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Hi, everyone. Welcome to the endocrinology talk. We'll be starting shortly. Just waiting for everyone to join. Okay, guys, if you wanna start to talk. Hi, everyone. My name's idea and everyone. I'm Sandra and we're both fourth years, And today we're going to just be going through a few endocrinology topics, so I'm going to be starting with diabetes and some adrenal topics. Um, I'm going to do some parathyroid, a bit thyroid and some quick conditions at the end as well, so we'll just be swapping over halfway. We'll have loads of STDs throughout the whole talk. And then if you guys have any questions, just write them in the chat box. Yeah. Enjoy. Yeah. Good. Okay, so we're just going to start with an S V A. So, um, Mohammed presents to the emergency department complaining of nausea and vomiting over the past day. He complains that before this has been excessively thirsty and passing large amounts of urine on examination, he has dry mucous membranes are prolonged capillary refill time and deep labor breathing. And his blood results are serum. Glucose is 27 so it's raised and serum ketones are also raised. So what typical finding will be seen on an ABG. So I'll give you guys a minute or so to just do this. All right? So I'll do you want me to share the polls? Are you watching them? Yeah. If you can watch them, that you can take over there. Okay. So I'm going to stop the pole now. The majority of people said C, which is the right answer. So it's raised onion gap. Um, metabolic acidosis. So the patient is in DKA and this is because of the history. So they have polyuria polydipsia. They're dehydrated there in ketosis and also the hypoglycemic. And you can also see that they have the deep labored breathing. So this is the castle breathing, and this is to basically compensate for the metabolic acidosis by blowing off the excess carbon dioxide. So now DK will typically result in a raised onion gap metabolic acidosis because of the production of excess Keto acids that will lower the pH um and then the other options. So the mixture of spiritual metabolic acidosis That's incorrect because it's completely metabolic. And then the normal onion gap, metabolic acidosis that usually because we have the decreased bicarbonate in DKA. We have the increased onion gap, so it's not normal, and then gap. Um, the reduced onion gap. Metabolic acidosis is incorrect because, um, a low onion gap is usually due to other causes such as decreased albumin or hypocalcaemia. And respiratory acidosis is incorrect because in DKA, the excess acidosis is because of the metabolic cause, not respiratory cause. So what is D. K? Um DK occurs in Type one diabetes. It's a life threatening diabetic emergency, and it occurs when the person is not producing adequate insulin themselves or they're not adequate not injecting adequate insulin to compensate for this. So it occurs when the body doesn't have enough insulin to use and process the glucose. So it's like defined by three main factors. So you have your ketonemia above three. You have acidosis with your bicarbonate being below 15, and you have hypoglycemia above 11 millimeters per liter. So there's three main domains that I thought would be useful to go over just to talk through the pathophysiology because then that will also help guide us with our treatment. So number one we have our metabolic acidosis, so when you have the lack of insulin, your cells are in starvation mode, essentially because of the lack of absorption of glucose. So they then start to start to release glucagon and other hormones, causing gluco neogenesis and like pollicis, which produces free fatty acids. And now, when there's a lack of insulin, the free fatty acids become ketones and ketones are weak acids, and this essentially leads to the metabolic acidosis. And then secondly, we have osmotic diuresis, so now that this is because of the hypoglycemia, so you have a really high osmolality of your blood, and what happens here is you have fluid shifting from the intracellular space to the intravascular space, and this increase in fluid is now going to be excreted via osmotic diuresis in the kidneys and then alongside the fluids. Electrolytes will also be dragged out of the filter and excreted. Now this leads to a depletion of potassium and also a mask hypoglycemia. So there's, um, a potassium imbalance, which is also really important to know about with DKA, because when insulin is lacking, potassium is moving out of cells and then this is raising the plasma potassium levels, even in the presence of total body potassium deficiency. So now these are the most dangerous aspects of DKA are the dehydration, the potassium imbalance and acidosis. And these are the three key aspects that we need to manage like and this will help us guide our management. So the key symptoms for DKA are nausea, vomiting, You have polyuria. You have polydipsia, you have abdominal pain, cause more breathing pair, drop breath and headache. As I said before, the costal breathing is due to you know, the excess so blowing off the carbon dioxide to reduce the acidosis almost to compensate. And you have the pear drop breath, which is due to the acetic acid to the ketone, is basically being converted to acid acetone producing this pair drop breath and the diagnostic criteria. So you have the lower glucose above 11 millimeters per liter, pH below 7.3 and ketones above three. And for management, I usually just remember this is Phillip. So you have your fluids. You have insulin and potassium. So with fluid, you want to start off with isotonic stadiums, so you want to start off with 0.9% sodium chloride. You also want to make sure to avoid giving a fluid bolus because if you give a large amount of fluid really quick, this will increase your risk of getting a, um, cerebral edema. And then, with insulin, you want to start as a fixed intravenous infusion at 0.1 unit per kilogram per hour, and then with potassium you. Also it's really important to monitor the cardiac function so serum potassium is often high on admission, despite your total body, potassium being low and then this often falls quickly following treatment with insulin. And this results in hypochelemia. So it's important to add potassium to replacement fluids. And if you start increasing your potassium infusions by quite a lot, then you need to start doing cardiac monitoring just because hypochelemia can affect your heart. And now Deke, a resolution so DKA is known to be resolved. When the pH goes above 7.3, the ketones are below 0.6 and bicarbonate is above 15. Now, when these criteria met, you can now, and the patient is also eating and drinking. You can move them to subcutaneous insulin. Um, the ketonemia. An acidosis should have settled within 24 hours, but if they haven't, you should think about referral to an endocrinologist. And then it's also important to know about a really big complication of DKA, and this is cerebral edema. So if you notice that the patient begins to have headache, irritability, visual disturbances or any changes the focal neurology you need to start thinking about the cerebral edema. And Children and young adults are more more vulnerable to this following fluid resuscitation. So you need to do a CT head and senior review. Um, and just really quickly to go over what cerebral edema is is, um, so dehydration with your D K and hypoglycemia causes water to move from the intracellular space in the brain to the extra cellular space. So then the brain cells shrink and they become dehydrated. So when you give, really like you give a high amount of fluid very quickly, you get a rapid shift of water from the extra cellular space to the intracellular space, and then the brain begins to swell and become edematous, which can lead to brain cell destruction and death. Now I'm going to move on to the next S p A. So Rahul, a six year old boys brought to the GP because he has recently started to wet the bed again. He gained continent overnight at age four, and he's been fine overnight since. But he's wet the bed every night for the last two weeks. Also, he's always pestering his parents for water and juice. Otherwise, he's a healthy boy, and he's getting on well at school. On questioning, his father notes that his son has lost weight recently. His mother has a thyroid condition and can't eat bread or pasta. On examination, the boy appears thin and a urine dipstick shows positive for glucose. So which cell type has been destroyed by the immune system? I'm going to try, and I'm sure I can Yeah, okay, I'm gonna stop the pole now, So the majority of people said See, which is pancreatic beta cells and all of you. All right. So, um, pancreatic beta cells are depleted in type one diabetes, so you have a child with nocturnal enuresis polydipsia and weight loss with a family history of autoimmune disease. So this is most likely diagnosis of type one diabetes. So that's autoimmune destruction, um, and pancreatic alpha cells. For those of you who said that those produce glucagon and not insulin so, um, just a bit more in type one diabetes. So this is characterized by an inability to produce all secrete insulin because of automation destruction of the beta cells. And this is the production site of insulin in the pancreatic islet of language on, um so the absence of insulin, least an increase in the rate of glucose production from the liver and reduced peripheral uptake of glucose. So this is exacerbated by the high levels of glucagon and other counterregulatory hormones, and this results in an osmotic diuresis like I mentioned before four d. K. So this results in the three key symptoms. So we have polyuria, polydipsia and weight loss. And for investigations, you usually do urine dip, the ketones and glucose. You do random and fasting glucose, and you might. You might need to do C peptide and diabetic or two anti antibodies, which I'll talk about bit more later. You don't regularly use HBA one C as it's not accurate for Type one diabetes that's usually used for type two. So, um, the diabetic auto antibodies. So these are further tests needed when Type one diabetes is suspected. But the clinical presentation include some atypical features. So, for example, if the patients above 50 or if they have a bm I of 25 or above, or if they have a slow evolution of the hypoglycemia. So examples of some of these auto antibodies you have your anti guard so antibodies to glycemic as the decarboxylase you have. I see a I A two and I eh, eh and, um, in terms of random and fasting glucose. So Type one diabetes is diagnosed with a fasting glucose of above seven or a random glucose above 11. But it's really important to know that if the patient is asymptomatic, you must have these demonstrated on two separate occasions. So one reading of a fasting glucose of above seven in an asymptomatic patient will not diagnose Type one diabetes, and um, in terms of the management. Management is typically multiple daily base basal bolus insulin regimen. So the basal refers to an injection of a long acting insulin, typically in the evening, which gives constant background insulin throughout the day, where, as the bolus refers an injection of a short acting insulin, usually three times a day before meals. Um, and it's also injected according to the number of carbohydrates consumed. Insulin pumps could also be given to patients above, above 12 or if they're struggling to control the HBA one c. Another thing that's quite important to know about that sometimes questions are about is about lipodystrophy. So if you inject into the same spot repeatedly and you can get this condition where the subcutaneous fat is hardened and this prevents the normal absorption of insulin when further doses are injected to this area. So for this reason, patients should cycle their injection sites, and it's also important to know the blood glucose target so on. Waking the blood glucose should be between 5 to 7 millimeters per liter, and before meals and any other times of the day, it should be 4 to 7, so the next s be a pre A. A 63 year old diabetic woman is admitted to a hospital in order to have intravenous anti antibiotics for community acquired pneumonia. On Day three of admission, she becomes confused and drowsy, after which she has a short seizures which spontaneously resolved. Her capillary glucose is noted at $3.1 million per liter, and she's unconscious. What is the most appropriate management of this patient. All right. Okay. I'm going to stop the pole now. Majority of you said I am glucagon, which is the correct answer. But a lot of you also did say IV glucagon. But I'll just talk about why that was incorrect. Answer. Oh, sorry. IV glucagon was around. Um, so this is the most rapid method of reversing hypoglycemia, and it's indicated as a patient is unconscious and has had a seizure. I am glucagon is acceptable, but it's not as rapid, so it's reserved for times when I've access isn't possible. You wouldn't give oral glucose tablets because the patients unconscious Um IV lorazepam will be wrong because this won't tackle the cause of the seizure. The cause of the seizure is the hypoglycemia, and stopping all diabetic medications wouldn't treat the current situation, but it may prevent further hypoglycemic episodes. So what is hypoglycemia is when it's a low blood sugar level, and it's defined as glucose being below four millimeters per liter. So in diabetes, this is caused by too much insulin or not enough carbohydrates or not processing the carbohydrates properly. And this could also be due to alcohol. So sometimes alcohol causes exaggerated insulin secretion. Um, and this is just because alcohol causes redistribution of some of the circulation in the pancreas, causing leading to excess insulin. So your typical symptoms would be hunger tremors, sweating, irritability, dizziness and Palo. But as as you can see here, the lower the hyper the lower the sugar levels, the worse the symptoms tend to be. So if you have a blood glucose level below 3.3, you'll get autonomic symptoms like sweating, shaking, hunger, anxiety, nausea. If your blood glucose levels for below 2.8, you'll get neuro neuro glyco Penick symptoms due to inadequate glucose supply to the brain. Um, so you'll get things like weakness, vision changes, confusion or dizziness, and then some severe and uncommon features of seizures and coma. And a lot of times, questions will ask you what the first thing you want to exclude is, and it is hypoglycemia. So, for example, and strokes, you would wanna exclude hypoglycemia first, because a lot of the symptoms can overlap, Um, in terms of the management of hypoglycemia. So it depends on whether the patient is conscious, whether they can swallow, so if they can, can do both. You want to give them 50 15 to 30 mg of a fast acting carbohydrate, glucose tablets and a drink. If they're conscious but can't swallow, you want to give them glucose gel around their teeth, so glucose gel or dextrose gel. And if they're unconscious, you want to enable IV access and give an IV glucose load and you want to consider I am glucagon if it's difficult to get them to establish IV access. So the next SBA we have Abdul, a 75 year old male, presents to the emergency department with 11 day history of Polyuria Polydipsia, increasing drowsiness and confusion. He has recently been started on oral antibiotics by his GP for a urinary tract infection. His past medical history includes Type two diabetes and hypertension. His medication history includes metformin, 1 g twice daily and ramipril, 5 mg once daily on examination, his Glasgow coma scale is 13 and 15, um, his apyrexia tachycardic and hypertensive with dry mucous membranes, and decreased the Integra. So which of the following investigation results would confirm a diagnosis of hyper as Mullah Hypoglycemic state. I'll stop the pole there then, So the majority of you have said serum osmolality of 330. And that's correct. So this is, um so this is HIPAA is more hypoglycemic state, and it's characterized by volume depletion in the absence of ketoacidosis. So so that for that reason, being is wrong. So you wouldn't get any ketones in your urine. Um, and you also see is correct because you have the triad of significant hypoglycemia, hypersexuality and volume depletion. So, um, a chair. So what this is is an acute diabetic emergency in patients with Type two diabetes mellitus. So the lack of insulin is coupled with a rising counter regulatory hormones such as cortisol. You have growth hormone and glucagon, which causes a profound rising glucose that's meant to say glucose glucose monitoring. Um, and then a certain amount of insulin is retained, and this prevents the development of ketosis that defines DK. And some common precipitant of this include infection, high dose steroids, my cardio infarction, vomiting, stroke or poor treatment concordance. So, um, the excessive glucose leads to a massive osmotic diuresis within the kidneys with the loss of essential electrolytes such as sodium, potassium. So this is because the proximal tubules in the kidney only have a certain capacity for reabsorption of glucose. So once this is reached, the remaining glucose is just passed through. The renal nephron is just causing diarrhea versus so as this water is lost, there's profound dehydration and there's a reduced circulating volume, so you get a really high osmolality and marked hypoglycemia. Um, sometimes patients with this condition may lose up to nine liters of water, so and the increase in osmolality will increase some compensation mechanisms, so you'll have more ADH release, which which will stimulate your thirst. But if this can't compensate for this extreme regional water loss, then the hypovolemia will just progress to an A k i electrolyte disturbances or even eventually, hypertension in coma. Um, it's also important to note that the hyposmolality state of the condition leads to hyper viscosity that will increase your risk of arterial venous thrombosis. So a lot of the patients are put on compression stockings just to prevent the risk of DVT. Um, so just going through some of the symptoms of this So you some general symptoms of fatigue, lethargy, um, nausea, vomiting, polyuria, polydipsia, neurological symptoms. You can get altered consciousness, headaches, papilledema weakness. So hematological symptoms, like I said before the hyper viscosity of the blood leading to potential stroke or peripheral arterial disease and functions and some cardiovascular symptoms like dehydration, hypertension and tachycardia. So the three main things that define H. H s. So you've got hypovolemia increased serum osmolality above 320. This is an important number to remember and hypoglycemia above 30 with no ketosis or acidosis. So because of the significant fluid deficit, your initial management will usually just be fluid resuscitation to restore the circulating volume. And the initial fluid of choice is intravenous. 0.9% sodium chloride, Um, and at least one liter should be given over an hour. Um, if you have significant hypertension, you'll increase the amount of fluids that you're going to use. But if the serum osmolarity is not declining despite the 0.9% sodium chloride, then the fluid should be switched to 0.45% sodium chloride, which is a lot more hypotonic relative to the patient's serum osmolarity, and then it's really important to also monitor the management so rapid changes of ceremonies minority are dangerous and can result in cardiovascular collapse and central Ponty Mile mile analysis. Um, so monitoring and replacing potassium is particularly important if insulin has started. And this is because, just like I was talking about in DKA, insulin drives potassium intracellular early, leading to a lower plasma concentration that could cause dangerous arrhythmias and rapid changes has to be You have to be avoided. So a safe rate of fall of the plasma glucose of between four and six millimeters per hour is recommended, and the rate of fall of plasma sodium shouldn't exceed 10 millimeters per liter in 24 hours and then in terms of insulin for this you would have to check the patient's ketones to see if the insulin is actually needed. Um, and it's only used if ketonemia is present, so this would be in a mixed picture of DKA slash h h s. So, for this, you would give a fixture insulin at half the amount that you would use for DKA. So I would use 0.5 units per kilogram per hour. Um, yeah, So the next SBA. So we have our CIA 62 year old female presents her GP for a diabetic review. She was recently diagnosed with diabetes, and she's trialed lifestyle changes. So today her HBA one c is 58 millimoles and at the time of diagnosis, her HBA one c was 51. Her past medical history comprises CKD with an estimated G fro of 22 chronic pancreatitis. She recently underwent PCI. So what is the appropriate management option? Okay, so I'm going to stop the pole there. So 48% of you have said prescribed kind of blood flows in, and that's the correct answer. So this is a patient with a diagnosis of type two diabetes. Who's trial lifestyle changes already, and these approved Ineffective, as shown by her HBA one C Um so he's all this patient is also gone, undergone a PCI, and they they have established cardio vascular disease. So in this case, then metformin is contraindicated due to the severe CKD as well. So the nice guidelines then say SGLT two inhibitors should be introduced as monotherapy. But I'll talk about that a little bit more later. Some people also said, um, so for the other options, um, A is incorrect because the patients HBA one C has risen to 58 despite the lifestyle changes. So this indicates a suitable medical that's suitable medications should be added now rather than rather than six months. See is incorrect because nice guideline suggest that those patients with established cardio vascular disease and can't tolerate metformin should have SGLT two mono therapy rather than an SGLT two with another drug and D is incorrect because the patients G F R. Is 22 indicating severe chronic disease and metformin can be prescribed in this category of patients. So, um, Type two diabetes essentially repeated exposure to glucose and insulin, which makes the cells resistant to the effects of insulin. And now this results in the pancreas becoming fatigued, and the pancreas eventually starts to produce less insulin, leading to a chronic hypoglycemia. So the symptoms of this would be fatigue, polydipsia, polyuria and unintentional weight loss. Um, so some of the risk factors of this would be ethnicity. Um So, for example, some non modifiable ones, like black Chinese or South Asian ethnicities, also being having an old being older, also having a family history of Type two diabetes. Some modifiable risk factors are obesity or having sedentary lifestyle or a high carbohydrate or particularly refined carbohydrate diet. Um, so to diagnose this, the fasting glucose should be above seven random glucose above 11.1 and HBA one C above 48 now the same as type one diabetes. This needs to be shown twice if the patient is asymptomatic for, um, a proper diagnosis. Um, and I'm just going to talk a bit about pre diabetes or prediabetes is an indication that the patient is heading towards diabetes, but they don't yet fully fit the full diagnostic criteria. But they should be educated regarding diabetes and begin to implement lifestyle changes to reduce their risk of getting to that stage. So they're not currently recommended to start medical treatment at this rate. So, um, you can have you can test this via impaired fasting, glucose or impaired glucose tolerance. So the impaired fasting glucose is actually means that the body struggles to get the blood glucose in a normal range, even after a prolonged period without eating carbohydrates. So the body struggling with the homeostasis of just getting your glucose to a normal level and then impaired glucose tolerance, is when the body is struggling to cope with processing a carbohydrate meal. Um, so the levels for this would be HB a one C between 42 47 impaired fasting glucose of 6.1 to 6.9 millimeters pelita and impaired glucose tolerance of 7.8 to 11.1 on an oral glucose tolerance test. So now I'm going to talk about the management of Type two diabetes. Um, I also have a flow chart on the next slide, which will explain it a bit. A bit more detail, but just briefly. You start with lifestyle measures, and then you go to lifestyle plus metformin. And then when the HBA one C will increase to about 58 that's the indication to add a second drug. And now this drug would be a hypoglycemia, causing drugs such as a sulfonylurea pioglitazone or an SGLT two inhibitor. And then, um, when the HBA one C is not decreasing, that you need to add another drug from the prior list, or you need to think about insulin based treatment. So this is the flow chart that I was talking about. So if your HBA one C is above 48 you need to add metformin standard. Release it. It's also sometimes a lot of questions are about patients having GI eye symptoms on on metformin. So if this happens and you need to trial a modified release metformin instead, um, and then if the HBA one C rises to above 50 58 then you can introduce a second drug. So a DPP four, um, an SGLT two inhibitor, sulfonylurea pioglitazone. And then, if the HBA one C is still equal to or above 58 then you need to try a triple therapy with the above drugs. And if this is not effective, not tolerated or contraindicated, then you need to add metformin, sulfonylurea and a GOP one agonist. So that's something like sanitizer. But there's a few. Um, there's a few things that you need to know about this. So for a GLP one agonist, you only add that if the B m I is above 35. So for people who have problems with obesity or if the B M I is below 35 weight loss would help the patient's comorbidities, um, and going back to the top, it's also important to know that if metformin is contraindicated, um So, for example, um, in CKD and the patient also has heart failure or cardiovascular disease. You need to do, uh, SGLT two mono therapy because that's shown to have a really good cardiovascular outcomes. Um, and if not, then if they don't have any heart failure, if they don't have cardiovascular disease, then you want to do a DPP four or myself and diarrhea or pioglitazone. And then this is just a summary slide of all the different diabetic drugs. I just thought it would be good to go over so metformin. It's important to know that it's weight neutral, and it doesn't cause hypoglycemia. Some side effects are diarrhea or abdominal pain. And like I said before, you would give modified release metformin in this case. But it can also cause lactic acidosis and contra. Indication of metformin is also lactic acidosis. And then there's also caution in renal impairment. Um, and then we have DPP four. So an example of this is sitagliptin, which is also weight neutral and doesn't cause hypos. Some side effects of this are GI tract upset, upper respiratory, respiratory tract infections or pancreatitis. Um and then we have pioglitazone, which is from the group that thiazolidinedione, which increase insulin sensitivity and also decrease the liver's production of glucose. Some notable side effects of this, um, I use the pneumonic elbow, So this is edema, so fluid retention, which is why it's contraindicated in heart failure. Then you have liver impairment, bladder cancer, a written osteoporosis. But it doesn't directly cause osteoporosis. It just increases your risk of fractures because it decreases your bone mineral density, and also it causes. It causes weight gain. So elbow, um, and then it's contraindicated in heart failure and active bladder cancer. And then we have cell phone diarrhea's, um, and this is the most common. One is the Gliclazide and Sulfonylureas will stimulate insulin release from the pancreas and some notable side effects to know about this causes weight gain and hypoglycemia, and also it's a voided in pregnancy, and once at night, areas are used as monotherapy. Also, they can increase your risk of cardiovascular disease, Um, and then GLP one mimetic So examples exenatide, which is given as an injection. It's also important to know that because sometimes questions will ask you, um, when patients don't really want to be given an injectable drug so it's important to not choose this one. Um, so this will cause weight loss. So it's really helpful in some obese patients. And also it doesn't cause hypoglycemia. Some side effects a g I upset weight loss and dizziness, and, like in the previous slide, it's considered of triple therapy is ineffective in these certain cases. And then lastly, we have, um, SGLT two inhibitors. So these will end with the suffix guaifenesin. So, like empagliflozin canagliflozin or dapagliflozin. So how they work is the SGLT two SGLT two protein is responsible for reabsorbing glucose from the urine into the blood into the proximal tubules of the kidneys. And these inhibitors will block the action of this protein and then cause glucose to be excreted in the urine. So, um, one really bad side effect of this is that can cause bony is gangrene. So this is necrotizing fasciitis of the genitals because of the glucose urea, and it can also cause normal glycemic ketoacidosis. Now I'm going to be moving on to, um, adrenal. So Hannah, a 42 year old woman, presents her GP complaining of weight gain. She's gained 10 kg in the last month despite exercising and a balanced diet. Additionally, she noticed an increase in her body hair and a new answer. Acne on her face on examination, centrally localized capacities noticed. And she has recently been prescribed oral corticosteroids for her adhesive capsulitis of the shoulder. So given the most likely diagnosis, what acid base and balance would you expect? So I'm going to end the pole there. There was a few mixed results, but the correct answer is e so hyperkalemic metabolic calculosis So I'll just go through the answers now. Um, so the answer is, um this is Cushing's disease. So this causes a hypokalemic metabolic ankylosis because when the levels of cortisol are high, um, so the cortisol is 10 free to bind to mineral mineralocorticoid receptors, which causes an increase in water and sodium retention. Also increase potassium excretion and increased high hydrogen ion secretion so leading to the alcohol OSIs and also leading to the hypochelemia lower levels. Yeah, Like I said, um, so then the other answer is incorrect because a hypoglycemic metabolic alkalosis will result from bicarbonate loss. So, for example, from diarrhea. But this patient isn't complaining of any GI symptoms, so it's not that and B is hyperkalemic metabolic acidosis. This is usually due to type for renal tubular acidosis. C is wrong, um, and D is hyper metabolic alkalosis, and this is commonly due to vomiting. But in this case, the patient hasn't complained about vomiting. So, um, Cushing's syndrome is caused by prolonged exposure to an excess of glucocorticoids and the cause of this maybe endogenous or exogenous. So exogenous means it's derived externally. So due to the administration of glucocorticoids, either as a medication or misuse, and this is by far the most common cause of Cushing's syndrome, um, you can also have endogenous causes of it. So this is derived internally, and now this is due to excess production of glucocorticoids within the body itself. But this is very rare. Um, and Cushing's disease, which refers to cases caused by a pituitary adenoma, are responsible for the majority of these cases. So the presentation of Cushing's disease would be around in the middle with thin limbs. Um, so you have a patient with a round moon face, central obesity, abdominal Australia, buffalo hump, proximal limb muscle wasting, easily bruising, reduced libido amenorrhea. And this is an example of some of the symptoms and what a typical patient would tend to look like. So, um, questions. Disease can be a C T H dependent or ACTH independent, and that's how it's split. So ACTH dependent, um, causes of it, uh, when ACTH is directly involved in, um, Cushing's syndrome. So that would be things like Cushing's disease. So pituitary adenoma ectopic ACTH production. So from Paraneoplastic syndrome, like small cell lung cancer or ectopic corticotropin releasing hormone production. So when it's produced by malignant tissue, um, some ACTH independent causes can be things like prolonged exposure to exogenous stories. Like I said, the most common cause of crashing syndrome adrenal tumors like adenomas, carcinomas and hyperplasia is that result in cortisol excess. So to investigate this, we use 24 hour urinary cortisol and the lower high dose dexamethasone suppression test, which I'll talk about in more detail. So, um, the dexamethasone suppression test is basically the choice for diagnosing Cushing's syndrome, so this involves giving the patient the low dose test initially and which is kind of like a screening tool. So if the low dose test is normal, Cushing's is excluded. But if it's abnormal, then the high dose test is, um, performed to differentiate between the underlying causes. So to perform the test, the patient would take a dose of dexamethasone, which is a synthetic glucocorticoid at night. And then the cortisol and the ACTH will be measured in the morning. And the intention is basically to find out whether the dexamethasone is suppressing, um, the spike, the morning spike of cortisol. So the low dose dexamethasone suppression test would use 1 mg of dexamethasone. And a normal response is for the dexamethasone to suppress the release of cortisol because of the negative feedback because of the increased cortisol, um, stopping the hypothalamus from producing corticotropin releasing hormone and from the pituitary response to stop producing ACTH. And then these low levels of Crohn's ACTH will eventually result in a low cortisol level. But when it's not suppressed, you know, this is the abnormal result, and then the high dose dexamethasone suppression test is then performed after an abnormal result. So, um so what? You would see So in the different causes, So in a pituitary adenoma. So this is on the pituitary gland. 8 mg is enough to suppress both the cortisol and ACTH. My negative feedback so it wasn't enough in the low dose test. But in the high dose test, this is actually enough to stop and suppress the cortisol. So then here you would see a low cortisol level and a low ACTH level in an adrenal adenoma. So you have a lesion here on the adrenal gland. Now, in this case, cortisol production is separate from the pituitary, and it's coming from the adrenal glands. So it's kind of out of the hate, like it out from the hypothalamus and anterior pituitary. So suppression of ACTH is seen through negative feedback. But the cortisol levels are staying high because cortisol just keeps being produced from the adrenal gland separately. So in this case, you would see a high cortisol, but low ACTH and then lastly in an ectopic ACTH tumour. So a small cell lung cancer. Um, neither ACTH or cortisol are suppressed here because the ACTH is being produced from the lung, and it's kind of coming from outside of the HPV axis and is unaffected by any dexamethasone. So here you would see high cortisol and high ACTH, and I just have a little diagram here, So a low dose dexamethasone test and what the normal result would look like. So you get a low suppressed cortisol or high cortisol would be indicative of Cushing's syndrome. And then, with the high dose test, um, Cushing's disease would be have a low cortisol, um, and high cortisol and a low ACTH would show an adrenal adenoma. High cortisol high ACTH would be ectopic ACTH secretion. Um, I don't know. I went that went through that a bit fast. But if you want to just look back and I've written a lot of notes as well, so you can just have a look and just clarify that. So in terms of the management of Cushing's disease, so the management of exogenous Cushing. So what you would do is you would withdraw the cortical steroid. But one thing is that it's really important to not stop this abruptly because you can, um, the patient will. Then you develop suppression of the normal endogenous glucocorticoid production and then result in an Addisonion crisis. Instead, the patient should gradually stop and have a regimen with clothes, safety netting and monitoring. And for the rest, Transsphenoidal surgery is the gold standard treatment for questions disease. So this is basically when you go through this whole process and you go through the nose to remove the tumor. So for questions, disease. So the pituitary adenoma you're going to resect from the pituitary gland. And it's also important to do a pituitary MRI for an ectopic ACTH cause you wanna surgically remove the source and also chemotherapy for adrenal lesions. You want to do adrenalectomy or even just resection of the tumor itself. So, um, the next s be a an A. A 39 year old woman is referred to an endocrinology clinic. So for the past six months, she complained of fatigue, weight loss and dizziness on standing. She has a range of blood tests and the following results found to be significant. So she her nine AM cortisol is low. So it's 312 no animals. Pelita. So what is the next best step in management? So I'll stop that the majority of you, said E, which is a shorter acting test, which is the right answer. So this is Allison disease, and the short acting test can be used to confirm adrenal insufficiency. So it's ideally performed in the morning when the adrenal glands are the most fresh, and the test involves giving Xanax, then, which is synthetic ACTH, Um, and then I'll talk a bit more about what this test actually is later on. So Addison's disease is primary adrenal insufficiency, and this is caused by destruction or dysfunction of the adrenal cortex. So the adrenal glands sit at the top of each kidney, and they were really important organ responsible for the release of catacholamines, the adrenaline, adrenaline, glucocorticoids, mineralocorticoid and sex hormones. And the most common cause of the adrenocortical cortical insufficiency in the Western world is autoimmune adrenal itis. So this is when auto antibodies will target enzymes involved in the bio synthesis of steroids. Um and then, like the whole world, the most common cause of Addison's disease is TB, so primary adrenal insufficiency. So this occurs when there's a reduction of glucocorticoids. Um, and when they're normal, physiology is interrupted. So, um, as I said, it's when there's destruction or dysfunction of the adrenal gland. And so in this test you would see decreased blood cortisol and also increased or normal ACTH production, um, and then secondary adrenal insufficiency. So here you have a reduction in a C T h. So this is affecting the pituitary gland, not the adrenal gland as, um, like primary adrenal insufficiency. And this is seen as part of panhypopituitarism isolated deficiency after brain injury or due to all do two drugs. So in this case, you would have low cortisol and low ACTH, and then a tertiary. Adrenal insufficiency is caused by a reduction in CRH, so corticotropin releasing hormone. And this is usually seen following chronic glucocorticoid steroid use, um, and then in terms of the features. So for Addison's disease, specifically, you would have non specific symptoms sometimes so lethargy, weakness, anorexia, um, vitiligo is a common finding. Also seen in Anderson's. I've seen this in quite a few questions. Um, you have a salt craving because of the hyponatremia. You get hyper pigmentation in the Palm a crisis. But it's also important to know that the this hyper pigmentation doesn't happen in secondary adrenal insufficiency. And that's a good way to kind of differentiate between the two. Um, and this happens. This hyperpigmentation happens because of the stimulant effect of the excess ACTH on melanocytes to produce more melanin, Um, you would also have hypertension hypoglycemia. Um and this happens because of because of the testosterone being low, so you would have you would have hyponatremia and then you'd have an Estonian crisis sometimes. So this is a potentially life threatening presentation of Addison's disease, and it's caused by a significant deficiency in glucocorticoids and mineralocorticoid. And it's commonly seen in tertiary adrenal, um, sufficiency. And as a result, um, of exhaustion, steroids and and Addison's disease. That may occur following an acute decompensation where an additional stress So, for example, infection results in an exacerbation of pre existing deficiency. So the short acting test So, um, is synthetic ACTH. So this is given in the morning, and serum cortisol is unmeasured zero through 30 and 60 minutes after administration. So in a normal individual, you'd see cortisol level doubling in response to the synthetic ACTH because of ACTH, stimulate stimulating cortisol production. However, Addison's you have the failure of cortisol to rise. Um, and this is when it's rising less than double than the baseline. Then you know this is Addison disease. You can also do other tests like nine AM serum cortisol or adrenal antibodies. Also VBG s A. P gs and your knees. Um and then acute management. So for the dystonia in crisis, so you manage this with IV hydrocortisone, 100 mg and IV fluid. Rehydration. Um, you also should do cardiac electrolytes and blood sugar monitoring. Um, you use 100 mg because that's sufficient mineral called called activity, and you don't really need the hydrocortisone. Acutely. For patients that already have Addison's disease, you should double the glucocorticoid dose and keep the fluid records own. Dose the same. So someone with chronic Addison's disease. You manage this with hydrocortisone in two or three divided doses, so you want to give 20 to 30 mg per day, with the majority given in the first half of the day, um, you and then hydrocortisone and also patient education. Addison's disease is very important, so to inform patients to never miss doses and also hydrocortisone injections, medic alert bracelets and steroid cards. So the next SBA and this is the final condition from me. So Ali, a 48 year old man, presents his GP with the three year history of hypertension that has been difficult to bring under control, no medication has been successful in reducing his BP, significantly accompanying the high BP, a muscle weakness and knocked down and bacteria so on examination. His BP is 164 over 82. Blood tests demonstrate low potassium and high LDL stone to run in ratio. Given the likely diagnosis, Which of the following is the most likely cause of this patient's presentation? So I'll stop the pole there. The most common answer was A, which is adrenal adenoma. But that's actually the incorrect answer. The correct answer was. See, so bilateral idiopathic adrenal hyperplasia. Um, so the history and examination findings indicate primary hyper all the strength of the steroid is, um so this is constant drome, and this is also the most common cause of secondary hypertension. Um, the most common cause of this is bilateral idiopathic adrenal hyperplasia in approximately two thirds of cases, and the rest is usually an adrenal adenoma. And classically, this presentation will include hypochelemia. But in reality, most patients tend to have normal potassium levels. But in SPNS, they do say that's usually hypochelemia. Um, previously, adrenal adenoma was actually the most common cause of primary hyperaldosteronism, but now it's changed to bilateral idiopathic adrenal hyperplasia. So apparently hyperaldosteronism is basically increased aldosterone. And what this does is it will increase your sodium re absorption from your distal tibia. Well, resulting in hyponatremia. Um, it will cause increased potassium secretion from the distal tubule and increased, um, hydrogen ion secretion from the collecting ducts. So this would give you a picture of, um this would give you hypokalemia hypertension and alcohol OSIs so you can test this and differentiated from secondary aldosteronism. So via the ALDOSTERONE. Brennan ratio, because in primary aldosteronism, you will have a high aldosterone and Lauren in because Brennan is only raised when the BP is low. Um, but in cons, you have you have high BP, so your BP is always high and you're running will remain low, whereas in secondary hyperaldosteronism, excessive running will stimulate aldosterone production. But in this case, Brennan remains high because secondary hyperaldosteronism is usually do two things like renal artery stenosis, where the BP and your kidneys are significantly lower than the BP in the rest of your body. So therefore you have high aldosterone and high Renan. And once you've done this initial aldosterone Renan ratio, then you'll do a high resolution CT scan of the adrenal glands. Um, this will tell you what kind of cause you have for your primary hyperaldosteronism. And then you will do Some patients choose not to have this but adrenal sampling. It's quite an invasive test. Um, and then you'll find out whether it's an adrenal adenoma or bilateral adrenal hyperplasia, and this will guide your management. So for an adrenal adenoma, you tend to do surgery for removal of this or in a bilateral adrenal hyperplasia, you will usually give aldosterone agonist such as brain uh, lacto. So, um, that's the end of my part. Now pass on to Sandra, who will be going through some more parathyroid and thyroid conditions. Hey, hi, guys. So, like I said, I'm just gonna be going through a few more conditions. Um, really quickly as well. So, like, she said, it's going to be a few more SBS. Um, so let's get straight into it. So the first s be a is prayer is a 72 74 year old female with end stage renal failure who presents to the E. D with severe abdominal pain, constipation, frequency of urination and dysuria. For the past week, blood tests show that she's got a high corrected calcium level. Her phosphate is also high, and her P T H level is also high. So, given the most likely diagnosis, what is the definitive treatment for this patient hyper parathyroidism. So I'll just open the polls one second. Okay, Okay, I'll send the pole that it. So the majority of you went forward Option D, which is Oh, which is correct. So for this question, we first we need to identify what the diagnosis is. So in this case, with the symptoms that the patient is presenting with the end stage renal failure, abdo pain, constipation and all the other symptoms along with the blood test, it shows a picture of tertiary hyper parathyroidism. So I'll go into that in a bit more detail later. But once you get this diagnosis, you need to know what the definitive treatment for this is. And it's parathyroidectomy, which is the removal of the parathyroid hormones. Hence where the answer is deep. So let's go into a bit more detail on what parathyroid hormone does. So Parathyroid hormone is a hormone secreted by the chief cells in the thyroid gland, and it responds to Hypocalcemia. So there are four parathyroid gland situated in all four corners of the thyroid gland. Um, and the parathyroid hormone is decreased by the chief cells like I mentioned. So the role of P. T. H. There's three main roles I break it down into the first one is increased activation of osteoclasts. So in simple terms, osteoclasts are essentially the cells in the bone that break down bone. And that means that they increased calcium and phosphate reabsorption in the bone. So you're increasing the levels of calcium. You've then got the increased reabsorption of calcium from the kidneys. So this occurs by inhibition of reabsorption of phosphate from the proximal convoluted, trivial. So that means there's an increased amount of exclusion of phosphate. So you've got low phosphate levels, and that actually increases the calcium reabsorption at the ascending loop and the distal convoluted tibial. And the last roll of P. T. H is that it increases vitamin D activity. So vitamin D activity so vitamin D increases calcium absorption from the gut as well. So all three of these things are increasing the levels of calcium that you have in the blood. So in a question when you need to identify hyper parathyroidism. There's a pneumonic that's really helpful to remember which some of you might already know, And it's stones, bones, groans and moans, so to go through those in a bit more detail. So for stones were talking about things like renal stones. So symptoms related to renal stones might show up in the question for bones. It's often things like bone pain and groans, abdominal groans. So things like constipation, nausea, vomiting and my bones are psychiatric moments of symptoms that would include things like depression, fatigue and psychosis. So this slide is talking about the different types of hyper parathyroidism. Uh, we'll go through each of them in a bit more detail. So primary hyperparathyroidism. It's caused by uncontrolled parathyroid hormone, which is produced directly by tumor of the parathyroid glands, and that leads to hypercalcemia. So an abnormally high level of calcium in the blood and, um, this essentially is treated by surgically removing that tumor. And then you've got secondary hyperparathyroidism. And the main causes for this are low vitamin D or chronic renal failure, which leads to actually a low absorption of calcium from the intestines, kidneys and bones, which is why your calcium level is low and sometimes it can be normal as well. And the parathyroid glands react to that low serum calcium level by excreting more parathyroid hormone, which is why your P T H level is high. And over time the total number of cells in the parathyroid gland actually increases, and this hyperplasia and the glands become bulky. Um, and the parathyroid hormone is essentially very high, and you treat secondary hyperparathyroidism by correcting the vitamin D deficiency or by performing a renal transplant to treat the renal failure and then, lastly, tertiary hyperparathyroidism, which is what the question was on. So that actually happens when secondary hyper parathyroidism goes on for too long. So we mentioned the hyperplasia of the cells earlier, so that high level of P T. H is now in the absence of any low vitamin D or CKD. And so that means that there's a high absorption of calcium and intestines, kidneys and bones, which causes the high hypocalcemia shown on the table. And to treat that like in the question, you surgically remove part of the parathyroid tissue so that you return the parathyroid hormone back to an appropriate level. So these are just some other M S K conditions that you might want to have a look over, but we weren't able to cover in a lot of detail, but they're also associated with calcium levels. So firstly, you got renal osteodystrophy. So this is a metabolic bone disease in patients with chronic renal failure, and they will present with symptoms of hypocalcemia and hyperparathyroidism, and they also have symptoms like osteo Malaysia, osteonecrosis and pathological fractures. Then you have osteomalacia, which is a bit more common you might have heard of again. This is another metabolic bone disease. And, um, what happens in this one is that there's incomplete mineralization of the bone matrix and the most common cause of osteo Malaysia is a vitamin D deficiency, and patients often complain of sort of bony pain, and they might have limited sunlight exposure. Hence the low vitamin D. Um, and diagnosis is normally made, and you get a low vitamin D with normal calcium or high P. T. H. And then the one that is quite often comes up in question has Paget's disease, and this is quite an easy one to remember. It's a disorder of bone turnover. So there is increased activity of osteo class and osteoblasts. And how to identify in the question is that when you're looking at the blood tests, all the levels will be normal, apart from a L P, which will be significantly raised. Okay, so let's move on to the next SBA. So Hannah is a 35 year old lady under the care of the neurosurgeons for treatment of a pituitary adenoma following endocrine testing. This is found to be nonfunctional. However, prior to the surgery, she's found to have a higher serum calcium level of 3.8. A diagnosis of hyper parathyroidism is then made, and it's suspected that she may have an endocrine syndrome affecting multiple parts of her body. What investigation should you undertake next? Okay, I'll send the pole there. So this question actually, the answer is sorry. Let me just is CT pancreas, so I'll explain it in a bit more details. So for this question, you need to know that pituitary tumors, parathyroid hyperplasia and pancreatic tumors all come under the umbrella of the multiple endocrine neoplasia one syndrome, the men's syndrome. So a lot of your e and um I can see why you said that, because there's different types of multiple endocrine neoplasia. But actually, thyroid ultrasound would be more for if you're looking for things like thyroid medullary cancer, which is actually found in men too, and not men One. Um So if you go through all of them in a bit, um, the options A with CT adrenals. So that's, um, also found in men, too, for pheochromocytoma is not in men. One, which is what this patient has. Uh, CT chest is not normally, um, sort of done for multiple endocrine neoplasia is it's more for things like Cushing's disease to see if there's any topic ACTH production or anything like that, but not really done for many conditions. And it's not an upper GI I endoscopy because again is not normally that commonly found with men's syndrome. So I'll go to through the men's syndrome is a bit more detail, So multiple endocrine neoplasia. So these are a group of conditions where there's formation of hormone producing tumors in different organs around the body. So there's three subtypes. You've got 12 a and two B, so starting off with one, this is a mutation in the men one gene, and it affects three things in particular, so it affects the parathyroid. It affects the pancreas, and it also affects the pituitary. And I've also written their ways in which that it can affect these organs. Um, and it's really important to remember these, because often in questions you can it might come up as hyperplasia or not, that is, affected the parathyroid organ and then men to a is different incentives mutation in the R. E t G, and it affects the thyroid. So this is where you get your medullary thyroid cancer, which very commonly comes up in questions. It affects your adrenal glands. You can get a pheochromocytoma is, and again it can affect your parathyroid glands. You can get hyperplasia and adenomas. You've then also got multiple endocrine neoplasia to be so this often, um, presents with mucosal neuromas mucosa. Neuromas are benign tumors of nerve tissue, and there are characteristic future of men to be particularly, um, it also affects thyroid, adrenal and parathyroid, similar to to a. But another distinguishing factor between the two is that you can get something called marfanoid body habitus in to be which is basically a term used to describe people with a very particular body shape. So you've got tall, slender physique with long arms, hands, fingers, legs and things like that. So there's another SPL. So Joanna is a 33 year old female who has been unwell for some time with symptoms of fatigue, headaches, double vision and intermittent blackouts. She has been found on the latest occasion to have a random blood glucose of 2.2. She recovers from these episodes. When she takes sugary sacks, it is suspected that she has an INSULINOMA. What is the best test for establishing this diagnosis? Okay, okay. And the pole there. So the correct answer for this one is Oh, okay, deep. So it's quite mixed with the answers, and this is quite a hard question as well. So I'll go through each one of them and why? The answer is deep. So firstly, um, it was 72 hour fast test. So in the question, it mentioned that the patient is expected to have it into lymphoma. Um, and the gold standard test for insulinoma is the 72 hour fast test. So I will go into an Insulinoma is in a bit more detail, um, in a couple of slides. But it's essentially a tumor of the pancreas, which makes excess insulin that your body can't use. And so you get hypoglycemia and you get a triad of symptoms, and the 72 hour fast test observes any drops in your blood glucose levels. And at the point of proper hypoglycemia, you take insulin and other hormones to identify whether you have this condition. So a lot of people put E as well, which is the three times, 15 hour fast test. So this is also, um, I think the test is used, but it's so it's not to be as gold standard as a 70 12 fast test. And it's not as good as the prolonged test, either. Um, a lot of people also a so measuring serum insulin levels so plasma insulin levels can fluctuate all the time, and so it can often give you a misleading figure, especially in the case of an insulin oma. Um, the Glucagon test is not really often used for the insulin oma. It's normally used to assess things like the HPA access, um, and see the insulin tolerance test is actually a screening test that's used for pituitary disorders, where you assess the body's hormonal response to stress instead. Okay, so there's a lot of S p A questions in this section. So the next one is. Jamal is an 18 year old boy who is in the 97th percentile for height and is on the 75th percentile for weight. He reports headaches and greasy skin with acne. He recently presented the GP complaining of pain in his hands, especially at night. He denies diarrhea and has a normal bowel habit. He denies feeling hot or cold, and his BP is 150 over 85. What is the most appropriate initial investigation to support the diagnosis? Okay, I'll end the polar so well done to everyone that said Nope. Be, um so yeah. So for this question, um, you need to identify what the diagnosis is from all the symptoms. So the getting larger, the headaches, the greasy skin, the increased BP, all sort of points towards the diagnosis of acromegaly. Um, and with acromegaly, the gold standard test for diagnosis is serum I g f 10 insulin growth factor one, Um, and in a couple of slides, I'll go into this in a bit more detail. We just got one more SBA to do. So the next one is Luke, a 25 year old man who presents to the GP with episodes of flushing and sweats. He describes these occurring intermittently and reports that he has periods of diarrhea that coincide with these symptoms. During these episodes, he feels that his heart is racing. He does not report vomiting or a temperature, and on examination of his abdomen and mask is noted in the right upper quadrant. He is normotensive. What is the single most likely diagnosis? Okay, I'll send the polar. So this is also quite split. But the answer to this one is E carcinoid syndrome. So this one is quite a difficult question. So in this, um, you sort of need to identify, obviously what? The diagnosis. Is that what you're asking? But the key thing to identify here is that the fact on examination of the abdomen, you can feel a mass noted in the right upper quadrant. So, um a This is indicative of a carcinoid tumor that's metastasized to the liver and that's led to systemic symptoms. Um, and it hasn't undergone metabolism in the portal circulation. So in terms of I know an option is the carcinoid tumor as well. But it wouldn't be see purely because, um, it doesn't take into account of systemic symptoms such as diarrhea and flushing and sweats and things like that. And I know a lot of people put a pheochromocytoma as well. Um, and obviously, with the chroma a pheochromocytoma, you do get symptoms like a flushing and sweating and things like that. But Pheochromocytoma is a over activation of the sympathetic nervous system. The patient in this question is normotensive, and when you get a pheochromocytoma, this wouldn't be the case. So that's why it's not D. Um, it's not a hepatocellular carcinoma because there's lack of any risk factors like hep B or Hep C. Um, and it's also not be infected gastroenteritis, because again, there's nervous factors like a fever or vomiting, so that makes that less likely. So we went through three conditions really quickly there with some SBA, so go into a little bit more detail now, So let's start off with the insulin Oma. So like I mentioned earlier, and Insulinoma is a neuroendocrine tumor of the beta cells of the pancreas and that result in inappropriate insulin secretion. So you're producing too much insulin the body doesn't need, and so you get symptoms of hypoglycemia, like sweating or feeling tired and dizziness as well. The cases are usually benign and our managed surgically, but they present with Whipple's Triad, which is something really important to identify any questions. So Whipple's Triad includes signs and symptoms of hypoglycemia, Um, serum glucose levels of less than 2.2 and symptom reversal upon glucose administration. And then the investigation, like we found out in the question, is a 72 hour fasting glucose test. Okay, now moving on to acromegaly. So acromegaly is when you've got excess amount of growth hormone, and growth hormone is produced by the anterior pituitary gland, and the most common cause of acromegaly is unregulated growth hormone secretion by a pituitary adenoma. And you need to know some of the key symptoms of acromegaly can come up in a question, one of them being bitemporal hemianopia. And this is when you can't see or you have loss of vision of the outside. Um, the outer sides of your vision. So this is because the optic chiasm it's just above the pituitary gland. And if there is a tumor in the pituitary gland, it can be big enough to press on the optic chiasm and the optic chiasm is where the optic nerves cross. Hence why you get this sort of visual field defect and then other sort of symptoms. You can get our prominent forehead, large hands and feet, et cetera, et cetera. So the definitive test is or the initial test. Sorry is the insulin growth factor one. And then you can also do an oral glucose tolerance test because high glucose can normally suppress the growth hormones that can help you identify whether the patient has a condition or not, and then definitive treatment is transsphenoidal surgery. So I think you mentioned earlier. But you go up through the nose and you use that to remove the tumor and then, lastly, Carcinoid syndrome. So Carcinoid syndrome is, um, essentially, you have carcinoid. Tumors are very rare, and they're very slow growing malignant tumors, and they develop in your endocrine system, and 5 to 10% of these tumors secrete hormones in particular. serotonin and the symptoms that you see in carcinoid syndrome are actually because of the effects of serotonin, and it's breakdown products on the systemic circulation. So this is why you get diarrhea, flushing grease and abdominal pain. Um, the test for this condition is a 24 hour urine. Every five h I A five h a is, um, a metabolite of serotonin and that sort of mediates the effects of carcinoid syndrome. Um, and then the management can be pharmacological, so you can use agent such as octreotide, which is an analog of somatostatin, and that inhibits tumor products. Or you can use surgery to decrease the tumor site. Okay, we've got more STDs now, so a 30 year old woman presents her GP with a lump in her throat. It lies just below below her thyroid cartilage and measures two centimeters by two centimeters. It is firm and moves on swallowing, but not on tongue protrusion. She has also noted that some of the glands in her neck are enlarged and lymphadenopathy is palpated in the anterior neck. What is the most likely diagnosis? Okay, I'll end up there. So, um, the answer to this one which a lot of you did actually get is papillary thyroid cancer. Um, so I'll go through all the options and explain why it is why it isn't so. Firstly, the answer was papillary thyroid cancer. And this is actually the most common malignancy. And in this question, the things that sort of point towards it is that it's a lot more common in women, and it presents in the third to fourth decade of life. So this fits this lady perfectly. It caused some sort of solitary nodule, and it metastasizes early in disease. So this is actually why she's got some of the glands in your neck are enlarged, and lymphadenopathy is also palpated in the anterior neck. Um, it was an eight, which a lot of you also put as well, because this doesn't sort of fit the demographic of the patient that we're looking at. So thyroid lymphomas actually present a lot later in life. So the 6th 7th decade of life, um, and it presents with an enlarging gotta and cervical lymphadenopathy. So she does have a sort of lymphadenopathy, which doesn't really fit any of the other criteria. So it wouldn't be thyroid lymphoma um, medullary thyroid cancer like we mentioned earlier. It's associated with the men to syndrome where parafollicular cells of the thyroid, and it's from the follicular cells of the thyroid. Sorry, and it has calcitonin is a tumor marker. Um, it's not the it's not anaplastic thyroid cancer, because this presents much later in life compared to the age of this lady. And it's a very, very aggressive tumor as well. And it doesn't really show any signs of that in the question and then follicular thyroid cancer. So this is actually the second most common thyroid malignancy. Um, it's more common in women as well, but again, it presents a lot later than papillary. Thyroid cancer does. Okay, um, another SBA. So a 37 year old lady presents with sweating, palpitations, tachycardia and acute confusion. On examination, she is warm to touch, has an irregular pulse, a heaving apex, evidence of pulmonary edema and a smooth, symmetrical swelling of the anterior neck. So the question is, what is the most appropriate initial management of this patient? Okay, I'll end the pull up. So the answer to this question, which again a lot of you did get, was IV propanolol so in this question, and we sort of identify what the patient has. So she's actually presenting with Thyroid Storm, which I've got slide on in the next. The next labs on this, basically, but it's IV propanolol because I asked for the most appropriate initial management of this patient. So with thyroid Storm, it's very important to control the cardiovascular symptoms, um, and the other peripheral symptoms as they lead to the most immediate complications of thyroid storm. And that's what Propanolol is. Therefore, um, I'll explain again in a little bit more detail in a second. I'll just go through why it's not the other ones. So it's not IV digoxin because it's actually the second line. So you use IV propanolol first, and only if, um, the propranolol is contraindicated. You actually use the Cytoxan. Um, but it's again. It's not ideal because one is second line and to the patient is very young. And this drug, actually overall increases mortality, so we wouldn't really be wanting to use it in a 37 year old patient. Um IV thyroxine will actually worsen the hyperthyroid state, so you definitely don't want to be using that one um, and logo. Ziauddin is actually used as ultimate management for thyroid. Um, and it's not used as the initial step and IV hydrocortisone again. It's very important to use it, and it is used in the management of thyroid Storm. But it's not the initial management. Because of the effects of the I IV. Hydrocortisone are immediately take a few hours for the actually work. So let's go through the management of thyroid storm. So thyroid storm is an acute, life threatening state where the body produces excess, uh, thyroid hormones. Um, and so this is actually due to long standing untreated or undertreated hyperthyroidism, for example in graves. So, um, it could be precipitated by infection. Um, surgery and trauma and the lab finding that you get are similar to hyperthyroidism so you can get a low TSH with high T four and t three. Um, so the main presenting symptoms. They're not very specific, but it's still important to know what they are. So you've got pyrexia. You've got fevers, hypertension, tachycardia and delirium, Um, and then in terms of the management, So the first thing you need to do is you need to sort out symptom control first. So, like in the question, the first line is IV propanolol. So beta blockers are used to inhibit the conversion of T four to t three. And like I mentioned earlier, the second line is IV digoxin. So, um, if the patients got asthma and they've got a low BP, you can give the digoxin instead and then step to the main. A misstep, too, is to reduce the thyroid activity, because this is due to hyperthyroidism. So the first line is propylthiouracil, which blocks new hormones enthesis and inhibits peripheral thyroxine conversion. You can also give local Ziauddin four hours later, and that's an iodine solution that blocks thyroid hormone release. Um, so again, you're reducing that thyroid activity. And then, um, you're also written down. What second line is there as well? Just to be aware of that. And you also give IV hydrocortisone, Um, not initially as step two, because it reduces the thyroid inflammation. Um, and again, it reduces peripheral conversion of T four to t three. And the last step is also to treat any complications that might actually arise from the thyroid storms. If the patient goes into heart failure or hypothermia. Those kind of things you should treat at this point. So the next s p a is prayer. Is a 45 year old lady being seen in the endocrinology clinic. She complains of a one month history of always feeling hot, sweating constantly and experiencing palpitations. The following tests were carried out. So TSH is low free. Thyroxin is high and her TSH receptor stimulating antibodies are positive. So what other findings would support the most likely diagnosis? Okay, I'll send the pole there, So yeah. So the majority of you got this one correct as well. So the answer to this one is pretibial myxedema. So with this, you can identify that the patient has, um, Grave's disease. So in this the most, the the finding that would support the diagnosis the most is pretibial myxedema because this is the sort of the symptom that is only really found in this condition. Weight gain and thinning of hair, um are found in thyroid conditions, but it's just looking at the question in particular, What finding would support the likely diagnosis the most, which we'll see. And then I've got one more on the thyroid. One less be on the thyroid. So a 35 year old woman with a history of graves' disease has had a previous thyroidectomy. She is on levothyroxine 75 micrograms a day, and she admits to a poor compliance with the therapy. So choose from below the thyroid function test you would expect to see in this patient. Okay, I'll end the pull up. So again, the majority of you did get this all right, so the answer is deep, so I'll just explain why it is deep. So in this question, the patient admits that she's got poor compliance with the therapy. So with Levothyroxine, Levothyroxine is T four, and it's got a half day of seven days. So in this option, TSH is not normal. It's still raised, which is what you'd expect in Grave's disease and the T four replacement, which is what the levothyroxine is because it's been intermittent. It's not been able to suppress the T TSH, so you've got a normal T three t four. But because the patient isn't using it regularly, you've not been able to suppress the TSH. Hence why it's still raised. So, um, I've made a quick like sort of a diagram of the thyroid tests and what the different different levels mean in terms of diagnosis. So in if we start off with hypothyroidism, so if you start with TSH level, you need to check whether it's high or low first. So if the TSH level is high, you then need to check T four and t three. So if the TSH level is high and you've got a low T three and t four, that is primary hypothyroidism. So that's when the thyroid gland itself is not able to produce adequate amount of thyroid hormone. However, if you've got a normal T three and T four, which is what was in the question that subclinical hypothyroidism. So that's mild thyroid failure, where your TSH levels are varied and sort of your T four and T three levels are varied as well. In the if you've got a low TSH level and then you check it the T four and T three, and you also got low T three and T four that secondary hypothyroidism. It's less common, and it sort of occurs when the problem isn't with the thyroid gland itself, so the thyroid gland is working fine, but the pathology is actually related to the pituitary gland or the hypothalamus. Um, and then you've got hyperthyroidism. So essentially it's the same thing, but the opposite. So your TSH levels you need to identify whether they're high or low, and then if the TSH level is high and you've got high T three and t four that secondary hyperthyroidism. So again, um, it's when the problem is not with the thyroid gland. The thyroid gland is working fine, but the pathology is with the pituitary gland to the hypothalamus, which means you're producing too much thyroid hormone. If your TSH level is low and you check your T four and T three and they are high, that's primary hyperthyroidism. So that's a problem with the thyroid gland, or it's producing too much thyroid hormone. And if it's actually normal, T three and t four that subclinical hyperthyroidism. Um, so you also made a quick list of other conditions that we weren't able to fit into this talk in a lot of detail, but it's important to have a look over, um, so myxedema coma. That's a hypothyroid state, and I just put key symptoms down here that often when you can see them in questions. You can identify what the diagnosis is. And that's just hypothermia, bradycardia and confusion. So just make sure you remember those three symptoms SIADH the syndrome of inappropriate ADH is something to look over diabetes insipidus We do actually have a slide on this, uh, in in a few slides, um, and then also again, look over prolactinomas and congenital adrenal hyperplasia is as well. So now we just got some really quick conditions, um, that we're going to go through. So first of all, a pheochromocytoma. So what essentially is this? So to start off with, we need to know the pathophysiology. So adrenaline is produced by chromaffin cells in the adrenal medulla, and a pheochromocytoma is a tumor of these chromaffin cells. So that means you get an increase in the amount of adrenaline produced, and the adrenaline actually is secreted in bursts. So that means that the symptoms are worse when you've got too much adrenaline and they can be worse at certain points. And so the symptoms of sort of what you'd expect if you've got too much adrenaline in your body. Things like anxiety, sweating, headaches, hypertension, um, and things like that. The diagnostic criteria or how you diagnose it is with 24 hour urine catacholamines. Um and you don't sort of measure serum catacholamines because these are unreliable and they naturally fluctuate. And so it's quite difficult to interpret the results. Um, and then you also measure plasma free medicine difference. Um, and this is better because it tells you how much adrenaline is secreted during the 24 hour period. So metanephrine is actually a breakdown product of adrenaline, and they have a long half life, so you can actually measure it in the blood, uh, in the plasma. Sorry. And then, um, that makes them less prone to dramatic fluctuations throughout the day. So you get a bit more of a reliable tool and then very quickly, the management is alpha blockers like phenoxybenzamine. And if you're on alpha blockers, you can also add beta blockers as well. But the definitive management for pheochromocytoma is an adrenalectomy to remove the tumor that is on the adrenal glands. The next condition is diabetes insipidus that we did as well. So the pathophysiology is You can have two types of diabetes insipidus, cranial nephrogenic. So these can be due to a lack of a D H antidiuretic hormone or a lack of response to a D. H. Um, so, like I mentioned, that can be nephrogenic or cranial nephrogenic is when the collecting ducts of the kidneys do not respond to a D. H and cranial is when the hypothalamus does not produce enough ADH. So the key symptoms are polyuria, polydipsia and hyponatremia. So if you see these three and a question, you can be pretty sure that it's diabetes. Insipidus, um, and the management. Oh, sorry, let's do the investigations first. So the investigations are looking at your hospitality and cereals morality. So you got a low urine osmolality and a high serum osmolality, and you diagnose it with the water deprivation test. So what happens in this test is that the patient doesn't drink any fluids for around eight hours, and then they're given synthetic ADH desmopressin, and the urine osmolality is measured eight hours later, and depending on what type of diabetes insipidus you get, you have different results. So for cranial diabetes, initially the urine osmolality is low because the hypothalamus is not producing enough a d h. But once you give the ADH your urine osmolality becomes high because in patients with cranial diabetes insipidus um, they're collecting ducts in the kidneys are working fine. Hence why the urine osmolality becomes high and then nephrogenic diabetes. Uh, initially, your urine osmolality is low, but with after after you've done the water deprivation test, the urine osmolality still stays low because the problem is with the collecting ducts, they no matter how much ADH you give them, they're not going to respond to it. So the urine osmolality stays low, and then the management is sort of treating the underlying cause of the nephrogenic. A cranial, uh, desmopressin can be given in cranial diabetes, and also things like low salt protein diet and thiazide can be given in nephrogenic diabetes insipidus so sort of getting onto the last two slides now. So hyperglycemia, um, is very important to be aware of. And it's essentially when potassium levels are more than 5.5 millimeters per liter, there can be many causes. Um, sort of split them into three. So first one is an impaired exclusion from cells, Um, and that can be due to acute kidney injury, chronic kidney disease ace inhibitors things like that, um, or you can have increased release from cells such as lactic acidosis, rhabdomyolysis, my dialysis or insulin deficiency. Other causes, um, like human ESIs. So if you've got traumatic venue, puncture or the tourniquet is too tight, that can actually cause hypochelemia in the blood. Um, a delayed analysis of the blood once you've taken it, but I can actually leak out of the cells causing a hyperkalemia. Um, and something very, very important to be aware of is E c G changes. So you can get to all tented T waves, which is very characteristic of hyperkalemia flat P waves and prolonged PR intervals. Um, and it's actually a life threatening electrolyte abnormality, so you need to treat them if the levels are over 6.5 or any E c g changes are seen. So that's really in the in the notes as well. Um, and then the management for hyperkalemia is calcium gluconate. So you give 10 mills over 10 minutes because that stabilizes the cardiac membrane. So it's sort of like the initial treatment, especially if you see any changes on the EKG. You can get IV insulin, 25 g of glucose, so the insulin causes the potassium to shift into the cells, and the glucose is required to prevent any hypoglycemia that may result because of this. And you can also give nebulized albuterol because again, that causes an intracellular shift of potassium. And then the last slide is just a quick side on hyper calcemia. So the hypercalcemia sort of defined when calcium levels are more than 2.65 millimeters per liter. Uh, there's very different causes. So, as I mentioned earlier, primary Hyperparathyroid is, um, can cause hypercalcemia malignancy. So if you've got a tumor sequencing calcium somewhere, osteolytic bone lesions so that's softened sections of the patient's bone. Um, so that's for me is a symptom of specific diseases that can secrete calcium medication like lithium and thiazide and thyrotoxicosis. So thyroid hormones are known to cause, um, bone reabsorption and moving calcium from bone to the circulation, which can lead to hypercalcemia and investigations. Hypocalcemia is sort of CCGs LFTs full range of BP T. H for primary hyperparathyroidism and then management. So first time management is essentially IV fluids, so it corrects the dehydration. It protects your kidneys from the high levels of calcium, and it also increases the calcium excretion as well. You can give bisphosphonates like alendronate, so that inhibits osteoclastic activity and osteoclasts like we talked about earlier. They break down the bone so you're reducing calcium release by giving the bisphosphonates, and you can prevent recurrence. So if it's from a tumor, you can use chemotherapy or radiotherapy for tumors. And if it's steroids, sorry if it sarcoidosis and things like that, you can use steroids instead. So that's actually the end of our presentation. We hope you found that useful, and I'll just get you back as well. Um, did anyone have any questions? Sorry. That's true. Thank you. Yeah.