covered today will make you good at both. So um bit of audience interactivity now I've prepared five single best answer questions. SBA is the predominant exam style question structure that we use in Britain. It can see unless if you didn't already know these questions and you'll recognize these, the moment we talk about it, they have a stem in which the minimum amount of clinical information is presented. They should never give you any information. It leads you astray or any extraneous or superfluous information after the stem, the question is presented and then you're presented with options. And the important thing to remember that differentiates single best answer from multiple choice is that more than one answer may be appropriate or correct. There may not even be any wrong answers, but your task is to work out which one of these answers is the best thing. So the question will be, will often be presented not as which of these is the right answer, but the question will often be presented to you as which of the following is the most appropriate or which of these would you do first? That's what an SBA is like. And that's how you need to be thinking about these questions. So we'll run through the five, we'll do it like an exam. I'll give you a minute per question. I won't necessary. I won't read, read it out loud. If people do desperately want it to him, you read the questions out loud. I can do. So, just let me know, I will give you a minute and Livia will put up the, the poll after a minute. We'll have, we can have a look at the poll answers then or we can go back to them after all five. And then once we've been through all five questions, we'll work through the answers. Uh Does that sound like a plan if anybody has any burning indignance, contrarian views on that approach to you? Let me know grand stuff, right? And so I'll start my time and live if you're happy to put up the pole for this first question, and I will start the timer in a moment. We'll give you a minute to have a look at this. If anybody desperately needs longer, just message on the chat, I'll give you a 12th warning. So, and you can click on answer later here if you if and it will appear in the chat so that you can still answer it and look at the screen at the same time. Glen, you can see the total responses at the bottom of the in the, in the chat. Just to give you a gauge on the amount of people that are engaging in answering before you move on you. Uh Grand stuff. Thank you. If you, I can see, I've got six responses so far. Excellent. I've got 31 responses. We've had about a minute. I'm more than happy to give you another 20 seconds. See if we can get those responses up and bear in mind. This isn't, this is an assessment for learning if you get these answers wrong, that just means that it gives us an opportunity to, to talk about these because these are not easy questions. So don't worry about getting them wrong. They are difficult and some of them are, I think quite Trixie and I'm doing that on purpose. Hopefully. So that when it comes to your final exam, you'll have something a bit easier, right? We've got 44 responses. I'll give it a few more seconds and then we'll move on to the next question. Okay. Moving on to question too. Same again. OK, brilliant. We've got 45 responses there and we shall move on to the next question. Question three. Oh, somebody's asked, somebody is asking me to move on to question three. Is, can you not see question three on the screen? I have moved the slide. Now let me go back and forward. Did anybody not see question three? Do let me know it's, it's showing for me, Glenn, everything's changed. Grand Oliver Collins. I apologize. Can you now see question three? I think it might be, it may well be an issue at your end. Uh Grand. OK. Sorry Oliver. Does that mean you, you can you see question three? Now background to publish, we'll give you longer to answer this, this question. Then how are we doing on the pole? Got a lower number of responses on this one and we've split the room with, with our responses, which is not surprising. This is probably the hardest question out of the five and we'll probably spend a while talking about this one. Got 38 responses. I'll wait until 40 and then we'll move on. Are we going at the right speed for people doing? Does anybody want me to slow down? Grand? We're up to 43. I shall move on to question four. Thank you, Olivia. Okay. We are up to 43 responses. We'll move on to our final question. Thank you. And I think I did put it on a later draft of this slide. Unfortunate. Think I've, I've uploaded an older one um just for any of you who are wondering this lady's saturations, her oxygen saturations are 98% on room air. If you're able to, if that changes any of your answers, you're more than welcome to do so. Right. We've, I think that's a reasonable amount of time before we move on to our answers. And a bit of a discussion, would anybody like to spend 30 seconds looking at any of the, any of the questions that we've been through? We could perhaps perhaps spend another minute or so, uh looking at any of the other questions so that you can work out your answers before we move on. Any specific answers that people want to look at or should we move on to the answers? Okay, then. Grand. Thank you. Thank you, Sophia. Right. Let's move on and work through these. You may well disagree. Uh I think that these are the answers that that I'm giving here are the most reasonable in the single best answer in each instance, if you have any burning opposition or any major questions, more than welcome to, to raise them and we can discuss it. So question one, a 57 year old woman presents with recent weight gain lethargy and constipation consistent with a possible diagnosis of hypothyroidism. Now, this is indeed confirmed. Thank you. Uh This is indeed confirmed with a low T four level. Now, which of the following investigations is most likely to be diagnostic in this case. Now, this question requires you to be able to differentiate your primary and secondary endocrine disorder. Now, the thyroid gland works through stimulation. So it's a swing mechanism. Big input gives a big output, little input is a little output. And you can see here that you've got a low T four and also a low TSH, the thyroid gland is working as it should. It's producing a low amount of T four in response to a low amount of stimulatory hormone. Therefore, I would suggest that in this instance, it's not a problem with the thyroid gland. This is the profile of a secondary hypothyroid disease. So therefore, there is only one of those options that doesn't look at the thyroid gland and look somewhere else. And that's imaging of the brain where the hypothalamus and pituitary gland sit. And I would suspect that this is more likely an issue with the hypothalamus and opportunity grand, potentially a pituitary adenoma. I hope that makes sense. See imaging of the brain is the only one that looks somewhere other than the thyroid gland. And the fact that this is a secondary disease looking at the hormonal profile suggests that it's not the thyroid, it's somewhere else. That's the problem. I hope that makes sense. I saw some people mention an anti thyroid antibody screen, um reasonable. Uh If you're thinking about an autoimmune disease. So potentially graves' disease, which would be hyperthyroidism or potentially hashimoto's thyroiditis, you would still expect a raised TSH in that instance, as because as the pituitary gland is attempting to encourage the thyroid gland to work when it's underactive. So, question too, the answer here uh is a, this patient is presenting with acute kidney injury, a very, very high calcium. And what I would suggest here are features of multiple myeloma. We've got high calcium, we've got renal disease, we've got uh aches and pains from high calcium and we've got evidence of bone fragility and bone illness. The only thing we haven't got here is anemia to fix the typical four um cardinal signs of multiple myeloma. And this question is asking you to check that you remember the, the acute initial work up for a presentation of hypercalcemia. So you, you want to do the P T H to check whether or not this is a primary or secondary disease. And in the instances where parathyroid hormone is actually working correctly, you want to be looking, is there a malignancy going on here? And whilst body imaging may well be appropriate later on down the line to look for any solid solid issue tubers, you would at least in the first instance, want to do a myeloma screen the BJP and serum electrophoresis. That would be the most appropriate initial work up. Although I can understand why later on some other hormone queens and imaging would would also be reasonable. But this is the most appropriate initial work up. Question three. The really, really tricky one that split the room. Now, you can see the answer there that I suggest is the fluid resuscitation. Now, I've deliberately not given you all the information you could have here. But if you'll permit me to spend a couple of minutes talking through how I would answer this question, hopefully you'll see why I think that this is the correct answer. So this is a lady who's hyponatremic. So how are we going to work through this question? One? Is this definitely a hyponatremia? Is it a true hyponatremia? Well, could she be pseudo hyponatremia? Could this be a hyper or Norma tonic? Well, there's nothing in her history that would suggest that she's floridly hyperglycemic or very, very high cholesterol or very, very high protein. I've deliberately said there's nothing in the past medical history on drug history that could be driving that. I think it'd be very cruel if this question expected you to guess that she had a, an occult hyperglycemia or, or an occult hyperlipidemia here. So let's assume it's a true correct hyponatremia. Now, is the body retaining water? Now, we don't have any osmolality is here. But is there anything to suggest that she might be hypo valentic? Well, she's collapsed during physiotherapy. So that suggests to me that she may well have a postural drop. So she may well be hypothalamic in this instance and won't the moment, you know, she's hypovolemic and in the absence of any obvious heart failure just as we discussed earlier as an aside, the most reasonable thing to do, he would be to try and treat her hypovolemia with fluid resuscitation, working through the other ones. Yeah, she may well have an occult adrenal insufficiency. So, hydrocortisone, you know, you wouldn't do any harm, fluid restriction. There's certainly nothing here to suggest that this lady has any heart failure or syndrome of inappropriate anti diuretic corner and secretion. You certainly need a lot more information before you could make that diagnosis. IV Furosemide again, is there any indication here that she's fluid overloaded? And indeed, sometimes furosemide can cause hyponatremia to worsen. But that's more common with your thiazide diuretics and fixed rate insulin. Is there anything here to suggest that this lady is acutely hyperglycemic? No. So I'd say that the only reason, the most reasonable uh answer here, the only one that you have perhaps enough information to, to reasonably work off is fluid resuscitation. And this lady had a fractured hip. Now that I have seen a couple of instances in which this has occurred during my orthopedic placement. One was a lady who had some insensible loss is through a d hist wound. So she had a large open wound that ran down the length of her, her lateral thigh and she was losing a lot of both salt and fluid through that. So she had a relatively low urinary sodium, but she was that her urine osmolality was high as she was trying to retain it. And in another instance, we see this lady is in a side room. Why might be she she, why might she be in a side room? Well, frequently patient's come in on to an orthopedic wards. They're put on automatic codeine and automatic laxatives. Maybe this lady has diarrhea and there's insensible losses that way. That's accounting for the hyponatremia. I've deliberately not given you all the information here, but hopefully this question has sparked you to, to start thinking through those answers. DMV, potentially. Yeah, it's, you can't really work on a ward these days without some form of norovirus outbreak going, doing the rounds very reasonably here. That could be what's going on here. So I'm just, this question is more of a springboard to prompt you to practice working through those questions and seeing how even without all the information you can start to rule out through, through relative likelihood, what could be going on well done to anybody who got that right. And to those who didn't, I hope this was still a useful question to start prompting you to work through that question for the answer is a venous blood gas. Um This gentleman is on Metformin and glipiZIDE, which I had in my dastardly ways, hoped to trick you into thinking it was pretty was a confirmed type two diabetic. He may well have some latent onset autoimmune diabetes or he may well be a type two diabetic who nonetheless develops DKA with high ketones and high glucose like that. You would want to rule out acidy bia. So a venous blood gas here is very reasonable. Of course, later on a diabetic antibody screen to confirm diagnosis would be reasonable. Chest X ray to look for any infectious cause for this could well uh drive, drive that, but it's a venous gas that you'll need to confirm a diagnosis of decay and initiate correct treatment. And finally question five, this lady with what looks like a pretty excessive COPD history. So you could infer from that as you've been on lots and lots of prednisoLONE. Never really quite green being on a higher reasonable dose of prednisoLONE for a while present with what sounds like could be a chest infection, really low blood pressure, a relatively low cap glucose and hype on a tree mix. This should be ringing alarm bells for adrenal insufficiency, critical adrenal crisis. So which of the following is the most urgent initial step. As I said, it's the life saving treatment which is step one stat 100 mg of IV hydrocortisone. And you can see here that C and D are also correct, you know, eventually you want to give them fluid resuscitation alongside the uh the follow up hide records. So you may well also want to give IV amoxicillin. This could well be a chest infection. And for those of you who put 15 liters per minute, if you're doing, you're a to a assessment. Um Then of course, you'll be popping her on oxygen if her oxygen saturations are low. So grand if you're putting the, that's not necessarily a wrong answer. So that's all the questions. I hope that's all been useful. Um For any for, for going forward from here, trust guidelines will offer some very good general Izabal advice. Um Nice clinical knowledge, summaries. Actually, once you get your head around, it do offer some good workups for hyponatremia diabetes. UK, both for patient's and for, for doctors and medical students has excellent resources and well, a little bit of a plug mind the bleep if I may say so myself has some excellence, endocrine it, endocrinological endocrinology articles for you folks. So we'll um we'll finish it there, quick addendum session. Nine Olivia, am I right? And remembering that it's actually the 29th of March that the gastroenterology lecture is. Yeah, that's right. So this Wednesday, we've got cardiology and next Wednesday, which is another 29th will be gastro um if everyone can scan Glenn's feedback code and I'll also put like a link for it in the chat as well. It just be really useful and it really would. I I I'd really appreciate some feedback from you folks. Thank you so much. Um It's two minutes past eight. I think we've run relatively to time. Uh Thank goodness. Um I am more than happy to stay for another 5, 10 minutes. If um If anybody wants to ask any extra questions or go back, go back over any burning issues from the presentation. Thanks very much folks. I'll start having a look through the chat. So, um let's have a quick look through here. Could we please catch up on this and go back to this video, please? Uh I don't know what videos, sorry, what video I'll add, this is all recorded gun and uh content. So it'll be up in the next couple of days that people can rewatch it. Grant noise. Oliver Collins says, but you know, I mentioned that I am is preferred to IV hydrocortisone, an adrenal insufficiency as it acts like it's more about the half life and the rate at which it's used up if, when you're supplementing over that 24 hour period. Um The Endocrinology Society recommends that I am. Um if you're giving it over four equally spaced doses, um it just sits around a bit longer so that person is less likely to, to tip back into hypercortisolism. How lowered historic Atoby to prioritize this over the hydrocortisone? Do you mean how low would historic have to be to prioritize fluid resuscitation? Uh That's an excellent question. Um If you're strictly going through your eight, we approach you notice they've got a, a low BP. Uh Of course, it's very, very reasonable to, to, to whack up fluids, you know, start to keep them mechanically perfused whilst you whilst you come to your diagnosis. That the function of that question primarily was to, to ensure that you knew that stat dose of hydrocortisone was the life saving treatment. Yes, it's giving them fluid resuscitation will mask, will, will help correct that low BP. But the thing that's going to stop that process from happening um and reverse it is giving them a hydrocortisone. So yes, very reasonable to walls that you may well want to prioritize that the fluids depending on how you work them up. A couple of questions from Emma cutting. When do you consider using treatments such as bisphosphonate or denosumab in the hypercalcemia? Great question. Um to give a, to give a, I suppose a session focused and albeit slightly flippant answer is as a foundation year to doctor and for anybody who revise is for their finals. Um It's not something you need to be considering. Um the monoclonal antibody and bisphosphonates should in the instances of hypercalcemia and refractory hypercalcemia um driven by perhaps malignancy. This should be at least a registrar endocrinology decision. But it's absolutely fantastic that you know about those things. I do not think that a finals question should ever ask that. But if you know about it, it's certainly something that you can raise for ongoing management in patient's. Perhaps you have refractory hypercalcemia. Excellent. I was told the graves' disease can result with hyper hypo and euthyroid state as the eye disease specific to graze and it doesn't move on thyroid just in case. So, Graves disease, um, it can fluctuate, Olivia. You may well know the answer to this question. Is there a specific pattern in which the, the thyroid hormones drop and rise in response to two Graves disease? Um I've really not done that much. Enter Crown in my foundation programs. Oh, sorry. No, basically covered. Kind of the basics that you've covered throughout this uh, would struggle to answer. I no worries, no worries till and I don't know the answer to that. I do know that it can fluctuate and throughout the course of disease, it can drop and then rise. There may well be an initial spike but grazed it and then a drop. Um I don't know specifically for the answer that question. I do apologize. But if, if you do find out, please um please send us an email and let me know that's a good question. Um Could I mention again what we need to look at for steroid use? Um I'd say that asthma and COPD approach. When it, when it comes to long term communal use of steroids, even an inhaler can trigger adrenal insufficiency, chronic rheumatological and inflammatory diseases. So potentially, I'd say potentially inflammatory bowel diseases, Crohn's or ulcerative colitis, rheumatoid arthritis, aids, arthritis, vasculitis, things like lupus. Um I'd say any condition that is managed with anti inflammatories by which I mean, steroids specifically could Welchol cause it when it comes to somebody with lupus or quite significant arthritis or Crohn's disease. The steroid use will be excessive and people that will trigger the red flag, what I would say is the caveat to that question is people don't tend to think as the steroid use. Um uh in asthma and COPD is as particularly high. Um But it is every day and it could be life long. So I'd always have a low threshold of suspicion in people with asthma or COPD long term accession. Um Yes. So the mechanism by which it, it's suppressed is that you're giving the body steroids which acts. So even though the body didn't make them, the hypothalamus and pituitary still register them. And so that negative feedback loop causes drop, which event which causes a reduction in the stimulation of the adrenal glands, which effectively, if you get, if you do it long enough or high enough levels will effectively send the adrenal glands to sleep. So that when you remove that exogenous steroid or when the body becomes acutely unwell. So that's it requires an acute rise in those steroid levels. The adrenal glands cannot provide it. They're, you know, they're on holiday, they working grand and I'll answer one more question cause we're coming up to 10 past, what are the long term risks of taking bisphosphonates like alendronic acid? Um I can give you a brief overview of that question as a final answer. Um It's more of a meds management question. Um So the I would say that when it comes to significant risks, the first one that I suppose we should all know about is the risk associated with the administration specifically of oral bisphosphonates can cause burning inflammation, horrendous, um osteonecrosis of the jaw there when you take it. So when people take an all bisphosphonate, they should take it with plenty of water and sit upright for 10 minutes, 20 minutes, maybe even half an hour to make sure that that tablet has made it safely into their stomach. If there's any chance it could stick in their esophagus, then it can irritate caused really quite catastrophic damage. Um The second main one, of course, uh I think that we should know about is yes, bisphosphonate to reduce the long term risk of fracture. And remember, there's bisphosphonates can be used endocrinologically speaking to long term reduce hypercalcemia. Um And then there's the more common use of bisphosphonates, which is in people with osteoporosis. And you want to maintain their, their, their bone modeling and the bone structure by by inhibiting osteoclastic activity. Um whilst bisphosphonates do reduce the risk of a fracture, um if you do happen to fracture your hip, for example, when you are on bisphosphonates, the chances of that being quite a bad fragility or uh I suppose atypical fracture are quite high because the normal bone remodeling, plastic and plastic activity constantly keeps the bone healthy and forming nice lamb alone. Nice trabecular structures. Um And when bisphosphonate inhibit that, yes, the bone is set in cement but it's not going to remodel and stay healthy. It may well be strong but it may well not be structurally sound. And so in those instances, when you do fracture, it may well be all the nastier fracture for it. And bisphosphonate fractures do have to manage slightly differently. Um So bisphosphonate, reduce your risk of fracture, do not necessarily reduce your risk of atypical fracture. Um I hope that answers your question, Jonathan Bruce. Um I think we shall leave it there folks because it's getting 10 past and you've certainly done more than your fair share of revising this afternoon with a fairly intensive our in 10 minutes of endocrinology revision. Well done folks. I hope this was useful. Please do fill in the feedback form cause I'm constantly trying to, to improve these sessions. We'll leave it there. Thank you so much. Enjoy your evenings and good luck with your upcoming, your upcoming exams and your foundation here. Thank you. Thanks Glenn. That was really useful. I think we've definitely all learned something.

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