DIP Episode 75 - USMLE Step 3/Medicine ITE/ABIM Board Review Series 2 (Endocrinology)

Welcome. This is episode 75 of the Divine Intervention Podcast. This episode will be targeted towards preparation for step 3 and the medicine-entering exam. And I will say because I closely try to follow the curriculum from the American Board of Internal Medicine, this will also potentially help for the medicine board exams. And today I'm going to primarily be covering now endocrinology. The thing I will say is I've done some reflections since I meet the first series in the podcast. And again, just thinking more about concerns of being efficient, being more timely and being as targeted as possible in the reviews. So I'm going to change things around with this podcast. I will still try to cover the same amount of material. I mean, obviously, I'm not going to recover the same thing already covered in the first part of this series. But I'll cover new material today. But I'll use a slightly different approach to try to be a little more efficient with my coverage. So, and today I will just keep discussing a lot of scenarios and interspersion the content as we go along. So this will be more conversational. So the first thing I'll tackle today is a Whipple Stryard. So Whipple Stryard, you've heard of this, is one of the easiest trials to memorize in all of medicine. So basically, it's like the person is hypoglycemic. They have symptoms of hypoglycemia and then those symptoms improve with the administration of glucose.

And the thing is, classically, why would you want to think about Whipple Stryard for exams? You want to think about Whipple Stryard in the context of three high-yield causes of like neuroglycopinic symptoms. So for example, the classic exams in areas to try to differentiate between a person that's injecting insulin or a person that has an insulinoma or a person that is facticiously taking a sulfonial urea to create symptoms of hypoglycemia. So clearly, if a patient is injecting insulin, the insulin that you can buy in a store, or at least in a pharmacy, does not have a CPF type of niche. So the person's insulin will be high, the CPF type will not be elevated. Right? You'll be able to tell the person, stop doing that. And again, you just give them glucose and this should get better. If a person has an insulinoma, right? So think about it probably like in the context of an immune one syndrome. They will have, again, the hypoglycemia, they will have high levels of insulin, but the CPF type will also be elevated, right? Because the insulin that's causing the symptoms is endogenous to the body. Whenever you have an endogenous increase in the release of insulin, that your CPF type will be elevated at the same time. For insulinomas, I mean, classically, you can give like diazoxide, as treatment, diazoxide is a drug that's very good at opening up potassium channels.

If you remember from med school, whenever you open up potassium channels, especially in the pancreatic beta cells, that will prevent the pancreatic beta cell from depolarizing and that will shut down the release of insulin. Alternatively, you can give an alkaliting agent known as streptozosing. Streptozosing is a very good drug for the treatment of insulin as well. Although, obviously, if you could do surgery to pull out the tumor, that will also be an ideal outcome there. So your insulin and CPF type levels are elevated. If a person has an insulin number, now if a person has is taking a, like taking a sulfonyl urea, right? Sophonyl urea, right? The aminezbombaction, they block that potassium channel again, that you find in the pancreatic beta cells, the cell depolarizes, you square out a ton of insulin. As a square now that insulin CPF is also re-easier, so you may ask yourself, divine, how do I differentiate between a person that's taking a sulfonyl urea and a person that's injecting insulin? Well, you do a sulfonyl urea screen, right? So you can basically check the urea for like a sulfonyl urea, like mid-glidinite, mid-tabolite, mid-glidinite is basically drugs that work like sulfonyl ureas, they just short are acting. So you can check for those mid-tabolites in the urea and that should be able to solve whatever dilemma. Okay, now what if you get a question about a person that hasn't insulinoma, right? And you're thinking about diagnostic testing.

So the thing is first thing is, right, you want to go ahead and confirm, you want to go ahead and confirm that you have an insulinoma first, right? So you do that testing and then after that you need to do like some kind of scanning of the abdomen, right? So you do like a CT scan of the abdomen to detect the insulinoma and then you should be good to go with that, right? So the insulin will be high, the CPF levels will be high and then you just don't have no CT scan to localize the lesion. Now, what if you get a question about a person that gets kind of dizzy after a meal? Now let's assume they recently had like gastric bypass surgery, right? So whenever you see stuff like that, then you're thinking more about a person that, because I mean, this is something that happens classically after a person gets gastric bypass surgery, they have like very quick reabsorption of whatever they consume. So for those people, that post-prenial hypoglycemia they get, you would want to recommend eating smaller meals and you actually want to recommend meals that have like more, just think of it as a more like balanced meal, right? So a meal that contains like proteins and carbs and fat and stuff like that, you just sort of want them to have meals that, I mean, not necessarily cause just such a huge insulin surge after they eat.

So small meals, small frequent, smaller meals, but again, meals that are not just predominantly carbohydrate, just have meals that have a mix of other things besides just straight-up carbs. Now let's assume you get a question about a person. So again, this is all endocrine. You get a question about like an old guy and his hats don't fit anymore and he has like bone pain and hearing problems. I'm really hoping that with this you're thinking about about a Pudgex disease, Pudgex disease classically presents in this way, right? And basically the thing that happens with Pudgex disease is that you have like, you know, sort of like disorganized remodeling of bone. And I mean, if you want to make the diagnosis, right? The diagnosis classically, you want to do something called a bone scan. A bone scan will show you those weird lesions that define that characteristically define a person having a Pudgex disease. Occasionally, if a patient has like really bad bone pain, you can also do an X-ray of that region that they have the bone pain in. But I'll tell you that the big, big test you want to order for patient as Pudgex disease on the exams is a bone scan. And I mean, if a patient is a symptomatic and they have Pudgex, you're going to do any kind of treatment. But if they are symptomatic, you want to go ahead and give them a bisfoss for need. Bisfoss for need is the treatment of choice for Pudgex disease.

And don't forget that Pudgex disease, right, is associated with a person having an osteosarcoma. Pudgex disease is actually a risk factor for the development of osteosarcoma. Don't forget that there are some drugs like a terryparatite that also increase the person's risk of osteosarcoma. And also, there is having like an RBG mutation, right, also does increase the person's risk of osteosarcoma. Now, Pudgex disease, right, I mean, classically on labs, there is no abnormality. The only abnormality is usually just an elevation in the person's alkaline phosphatase. And I mean, if you do imagine, you may see like the hair and end appearance to the bone, like a cotton wool appearance to the skull. Remember that you can also find that appearance in a person that has like severe hemolytic disease from like thalacemia, for example. And because people that have a Pudgex disease, right, they have like hypervascular bone marrow, they can ultimately develop high-up or heart failure. So Pudgex disease is just one of those things, you kind of want to pay attention to. And it's also, again, very commonly tested on exams. Now, let's talk about some more scenarios here, right? So let's assume a person has like a fat soluble vitamin deficiency, right? So hopefully, remember, your fat soluble vitamins, right? Those are vitamins like ADE and K, right? So if you have a vitamin K deficiency, it could bleed. If you have a vitamin E deficiency, right, you can have problems with your cerebellum.

If you have a vitamin D deficiency, you have like secondary hyperparthyroidism, you can have like osteomalysia. If you're an adult, you can have rickets if you're a kid. And if you have a vitamin A deficiency, right, you can have like night blindness. So what are the classic things on exams, on like the intranaxam or step three of the medicine boards that cause vitamin D deficiency, right? So one classic one is Celiac disease, right? Celiac disease, pretty classic, right? So these people, I remember Celiac disease has a pretty election for the small intestine, especially the terminal helium, right? So remember, it's a terminal helium that is the primary side of reabsorption of those fat soluble vitamins. So you can run into trouble there. Also, think about a person that has like pancreatic insufficiency, like a patient with cystic fibrosis, right? Because the economic pancreatic enzymes, they can not emulsify fat, so they can not reabsorb fat soluble vitamins. So those people can also get into trouble. Another classic situation is a patient that has Crohn's, right? Again, remember, Crohn's has a pretty election for the terminal helium, so that can sort of lead those people towards those problems, right? Then I just said that if a person has vitamin D deficiency, right, they can have like a secondary hyperparthyroidism, right? So it begs the question that how would you differentiate? I guess this will be another nice exam scenario.

How do you differentiate with throwing chronic kidney disease and chronic liver disease as the cause of secondary hyperparthyroidism? The thing you want to know that those circumstances is to check the phosphate, right? So let's deal with each scenario one by one. The thing is if a patient has chronic kidney disease, right? As the cause of their secondary hyperparthyroidism, the mechanism there is that they don't have one alpha hydroxylis working, right? So if you don't have one alpha hydroxylis working, you cannot make active vitamin D. You cannot make calcium trial. And if you don't make calcium trial, you will not reabsorb calcium and phosphate in the gut, right? So you'll be hypocalcymic. If you're hypocalcymic, you'll vitamin D. I mean your PTH levels will go up, right? And we know PTH is known as the phosphate trashing hormone, right? So you would expect that your phosphate should go down in chronic kidney disease, I mean in secondary hyperparthyroidism. But the thing is if that secondary hyperparthyroidism is arising from CKD, then your phosphorous will actually be high because the primary phosphorous is critical organ of your body is your kidney. So if your kidneys are not working, your phosphate is not going to go down. So in CKD, in CKD, induce the secondary hyperparthyroidism, your PTH is high, your calcium is low, but your phosphate is actually high because you cannot get rid of it. Contrast that with chronic liver disease, right?

So if you look at normal vitamin D metabolism, you'll be in the sun and then there is an enzyme in the liver that helps you make calcium diol, that's like 25 hydroxy vitamin D. And then you go to the kidneys and then that calcium diol is converted to 125 dihydroxy vitamin D, also called calcium trial. So if your liver is not working, you're not going to create feedstock for the kidney. For the kidneys, the one alpha hydroxyl is to work on. So actually chronic liver disease, right? So like cirrhosis can also cause a vitamin D deficiency, right? And the associated as secondary hyperparthyroidism. Only big thing there is that. So let's sort of walk through this, right? So you're not making the vitamin D. If you're not making the vitamin D, again, you will not reabsorb calcium in your phosphate in your gut, so your blood calcium levels will be low, so your PTH will go up. If your PTH goes up, right? Your phosphate should be outtrashed, right? And because your kidneys are working, well, your phosphate will be appropriately trashed. So in secondary hyperparthyroidism arising from chronic liver disease, your calcium is low, your PTH is high, okay? But your phosphate will be low because your kidneys are working. Very high, you to know and understand those are two scenarios. Now, again, vitamin D, I guess I'll just say this, right? Since I'm talking about calcium diol, actually if you want to assess a person's vitamin D status, measuring their calcium diol levels, right?

So they are 25 hydroxy vitamin D levels, is actually the best measure, okay? Of assessing a patient's vitamin D status. And then if if a person has vitamin D deficiency, right? If, for example, they have CKD, you want to give them calcium trial as treatment, right? And then you can give like a 25 hydroxy vitamin D as treatment for patients that have a chronic liver disease to sort of fix their secondary hyperparthyroidism. Now, let's talk about osteoporosis, right? So osteoporosis is a very big topic for these three exams that we're targeting here. And the first thing you want to know with osteoporosis, first things first are your screening guidelines, right? So if a woman is more than 65 years old, right? You want to go ahead and screen her with a dexasca, right? And I mean, the key value you're looking for is a T score having been less than negative 2.5. If your T score is less than negative 2.5, that defines osteoporosis and you go ahead and treat. But the thing is they know that most people have memorized that guidelines. So they begin to present some atypical guidelines on exams for people that potentially less than 65 years old would also deserve screening for osteoporosis. Now, the big ones you sort of want to keep at the back of your mind are people that, for example, have like anorexia nervosa. Those people certainly deserve osteoporosis screening before the age of 65.

If a person has a primary hyperparthyroidism, remember, if high levels of PTH literally leaches away at your bone, if those people are less than 65, they also deserve screening for osteoporosis. If a patient has been on steroids for a very long period of time, so see, for example, for like an autoimmune disease or for rheumatologic disorder, those people certainly deserve screening for osteoporosis again with a dexasca. Or if a person is like a long-term smoker, right? So let's say they've smoked for a very long period of time, smoking causes problems with a bone reabsorption, so you can also get osteoporosis that way. So those people again deserve screening. Another classic one is a person that has like a history of hyperthyroidism. Again, remember, thyroid hormone has a direct reabsorbing effect on bone, okay? So you want to again scream those people for osteoporosis. And I guess another one that's probably a little low yield, but it means shop on an exam, is if for example they have like a very strong like family history of like hip fracture, or they've had like fractures that are kind of like weird, right? So it's like you're present that you just like fell from like a standing height and then you get like a big, big, big fracture. Those people potentially also deserve screening for osteoporosis, even if they are less than the age of 65. Now again, remember if you're negative 2.5 or lower with a dexascan, you have osteoporosis.

And again, usually in osteoporosis, there are no lab abnormalities, right? So contrast to the surface disease where the alkaline phosphatism may be elevated. Classically, in osteoporosis on exams, there are no lab abnormalities. Again, actually very high high yield to know that. And really why you may ask yourself like, why do so many women get osteoporosis? The thing is, as you get older, right? Your ovaries sort of stop working. As you over stop working, you stop making estrogen, right? As you stop making estrogen, at least the very potent estrogen, because I mean, if your postmenopausal, you still have a kind of estrogen that's made by your dippocytes on their activity, on the action of the enzyme known as aromatis. But it's not as potent as the estrogen that comes from your ovaries, right? So once you hit like that magic age of like 50, you over stop working, you over stop working, then by some mechanism that you probably remember from step one, involving osteopor Tegrine, your bone begins to resorb, right? So you begin to get into trouble with osteoporosis. Also, if you're a guy, if you have like low testosterone for any reason, that also increases your risk of osteoporosis. And in general, right, if a patient has osteoporosis, you want to go ahead and treat them. And your treatment usually revolves around giving this phosphonids. I mean, if a patient has that low T-score less than negative 2.5, that's an indication for studying this phosphonids.

If a patient has like a fracture that is deemed to be secondary to osteoporosis, you also want to go ahead and treat those people with this phosphonids. And there is something called like, I think it's called like a fracture risk assessment score. It's called like a fracture score. It's something that can be calculated. If your fracture score is more than 20%, you also deserve this phosphonid treatment for osteoporosis. And I mean, again, like I said, this phosphonids are first line, but don't forget that this phosphonids have some side effects, right? So, if for example, a person has really bad kidney disease, they probably should not be put on a phosphonid. If a patient has really bad esophagitis, they also probably should not be studied on a phosphonid, right? Because remember, this phosphonids can cause a pill of esophagitis. In fact, you need to basically like take them on an empty stomach and you need to stand for like 30 minutes after taking a phosphonid and take a lot of fluid so that it does not interact extensively with the esophageal milk, which cause a lot of trouble. And don't forget that this phosphonids, they can also cause osteonecrosis of the jaw, okay? So that's one thing you sort of want to avoid with this phosphonids. If people have like any of these like problems or contraindications I'm mentioning, you probably don't want to study monobisphosphonid on exams.

And then, if a patient obviously cannot tolerate a phosphonid, one thing you can consider doing is to give those patients like a relox effect, right? Relox effect is a great drug, it's a serum. It kind of works like tamoxifen, but it's kind of different in the sense that so I guess let me sort of compare and contrast both for you, right? So tamoxifen is a serum, it's used as chemoprophylaxis for breast cancer, right? It's like an estrogen receptor antagonist in the breast, but it's an agonist in the uterus and bone, right? So because it has like proestrogenic activity in bone, it's great for osteoporosis, right? But tamoxifen is not used to treat osteoporosis, reloxifen can, okay? Reloxifen is an estrogen receptor antagonist in the breast, although it's not as great as, it's not as great as relox, as tamoxifen, but reloxifen, it actually has, it doesn't have the same estrogen agonist activity in the uterus that tamoxifen has. So you actually have no increased risk of endometrial cancer with reloxifen compared with tamoxifen, but reloxifen does have estrogen receptor agonist activity in bone, so it's actually good for osteoporosis. Only problem is it also increases your venus thrombone polychrist, so that's something you sort of want to watch out for.

So if, for example, on the exam, again, a patient cannot take this phosphonate for some reason, you can strongly consider using reloxifen, but in the weird, weird scenario where, for some reason, your patient cannot take a phosphonate, your patient cannot take a, cannot take a reloxifen, then one thing you potentially want to consider in your test is studying them on terryparatide, although again, I will say that terryparatide will be a very rare correct answer on these exams, but it is certainly useful in the treatment of osteoporosis. Now, what are some key things you want to know about terryparatide? So the thing is terryparatide, you give it in a pulsatile fashion, when you give it in a pulsatile fashion, it actually encourages bone production, if you give it in a continuous fashion, it actually encourages bone resorption. Remember, terryparatide is a PTH analog. Now, the thing is terryparatide though, I mean, there's the risk of tachyphylaxis, right? So after a while, it stops working. In fact, I'll say most times, you don't prescribe it for more than two years, because one, it stops working after a while, and two, you also worried about osteosarcoma with terryparatide, because remember, we essentially give it a growth factor, a stimulating factor to bone, right? So you can potentially envisage that cause in malignant degeneration of bone, right? So like osteosarcoma. So obviously, you don't want that, that's not a, that's not a reasonable outcome.

Now, one thing they may do on exams is they may give you a question about a patient that has like osteoporosis, and they're like postmenoposal, but they don't have like hot flashes, they don't have like any like serious postmenoposal symptoms, and then they try to trick you into giving those patients estrogen replacement therapy for osteoporosis, resist that temptation, okay? The only time you give people estrogen replacement therapies, if they have very severe postmenoposal symptoms, estrogen replacement therapy is never the right answer as the treatment for osteoporosis. No, that is not a, that is not a great strategy on exams, you'll get those questions wrong. So just just never do that. Now, let's assume, let's sort of jump to another scenario. Let's assume you get a question about a patient that has a kidney stone, right? And they have a history of MEN1, right? Hopefully you're thinking about a primary hyperthyroidism, right? Causing like hypercalcemia and like a calcium kidney stone in those people, right? So calcium nephrolithiasis. Remember, MEN1, it arises from like a meningin mutation. It has a rosomodominant inheritance, and remember that there are three basic antigens with MEN1, right? So those people can have like primary hyperthyroidism, right? In fact, the pneumonia is like parapanthit, right? So they can have primary hyperthyroidism, which is actually the most common presentation of MEN1. They can have pituitary tumors, right?

So they can have like a pituitary adenoma. Classically, it's a prolactinoma, although they can also have a tumor that's secreted in a ton of growth hormone. And then they can also have pancreatic neuroendocrine tumors, right? So they can have insulinomas, they can have, so they can present with like weeple striat, they can have glucanomas that can present as diabetes, and then like a rash, I mean the classic boss freeze for the rash on the exams is a necrolitic migratoryory and then they could also have um, um, vipermus, right? Remember vipermus can present as the WDHA syndrome, right? So where you have like watery diarrhea and they have like a potassium problem so they can have like hypochylinea, and then they could also stop making gastric acid or so echlohedria, does the WDHA syndrome that's characteristic of a vipermus? And then alternatively they can also have a zollinger elicin syndrome, right? So they have a gastrenoma, right? So those people have like virulent ulcers in the stomach, and those ulcers tend to be like in weird locations, right? So like if you see like a distal, gigenol ulcer, that's pretty, that's almost like pathonomonic for zollinger elicin syndrome. Um, so if you see kidney stones, a vision of the histrovenian one syndrome, you're thinking about primary hyperparthyroidism, right? And remember that the most common cause of hypercalcemia, right? Like in the US, at least in a patient that is not in the hospital, is primary hyperparthyroidism.

And the thing is in those patients, the most common cause of primary hyperparthyroidism is a parthyroid at enoma, okay? But if you want to contrast with a patient that has a immune one syndrome, the most common cause actually, and this is actually very high yield, to know for example, the most common cause of primary hyperparthyroidism in a patient that has a immune one syndrome is actually a parthyroid hyperplasia, not a parthyroid at enoma, okay? That's a, it's kind of like a subtle difference, but it's actually very high yield to know for example. Now, what if you get a question about a patient that has a primary like has hypercalcemia, and then impatient in the hospital, right? What's the most likely cause on that of circumstances? Well, I hope you're thinking about malignancy. Malignancy is the most common cause of hypercalcemia in a hospitalized patient, right? So if you see hypercalcemia in the impatient setting, you need to begin to worry about a potential malignancy causing that hypercalcemia. And I mean, you may say, okay, divine, how light difference between primary hyperparthyroidism, as the cause of a patient hypercalcemia, and like hypercalcemia of malignancy, as the cause of a patient hypercalcemia. Well, one way you can do that is to sort of look at labs, right? So, if a patient has primary hyperparthyroidism, obviously the pth will be high, right? If the pth is high, the accostomy will be high as well. I mean, that's why they are presenting, right?

That's why they have the hypercalcemia in the first place. And then, the aphosphate will be low, right? Because again, another name, another like a mnemonic, right? For pth, it's a phosphate trashing hormone. So if the trash phosphate, right? The phosphate levels will be low, okay? And I guess if you're looking at the levels of calcium in the urine, right? If you have a ton of calcium in your blood, guess what? You're going to have a ton of calcium in your urine, right? So, those people will have high levels of urinary calcium, okay? That's what defines those that sort of like the values you observe in a primary hyperparthyroidism. Now, contrast that with hypercalcemia of malignancy, right? So, if a patient has hypercalcemia of malignancy, the accostomy levels will be high, but the thing is, in hypercalcemia of malignancy, it's not usually pth itself that causes the hypercalcemia. It can be something else that activates bone resorption that causes that hypercalcemia, right? So, for example, say, for example, a patient has like a squamous cell cancer of the lungs, that squamous cell cancer of the lungs, right? Can produce pth RP, right? So, like pth RP is a peptide, and that pth RP, right? I mean, pth RP is a peptide, that already tells you what it does. It acts just like pth, right? So, you release a ton of a pth-like substance that works just like pth, so you absorb bone, right?

So, you have like elevated calcium levels, you have low phosphate levels, and you would have, so high calcium, low phosphate, but those people's pth levels will actually be low, because the pth will be appropriately suppressed, because they have a hypercalcemia, okay? Again, that's a very high-ealth thing to know for, for example. So, that's how you differentiate between, again, hypercalcemia of a malignancy, right? Or hypercalcemia rising from primary hyperparthyroidism. I mean, another classic scenario may be like multiple myeloma, right? So, in multiple myeloma, right, those people, the plasma cells, the secret, the atom of interlooking one, in fact, the anodinine from interlooking one, of interlooking one is osteoclasts activated in fact, right? So, those people directly again, result bone, so the calcium will be high, but the pth will be low, because they will be appropriately suppressed, okay? And, if for example, patient has primary hyperparthyroidism, right? How do you want to treat those people? In general, you can treat those people with like this phosphonids, although I will say that for the purposes of your exams, you probably want to go ahead and do a parathyroidectomy. You probably want to go ahead and do a parathyroidectomy. And the thing is, this is one of those annoying things that just pops up on exams all the time, but there are certain indications for parathyroidectomy, right? So, you want to know who should get a parathyroidectomy.

The classic ones that are tested on exams are people that have, that are aged like they're less than 50 years old, so if you have a patient that's less than 50 years old, those people deserve a parathyroidectomy. If you have a patient where their blood calcium levels are more than one, like, greater than one, I believe it's like milligrams or grams per acid, they're above like the upper limit of normal. Those people also deserve a parathyroidectomy. If a patient is beginning to have problems from having that hyperparathyroidism, right? So, like kidney stones, for example, you would want to go ahead and you'd want to go ahead and recommend a parathyroidectomy for those people. If a patient has, like, the beginning to have problems with creatinine, right? So, like, they're beginning to have creatinine elevations from the chronic hypercalcemia, like kidney disease is beginning to develop. Those people also deserve a parathyroidectomy. If you have a patient that has osteoporosis from having the primary hyperparathyroidism, those people also deserve a parathyroidectomy for the treatment of that primary hyperparathyroidism. So, those are like the classic, classic scenarios. You sort of want to keep at the back of your mind for indications for a parathyroidectomy. And then you want to remember that if you perform a parathyroidectomy, right? Those people can have like hypocalcemic seizures after the surgery.

So, that's just something you sort of want to keep your eye on after surgery. Like, you don't just send those patients home immediately. Usually, you send them home with like, some kind of like very strong, like calcium prescription, just to make sure they don't get into trouble. Because hypocalcemia can cause lots of problems. It can cause seizures. It can cause a prolonged cutie interval. So, those are things you all kind of want to watch out. You want to watch out for. And again, I've talked about some high-yield scenarios here. Like, I've talked about how hypercalcemia can present in the setting of a MEN1 syndrome. And also MEN2 A, right? And then I've talked about how people could get hypercalcemia on malignancy, right? So, classicly on exams, you're thinking of like, scream or cell cancer of the lungs. You're thinking of multiple myeloma, right? And I've talked about like the different values that can help you differentiate between primary hyperparathyroidism and hypercalcemia of malignancy. I guess one sort of odd scenario I want to talk about here is something called familial hypocalcyria, hypercalcemia. So, this has relatively similar labs to primary hyperparathyroidism with one key difference, right? So, basically, the pathophysiology on the line FHH is that a patient has defect in the calcium sense in receptor, right? So, even if they're hypercalcemic, their parathyroid glands do not recognize that, maybe it's time to stop making all this parathyroid hormone.

So, these people actually have high levels of PTH. And because they have high levels of PTH, they'll actually have high levels of calcium in their blood, so they will have hypercalcemia, okay? And then these patients, they will also have low levels of phosphate because the PTH appropriately trashes phosphate. But in contrast with primary hyperparathyroidism, where your urinary calcium is low, I mean, it's high, right? Because again, high levels of calcium in the blood equals high levels of calcium in the urine. In patients with familial hypocalcyria, hypercalcemia, right? I mean, you can even see the name of the disease, hypocalcyoric. They actually have low urinary calcium levels. That's actually very high, you know, for example, because the thing is the calcium sense in receptor, again, does not recognize that, oh, if you're hypercalcemic, there's no need to reabsorb calcium in the urine. It doesn't listen to those signals. So, these people actually reabsorb a ton of their calcium from the urine. So, the end of being hypocalcyoric. So, the urinary calcium is a key distinguishing feature between FH and primary hyperparathyroidism. It is, the urinary calcium is high in primary hyperparathyroidism. The urinary calcium is low in familial hypocalcyoric, hypercalcemia. And, I mean, if a patient has hypercalcemia and they are taken on anti-hypertensive medication, hopefully you're thinking about thiazides, right?

So, remember that your lupes lose calcium, when your thiazides retain calcium, right? Thiazides are one of those classic drug causes of hypercalcemia. I mean, what if you also get a question about a patient that is hypercalcemic and they're like an African-American female and they have like symmetric bilateral, a hyla lymphatic anopathy on a chest x-ray? Well, I hope you're thinking about the sacroidosis with that. Remember, like the granulomas in sacroidosis can overexpress a one-offerhydrocelies, so they can make a ton of vitamin D and that can cause a hypercalcemia. And, I mean, if a patient has primary hyperparathyroidism, right? I mean, the way you can do the workup is you measure the blood calcium levels to confirm the hypercalcemia. And I will encourage you to not base your calcium measurement solely on the total serum calcium, right? Because if you have high levels of argument, that can make your total calcium high, right? The thing you want to do is to measure an ionized calcium, right? The ionized calcium will give you like a very true gauge as to the patient's calcium status because again, if you have a ton of argument on board, the total calcium will be high or the ionized calcium will actually be normal, right? So, you don't want to, again, base your decisions primary on total calcium. Measure your ionized calcium.

Once you confirm the hypercalcemia with the ionized calcium, then you can do like a technician systemy-based scan of the parathyroid lens to screen for the adenoma that is potentially causing the primary hyperparathyroidism. And just to round this out because this is kind of like a high-yield topic, let me say a few more things about some things already mentioned, right? So, I said that MEN1, they get like parathyroid problems, they get pancreatic problems, and they get pituitary problems, right? Don't forget MEN2 A and 2 B, right? So, remember that in MEN2 A, right? Those people can have parathyroid problems, right? So, they get the parathyroid hyperplegia, right? And then patients with MEN2 A also get pancreatic, I mean, they get fiochromosytomas, right? So, they can get fios, remember the episodic headache and hypertension. And then those patients can also get medallary thyroid cancer. In fact, medallary thyroid cancer is one of the most common manifestations of MEN2 A, for the MEN2 A syndrome, right? So, that's something you want to keep at the back of your mind. And it's also inherited in an arosomodominant fashion, and it's associated with a retogen mutation. MEN2 B, somewhat similar findings, they get like the fiochromosytomas, but they don't get like the primary hyperparthyroidism. They get the fiochromosytomas, they get the medallary thyroid cancer. Remember, that has calcytonin as a tumor marker. And then they also get mucusoneuromas, right?

So, they get like the neuromas usually around the lip. And then they also tend to have like a marphanoid of body habitus. And one high-youthenile, see for example, is if a patient has a history of MEN2, they actually need their prophylactic thyroidectomy, because they will almost certainly get met... Actually, the chances of getting a medallary thyroid cancer is like 100%, it's just a matter of when. Okay, so those people actually need a prophylactic thyroidectomy so that they don't get medallary thyroid cancer. And then I also talked about multiple myeloma, right? Obviously, for multiple myeloma, you want to do like your SPAP and UPEP to make the diagnosis, right? I remember multiple myeloma, you can treat it with drugs like a bortezomib, that's a pretty sum inhibitor. And you can also give thalidomide, right? I mean, you may say, oh, divine, thalidomide, birth defect, why are you giving it to a person? The thing is, the people that get multiple myeloma tend to be old people, right? So, those people are usually like past the age of childbeer, right? So, those are situations where thalidomide is fine, the clinical benefit, so that weasel risks, on that those are circumstances. And then there is one great calcium disorder as well that again, makes its way to exams. If you notice, I've probably been spending like the last 20 minutes talking about like calcium problems, but these are all things that you could potentially see on these exams.

And there's this condition known as a pseudo-hypo-parthyroidism, right? Basically, the pathophysiology of this disorder is that these people have like resistance to PTH. So, they have a ton of PTH on board, but the second messenger system for PTH just doesn't work. So, the PTH levels are high, but they have like a hypoparthyroid state, if you may. In fact, pseudo-hypo-parthyroidism is a cause of hypocalcemia, not hypercalcemia, right? So, these people that have pseudo-hypo-parthyroidism, you check the PTH levels, it's high, right? But even if the PTH is high, the calcium is actually low, because they're not getting any PTH effect. And it should make sense that their phosphorus should be normal or high, because again, they're not getting any sort of phosphate-trushing effect from PTH. And one weird thing that you may see on exams with pseudo-hypo-parthyroidism is measuring the cyclic AMP levels in the urine. The urine cyclic AMP is actually high in primary hyperthyroidism, because PTH uses cyclic AMP as part of the second messenger system. But if a patient has pseudo-hypo-parthyroidism, because they are not getting the effect of parthyroid hormone, their urinary cyclic AMP activity is actually pretty low. So, that's actually a very useful test to delineate primary hyperthyroidism where the urinary cyclic AMP is high from pseudo-hypo-parthyroidism where the urinary cyclic AMP is low. Okay?

That's one of those tests, this is just one of those questions that most people will get wrong on a test, but hopefully you don't get it wrong because you hopefully are listened to this podcast and actually are paid attention. And again, like I said, right, you do a parthyroidectomy in general for primary hyperthyroidism, I mean if the patient is like a bachelor's school candidate, that's where you can consider like a bisphosphonate or you can consider like this drug. It actually modulates like the calcium sensing receptors in a calcet. It can actually be used for the treatment of a primary hyperthyroidism. It decreases the endogenous release of a parthyroid hormone from the parthyroid gland. Now, what if a patient comes in and they have severe symptoms from their hypercalcemia? So let's say they're like volume down and they're like obtundate and they have like severe abdominal pain and poliria and all that stuff. How do you treat those people? The thing is your treatment of choices, the first thing you always always always want to do both clinically and on exams is to give them a ton of fluid, give them a ton of normal ceiling. Okay? And then as you're giving them that ton of normal ceiling, you can also give them, you can also give them a fewer semi-terrace, so lessyx. Remember that's a lube diuretic. Remember lube's lube's calcium. So that can sort of cause like a calcium diuresis to help them with the hypercalcemia.

Alternatively, you can also give those people a calcetoning. Calcetoning is actually a great drug for very quickly lowering a person's serum blood calcium at levels. Okay? So this is one of those weird things you want to keep at the back of your mind. Now, one thing though, if a patient has hypercalcemia and that hypercalcemia is arising from like sacoidosis or like multiple myeloma, steroids actually excellent, like an excellent choice for those, for these are particular scenarios because the thing is sacoidosis responds to steroids and multiple myeloma actually does respond to steroids. I mean, those are responding everybody. It responds somewhat. So that hypercalcemia from multiple myeloma can be treated very effectively with steroids. And to sort of like tee things up before we sort of move on here, let's sort of talk about a hypocalcemia for a bit. So hypocalcemia, right, can arise from, I mean, I just told you that hypercalcemia can arise with hyperparthyroidism. Well, hypocalcemia can arise with hyperparthyroidism, right? And I mean, if you want to ask yourself, what is the thing that commonly causes hyperparthyroidism in the US? It just arises if you scrub in surgery, right? So if you're having like thyroid surgery for any reason, and then by some mistake, although this doesn't happen commonly, you'll de-vascularize the parathyroid glands, right? You basically knock out your parathyroid glands, right? And then you can sort of get into trouble with hypoprthyroidism.

I mean, what if they give you a scenario about a patient that is like a newborn, has like truncose arteriosus, has like clef lip, has like hypocalcemic seizures, and let's assume like they have like a cell medated, like immune deficiency. Hopefully you're thinking about like the George syndrome. Remember, that's a chromosome 22 Q11 defect, right? It's called like the Q22 disorder. That can classically present with a primary hyper with a hypoparthyroidism, right? Because for those people, the third and fourth are pharyngeal pouches, do not develop properly. So they lose their thymus and they also lose their parathyroid glands. And what if you get a question about a patient that is a hypocalcemic, and the hypocalcemia rose because let's assume they were like found down. Let's say they were like an alcoholic and they were found down for a long period of time and you check their creatinines like super high and they have hypocalcemia, right? So what's causing that hypocalcemia? Well, hopefully you're thinking about a ruptomyolisis. Remember, ruptomyolisis can cause it's like myocyte necrosis, right? So as they have that myocyannecrosis, they spill a lot of potassium into the serum. So those people can actually have like hyperchylemia and like bad, bad, bad problems with hyperchylemia. But another thing they can have is hypocalcemia because those dead muscle cells can sequester calcium. Okay?

So those people you need to, basically if a patient has ruptomyolisis, you need to place them on telemetry, right? Because with the hyperchylemia they have, they can have like like peak t-waives, they can have the white QRS complexes that can progress to easily and death, which is not ideal, obviously. Another thing that can happen is they can have like problems with hypocalcemia. So remember, hypocalcemia can prolong a person's cutie interval and that can ultimately cause a torsada point. Again, which is not a good arrhythmia to have. I guess a while I'm even on the topic, right? Any major electrolyte disorder that has hypo in the name can cause a prolonged cutie interval and torsada point, right? So like hypochylemia can cause a prolonged cutie interval, hypomagnesemia can cause a prolonged cutie interval. Okay? And if you have prolonged cutie, again, that can cause a torsada point. Now, what if you get a weird question about a patient that has like, you know, like just recurrent throsh, you know, and they have like a primary adrenaline sufficiency, right? So they have like really bad adolescents and then they also have like hypoprathiridesim. If you see this, I really hope you're thinking about this weird disorder. It's called like autoimmune polyglondula syndrome. Okay? At least type one, there's a type two, but the big one that is tested on exams is type one. Type one is where you observe the triad of so in the type one, right?

They usually have like the chronic mechocotinous candidysis. That's why they have the throsh that I described in the QSTEM. And then they can have all these other like weird autoimmune diseases, right? So they can have like hypoprathiridesim, like an autoimmune hypoprathiridesim that can cause hypochocemia. They can get video LIGO, right? They can get like premature variant failure, right? They can get they can get adolescents disease with that versus I guess the type two form of autoimmune polyglondula syndrome where again, they can also have the hypoprathiridesim, but these people can also have Hashimoto's thyroiditis. In fact, I want you to associate Hashimoto's thyroiditis more with APS type two versus APS type one. These patients can also have like gravestisies. They can have like diabetes like type one diabetes, right? Because remember, that's an autoimmune insularitis basically. So they can have many of those problems, but usually the chronic mechocotinous candidysis not arise with APS type two. So let me try to make this clear for you. If you see hypoprathiridesim and you see video LIGO and you see chronic mechocotinous candidysis, think about APS type one. If you see hypoprathiridesim and you see like gravestisies and you see like Hashimoto's thyroiditis with no chronic mechocotinous candidysis, I really want you to think more about APS type two. The pathophysiology probably doesn't matter much for the exams you're going to be worried about.

It's probably just for step three. You may want to think of these disorders arising from like an air gene mutation. It's like AIRE. Basically, it's I think it's like a transcription factor that ultimately helps you present the antigens from your endocrine glands in utero, like in the process of embryology. So if you have a mutation in that enzyme, you don't present these antigens in utero. So your body recognizes them as foreign, so your body begins to destroy those different endocrine organs specifically. But again, I don't really see them testing that pathophysiology on exams, but I guess I'll just throw that in there. Just in case it wildly shows up on step three for some bizarre reason. Now, I mean one other thing I guess you want to keep at the back of your mind with hypocausine varieties. If a patient is hypomagnesiac, if you're repleting the acousure, the acousure may actually not replete appropriately. That's another problem with potassium as well. Basically, if you have mac problems, your calcium and your potassium will not replete as the as they should. And again, remember if a patient is hypoparathyroid, the epitage will be low. If the epitage is low, the acousure will be low. If the acousure, if the epitage is low, the phosphorus will be high. That's like easy. But if a patient has, again, pseudo-hypoparathyroidism, as I described already, the epitage is high, but the acousure is low, and the phosphorus is high. The half-high levels of PTH, but PTH does not work.

I've talked about how you can treat the hypocausine that are as chronic kidney disease. I said, give calcium trial. Versus if a patient had chronic liver disease, you give calcium dial. Let's switch out of calcium land and begin to talk about some more endocrine disorders. Let's talk about what if you get a question about a patient that has episodic headache and hypertension? That's pretty classic for a few chromosidoma. Few chromosidoma. Basically, the PATHLF is here, involved like a neurocells, like your chromafin cells, usually in the adrenomydola, producing a lot of caracolomins, so like a penephrane or a penephrane. It's actually very high to know for step three that those chromafin cells that lie your adrenomydola come from the neuro crest. Those chromafin cells have nicotinic acetylcholine receptors on their surfaces because, remember, they're essentially a modified kind of post-ganglionic sympathetic neuro. That is more for step three. It's not something that I see showing up on an intraining exam or medicine board exam. Well, if you showed up though, you'll get it right because, again, you hopefully have paid attention and listened to this podcast. Now, few chromosidoma actually has associations with a few like syndrome, so like neurofibromatosis type two has an association with pho. One hippolendal, so VHL, I believe that's like a chromosome three defect. That also is a social field. Remember, VHL is also associated with a brain tumor known as a hemanguoblastoma.

It's just one of those bizarre things. You want to keep in mind, for example. And then, fields can actually also be observed in the ME and syndrome, especially like ME and 2 A and ME and 2 B. So, just one of those, again, high-yield things you want to keep at the back of your mind. And I mean, obviously, if you want to make the diagnosis, the first thing you do is you measure the levels of like basically like a dicholamine breakdown products. So like like men and effrins, like VHA, VMA, you can measure those levels in the urine or in the cere. And then, if those levels are elevated, you're like, maybe this person has a feel. So, you try to localize the lesion by doing like a C2 and MRI of the abdomen. Usually, that will help you find the lesion. You may find it like in the adrenomy dollar, or you can find it like in a classic location where you may occasionally see these like neuro-based tumors. So, for example, in the posterior medias thine, a fibromosytomalculine actually shop in the posterior medias thine. Now, one thing you want to keep at the back of your mind, though, is, what if you, you're like, wait, the ME and effrins are high, but you do a CAT scan, you do an MRI of the abdomen, you don't find in the tumor. One thing you may want to proceed to is something called an MIBG scan. The MIBG scan is very specific for cells that, that like of like, of like neural origin that produce like a ton of caracolamines.

So, if you do that MIBG scan, it can actually help you localize a few chromosomes like tumor. I mean, it's, it's a necotary test and I mean, it's very, rarely done in the real world. In fact, I don't think I've ever seen it done, but if your CT or your MRI of the abdomen fills you with regards to localizing the field, you could actually proceed to that MIBG scan. It's a very nice radiological study. It localizes very specifically to, to, um, uh, few chromosomes like tumor. Now, how do you treat a field, right? I mean, you obviously want to do some kind of surgical resection, but the surgical resection is not the high-yield treatment that shows up on exams. The high-yield treatment that really does show up on exams is what you do pre-up, right? So, the thing is for those patients, um, it's almost like, uh, overdosing on cooking sort of scenario, right? Because, um, they will classically want to treat, treat you on exams into doing like beta block it for these patients first. Trust me, that is not the right thing you want to do. It's just like the classics step one question, oh, patient overdoses on cooking. What do you want to do for them? Right? You don't want to give them a beta blocker. That's a bad idea. They'll have like the unopposed alpha effect. They'll have like severe hypertension and then they can get like a hypertensive stroke and die. You don't want to do that, right?

Um, uh, I guess so since I mentioned cocaine, you want to give benzos, benzos are the first line treatment for a cocaine overdose. But back to this, uh, since we're talking more about endocrine and nuts like here, if a patient has a field and you want to send them to surgery, like two weeks before surgery, usually, yes, like a few days, usually like two weeks before surgery, you want to give them like an alpha blocker first, right? So like, you want to give them like phynoxybenzamin. Phynoxybenzamin is an irreversible inhibitor of alpha one receptors, right? So you block that alpha receptor so that you don't have those unopposed alpha effects. And then if you block those alpha receptors, then if you want to do beta blockade, fine, that's fine because you've already wiped out that alpha response so that again, you don't get a hypertensive or crisis. And then another classic exam scenario is if the patient with a field has like intra-hypertension, let's say like the blood pressure just shoots up to like 250 over 160 or something ridiculous. For those patients, you again, want to consider giving like an alpha blocker like phynolymen, alternatively you can also give a nitro-persite on on on exams.

Although nitro-persite, I guess since I mentioned it, one like dovetail question from nitro-persite is, let's assume a patient has been on like an nitro-persite for a long while and then they get like a lactic acidosis and then they become like on a responsive, hopefully you're thinking about a cyanide poisoning with that, right? Remember nitro-persite has a lot of cyanide groups so you can precipitate a cyanide poisoning. And classically for that, you want to treat with like emo-nitrogen like thiosophate, right? Actually, wait. Yes, you want to treat with emo-nitrogen thiosophate. Again, this is a podcast. Yeah, I have some general ideas of what I want to discuss about some things just crupper in my mind as I give these presentations. So you want to give emo-nitrogen because the emo-nitrogen will convert like your hemoglobin to methemoglobin basically to like ion in the 3-plus form. And in that ion in the 3-plus form will complex with the cyanide and then the thiosophate will form a thiosyanate and then you can get rid of it, I think you can get rid of it in like a urine or something like that. Okay, now what if you get a question about a patient that has like on-relenting hypertension and they have like a hypochylemia on labs like the epitome is like 3 and then they have like a bicarbon of like 28. So they have like a metabolic alkylosis. This should get you thinking about con syndrome, right? So like primary, high-proud dose, tyroneous, right?

So this will likely be like an adrenal cortical tumor. So again, don't make a mistake here. In con syndrome, the tumor that's making the aldosterone is in the adrenal cortex. It will likely be arising from like the zona glomerulosa of the adrenal cortex. Contrast that with a fiochromocyte tumor that can also again cause like the on-relenting hypertension, will that tumor will be more of like an adrenal medallary tumor. Okay, so please don't make those mistakes. Remember, the adrenal medallarizes from uro crest. The adrenal cortex does not arise from uro crest. So how do you make the diagnosis of con syndrome, ready? If you suspect con syndrome, you will classically want to measure the plasma levels of our dusterone, measure the plasma levels of reigning, right? And then you calculate something called the plasma or dusterone to reigning ratio. If it's more than 20, that is pathonomonic for primary, high-proud dusteronism. Although you don't stop there, right? The thing is you want to sort of like, I mean, for every screening test, there's almost always a confirmatory test in medicine, right? So for these patients, after you've measured the plasma or dusterone to reigning ratio and it's more than 20, you would want to confirm those results with something called like a salt suppression test. So you basically give those people a salt load. Usually if you give a person a salt load, right? That will cause like intravascular volume expansion.

So that should ideally decrease your production of our dusteron. But if you have a failure of our dusterone to suppress with the administration of a salt load, that is confirmatory for con syndrome. So the next thing you do after that is to do a CT scan to basically localize the source of the lesion, okay? And if you do a CT scan and let's say you find like an adrenaline enoma that is making all this out of the dusterone, then you've basically made your diagnosis there. But here is where you really want to be careful on exams. The thing is if a patient has con syndrome, con syndrome can arise from an adrenaline enoma, but con syndrome can also arise from adrenal hyperplasia, right? So like adrenal quadricul hyperplasia. So the thing is let's assume you're like, oh, I just saw an adenine, I've done the plasma or dusterone to re-resure it's more than 20. I've done a CT scan and I see this, you know, just nice classic adenoma in the right adrenaline, you're like, okay, time to go ahead and resect this right adrenaline gland, fix this patient's problems and send them on their way. That is a bad idea. Before you take a patient to surgery for con syndrome, one thing you definitely want to do is to do something called adrenaline sampling. You see how divine, why would I want to do adrenovine the thing is think about it.

Let's just what if the right adrenaline adenoma you're seeing is a non-functioning adenoma, but you actually have hyperplasia in the left adrenaline gland that is actually causing the con syndrome. Well, if you just cut out that person's right adrenaline, and you're like, wait, this person's problem is it's not fixing so much. And you're like, oh no, now I have to cut out the left adrenaline gland as well. That will obviously not be a good thing, right? Then again, there'll probably be a lawyer that will be very willing to collect your medical license on that those circumstances. So the thing you always do before you take a patient to surgery for con syndrome is, I mean, you start them like, you'll first start them on like an audition receptor antagonist, right? So like spermolactone or a pleronone, right? To sort of like co-demoverty of surgery. And then before you do the surgery, you actually want to do like sort of like a localization sort of business, right? So the thing you do for those patients is you check the adrenal vein on both sides to see the site that has higher levels of our dostero. That helps you sort of like localize that, okay, this is the adrenal site that is over producing this outdoor serum so that you are going after the right adrenaline gland. You are doing the right adrenaline, okay? And again, you definitely want to do that before you go to surgery.

In fact, I will talk about another venous-like structure, probably in this podcast or in the next podcast that targets like the medicine board's IT step three, when I continue discussing endocrine, when we get to like a pituitary problems with like the sampling the inferior petrocellal sinus. That's one other thing I'll talk about. That's like another nice localization tool you can use in endocrine. That classic issues open exams. And remember, I said that if a patient has con syndrome, right? The plasma or dostero and terinine ratio will be more than 20. The thing is you also want to compare this with a patient that has like fibromuscular dysplasia, right? So there'll be like a young female that has onrelenting hypertension that is not responsive to like three different anti-hypertensives. And you may hear like a brewy when you like a flung brewy when you are scotting the abdomen alternatively can be an old guy with renal adristinosis, right? Those people will also have like a flung brewy. Although they don't give you that flung brew on exams, they may give you like the fondoscopic finding of arteriovinoz niquin. That's classic for renal adristinosis. Remember if a patient has renal adristinosis, right? They are not profusing, they are afraid materials very well. So their GG cells begin to freak out. So they release a ton of reneine. And addition to releasing a ton of reneine, they will also release a ton of outdosteroane, right?

Because remember reneine is like the gig keeper to the reneine and dotheroine system. So in renal adristinosis and fibromuscular dysplasia, you make a ton of reneine. That reneine will convert and dotheroine to and dotheroine to and dotheroine to and dotheroine and then the endothelial cells in your lungs, right? That around like your pulmonary capillaries will convert and dotheroine to and dotheroine to and then that and dotheroine to we go to the zonal glomerulosa of the adgenial cortex and increase the release of outdosteroane. So your reneine will go up, but your outdosteroine will go up at the same time as well. So your plasma outdosteroane to reneine ratio usually will be less than 10 in the setting of renal adristinosis and fibromuscular dysplasia. Contrast this with con syndrome again where that ratio is more than 20. So actually in con syndrome your outdosteroine level is high and because your outdosteroine is high your absorbing sodium in the distant nephron or your absorbing fluid at the same time you become hypertensive. So your reneine and dotheroine system is actually dialed down. So your levels of reneine are actually low in the setting of con syndrome. That is why your plasma outdosteroine to reneine ratio is more than 20 if you have a con syndrome. Now let's I guess this podcast has gone on for more than an hour, but you know there's some other high-yield stuff I think I want to get through to this. I'm going to just keep going.

So I'll just give you a bunch of clinical scenarios and then you tell me what the most likely diagnosis is. And actually yeah yeah let's go ahead and do it. So let's assume you get a question about I don't know this point just keeps nagging in my mind. Let me just go ahead and discuss it right now. Before I go to these scenarios. So if a patient has adicence disease, right there again this is this is almost like a freestyle podcast. It's but again like I don't just show up and like start like talking now. Yeah it's a freestyle podcast but I also did some preparation before I started with this rendition and all these things I promise you they are very high you to know for the exams that this podcast is a targeted towards. So back to the story. So but I want you to be conversational so you can be something and just listen to and just learn as you're like driving home from a long day at work or taking a shower or working out at the gym or something. So if a patient has adicence disease right that's also known as primary adrenaline sufficiency. So the adrenal glands don't work. If your adrenal gland is not working your zone of lumeurilosa, fascicular and reticularis is not working right. So for those people they obviously have low levels of our dostura right and they will also have low levels of cortisol right. So they will have like a mineralocorticoid and a glucocorticoid deficiency.

So for those patients you don't want to treat them with like flujocorticoid zone to replenish the mineralocorticoids that are missing and you would also want to treat them with a glucocorticoid to replenish the cortisol that you are missing. Now contrast this to the patient that has a secondary adrenaline sufficiency right. So let's assume a patient has I don't know let's say they have like a pituitary the normal that is like sort of like growing and causing a decreased production of acth at the level of the anterior pituitary. If people are not making acth right those people would have trouble making an offer cortisol right. So they will have a glucocorticoid deficiency but shockingly they will actually not have a mineralocorticoid deficiency. So why is that? The reasoning behind that is remember your zone of glomerulosa is actually not under the control of acth. It's actually under the control of your renein and your tensin outosterone system okay. So if you have primary and general insufficiency your general gland is gone. Whether your renein and your tensin system works it doesn't matter. You have a glucocorticoid and a mineralocorticoid defect.

But if you have secondary adrenaline sufficiency where the problem is more upstream at the level of the anterior pituitary your general gland that working just fine is just like the fasciculata and reticularis that will not work well because you are not stimulating them with ECTH but your renein and your tensin outosterone system will be working well and good okay. So for those people you actually do not need to give them fluzocorticoid. You just need to give them glucocorticoid. If you have a secondary adrenaline sufficiency. Okay so let's jump to a few scenarios and I guess we'll probably around this up. So this does not go on for much longer. I'll pick up from the other things I wanted to discuss in the next step in the next podcast that's targeted towards these exams. So what if you get a question about like a foe foe toe female okay that has never had mencees and she has like recurrent pylonofritis. Hopefully this gets you thinking of a toner syndrome right. Remember these people are 45 eggs skull. It means as like divine way do they have a primary manorera. Why they not having mencees? Well they have strict ovaries right. So if you have strict ovaries right you're not going to have mencees in the first place and you may ask divine why do they have recurrent pylonofritis. I'm just using that to tie in the facts that patients with toner syndrome right. If you see recurrent like urinary tract infections you really want to think about horseshoe kidney right.

So remember those people like the inferior pores of the akibnis remain fused right. So you sort of stay stuck under the inferior mesenteric artery in embryology right. So those people can now get like recurrent urinary tract infections with that. And I mean I guess what are some other classic things that are such as toner syndrome that you want to know for these tests. You want to know that patients with toner syndrome tend to get like bicospidiotic valves right. So if they describe like a systolic ejection murmur in a patient with toner syndrome and they're like 45, 50 years old like basically like early eodic stenosis. Think about a biose bicospidiotic valve with those. And remember that having biose bicospidiotic valve actually increases your risk for eodic dissection or any of the other like acute eodic syndrome right. Bicospidiotic valve for some reason it increases your risk of like eotopathy that can ultimately lead to like an eodic dissection. So that's just one of those weird things you may also see in toner syndrome. Now patients with toner syndrome can also get like quotation of the order right. So classically you'll see like upper extremity hypertension and low extremity hypertension right. And then if you do like a chest x-ray you may see like that classic three-sided okay. That's on that classic association with with a toner syndrome. And the thing is right these people who patients with toner syndrome the hypogonadol right.

But the thing is they have more of a hypergonadotropic hypogonadism right. And the reason that's the case is because the ovaries are not working they are not making estrogen. They're not making estrogen. There's no negative feedback at the level of the hypothalamus and the anterior pituitary right. So they are levels of GNRH and FHH and LHT will all be okay. So they will have a hypergonadotropic. So they are gonadotropins are high. But the their estrogen is low right. So the hypogonadol but the hypergonadotropic okay. Those tropic hormones for the gonads will be elevated because there's no negative feedback. And the thing is right if a patient has toner syndrome right. They will have like under developed breasts like very under developed secondary sexual characteristics right because again they're not making estrogen. In fact I will tell you this because these these um e-menorial questions and all that stuff they love to mess with people's heads by telling you oh they have like toner one breast and they have no pubic auxiliary hair. Let me just give you a simple trick that makes the analysis very easy. Basically if a patient does not have pubic or auxiliary hair right off the bat you should begin to think about disorders where they either have low levels of testosterone or they have testosterone and it's not effective for example like an angiogenic sensitivity syndrome.

But if a patient has under developed breasts or like uh um yeah I'll say primary like under developed breasts or like tanner one breasts um you really want to think more about like having like an estrogen deficiency. So under the circumstances you want to begin to think about situations where estrogen may be low right. So for example if a patient had like toner syndrome there'll be a cause of like uh primary menorial with uh like tanner one breasts for example. So let's jump to some other scenarios right. So what if you have like a 4.0 GPA like female athlete that has a primary menorial right. So this will be more of like you know like a functional hypothelemic insufficiency because the thing is if you're working out a ton or you're under like tremendous amounts of stress guess what that does to your HPG axis is short okay. And when your HPG axis is short, shots down right. Your generic levels will be low, your FSH levels will be low, your estrogen levels will be low right. So those people can uh get like uh basically like a hypothelemic in menorial okay um another classic um I guess scenario let's assume a patient has like breasts so they have like tanner three tanner four breasts uh they have like a vagina although it's like a blinding thing vagina but you do an ultrasound you don't find the uterus um and you don't see any pubic or axillary hair um if you see this um I really hope you're thinking about undergaining sensitivity syndrome.

So you get like a complex disorder tends to screw with people's heads on tests so let me sort of talk about it uh in some detail right. So if you have AIS your genotypically male we have phenotypically female okay. So these people actually have like a 46 X Y um carotype okay. The problem is these people are making testosterone but the testosterone is just not working okay. So if the testosterone does not work guesswork they wouldn't have anything for five alpha reductives to act on to convert the testosterone to DHT. So if you're not making DHT the external genitalia will not very nice so you will go down to the fourth female pathway okay. So that's why they'll have like external female genitals but these patients will not have a uterus right because remember these people are genotypically guys so they have a testis and because they have a testis they are making anti-malirium hormone right and that anti-malirium hormone will kill the malirium duct and everything that's derived from it right. So like the uterus will be gone the fallopian tubes will be gone as well. Now you may ask divine where would these people have breasts? Well the reason they will have breasts is because they have aromatis so that aromatis will take their testosterone and convert it to estrogen and that estrogen would help with the developmental breasts okay.

So and these people actually have no axillary hair because again they have testosterone remember I told you a telltale sign that you either have a testosterone deficiency or testosterone is not doing his job right you have like like basically like a functional testosterone deficiency which is what you have with the IS is having the absence of axillary or pubic hair okay. These people will actually not have axillary or pubic hair and I guess to sort of tee things up here. What if you've got a question about a patient that has you know they have breasts they have like a blind ending vagina you do an ultrasound you actually spot some nice nice looking ovaries but you don't see like a uterus or you don't see fallopian tubes you don't think about malirium egenesis for that. I believe that's also known as Meyer Rockitansky Costerhousers Syndrome or malirium egenesis for short. Basically these people just for some bizarre reason just don't develop the malirium duct the malirium duct right. If you have malirium egenesis everything that's derived from the malirium duct right so like the upper two thirds of the vagina the uterus the fallopian tubes don't develop remember your ovaries your ovaries your ovaries are not embryologically derived from your malirium duct so those people will have ovaries and guess what if you have ovaries you have estrogen if you have estrogen guess what you have breasts okay so those people have breasts they just have no uterus.

Now what if you get a question about someone that has phenotypically developed as a girl and then like over like a one year period in puberty they just rapidly begin to viruli and then like over like a one two year span they almost quickly become males.

If you see that you want to think about five alpha reductis deficiency right I mean like you've probably heard of this things like a Spanish term I think it's like Guave Doches it's a relatively common problem in like like I think I don't want to butcher this but it's like either like a central or a south or this it's like it's like like some kind of like south or central American country basically they have like the five alpha reductis deficiency remember five alpha reductis helps you convert testosterone to DHT and DHT is primarily responsible for the virulization of your external genitalia right so if you see those kinds of if you see that kind of problem think about that deficiency but you may see divine okay if they develop as females all through their lives on to puberty why do they suddenly become male at puberty the reasoning behind that is that puberty you'll see just ridiculous amounts of testosterone so those ridiculous amounts of testosterone just basically force virulization okay so it doesn't matter even if they don't have the HD they just become virulized with a super high levels of testosterone that characterize puberty and then I guess just as a just to throw your bone here what if you get a question about newborn with ambiguous genitalia right if you see a newborn with ambiguous genitalia hopefully that gets you thinking about congenital adrenal hyperplegia right that classically arises from a 21 hydroxylisa deficiency now what if you get a question about a lady this is had mencise in the past but let's see you know she had like a DNC like a dilution and cure attached like a year ago and then she's no longer having mencise for those patients you want to think about asherment syndrome right so asherment syndrome basically this if let's assume you have like a DNC and let's see whoever did the DNC like you know maybe scrub the little too hard you can ba

sically strip of the the basal endometrial the basal endometriop right so you basically have nothing to regenerate the endometrial cavity okay so these people classically you would want to go ahead and like like the buzzword they are looking for for treatment on exams is something called like hysteroscopic lysis of adhesions because those people basically form a lot of scar tissue in their in their uterus along the endometrial lining so generally the way you want to treat these people is you know you go ahead and lie those adhesions and then you give them estrogen to sort of build up the endometrial and then you they can return to like fertility and they can start having like like normal menstrual cycles again one thing I would say here is they may give you like an experiment style question on these exams and tell you that oh if a patient like they may give you this thing called like the progesterone we draw challenge test right and then I mean I can't really think of a way they would design a question but I have certainly seen this tested where you're sort of like supposed to deduce like oh if a patient has ashram syndrome how would they respond so let's let's assume they have ashram syndrome that has not been treated how they respond to like a progesterone we draw a challenge test the thing is they will actually not have the withdrawal bleed because again the thing is when you give progesterone and we draw it you will get bleeding if you have a built up endometrum right so if that bezel in the metrum is gone you're not gonna build up the endometrum in the first place so there's nothing for progesterone to stabilize and then for you to have like bleeding when you withdraw that progesterone so they will have a negative response to that challenge contrast out of the patient that has PCOS in PCOS those people they are a cigarette ton of estrogen but they don't have much

of progesterone like enough progesterone around so those people if you actually do like that progesterone we draw a challenge because they have high-pressurgynesium they have like this super built up endometrum if you give them progesterone and we draw it they will actually have a withdrawal bleed so make sure you can interpret progesterone we draw challenge tests in the context of these disease like PCOS and the ashram and syndrome I can really see them like sort of like saying oh you know cuse them like oh the progesterone we draw a challenge test did not give any like we draw bleeding and then they will give you like maybe like four or five options where like of those like of those five options like four of them have like a positive test and then one has a negative test and they sort of have to like reason through like oh for this disorder this is what will happen for this is sort of this will happen right so just sort of keep those things at the back of your mind now what if you get a question about a patient that has again stopman's treating and let's assume they are patient with like schizophrenia right guess a diabetic gastroparesis why would they stop having men's it right so these people likely have a likely taking you know some kind of dopamine antagonist right so if your patient has schizophrenia they are probably taking like an anti-psychotic like respiratory don't of something right remember these things are dopamine antagonists and remember that normally dopamine's job is to inhibit the release of prolactin okay in fact think about dopamine as prolactin inhibiting factor so if you're taking a dopamine receptor antagonist your levels of prolactin will go up because you are blunting the effects of dopamine so you will have hyper-prolactinemia remember that's classical as with your respiratory don't on tests so you get hyper-prolactinemia and prolactin sup

presses the HPG access right so you stop having menstrual cycles and with regards to the diabetic gastroparesis remember one treatment is metoclopromide right metoclopromide is a dopamine antagonist so you can also get hyper-prolactinemia because again we effectively shutting down the tuberoinformed developed pathway that relates to dopamine now obviously you want us potentially you know maybe stop these medications and the problem will sort of fix now what if you get a question about numin C's in a woman that has like tonal vision right so this is basically like a bite temporal like a heteronimosa hemi anopsia for these patients right they likely have like a pituitary adenoma right that's you know compressing the optic chiasm causing those visual field defects but the reason they've stopped menstruating is again they probably have they have like a prolactinoma right remember prolactinomas um it's a like a pituitary adenoma it's not a it's not a secret so pituitary adenoma that's making a tonal prolactin okay um in general the way you make that diagnosis is you know you measure the levels of prolactin right it will classically be elevated and then after you detect the prolactin elevation you then go ahead and you know do like an MRI of the pituitary gland and you'll see the adenoma and I'll tell you this I'll say like 99.9% of the time choosing surgery is the wrong answer for the treatment of a prolactinoma in general for prolactinomas you explore medical management first medical management almost always works and like shrinks a prolactinoma in most people right so you want to choose a dopamine remember I told you that I just told you that dopamine shots down the release of prolactin right so you want to give a dopamine agonist like cabregulin or bromo cryptin those are very nice drugs for the treatment of a prolactinoma as although if you've got an evil example quest

ion where cabregulin was an answer choice and bromo cryptin was an answer choice pick cabregulin of a bromo cryptin cabregulin is better tolerated of a bromo cryptin now um if for example though let's say you've tried medical therapy it's not working you know then you can try resetting the prolactinoma and the boss phrase you're looking for an exams for resetting pituitary adenomas in general is something called a transphenoidal resection okay that's the boss what you're looking for in tests now what if you get a question about a 39-year-old female you know she has no men she like with the past two three years she has no mences and she has a history of like type 1 diabetes she has a history of like addison's disease so that's like primary and adrenaline sufficiency um for those people you want to think about you know uh like a premature variant failure so they basically had like autoimmune destruction of their ovaries essentially just remember right you're not supposed to you know it you're not supposed to be menopausal before the age of 40 right so uh 39-year-old female this is likely premature variant failure and classically we present on exams in a patient that just has like a very strong autoimmune predisposition right so like autoimmune adrenalineitis autoimmune insularitis that's like type 1 diabetes and stuff like that so for those patients um think about premature variant failure and again this would be another good example just like toner syndrome of hypergonnaidotropic hypogonnaidism okay because the ovaries are not working the levels of gen RHFHLH will all be high now what if you get a question about a you know patient that has no mences and let's assume they recently got like a total thyroid dectomy for follicular thyroid across the normal remember this is one of those weird thyroid cancers that usually doesn't spread to lymph nodes usually spreads hematoc

inously right um for those patients um I really really hope you're thinking about um hypothyroidism that's causing hyperprolectinemia right so remember um if you recite the thyroid gland well bye bye thyroid hormone uh if you don't have thyroid hormone on board anymore right your levels of TSH will go up your levels of TRI will go up right um so thyroid tropin release in hormone one of that term you can use to describe thyroid tropin release in hormone is prolactin release in factor okay so if your thyroid hormone is low so if you're hypothyroid for any cause your TRI will go up if your TRI goes up you will increase the release of prolactin and if you increase the release of prolactin well guess what uh you will shut down your HPG axis and you will also stop again having a menstrual cycles and in general um I mean if you if you traded the hypothyroidism that conditions should technically uh resolve now what if you got a question about I guess this is sort of related to like losing menstrual cycles but let's assume like you get a question about a lady that just delivered um let's see she had like really bad placenta previous had like a ton of bleeding and then she cannot lactate right so she cannot like you know breast feed her baby um you want to think about she hand syndrome right so these people have potentially had like a you know like a pituitary necrosis if you may because of the blood loss so they basically had like almost like uh like uh like uh like an ischemic stroke I think of um she hand syndrome of as an ischemic stroke of the pituitary versus um pituitary apple plexi that I think more of like a hemorrhagic stroke of the pituitary gland so this patient in this case has a she hands syndrome now what if you get a question you know about a like a hersute female you know has a bmi of like 37 and she's having trouble becoming pregnant uh it's a pretty classic q

uestion right you want to think about PCOS please don't get this wrong on an exam ever okay this is PCOS remember PCOS right you it's actually something that you don't necessarily need imaging to make the diagnosis uh you can actually make the diagnosis like super clinically um in fact there's like three diagnostic criteria you just need to meet two out of three and boom the diagnosis has been made right so uh one of the criteria is like um you know um simple cystic ovaries on ultrasound another one is you know seen like size of height signs of like hyperanogenism so like really bad acne like nodulocystic acne or like hersuteism and then the third criteria is like evidence of an ovulation right so like uh immune-oriented stuff like that so if you see that um think about PCOS and if you meet two out of those three criteria you've met your diagnosis now you want to be careful here though if you see it like kind of like a similar presentation to what I just mentioned but you see it like rapidly progressive over like a very short period of time uh sort of think about more of like you know some tumor maybe in the adrenal gland that's making like DH As okay that is causing that hyper androgenism so maybe like oh you could also be like a ladyxel tumor for example um in general for PCOS you pursue multi-modal treatment right so you you know weight loss um that can help with like the insulin problems that they tend to have um if they have like diabetes um you want to go ahead and give them it forming in fact there are some patients with PCOS that um they're like oh they have infertility and give them it forming and that actually like fixes the infertility but on exams though if a patient has infertility and he desires pregnancy and they have PCOS you want to go ahead and give them clumifin um clumifin is a serm um that helps with um promoting a fertility about 75 to 80% of wome

n with PCOS that take a clumifin they actually have a return to fertility and then if the woman is worried about like the hyper androgenism uh like the hersotism and all that stuff you know you can give them like OC Ps that can help you can also give them a spironolactone spironolactone inhibits an enzyme known as a five-offer adoptees but it does that in the skin and it really helps with that hersotism now um if a patient with uh you know long history of PCOS has like vaginal bleeding on exams your next step in management for those patients is to do an endometro biopsy because they could potentially have endometrial cancer right remember one of the cardinal features i mean it's not part of the diagnostic criteria but it's one of the cardinal features of PCOS is hyper estrogenism like on opposed hyper estrogenism so that can increase the risk of endometrial hyperplegia and endometrial cancer so you want to go ahead and do an endometrial biopsy for them even if they are not uh even if they are like 37 years old for example you want to go ahead and do an endometrial biopsy because they will try to mess with your head on exams and say oh usually the people who do endometrial biopsies for people that are more than 50 no if you have like very big big risk factors like if you have PCOS or you're like super obese and you have like vaginal bleeding and you're less than 50 even less than 40 it doesn't matter go ahead and do an endometrial sampling for those people to make sure they don't have an endometrial cancer now what if you get a question about like a six foot tall guy that has like small testicles and has gynecomastia and has like difficulty getting his wife pregnant uh this is pretty classic claim filters right um the next step in that notice is you really just to get a carrier type you will detect like 47 xxy okay they have like an extra x chromosome so they'll have li

ke a bar so if you see like a bar body um so they give you a question they say oh they did like genetic analysis they saw like a bar body in a guy that's claim filters syndrome in exams that's just good uh testic in strategy right there now what if you get a question about an immigrant that is having trouble you know getting his wife pregnant and his immunization history is unknown think about mumps under those circumstances remember right mumps can cause like an epidemore or chitis right so you can basically look at the testicles under those circumstances and that can cause infertility meaning if you're a testicles they're working uh then well bye bye spur okay now what if you get a question about a guy with a hemoglobin E1c of 9 okay that is having trouble getting his wife pregnant and then they tell you that oh you don't physical exam and you see skin hyperpigmentation um for these patients uh you really want to think about um so you're seeing hemoglobin E1c or 1 right that's diabetes and you're seeing skin hyperpigmentation right so like bronze diabetes that should hopefully get you thinking about a hereditary or hemochromatosis remember those people can have the position of um iron in the apancras right so they can get diabetes from that because they're no longer making insulin they can also have the position of iron in their hearts they can get a restrictive cardiomyopathy with that although they could take also get a diluted cardiomyopathy and then they can deposit iron in their in their levers and get cirrhosis right alternatively they can also um deposit that iron in their in their testicles and they can get like testicular trophies and fertility with that so that's why I brought that up here remember the way you treat hereditary hemochromatosis is to um is to um what am I thinking about here flip bottom right so it is like blood let's those patients and that

will help with that iron overload state remember classically on exams your first step in diagnosis is to go ahead and check their levels of ferritin the ferritin will be very high okay and then um you can confirm the test by doing like some genetic analysis for the HFE gene mutation and I guess to sort around this up let me just talk about like you know hypogonadysamine guys I feel like I've been focusing on women for the most part let me give the guys some love here so um in terms of like hypogonadysamine males right so any presents like you know like erectile dysfunction or like lulabido and stuff like that usually the way you sort of make your diagnosis you know check the total levels of testosterone in the morning um if it's low then you have your diagnosis there um if it's sort of like borderline you can do something called like a free testosterone level so actually if your total testosterone level is not diagnostic go ahead and check a free testosterone level that will help you make your diagnosis and I mean in general you can do like testosterone replacement therapy for these people you can give it as like you can give like the testosterone as a patch um actually in my residency program we just had a discussion on like erectile dysfunction and stuff like that um it was actually a pretty useful okay so uh because this is something you encounter a lot in primary care and uh many people don't know how to treat it they don't even know to work it up uh but guys will not come out and see that oh they have erectile dysfunction right um so it's just one of those things if you're going into internal medicine it's just one of those things you want to keep in your back pocket because it's something that again guys will not share if you don't ask so ask about these things a primary care visits and you'll be surprised that how many guys will say oh yeah I'm having trouble

getting it up uh green intercourse and all that stuff right and you may want to sort of pursue some diagnostic testing with them okay um and I guess like you know like someone is uh before you start treating testosterone deficiency right you want to you know sort of get a CBC first you know check the hematocrit because remember testosterone replacement can actually cause a rethroughcytosis right so you want to sort of have like a baseline CBC and another thing you also potentially want to do is to you know check and cover baseline PSE level because remember testosterone can drive prostate cancers right um in fact that's why some prostate cancers especially like the metastatic kind are respond to um angiogen receptor blockers right like bicaridumide and fluidumide now uh uh two more scenarios and I promise will be done what if uh uh guys having difficulty getting his wife pregnant right and he's like a super buff guy has like large biceps amazing abs basically think about a guy using anabolic steroids right uh usually those people have like testicular trophion exam that's like the classic thing they put on on in a q-step and then the very last scenario uh what if you get a question about a guy you know comes in says he has trouble uh getting up in green intercourse but he has like morning erections right this is like a psychogenic erectile dysfunction that's a very classic uh exam question so did a guy head and stop here um I'll pick up from here in the next podcast but uh again for those that have listened to the first one that is into this one comparing contrast which one do you prefer I feel like in this one I was able to cover a lot more material um in comparatively in about the same amount of time so I feel like this is probably a more efficient format because I'm talking about like pathophysiology talking about treatment talking about workup but I'm just sort of

interspersing many different things so just let me know if you prefer this format this is likely the format I will stick with for the foreseeable future and again like I said I'll keep making more and more of these uh of these are podcasts to prepare for like the medicine boards the medicine in training and uh the USM L step three exam so I wish all the best I'm really hoping and praying that the leakers win the again tonight and again I'll throw it out there that I offer one on one tutoring for all the USM L exams step one two CK two C S step three the medicine in training exam and the medicine and um also the application prep so ira's applications for residency and case applications for med school mock interviews and stuff like that I have a lot of experience after you're thousands of people in this life so um just reach out to me divine intervention podcasts with an s and gmail.com uh or you can email me through the website and I'll point you in the right direction so have a wonderful day I'll see you in the next podcast god bless thank you

Must block alpha receptors first (e.g., phenoxybenzamine) before beta-blockers to prevent unopposed alpha effects and hypertensive crisis.

Sarcoidosis/Granulomatous disease.

Parathyroid hyperplasia (not parathyroid adenoma).

5-alpha reductase deficiency.

PHPT will have high PTH; Multiple Myeloma will have low/suppressed PTH.

Urinary cAMP measurement. High in PT HrP, low in pseudo-hypoparathyroidism.

Malignancy.

Hypergonadotropic hypogonadism (e.g., Turner Syndrome).

Measurement of metanephrines in urine/serum; MIBG scan.

Low or suppressed.

Oligo/anovulation, polycystic ovaries on ultrasound, and hyperandrogenism (acne/hirsutism).

Mineralocorticoid receptor antagonists (e.g., spironolactone or eplerenone).

Malignancy.

Hypergonadotropic hypogonadism (e.g., Turner Syndrome).

Measurement of metanephrines in urine/serum; MIBG scan.

Low or suppressed.

Oligo/anovulation, polycystic ovaries on ultrasound, and hyperandrogenism (acne/hirsutism).

Mineralocorticoid receptor antagonists (e.g., spironolactone or eplerenone).