DIP Episode 93 - USMLE Step 1 Rapid Review Series 4 (Endocrine)

Okay, welcome. My name is Devine. I'm a PGY-1, a transitional year resident that's going to radiology. This is the 93rd episode of the Devine Intervention Podcast. This will be a rapid review for the USML staff one. I guess this will be serious for. I mean, this podcast I'm going to be talking about endocrinology. Okay. You'll be a rapid review. I'll just review like a lot of high opathologies in a very short period of time. Right, so now make them as case presentation. So let's just go ahead and jump right into it. So what if we get a question about a patient, you know, that, you know, recently received a transplant and now they have proposed try. What are you thinking about? I really hope you're thinking about like a local court decoy to induce like pushing syndrome, right? So like an Iatrogenic or pushing syndrome. Remember, right, if a person receives a transplant, they typically need a immunosuppression, but you know, there's can cause a lot of problems, right? They can cause like osteoporosis, they can cause like osteonecrosis of the jaw, osteonecrosis of the hip, right? They can cause a metabolic syndrome, they can cause a lot of bad things, right? So and if a person is on steroids for longer enough, they can actually get pneumonia with an immunosuppression. So you just want those higher things you want to keep at the back of your mind.

Now, what if a patient has like, you know, like higher in osmolality and they were recently, and they recently started treatment for diabetes? I really hope you're thinking about one of the sofoneal urias, clopropomide. Clopropomide is actually one of the sofoneal urias that has a pretty strong association with a SIDH, okay? So remember, if you have SIDH, you basically have a uvolemic hyponitrimia. So you have low serimosmolality in the setting of a high urinosmolality, right? Because you're resubbing a crap ton of fluid from your, from your urine. Now, what if you get a question about a child? You know, that has technique and has like a clear thymic shadow on chest x-ray. I really hope that gets you thinking about like the George syndrome, okay? Remember, the George syndrome, your third and fourth afferent geopouches don't form. So your third and fourth pouches don't form. You will not form your thymus and you also not form your parathyroid. Try not to remember your parathyroid. Lens make parathyroid hormone. And their job is to raise your blood calcium. So if those are not there, you won't make parathyroid hormone. You'll be hypocalcymic and that can cause like signs of hypocalcymia like, like technique. They can even have like hypocalcymic seizures as a newborn. That's a classic way that shows up on exams. Now, what if you get a question about and they give you this buzzword? So period still res option along the lateral aspects of the middle phalanges, right?

This is classic for primary hyperparathyroidism. Remember, the most common cause very high you to know this. The most common cause of primary hyperparathyroidism in the US is a, is a parathyroid adenoma, right? Although you want to be careful in the setting of the MEN and DRUMS, the most common cause of primary hyperparathyroidism is a parathyroid hyperplasia, right? Remember, if a person has primary hyperparathyroidism super high, you'll actually know that their pth levels will be high, right? So if their pth is high, you already know that their calcium is going to be high, right? And remember that pth is known as the phosphate trashing hormone. So if their pth is high and the calcium is high, their phosphate will be low because you will appropriately trash the phosphate. But because there is a ton of calcium in your blood, there will be a ton of calcium in your urine, right? Contrast that with a FHH, right? So for the familial, a hypochalcyoric, hypercalcymia, we're basically the values are the same, right? So they'll have like high pth, they'll have like marginally the very blood calcium, their phosphate will be low, right? But the urinary calcium will actually be low. So that's actually a very high, high yield way to differentiate familial hypochalcyoric, I mean, even the name tells you, hypochalcyoric, hypercalcymia. So it helps you tell that apart from a primary hyperparathyroidism. So that's what answers my next question, right?

So if a person has like very low urine calcium in the sense of a very high serum calcium, that should get you thinking again about familial hypochalcyoric, hypercalcymia. And then what is a, I guess a nice way that you can, this will be like a 270 plus sort of question in the USM list, that one. So how can distinguish person, how can distinguish like a parathyroid hormone, relitheptide from a non-parathyroid hormone, relitheptide oncologic cause of hypercalcymia? You can actually do that by checking the urinary cyclic AMP. So some of you may say divine, how does that make any sense, right? So remember, so say for example, if a person has like a scum of cell cancer of the lung, right? Well, you make pth relitheptide, remember that pth, so that acts through like a GS, G-pertine copalt receptor. So your, that basically, there is your levels of cyclic AMP, right? But if a person has hypercalcymia from like, like an osteoclast activity factor like interlooking one in the setting of like multiple myeloma, for example, those people will be hypercalcymic as well in the setting of maligancy, but the urinary cyclic AMP will not be elevated, right? So because I own just not work through that pathway, right? So it's just one of those weird things. Me see on the exam pretty much everyone get it wrong, but you wouldn't. Hopefully because you listen to this podcast. Now, what if you get this question, this is something, if you get it wrong, you should go home and cry after your test.

But what if you get like a person that has like, you know, symptoms of hypercalcymia, and then they have hypercalcymia, and then you give them glucose and they are symptoms sort of go away? I really hope that's getting you thinking of like whipples, try it, right? And that's pretty classic for a friend in solinoma, remember in solinomas, right? You classically find them in the setting of a MEN1 syndrome. That's just a high-youth thing to know. Now, what are the organs, right? That I guess, classically affected by MEN1, right? So remember, it's your pituitary parathyroid and pancreas, right? So these people can have like pituitary at the nomas, they can have like parathyroid hyperplegia, right? Presenting as primary hyperparathyroidism. In fact, it's very high-youth to know that the most common presentation of MEN1 syndrome is primary hyperparathyroidism. From remember, I said it earlier, a parathyroid hyperplegia, right? And then they can also get problems with the pancreas, right? So like this pancreatic neuroendocrine tumors, like in solinomas and whipples, try to just talk about that. Look how good nomas, remember your necrolitic migratoryorythema, right? Where they have like a rash, you basically see like a neon set, like it's usually on the bottle, like nasty nasty rash, like necrotic rash, and then neon set diabetes really want to think about a glucanodroma. They can also have vipermas, right?

Remember that can present us as a WDHC syndrome where you have like watery diarrhea and hypochylibia and acrohedria. And then if you're thinking about MEN2 A, right? Remember that those people will have like medallarythioric cancer. Remember basically, you need to prophylactically resect those people's thyroid because it's not a matter of whether they will get medallarythioric cancer. If you have MEN2 A, you're going to get it, right? Like the MEN syndrome, see if you're going to get medallarythioric cancer, it's like 100%, you're going to get it. It's just a matter of what, okay? So those people need like a prophylactic, a thyroid, that's actually a pretty good USM and this step one question. And then remember that in MEN2 A, you can also see like a fiochromositoma. Remember that's a tumor that arises from the chromafin cell, so the adrenaline right? So remember that the adrenaline, those are chromafin cells that basically are modified, post-canglonic, sympathetic neuron, right? So basically they can basically turn that fio question into like an embryology question because those cells are actually derived from neurocrest, okay? And remember that they have nicotinic acetylcholine receptors on their surfaces, just one of those like nasty nasty things they love to test on exams. And then another thing with MEN2 A, don't forget the hyperparthyroidism and again remember that parthyroid hyperplasia, not that the norma is what is implicated there.

Now what if you get this triad, right? So what if a person has like like mucocutinos acandidiasis and they have like adrenaline sufficiency, right? So like adhesis disease and then they have like hypoparthyroidism. I really hope you're thinking about this thing known as the autoimmune polyglondrylis syndrome, okay? Shows up pretty commonly on exams, and then what if you get a question about a person that has like episodic headache, hypertension, like that freesis, like they're sweating a ton, and they have like these palpitations. I really hope you're thinking about a fiochromositoma, okay? Remember again, adrenomadolary, chromofin cells, tumor from that region. Remember fios, as I said, like MEN2 A, okay? Very high yield to know that, and don't forget that before you take those people to surgery, it's very high yield to remember that you want to do like alpha blockade before you do beta blockade, right? So you want to give them an alpha blocker like a phenoxybenzamin. Remember phenoxybenzamin is an irreversible alpha one antagonist, or you can also give them phentolamine. Phentolamine is a reversible alpha one blocker, right? So you can already see how they could test that in the context of amykelysmenting kinetics, like, oh, this one is irreversible. Oh, this one is reversible, right? So those are kind of high yield things you want to know for your exam. So you do the alpha blockade first before you do the beta blockade, right? So again, high yield to know that.

And then, um, um, what if a person has, um, and no, let's say I sort of sort of kind of talked about this in the podcast, but it's actually kind of high yield to know. It's sort of is a nice way to tie in a neurology, right? So what if a person has like a ton of like, you know, visual constriction, they have like hypothermia, um, and they have like a tacky cardia, right? These people are like, maybe these people like over sympathetic, right? So the way I think about it is these people over sympathetic because they have like essentially like a parasympathetic lesion, right? So it's like the sympathetic system is working on a post, right? So what's the nucleus of the hypothalamus that's kind of like screwed up, right? So I hope you're really thinking about a lesion to like the end, like the anterior hypothalamus, okay? That's a very nice way to contest that on exams. And then, what if a patient has like a ton of visual dilution, their hypothermic and the abridicardic, right? You're like, hmm, these people are over parasympathetic, right? So if they are over parasympathetic, that means, um, their sympathetic nervous system must have been lesion, right? So imagine that the posterior hypothalamus has been all screwed up. Remember in my neuro podcast, right? So the comprehensive neuro podcast I talked about, um, I've been, I studied it recently.

I remember I said that, um, your sympathetic nervous system, in fact, your autonomic nervous system in general, both sympathetic and parasympathetic, they actually both start in the hypothalamus. That's actually a very high yield thing you want to know for tests. They actually both start in the hypothalamus, okay? Um, so if you sort of lesion like specific parts of the hypothalamus, if you lesion your parasympathetic, you'll be over sympathetic in your response. If you lesion your sympathetic nervous system, you'll be over parasympathetic in your response, okay? That's a very nice crafty way to be considered like run circles around that concept on the USMLE step one exam. Now, what if you get a question about a child that has like precocious puberty, they have like coffee or lace spots, and then they have like all this like boony lesions, right? So the boss phrase on exams is polio-studic fibros dysplasia. What kind of syndrome are you thinking about? I really, really hope you're thinking about my CUNO bright syndrome, okay? My CUNO bright syndrome, right? So that's kind of like a high yield thing you want to know, right? So polio-studic fibros dysplasia, a coffee or lace spots, right? And they'll have like precocious puberty. Now, um, um, let's see. So what is the only I guess the only anterior pituitary hormone where their release is basically inhibited by positive feedback, right? I hope you're really thinking about a prolactin, right? I remember that prolactin, right?

Kind of like activates a dopamine. And, um, let's see. I guess what if you get a question about a hormone that you know sort of kind of like activates the anorexigenic pathway? Um, what hormone are you thinking about? I really hope you're thinking about leptin, right? So leptin is one of those things that kind of like suppresses a suppresses a appetite, okay? Now, um, what is like this classic feature you'll find on histology in a patient that has a pylocytic astrocytoma, right? Again, I hope you're really thinking about those rosin thyl fibers, right? So they're like pink cox-sure fibers. They love to test those on exams. Now, what is I guess the hypothelamic, let's assume, you've, uh, lesion, the nucleus of the hypothalamus. And this person has like a super, super, super low BMI, right? So what are you thinking about? I really hope you're thinking about like lesion to the lateral nucleus of the hypothalamus. So remember the lateral nucleus of the hypothalamus actually encourages you to eat. So if you sort of shut it down with a lesion, then you will not eat and then you have a small BMI. The reverse is the case for, um, a ventral medial lesion of the hypothalamus, right? So a lesion to the ventral medial nucleus. And it's kind of high up to know that because, right, uh, if you lesion the ventral medial nucleus, that actually promotes the tidy. So if that's all screwed up, right? You will not be, you will not be associated if you may, right?

So you eat a ton, so you have a super high BMI. Now, um, what is the classic description of like a cranial faringioma on, on exams, right? So remember, right? You'll tell you that you see like, uh, uh, right? You can tell you that you have a person has like an intracranial mass. It's usually supercellar, um, and it has like calcifications, right? Don't imagine. And remember on pathology, you see like the classic like modal oil, modal oil fluid. Um, one of the classic things, right? Remember those cranial faringiomas, they can cause like a bite temporal, uh, heteronimosa, hemi anopsia, okay? So that's a nice time with, neurology there. And remember that those things that derived from my rathkis pouch, right? So that's a very nice way we can sort of throw in a embryology there. Now, um, what would you find on histology in a patient that has sacroidosis? I really hope you're thinking about the nonchysheding granulomas, right? And what if a person has sacroidosis? Is there a particular calcium imbalance you may notice on an exam? Um, I really hope that you may, you're thinking about like hypercalcemia, because remember that in sacroid, right? You tend to release a crap ton of one alpha hydroxylase. And remember that one alpha hydroxylase, its job is to convert calcium diol or 25 hydroxy vitamin D to calcium trial or 125 dihydroxy vitamin D.

So if you're releasing a crap ton of one alpha hydroxylase, you'll activate a ton of vitamin D, you absorb a lot of calcium and phosphate in the gut, so it'd be hypercalcemia. So hypercalcemia can actually be a feature of of a sacroidosis. Now, what's like the classic feature you would see on histology in a patient that has longer hand cell histiosytosis? I really hope you're thinking about those, those are Burbek granulomas. Okay? Now, um, let's see. What if you get a question about, you know, like, I guess a lady, you know, that has like leaky breasts and she's being treated for schizophrenia? Um, I really hope with that, you're thinking about like, like, hypercalcememia, induced by an anti-psychotic, right? So remember that dopamine, right? Uh, one of its jobs is that it inhibits, um, pingo. Let me think about this for a second. Okay, so one of dopamine's jobs relates to, okay, let's put it this way, right? So one of the things prolactin does, right, is to promote like a milk lid down, right? So if you have hypercalcememia, you have more milk lid down, so you can have gallactory. So the president is taking an anti-psychotic, again, I apologize for all this, thinking I have to do like in the, in the while I'm giving these lectures, uh, many of these things again, I sort of discussed them from memory. That's why it's a rapid review in the first place. But basically, if a person is taking an anti-psychotic, remember those are dopamine receptor and antagonists?

I remember that another name for dopamine is prolactin inhibiting factor. So if you're taking a dopamine receptor and antagonist, uh, like an anti-psychotic, like calopere don't, for example, basically you're taking it with the effect of prolactin inhibiting factor. So prolactin will no longer be inhibited. You have a corruptona prolactin and prolactin, you then begin to like have gallactory and all that stuff, right? I remember that the connection, the pathway that connects dopamine and prolactin is known as the, uh, the tubero-informedibular pathway. Okay? Just one of those weird things you want to keep in mind for, for example. Okay. Now, um, what if you get a question about like an individual that is leaky, basically using the restroom aton and they're being treated for bipolar disorder, right? So I really hope with that, you'll think about like lithium and like the nephrogenic adabitus and syphidus. Remember that lithium, right? It sort of goes in. Uh, remember if you sort of go back to, uh, polish chemistry, I know this is probably like, uh, like, well, like six years away, ago for some of you, although I'm kind of obsessed with chemistry. But if you remember from chemistry, right? So remember like the periodic table, if you look at group one, we have like a lithium, right? Remember lithium has is like element three. So if, uh, it sort of has like one electron in its alpha-mole shell and then you drop down to sodium, sodium is like element 11, right?

Because it has like three like op orbitals or whatever that crap is called and it also has one electron in its alpha-mole shell. So they're kind of like similar in terms of chemical property. So that in the channel that you'll find that the principle cell of the collecting duct, uh, sodium can go in through those channels. Well, guess what can happen as well? Lithium can go in through those channels and if lithium goes in, it can sort of scrub the signal link cascade of, um, of, um, what is it called? It can scrub the signal link cascade of 88, right? So you scrub that signal link cascade. You no longer respond to the 88 you have, right? So you have a nephrogenica diabetes in syperus with that. So basically, um, you'll be, you will not have the ability to reabsorb water from your urine, right? And guess what? Uh, you'll be a ton, right? So those people will be hypernatremic. So they'll have a high serum or smallality, but you'll have a low urine or smallality contrast that with SIED, where you have a low serum or smallality and a high urine or smallality. I can see how they can try to like mess up your brain with that on the USML East. Okay. Now, um, uh, let's see, is there any other thing I want us to talk about? Um, so what's, I guess the gene mutation, right? So this would be a nice way to test the sun exams. What is the gene mutation?

That'll be associated with a patient having like, you know, like feel chrome, like this, let's see, it's a triad, feel chrome, cytoma, medallary thyroid cancer, and like, uh, primary hyperparthyroidism. I really hope you're thinking about ME&2 A or one of the ME&2 syndromes, right? Uh, more so ME&2 A, right? Remember, it's a red, uh, genum mutation. Okay. Now, what is the HLA associated with like, you know, like, the tell you that, oh, you do histology and you're looking at the, you see like a lot of like, germinal centers in the thyroid gland. Um, I really hope that gets you thinking about like HLA DR5 and Hashimoto's thyroiditis, right? Okay. Now, what is the HLA that's associated with like lymphocytic infiltrates in the eyelets of longer hands? Um, I really hope that gets you thinking about like HLA DR3 and DR4, right? So you're thinking about like, uh, uh, uh, type 1 diabetes, right? Remember, that's like an autoimmune destruction of your pancreatic eyelets. Okay. Now, what are the antibodies that are associated that, you know, you can sort of detect in a, you know, like a two-year-old with diabetes. Um, I really hope you're thinking about like antibodies against like GAT65. Um, that's like glutamate to decarboxylase. Um, remember, those are one of those high-yield antibodies you can observe in the setting of type 1 diabetes. Remember that glutamate decarboxylase, if I'm not mistaken, um, converts, um, command, divine thing. Yes, yes, yes.

glutamate decarboxylase converts, uh, glutamate to GABA. Okay. And remember that glutamate decarboxylase actually uses vitamin B6. I believe vitamin B6 is also known as a paradoxal phosphate. Use vitamin B6 as a cofactor. So if you have, um, I don't know if you're being treated for TB, right? Uh, you don't take the doctors advice. And when you ask for the doctor, I'll just take my INH for nine months, no issue, right? So you take your eyes on it, you don't take B6, you deploy your B6 pool, you deploy your B6 pool, there's no cofactor for glutamate decarboxylase. So guess what? That fancy reaction where glutamate is converted to GABA doesn't work so well anymore. If it doesn't work so well, guess what will happen? The levels of glutamate will go up and glutamate is an excitatory hormone. GABA is an in, sorry, glutamate is an excitatory neurotransmitter. GABA is an inhibitor neurotransmitter. So if your levels of GABA going down, when your levels of glutamate are going up, guess what happens? Seasures. Okay. So that's the potential pathophysiology behind people getting seizures whenever they basically have a vitamin B6 deficiency. And remember that a classic cause of that on the USML is an INH toxicity. In fact, a very nice way they can actually test INH toxicity on your exam is to describe a patient that's being treated for TB and the patient also has like concomitant depression. You probably want to avoid a bupropium in those patients.

Remember that bupropium actually has the ability to lower your seizure threshold. So basically anything that predisposes you to seizures, so the kind of is a relative contraindication to the administration of a bupropium. I remember bupropium is an NDRI. It's an Norepinephrine, a dopamine or a reoptic inhibitor. So if a patient has anorexia nervosa, for example, remember those people tend to get like these weird electrolyte anomalies that can increase the risk for seizures. You don't give them bupropium. Another classic one is bulimia, right? Another very nice crafty one again. That really the USML is you want to think about it as just an exam where can you sort of see through the integrations of concepts in questions. If you can sort of see through those integrations, you'll be able to do pretty well on your test. So again, that's a very nice way they can tie isoniazide and bupropium together. And then one thing you also don't want to forget is that remember that isoniazide can also cause a cyderoblastic anemia, right? So you say like, hmm, divine, how's that happen? Right? So remember again, this vitamin B6 sterve been talking about. If you think about the first step in the synthesis of hym, remember that you combine glycine and my belief succino-coe, under the action of this enzyme known as amino-levelinic acid synthase to make delta-milo-levelinic acid, right?

So basically if you have a B6 deficiency because you're not listening to your doctor and you're taking your isoniazide and not taking B6 as a supplement, you'll deplete B6. If you deplete B6, guess what doesn't happen? Your alas, doesn't work. Doesn't work so well. It doesn't work so well. The first step of hym synthesis won't work. If the first step of hym synthesis doesn't work, then you will not be able to make hym. If you don't make hym, basically if you screw up your hym synthesis pathway, you're essentially getting a cyderoblastica anemia as a kind of like a side benefit. Okay, so enough with isoniazide and also don't forget it can cause a drug-induced lupus, right? Remember the association with the anti-histona antibodies? Okay, so I guess let's sort of jump back on an antibody story, right? So what are the antibodies that will be detected in a patient that has exopthalmos? I really hope that gets you thinking of what Graves disease, right? And remember the association with anti-theroperoxidysa antibodies? Although remember that patients with Graves also have like the antibodies, like stimulated antibodies against like the TSH receptor, okay? Now, let's see, what if a patient has like decreased the deep tendon reflexes and they recently got like an iodine load? What effect are you thinking about? I really hope you're thinking about the wolf chikof effect, right? So basically these people have like hypothyroidism in the setting of an iodine load.

Remember like the analogous concept will be the the iod-based alpha phenomenon where a person has like hyperthyroidoxicosis symptoms because they recently got an an iodine load. Okay, and then what kind of tests would you want to use? You know, sort of to sort out why a patient may have like massive polyurean polydipsia? I really hope you're thinking about like the water deprivation test, right? Remember that is a test for what is this thing called? That's a test for diabetes and sypidus, right? Diabetes in sypidus, right? Because remember in diabetes in sypidus, you're not making basically your kidneys have an ADHD problem. And if you have an ADHD problem, you will not reabsorb water, right? So you'll be hypernatremic and then, um, so your serum will have like, you have like high serimosmolality, but you have like low urinose molality, right? So you're like, that's not normal. Maybe this person has diabetes in sypidus. So the first step thing you do is the water deprivation test. And literally what you do, deprive the patient of water. And the thing is, if you deprive a patient of water, the way the body will respond is, hmm, I'm being deprive the water. So your body will try to make a ton of ADHD in response. If your body makes a ton of ADHD, so this is the normal response I'm describing. Your body makes a ton of ADHD. You will basically start reabsorb in a crap ton of water from your urine. Okay? And by doing that, your urine will become hyperosmolar, right?

As a response to that order deprivation test. But if for example, your body does not respond to a purview, you're like, hmm, after you prepped this person of water for a few hours and your urine of molality is still like relatively low. And the serum of molality is relatively high. If you see that, then you're like, okay, I think I've sort of kind of like decided that this person has diabetes incibidus. So your next step was then to determine, is this a central diabetes incibidus where you're not making ADHD or is this an effiging diabetes incibidus where you're making a ton of ADHD, but you're actually going to respond it, right? So the way you figure that out is you do allow to decimal pressing. If you give decimal pressing, remember that decimal pressing is an ADHD on a log. So if giving decimal pressing fixes the issue, boom, that tells you that, okay, it's an ADHD deficiency that was causing this problem, right? So guess what? That tells you you have a central diabetes incibidus. But if the administration of decimal pressing does not fix the problem, then that tells you that you're dealing with an effigyneca diabetes incipidus, right? And remember the classic drug causes like letheum and also don't forget your tetracycline, a demeclocycline, right? Demeclocycline is also associated with a nephigyneca diabetes incipidus. In fact, remember that that nephigyneca diabetes incipidus with a demeclocycline is actually used as a treatment for SIEDH.

You will basically be using the side effects of a drug to treat another pathology, okay? Yeah, so let's leave it at that and keep going. Now, what if a patient, you know, is has a history of hypothyroidism and they are presenting with opportunistic infections. So what are you thinking about, right? So sorry, so let's assume a patient with a history of let's put this way, hypothyroidism is presenting with opportunistic infections. What are you thinking about with that? I supremely hope you're thinking about so hypothyroid patient being treated with like p2yomethymazole, those anti-fyroid medications. Remember, those are associated with like egg granulose, like tussis, right? So they can, if you're if you're if you're white cells are not there, right? Compredate yourself against infection, right? So you can get into trouble with that. Remember, they can also make that into a cyclosyping, right? So those are always the contests, those are fancy, fancy concepts. They can actually also make it into a neuro-question with carbamazepine, right? Because remember, carbamazepine is that thing we used to treat a tigdolary, it's like trigeminal neuralgia. Those those are like the four high-yodrocks that can cause a egg granulose, itose, p2u, methymazole, carbamazepine, and also when I just mentioned, closyping, and also don't forget, right? Closyping is one of those drugs in psych that has been associated with a decreased risk for suicide.

The only other drug inside that holds that clint to fame is a is a lefium. Okay, now what if you have a patient that you know, so the has like tetany after you know like recent surgery where the you know kind of remove the cancer that's associated with someoma bodies. If you see that what are you thinking about? I really really really hope you're thinking about you know like inadvertent removal of the parathyroid glands, right? So what's the cancer I'm referring to with someoma bodies? I hope you're thinking about like popularly thyroid cancer, right? So, popularly thyroid cancer is as just someoma bodies, right? So remember that if you're removing the thyroid gland, you can inadvertently also devascularize the parathyroid, and you can get into trouble with that, right? So, and then you basically lose your source of PTH, and then you can get hypocalcemia and get like seizures, and the other signs of hypocalcemia like a prolonged cutie interval, they can get like tetany and all that all that crap that shows up on test. And remember your cancers with someoma bodies, right? This is something you definitely need to know for exams, right? Don't forget your popularly thyroid cancer, don't forget your main engeoma, right? And don't forget your, your, come on divine think.

Don't forget your, so popularly thyroid cancer, meningoma, misotheloma, this one, this last one I guess the number four one, I'm not super sure because this was years ago I reviewed this, but you probably also want to think about like a serious cystadneucarcinoma. I believe those are also associated with someoma bodies, I'll have to look that up, I can, I guess I can confirm it in my in a future podcast. Okay, now what if you get a question about a patient that is hypertensive after consuming a licorice, right? So hypertensive after consuming licorice, I really hope you're thinking about like, you know, like this is called like the syndrome of apparent mineral recordicoid excess, right? So remember that licorice contains the stenosis like glyceretic acid, and that has the ability to inhibit like this enzyme known as 11 beta HSD2, I think 11 beta HSD2 stands for like 11 beta hydroxy steroid, hydrogen yeast too. Remember that that enzyme converts cortisol to cortisol. So remember that normally the natural, I guess the preferred agonist that may or quadicoid receptors outdoastro, but the thing is it so happens that cortisol also has like you know decent ish agonist activity, amino or quadicoid receptors. So your body is like, you know what, I don't feel like being hypertensive all the time. So let's make this enzyme that converts that cortisol to cortisol. Cortisol has the agonist activity at mineral recordicoid receptors. Cortisol does not have that activity.

So the thing is if you consume licorice like a Krypton aliequerish for whatever like bizarre weird reason, consumer Krypton aliequerish, you'll inhibit 11 beta hydroxy steroid, hydrogen yeast too. When you inhibit that enzyme, you do not convert cortisol to cortisol, cortisol builds up. You have that agonist activity, mineral recordicoid receptors and boom, you get hypertensive. So in fact, if you want to sort of stretch that concept a little further, those people will be hypertensive because remember that whenever a austroid increases your absorption of sodium at the inech channel of the collecting duct, so water will come in alongside, so it becomes hypertensive. And then in addition to that, remember that you will also get like a metabolic alkalosis. They will get a metabolic alkalosis because remember if you're taking a look at the alpha intercalytic cells of the distal nephron of the collecting duct, remember that those cells have a proton ATP pump on the urine side that actively pumps out protons and that proton pump is activated by austerem. So if you have a deficiency, if you have a ton of and that outdochstern, right, it accomplishes its due diligence by activating mineral recordicoid receptors. So guess what happens? When you have a crap ton of cortisol, right, from this syndrome of operating mineral recordicoid excess, you will activate that proton pump and you basically peel out a ton of protons and you recover metabolic alkalosis as a side benefit there.

You will also get hypochemic, right, because remember that if that inech channel at the principal cell of the collecting duct is working super well, then you you create like a negative on the urine side and that will draw potassium, right? So you get hypochylemia as a side benefit there. So you get like a hypochylemia metabolic alkalosis with hypertension. If you have a syndrome of a apparent mineral recordicoid excess. Okay, and remember that people that have like acromegaly or like a growth hormone, like a growth hormone secretion or tumor, right, those people tend to get cardiac issues, right, because they have like growth of your heart and their visceral organs and all that crap. Okay, and I guess what's the most common location for an ethypica, like I guess let's say like ethypica thyroid tissue, right? So that's something called like lingua thyroid. So usually around the tongue, that's like the most common location for like ethypica thyroid tissue. Okay, now what if you get a patient, right, that has you know like failed to lactate and she recently just gave birth, right? So basically like signs of like hypochyturism and there is setting of like recent delivery. You really want to think about like she has syndrome, right? So remember that, you know, you get like super hormonal whenever you get pregnant, right? So guess what happens? Your pituitary gland, it like doubles in size when you get pregnant.

So that means it probably needs a little more blood flow than normal, right? So if for example you have something bad that happens and you become like hypo-tensive. So there's like low flow to the pituitary gland. Well, the bad thing that may happen is you can infarct your pituitary and then basically get like signs of hypochyturism, right? So basically if you have like, let's say you have like, you know, delivery that doesn't go as planned and you lose like a crap ton of blood, you can basically like have like a like ischemia of your pituitary gland and you can get like she has a syndrome. And I guess what's the kind of diabetes that has the strongest genetic concordance? I hope you're thinking about like type 2 diabetes, right? What if you see like, they tell you that oh, you're performing histology and you see like apple green by refringence in the pancreatic eyelets of longer hands? I really hope you're thinking about like type 2 diabetes. Remember that type 2 diabetes is the kind of diabetes that's showed like amyloid deposition in the thyroid gland, I mean sorry in the pancreatic eyelets. So don't forget your apple green by refringence on a congorida steamy. Okay. And I guess what's the part of the brain that if you lesion it, you can sort of like scrub your steep cycles. That's more like the superchancemeric nucleus, right? That's kind of easy. Let's see.

Now what if a patient has like very high levels of PTH and they also have like very high level like BUN and very high creatinine? I really hope you're thinking about like secondary hyperparathy or disease, right? So remember that if your kidneys don't work, if your kidneys don't work, guess what guess what happens, right? Your one alpha hydroxylase is like bye bye. If your one alpha hydroxylase is bye bye, then you will not be able to convert a calcium dial to calcium trial and if you're not making vitamin D, so basically active vitamin D, you will not have the ability to reabsorb calcium and phosphate in the gut, so you become hypocalcemic. If you're hypocalcemic, your levels of PTH will go up, right? So your phosphate trashing hormone will go up. If your PTH goes up, you will think that, maybe you know what, my PTH is up, I'll probably appropriately trash the phosphate. That's not what's actually going to happen, right? Because if you think about it, if you have like chronic kidney disease, your kidneys like the primary excretor of phosphate, so if your kidneys are all screwed up, even if your levels of PTH are high in secondary hyperparathy or disease, from chronic kidney disease, your phosphate will actually be high as well. It will not be appropriately trashed because your kidneys don't work.

And while I guess we're on this topic right, I guess it will be a nice segue to helping you differentiate between secondary hyperparathy or disease that arises from liver disease versus secondary hyperparathy or disease that arises from kidney disease, right? Because think about it, that 25 hydroxy vitamin D that I talked about that is acted on by one alpha hydroxylis. Do you know where it comes from? It comes from the liver. So if your liver is not working, you would not make calcium diol and if you're not making calcium diol, you have no feedstock for calcium trial. So if you're not making calcium trial, you will not reabsorb calcium and phosphate in the gut, you'll be hypocalcemic and your PTH will go up. If your PTH goes up, you will not properly trash phosphate because the problem is not that you'll liver, it's that you're kidney. Okay, versus chronic kidney disease where your kidneys don't work, so you cannot convert calcium diol to calcium trial. So you have low calcium trial, so you are not reabsorbing calcium and phosphate in the gut. So if you're not doing that, you'll become hypocalcemic, so your PTH goes up in response, but your PTH cannot appropriately trash the phosphate because your kidneys don't work. Okay, because remember, if you want to appropriately get rid of phosphate, your kidneys got to work. If not, you're not getting rid of that phosphate in any way shape or form.

So basically the levels of phosphate help you differentiate between secondary hyperprout thyroidism from chronic kidney disease versus secondary hyperprout thyroidism from cirrhosis, for example. Okay, now remember hypocalcemia, the classic physical exam findings, so like the chrousosine, where you tap the cheek and the jostec sign, sorry, the jostec sign is where you tap the cheek and wait, jostec and chrousosososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososos ososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososososos The insulin can buy a drugstore that doesn't contain CPAP type. The insulin can buy a drugstore that doesn't contain CPAP type. The insulin can buy a drugstore that doesn't contain CPAP type.

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Hypercalcemia, symptoms of hypercalcemia, and symptom relief upon glucose administration.

MEN1 syndrome.

Parathyroid adenoma (though hyperplasia can also be a common cause).

Antibodies against GAD65 (Glutamate decarboxylase).

Noncaseating granulomas.

Alpha-blockade first (e.g., phenoxybenzamine), followed by beta-blockade.

Inadvertent removal or devascularization of the parathyroid glands, leading to low PTH.

Lesion to the lateral hypothalamus ("hunger center").

To convert 25-hydroxyvitamin D (calcidiol) into 1,25-dihydroxyvitamin D (calcitriol), which is the active form.

Pituitary gland, parathyroid glands, and pancreas.

In nephrogenic DI, the urine osmolality remains inappropriately low despite high serum osmolality (failure to concentrate).

Bupropion (NDRI), because it lowers the seizure threshold.

Rosenthal fibers (pink, eosinophilic hyaline material).

In CKD, phosphate levels will be high because the kidneys fail to excrete phosphate effectively, regardless of PTH levels.

Lesion to the lateral hypothalamus ("hunger center").

To convert 25-hydroxyvitamin D (calcidiol) into 1,25-dihydroxyvitamin D (calcitriol), which is the active form.

Pituitary gland, parathyroid glands, and pancreas.

In nephrogenic DI, the urine osmolality remains inappropriately low despite high serum osmolality (failure to concentrate).

Bupropion (NDRI), because it lowers the seizure threshold.

Rosenthal fibers (pink, eosinophilic hyaline material).

In CKD, phosphate levels will be high because the kidneys fail to excrete phosphate effectively, regardless of PTH levels.