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Hello, everyone. I'm Dia. I'm one of the f ones um who went to Imperial. Um So I'm going to be giving you a talk in Endo. Um So just to start off with a few disclaimers. Um So I've tried to um go with nice guidelines and I try to update everything for 2024 slash 2025. Um But if there's anything from your placements or anything from your teaching, that conflicts what I say, then obviously go with that. What I'm going to do is I'm going to go through how to structure your history for patients. So you have a diabetes and Endos station. Um And then I'll give you an idea of the main conditions and presentations that you have in Endo as well. Um But I won't give you details on everything that you need to know and give you all the information that you need for a distinction. Um If you have any questions then feel free to type in the chat or mute yourselves. Um So just to go through the second structure, so I'm going to be going through Goiter slash neck, swellings, weight loss, polyuria, polydipsia, weight gain bones, bones, stones, and grown's pituitary tumors emergencies, an endo and I'm gonna go through some BS with some test results as well. So for your ENDOS station in cases you have a patient with a presenting complaint, you'll be asked to take a history and then say some relevant investigations come up with some differentials and say a diagnosis, then say what the management is and counsel the patient on that. And then you have four domains for that as well. So the four domains are clinical skills, formulation of clinical issues, discussion of management and then professionalism and a patient centered approach. So starting off with goiter neck swellings. So this is the first case. It's a 43 year old patient who is presenting to the endo with swelling in their neck. Um So if someone wants to say what they think the differentials are for someone who has a goiter thyroid, yeah. And specifically when you think about thyroid, what sort of differentials are you thinking? Graves disease? Exactly. So the main thing that you're thinking is graves disease, um there's a few others as well. So thyroid cancer dec veins or viral thyroiditis, you have toxic nodular goiter or plummer's disease and then toxic thyroid adenoma. And then in terms of investigations that you want to do for this patient. So whenever you are saying it in cases, you want to say that you are taking a bedside bloods and further investigations approach. So bedside you want to do your basic examinations. So you want to do a cardio exam, an ABDO exam, a thyroid exam, and neuro exam. And then you also want to perform an ECG for this patient. And then in terms of bloods, you want to do your basic set. So you want to do your full blood count, your eer and your LFTs. You also want to do your thyroid function test. I would say that's the most important one. And then um you want to do TSH receptor antibodies as well and then you want to do imaging. Um So you can do radioactive iodine technetium scans and then thyroid isotope scan and then you want to check for any auto antibodies that the patient might have. So anti TPO and antithyroglobulin. Um So, like I said, the main thing that you want to do is your thyroid function test. Um So I've got some of those levels for you. Um And if you want to just say what the differentials are for each one, so, starting off with the top line. So if a patient has high TSH and low T four, what would you say the differentials are for this patient? I go to a mean th exactly. So all of the things that cause destruction of the thyroid gland. So, thyroiditis. So you've got your atrophic thyroiditis, hashimoto's de core veins, postpartum and renal thyroiditis. So that's because of the destruction of the thyroid gland. It's sort of causing that release of T four and then the T four gets depleted, causing high TSH. Then if you have a high TSH and normal T four, what are you thinking? Subclinical? Exactly. Yeah. So, either the hypothyroidism is treated and they now have a normal T four level but they still have the high TSH again because of negative feedback or subclinical hypothyroidism. Then if they have high TSH and high T four and I could. Ok. Exactly. Yeah. So if there's, um for example, if there's a tumor that's secreting TSH, or if they have any resistance to thyroid hormone that would cause high TSH and high T four. And then if they have low TSH but high T three and high T four, then what would you say the differentials are graves disease? Exactly. So graves is one of them. But it's all of the things that I've already gone through. So graves toxic, multinodular goiter, toxic adenoma drugs can also cause it. So there's your thyroxine and your amiodarone and then any ectopic sources of um tt three and T four, for example, a trophoblastic tumor. And then if you have a low TSH and normal T three and T four. Mhm. So, subclinical hyperthyroidism. Exactly. So your subclinical hyperthyroidism. So you have normal T three and T four. But again, because of the negative feedback, you're going to have low TSH. And then if you have low TSH and low T four, secondary hypothyroidism disease. Exactly. So, you have your low T four that's caused by the low TSH. And then if you have high slash low TSH and then low T three T four. So your thyroid, yeah. Exactly. So sick, your thyroid syndrome. So, this will all be familiar to you from PA. Um, so I'd say just for your finals just to go through all of this again, it's important to know with differing TSH and uh T three T four levels what your differentials are. So, for this patient, their TSH is low, their T three is high and their T four is high, they also have anti TSH receptor antibodies and their scans shows high diffuse uptake, which you can see on the side here. So what would you say the diagnosis is for this patient? Graves disease? Yeah, exactly. So the diagnosis here is Graves disease. And then when you're managing this patient, um you want to give them some symptom relief first. So you want to start them on any beta blockers, give them topical steroids for dermopathy and then give them eye drops for exophthalmos. Um You can also start them on anti thyroid medication. So the main one will be your carbimazole, which um you start at 40 mg and then you continue for 12 to 18 months. And there's two approaches to that. You can either start at 40 then sort of trit it um until you get normal um thyroid function test levels or you can block and replace, you've got your radio iodine and then you've got your surgical approach. So your surgical hemi or total thyroidectomy. So the patient now presents with confusion, pyrexia and shock and you didn't manage their graves in time. So you didn't give them their car in time. So what would you say the diagnosis is now? So like a cytokine stone? Yeah, exactly. So you're thinking thyroid stone. So in terms of presentation, um the patient will have shock pyrexia confusion. They can also have vomiting, fever, tachycardia. They could also then have hypertension and heart failure as well. So the most important thing for this patient is that you admit them either to HD or to ICU, you then want to manage this patient. So you start off with some cooling for their fever. So you can give them some paracetamol and some fluids. You want to start them on high dose antithyroid medication. You want to give corticosteroids. So you can get dexamethasone, which is going to block the conversion of T four to T three. And then you can give some circulatory and respiratory support, for example, beta blocker and glucose iodine. Um So I have an SB I'm just going to read it out. So it's a 32 year old woman um who's had palpitations and hot flushes for four weeks. Um She's noticed a painless swelling in her neck um in the same time and her weight has decreased by 2 kg. She gave birth four months ago, um, after a normal pregnancy and she's not breastfeeding, she has a high pulse, high BP, she's tremulous and restless and then she has a large, smooth and nontender goiter and then they've got her investigation results as well. Um, so if you want to take, um, a minute to reread it and go through investigations and then say what the most appropriate initial treatment is. So we have a bee. Yeah, exactly. So, um, the answer is propranolol. Um, so the reason for this is that this lady has palpitations and hot flashes. So she's showing signs of hyperthyroidism. She's lost weight. She has a goiter and her T four and T three are high and then her TSH is low. She also has thyroperoxidase antibodies. Um, she's given birth four months ago. So you're thinking postpartum thyroiditis. Um, so you give propranolol which is going to block the effects of thyroid hormone on the heart and peripheral tissues and then you want to control the symptoms as the most appropriate initial treatment before you go on with any further investigations and management. Ok. Moving on to polyuria and polydipsia. So we have our second case who's a 58 year old patient who's presenting to the GP for excess thirst and urination. Um, so, um, again, in cases, they'll ask you to take a focused history state, any key investigations and discuss management. So, what would you say the differentials are for a patient with polyuria and polydipsia diabetes. Yeah, exactly. Diabetes. When you say diabetes, um, what type of diabetes? Both and we also have diabetes insipidus as well in nature. Yeah, exactly. So you've got your three diabetes. So, type one diabetes, type two diabetes and diabetes insipidus. And you've also got hypercalcemia in terms of investigations. Again, you want to do a bedside bloods and further investigations approach. In this case, it's mainly bedside and bloods. So bedside, you want to do a urine dip and then urine M CNS as well. And then in terms of blood, again, you want to do your baseline blood. So full blood count and LTs, then you want to do more um, bloods depending on your differentials. So glucose and HB A1C, you also want to do parathyroid hormone and calcium levels and then urine and plasma osmolalities. So for this patient, her HBA1C is 58 random plasma glucose is 13.7. So, what's the diagnosis here? Type two diabetes? Exactly. Yeah, it's quite easy. But, um, in terms of diagnosing type two diabetes, it's important to know um, the approach to it. So whether they're symptomatic and asymptomatic, if they're symptomatic, then you want to check either if their fasting glucose is more than seven or if their random glucose is more than 11.1. Um, if they're asymptomatic, then you need to have that on two occasions. Um, you can also use HBA one C to diagnose diabetes. So if it's 48 then it's diagnostic. If it's less than 48 that doesn't exclude diabetes, you just have to do more investigations to um, diagnose it. So in terms of management of diabetes, obviously, you've got your medications, but you also want to take a more holistic approach, especially when you're explaining it in your cases or counseling a patient. So you want to refer um the patient to a diabetes specialist for an individual care plan. You want to refer to support groups such as diabetes, UK, obviously, you give lifestyle advice as well. So giving weight loss advice, exercise and diet strategies, you want to make sure that they're vaccinated against influenza and um have the pneumococcal vaccine as well. And then you want to monitor the HB A1C every 3 to 6 months. Um And then you want to do that until they're stable on unchanging antidiabetic medication. So you might be adjusting that um medication until the HB A1C is at a stable level. And then you monitor every six months to maintain good glucose control in terms of management for type one. you're just going to have insulin therapy and you want to make sure to educate um the patient on self monitoring of glucose. And so they know the optimal targets for glucose as well. Then for type two, there is sort of an algorithm that you want to memorize and this is really important for both your writtens and your papers. So I would say make sure to memorize this. Well, um so first you want to see if the patient has a cardiovascular risk. If they do have a cardiovascular risk, then you want to prescribe Metformin and an SGLT two inhibitor. If they don't, then you just want to give Metformin. If they're experiencing gi side effects from it, then you change it to modified release Metformin. If Metformin is contraindicated, again, it depends on if they have a cardiovascular risk or if they have heart failure. In that case, you give SGLT two monotherapy. If they don't, then you want to start them on one of the other um diabetes medications. So DPP four inhibitor or a pioglitazone or Sulfaurea. Um So that's your first line. And then your second line is that you're going to add a DPP four inhibitor, pioglitazone, sulfonylurea, SGLT two inhibitor, then your third line is that you are going to add another one of those drugs on top of that or you start insulin based treatment. And then fourth line is that you switch one of those medications if one of them is not working or the glucose HBA one C is still not controlled or you can switch to a GLP one mimetic. Either if the BMI is over 35 or there is any occupational reasons why they can't be on insulin. Then you also want to consider if their BP is controlled. So if they are taking any BP medications, if they need to be on any antiplatelets and lipid control as well. So, if their cure risk is over 10% then you want to start the patient on statins. So the first line would be 20 mg of atorvastatin. Um, then in terms of, um, your diabetes medications, it's important that, you know, um, for each one of the types of medications, the contraindications, the effect on weight and hyperglycemia risk and then, um, effect on kidneys and liver are sort of circled. The ones that are, I would say the most important on the nice guidelines. Um So just to quickly go through it, DPP four inhibitor, GLP one SGLT two inhibitor and sulfonylurea, they all cause um ketoacidosis and then you don't give, um, also they're, they're contraindicated in ketoacidosis. And then pioglitazone, you don't give if a patient has a history of heart failure, previous or active bladder cancer or if they have uninvestigated microscopic hematuria. Um, the two medications that cause weight loss are G LP one and the SG SGLT two inhibitor. And then, um, the medications that cause the highest hypoglycemia risk are insulin and also sulfonylurea, especially in elderly patients. And then the only medication that you don't have to consider, um, for renal impairment is pioglitazone. So I'd say again, make sure you know this quite well. And then on nice guidelines, there's sort of an algorithm for um, which medications to start on and things like that. But I've already gone through that anyway. Um, and then moving on to complications of diabetes. Um, so DKA is one of the complications that's more common in type one diabetes. The patient will present with abdominal pain, vomiting, nausea and lethargy. They'll have kal breathing. And then when you do your investigations in urinalysis, they'll have ketones in their urine. Um, and then you check the blood glucose which is high, but it can be normal. And then in terms of management, generally, you want to admit them, give them IV fluids. Um and then IV insulin and potassium replacement. That's quite general. But you do need to know the whole guideline for DKA management as well. And then the complication that's more common in type two diabetes is HHS. So hyperosmolar hyperglycemic state. So in terms of the presentation for these patients, they'll have confusion, polyuria, polydipsia and nausea. Um in terms of signs, they'll have dehydration and hypovolemia. And then when you do investigations, they'll have normal ketones in their urine and their glucose will generally be over 30. So very high. And again, management is you admit you give IV fluids and then IV insulin and potassium replacement. And then this is the algorithm that you guys will need to know for DKA. Um I'm not gonna go through it now because it's quite a lot of detail, but just uh make sure to memorize all of that for your exams as well. And then moving on to the next SBA. Um, so this is an 83 year old woman who has recurring dizzy spells. Um, the episodes are associated with transient shaking of her hands, which is most noticeable before lunch and evening meals. She has hypertension and type two diabetes and those are the medications that she's on. Um, her BP is slightly high. Um, and there's not much difference between lying and standing and then her blood glucose is six and they've also got her blood results. Um, so again, if you want to take a minute and then tell me what, uh, the most appropriate therapeutic change for this patient is. You see. See, exactly. Yeah. So you want to reduce the glipiZIDE dose. That's because this patient is presenting with shaking of her hands, um, which shows that she's hypoglycemic, especially before meals. Um, anti HB one C is 50 which is within the target range. Um, so if you control the glucose too much, then that can increase the risk of hypoglycemia, especially because she is on a glycoside, which is a sulfonylurea and that's more prone to causing hyper as well. So you definitely want to reduce the glycoside dose. Ok. Moving on to the next SB, so this is a 24 year old man. He has two days of vomiting. He has type one diabetes. He's drowsy but maintaining his airway. Um, he has a low BP, high pulse, high respiratory rate, normal oxygen and then they've got investigations. So again, if you want to take a minute and say what the most appropriate initial treatment is. Mhm. Is it a? Yeah. So it's a, so you want to give fluids because there's patients in DKA. Um, so you want to um, correct their dehydration and hyperosmolality first. Um, you'd give insulin but that would be later. And then the next b so this is a 36 year old man. He has type one diabetes and has a pilonidal sinus. Uh And then it goes through which um how many units of each insulin he takes? Um He's scheduled for an excision of the sinus under general anesthesia. He's first on a morning operating list and he's asked to fast from midnight the night before. Um So again, if you want to take a minute and say what the most appropriate plan for managing his insulin preoperatively is we have e exactly e um So the reason for that is that you want to balance the hyperglycemia risk with the hypoglycemia risk. Um So if you omit the insulin, um then there's a risk of hypoglycemia. But if you take insulin while fasting, then there's a risk of hypoglycemia. So you want to keep the long acting insulin and then because this patient is first on the list and they're starved as well. You want to omit the morning incident and then resume that when they start eating and drinking again and then it's important to monitor glucose during surgery. Um, so there's three BS there that are related to diabetes. I've taken these SBS from the UK MLA Paper Bank. Um, so because three of them relate to diabetes, I would say really focus on diabetes, investigations management, just know it really well because it's most likely, um, to come up a lot in your finals. Um, moving on to weight gain. So this is a 45 year old patient who's presenting to the Endo clinic with weight gain. Um, so again, in cases, we will ask you to take a focus history, state, any key investigations and then discuss management. Um, so when you're going through a weight gain history, there's a few really important things to go through and ask. So you want to go through the timeline of the weight gain, the site and distribution impact of exercise on weight gain, the impact on the patient's quality of life if they have any stria easy bruising thin skin, if they have any cold intolerance, if they have constitutional symptoms, and then you want to do a general assistance review. So ask about their mood, any shortness of breath, vision changes, change in bowel habit and recent illness. Um, you might wanna ask about menstrual history as well, check their drug use. So if they're using steroids, um, if they have alcohol excess in their social history, and then if they have any family history of thyroid disease. So, this patient has dry eye across the tummy, centripetal obesity and is on long term stories for rheumatoid arthritis. So, what would you say? Um the differentials are for this patient? Cushing's? Yeah, exactly. So you've got your Cushing's syndrome, your Cushing's disease. And then another differential for weight gain is hypothyroidism. So, just to go through the courses of Cushing's syndrome, you have your ACTH dependent ACTH independent and Pseudo Cushing's. So under ACTH dependent, the most common cause is Cushing's disease. Um So that's a pituitary adenoma releasing ACTH. But then you can also have ectopic ACTH release, for example, from a small cell lung cancer. And then you've got your ACTH independent. So that's steroids as the most likely cause and then 10% from adrenal adenoma. And it can also be caused by adrenal carcinoma. Then you've got your pseudo Cushing's. So if a patient is taking alcohol excess, then investigations would find deranged LFTs and macrocytosis and then severe depression could also cause Pseudo Cushing's. And then you want to think about your investigations for this patient. Um So again, you do your bedside bloods and further investigations approach. But in terms of more specialized investigations, first line, you want to do an overnight dexamethasone suppression test or a 24 hour urinary free cortisol second line, you would then move on to a low dose or a high dose dexamethasone suppression test and you do your inferior pituitary sinus sampling. And then you might also want to um ask for a CT or pet scan to identify the source of ectopic ACTH. Um So just to go through um the high dose dexamethasone suppression test, um and what sort of results you have? So either you're going to have suppressed or not suppressed levels and then that's going to help you um figure out what the diagnosis is. Um So for pituitary adenoma, um what would you say about the cortisol and ACTH levels, whether they would be suppressed or not suppressed, both would be suppressed. Exactly. Yeah. So they'd both be suppressed. So the pituitary adenoma is releasing ACTH. So when you give a high dose of dexamethasone, it's going to suppress both the cortisol and the ACTH levels. And then for ectopic A CT and neither of them are suppressed. Exactly. So both of them are not suppressed. So the ACTH is coming from a source um outside of your normal access. Um And then that's going to cause both the ach and the cortisol to not be suppressed when you give high dose dexamethasone. And then for adrenal adenoma, the ACTH is suppressed. Yeah. Exactly. So ACTH is suppressed, but cortisol is not suppressed. That's because the adrenal adenoma will release cortisol. Um So when you give high dose dexamethasone, it's not going to suppress that cortisol because there's so much, but it's going to suppress the ACTH and then this is um, just a flow diagram. I'm going through the investigations for Cushing's syndrome. Um So it's split between ACTH independent and ACTH dependent. If it's ACTH independent, then you want to do your adrenal ct and check for any micro macro nodules. Um And then if it's ACTH dependent, then you want to do a pituitary MRI crh test and then eight mill G on dexamethasone test. Um If the pituitary MRI um shows that there's a lesion, then you can say it's Cushing's disease. If it's negative or inconclusive, then you want to do your um I PSS um then you want to check the gradient. So central to peripheral gradient, if there is no gradient, then you want to do some further imaging. And then that will tell you if there is an ectopic ACTH secreting tumor, if there is a gradient, um then you diagnose Cushing's disease. And then in terms of management. Um so for Cushing's disease, um the first line is a transsphenoidal pituitary adenomectomy. And the second line, you can try medications as well. So, somatostatin analogs um and then dopamine agonists as well like Berlin. And then for ectopic ACTH, the management would be um surgical resection or ablation. And then for ACTH independent, you'd remove the adrenal gland if it's a tumor. Um and then give steroids if you um need to. Um there is a risk of Nelson's Syndrome. Um There's actually two complications with the surgery. So one of them is Nelson's Syndrome. Um Nelson syndrome is when you don't have any cortisol. Um after you remove the adrenal glands, especially if you remove both and that will cause a massive release of ACTH, which is going to increase the size of the pituitary gland. Um because of negative feedback that will cause um a growth in the pituitary gland and then that can have mass effects and cause skin hyperpigmentation. You can also have a hypoadrenal crisis. If that happens, then you need to prescribe lo lifelong glucocorticoid. Um So, hydrocortisone and Mineralcorticoid. So, fludrocortisone um replacement and then if it's caused by steroids, then you need to um wean the steroids. Ok, moving on to bones mos and groans. So a patient um presents to the endo with bone pain. So again, they'll ask you to take a focused history, say any investigations and discuss management. So, for this patient, um she has constant lower back pain for six weeks, which is an eight out of 10 in severity. This occasionally um happens in her hips as well. Um She's tried paracetamol and Ibuprofen gel, but they've not helped with the pain. She has some associated symptoms as well. So, drinking lots of water, passing urine eight times a day and napping frequently, um went through menopause five years ago. Um And then a past medical history of renal calculi. So what would you say the differentials are for this patient like multiple myeloma? Yeah, exactly. Um can you think of any other differentials if we've already gone through it? But if they're drinking lots of water and passing urine, um, frequently, then what other differentials are you thinking about? The diabetes mellitus and insipidus? Yeah, exactly. So, those, those are the differentials that you're thinking about. Um, another one would be primary hyperparathyroidism. Um, that's because she's showing, um, this bone pain, um, that she's had, um, for a long time and that can be um a sign of hypercalcemia. So, primary hyperparathyroidism is one of your differentials, multiple myeloma, diabetes, insipidus, and diabetes mellitis. And then um the most likely diagnosis here is primary hyperparathyroidism because of the bone pain she's having, she has a history of kidney stones and she's postmenopausal as well. So when you're taking a history of a patient with stones, bones, abdominal grown's and psychiatric bones, um there's a few other questions that you want to ask this patient. So whether they have polyuria and polydipsia, if they have any renal symptoms, like stones, polyuria and dehydration, if they have any bone resorption, effects of parathyroid hormones or any pain fractures, if they've ever had osteopenia or osteoporosis in the past, um if they have any abdominal pain, so they could have constipation, uh pancreatitis and peptic ulcers. So it's more likely to be duodenal ulcers rather than gastric ulcers and then any change in mood concentration and confusion. And then you will also want to ask about any palpitations chest pain and any arrhythmia. Um and then you want to do investigations again for this patient. So again, you want to do your bedside bloods imaging approach. So bedside, you'd want to do urinalysis, 24 hour urine calcium and you want to do an ECG as well. And then bloods again, you want to do your baseline bloods, but you also want to do a bone profile and then parathyroid hormone HB A1C, you wanna check their Vitamin D levels, you want to check their glucose and serum and plasma osmolalities and also protein electrophoresis. That's gonna help you rule out all of your differentials. And then imaging wise, you want to do a bone density scan and do X ray if they have any fractures and then in terms of your pth and your calcium levels, um that's going to help you with your um diagnosis. So if you look at the first line, if a patient has high calcium um low phosphate and then high slash normal pth, high slash normal alkaline um phosphate, then what would you say the um differential is say primary hyperthy parathyroidism. Yeah, exactly. So you have your primary hyperparathyroidism. Um So that's when you have high calcium um and high um parathyroid hormone, but it can also be um inappropriately normal as well. Um And then I'll probably show you the answer. But for the second line, um so if they have low calcium, high phosphate, high parathyroid, high alp and then low Vitamin D or normal Vitamin D then what would you say? Secondary? Exactly. Yeah, I've shown it. Um, but that can most likely be caused by either CKD or Vitamin D deficiency. Um, so something outside of the parathyroid gland, um, that's gonna cause low calcium, which in turn is gonna cause high PTH and then, um, if they have high slash normal calcium ap and Vitamin D and then high PTH. And what are you thinking? Tertiary? Yeah. Exactly. Tertiary. Which is your autonomous um parathyroid hormone secretion. And then um if you have low calcium, low parathyroid hormone and high phosphate, what are you thinking? Hypoparathyroidism? Yeah. So, hypoparathyroidism. Um, if they have low calcium, low, um Vitamin D and high PTH, what would you say? Vitamin D deficiency? Yeah. Exactly. So, a stimulation or Vitamin D deficiency, if everything's normal apart from the ALP, then what would you say Paget's disease? Yeah. Exactly. Paget's disease. And then if everything's normal, but they still have that um, bone pain, then what would you say osteoporosis? Exactly. Osteoporosis. Um So again, I would just make sure that, you know, all of these um different levels and what the condition is as well. Um Moving on to management of hypercalcemia. So, initial management you split it into if it's mild or if it's moderate or severe. So, if it's mild, then you advise fluid intake and then you want to avoid things like thiazides and Vitamin D and then you can review again in six months. If it's moderate or severe, then you want to admit the patient. The most important thing is that you give fluids for this patient. Um So you give IV naught 0.9% sodium chloride and you want to give 4 to 5 L in 24 hours. Um If the hypercalcemia is persistent post rehydration, then you want to call your senior and give IV bisphosphonates. So either zoledronic acid or pamidronate. Um And that's so the reason why you give it is because it's an inhibitor of osteoclastic activity. So it's going to reduce your serum calcium levels. And then you can also try loop diuretics, but that's only if they can't tolerate aggressive fluid rehydration because it can worsen electrolyte disturbances. And then you want to find the cause of the hypercalcemia. So if it's because of granulomatous disease or lymphomas, then you can give corticosteroids moving on to hypocalcemia. Um when you take a history, you want to ask things like if they have any fatigue or weakness, whether they have any perioral dental paresthesia, any tetany or seizures, um you want to ask about the medication history. So, if they've been on PPIs bisphosphonates, if they haven't had any chemo or radiotherapy or if they are on any anticonvulsants, so they can all cause hypocalcemia, and then you want to ask about surgical history. So if they've had a thyroidectomy or a parathyroidectomy, and then it's quite rare but any family history of hypocalcemia, for example, in congenital Digeorge syndrome. And then on examination, um, the main findings that you have Arusal sign and chopstick sign in terms of investigations for a patient with hypocalcemia. You want to do your bedside, um, ECG. So you want to check for any arrhythmia or prolonged QT, you want to do your bloods. So that's your whole bone profile. And then you want to um consider an X ray if you're suspecting any fractures or osteomalacia. And then management wise, you want to give IV 10% calcium gluconate, 10 mL over 10 minutes. And then you want to monitor with telemetry or ECG and then you can consider oral calcium supplements. And then on senior advise, you can also give calcitriol or synthetic P th. So, moving on to another ba this is a 45 year old man who's had weight loss, fatigue and polyuria for three months. He takes many multivitamins and then they've got his investigation results as well. Um So again, if you want to take a minute and then say what the most likely diagnosis is we have. See. Yeah, exactly. So, um in this case, it's primary hyperparathyroidism. That's because they have increased calcium. They also have high ALP and it's only a slightly elevated parathyroid hormone even though the um calcium is really high, moving on to pituitary tumors. Um So a patient presents to endo clinic with vision changes again, they might ask you to take a further history investigations and then go through management. So, for a pituitary adenoma, it's very similar to what you've gone through in path already. But you can either have a secreting or a non secreting pituitary adenoma. You can have a microadenoma, which is less than 10 millimeters. And that's most likely to be benign or a macroadenoma, which is more than 10 millimeters and that's most likely to be aggressive. Um If it's large, then it can compress the optic chiasm which causes bitemporal hemianopia. In terms of it, when you're taking a history, you ask about any vision changes and they might tell you um that they um have any, they have reduced vision. So that's a bitemporal hemianopia. They might have headache and they might have excess hormone. So they might have excess ACTH, which is your Cushing's disease. They might have excess growth hormone, which is a megaly or they might have excess prolactin which causes amenorrhea or galactaria. Um On the other side, you can also have deplete did hormone which is caused by the compression of the pituitary gland which causes generalized hypopituitarism in terms of investigations. Obviously, when you do your paces, just run through your bedside bloods and further investigations approach. Uh But more specifically, you want to do a combined pituitary function test any formal visual field testing. And then you want to do an MRI brain with contrast as well. And then going through the differentials. So um first one is prolactinoma uh for a prolactinoma, the prolactin is going to be really, really high. So in the thousands, so usually about 6000, there's going to be no rise in growth hormone and cortisol. And then first line management is to replace any hormones that are deficient. So for example, hydrocortisone T four estrogen and growth hormone and then uh dopamine, I think it should say agonists. So, Kerlin and bromocriptine and then second line management is your surgery. So your transsphenoidal surgery, um if the visual symptoms um are not responding to medication, um then nonfunctioning pituitary adenoma. So, um findings are that the prolactin is between 1000 and 5000 and management. You want to do your cabergoline Bromma creatine again. You can also watch and wait. If they're asymptomatic, then you also have acromegaly. So in that case, then you have increased growth hormone, increased prolactin and no rise in cortisol. And then in terms of investigations, your gold standard is an oral glucose tolerance test. But you can also do um IGF one and they'll have a high glucose, calcium and phosphate and then management wise, it's your transsphenoidal surgery. Um and then you can do pituitary radiotherapy again, give cabergoline octreotide or a growth hormone antagonist. The um so moving on to prolactinemia, we've sort of gone through it already, but splitting it into whether it's less than 1000 between 6000 and over 5000. So if it's less than 1000, um then the differentials you're thinking are it could be due to stress, a recent breast examination or vaginal examination or hypothyroidism or PCOS. If it's between 6000, and you're thinking hypothalamic tumor, a nonfunctioning pituitary tumor, microprolactinoma PCOS or a drug. And then if it's over 5000, then you're thinking macroprolactinoma. So, moving on to the next SBA 45 year old man has six months of tiredness, reduced libido and erectile erectile dysfunction. Um This is the investigation results. Um It's kind of obvious because I've already gone through what the presentation is. Um But what's the most likely cause of his presentation? Is it? E Yeah, exactly. So it's a pituitary adenoma. Um So moving on to emergencies and endo I've already got a few. Um So I've already gone through a DK A um and HHS. Um but there's a few others that you need to know. So one of them is Addisonian crisis in terms of features. Um They'll present with shock confusion and they'll usually have known Addison's disease and then they'll have triggers that cause this Addisonian crisis. So for example, if they have intercurrent illness, if they're not compliant with their medications, if they've had any recent surgery or trauma as well, and then in terms of management, you want to do your a to approach. So when you're presenting as well, you always want to say, start with airways breathing, etc. Um And then if you are suspecting an Addisonian crisis, you treat it even before you get any biochemical results. Um and you want to start them on hydrocortisone, 100 mg IV um right away. And then you also want to um recess with IV fluids. So you can give 500 mL of sodium chloride um that will support the BP. And then if they need more fluids on top of that, then you can give that as well. And in terms of investigation findings, you'll find a low sodium, high potassium and low glucose. Um You also want to screen for infection, um establish the patient on a long term steroid regimen. And then if they're al aldosterone deficient as well, then you want to start them on fludrocortisone. Um The next emergency is a fe so the patient will present with pallor, a pulsating headache, hypertension and pyrexia. Um You want to do an ECG for patients with po that will um show left ventricular hypertrophy or ST segment elevation BT or cardiogenic shock. Um in terms of management. Again, at V approach, um you want to admit the patient um get help. Um you can take the patient to ICU as well. Um You want to do alpha blockade first. Um So you can give IV alpha blocker like phentolamine. Um and then you repeat until it's a safe um BP and then when controlled, you can use a long acting alpha blocker like phenoxybenzamine. Um And then you give 10 mg of that once a day orally and then you can increase that by 10 until 30 mg. And then you give a beta blocker which will control tachycardia or mi slash dysrhythmias. Um And then you want to then do a surgery for them that will be elective and it'll be around 4 to 6 weeks later, which will allow for full alpha blockage and volume expansion. Does anyone know why you do alpha blockade um blockade before um, you give a beta blocker? Ok. If you're not sure that's all right. Um But the reason why you want to do alpha blockade first before you give a beta blocker is if you give an unopposed beta blocker first, that will worsen um the high BP that they might already have from the VA. So you always want to do alpha blockade first. Um moving on to hypopituitary coma. Um So in terms of the presentation, they might have hypothermia, refractory hypotension, they might have headache and loss of consciousness. They might have a hypo and it's usually present in someone with known hypopituitarism. For example, if they have a pituitary epilepsy or Sheehan syndrome, in terms of investigations, you want to do cortisol levels, ACTH glucose thyroid function tests, and then a CT MRI as well. And then when you're managing this patient, you want to give hydrocortisone, um I va 100 mg four times a day, you want to replace their thyroid hormone and then if they have pituitary apoplexy, then you can do surgery, but that's quite specialist and it's usually done on a case by case basis. Um I'm just gonna go through a couple of SBA S for test results as well. Um, so this is the first one. So it's a 74 year old man. Um, he's been increasingly unwell with progressive thirst and nausea for two weeks. Um He initially described needing to pass urine more frequently than usual, but has not passed urine for 24 hours and he has type two diabetes. Um So it's asking to calculate the serum osmolality. So again, if you want to take a minute and then say what the answer is. D Yeah, exactly. Um So the way that you calculate serum osmolality is by um multiplying the sodium by two and then adding the value of urea and glucose. So that's 149 times two. Then you add the H 15.4 and the 41.7 and that will give you your 355.1 moving on to the next SBA. Um So it's a 65 year old man. Um He has constant back and right knee pain for six months, partially relieved by analgesia. Um He's an exsmoker and otherwise, well, they've got some blood results for him um including X ray and isotope bone scan. Um So again, if you want to take a minute and say what the most likely diagnosis is. We have B Exactly. So it's Paget's disease. That's because of the elevated alp. Um even though they have a normal calcium and phosphate and then the bone scan also um says areas so it will be like patchy uptake, um or like patchy areas of increased uptake um in the femur lumbar spine and skull. Um So that was my last SBA. Thank you so much for coming. Um If you have any questions, then I'm um free to answer them. Um And then please, if you can fill, fill in the feedback form as well. Thank you.