DIP Episode 514 - A Framework For Understanding Endocrine Testing (for Step 1-3)

Welcome, my name is Devine. This is going to be a quick podcast, but it's something that I think is going to be very helpful for people that are studying for step one to step three. And in this podcast, this is episode 514. We're going to be talking about the framework for endocrine testing. The framework for endocrine testing. This is just something I would truly generally in my heart want you all to get downpour. If you understand this, it will just make so many things in endocrinology make a lot of sense to you. Instead of you just blending and rising things. So there are two major rules I want to go over here. And I'll try to give some examples to really buttress these points. Now, we know that whenever we're dealing with an endocrine disorder, there's usually one of two problems we face. Either you have excess of a hormone or you have a deficiency of a hormone. I'm going to say that again, you either have excess of a hormone or you have a deficiency of a hormone. So the thing is typically in endocrinology, endocrinology is one of these disciplines that follows very set principles. Typically in endocrinology, when you want to diagnose something, you'll usually start with some kind of screening test. And then if that screening test is positive, you will then proceed to a diagnostic test, a confirmatory test. So the rule here, the two rules here is a number one. Whenever you're dealing with an endocrine disorder, that involves a deficiency.

Whenever you're dealing with an endocrine disorder, that involves a deficiency. Your confirmatory test, your diagnostic test, usually is going to be some kind of stimulation test that's rule number one. Rule number two is that if you're dealing with an endocrine disorder, that involves some kind of excess of a hormone, your confirmatory test is going to be a suppression test. And again, this makes sense. If you have a deficiency of something, you want to figure out why am I deficient in this thing. So you will try to force that gland to secret that thing. That's a stimulation test. If you have excess of something, you want to try to see what's going on here. You will try to force that gland to stop secreting excess amounts of that thing. So for example, let's try our rule number one. Rule number one, we said, ooh, you have a deficiency of something. Well, one way you can test to see what's going on. Your confirmatory test, your diagnostic test can be a stimulation test. For example, think of a question about a person that has a history of Hashimoto's. Because usually when they test an autoimmune disease, they love to give you a pass medical history of another autoimmune disease. And the tell you in the queue, stem that this person has skin hyperpigmentation. And this person is hypotensive. And this person is hypoglycemic. And this person, you know, the hostility this person has not been feeling well for a while.

Well, if you see something like this, I would really hope you're saying, ooh, divine. It sounds like this person has adicence disease. Remember, adicence disease is a primary adrenaline sufficiency where you pretty much make autoantibodies and destroy your adrenal cortex. Remember, the adrenaline dollar is generally not damaged in adicence disease. But in adicence disease, the major thing we care about is the cortisol being low. So again, we have reduced secretion of something. So how can we confirm that diagnosis? Well, we'll confirm that diagnosis by doing a stimulation test. That stimulation test is called a co-synchropin stimulation test. Co-synchropin is an ACTH analog. A normal person like me and you, if I give you, well, a normal person, I guess, if you get co-synchropin, the thing that is supposed to happen is that your cortisol is supposed to rise because it's an ACTH analog. But if a person's cortisol fails to rise, even with the administration of co-synchropin, then that's the agnostic, that's the confirmatory of primary adrenal insufficiency. Simple as that. Now, another situation where you may see this stimulation, some of you may be wondering, I guess, that divine. Why did this person have skin hyperpigmentation? Well, if you think about it, if you're not making cortisol, there's no negative feedback in the brain. So your ACTH is going to rise. But ACTH is not made in isolation. It's made together with MSH, melanocytes, stimuli, tin hormone.

And from a compound called pom-c, pro-upio melanocortin. So that's going to cause you, since you have high levels of MSH, that's going to cause skin hyperpigmentation. Now, what if they give you a question about a person that has precocious puberty or delayed puberty? Well, one of the ways that we figure out what may be going on with this person is to do something called a GNRH stimulation test. Many times for this test, they'll give something called luper light. Luper light is a GNRH analog. Again, if you notice that's why I'm giving this person luper light and they're going to drop in's rise. They're FSH rises, they're LH rises and things like that. Then that tells you that they have an intact HPG axis. That tells you that, hmm, maybe this person has the HPG axis activated a little too early in life. That's why they have precocious puberty, for example. But if you notice that you give luper light in doing the GNRH stimulation test, and the person's FSH or LH does not rise, or you notice that, so let me give you two sets of results. So what if the FSH and the LH does not rise? So you notice at the end of the test, let's say you're doing this in a woman. FSH does not increase, LH does not increase, her estrogen does not increase. After doing the test, then that tells you that, ooh, there must be some kind of pituitary failure that's causing the problem.

There must be some kind of anterior pituitary failure that's causing the problem, because FSH and LH are released from the anterior pituitary. Obviously, if you're not releasing your gonadotropins, then your gonad, your gonad, your ovaries will not be making estrogen from the granulosa cells. But what if you give luper light? And you notice that the FSH and the LH increase, but the estrogen does not increase. Then that tells you that the person likely has some kind of primary gonadotropilier. Like for example, in Turner syndrome, the gonad pretty much does not work. You have strict ovaries. So even if, okay, your anterior pituitary is responding normally. You're making FSH, you're making LH, but the gonad itself cannot respond to those increased amounts of FSH and LH. So in that case, that person will probably have some sort of delayed puberty, some sort of delayed puberty. So again, that's important to understand. I think I've given enough examples there. Now, if you have excess of a hormone, again, that's rule number two. Your diagnostic test, your confirmatory test, is going to involve some kind of suppression. If you're making too much of something, it would make sense to try to see, can I shut this thing down? Like for example, they give you a question about a person that has tried multiple anti-hypertensives. And this person's blood pressure is not being well controlled. And they have metabolic alkalosis. They have hypochylenia.

That's probably a question about con syndrome, or primary hyper-adjusteuronism. So how do we handle this? How do we confirm? How do we diagnose this? Well, there's this thing called the salt suppression test, the salt suppression test, or some people call it a silly infusion test. But basically, you give a person a salt load, and you try to see those the out-dosterone suppress. Because normally, if I give you a ton of salt, or I give you a ton of fluid, like normal saline, your blood volume is going to rise. If your blood volume rises, well, your blood pressure is going to rise as well. So if I give you those things, the blood volume rises, your blood pressure rises. Your body is going to be like, wow, my blood pressure is a little too high. So let me go ahead and turn down the reading and utensil in our dose-turing system. So your dose-turing is supposed to suppress. But if you notice that, man, a person, I give them salt, like normal saline, like a salt load, and their dose-turing feels to suppress. That's confirmatory of consangular. That's confirmatory of primary hyper-adjusteuronism. Or what if they give you a question about a person that is having increased spacing between his teeth? And he's, they tell you that he has generalized visceromagaly. His hearts don't fit very well anymore. His face looks very different across pictures for me, years past. And that tells you, the person probably has some kind of acromegaly.

So growth hormone excess, again, making too much growth hormone. So again, how do you confirm? Because yes, you're going to measure the IGF1 levels to start. But how do you confirm the diagnosis of acromegaly? Well, you're going to do an Oro glucose suppression test. Sometimes they call it an Oro glucose tolerance test. But basically, in a normal individual, when you get a glucose load, because remember, one of the jobs of growth hormone is that it raises your blood glucose levels. It's a diabetes genic hormone. So once the way a normal person works is growth hormone will raise their blood glucose levels. And then as those blood glucose levels rise, that will then suppress the growth hormone production. So in a normal person, the administration of glucose, a glucose load, shoots or presses your growth hormone production. But in a person that has acromegaly, that's an adult, or gigantism that's in a child, basically, their growth hormone will feel to suppress. Their growth hormone will feel to suppress with the administration of a glucose load. That's confirmatory. That's the agnostic of gigantism or acromegaly. Now, the final one I'll talk about, right? If you're thinking about a person that has pushing syndrome. Remember, pushing syndrome, one of the ways we, that's a cortisol excess. One of the ways we can confirm or diagnose your pushing syndrome, is to do these dexamethasone suppression tests. Like, for example, the high-dose dexamethasone suppression test.

If you give a person high-dose dexamethasone, measure their cortisol the next day, and you notice that while this person's cortisol has suppressed, that tells you they have cushing's disease, tells you that they have a pituitary adenoma that's making a ton of ACTH. In fact, I will mention a caveat here. This is probably the only situation in, for USML purposes, where a suppression test could be a screening test. And that's the load-dose dexamethasone suppression test. That's one of the ways we screen for cushing syndrome. Remember, if you want to screen for cushing syndrome, you can check a person's 24-hour urinary cortisol. We can check the alictmite saliva recorder, or you can do a load-dose dexamethasone suppression test. In cushing syndrome, if you give that load-dose dexamethasone, you'll notice that the next morning the cortisol did not suppress. That pretty much applies to every case of cushing syndrome. I'm going to say that again. Failure of cortisol to suppress with the administration of load-dose dexamethasone is a good screener for pretty much every cause of cushing syndrome. But the high-dose dexamethasone suppression test is going to be a confirmatory test. It's going to be a diagnostic test where you try to tease out the major causes of actheptic cushing syndrome. I've made podcasts on this stuff that you can easily check out. If your cortisol suppresses, that tells you that, okay, this person has cushing disease.

They have a pediatric adenoma that's a critical tone of actheptic. But if the cortisol does not suppress, obviously, you're going to be getting that chest CT to look for the small cell lung cancer. So again, I think hopefully you'll finally get this point. This is one of those things that I wish that more instructors will go over as like a basic concept before you won't start learning endocrinology. When you have this foundation in mind, it's going to make things a lot easier when you're learning a lot of these pathways. But again, to summarize, if you have an endocrine disorder where you have a deficiency of a hormone, the confirmatory test, the diagnostic test, is going to be a stimulatory test. You're trying to see if you can stimulate production, stimulate production of that hormone. We give the example of the co-synchropin stimulation test and for other sense disease, primary adrenaline and sufficiency. And the GNR stimulation test would looper light for precocious or delayed puberty. And then the rule number two was that if you have excess of a hormone, then the way you're going to confirm, the way you're going to diagnose that disease, is by trying to do some kind of suppression test. We talked about the salt suppression test or the silly infusion test for con syndrome. We talked about the oral glucose tolerance or suppression test that we use for giganticymarchrometalline. And then we talked about the Dixamethasone suppression test that we use for cushing syndrome.

So thank you for listening to me today. I have review courses for all the USMEL exams. The one that's coming up pretty soon is from March 1st, I have a step one review. So people taking step one or complex one is a 25 hour class or people that are taking step two or step three or complex two or three bad foundations. I also offer courses for step two, step three, have a test taking course, a bio stats class, a social sciences ethics and QI class. I've made a podcast on those you can listen to that. If you're interested, shoot me an email, the over Zoom. It can give you some more information through the website. The courses are not lectures. They're pretty much all scenario-based because that's more realistic to your exams. Also, for one or one tutoring for all the USME Ls and pre-clinical exams, 30-ish-shelf exams, I help with mock interviews and era's applications. And I have this podcast on Apple Google and Spotify. And I have another website called divininterventionalifelessons.com. Wherever we can post two podcasts and from a political perspective, I try to address a life lesson. There's actually an Apple podcast associated with that, divininterventional life lessons podcast. Okay, and also of a You Tube channel, as I've said, where I post the videos that I make for this website. So thank you for listening to me today. I'll see you next time. Have a wonderful rest of your day. God bless you. Bye for now. Thank you.

Use a stimulation test, attempting to force the gland to secrete the hormone.

Use a suppression test, attempting to shut down or suppress the excessive hormone production.

Cosyntropin stimulation test (ACTH analog). Failure of cortisol to rise confirms deficiency.

MSH (Melanocyte Stimulating Hormone), which is co-secreted with ACTH.

Salt suppression test or saline infusion test. Failure of aldosterone to suppress confirms excess.

Acromegaly/Gigantism.

Stimulation test (e.g., Cosyntropin for cortisol).

Suppression test (e.g., Dexamethasone or Glucose load).

To see if the adrenal cortex can mount an adequate cortisol response, confirming primary failure if it fails to rise.

Failure of aldosterone to suppress despite increased blood volume/salt load.

If FSH/LH rise but estrogen doesn't, it suggests primary gonadal failure (e.g., Turner syndrome). If FSH/LH don't rise, it suggests pituitary failure.

It helps differentiate between pituitary ACTH excess (suppression expected) and adrenal/ectopic ACTH excess (suppression often fails).

Stimulation test (e.g., Cosyntropin for cortisol).

Suppression test (e.g., Dexamethasone or Glucose load).

To see if the adrenal cortex can mount an adequate cortisol response, confirming primary failure if it fails to rise.

Failure of aldosterone to suppress despite increased blood volume/salt load.

If FSH/LH rise but estrogen doesn't, it suggests primary gonadal failure (e.g., Turner syndrome). If FSH/LH don't rise, it suggests pituitary failure.

It helps differentiate between pituitary ACTH excess (suppression expected) and adrenal/ectopic ACTH excess (suppression often fails).