Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Perfect. Thank you, Tess. So, going through the learning objectives for today, um which you were sent before the session, it's to understand the most commonly occurring endocrinology presentations and the conditions required for medical finals and also for cli clinical practice when you become F ones in the not so distant future. I also looking at a structured approach to diagnosing and managing endocrine disease is frequently seen in exams and enhancing clinical reasoning skills related to endocrinology and then gaining insight into the key endocrinology topics that often appear in exams and the last bullet point which I'm sure you can read. Um So looking at the MLA Curriculum, me and um Joanna have split into two halves, I'm going to cover the first half and then she's going to cover the second half. I'm focusing on thyroid pathology in the first half. And then um Joanna's gonna focus on diabetes and um diabetic emergencies. So firstly, we're gonna start with a pole just to get your brains in gear after a long day. I'm sure of placement. So, are you able to share the first round tests? Um We can make it interactive. Sorry about my dog in the background. Now we get it. So you've got a 42 year old woman with a three month history of weight loss, insomnia and palpitations. She's got a fine resting tremor and bilateral proptosis. So, what is the underlying underlying pathological mechanism? So, there's three people. This answer so far, I think there is 21 people so far. Everyone's getting the right answer. Any other guesses. OK. So we'll move on in the interest of time. So the answer is b an antibody directed against the thyroid stimulating hormone, that is the TSH receptor. And we'll go through um a bit of the physiology behind that. So, looking at the um thyro physiology, if we're thinking about how it all happens and how we can relate this to clinical practice, we've got to understand the basics of the physiology. So the hypothalamus releases the trh which stimulates the anterior pituitary pituitary gland to release TSH. And this in turn stimulates the thyroid gland to release both T three and T four. And then there's a negative feedback loop which I'm sure you all learned in your preclinical years as to T three and four, suppressing trh and TSH um when you've got too much of it, but we'll move on from that and look at the clinical features, which is what's going to be relevant when you become F ones. And also in finals. So this table you should be familiar with as to the thyroid clinical features. So with hyperthyroidism, we're looking at weight loss, restless heat, intolerance, um thyroid Apache. So that is in the left bottom, left hand picture. You can see, you'll see it's a rare skeletal manifestation of graves disease. So clinically, you'll see clubbing and you will be able to see some X ray changes. Although don't ask me what they are because I'm not a radiology expert, but I've been told that you can you also get pretibial myxedema, which is in the bottom right picture and um atrial fibrillation along with diarrhea, anxiety and oligomenorrhea and then kind of the opposite for hypothyroidism. So weight gain, constipation, menorrhagia. So those are the clinical features for thyroid disease. And then if we are thinking about thyroid function tests, again, this is a table which you need to be familiar with for your exams. So we'll go through each one in turn, I'm going to skip over the first few, but I had a patient today, um who is a nursing home resident and she had a really high TSH and a normal T four. And we were thinking, hm, what could this be? Could it be subclinical hypothyroidism? Well, the answer to that is probably not because she's diagnosed with hypothyroidism and is on levothyroxine. So then we have to think, well, is she actually been taking the levothyroxine? And we looked at her medication record from the, from the nursing home and it showed that she hadn't really been taking it. So hence why poor compliance with Thyroxine is something to consider. But moving on, we're gonna go on to um question two. Are you able to share that one? So you've got a 32 year old female who was advised to visit her GP as her vision was worsening. So the optician noticed redness and watering of her eyes and noticed that her eyes appeared to be bulging out as described by her husband. She also stated that she's incredibly, she's feeling increasingly tired and often feels that her heart is racing. So the GP ran some thyroid function tests and TSH receptor antibodies were detected which of the following would not be a typical sign of graves. So thinking back to that table of clinical features, which would not be a typical sign of graves disease good. So most of you are getting the right answer. So it is see weight gain. Um and you can refer back to the clinical feature table when you get the slides after this presentation. So going through hyperthyroidism. So there are two key definitions. So, hyperthyroidism is a condition where the thyroid gland is overactive, leading to production of excess thyroid hormones. But then thyrotoxicosis is sometimes used interchangeably. But technically, it's a syndrome resulting from the presence of excess thyroid hormones in the body. So it's not always due to thyroid gland overactivity. So if you are considering someone's got hyperthyroidism, when they're presenting to the GP practice or you've got them as an inpatient or you're seeing them in the acute setting. The investigations that we'd want to look at performing are firstly thyroid function tests. So looking at the TSH levels, the T three and four, then looking, then arranging some blood tests for thyroid antibodies. If the thyroid function tests come back abnormal and then considering further down the line, an ultrasound scan of the thyroid and a radioiodine uptake test. So, I've created this little summary slide for the causes of hyperthyroidism. So the the most common cause is Graves disease. And this is an autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism by mimicking TSH on the receptors. So that's why the first question related to Graves disease in terms of the thyroid, the thyroid receptor antibodies mimicking TSH. And that has some three unique features which is exophthalmus, pretibial, myxedema and thyroid Apache, which are unique to Graves disease. Um Sometimes exams can test you on thyroid scintigraphy which shows diffuse homogenous, increased uptake of radioactive iodine. Um And nice guidelines recommend that everyone who has a diagnosis of Graves disease is referred to secondary care. So, endocrinology for ongoing treatment. Another cause is toxic, multinodular goiter, sorry. So this describes a thyroid gland that contains autonomously functioning thyroid nodules resulting in hyperthyroidism and the thyroid scintigraphy with the radioiodine uptake test reveals patchy uptake and the treatment choice would be radioiodine therapy for this. Um and kind of similarly with solid toxic thyroid nodules. But I want to touch on amio amiodarone therapy. So, amiodarone can cause thyroid dysfunction due to its high iodine content and its direct toxic effect on the thyroid gland. So, whilst patients who develop hyperthyroidism with amiodarone should stop taking amiodarone. Those who develop hypothyroidism can continue amiodarone with levothyroxine. That's quite a commonly tested factor in exams that's worth, that's worth remembering. And then the final, one of the final causes of hyperthyroidism is subacute thyroiditis, which is also known as de veins, thyroiditis. Those terms of used interchange of brain exams and this often follows a viral infection. So when you're doing your sbs and your multiple choice questions, a patient's got a viral infection and then has deranged thyroid function tests. You think about subacute thyroiditis where they'll initially get a painful goiter and a hyperthyroid episode, then they'll become e thyroid and then they'll become hypothyroid. And if you're treating this um later on in your careers, then we'd start, we'd consider nsaids such as naproxen. So the management of hyperthyroidism is initially with propranolol. So a beta blocker um to block the adrenaline related symptoms of hyperthyroidism, you can then start considering antithyroid drugs such as carbimazole if symptoms aren't controlled and GPS are um recommended by nice to start patients on carbimazole. But um a nice little tip for exams is that propylthiouracil is preferred in the third trimester of pregnancy. Um But the definitive treatment if it's not responsive to carbimazole is radioiodine therapy, but just note that again, this is contraindicated in grade eye disease. And then thyroidectomy is an option for those with large goiters. But again, those three common risks of hypocalcemia, laryngeal nerve damage and bleeding are risks that are worth remembering when doing your ps. So, complete remission and the ability to stop taking carbimazole is usually achieved within 18 months of treatment. But the key factor remember with taking carbimazole is that it can cause agranulocytosis. So, if you have a patient who develops a sore throat or a high fever, whilst taking carbimazole, it's really important that they seek medical advice because that risk of a low white blood cell count and they'll need further investigations for that. So this, I've just summarized the nice guidelines for hyperthyroidism. Um I'm not gonna go through this now, but this is um for relevant for future clinical practice and for your exams. So, thyroid eye disease, the there is a difference between exophthalmos and proptosis. I didn't know this until I was doing my finals. Um but it is a key difference worth remembering. So, proptosis refers to the anterior displacement of the eyeball, whereas for exophthalmos is proptosis associated with thyroid disease. So they're not interchangeable. Exactly. Um and exophthalmus is thought to be caused by an autoimmune response against an auto antigen, possibly the TSH receptor which causes um retroorbital inflammation and remembering from a key point from earlier radioactive iodine is contraindicated if patients have thyroid eye disease as it may cause a worsening of the inflammatory process. So, moving on from hyperthyroidism to hypothyroidism again, just going back to the um the thyroid physiology where primary hypothyroidism is caused by thyroid gland insufficiency. So, thyroid hormones such as free T three and T four will be low TSH will be high because there's no negative feedback to the brain. So the pituitary produces lots of TSH to try and get the thyroid working. Secondary hypothyroidism is caused by pituitary pathology that results in low production of TSH. And therefore, because you've got low TSH, you'll have low T three and T four. So just summarizing the causes of hypothyroidism. So, the most common associated cause is hashimoto thyroiditis, which is associated with antithyroid peroxidase, anti TPO and anti thyroglobulin antibodies. This will initially cause a goiter before atrophy of the thyroid gland. And a key fact, a key link to remember for your exams is that it's associated with the development of mortar lymphoma. Um iodine deficiency in the developing world is another cause of hypothyroidism as well as medications. So, we've spoken about amiodarone and as I said earlier, if a patient develops hypothyroidism, taking amiodarone, they can continue taking it, but they should take it with levothyroxine. Um there are central causes which cause a secondary hypothyroidism. So this is where the pituitary gland is failing to produce enough TSH. So it's often associated with a lack of other pituitary hormones such as ACTH. And this is called hypo tourism hypopituitarism. And it has many causes such as vascular causes where you've got Sheehan syndrome, which is worth reading up on if you've not heard of that before, as well as radiation infection and pituitary gland tumors. So, the management of hypothyroidism is easier than the management of hyperthyroidism. It's simply with levothyroxine and that is a synthetic T four which metabolizes to T three in the body. And when you're starting patients on levothyroxine, we titrate the dose until the TSH is normal. Now, the side effects of levothyroxine which are worth remembering are osteoporosis and atrial fibrillation because they are um clinical features of hyperthyroidism. So, if you're increasing the levels, the thyroid hormones in the blood, then you're going to start seeing the side effects of osteoporosis and atrial fibrillation and the other clinical features of hyperthyroidism potentially and worth just linking this to other specialties such as in obs Andy, where if you've got a patient who's pregnant on levothyroxine, their dose needs to be increased by at least 25 to 50 mcg due to increased demand on the maternal body. So that's a key fact, worth remembering as well. Let's do um question three to see if we were still paying attention. So what is the most likely diagnosis for this patient bearing in mind? This is a talk of endocrinology. 14 people out 20 on anyone else. Ok. So this is a presentation of thyrotoxic crisis. So, the key clue here is the withdrawal from carbimazole and the treatment for hyperthyroidism. So, cocaine intoxication would present in a very similar way. But the history is more suggested of previous hyperthyroid diagnosis. Common syndrome is primary hyperaldosteronism due to an adrenal adenoma which would present with hypertension, high potassium levels and a metabolic acidosis. Um and myxedema coma is a hypothyroid emergency which can present with hypothyroid symptoms relating to any body system that commonly affects mental state. And patients would be hypothermic, hypotensive and bradycardic. So let's quickly go through the thyroid emergencies. So, we've just touched on thyrotoxic crisis, which is an acute hypermetabolic state induced by excess release of thyroid hormones. So, the symptoms, as we just saw were pyrexia, hypertension and tachycardia and the management, you can read up more on the management because it's quite complicated how you've managed this. But in summary, we'd start with either propranolol or digoxin. If they're a more sedentary patient with comorbidities or asthma, you then start considering propylthiouracil leco iodine and IV hydrocortisone. On the other hand, you have myxedema coma, which is severe hypothyroidism, which as I just said would cause symptoms of reduced mental state and hypothermia, bradycardia and their management is IV thyroid replacement, ie hydrocortisone, mechanical ventilation, IV fluids and rewarming because they're hypothermic. So, just quickly before I hand over to Joanna going through osk thyroid examinations, which is um a thing is an examination that can be tested during final year. Osk. So just giving a quick summary of introduction, I'm sure you're all familiar with OSC now and you know how to introduce yourself and start an examination. But then we're generally inspecting the patient whilst they're at rest. And as always with most examinations, we start with the hands with palpating of the radial poles. We're looking for those clinical features of thyroid disease such as thyroid acropa or clubbing within inspecting the face. So, um there are, if you look on geeky medics for a video of thyroid examination, it's a really good run through of this and this is kind of a summary of that. So when they, when they inspect the face, they're inspecting the eyes from all angles. So from the lateral aspect, superior aspect, inferior aspect for looking for signs of thyroid, eye disease, assessing for lid lag and eye movement abnormalities and then then inspecting the thyroid. So you're going to inspect first, you're going to inspect whilst they swallow water and protrude their tongue to see. I think that's to see if they've got a hypoglossal cyst. Someone might be able to correct me if I'm wrong with that. Um Then we palpate. So we palpate the thyroid gland from standing behind them and feeling their thyroid gland to see if there's any nodules or a goiter palpable again, whilst you're palpating, get them to swallow some water, get them to protrude their tongue, then palpate for lymphadenopathy, inspect their for tracheal deviation, um, assess for retrosternal dullness, osc will take the thyroid gland. See, there's a bruit and then there's three special tests which you can do to score some extra points in an oscopy if you remember and you have time at the end is to assess the biceps reflex, inspect of pretibial myxedema and assess for proximal myopathy. So, um I'm now going to hand over to Joanna if she's managed to log in and she's going to go through other endocrine emergencies. Yeah, great. Um Can you hear me? Yes, perfect. Thank you. Um Is it OK, James, if you continue to share the slides, of course. Um Perfect. Ok, thanks very much. Um So yeah, my name is Joe. I'm another F one at Conquest Hospital. Um So the second half of this session is focusing on endocrine emergencies. Um So there are four that we're going to go through. Um the first three relate directly to diabetes. So those are DK A HHS and hypoglycemia and then lastly, we'll touch on um an Addisonian crisis or adrenal crisis. Um So we'll come to the next SBA question. Um So this is a five year old boy um with a history of type one diabetes presents with 12 hours of vomiting and abdo pain. You can um read there the results of his ABG and uh urine dip. He's treated with IV fluids including potassium and an insulin infusion. Um but after three hours he has a seizure. Um So what's the most likely underlying cause of this seizure? I've only just managed to join the events and I actually don't know how you see the results of the polls. I'm not sure people are doing that. Yeah, we can, we can read it out to you. So I've got 62% or 66% saying cerebral edema and then we've got a couple of votes for each of the other options as well, but the majority have gone through brilliant. Ok, thank you. Yeah. So um that was correct. So, cerebral edema. Um So hopefully you picked up that this is a case of DKA. Um And in a moment, we'll come to why the most likely answer here is cerebral edema. Um So if we move to the next slide, thank you. Um So, DKA um is a chaotic metabolic state in which all three of hyperglycemia, acidosis and ketosis are present. Um It's usually either first presentation of type one diabetes or sometimes there's a complication of type one diabetes. Um in rare cases, it might be associated with type two diabetes under conditions of extreme stress. Um and triggers might be things like infection, um missed insulin doses or acute cardiac events like an MRI um and just very briefly, biochemically, um DK A involves reduced net insulin action and then elevated levels of opposing hormones. Um And the result of that is, you get increased breakdown of glycogen, increased gluconeogenesis and decreased uptake of glucose by peripheral tissues and those all cause hyperglycemia. Um And then you get breakdown of triglycerides and ketogenesis in the liver. Um That's what causes the ketosis and acidosis. Um The diagnostic criteria you can see there. So glucose of more than 11 or known diabetes. Um p eight of less than 7.3 bicarb of less than 15. So it's a metabolic acidosis and raised ketones. Um And the symptoms are less today. You might well be familiar with those. Uh So we move on to the management of DKA. Um So the first and most important aspect of management is fluid resuscitation. So DKA is a state of extreme dehydration. It's an average of a 6 L fluid deficit. Um So resuscitating with IV um Saline is the most important initial step. Um And then secondly, you give a fixed rate um IV insulin infusion and then later add 5% dextrose to that um to enable the insulin to continue to correct the ketosis. Um but without causing hypoglycemia. Um And then thirdly, you want to continue the patient's long acting insulin um but stop the short acting insulin in the acute management of DK A. Um you want to think about adding potassium to the replacement of fluids as insulin will drive potassium into cells and can cause hypokalemia. Um then PT profen axis because DK A is a prothrombotic state Um And then think about identifying and treating the precipitating factors like infection or like an M and then regular monitoring of glucose ketones, electrolytes, particularly potassium um is really important and keeping on accurate fluid balance charts. Uh So we move on to complications of DK. So these can be divided both into um complications from the DK itself. Um So those can be um VT we mentioned the prothrombotic states, acute respiratory distress syndrome. AK I arrhythmias from hyperkalemia. Um because the acidosis causes an extracellular shift of potassium. So you can get hyperkalemia, um and gastric stasis and then there are complications um which are more iatrogenic, so related to the treatment and those can be hypoglycemia from the insulin hypokalemia again from the insulin. Um and cerebral edema. Can you go to the next slide, please? Thank you. So, cerebral edema is a complication that occurs in about 1% of DKA cases. Um But especially in young patients like in that question. Um and it's caused by um the fluid resuscitation being too rapid, causing fluid overload. Um And if you're suspecting possible cerebral edema, um then an urgent ct head is really important and an urgent senior review of your patient. OK. So that's everything on DKA. Um So we're moving to the next endocrine emergency. Um And this one does relate really directly to a patient on the wall that I'm working on. Um we had this sort of exact scenario. Um a couple of weeks ago. So, um these emergencies are really relevant to real life as well as relevant to exams. So, this is an 82 year old lady on a DAS ward being treated for urinary sepsis. Um, a couple of days after her treatment, she becomes unwell with thirst, nausea and lethargy. Um she's very dehydrated. She's stopped passing urine and she's got very poorly controlled type two diabetes. Um, so you can see her um electrolytes um and urea creatinine glucose there. Um So what is the patient's serum osmolality? Don't worry if you don't know how to calculate that. So we'll go through it in a moment. Um But this is something that I did on the ward a few weeks ago and it's also something that you can be asked in the UK MLA exam um test. Do we have any answers from that? Joe? Can you see the three circles on the right hand side? Uh Yes. If you top the click, if you click the top one, which says chat. Yeah. And then you can go to messages. Perfect. OK. Thanks so much for that. OK. That's helpful. Um OK, I'll just give you another few seconds to think about that question. OK. Um So we move to the answer and how you calculate this. So the answer here is d um So this is a formula that we use it. It's quite straightforward. So it's two times the sodium plus the urea plus the glucose and the normal range is between 275 and 295. Um You might see some variation in the formula. Sometimes it includes potassium as well. Um But I think this is the most standard one and it's also the one that we've used um in a UK MLA question. So I'd, I'd stick with this formula. Um So moving on then to a bit more about HHS. Um So it's a medical emergency um in which hyperglycemia results in osmotic diuresis and severe dehydration. Um it's associated with a 50% mortality rate, so really significant there. Um and it typically occurs in elderly patients with type two diabetes. So, unlike DKA, which is much more type one diabetes, often younger patients. Um HHS is more elderly patients with type two diabetes and often with lots of comorbidities, um precipitated by illness like infection or an acute cardiac event. Um The diagnostic criteria is less well defined than a DKA. Um But the two most important factors uh are marked hyperglycemia so often over 30 a significantly raised serum osmolarity. Um So over 320 but there's not usually a significant ketosis or acidosis with HHS. Um So in terms of clinical features, you get polydipsia and polyurea initially, but then later reduced urine output. So that's the osmotic diuresis and then severe dehydration and you get lethargy, nausea and vomiting, focal neurological deficits and it again, it's a prothrombotic state, you get hyperviscosity of the blood. So risk of stroke and MRI S there um in terms of the management principles of management are similar to DKA. So again, the first most important step is fluid replacement um with normal saline, um closely monitoring the potassium and adding potassium um to the saline as needed. Um And then secondly, IV insulin, um if the patient remains hyperglycemic and you follow a protocol, a local protocol for how much insulin and how much potassium to give. Um again, bt prophylaxis is important and then important again to treat, to recognize and treat the underlying cause. Um And then just again to highlight that gradual and correction of metabolic disturbance is important because there's risks of cerebral edema and also osmotic demyelination syndrome if she corrects particularly sodium um too rapidly. Ok. So that's everything about HHS. So on to the next endocrine emergency. Um So this one is a 40 year old patient with type one diabetes being treated in hospital with IV antibiotics. His oral intake has been significantly reduced and when a nurse tries to wake him in the morning, he's unarousable and his glucose is 2.4. Um What do you think the most appropriate management for that would be? Ah So the question um this relates back to HHS. Um So can you confirm the difference between serum osmolarity and osmolality? Um I'd have to look that up. Actually, I did used to know that, but I can't remember off the top of my head. They're very similar. I think it's relates kind of to the um to the units we tend to refer to osmolality. Although actually, I think the previous slide said osmolarity, which was a mistake. Um I don't know if James or Tess or Cash can clarify that. I'd have to look it up, I'm afraid. Um So just coming back then to the question on hypoglycemia. Um um yeah, so we've got a range of responses there. The answer is d so IV glucose 20%. Um And in a moment, we'll come to why. That's the correct answer. Um So hypoglycemia is plasma bers of less than three, although the threshold for symptoms varies. Um It's most commonly in insulin dependent patients um caused by insulin or by other um oral hypoglycemics like glipiZIDE, which is a sulfonylurea, um often associated with increased activity, missing meals or overdosing um on the insulin treatment. Um more rarely it can occur in nondiabetic patients. Um and that can be through non diabetic patients, misusing insulin or through alcohol excess and missing meals. Um through an insulinoma which is usually a benign tumor of the pancreas, uh pituitary insufficiency, addison's disease and liver failure. Um in terms of symptoms, these can be divided into autonomic symptoms which result from the release of Glucagon and adrenaline. So that's the sweating, anxiety, hunger tremors kind of thing. Um But then you also get neuroglycopenic symptoms. Um and those occur with more severe hyperglycemia um resulting from inadequate glucose supply to the brain. So that's when you can get confusion and reduced G CS seizures and then um in most severe cases of coma. Um Thank you, Tess for looking into that. So, yeah, Tess has put an explanation in the group chat of osmolarity versus osmolality. I was, yeah, I think they are very, very similar. OK. Um So in terms of management, then of hypoglycemia, um we can divide this into in a community setting and then in a hospital setting. Um So in a community setting, if the patient is awake, then our first step would be to give oral glucose and that can either be in a liquid gel or tablet form. Um But if there's a decreased level of consciousness, um then the patient might have what's called a HypoKit um which contains a syringe of um glucagon um that someone can give to them either im or subcut. Um And then in a hospital setting, um if the patient is conscious and able to swallow, then again, you'd give um an oral glucose. Um But if the patient is drowsy or unconscious, um then your first line option would be to give IV 20% glucose through a large vein. Um can also give 10% glucose. Um But you wouldn't give 5% because that's not really going to be effective enough. Um And you wouldn't give 50% because that's hypertonic. Um So, ideally 20% or 10% glucose. Um But if you don't have any easy venous access, um then you would give um im or Sub Glucagon. Um but IV glucose is preferable. Um because uh Glucagon has some side effects of nausea and flushing. Um So if the patient has venous access or you can easily establish venous access, um then that will be your first line option. Um In this case, the question that we answered, um the patient was on IV antibiotics. So, um they had venous access. So it would be easy to give IV glucose for that patient. Um And in this question again, the patient was unarousable. Um So we wouldn't want to give oral glucose or buckle gel um because there's a risk of aspiration there because of the unsafe swallow. Ok. So this is the last one. Now, the last endocrine emergency. Um So this is a 31 year old woman with Addison's disease. He's been unwell for two days with vomiting and diarrhea. She's brought to with reduced consciousness and found to be hypotensive. Um There is the investigations. So sodium uh of 132 potassium of 5.8 her urea and creatinine are also raise and her glucose is 3.1. Um So what do we think is going on here? What's the most appropriate immediate step in the management of this patient? Yeah, great. So most people have gone for 100 mg of hydrocortisone IV or IM and that's the correct answer. Um So what's going on here is an adrenal crisis. Um If we move to the next slide, thank you. Um So, adrenal insufficiency is failure of the adrenal glands to produce sufficient steroid hormones. Um And so the steroid hormones are cortisol which is produced by the adrenal cortex um in response to ACTH. So that's part of the hypothalamic pituitary adrenal axis or HP axis. And then the other, the other main one is aldosterone, which is produced by the adrenal medulla in response to angiotensin two. So I'm not gonna go any more into the physiology now. But um if that's not something you're confident or familiar with, then definitely um it's worth looking over. Um And then an adrenal crisis is when you get an acute presentation of severe adrenal insufficiency. Um And there are lots of causes of adrenal insufficiency. Um They can be divided into primary secondary and tertiary causes. Um But for today, we're just going to mention um the two that are most relevant. Um and these are Addison's disease, um which is an autoimmune condition where you get destruction of the glands. Um And then secondly, stopping long term or high dose um steroid therapy. Um that's because steroids suppress the HP access. And so if you suddenly stop steroids, um that can lead to acute adrenal insufficiency. Um in terms of the presentations, you get reduced consciousness, hypotension, hypoglycemia, um electrolyte abnormalities. Um In the case of primary adrenal insufficiency, you lose both cortisol and aldosterone. That's the mineralocorticoid activity. And when you lose aldosterone, you get hyponatremia and hyperkalemia. Um This is a slightly confusing point. I think that in cases of secondary and tertiary um adrenal insufficiency when the problem is with the pituitary gland or the hypothalamus, you then don't get that kind of hyponatremia hyperkalemia picture. Um because aldosterone activity is normal because that's not part of the HP axis. Let me know if that doesn't make sense and it's a slightly confusing point. Um But in Addison's disease, you get hyponatremia and hyperkalemia. Um It might be the first presentation of Addison's or it might be in a patient with known Addison's disease and the um adrenal crisis is triggered by infection or trauma or some other acute illness. Um or as we said, in cases of suddenly stopping long term steroids. Um So in terms of the management, um so the management will involve an A to e approach um immediate transfer to hospital. And then the first step, most important step is giving either IM or IV hydrocortisone. Um We need to give initially a 100 mg bolus um followed then by a continuous infusion. Um and then you need to give IV fluids as well. So you need to give a bolus probably 500 mils of normal saline over 15 minutes and then ongoing rehydration. You'd correct the hypoglycemia before we talked about how we would do that. Um And you carefully monitor the electrolytes and the fluid balance. Um The patients who are on long term steroids are steroid dependent and they should carry one of these steroid alert cards so that anyone who comes into contact with them um, is aware that they're um steroid dependent. I'm sure that their steroids are prescribed. Um doses of steroids are normally uh doubled during an acute illness uh to mimic the body's normal steroid response. Um And uh exogenous steroids must be stopped slowly. Um If they've been going on for more than two or three weeks, they should be tapered slowly to allow the H PA access to regain its normal function to avoid adrenal insufficiency. Ok. So, um this is just a summary of some of the key points um for exams, but also um for real life. Um I've only been an F one for a few, well, just less than two months, but I've already had to use these things in practice, they're really important to be aware of. So just to summarize DKA, you get hyperglycemia acidosis and ketosis in an exam question, it will probably be in a patient with type one diabetes, often in younger patients versus HHS where you get hyperglycemia, high serum osmolality. Usually in a type two diabetic patient, often in elderly ill patients. Um just a reminder of how you calculate serum osmolarity and then the most important immediate management step in both of those scenarios is IV fluid resuscitation. Um and then a quick summary of the management of hypoglycemia. So if they have a safe swallow, then it's some form of oral glucose. Um if they have reduced consciousness and they have venous access, then IV glucose 20%. If they have reduced consciousness and no venous access, then I am Glucagon and then just finally, um in the cases of adrenal crises, the most important initial management step is 100 mg of hydrocortisone, either IV or IM and that is everything I think. Um Yeah, feel free to leave any questions in the chat and we can try to answer them. Um Yeah, otherwise thank you very much for listening and I hope that was helpful for your er exam preparations. Thank you so much for coming everyone and thanks to Joanna and James for a really nice um succinct and clear talk. Um If you guys fill in the feedback form, you'll get access to the slides. Um and there will also be a recording of the session if you want to watch them back in perpetuity. Um If people are