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Endocrine Emergencies Part 1, Dr Isra Ahmed Mohamed, Consultant Endocrinologist and GIM consultant - Cambridge University Hospitals NHS Foundation Trust

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Summary

This on-demand teaching session is aimed at medical professionals and will provide an in-depth look at a patient who has presented in an adrenal crisis. It will cover the importance of timely shifts in medication dosage, different causes of adrenal crisis, and how to assess a patient's vitals and look for signs of infection or other causes. It will include three case studies and interactive activities, so volunteers are encouraged to participate.
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Learning objectives

Learning Objectives for Medical Audience: 1. Identify symptoms of an adrenal crisis and formulate a treatment plan. 2. Describe the effects of thyroid hormone and cortisol on the body. 3. Demonstrate knowledge of the ABCDE approach as it applies to a medical case. 4. Explain how hyperthyroidism can affect cortisone levels and lead to an adrenal crisis. 5. Evaluate lab results and determine how they are related to an adrenal crisis.
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Computer generated transcript

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

Be able to um join you today on this session and I'm hoping that it would be a useful one for you. Uh So I can see. So a few of you started writing um where you are from and I think I might just enable my camera just to see my face for the first time. Just one minute. Uh They got here, Lina from Ahad University, they got er Za ah Islamic University. Um What else? Uh the rest of you? I think you haven't written yet. Um OK. So I think we are already uh one minute. Uh shall we uh start or wait for a few minutes for more to join? So it's OK. So uh what we have uh here. So um I will be sharing with you a total of three cases. We will be going through them. Um I need it um and it will be more useful to be interactive. Uh So at each uh time I will need two of you to help me. So, can I have a couple of you as volunteers to start this place and I will guide you? So it will not be anything difficult and I'm trying to uh make it at an appropriate level so that everyone can uh find something out of it. Hopefully any volunteers, uh if you are able to volunteer, say your name and it's not gonna be for the whole time. So it's just uh first two for maybe uh all or part of the first case and then so on. No one coming forward work. OK. I'm not sure. Um OK, someone put through me, Anna. Thank you, Anna. So um uh so in a minute, I will share the slide. Anyone uh would be with Anna. It's usually actually helpful to have two people around the same time. It reduce the pressure from the person. So I got Anna from Ukraine and then, and someone else, please got someone from India PS A OK. Anyone else please? It wouldn't be difficult. OK. So, um I know would you like uh to admit yourself uh please and um tell me what your level you are and we kinda start from there. Uh Well, each and every one of us has uh written uh years of designation in the chat as well, like I'm from final year. OK. Hello. Sorry. OK. Uh So what's your name you say has a Hasan Azad Azad Asad. So Asad that you gonna help Anna you shared with her? So got uh so let us see, she's going to arrive soon because the last lecture just, just finished, she's going to arrive soon. Oh, ok. So you were logging in on her name. Fair enough. Ok. So let's just, let's start on. So what we have here, uh So the slides are not going through, I will stop the camera if it helps. And ok, so we got a patient. So this is a GP letter. So, uh I think the system in different countries might be different. So here in the UK, we do have general practitioners uh who own patients and then um they get contacted most of the time by the patients if they have issues. So this patient has contacted her GP because she wasn't. Well, and the GP sent her immediately to the emergency department. And this letter uh saying that um she has been unwell hypotensive. She's been vomiting, she's been having some headaches, she wasn't stay on her feet. Uh Her uh BP when she was sitting was 160/90. But when she stood, her BP was uh dropping down to 80/60. She was tachycardic. Um She did have an ECG showing uh tachycardia with the heart rate up to 1 40. So he mentioned to us that this patient taking hydrocortisone and fludrocortisone. Could um someone tell me um is it um asad, would you please tell me what is in your mind about what's going on decreased level of cortisol in the body due to Addison maybe. Yes. So, so yes, with the hydrocortisone fludrocortisone, this suggests that the patient is likely has a disease and the patient having these symptoms. Um They just say that, ok, she looks like she's getting into an adrenal crisis. So uh wait, it's not going uh next. So what she arrived in the emergency department, um the first person, um she is seen by the nurse, she documented that uh her age, the presentation BP was actually lower. Now, uh she could, the, the person please mute. Is there is some noise I can't speak. OK, muted. Thank you. So uh so we got the, so the BP is even lower. She is still tachycardic. So what is your approach at this point? What do you want to do first? First, we'll go for the vitals, try to break the vitals for normally. So when you are, yes, you need to correct this vital. So when what is the process that you are going to do? What, what do we call it when someone is acutely unwell? And you are going to yeah, fluid uh rehydration because patient who is vomiting and uh ABC is she lot airway breathing and circulation, correct? So we need to get uh the AB C always when you have anyone unwell, you are in the hospital. Um you are a junior doctor there at any level. You are going to think about ABCDE. You are not gonna be wrong. If you start there, we will make sure that the patient is safe So the airway, we didn't have an airway issue for this patient. Um the breathing um she was saturating, ok. The circulation is the issue. So we have a low BP and we have a person who is tachycardia, correct? The person told me that they need dehydration. So you're going to immediately put uh two white or cannula in both arms, you uh take them uh you will be taking blood sample, of course, immediately as you do that and you give the patient some fluid preferably, you are going to what we expect you, they are going to give crystalloid fluids. So 0.9 per percent sodium chloride or solution and you are going to assess the next one with the disability. Her G CS was not impaired at the time. You will check the blood sugar, the blood sugar wasn't low and you will do the full exposure to see if there is any other issues uh causing the BP to drop, including sometimes it can someone would be bleeding but not this patient. However, when the patient was viewed, she was uh hyperpigmented. So the once. So this is you the ABCD start in the beginning because she is acutely unwell. Then after that, after you start that, of course, you are going to be collecting information as you are seeing the patient, but the full clocking requires first patient is stable. Um So you have done your ABCD. So she uh when you the person, the doctor who starts clocking her, she had a dino of in May 2021. Her presentation actually was in November 21. She as well, uh, had a diagnosis of, uh, overactive thyroid back in September 2021 and she's been already on treatment any before I go to the next line. Anything that, um, brings any relevance for the thyroid and Addison and her presentation with the adrenal crisis, maybe it's the overactive thyroid and the these are both autoimmune. Uh it is. Yes, both of them are autoimmune disease. Yes, that is one. What else? What does the thyroid hormone does to the cortisone overactivity, the contra insular part, two contra ins insulin, contra insulin daily. Ok. So, so in this case, so when you have too much thyroid hormone, it increases the metabolism of cortisol. So you run out of the cortisol quicker and um when you have too much thyroid hormone. So she, it depends uh what we will look shortly in the results, how they were looking and if that has been contributing to the presentation. So she mentioned that she wasn't feeling well for actually 4 to 6 weeks telling that she might not, she hasn't been taking a liquid replacement. So though she was taking an appropriate dose according to her body, the weight and the diagnosis, however, it wasn't appropriate for someone who had thyrotoxicosis because if you are, we are relatively sick, you might require double the usual uh steroid dose while your thyroid function is not. Uh Right. So she has said that she's vomited 23 times the last uh week, uh or so. And then she was nauseous. Um and she was trying to eat not much though, uh but she managed to keep her tablets down. Um, she didn't have other symptoms but she was feeling weak and dizzy. So the rest of the background we already mentioned about add hyperthyroidism. She had a previous diagnosis of asthma. She's been taking fludrocortisone 50 microgram for her age and by the way, is slightly relatively lower dose than usual. Most people actually on 100 microgram. However, some people might be OK with the 50 microgram and then the hydrocortisone, she was taking a total daily dose of 20 mg. This is in divided doses. We usually ask them to take 10 mg first on waking in the morning, first thing to do. And then they take another five mg uh around midday, four hours after the morning dose and then another uh five mg four hours after the dose after. So it will be around early uh evening between four pm, six pm. So she's been taking the carbimazole which is for the hyperthyroidism. Um and that is um in he we will have a thyroid session. Uh I think in July if you mean attend it, but this is uh thyroid peroxide inhibitor and inhibit the sensitive of thyroid hormone and she's been taking that at a dose of 20 mg and she has been taking the propranolol for the tachycardia induced by the thyrotoxicosis. So she had that from, as she lived with her parents, she wasn't a smoker. So um the com the uh doctor examined, her BP has improved and the heart rate improved after receiving the f uh bag of fluid, her G CS remained 15 out of 15. Um Anyone tell. Um uh So the levels I just the glass G comma scale. So I will just take it short because uh so the GC is a class uh comma scale to assess consciousness level. Uh We measure um uh so she had it completely fully normal. She chest examination was fine cardiovascular examination. Um No evidence of um cardiovascular compromise. Apart from actually, of course, we have the BP, it's low because of the um lack of cortisone. She had the uh uh no uh G I uh signs. Um And she was clearly hyperpigmented as we would see in someone who is not adequately replaced, um who has add are not adequately replaced. Uh The plas here are very, I'm sorry, it's very small print. Um So I will take you through it. So this, we say that was November the 11th. So when you have an adrenal crisis, um sometimes it, it could be predicated by someone who's not taking enough uh replacement or it could be pred by other things like, um, infection, trauma, any kind of injuries. Um, if you are going to surgery and you didn't have the replacement, of course, that is a ma major issue. Um So if you, uh, if you have infection, so we are going to assess for if, uh, or if you had a cardiac event. So, and other causes, of course, uh, so the white cell count uh, was uh normal. So, and then, uh, she did have AC RP uh done that was normal. So if we go from the fest on the left side of the screen, the w white cell count, this is uh normal. We say the hemoglobin, she's slightly anemic, it becomes relevant in a minute. I will tell you she has uh the MCV is just borderline on the lower. Um Then uh this is for the size of the um blood cell platelet count was normal. Uh neutrophil percentage uh number um are normal. We got uh she had the liver calcium checked for her. The calcium was high. Um So the calcium can actually be high in um adrenal insufficiency. It could be as well um high if the patient is dehydrated, which she's been. But of course, if this does not correct at IV fluid correction, you need to start thinking about other causes of high calcium. Can anyone shout to me what other causes of high calcium hyperthyroid, parathyroidism? Hyperthyroidism? Yes, hyperparathyroidism can cause it. And what else can cause hypercalcemia. Osteoma, breaking, ostomy, cancer, multiple myeloma. Yes, bone y it could cause hypercalcemia. Ok. So this can work. These two can cause a hypercalcemia. Um any kind of malignancy and bone metastasis can cause hypercalcemia. This is less likely in her condition. Renal impairment can cause hypercalcemia. But in this patient, the reason of her high calcium is uh likely dehydration. The adrenal insufficiency that we would expect to be normal uh to normalize after IV fluid hydration. But with this uh level, the patient will need to have an ECG to make sure that no ecg changes um of hypercalcemia, which she did not have, but she had sinus tachycardia. So we have a sodium low potassium high and that is expected to be seen in adrenal insufficiency. What is the part of the adrenal hormones that would be impacting this most aldosterone and three aldosterone? So, yes, aldosterone. Um when you have lack of aldosterone, you can have uh sodium being very low potassium, very high. It's one of the features of adrenal crisis as well. Adrenal function was fine. Your creatinine was fine, was raised the um as per um dehydration, the CRP was slightly above the range but not enough to say that OK, there is significant infection going on. As you read, it was the white cell count as well and you got the liver function was fine. So she did have a gas done for her as well. The PH was normal 7.38 she had the normal bicar uh she did have um as we know the sodium potassium were uh sodium was low potassium high. So the the gout shows you all these features, these are the most important points you see them in this patient condition, gout and then the lactate was slightly raised again because of uh uh dehydration. So, so she had the ECG as I mentioned and it shows sinus tachycardia for completion to rule out infection. She had a chest x-ray that uh showed uh no evidence of infection. Um So going uh to next, the treatment she you mentioned already about IV fluid, but you have mentioned that she has cortisol insufficiency. So then you will need to treat her with hydrocortisone immediately. So if you see someone in the emergency department, non add disease, low BP, do not delay giving that. So you give you get this treatment I hydrocortisone from here on. What is your next step in the treatment? What are you gonna do from here? Continue treatment with hydrocortisone and monitor patient BP. Exactly. Yes. So OK. And how much hydrocortisone are you gonna give this patient after this? Morph? MMG sorry. Every six hours. Uh 50 M. Yes. So you can give 50 mg uh every six hours. Some places might give uh IV hydrocortisone infusion 200 mg over 24 hours. But in most places, this is not convenient. So 50 mg uh four times a day. So, so far in, in a place where you have limited resources, the most important thing is that you have done your ABC D, you have uh of course, if she had low oxygen, you would have had given her oxygen. Uh And then if you had the low BP, you were given her fluid. And I'm hoping that you will have access to hydrocortisone so that uh you can get it because it is what is going to save her life, the hydrocortisone and the IV fluid. And then as you said, you will continue with the um uh I va 50 mg um four times a day, she had more fluid. Uh She is the you need. Yes. Uh You need to think about if there are other precipitating factors, pregnancy test is important. Um So the person has sent as well as for uh further blood to be sent to assess about if the replacement uh prior to presentation was OK, has sent for ac and in the morning. Uh although in the acute phase, you already um made the diagnosis, you started the treatment. That is what you need. The if you have a, a choice of uh blood test that you need to do and you can't do many blood tests. The most important in this presentation since you have made the clinical diagnosis of adrenal. Uh insufficiency is doing a urea and electrolyte to check the sodium potassium level. And the renal function. And then if you have more to do, then you are checking the full blood count and CRP I, there are so many places where they don't have the gas. Um If you don't have it, uh you would uh I think ideally have it, but if you don't have it, these three tests are the most important and on top of them is the uterine electrolyte. So the uh then she wasn't pregnant. Um There was a plan to repeat her bloods later after hydration. Uh In some places we do have here, we have a response team like team who are associated with the intensive care, uh who would be able um to help in case the BP was refractory to hydration. But in her case, she responded to fluid and the hydrocortisone the person. And this is actually just the plan for the person who saw the patient in the first place. I didn't make any modulation in this. Um They were thinking about if the BP is not improving, do I need to think about cardiac event? Which is a good thought to think about when patient coming with other crisis as a possible perception. But as we mentioned, for cardiovascular examination, apart from the low BP was fine. Um So, uh she, we looked again at the same time, we mentioned about she has hyperthyroidism, we should have had a thyroid function that is gonna be another fourth important blood test. Um And then again, actually in the white cell count, uh uh is important um to do because the Carma lately can cause complication with uh bone marrow suppression and a grams. This is very rare 3 to 5 in 1000. So the thyroid function, can anyone comment to me on the thyroid function, please? Ts is low. Uh TSH is low. Yeah. Uh and free T four is high, a little bit high. Yeah, the uh free, free thre is also high and this thyroid per so, so th thyrotoxicosis. Yes. So this patient is thyrotoxic which is we mentioned that it's gonna be consuming her um her thyroid uh hydrocortisone. The cortisol level was actually a good level detectable, but the patient had hydrocortisone. So the sample wasn't taken before thyroid peroxidase antibody. Um And T si uh they will be important if you are going to make the diagnosis in the beginning. But this patient has already had a diagnosis of uh graves disease from before if we didn't have that information. Yes. The T si this is um that is um what is it? Um one of the indicator of what if, what is the cause of thyrotoxic disease. And in this patient, it was grave disease, strongly positive in some other areas. This is equivalent to TSS receptor antibody. So, for completion screening for infection, she had a urine uh di and her urine uh showed uh that uh her uh uh nitrate and leukocyte were negative, suggesting no evidence of um urine infection. Uh They, it was around the COVID time. So the COVID screen was negative and the pregnancy test was negative. An important other point in this urine test is her glucose, urine glucose is negative. Although the ketones are slightly detectable. Um but that is because of dehydration rather than um a concomitant. Uh rather than that the patient has diabetes. Having said that this patient, same patient later in the course of her illness actually developed diabetes. So we went back to some of the her previous investigations at the time of diagnosis, she did have a positive Adal cortex antibody confirming the underlying cause of uh uh uh adrenal insufficiency in her. Um which is Addison disease. She had a strongly very high uh a as we would see, normally when you don't have cortisol uh produced due to destruction of the adrenal gland. And if you don't have enough fluid cortisone and aldosterone in the blood, the radium will be high as uh linked to the renin angiotensin system. Um For uh around we looked again around the time of um uh presentation earlier. Um uh diagnosis is it actually this is later actually, I don't know why I put it here. Uh But one point I have to mention that as you mentioned, she has two autoimmune diseases. She is at risk of developing other autoimmune diseases. Part of the assessment, you need to think about what other autoimmune diseases could come uh to could happen because she likely has a polyglot autoimmune syndrome. So, uh pernicious anemia is one of them. So you will need to at least annually screen this patient uh with a vitamin B 12 level. Uh that was normal folic acid was low. Uh you, when it is low, you need to think about again, if there is evidence of celiac disease. Again, another autoimmune disease which you do tissue transglutaminase for that, that was uh um normal um DHEA, this is adrenal and and it is low. Uh the HBA one C was tested. This is around the time in January when she developed the diabetes for the diagnosis of diabetes to be made, you need the HB A one C more than 48 and more than one occasion um in the absence of symptoms. But if you have symptoms and a very high HB A one C, this is diagnostic for diabetes in January 2022 which was a two months visit or two months after that three months, two months after her presentation in emergency department, she actually developed diabetes. She had the gastric peral antibody, intrinsic factor antibody, not all places have them available, but when they are available, you will do them uh for a screening for pernicious anemia. Annual one. So the outcome of this patient, she recovered on IV hydrocortisone and IV fluid uh when she stopped vomiting and she started eating and, and drinking. Uh So uh she had a double dose of oral hydrocortisone. Uh The fludrocortisone was not given in the beginning. She was on a high dose of hydrocortisone. Uh So she was on 50 mg Q one. They are on 50 mg QD that has the mineralocorticoid activity as well. Um So, but once uh she's no longer taking the hydrocortisone, she needs to be commended on the flu. Uh taking the IV high dose of hydrocortisone, she needs to be uh to start back on fluid cortisone. The carbimazole, we continued around the uh on the same dose. However, we start her on double dose of hydrocortisone because she is thyrotoxic cytotoxic. And we aim to continue on double dose for the rules. We tell patients who, when you have acute illness, you double your dose of a steroid, we send her home on double dose until the thyroid function becomes normal. So the adrenal cri uh so before I go next, any question, before I go to the next slide, let's see if I can see the chat. Oops, sorry. Uh Could you please specify um um a an analysis, the test that we have to provide for our patient when we suspect um adrenal insufficiency. Uh Could you please repeat that? Uh what is that? Uh what test? Uh what test usually uh you recommend to when you suspect adrenal insufficiency? Ok. So what test? So um we're gonna repeat that what test I would recommend when you suspect adrenal insufficiency. Ok. So it depends, uh it depends what you are looking at. So if you are looking at someone you are trying to diagnose for the very first time, if they do have adrenal insufficiency or not, of course, you will need to do um a 9 a.m. cortisol though early morning cortisol. So the level of this uh to say that if this patient is likely to have adrenal insufficiency or not is based on the lab. So for example, in our lab here, the level more than 3 50 um would say that um unlikely adrenal insufficiency, less than that, more likely adrenal insufficiency. This is not in a nonpregnant lady. In pregnant ladies, they have higher cortisol level. Um that's normal. So, yes, a test screening test will be early morning cortisol. If you very have very uh high suspicion, uh you can send around the same time a level. Uh because if you have a low cortisol and raise adrenal, uh a level, you can localize the level of adrenal insufficiency to the adrenal gland you will need as well. Uh Once you have uh So the screening test, you can confirm it with the short sin test, which is not done in the acute phase of this patient coming in adrenal insufficiency. But uh if uh if the patient have, of course, the key thing is that you have treated in the acute phase uh this is now you are trying to investigate the underlying cause. So the early morning cortisol, if the patient is already taking a steroid, because someone thought that they were acutely unwell, they wanted to save their life and they gave the steroid. Ok. There no harm uh in waiting for the early morning dose to uh cortisol to be done when the patient is more stable and you do it uh before the morning dose of. But usually they need to be on a little dose of before you take that. And not more than um uh 57.5 mg of prednisoLONE, which is gonna be an equivalent to 20 mg. So, no more than 20 mg of hydrocortisone. So the early mono cortisone um as a screening test, if you have high suspicion as it, as you send it, you send it because you need to send to say what level uh of a uh the adrenal insufficiency in um I will go through the rest of the slide. It will show me other things there. Uh Someone said was it uh was it the long term I CS causing adrenal suppression or an autoimmune cause? Uh This patient had adrenal cortex antibody positive. So the Adreno cortic uh uh adrenal cortex antibody positiv, it is an autoimmune disease. This patient has primary adrenal insufficiency given that she's on fludrocortisone and hydrocortisone. But I will come to that in the following slides. So, as I mentioned this. So this is a life-threatening in the current emergency, you need to correct um uh this and treat appropriately. Otherwise, the patient will die. Then this treatment to IV Fluid IV Hydrocor is um the adrenal briefly so that I other people at different level, the adrenal glands um are or the other name for them, suprarenal glands on top of each kidney. Um So they are supplied, blood supply comes from uh it's three superior and inferior adrenal arteries which come from nic artery and from renal arteries. Um This is how they look actually in a cadaver. This is um the left adrenal gland, the right adrenal gland. Um And then you do have uh again, it is retroperitoneal with the kidney. They are enclosed with the kidney in the uh perinephric Fassa, but they are separated from the kidney by the peri uh renal uh fat. Um This is how they look on the adrenal ct scan. This is a normal adrenal gland. We have the arrows showing where they are. And this is um when you break down the histology of the adrenal gland, you have the adrenal mema and then you have the adrenal cortex and the adrenal cortex, you do have the capsule and then you have the zona glomerulosa where you have the ald is produced, which is the mineralocorticoid, which will uh control the sodium potassium. Then you got zona fascia where you have the production of corticoid glucocorticoids and then the zona reticularis where you have the production of um uh of the ad adrenal androgen, including thes. We're just checking this uh someone put here, OK? That's fine looking on the chart. So uh this one, I, I don't think we have much time to go through it, but this is one thing homework for you uh is to look on the normal human steroid genetic pathway. The adrenal uh hormones are steroid hormones and produced from the cholesterol. Different enzyme pathways produce different uh parts of the adrenal hormones. Um So you get uh here uh from uh on the side, starting ending with the cortisol production going pathway through 17 hydrox uh hydroxylase. You got the predone, then they go to adrenal androgen. Um A cortisol here. Actually, the first line is aldosterone. So um this one, I will leave it for you as a homework to review later. So the uh this is when you are thinking about secondary and uh primary adrenal insufficiency. And what do you think about the negative feedback mechanism in the hypothalamic pituitary adrenal axis. So you get the adrenal cortex producing the adrenal uh cortisol. So, so, and then I think before I go there, I need to say that the adrenal Glucocorticoid are controlled by the pituitary, which is when we are speaking about the hypothalamic pituitary adrenal axis. This is the one that is uh can be impacted by the long term um use of a steroid either oral or inhaled or any kind of potent topical one. or if you have of course, or hypothalamic disease. Um, so if you have the, here, the hypothalamic pituitary adrenal axis, uh, the hypothalamus produce the cortrophin releasing hormone. Uh, ok. So, uh, so you get, uh, the hypothalamus producing cortrophin releasing hormone that stimulate the pituitary to produce uh, the ac uh end coric hormone. Um, there is someone speaking on the background. Uh would you mind muting yourself? Ok. And then the adrenal gland would using uh the cortisol uh for the al um aldosterone, the mineralocorticoid, it is controlled by a different system which is the rein angio can see aldosterone system. Um So again, this is some other thing. These are two slides. I think there is a third one that I will ask you to have it as homework. You need to know them by heart. So primary it normal, we have the negative feedback mechanism. You got uh once you have adequate cortisol produced from the adrenal gland, it has a negative feedback on the pituitarum hypothalamus so that they don't send too much crh or if you have a primary adrenal insufficiency, that is primary adrenal disease, that is the adrenal gland itself is not producing, there is a problem with it. You don't have anything going back to have a negative feed back. So you will have high ac you will have high crh. In this happens when you have a disease of the adrenal gland, any cause of destruction, other autoimmune like in Addison disease or it is caused by hemorrhage or tuberculosis or um uh you have um what is in other infection? And recently, there are some uh new drugs like immunotherapy can actually cause adrenal Luis and uh primary adrenal insufficiency for the secondary adrenal insufficiency. The you, the adrenal gland itself in the beginning is not, is, is fine, it's able to produce cortisol if you stimulate it, but you don't have enough uh hypo um what any product enough? Uh adrenal cor atrophic hormone coming from the pituitary gland. Usually, if you measured the cr which we don't usually measure the test test if you, you measure that the crh will be high. But what we'll be measuring here, the a the ash will be low and because the ash is not enough there, the adrenal cortex will not produce cortisol. So both A and cortisol will be low in secondary adrenal insufficiency. So then uh we do have again, primary versus secondary a insufficiency. We have it uh 80% of the cases. Um our uh primary uh we got uh autoimmune of uh cause of that, of which Addison disease of the primary is 75%. We say the A is high in primary, not in secondary, the Glucocorticoid and the mine corticoid. Both of them are deficient in the primary. But the second in secondary adren insufficiency because of the mine corticoid control is separate from the a uh that would be preserved, but you will have a low cortisol. The sodium would definitely be low in uh primary adrenal insufficiency if not replaced with the high potassium, uh that would most of the time have be not present to have a normal potassium, but you might have a low to low normal sodium. Uh The treatment for primary insufficiency, you need to give both hydrocortisone and fludrocortisone, hydrocortisone to replace the gluc and fludrocortisone uh to replace uh the steroid. You don't need fludrocortisone adrenal insufficiency. And uh as I mentioned, you need to think about other association. So, autoimmune Gland syndrome, like in this patient, she has um graves disease. She had diabetes. Uh she might develop other immune disease as um the course of her illness, but we will be monitoring her. Uh the adrenal uh S deficiency mostly hypo uh pituitaris. Uh What time is it? Now? What I think I will just get my phone to half the time in one minute, please. It's 22 3. So you've got about 20 minutes. Uh Hello. Hi. So it just uh this is a photo I got from internet. Actually, the patients uh who don't have enough adrenal uh hormones uh because of a decent disease, they will have pigmented the skin because of the AC will be very high. Um And then you would feel you weak, thin uh BP, low blood sugar can drop, you can lose weight and you said the adrenal crisis, um, the feature of fatigue, uh, if someone is very unwell, uh, fatigued and then you have, uh, found them to have low, uh, any of these symptoms. If some places say that, ok, if you have someone with adrenal suspected or confirmed adrenal insufficiency and, uh, you had, uh, uh, they come very unwell. You have as well on top of that too. Other things like hypo uh hypotension or hyper uh hyperkalemia or hyponatremia. Uh postural dizziness. You would think about a an insufficiency. Uh You can uh the symptom presentation could be with nausea, vomiting, abdominal pain. Um They usually would be a history of weight loss if there is protracted history without adequate control um without adequate replacement. Uh We can have other symptoms like fever, but it could be an infection causing it. If you are the patient who had a prolonged episode without intervention, they can lose consciousness, they can go into coma and they can die. Um So the uh lab finding, lab finding in adrenal crisis, you, as I mentioned again, low sodium, high potassium, you might have renal impairment because of the dehydration, but chronically untreated, you can have cytic anemia. Uh you can have a low blood sugar in adrenal crisis. We mentioned already about the treatment and once uh they are well, you can keep them initially on double dose and you taper it down. But usually the endocrinologist will be involved here. Um So, and then we go, but um, you need to be sure that your patients who have adrenal insufficiency are um aware of strict, their rules and aware that if they are going for an operation, they will need to have a, a steroid plan. So the strict the rules, uh you always tell them if you are unwell, you have fever or you have diarrhea, you need to double your dose of the steroid, the usual one. So if they take 10, 55, you go 2010 um and double, if they are on a higher dose, just double it. Uh if they are unable to keep the tablets down, they need, every one of them has an emergency hydrocortisone injection that they can give it intramuscularly. They give themselves 100 mg and seek urgent medical help if you are, they are still unwell. But for surgery, uh they need to, if uh especially either elective action or emergency surgery, you need to make sure that the patient with adrenal disease, adrenal insufficiency is replaced um with uh adequate hydrocortisone for major safety. Does that means that you give 100 mg um on induction. And then after that 50 mg qs, there are some uh minor uh procedures um that not to IV hydrocortisone. So you can just double dose on the day. They are, they are going to have dental surgery. They will uh which is not requiring anesthesia apart just from local anesthesia, they can double the dose for 24 hours and so on. Um during Coronavirus in time, the patients with a insufficiency were required not just to double the dose if they have a COVID infection. Now, it is weaker than before with the virus. Uh but if someone is very unwell with COVID infection, they might require uh quadrupling the dose if they are, they are normally taking a total of 20 M cortisone a day in divided doses. When they have COVID, it needs to be 20 mg, four times a day. Some people replace the steroid, the gluc corticoid with prednisoLONE rather than hydrocortisone. Uh That should be um on case by case basis. But the um most the physiological one for replacement is hydrocortisone. Some places I know they don't have hydrocortisone. PrednisoLONE is the replacement, usual replacement dose will be around five mg. Uh And then if they are unwell, then they will need to double that. And if they have COVID infection, we were asking them to take 10 mg twice a day. I uh so for so the answer to answer your question about how you diagnose adrenal insufficiency or you suspect it three dose 9 a.m. Cortisol as a screening test with ach rein level. And um if, if, if and if you have more extra resources, you do at the same time electrolyte because you will see if the sodium and potassium are impaired. If you have access to al you would do that. But the minimal test will be an iron three dose 9 a.m. cortisol. The that will tell you if you have enough a uh a uh cortisol or not, uh if you don't have enough cortisol, you need to find to confirm that with the short acting test. So the short action test, you would give the person sens synthetic adrenocorticotropic hormone. Usually you take a zero sample cortisol with a level, you give the injection which is 2 50 microgram. You can give it either IV or IM and then you take a sample for cortisol 30 minute. After that, you would expect to be at least more than 1 50. And then there is a cutoff point based on the labs. For example, our lab here, you need to the level to go above 4 50 to localize if it is a primary adrenal insufficiency or a secondary adrenal insufficiency, of course, the history is most important. Uh But if it is still not clear for you, the ash will be high in someone with a primary adrenal disease. It will be low in a patient with uh secondary adrenal disease. If you have a suspicion of secondary adrenal disease and you don't have a clear cause like the patient being on long term steroid, you need to do adrenal imaging through adrenal um pituitary disease or hypothalamic disease. You need to do an um pituitary MRI um where available if it's not available, um a compromise, it's going to be a pituitary ct scan, but pituitary MRI will uh give more information. And then of course, in that case, if you are thinking about standard adrenal insufficiency with no clear cause like long term steroid, you will need to send adrenal um the rest of the pituitary hormones which are the LH FSH um uh with the for the female or testosterone for the male. Uh you send prolactin um uh level um and igf one level. Um So uh we have uh 15 minutes. So uh can I have two other volunteers or actually I might just uh shout and whoever feel like wanting to say it? Uh Tell me. So this is the second case of 2nd 22 year old male. He was admitted to the emergency department. He had 12 hours of headache, vomiting and photophobia. He was drowsy. Uh He had no fever but he had possible likely from the clinical examination. Um the uh left uh 3rd and 6th nerve py. What are your thoughts of the likely diagnosis? Here? There's a possible pituitary tumor here. It is possible pitu tumor and patient. Um What you are thinking what is happening with the pituitary tumor? They are presenting acutely unwell what like the at the optic Chima which is might be pressing the optic nerves causing the disruption the uh optic pathway and we might be pressing towards the pe pe or somewhere, which is, you could say that yes. And then if they have the tumor for a long period of time and they had any bleeding and it, they can, or infection, they can present acutely with a headache, vomiting and photophobia. That is the, that is in this case, actually, the diagnosis is they have what we call pituitary apoplexy. We'll go next on the slide if we have time. Uh, is it possible it could be Foster Kennedy, Foster Kennedy Syndrome or it's too specific for this? I think I too specific. I think what I would want is if you just make a diagnosis of likely pituitary a prop, that is what you need to save the patient because you will need to give him treatment vital for him here. What would it be very vital treatment with him? Feeling unwell vomiting with? Again, we go with the ABC D and uh, yeah. And uh, and the, we get it as fast as we could, we could get the MRI of the skull itself. What is gonna be, what are you gonna do before the MRI? If you take them to the MRI without the Medica, this medication they could die on. We try to, we try to reduce the cranium pressure if the cranium pressure is causing the vomiting and the, if you are thinking about pituitary apoplexy, what is more likely to cause the vomiting than the com than the increased pressure? What is the pituitary, uh, uh, uh, gland is doing. What hormones is it producing? Which one? If you don't have enough, you die possible. It's really re using all sorts of, uh, stimulating hormones such as thyroid and adrenal and, uh, every possible. So the, yes, would the thyroid kill them immediately if it's not thyroid hormone? No. What, uh, what, what is the thing that is gonna kill them immediately? If they don't have the treatment, we come again to the hydrocortisone. So the ace, the you would yes, the ace deficiency, but you wouldn't replace with ace is short live uh and it is not given as treat. You give cortisone. So if you think that this patient have a pitu, yes. ABC de give hydro take the blood samples including the cortisol level. Or if you can if you can ace and other bloods and give the hydrocortisone while you investigate more. In this case as well, you need, we are discussing other endocrine emergencies. But you, I would want you to remember other differentials including intracranial bleeding can cause again, headache, vomiting, photophobia, uh or uh intracranial infection as well. So uh what we have next year, the patient uh had the ABC D, they sent some blood and some of the bloods came back with the sodium of less uh of 126. It was low. The full blood count was fine. CRP was not raised. The person seeing them thought about the aid hem and meningitis, they gave them treatment for that. They sent the person for CT, the person did not think about prop at the time. But if they thought about it, they should have given hydrocortisone. But the CT scan showed something. Can anyone tell me what it shows? So it showed a pituitary tumor here in the uh and it is bulky and there is some bleeding to it, which is what we call a pituitary prophylaxis, immediate action, hydrocortisone was given IV fluid were given, which is uh the IV fluid would be as part of the ABC D assessment. And uh so the endocrine team of, of course, the initial treatment, you would expect all doctors to be able to give it. But further investigation, we need involvement of the endocrine team to send uh to assess the rest of the pituitary profile. The patient actually full assessment showed that um uh what is it called? Um evidence the with the puberty, they were not well developed. Um The thyroid hormone was very low. Um four different range we have with 10.5 to 21. So no, nothing of the thyroid hormone is there. Cortisol is very low 16, the prolactin was very high. So this is a likely prolactinoma. And as you say, we want to save the vision. So you will need to do a formal visual field assessment and you need to involve the neurosurgeons because visual neutrophils are impaired. Uh uh because the patient has palsy uh or if they have a temporal Hemon, they might need to operate on him. Um The uh we said it is a medical emergency caused by hemorrhage or infection in the pituitary tumor in a pituitary tumor. Uh You need to have a high index of suspicion to diagnose it and save the life of the patient. This is the image of the pituitary gland in the um cella. Uh You have an interior and posterior pituitary. You got the hypothalamus and the infundibular of the chasm on the top. If you do have a um a very um uh en enlarged tumor, it can compress on this and caused by temporal hemianopia. I missed putting the versus um anatomy there. This is the third slide that is for your homework. I need you to look on the anatomy of the cavernous sinus. What are the vessels and the nerves that pass through that? And that's why the patient had the nerve palsy of the third and the um sixth because of infiltration of the cavernous sinus. And then the pituitary hormones, anterior pituitary produce growth hormone. Uh It's important for the bone muscle organs, prolactin for uh lactation, uh LH and FSH for gonadal um product, gonadal hormones, production and development of the gonads. Uh We got the TH TSH, stimulating your thyroid hormone, stimulating the adrenal cortex and the posterior pituitary will produce OOPS oxys. And uh it produces the vasopro which is antidiuretic hormone, um the excess of uh which can cause this idea low sodium. And then um so that is the hormones produced by the pituitary gland. This is how the pituitary gland looks on an MRI. This is a second for you. We got the sphenoid sinus. This is the pituitary gland. This is the bone cli there and then um a coronal um view you have, this is uh the pituitary gland, the pituitary stoke the optic Chism on the green, uh the uh carotid um the the vasculature and then the vernal sinus, uh the sphenoid sinus here. Um So, um we considered the particular a plex um in patient who had acute severe headache. And if uh as well, the clinical, you have a differentiate of course of sub hemorrhage. Again, you need to think about that the patient had neuro thal signs like our patient. And if the patient is known to have uh pituitary tumor and the symptoms of sign, we already know some of them. Um the most common with the, the, the headache, but you have the could be nerve palsy called including third nerve palsy. And uh that is because the vernal sinus will be involved. And this is you need to look on the anatomy of the carnal sinus. Uh you can have reduced visual acuity, visual field impairment because you press on the optic chasm, then you have bit temporal he and then if you have a fever neck stiffness, photophobia or uh these are some of you can think about maybe there is an infection. But again, you need to think about uh pituitary xy. The things that can precipitate it. Major surgery can precipitate it. Anticoagulation therapy can precept it, pregnancy, um, injury, head injury, very high uncontrolled BP. Um So, uh there are some uh guidelines on um the uh how uh you treat and so you start, if you suspected it, you mentioned ABCD and supportive measures, you give the hydrocortisone, you send it with. Um of course, you would have sent the sa once you put the Cannula, you sent for imaging and then you would liaise with the other team. And if the patient has a severe reduced visual um acuity, uh visual field deteriorating or GCS uh uh reduced, this is an indication for uh for urgent um surgical management. And if, 00 sorry, this is some of the guidelines. And if you have um and you don't have this, you might consider just continuing on conservative management to stabilize the patient and get more assessment. And once to stable the patient, they would usually most likely require some uh surgical intervention. If the tumor is very large and impacting of the chasm, these guidelines are available online. Uh If you don't uh have them, we can send them to you. I think I have just slightly just repeated it. Uh I don't think we have time for the third case, but it is about thyroid and this we have, I have a thyroid session coming in July. Any question? Um It will help me if you give feedback so that I do have emergency uh endocrine emergencies. Part two coming, I think this month um I would go through other emergencies. Everything, everything was listed. Thank you. Thank you. Thank you. Uh May I have a question please? Of course, uh uh regarding the pregnant women, uh uh how often uh do you see such a patient with adrenal insufficiency in pregnancy? You mean that if someone came with suspected a insufficiency during pregnancy, uh maybe some of them are pregnant and they are they uh take uh medicines due to add this disease. Ok. So, so, so how they do it? So the medication you, of course, they can continue with the hydro, they should continue actually the hydrocortisone. So, so you have to, I know primary insufficiency, they must continue on the fludrocortisone. They must continue on the steroid. Normally pregnant ladies would have, if they have the adrenal gland working fine, you would have much higher level of cortisol uh in them in their blood. That is because uh there is increase in the um production itself of cortisol, but there is the increase in the uh uh uh cortisol um corticosteroid, the cortisol binding globulin. So they would have higher level and then the CRF cr will be stimulated during pregnancy. So you would have much higher cortisol. So, you would expect in pregnancy by the second trimester, you would require a, a 20 to 40% increase in the dose of hydrocortisone. The dose of fludrocortisone is difficult to assess because the renin will be high anyway. Um because of uh the progesterone uh production causes some degree of resistance. So you can't measure if you have enough with the renin. But if the patient has uh high potassium uh low sodium or they have significant postural drop, they might require adjustment with increasing the dose of fludrocortisone. If their start to come down, then you need to think about. If the uh and the uh the BP is high, you might need to cut down on the dose of fludrocortisone for secondary adrenal insufficiency. You just need the steroid in the human. Uh uh the human fetus unlikely to be affected by higher doses of steroid because you do have uh an enzyme in the placenta that breaks down the steroid. So the the fetus will not have excess uh steroid. If the patient requires higher steroid, she needs to have them. She needs to have a review of the rules that she if she, for example, but she has hyper gravid uh vomiting. If she vomited the dose, she needs to take it again. Uh If she is generally unwell, she needs to double her dose. If she's unable to keep the steroid down, she needs to go to the hospital for IV steroid. Thank you. Thank you. Ok, so could I just take this moment to thank you, Doctor Mohammed for your session today. Uh We're just running out of time. The next session will start in approximately two minutes. Thank you. And could everyone just please be reminded to complete the feedback form if they haven't done so already? Thank you. Bye.