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Hi guys and I think you might be muted. That's so sad because it was such a good intro. Hi, everyone. Welcome. Good evening. Um, to our endocrinology road to final session this evening. Thanks so much for coming on if you're here live and if you're not. Hi. And from the past, I guess my name is Anna. I'm an F one at Manchester Infirmary and I've got with me, Tess. Um I'm a, an F one at Conquest Hospital in Hastings. Um We've got 10 lovely MC QS to go with you. Um, Tess is going to start us off with the first five and there's obviously a very huge topic, so we've not hit every single thing we could possibly hit. And it's to be honest, mostly at least my questions, I didn't have to look through tests as well, mostly focusing on um sort of management and that kind of thing. So we won't get into the nitty gritty of physiology and things just because this would go on for two hours and I'm sure no one wants to do that on their Thursday evening. So, um, we'll try to keep it as succinct as possible. Um, so we're Thursday. Well, we were originally called Thursday 15. We're now mimetic teaching. We host a sort of teaching session every Thursday, usually about an hour long where we go through different topics and it's all on demand. So, if you go through our metal account, we've got loads of different videos on loads of different topics. I think most recently we had a gastro session on Tuesday. Um, and the next one I think is Peds next Thursday as well, but you can always check out our Instagram account. I try to keep it updated as much as I can um or just follow us on medal and you'll get the exact dates. Um So is everyone ready to go? Can everyone hear us? Ok. Are we ready? That's good. All right. Next slide then please test. Um So yeah, I forgot to mention this is mapped to the UK MLA curriculum. So it should be quite comprehensive for what comes up in med school finals and how it works is we'll give you a minute for each M CQ and then at the end we'll go through each answer and sort of cover the topic surrounding the M CQ as well. Ok. Are we ready to go? First question? Next question, please? Tess I'm just going to read it out as well. A 65 year old female presents to her GP, complaining of weight gain weakness, bruising and low mood. She has past medical history. Of COPD, 20 pack year smoking history. She takes salbutamol PRN on examination. She's a round face, central obesity, bronze, pigmentation of the armpit and bruises on her arms and legs. Her BP is 160/100 and 37 and her blood sugar is 13. Given the most likely diagnosis, what investigation will be most useful for determining the underlying next slide, please. Tess 45. 0, sorry. That's my timer. 45 year old male seen in the renal clinic for treatment resistant hypertension. He's made a positive lifestyle changes and is on optimal antihypertension medications. He's otherwise fit and well. Although does complain of some regular headaches. Examination is unremarkable bloods are as follows. And what is a podcast? Most likely to show next slide, please test 35 year old female seen by her GP for frequent urination. She denies any dysuria or hematuria and reports that she is thirsty all the time. She has a past medical history of bipolar disorder. She takes lithium. Her blood are as follows. Her urine dip is negative glucose and blood in nephrogenic diabetes inhibitors. What will the desmopressin stimulation test? Show next slide. Please test 37 year old female seen by her GP for anxiety. She describes frequent headaches, anxiety, palpitations and sweating. Past medical history of significant for neurofibromatosis type one on examination. She is found to have a tremor heart rate. 114 and BP. 151/100 and 20 bloods are as follows. And what is the first step in managing? Next slide, please test a 32 year old female presents to a GP with a six month history of lethargy weight gain. She's also noticed she's losing more hair in the shower than usual. Her vital signs are as follows. Heart rate. 58 BP of 100 and over 71 temperature of 36 7 under respirate. 20. Clinical examination reveals a loss of the outer road of the eyebrows and periorbital edema. Blood test results reveal a high TSH and low T three and T four which antibody test is most likely to be positive in this patient. Next side please. Ts 67 year old male presents to A&E with nausea, vomiting confusion. He has a past medical history with type two diabetes, hypertension, peripheral vascular disease. He initially was suffering from the flu which seemed to resolve a week prior, but he has since deteriorated again. Vital zero as follows heart rate of 102 BP of 99. Over 64. A temperature 36 4 and a respirate of 28. An ABG is done which shows the following which of the following medications is likely to have precipitated. The above presentation. Next side please, an 82 year old woman presents with confusion and disorientation. Labs reveal persistently low serum sodium despite normal saline administration examination findings show that she's well perfused has moist sperm rings, non raise JVP and no signs of peripheral edema. Her medical history is significant for congestive heart failure but no diuretic use which of the following suggests a diagnosis of si DH. Next time, please. 67 year old male presents to A&E with nausea, vomiting, confusion, past medical issue with type two diabetes, hypertension, peripheral vascular disease. He's initially suffering from the flu which meant he was not able to get his repeat prescription from the pharmacy. Vitals are as follows heart rate. 102 BP of 99 of 64 temp of 36 4 and a respirate. 23 an ABG is done which shows the following which statement is false about the fluid deficit. And HHS next slide please. 24 year old woman presents to a GP after not having her period for the past six months. Past medical history of celiac disease and asthma on further history taking the patient real. She's also been suffering with tiredness, irritability and has lost 5 kg in the past three months. Unintentionally, vitals are as follows heart rate of 100 and two BPM, irregular BP of 100 and 39/91 temp of 37 respirate of 15 and oxygen starts 100%. Which of the following would suggest this patients symptoms are specifically due to the presence of anti TSH R autoantibodies. And I think that's all the questions. Absolutely. Ok. So we're gonna now go through the questions and it'd be amazing if you guys could put in the chat once you hot. Um But don't worry at all about being right. That's the whole point of, of this talk. Um And then basically, we're gonna use each question as a little springboard to look up certain conditions in within endocrinology. Um So for the first question, if people could just put in the chat before we think about how we're gonna manage this patient, what diagnosis do we think is the most likely here? So we've got someone that's been unwell for a few days but has now come in sort of confused. Um They, they've got high heart rate, low BP, low sugars. And if you look at their bloods, we've got high potassium and low sodium. Has anyone got any ideas what might be going on here? Ok. Um We'll move on. So, um what I'm trying to get out with this question is that the most sort of likely um diagnosis? Um Let me just sorry, my computer's frozen is an Addisonian crisis. So they've got tummy pain, they've got the low sodium, they've got a history of um like sort of family history of autoimmune conditions and they were a bit unwell in the preceding few days. Um So what answers did people put for managing this patient? Did they think insulin maybe bit of glucose if we've got the low blood sugar fluid antibiotics or hydrocortisone. Ok. Um So first question, most important sort of urgent thing is we need to give the patient a hydrocortisone that's gonna rev reverse the Adison crisis and fix a lot of the other things. Um As part of treatment for Aerian crisis, you absolutely do also give IV fluids. Um But if you look, this patient is reasonably stable, it's a young person so that BP is not super, super low. The, the capillary refill is OK. So the first step of the algorithm is getting that IM or IV hydrocortisone in, OK. I've sort of bolded all the things in the question that lead us to thinking it might be an Addisonian crisis, especially that low sodium and the the tummy pain, the low sugars, that's all quite suggestive of Addisonian crisis. Um So if we just take a step back and just remember what the steps are in the adrenal axis. So, in your hypothalamus, you have um C Rh and that stimulates the um production and release of ACTH adrenocorticotrophin. Oh, what's the word adrenocorticotropic hormone from the anterior pituitary? And that's gonna cause you the release of your cortisol, your stress hormone from the adrenal glands and the cortisol will give negative feedback back to the brain to reduce the pathway. Um So it's life and it's really helpful in endocrinology. If you remember what the hormone does, then you can think about what's gonna happen if there's too much of it or not enough of it cos it will literally just be sort of a plus minus effect. So, thinking about cortisol, um it's the stress hormones, it's gonna increase your alertness, increase your blood sugar and your metabolism, getting you ready for thi doing things, it's gonna suppress your immune system and it also suppresses your osteoblast activity, which is important when we think about um when we have too much of it because that can cause osteoporosis, aldosterone. We'll talk about the pathway that causes release of aldosterone in a bit. Um But it essentially causes you to keep all your sodium in which keeps your water in it and increases your BP um in Addison's which we're gonna go on to. You don't have enough out um aldosterone. So you're losing all your sodium and you end up with a low sodium. Ok. The adrenal gland also produces um sex woman D hea and also epinephrine, which causes your sympathetic response, which we'll talk about in a little bit. Um So I just go to the next slide, adrenal insufficiency. That's what we were talking about in this question. That's a broad umbella term for when you're not having enough of your steroid hormones. So your cortisol and your aldosterone, um and when you have insufficiency, you need to replace them. Addison's disease refers to primary adrenal insufficiency. They've got a problem with the adrenal glands usually autoimmune in nature. Secondary is when you have a problem with the pituitary. So you've not got enough ACTH being produced maybe due to a tumor or radiotherapy. Um, and then tertiary is just the next level up of the axis. Quite easy to remember. It's a problem with the um, hypothalamus. Usually it's long term sort of oral steroids are causing negative feedback on your hypothalamus and you're not producing your C Rh adrenal crisis or Addisonian crisis, which we had in the question is your acute severe adrenal insufficiency. And that's a life threatening emergency. So it's really important um that we know how to um sort of treat that in the first instances. And like I say, the mainstay of treatment there is give them the hydrocortisone to replace it um and give them fluids and then correct things like sugars and electrolytes as you go along. And this is just a little bit of an overview of what symptoms people might have. Can you have someone in the chat mind just letting me know, have I frozen if Tess has disappeared for everyone else or is it just me? Let's see if I can get the slides up. I don't know if anyone can hear me. I'm here. I, I've reloaded the web page. Can you hear slash see me? You're back with me. I don't know if that was me or you, but Ting says it could, it could be me. It really could be me. I'm using safari and it like that. But it didn't like chrome either. Ok. I'm hoping everyone can hear here and see both of us now. Um, so I was just going through adrenal insufficiency. So if it happens over a longer, um, amount of time, you don't get this crisis, um, then your symptoms can be broken down by the sort of hormones affected. So you might have, when you have low cortisol, you might have fatigue, weight loss suppression cos remember it's your stress hormone, it's making you alert. So it's gonna do the opposite. Um When you have low aldosterone, um you're gonna have the low sodium which is gonna cause muscle weakness and cramps, dizziness, fainting. Um, you might be craving salt. Um You might have tummy pain, nausea and vomiting. Um And then if it's an adrenal problem rather than, you know, pituitary or hypothalamic, you might have low DD hea as well. So you might have reduced libido. Um And in Addison's because um there's sort of no negative feedback to the brain, you're gonna be producing lots of the um the higher hormones including ACTH and that causes bro's hyperpigmentation cos it stimulates, stimulates your um melanocytes. Ok. But you wouldn't get that in a problem where there's not enough ACTH, for example, um I was only in crisis like we said, you've got your reduced consciousness, your low BP, low blood sugar, low sodium and maybe high potassium. Um, investigations wise, your routine bloods might have already sort of led you down this path. And then the first sort of quick screening test you can do is an early morning cortisol. Um, although that's often actually falsely normal. Um, the next test you're gonna do is your short synacthen test. Whereas basically you use synthetic ACTH, um, which in a normal body should stimulate a doubling of your cortisol level. It, if, if it doesn't, then you've got some sort of adrenal insufficiency. Um, It might be a primary insufficiency is a problem with the adrenals, cos you're not responding to the ACTH or your adrenals have atrophied in secondary insufficiency so that they've become so used to not producing stuff that they are no longer able to essentially. And then you can look at your ACTH levels to distinguish between those two issues. Um a bit further down the line. You can also do autoantibodies to look at the autoimmune causes of the adrenal problem and you might CT or MRI the glands or the pituitary to see if there's a problem. Replacement is just um the main, sorry, the main part of management is just replacement and you're gonna want to double your doses during illness because that replicates what the body would naturally do. Um And they're gonna need a steroid card or some sort of ID to that. Healthcare professionals know not to stop their steroids. And we've already talked about the emergency protocol a little bit. Um Your adrenal crisis might be your first presentation of adrenal insufficiency or it might be triggered by some sort of infection or, or trauma. So, if you're suspecting it, but you don't know for sure, just start the treatment, um, while you're waiting for the investigations. So, if we go on to question two, this is a patient, um, complaining of weight gain weakness, bruising low mood, a bit of a smoking history, a bit of chest problems. Um, and then on examination, they've got rounding and bruising and that bronze pigmentation we've already talked about. Um So has anyone got any ideas of what the most likely diagnosis here is and or what investigation they would find most useful for determining the underlying cause of that diagnosis? If I say the diagnosis is Cushing's Syndrome, does anyone have any suggestions on how we might find out what's driving the Cushing's Syndrome? It's OK. It's been a long week for me too. Um So if we just go here, so just a Cushing disease. Very good. Um So it's quite a typical presentation of Cushing's disease, that sort of rounded face, central obesity, the bronze pigmentation again here is caused by um high ACTH levels. Um And unlike the last case where there was low BP and low blood sugar, we've got high everything because we've now got too much cortisol. Ok. Um We're gonna go on to the tests um on the next few slides. So I'll go over that a bit more. So, Cushing's syndrome is when you have too much, um, cortisol and the other glucocorticoids. Well, that's the main one. Um, and it's, it's not quite the opposite of Addison's cos you don't have aldosterone involvement but a lot of the symptoms to the opposite, um, causes are a pituitary adenoma. Um, that's secreting ACTH, that would be Cushing's disease specifically, um steroid use. So, oral steroids, etcetera, um, an adenoma of on one of your adrenal glands, um or one that we need to rule out is paraneoplastic syndrome. Um very commonly small cell lung cancers can be producing the ACTH. Um So if we identify Cushing's Syndrome in someone, we now need to figure out the cause the symptoms that might sort of lead us to thinking it's Cushing's syndrome can be visible as seen in this diagram, including proximal muscle wasting where they can't get up from a chair without using their hands. Um And it on it sort of examination. Um You might find that they've got hypertension. Um the sugars and stuff might suggest they've got diabetes, bloods might show dyslipidemia, they may have osteoporosis or even and even cardiac hypertrophy and then psychologically um excess um C um cortisol is gonna potentially cause anxiety and depression, insomnia, cos they're staying alert and rarely psychosis. So, in terms of investigations, I find these really hard to remember. So I've tried to lay them out as clearly as I can. Basically the m the the big biggest part of the investigations is dexamethasone suppression testing. If we think back to the pathway, um, steroids. So, cortisol in the body or dexamethasone that we're giving exogenously should suppress, um, give like negative feedback to the whole access. So, in a normal person, if you give them the dexamethasone, um I think it's, it's around 10 or 11 pm in the evening, the next morning at nine ama normal person would have no cortisol. Ok. Um But in, in any cause of Cushing syndrome, it's going to be high or rather not suppressed just normal. Ok, then if we, we wanna confirm that we, it's very likely Cushing's syndrome. We can use the low dose 48 hour dexamethasone suppression test. So they take um a very small dose of dexamethasone every six hours for eight doses starting at 9 a.m. on day one when you check the cortisol and then you check again on day three after the last dose. Um Now you're not gonna suppress the cortisol production if it's being produced by the adrenal gland um or by an ectopic ACTH, but you would be able to suppress a pituitary adenoma producing um ACTH. Um So now we're left with, well, is it adrenal or is it ectopic? And that's when we do the high dose 48 hour test. Um because using a higher dose of dexamethasone can suppress the adrenal adenoma. Um Let me just check thyroid that right. I think I might have just said that wrong. The high dose 48 hour test will suppress cortisol if there's a pituitary adenoma. Yes, I was reading the table wrong apologies. It will suppress a pituitary adenoma. Um, but it will not suppress an adrenal adenoma like a topic ACTH. So the high dose test distinguishes if it's a pituitary adenoma or if it's one of the other causes and then we can look at the ACTH level to see if it's an adrenal adenoma or something to do with the ACTH apologies. If that was confusing, I can go over that again and now I've got my brain turned on. Um So you combine the dexamethasone suppression test with the ACTH levels to figure out where the problem is along the axis. You can also do the 24 hour urinary free cortisol. Um If you can't, for some reason, do a dexamethasone suppression test, if it doesn't sort of indicate the cause, just shows if you've got high levels of cortisol being produced in the body, um your bloods um will show probably a high white cell count um and low potassium. If you've got an adrenal adenoma, that's secreting excess aldosterone imaging, that's useful MRI brain to look at the pituitary CT chest to check for cancer like small cell lung cancer and maybe CT ABDO as well. Management is gonna be removing the underlying cause. Um And then if that's an adrenalectomy, you might need lifelong steroid replacement. Um Another option is metyraPONE which reduces production of cortisol by the adrenal glands. But usually it's just remove the cause and replace if needed. Yeah, if everyone's happy with Cushing's syndrome, I'm gonna move on. Yeah. So question three. Does anyone have a suggestion for what the diagnosis is before we look at the blood gas? So this is a young person with treatment resistant hypertension, experiencing headaches but examination otherwise unremarkable. No real past medical history, slightly low potassium and high sodium. Um and otherwise of normalish gloves. Ok. So, this patient from their presentation is quite likely to have Conn's Syndrome. Um and in Conn's Syndrome for most, more broadly, hyperaldosteronism, you get a metabolic alkalosis and we're gonna talk about why. So, aldosterone is part of the re renin or renin angiotensin aldosterone system that responds to the BP if it's low. Um your kidneys are gonna sense that in the juxta glomerular glomerular cells in the afferent arterioles and they're gonna stimulate more production of renin. Ok. Renin is gonna stimulate the conversion of angiotensin in the liver to angiotensin one, which will then go to the lungs and be converted by ace into angiotensin. Two angiotensin two is then gonna work to increase your BP by three methods. Vasoconstriction, cardiac remodeling. So, more to allow more pumping and aldosterone release. And we talked a bit earlier about what aldosterone does. Does anyone remember what it does in the kidneys specifically about sort of sodium and water causes water retention and sodium absolutely very good. Um So if we go to this next slide, so the main way it's gonna affect BP is by reabsorbing sodium in the distal tubules of the kidneys, which means you will then also reabsorb more water and you're, you're more filled and then you have a high BP. Um So that contributes to this sort of pathway here by filling you more. So you've got angiotensin two is gonna cause squeezing of your vessels, pumping of the heart and retention of water by aldosterone, you then get the high BP and that gets negative feedback to running. So it it can sort of balance out um as well as that aldosterone is going to increase potassium secretion in the distal tubule and also hydrogen secretion um from the collecting dots which is gonna affect your ph hyperaldosteronism. Aldosteronism when you have high levels is when you have high levels of aldosterone, it actually accounts for 5 to 10% of hypertension. It's the most common cause of secondary hypertension. And Conn's syndrome specifically is when you have hyperaldosteronism due to an adrenal adenoma. Mm, the main presenting feature of hyperaldosteronism is hypertension. You often have no other symptoms or very sort of vague nonspecific symptoms like headache, weakness, fatigue, your bloods are gonna show a high sodium and a low or normal potassium sometimes. Um and you're gonna get a metabolic alkalosis cos you're secreting all of your hydrogen. So that was the answer to question three. In this case, it as it's the most common cause of secondary hypertension. You need to test for it in young patients with hypertension. If you've got a patient where treatment's not working or if the patient has also has low potassium cos that can be sort of a clue for you. Um Conn's syndrome is sort of one key cause, can anyone name any other causes of hyperaldosteronism? I know I'm gonna get used to answering the questions. Don't worry. I'm just joking. Oh, no, please is the reason I didn't come to this one. These are hard to be fair. I didn't even know all of this for finals. Like you keep learning when you get into F one. So primary causes where you've got adrenal overactivity, you're producing too much aldosterone. Um Most commonly would be a bilateral adrenal hyperplasia. Um You can also get adrenal adenoma con syndrome and more rarely familial hyperaldosteronism. Secondary hyperaldosteronism is caused by excess renin production, which might be due to renal artery stenosis, heart failure or liver problems. Um Basically, you have a disproportionately low BP in the kidneys. So you're producing lots of renin and that's producing lots of aldosterone, but it's not really helping the renal artery stenosis at all. You're gonna investigate by looking at the aldosterone to renin ratio. The A RR in primary, you'll have high aldosterone and low renin cos the there's negative feedback on the renin. But in secondary, they're both high because there's no feedback going on. The renin is independent. You, they might do a CTR MRI to look for adrenal tumors or hyperplasia. A renal artery Doppler or a CT angiogram or MRI angiogram to look for stenosis. Um And you can also do adrenal vein sampling um to see if what one gland is producing more than the other. Um But then essentially, once you've figured out the underlying cause, the treatment of hyperaldosteronism is to treat the underlying cause. So, remove the surgery, open up the stenosis, et cetera. You can also give aldosterone antagonists, something like Aleen or spironolactone. Um And they should counteract the aldosterone. Ok? Please feel free to put any questions you have in the chat as we go along or if I haven't explained something. Well, I can try and say it again in a different way. Um But we'll move on to question four for now. So this is a patient with frequent urination but no other urinary symptoms and thirsty all the time. Um Her medication is lithium and her bloods, you can see for yourselves, she's a little bit salty in her blood and has very dilute urine and thinking about differentials the HBA1C and the urin di don't suggest sort of diabetes as the cause of your polyurea polydipsia, uh diabetes mellitus. That is, and they also don't suggest um like a urinary tract infection. So this is a case of diabetes insipidus. Um And then the question has decided to go for nephrogenic diabetes insipidus. But there's also something called cranial diabetes insipidus, which is probably what this patient would be more likely to have with their lithium. Um So, has anyone got any idea what a desmopressin stimulation stimulation test is and what it might show in nephrogenic diabetes insipidus? I think I'll move on just on the interest of time. Um So we're gonna go through, you know why? But basically, they're gonna have low urine osmolality. So very dilute urine after desmopressin has been administered, I'm gonna look up why in a second. So again, taking a step back, just reminding ourselves of what the hormones do so that we can understand where the problem is. ADH antidiuretic hormone is produced in the hypothalamus secreted by the posterior pituitary gland and it causes water reabsorption. So stop pee don't stop the water going water reabsorption from the collecting guts in the kidneys. Um I think Anna's gonna talk about sa DH a little bit later, but that's basically when you have too much A DH. So you're absorbing too much water and we're gonna talk about diabetes insipidus now where you haven't got enough A DH. So you're not absorbing your water, you're peeing a lot. So you're gonna have very dilute urine and, and potentially concentrated um blood. Um And if you've got concentrated blood, you're gonna wanna dilute that. So you're gonna be feel thirsty. Ok. A problem with ADH can be pinned down to two pro places. You can either not be producing enough um in the brain. So that's cranial diabetes, insipidus or your kidneys might not be responding to the A DH nephrogenic diabetes insipidus. Ok. Um Problems in the brain can be anything can be idiopathic or brain tumor infection surgery, genetic mutations, wolfram syndrome and then nephrogenic wise um could be caused by uh so medications in my notes, I've here written here lithium. So that that would actually be nephrogenic. I was wrong apologies, hypercalcemia, hyperkalemia, and any kidney disease like polycystic kidney disease can cause nephrogenic diabetes and syphilis. I wonder if anyone remembers like the other name for A DH at all. This is not this very confusingly because in medicine, you just can't have enough names for things. Absolutely. I don't know. II kind of prefer this name actually for ADH um vasopressin, which is useful because has just mentioned that vasopressin is what we use to test for diabetes. And so it's just something to link in your brain, they're related. Absolutely. That's it's very helpful to know like various different names because sometimes the names tell you exactly what it does. Um There's another condition that I haven't put on here that might cause polydipsia and polyuria that's called primary polydipsia where you're, you've got excessive water consumption, but there's nothing wrong with your A DH system. So you're gonna have a, a euvolemic hyponatremia, low sodium, but you're also gonna have dilute urine. So everything's diluted because you're just drinking lots and peeing lots. Ok. So diabetes insipidus specifically, um, it's gonna present with polyuria, polydipsia, you're gonna feel dehydrated and you might have postural hypertension because peeing so much of your water out, your serum osmolality will be high or normal, potentially if you're drinking enough to sort of maintain it. Um And your urine osmatic low dilute. If you, they, if you decide to do a 24 hour urine collection, they're gonna produce more than 3 L over 24 hours. But the diagnostic test is gonna be a desmopressin stimulation test, which is also known as the water deprivation test. Um So you basically d deprive the patient of fluids uh for up to eight hours and then measure their urine osmolality. Um You and I would then have very concentrated urine. Um But in diabetes Insipidus, they're still going to have the dilute urine that they were having before. It's not gonna respond to water deprivation. So, if you've ruled out diabetes insipidus cos they've got um high urine asthma. Great. If not, you're gonna give your desmopressin, desmopressin. Um Pretty sure is just a synthetic version of A DH. Yes, synthetic A DH. Um And you're gonna then measure the urine osmolality over the next 2 to 4 hours to see if there's a response in craning your diabetes insipidus. It's just that you're not making enough. So if you give fake um A DH, your body is going to respond and you're gonna start concentrating your urine by reabsorbing the water. In nephrogenic diabetes, insipidus, your kidneys aren't responding to the A DH. So even if you give synthetic A DH, your kidneys won't respond. So your urine osmolality will remain low. Ok. Which is, I think what we had in the question, management wise, as with all the conditions we've gone through so far, you're gonna try to address the underlying cause if you can. So if it's caused by medication, stop that the tumor drop it out. Um Conservative management can work in more cases. Um And then in cranial diabetes, insipidus, you can give desmopressin to replace um the A DH levels, nephrogenic diabetes, insipidus is a bit harder to treat. Um, the endocrinologist will lead this, but they might suggest, you know, high water intake, high dose des desmopressin prescription thiazide diuretics and things like nsaids, but it's a lot harder to treat. Um, ok. We're on my last question. Then I'll hand over to Anna. So question five, this is uh an anxious lady having headaches, anxiety, palpitations, sweating. She has something called neurofibromatosis type one. Um A tremor, high heart rate and high BP, blood's actually kind of normal apart from the plasma metanephrine, what do people think might be going on here? And or how would they try and treat this? Excellent. Someone suggested pheochromocytoma, which is spot on diagnosis. Um How would you manage a phaeochromocytoma? I'm glad that no one said like thyroid because that was sort of my, my trick differential that people might jump on it. So management of phaeochromocytoma, the first sort of step is gonna be an alpha blocker like doxazosin. Um I've highlighted the sort of key parts of this question that are leading us to that diagnosis, but we're gonna talk about the presentation now. So pheochromocytoma is a an adrenaline secreting adrenal tumor, usually noncancerous. Um and 10% of them are cancerous and 10% are also bilateral. The chromaffin cells of the um adrenal gland, they produce excess adrenaline which is released in bursts and gives us intermittent symptoms of anxiety, sweating, headache, tremor palpitations, hypertension, tachycardia. Basically everything that you want the adrenaline to do in sh in a sort of a stress situation where you need to fight a bear or a man in the woods, but it's doing this uncontrolled. Um In burts 30 to 40% are genetic. I've put them sort of the common causes here. And in our question, it was a patient with neuro bromone. I can't speak today. Neurofibromatosis type one. Ok. Um Adrenaline is a catecholamine. Um You also got um sort of other names for it. Uh Noradrenaline or Epinephrine and norepinephrine if you're American and it's basically a fight or flight. So in chroma, you can look at the plasma free metanephrines which is the sort of metabolic breakdown of your um adrenaline. Um and they have a longer half life because the actual adrenaline is only gonna be in your blood for like a few, a few minutes. So it's not gonna be reliable if you test that at a random point in time. But your metanephrine um is gonna stay around and be helpful to measure. And you can also measure um 24 hour urine catecholamines. So, catecholamine is the umbrella term for adrenaline and noradrenaline. And you can capture um how much is being released in the urine to sort of measure how much might be being produced in the body. Ct and MRI can help you visualize the physical fair chromosoma tumor. Um And you can do genetic testing if you wanna think about a genetic cause management, like I said, is alpha blockers. First, the next step is then beta blockers and then surgical removal. Catecholamines work on both alpha and beta receptors. The their effect on alpha receptors is that they cause vasoconstriction whereas beta receptors cause vasodilation. So when you've got the effects on both receptors, it can kind of even out. But if you use beta blockers before you've given someone an alpha blocker in fair chroma cos, you want to reduce the heart rate, for example, um then the unopposed alpha mediated vasoconstriction can lead to a hypertensive crisis or pulmonary edema. So you always need to make sure you've blockaded the alpha receptors first with doxazosin or um, phenoxybenzamine, then you can start giving them beta blockers that's safe. And the reason we do all of this before the surgical removal, um is to make sort of anesthesia and surgery safer because you're gonna have a fight or flight response to having surgery. Um, and you don't want that to be uncontrolled. So we, we try and control all their symptoms medically first and then chop out the tumor when it's safe. Um, but like I said, it's usually noncancerous, um, producing g brilliant, if anyone's got any questions about the topics I've covered, um, hit me up in the chat, but I'm gonna hand over to Anna now for questions 6 to 10. All right, let's go then question six. A 32 year old female presents to her GP with a six month history and you and weight gain. She's also noted that she's losing more hair in the shower than usual as follows, quick, very quickly. Before I do this, I'll send out the feedback form in case anyone needs to drop out. Now, it would be really, really useful, um, for you to fill that out. It really helps me in tests, um, and us as an organization to see how we can better improve our sessions. Otherwise, if you've got a few more minutes to hang on for the rest of the session, um, that would be really great and we'll continue. Um, otherwise it will be on demand like I've said before. So don't worry if you can't say it's the end of the end of the session. But please do provide us feedback if you've got a spare couple of minutes. So, um we have um, so kind of a little bit bradycardic, I would say 58 not quite 58 BPM, BP touch low. Um temp normal respirate just about right. Um We've got some weight gain and lethargy loss of the altitude of the eyebrows. Um T TSH is high, T three and T four are low. Do we know what kind of diagnosis I'm trying to get at here. Anyone in the chat if anyone's still around. So I'm trying to get at, oh we've got someone and hyperthyroidism. Amazing. Thank you so much. Um So does anyone know which antibody test is most likely to be positive in this patient? I know this is someone, this is something that really got me confused in that student because there's so many different types. Um which is why I really wanted to just go over it in the case of um hyperthyroidism in the West. The most common cause is Hashimotos. And in that case, next slide, please, the answer would be dear antithyroid prostates. If it comes up on the next slide, I don't know if it's just my internet or not. Yeah, perfect. Next slide again. So we'll just quickly go over to our favorite. Um hypothalamic pituitary thyroid axis. So the hypothalamus, oh, no worries. Test the hypothalamus releases a thyrotropin releasing hormone which stimulates the anterior pituitary gland to release thyroid stimulating hormone, which then stimulates the thyroid gland to produce T three and T four, which is um very, they're very important hormones in your, in the regulation of your metabolism. Um T four particularly increases is the active form. Um T FTF for sorry, it's a pro hormone, but we've got 14 times more T four than T three in our body. And um T three increases the basal metabolic rate. It affects protein synthesis. Um It helps regulate long bone growth neuromata and increases the body sensitivity to catecholamines. And if we just put that in context of, well, what does it mean when our thyroid hormones are high or low? We can go to the next slide so we can get some hypothyroidism, which is what we were seeing with a lady in this question. Some weight gain, fatigue, bradycardia, cold intolerance, constipation, depression, mental fog, impaired memory muscle weakness, dry, coarse hair and skin, which makes sense if we slow down our metabolism all the way down, this is what we will inevitably get. Um And if we speed everything up, increase our metabolism, we'd get some weight loss. We'd be paradoxically the fatigued or hyper excitable. I mean, you can see how that would be if we're constantly feeling like we're on the go, we've got palpitations, tachycardia that can tire someone out or it could make us hyper excitable or and would be associated with mood changes like anxiety, irritability, insomnia, mood swings. Um we could suffer with some heat intolerance, diarrhea, diaphoresis and I sort of hinted to it earlier. Um where I suggest that the most common cause of hyperthyroidism in the West um is oh hashimoto's and um the most common cause of hyperthyroidism in the West is graves disease. Um Whereas in the developing world, it's an iodine deficiency next slide, please. Um So this, it takes a while to sort of get your head around this diagram, but once you get, it feels good, you've got um which different antibodies are related to which disease. So there's obviously an overlap, um which is annoying. But um basically, we've got thyroid peroxidase antibody and hashimoto's thyroiditis, which is present in 90% of people who have hashimoto's and 75% of Graves disease. Um And then we have our TSH receptor stimulating antibodies which are mostly present Graves disease. Um 90% to 100%. And then our thyroglobulin um antibodies on the top, right, which we can see 70% in Hashimotos and 30% in Graves. And sometimes you can see it in um thyroid cancer as well. Um And tess kind of alluded to it in her when she was talking about primary hyperaldosteronism and secondary hyperaldosteronism. It can sort of be applied to any endocrine disorder really So primary, any primary endocrine disorder is going to affect the gland that produces the hormone that we're talking about. So, in that case, primary hyperthyroidism would be affecting the thyroid gland. Um secondary hyperthyroidism doesn't even know what that would be affecting. Say, hypothyroidism doesn't remember would be affecting the anterior pituitary and then tertiary hyperthyroidism would be affecting the hypothalamus. You just take a step back and a step back and a step back. Um Great next slide, please. Oh yeah, just quickly. Um We've got hyperthyroidism. Some of the causes that I mentioned include hashimoto, which is the most common in the UK, which is an autoimmune disease. Um and it's got sort of various various mechanisms that cause its path issue. So I won't get into it too much. Um It's important to note that many diseases that will result in hyperthyroidism have an acute hyperthyroid phase. So that doesn't include hashimoto. So at the beginning, they might have all of these effects of hypothyroidism, anxiety, irritability, high heart rate palpitations, and then after the acute phase, it might then result, it will then result in the hyperthyroid phase. So that's true of Hashimotos, not all the time in some cases. Um and also true in postpartum thyroiditis and also subacute thyroiditis, which they're all um diseases that result in hyperthyroidism. Um And in terms of hyperthy hyperthyroidism, we've got graves disease um which is the most common cause of thyrotoxicosis or a thyroid storm. Um and also toxic multinodular goiter, which is when we've got independent sort of nodules in our thyroid that are releasing T three and T four. So willy nilly, regardless of what the hypothalamus and the pituitary gland saying um into the bloodstream causing a hyperthyroidism and the drug amiodarone as well can cause hyperthyroidism. And therefore, the treatment sort of depends on the cause. Um if it's hypothyroidism, all you really need to do is replace the thyroid that's not being made. Does anyone know which drug we use to treat hypothyroidism at all? Levothyroxine and in the case of hyperthyroidism. Oh yeah, perfect. Someone's got it in the chat. Um, hyperthyroidism. We use a certain drug to control the symptoms of palpitations, which is usually propranolol, which is a beta blocker or we can use, um, to specifically address the excess excess production of um, thyroid hormones. We use carbimazole, um, and that stops thyroid peroxidase. Um, from isdin tyrosine residues on um thyroglobulin globulin, which is used to um produced through T three and T four. the thing we can use is radio iodine therapy which um is used in things like thyroid cancer and toxic multinodule goiter to essentially render um these nodules from, um, from making the, um, T three and T four. And in extreme cases, you would need surgery. But obviously, once you have surgery to remove your thyroid gland, you need to then um, replace it exogenously with levothyroxine for the rest of your life. So we just tend to go from a conservative to, um, the last resort would be surgery. Great. Next slide, please. Um, so we've got a 67 year old male. I've put two questions in that seem quite similar, but they're getting at different things. So we'll see if we can sort of pull it out from this question. Um, so we've got a 67 year old male with type two diabetes who was, who had the flu a few weeks ago, but he's gotten worse again. And I was asking which of the following medications is likely precipitated to the above presentation. Um, so what can we get from this? So he's got a low ph, meaning he's ato um, he's got a low bicarb, he's got a low potassium as well. Well, the sodium's OK for now. Um I'm really sorry, I forgot to the reference ranges. So I feel like this is a bit mean of a question, but Tess has put them up before. So maybe, maybe you need to come down or something. Um, so we've got a metabolic acidosis. So, does anyone know what this gentleman might be suffering from at all in the chop? So it seems like a diabetic ketoacidosis, doesn't it? Which is unusual because he's got a type two diabetes and his glucose is normal. So we might call it a euglycemic diabetic diabetic ketoacidosis. And the drug that's most commonly associated with euglycemic ketoacidosis. Is dapagliflozin. Um, next slide please. There we go. Topical, frozen neck cloud again. Um, so I'll just quickly talk about the diagnosis of type two diabetes. So type two diabetes can be diagnosed in one of two ways. The first way is using HBA1C, um, which shows us sort of roughly the amount of glucose in our bodies and it's rough guide of, um, 3 to 4 months that because that's the lifespan of a red blood cell. So to be, to have a diagnosis of diabetes needs to be over 48 or we can do a fasting glucose or random glucose test as well. And if the fasting glucose is above seven and or the random glucose is above 11.1 we can say that this person has diabetes, but that's only if the patient is symptomatic. If they're asymptomatic, you would need to repeat the test two times um to confirm a diagnosis of diabetes. Now, nice wants you to know and I feel like this is quite high yield which conditions you mustn't use HP A1C. Um in and that includes Children and young people less than 18 years of age. Um pregnant women or women who is two months postpartum. Um and I know that there um anyone with um sort of a diseases hemoglobinopathies affecting their hemoglobin and therefore, the HBA1C, you wouldn't be able to use the HBA1C for them either to diagnose diabetes. Next slide, please. So, um we've got some different targets, depending on the therapy the patient is on. So, if we're thinking a lifestyle or a lifestyle, Metformin alone, we're trying to aim for a HBA1C of 48 or below. Um, and if it's lifestyle and any drug that can cause hyperglycemia and I'll get to which drugs can cause hyperglycemia. We're aiming for a HBA1C 53. And that's because we don't want too tight of a control with someone who's got, um, any drugs that can cause hyperglycemia because it could be indicating that they've got um, excess hypos, which in the elderly population, which is what type two diabetes usually affects, can be quite dangerous. Um, as you can imagine because symptoms of hyperglycemic can result in coma and therefore it falls and can even be fatal. So we really want to minimize the amount of hyper that we're having. That's why we tend to shoot for a bit higher target people who are, um, any drugs that cause hypoglycemia. Weirdly enough, this doesn't apply to people who type one diabetes and are still aiming for 48 millimoles per mil, which is unusual, I thought because they're taking insulin, which is definitely a drug that causes hypoglycemia. But that's what nice, um, suggests. So that's what we're gonna stick with. Next slide, please. Um, so in terms of how it treats diabetes, diabetes at first line, it's always going to be Metformin. Um, usually in practice, I've seen people prescribing Metformin modified release instead of immediate release. And that's just because the gastrointestinal side effects are best tolerated with the modified release. Um And in people who've got either chronic heart failure or any established cardiovascular disease, you want to really be adding an SGLT two inhibitor as well. Um And that's because they're proven to help um in terms of improving the mortality of people with heart failure and diabetes. Um And if that's not achieving our targets, then we would need to move on to our secondary drugs, which are including our SGL CT S if they're not already taking it, um DPP four inhibitors, pioglitazone and sulfon urea, but you really need to be checking the interactions as well. And um you can add on, for example, if you started them on a DPP four inhibitor and they're still not work, it's still not working. You can then add a sulfonylurea and so on and so forth. Um And if all of that's not working, we can consider GLP one agonist, um which is our, you know, some glutide or glutide or Ozempic. Um That's usually if there's other risk factors involved involved um because they're so short in supply in the NHS right now. Um So that includes BM I group 35 which needs to be just for ethnic group. And that's because they're shown to obviously um help with weight, weight loss or we can, we can then consider our insulin therapy. Um I've not really gotten into too much detail about insulin therapy in this because it's already quarter past eight. So um next slide, please. So I feel like, oh, it's just cut off there. That's quite sad. Um That's fine. You know what, I'll upload this to our Instagram because it's a very useful table that sort of summarizes what each different drug does. You know the ways to remember it according to the suffix, the mechanism and important things to know about each drug which I won't bore you by um reciting of the slide. Again, it's on demand. So you can either come back and watch this video or again, just look at our Instagram and I'll upload it there. Next slide, please. Um And this is just a diagram that I found on the internet explaining how SGLT two inhibitors, your Dapagliflozin, et cetera, chemical Gliflozin can cause a Lym DK which is unusual to see in someone with type two diabetes. And again, I don't bore you with going through all of it. But um it's there on the side if you would like to pause and read it next slide, please. Perfect. So again, D DK A management which you don't want to go too much detail about because it could be here for hours. But the most important thing is fluid, fluid, fluid people in DK are very, very volume depleted. Um So we need to do some aggressive fluid replacement. Um And this is sort of based on each trust, they've got their own guidelines. Nice, doesn't have specific guidelines on this. Um And obviously the next most important thing is insulin therapy. So everyone needs to be started on a fixed rate insulin infusion and that's usually 0.1 units per kilogram per hour. Um And when the glucose starts dropping below 14, which is less relevant than a euglycemic ketoacidosis, you need to add in your 10% glucose to prevent any hypos. Um As the insulin keeps running, um important thing to know is a lot of these um foods that we're giving will have added potassium in them. And that's because insulin causes um a decrease in potassium levels as well. Next side, please. Great question. Eight. an 82 year old woman presents with confusion and disorientation. Labs are real persistently low serum sodium despite normal saline administration. And um what do you think? I tried to sort of get onto the volume status of this patient? So, would anyone want to suggest whether they think this patient is hypovolemic UIC or hypervolemic based on the examination findings? So they've got, they're well perfused moist mucous membranes. J BP is OK. No signs of peripheral edema. Yeah, they seem a euvolemic, don't they? Despite the history of congestive heart failure, um they've not got any diuretic use suggesting they don't have a particular problem with peripheral edema. And that might be because they're suffering from, for example, left sided heart failure, which is less likely to cause um, peripheral edema compared to right sided heart failure. Um Which of the following suggests a diagnosis of si DH, does anyone know one would hazard a guess in the chat? It's ok. If not, I wouldn't have any idea if you asked me weeks before my finals. That's fine. Next slide. So you Osma, see your 400 M osmos per kilogram. Great. Next slide. hyponatremia. What exciting, exciting topic. You can definitely tell. I'm absolutely so interested in this. So my symptoms of hyponatremia, we can be tired, we can suffer with nausea and vomiting, headache, confusion, muscle spasms, dark urine and then extreme cases, if it's a very, very low, we can have convulsions or seizures and even behavioral changes. There's many potential causes and I'll try and go through a systematic way of approaching the hypernatremic patient. Um But Tess has kindly listed out a couple of reasons for hypernatremia including dehydration, heart, liver kidney disease, a high water intake, which Tess led to earlier when she was talking about diabetes insipidus. Um So let's let's see. How are we going to address the patient with hypernatremia? Next slide, please. So we're going to try to take it in three different steps. So, the first thing we really want to assess is a plasma osmolality. Um See how many solutes we've got on our blood. What's going on? Do we have a hypotonic um hypertonic hyponatremia eic hypernatremia or hypertonic hypernatremia. Um We're going to look at the volume status as well, which is why I included it in the question. Um Very important for any patient that you've got with hypernatremia. It's always important to do a fluid assessment on them, fluid balance assessment. Um And then uh finally, we can use the urine osmy to give us a final clue as to what's going on. So, next slide, plasma osal, let's see. So, like I said, we can either be hypertonic eic or hypertonic next slide. Um And if we're u tonic or hypertonic, this isn't really matching up, is it with our hyponatremia? Because if we've got hyponatremia, we would expect to be hypotonic because you've not got that solute in our bloodstream. So, in the cases where we've got a hypertonic or UIC hyponatremia, we need to think is there another solute that's causing us to be hypertonic ie hyperglycemia um which would cause hypernatremia because if you can imagine we've got loads and loads of sugar in our blood, our body will try and reabsorb water and therefore, dilute the sodium that's already in our blood. We may not actually have a low sodium, but it appears like we've got a low sodium simply just because of the balances of salts in our blood. Um or we've got a pseudo hypernatremia, meaning we might have um low fats, which is causing us to appear again, like we've got low sodium when we don't a true hypernatremia would have to be a hypertonic hypernatremia. So we go on to a set set which should be assessing volume status. Um And again, I went through, we can be hypervolemic eic or hypovolemic and that would mean slide. Um if you're hypervolemic and hypernatremic. Um So we've got, you know, we've got uh peripheral edema, we've got peripheral pitting edema, you've got um crackles on the chest, you've got R JVP. Um We could have Anasa if it's particularly bad, that's result that's due to renal failure, cardiac failure, nephrotic syndrome, and cirrhosis. Um If we had a hypovolemic hypernatremia, then we need to think about uh where is this? Where is it going? Are we vomiting it all up? Are we pooping it all out? Um Is it because of an Addison's, are we wasting away in our urine? Um or derma losses such as uh burns, is it all third spacing? Um And then if we're evola, we can go on to our next step, which is checking our urinary sodium. Um And we can either be over 100 which is a high urinary os, so very concentrated urine or very dilute urine under 100 osmoles per kilogram. So let's just, let's just think about it. We've got a hypernatremia or volemic concentrated urine or really dilute urine. And so the next slide got really dilute urine. We're thinking about water intoxication or inappropriate IV fluid therapy. That includes our primary Polydipsia, which Tess mentioned earlier, which can be, you know, the most common causes that we think about in our textbooks are psychogenic primary Polydipsia, which can be seen in conditions like schizophrenia, which they just keep drinking loads of water or beer potomania, which again, when you're just out and you just keep drinking those loads of water. Um And then we've got a peaceful, wonderful si DH. Um if we've got a UIC hypernatremia and we've got a very concentrated urine, si DH, um which was what the question I was alluding to. So, next slide, please, what is Si DH? Because as I said, I didn't really understand it ever in med school. Um So I'm glad we're going over it together. Um It's a syndrome of inappropriate and diuretic hormone secretion, which is very useful. So let's elaborate next slide, please. Um So syndrome of inappropriate antidiuretic hormones, you've got too much A DH or like I said before, I prefer vasopressin as a name. I just feel like that helps me visualize what a DH is actually doing instead of this double negative or whatever. So what is NH we the the posterior purity um releases ADH in response to low circulating volume of water. Um and it acts on the kidneys, increases aquaporin two receptors in the distal conv tubule and the collecting duct. And that means that we've got low circulating volume and the kidneys are trying to get the reabsorb the wall strip back from the urine into our blood. So we increase our circulating volume um which results in m more water in the blood, but then more concentrated urine, as you can imagine, cause you're taking it out of the urine and putting it into the blood. Next slide, please. I just thought like we do, we probably need to pepper in some flan into this. Um the nitty gritty of endocar. So there we go. Next slide. Yeah, next slide. Um So si DH involves continuous inappropriate ADH release um which is not affected by normal physiological physiological feedback. So it's just going to continue, continue to release. Um ADH um So the kidneys are reabsorbing more and more and more wall making our blood effectively more dilute and our urine really, really concentrated. So we just keep excreting that sodium out. Um And then all the excess you would think then where is all of this fluid going? Why aren't we getting any peripheral edema? Our bodies are just able to deal with it at the level that the proportion to the ADH is um distributed evenly across all compartments of our bodies. Um And it specifically dilutes our blood electrolytes, including sodium causing hypernatremia. And therefore, that's why we get the results that we get in si th next slide. Um There's many different causes. The main safe treatment is fluid restriction. Um And there's many different causes that I put up there. One of the most important causes. I think that you'll see day to day as a doctor, special foundation doctor is medications such as SSRI is antipsychotics, anticonvulsants, million different reasons. Um, but there we go next slide, please. Question nine. so we've got a 67 year old male with nausea, vomiting, confusion with type two diabetes. This is the one that was similar to the one that we've already been through, um, who had the flu and that meant he didn't get his repeat prescription from the pharmacy. So, whatever drugs he was taking for his type two diabetes, mellitus he's not been taking and he's been recently ill as well, which is important to know he's tachycardic, he's a bit hypertensive. His respirate is a bit high and he's confused, which is important as well. This is quite an unwell man which might prompt us to do an ABG which reels a metabolic alkalosis. Um, a very, very stunningly high glucose of 36 and a very high sodium of 100 and 60. So we're talking about HHS or hyperglycemic rows. My other states, which is a, a diabetic emergency senior type two diabetes. And the question is guessing out what is, which ones of these are not true about? Hs next slide, which is the first one. In fact, our losses are of fluid in HHS are much, much greater. Um, as you can imagine as we're trying to, um, we're just so so dehydrated from the high sugar content in our blood. Next slide, please. So it's a, as I said, diabetic emergency and this is very important, has significant mortality. I think something about 5 10% of people who have HHS. Unfortunately go on to pass away um due to this condition. Um and in its earlier stages, we're getting the urinary frequency, thirst, nausea, um severe dehydration and then it can lead to confusion and ultimately can lead to coma or even death. So there's no strict, hard and fast rules as to how you diagnose HHS. But you can usually tell someone might have it if they've got blood glucose of over 30 or a really high um raise serum osmolarity of over 320. And we can roughly calculate the serum osmolarity by um two times um sodium plus glucose plus urea. And if it's over 320 we're likely dealing with an HHS on our hands and those are the nice guidelines as well. Um About what suggests the diagnosis of HHS. Next slide, please. Um So yeah, like I said, in a person weighing 100 kg, we're looking at 10 to 22 L of fluid losses in HHS. So we need to be doing some aggressive, aggressive fluid resuscitation. And what's different from DKA versus HHS is that most of your glucose reduction is going to be from that um from that aggressive fluid replacement. And that's what's gonna lower our blood glucose um instead of the insulin um which is typically not needed in people with HHS only if their blood glucose. Um if they're not responding enough to the food replacement, can we consider further insulin therapy? But to be honest, this is kind of we're approaching past the level you need to know for your med school finals. Um The important thing for HHS is you really need to be involving a senior because it's a very complicated condition that needs sort of endocrinologist input or at least input from an acute medic consultant. Um So we also we need to consider prophylactic low molecular weight heparin. In most people, I mean, most people in hospital, all in patients usually get prophylactic low molecular weight heparin. But in people with HHS is a very high risk of clots including stroke and myocardial infarction, which is why it carries such a high risk of mortality. And other things we need to consider is not dropping the sodium too much. So, yes, the sodium is blindingly high at 160. But does anyone know what happens if we correct sodium too quickly? Does anyone know what condition that results in usually in cerebral edema? And that's because um we're correcting the sodium. So then the water moves into the brain cells and that increases your intracranial pressure and that can result in seizures um and ultimately herniation and brainstem uh death as it herniates to um the brainstem. So, that's one thing we need to consider. And that's why we usually use um 0.9% sodium chloride. So that's what we call eic sort of sodium chloride. And we can use consider using 0.04 or five or hypertonic sodium chloride after that, if the patient isn't shocked and we're not seeing much improvement with sodium chloride, 0.9% um great. And the form glucose shouldn't be more than five millimoles per liter per hour. And that's for a similar reason um to minimize the risk of neurological complications. Cool. And last question. Oh yes. Some precipitating factors before we move on of DK and HHS um infection, non adherence with um diabetic treatment which we got from the questions stem actually um new onset diabetes. So uh people who don't know they have got diabetes or people newly diagnosed with diabetes. Um Great. Uh next slide, please. Uh question 10. And this one isn't long at all. Um We've got a 24 year old woman with past medical history of celiac disease and asthma. So she's got a history of autoimmune disease, um suffering from uh amenorrhea. She's also suffering retired disability and has lost 5 kg in the past three months. Does anyone know what we're trying to get at here? Which, which disease might she have considering the antibodies, graves disease? So there, so there's, so this is there's some symptoms in Graves disease that are specifically associated with graves disease and not other causes of um hyperthyroidism and that's specifically linked to the presence of anti TSH R or antibodies. So, in this case, next slide, it's b swelling or clubbing of the fingers and it's also known known as thyroid ACR. Next slide, please. So these are specific features of grave's disease. Um that up Fathy, um the specific eye signs that are associated with grave's disease. Um We can also get a non pyma of the tibias, pretibial myxedema or a thyroid acropachy, which is a combination of clubbing and swelling of fingers and also new periosteal bone information. So very chubby, swollen fingers. Great. Thank you so much for listening. So, topic that we didn't mention the today as you know, it's half past eight. So we always run late, but there's a lot to get through hyperparathyroidism, which we covered actually in our real tool that tested that for us. Um acromegaly and sex hormones as well useful to cover um as part of the UK MA curriculum. Thanks so much everyone for joining us this evening. Um And thanks so much for all your feedback. Be really helpful. Like I said, if you could fill the form out, let us know what we could improve on what you would like to see from us next. Any suggestions. Um And I really hope that was useful for all of you. Thanks so much for hanging out with us. Um Spending your Thursday evening. Bye. Bye, thanks everyone. Bye.