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All right, cool. Um So hi guys. Sorry, I think I joined and then uh it wasn't, there's a few technical issues, but hopefully you guys can hear me now. Um And hopefully you can see my slides. Uh and if you can't, please let me know on the chat and then I can fix it, but hopefully, hopefully you can see everything now. Um So I think we can give it a start. Um So today we're gonna talk about uh adrenal disorders and obesity. Um just give me a second one, my laptop loads and then we can give it a start. Ok, so going through kind of the lecture timeline, um we have so introduction to adrenal gland disorders. Then we talk about adrenal disorders, main kind of diseases found. Um how we investigated diagnosis and management. Then we talk about introduction to obesity medicine. And finally, we'll go on to see kind of how to manage obesity and different drugs involved um and kind of what kind of uh strategies and approaches to be. Um So moving on. So we have adrenal glands, very basic introduction. So obviously, the adrenal glands are located on the upper poles of each kidney. And what I mean what I mean, poles of the kidney just means that the top of the kidney. So the adrenal glands basically sit on the top of the kidney. Um the adrenal glands has kind of two main layers, right. So we have the inner layer which is the medullar which kinda sorry, this this image is quite blurred but basically the inner layer which is the medlar and then the outer layer which is the adrenal cortex are kind of two main layers. Um And the adrenal cortex is divided into three main layers. So you have the zona glomerulosa which is the outermost layer and that produces aldosterone. Um We also have the two, the other two layers are the zona fasciculata, which is the inner layer which is the middle layer sorry of the cortex. And then the zona reticularis which is the innermost layer of the cortex. Um and the zona fasciculata and reticularis kind of the these do produce your um Cortisol cortisol. Um And we talk a little bit more about a strong and cortisol or what they do um in a, in a few more slides. OK. So talking about, I mean, I already talking about sections of the adrenal gland, the adrenal cortex and the mela um and talking about the arterial venous supply. So the adrenal gland kind of has only one vein that's important, not only has one vein, but it has many arteries OK. So what happens is the left adrenal vein drains into the right adrenal vein which then drains into the inferior vena cava. So, and then it goes off. So that, that, that, that, that's all you have to know. But the, the key thing here, I mean, has one vein. Ok. Um And in terms of, so what is cholesterol? So cholesterol is a steroid precursor when I say steroid precursor, I mean, it's all, most of the steroids are formed from cholesterol. So cholesterol, cholesterol is your base and then a lot of different reaction we we can talk about in a few slides, but a lot of different reactions happen with the help of enzymes. Um and that this helps produce your kind of steroids. So I strong cortisol and then sex steroids. So that's so everything comes from cholesterol. It's basically what I'm trying to get at. Ok. So adrenal disorders overview. So let's talk about the, the hypothalamic pituitary adrenal axis, which is the H va axis. OK. So the hypothalamus produces your corticotropin releasing hormone as show on the slides and the cortico corticotropin releasing hormone that acts on the anterior pituitary gland, which then helps the anterior pituitary gland produce ACTH, the adrenocorticotropic hormone and ACTH finally acts on your adrenal gland or the adrenal cortex in specific to produce cortisol. So cortisol and, and, and all this happens and there's a negative feedback loop right in this axis. OK. So the cortisol if it's, when I, when I say negative feedback, I'm sure you guys know what it is. But just to explain. So if there's high cortisol in the body, uh there's gonna be a negative feedback and it's gonna, it's gonna feedback back to the anterior pituitary and the hypothalamus as shown in the diagram to reduce the production of ach and crh because too much cortisol. So once to reduce the amount of cortisol and that's done by reducing the amount of crh and ach and that's what make the feedback means, right? Ok. So the main disorder is Addison's disease. What is Addison's disease? Addison's disease is basically primary adrenal failure. Ok. And primary adrenal failure, what happens in primary adrenal failure? The adrenal glands are not working, right? So, when the adrenal glands are not working, you're not gonna be able to produce cortisol. Ok? Because the adrenal glands are just not working, right? And now with the lack of cortisol, you're gonna have an increase in ACTH. Why? Because the negative feedback is going to kick in. Basically, there's low cortisol. So it's gonna, it's going to, it's gonna ask the anti pituitary to produce more ACTH because the body wants more cortisol. But despite the increased ACTH, cortisol is not gonna be produced because the adrenal glands have failed, right. So that's why you have increased ACTH and decreased cortisol in Addison's disease. Ok. Um Some of the kind of key symptoms of Addison's are things like hyperpigmentation, which I'll talk about why it happened. So, um you have hyperpigmentation, low BP, um and then weight loss, nausea, diarrhea, kind of basic symptoms. Um But I think the, the most, the most, I mean, uh all the exam questions I've seen is hyperpigmentation comes up. It's mostly absence, right? And why? Because it's basically ACTH how it's, it's formed from something called preopiomelanocortin, right? POMC. OK. And that's what's in the diagram here. OK. What happens is when, when, when there's increased ACTH, obviously, it's gonna increase the amount of POMC because it needs to produce more ACTH and with increase in POMC, right, that also produces um metal stim stimulating commerce, MS H. Um And with, with the increase in PC, there's gonna be increased MS H OK. And with an increase in MS H, it's gonna cause you to be tanned. OK? Because obviously melain is increasing in the body. So it's gonna melatonin. So, and it's gonna cause an increase and it's gonna cause you to be tanned and hence why you have hyperpigmentation because your MS H is increasing and that's gonna cause you to have pigment uh um on the arteries of the skin. So that's why you get, that's the basic mechanism of where hyper pigmentation comes from. OK. And not, not. So that's a very key symptom in addisons, right? OK. So uh moving on to testing for a, so what are the investigations present? Um for Addison's OK. So first we have the short synacthen test and when I say synac um it's short synthetic ACTH, OK. Basically, what they do is they inject synthetic ACTH im so intramuscularly into the body. And what happens with that is you would typically expect an increase in cortisol. OK? Because AC ACTH is gonna cause increase cortisol. So typically you would expect an increase in in cortisol. But with the short synacthen test, you're gonna have no increase in cortisol, ok? Because your adrenal gland failed. So it's not gonna do anything about it. OK? So that's a, that's a very important test for a, right? The next, the next one is you have high ac levels, obviously as talked about before and you're gonna have low, I'm sorry. And you're gonna have low early morning uh Cortisol. OK. So the thing is um Cortisol is usually quite high in the morning because it has a diurnal diurnal rhythm. Ok? So typically it should be really high in the mornings, but in this case, it's gonna be quite low because obviously your adrenal glands have failed. So it's not gonna produce Cortisone, ok? So, um this just died. I'm kind of explaining the synthetic ACTH test, but I kind of talked about it. Um And in terms of kind of treating this disease. So, treating Allison's right. So if you're treat Addisons, you're gonna have to use three kind of things. So you, you, you're gonna use fludrocortisone OK, hydrocortisone three times and prednisoLONE. So those are your, those are your three main stay of treatment in terms of AINS, ok? And that's important to remember. OK. Um and you may ask, you know why not just give aldosine, ok? In instead of in a and cortisol instead? Now why we don't give aldosterone and cortisol is because the half-life it's too short um for a safe once daily administra administration, it's, it's the cough is basically too short for it to actually act and it's not gonna be effective enough. OK? Um And hence why we do not give um a strong cortisone. OK. So that, that's why we don't give it now. Um Moving on to a few more adrenal disorders. OK. So this is your kind of, as I said, your steroid precursors cholesterol. Yeah. So and that, that's, that's you over here, right? Cholesterol starts off, everything starts off with cholesterol. OK. Your steroid precursor. Now, so how it forms this, this diagram basically describes how your different steroids are forms iron cortisol and you know your sex steroids, which you are and which is how, how they are formed the game. So let's talk through it. OK? The dim is quite simple. So, but we talk through it, right? So I love to start off with cholesterol. Uh cholesterol is, is just basically progesterone is formed from cholesterol. OK. And then progesterone now goes on from 11 deoxycorticosterone with the help of 21 21 20. It's 21 hydroxylase. Ok. That's the enzyme enzyme name is 21 hydroxylase. Ok. I'll just written down the number 21 but it's 21 hydroxylase. All right. Um And then le 11 deoxycorticosterone then goes on the form corticosterone which with the help of 11 hydroxylase and then corticosterone with the help of 18 hydroxylase um goes on to form aldosterone. Ok. Now that's how aldosterone is from not cortisol. So, progesterone is then changed to 1708 progesterone. OK, with the help of 17 hydroxylase. Um and then 1708 progesterone is then goes on to form 11 the oxy. Um.