DIP Episode 278 - The NBME and Amenorrhea (For Step 1-3)

Okay, welcome. My name is Divine. This is episode 278 of the Divine Intervention podcasts. And in this podcast I'm going to be talking about a super high-yield topic for all the USML exams actually. Like this is just one of these things. I got pretty much guaranteed you're gonna get a few questions on this on your test regardless of what you do. This is the podcast on Eminaria. Okay? Eminaria. Eminaria. So what is Eminaria? So Eminaria basically means you're not having your period anymore, right? You're not having your period anymore. And then you know, obviously if you're already age of 40, you know, you're beginning to think of things like Perimenopause or Menopause or I don't know, maybe as a woman you're trying to play a prank on your husband that, oh, it's my period just to, you know, freak him out a bit, whatever. I'm just kidding there. Or you're pregnant. Remember the most common cause of secondary menoria. And I'll talk about what primary menoria is or is a secondary menoria. So let's stop joking and let's get right to it. So Eminaria again, it means no period, right? So what are some big things about Eminaria? Well, you can divide Eminaria into being primary menoria or secondary menoria, right? So what primary menoria? Primary menorias means you've never had mences, right? You've literally never had mences. The only thing though with primary menorias, you need to know some age definitions.

So for example, if you have secondary sexual characteristics and you have no mences, we can wait till the age of 16 before we can diagnose your primary menoria. But if you have no secondary sexual characteristics, then unfortunately, you need to, we need to be a little more aggressive. So that's the age of 14, right? So that's primary menoria. Now, so again, to recap, primary menoria, you don't have secondary sexual characteristics and you've no had mences, we diagnose you at 14. You have secondary sexual characteristics will give you a little more leeway. You go to the age of 16. And then what is secondary menoria? Secondary menoria is basically a person that has had periods before. But for whatever reason, the periods stop, right? So in the case of a woman that used to have regular periods before, if she has no periods for like three months, that's going to be secondary menoria. But if we have a woman that has had irregular periods all along, so let's say like a PCOS patient, and then she has no periods for like six months, then we absolutely begin to worry about secondary menoria. So again, pay attention to timeframes. Secondary menoria means, oh, used to have periods before, but now normal periods. If your periods were irregular before, then we say, if you missed three cycles, that's kind of worrisome, right? If your periods were irregular before like a PCOS patient, and then you miss six cycles, then it's like, okay, this is really worrisome, right?

And six cycles is usually like six months, three cycles is usually like three months roughly, right? So what are some things that can cause immemorial? So there's a bunch, right? And the thing I will try to do here today is to try to give you mechanisms so that you are no memorizing these things, because to be honest with you, these are really not things you should memorize. These are things you really should try to understand. So let's talk about some causes of primary menoria, right? So what if they give you a question about a four-foot tall female, and she's never had main seats, right? Again, the fact that she's four-foot tall should tell you something, right? This person has Turner syndrome. Remember, Turner syndrome, those people genetically there are 46 X-Call, right? So these people, they have no bar body if you were to look at their cells on their electron microscopy, especially the nucleus. So internal syndrome, they have streak ovaries, right? And again, these kids, they will have like relatively normal genitalia, right? But again, they will have like really big time, the live puberty, right? Really big time, the live puberty. So essentially, because these people have streak ovaries, they're not making estrogen, right? So if you're not making estrogen, then guess what? What's going to happen to your FSH and LH? Well, your FSH, LH and GNI are going to be increased, right?

And in fact, Turner syndrome is one of those things that causes what we know as hyper-gonadotropic hypogonadism, right? So your FSH LH is elevated, but your estrogen is low, right? So they are hyper-gonadotropic, they are gonadotropins are high, but they are hyper-gonadot, right? The estrogen is low. Another thing that can cause primary menoria can also be a person that, let's say they give you a question about like 19 year old female, they tell you that she has never had her men's ears and they tell you that she has like, Turner's stage four breasts. So you know, she has pretty pretty legit breasts, but then they tell you that, oh, she has no accellerial pubic hair and then they tell you that, oh, that her vagina ends in a blind pouch and you can't see any uterus on a transvaginal ultrasound. When you're very see stuff like that, right? You want to think about testicular feminization syndrome, right? Remember, sometimes this is what's known as EIS, angrogenian sensitivity syndrome. So what's the pathophysiology there? Well, the pathophys is essentially the testosterone receptor doesn't work. It's actually like an ex-linked, ex-linked defect. So essentially the angrogen receptor doesn't work. So even if testosterone binds to it, you're not going to be able to respond to that testosterone, right? And the thing is testosterone controls your pubic anaccelerial hair.

If you have bad, like, underdeveloped pubic anaccelerial hair on an MBM exam, then you definitely, definitely should be thinking about AIS, right? So you may see, okay, why do they have like no uterus, no ovaries, no upper vagina? Well, that's pretty easy, right? So remember those test, because these guys, these people are males, they have 46x1. So they have testicles, right? So those testicles contain sertouli cells. Those are totally cells. The make anti-malignant hormone. Remember, sometimes it's called malirion inhibiting factor, or sometimes it's called malirion inhibiting hormone. So those things prevent the formation of the malirion dot. So everything that's a derivative of the malirion dot does not form. So the fallopian tubes one form, the uterus one form, and the upper vagina one form. Remember, the ovary is not derived from the malirion dot. That's extremely high, you know, the ovary is not derived from the malirion dot, okay? So that's how you diagnose AIS, right? And again, people that have AIS, essentially they're going to have low levels of FSC and LH, right? They're going to have low levels of FSC and LH, because that testosterone, that's not able to act on its receptor, right? Again, they're not really going to have, like that excess testosterone they have that doesn't act on the angiogen receptor in the periphery. Well, it's going to, in a sense, so actually, so let me, let me come back a bit here. So the angiogen receptor doesn't work, right?

I remember the angiogen receptors in the periphery, but they also angiogen receptors in the brain, right? Like for example, we know for sure that, what is it called? Testosterone can have some brain-like effects, right? So the angiogen receptors in the brain actually still don't work. But remember, these people, they have this enzyme known as aromatase, right? They have normal aromatase activity. So aromatase can convert that, those androgens that testosterone to estrogen. And then that estrogen can exert negative feedback at the level of the anterior pituitary. So these people are going to have low FSC and LH. These are really high autonone. People that have androgens in sensitivity syndrome are going to have low FSC and low LH, okay? Low FSC and low LH. And again, because again, they have this aromatase business taking testosterone to estrogen. That's why they're able to have great breasts, right? They're able to have great breasts as a result of that. And then what if they give you a question about a person, you know, they tell you that this woman is a female. She has never had mency. She's 19 years old. And then they tell you in the question that she has, you know, she has normal breasts. So like tonar five breasts. She has great pubic and axillary hair, tonar five. So just what you notice that she has never had a mency's and they tell you that all the vagina ends in a blunt, blind pouch and you do a transvaginal ultrasound, you see all your uterus, right?

So right off the bat, if you see that she has good pubic and axillary hair, that should help you exclude 100-inching sensitivity syndrome, right? Because if you have 100-inching sensitivity syndrome, that's going to, you're not going to have good pubic, you'll have underdeveloped pubic and axillary hair, right? So the fact that she has good pubic and axillary hair tells you that the testosterone is working. And the fact that she has great breasts tells you that she has estrogen and rock, right? So she has ovaries. So whenever you see stuff like this where the person is pretty much normal, but they just don't have upper vaginas and uterus, they want to think about something called molyrian egenesis, right? You want to think about molyrian egenesis. So remember molyrian egenesis, sometimes on the example is called MRKH syndrome, right? So my orokitansky costarhousers syndrome, okay? My orokitansky costarhousers syndrome. And again, because these people have no more regulation of everything, the uterus is, I mean, their ovaries are fine, making testosterone normally, making estrogen normally. Remember, estrogen is made by the gramolosa cells and then testosterone is made by the thicker cells, that estrogen is going to regulates the FSH LH normally, right? So their FSH and LH will be normal, right? Again, the reason I'm emphasizing these values is your friends at the end of the year, they're pretty smart, right?

So they love to occasionally give these questions and then they can try to see if you can differentiate between two or three different pathologies by the FSH and LH levels. Again, that's what I'm trying to explain pathophys. Most of these things you don't have to memorize, they just make sense, right? Okay, what if they give you a question about a patient and they tell you that, oh, this patient has a history of, she has a history of like some pelvic malignancy, she has on the con-reducion therapy, like three, four years ago, and then since then she has been in the name and rick, right? If you see that, I really hope that you're thinking about like ovarian failure, right? Think about ovarian failure. Remember ovarian failure is something that can happen because the ovaries, whenever you have a cell that is rapidly dividing, it's not going to be very happy when you're subjected to radiation or chemo. I mean, think about it, when people have cancer, why do you think their hair kind of falls off a lot? Why do you think they have a lot of GI problems? Because those are rapidly dividing cells, right? So your ovaries, at least if you're a woman that has reproductive potential, those ovaries are rapidly, contain a lot of rapidly dividing cells, right? So the thing that's going to happen is if you subject the woman to like chemotherapy or radiation therapy, that can cause the ovaries to fail, right?

And again, if the ovaries fail, unfortunately you're not going to be making any estrogen anymore, if you're not making any estrogen, then your FSH and your LH will be, will be normal. I mean, sorry, it will be increased because there is no more negative feedback from that estrogen, okay? So again, just one of these things that are very high you to know for purposes of exams. And then, what if they give you a question about a 30-year-old female, they tell you that she has a history of like Hashimoto's thyroiditis, and then they tell you that over the past year, she has been trying to have a child with a husband, and she's not able to, and they tell you that her Hashimoto's is well controlled with liver thyroxyl. In fact, they will give you thyroid hormone labs and they'll be normal. And then they will see which of the following is the most likely etiology of the patient's presentation. And they will try to trick you into picking hypothyroidism as the cause, but notice all I've given you in this Q stem literally tells you that the thyroid hormone is, the thyroid gland is, I mean, the, she has good control, right? So if they're telling you something in an in-be-me question, stop arguing with the in-be-me, they're not trying to trick you, okay? Stop arguing with them. Again, the other ones that literally control your scores. Whatever they tell you, just take it down and say yes sir, or yes ma, and move right along, okay?

So essentially, when you see a person before the age of 40, and you notice that these people, they are beginning to have like no man's teeth, and they're having trouble conceiving, and then in the question they can even tell you that their FSH is elevated, and they have a history of like an autoimmune disease, then I really want you to think about premature variant failure, right? Remember many times people don't have premature variant failure, they get that because they have like some autoimmune attack of their ovaries, right? And remember many times on ambient exams as a general principle, when they want to give you a question that has an autoimmune disease as an answer, they will give you the person having a pass medical history of another autoimmune disease. So obviously, for a person who has premature variant failure, remember, again the diagnostic criteria, this is a person where they pretty much stop having the appearance before the age of 40, right? And you notice that their FSH is elevated, right? So if you see that, I want you to think about premature variant failure, right? Pre-mature variant failure, and again, because the ovaries are filled, no more estrogen, right? So your FSH and your LH are going to be elevated, okay? FSH LH are going to be elevated.

Okay, what if they give you a question about 19-year-old female, they tell you that she's a competitive Olympic athlete and she has been having trouble conceiving and she has not had appeared for the last seven months, right? What's your diagnosis there? Well, I would really hope you're thinking about athletic immunaria, right? You're thinking about athletic immunaria. So remember, whenever you, unless you have BMI is like 18, you know, super slender BMI, well, the problem is whenever you don't have adequate nutrition, your levels of hormone known as ghrelin go up, right? Your levels of ghrelin, GHR, ELI, and go up. And when your ghrelin goes up, that actually shuts down the production of G&RH, right? Ghrelin is a very powerful inhibitor of G&RH secretion. So guess what? If your ghrelin is high because you're grueling with hunger, right? Then you're going to shrunk down G&RH. If your G&RH is low, then your FSH and ELI true both belong, right? And then your estrogen will obviously be low. So if you notice in this case, this person's going to do tropines are low, but the estrogen is low as well, right? So this will be a very good, nice, handy-dandy example of hypogonadotropic, right? Hypogonadism, okay? Another thing, and again, obviously this person just needs to start eating, start eating, get to a healthy BMI and they have situational largely for the most part resolved, right?

And then also remember, if a person has, they can give you a question about a person that has like a bighteum prohemia, anopsia, and again, gain fertile, right? Again, in those circumstances, please think about hyper-prolactinemia, right? So they have like a prolactinoma that's compressing the optic chiasis, and that's causing that tonal vision. But in addition to that, prolactin is a very powerful inhibitor of G&RH. So if you give a G&RH, again, your FSHLH will be low, your estrogen will be low, and you'll be immunarick, okay? So that's another example. So prolactinoma causes a hypogonadotropic hypogonadism. Remember, those people have like Galactoria and Gagnacomastia, and you can treat them with dopamine agonist, like bromo cryptinocarbrogoline, right? And then what if a person needs to give you a question about a patient, you know, three-year-old female, for the past year, she's only going to have kids, and then they tell you that, you know, they give you like some labs, you notice providers, some heart rate is 56, and she has like decreased dependant reflexes, has like a non-pidine edema of the lower extremities. If you see that, you should want to think about hypothyroidism, right? Remember when you're hypothyroid, that's going to make your TRH high, right? I remember, another name for thyroid, tripping releasing harmonies, prolactin releasing factor. So if your prolactin is then increased as a result of that.

So literally hypothyroidism causes hyper-productin need, right? So your prolactin is high, your prolactin is high, that's going to kill your GNRH. If your GNRH gets killed, then you're going to be immunoric, right? So again, hypothyroidism can cause a hypogonatotropic hypogonatism. I mean, what if they give you another question about a patient that has chronic malabsorption and the infertile, and they tell you that, you know, this person has this person has recurrent infections, right? Like recurrent, respiratory infections, that's obviously going to be cystic fibrosis, right? And cystic fibrosis, again, basically the guy on the gal that has cystic fibrosis will be infertile, right? For the guy's case, his vast difference is not there, right? You have a genesis of the vast difference, that's going to cause problems. For the lady in that case, she has like, remember people that have see of the very thick secretions, right? So have vaginal secretions will be like super, super thick. So because the vaginal secretions are literally super, super thick, she's not going to be able to let sperm in, right? So she's going to be infertile in those circumstances. So you may be like, define, why does this person have malabsorption? We'll think about it. If a person has CF, the apalchretic dot is all gunked up with like just nasty guppies, like very thick secretions, right? So they're not going to be able to put lipids in the in the GI tract.

So they're not going to be able to bring down fat. So they're going to have a lot of fat malabsorption, right? Now, what if they literally give you an identical presentation to what I said, right? Infertility, fat malabsorption, but you don't see all the stuff with recurrent or respiratory infections. And they tell you that, oh, the present symptoms resolve whenever she goes on a new diet or whatever. If you see that, that's going to be celiac disease, right? Ciliac disease is just almost like a malabsorptive cause of acolytic amenerate, right? Because think about it. If you have celiac disease, you've killed your your microbiology line in your small intestine, right? So you're not going to be able to reabsorb anything. So people that have celiac disease, they tend to be like have like really bad malnutrition. Well, if you're malmourished, well, guess what? Your grinning again is not really high. If your grinning is high, it's going to kill you and your age. So you're going to have a hypogonadotropic hypogonadism, okay? Hypogonadotropic hypogonadism. And then don't forget, people that are anti-psychotics, right? So what do anti-psychotics love to do to people? So remember, anti-psychotics, the blocked dopamine receptors, well, one area where they blocked the dopamine receptors is in the two-barrow infant developed pathway, right? So remember, another thing for dopamine is prolactin inhibiting factor.

So if you blocked the dopamine receptors, you're actually going to have an operation of prolactin, especially in people that are taking risk very low, right? So if you do that, your your prolactin will go up, your genital will go down, your fSHL will go down, right? Your estrogen will go down, right? So ultimately, again, that will lead to a hypogonadotropic hypogonadism, right? Another classic one that can give you again, they can even give you a person being treated for diabetic gastroperiesis that develops in menoria. Again, the thinking there is very easy. Again, we treat that diabetic gastroperiesis with metoclopromide, but the clopromide is a dopamine receptor antagonist blocks the dopamine receptor that will cause hyperpaparalactinemia and then that will kill genareach and then you have a hypogonadotropic hypogonadism, okay? Another one that can give you is the person that is hersute, right? And is infertile, right? That's obviously going to be PCOS, right? That's going to be PCOS. Remember, people that have PCOS, right? They tend to have like very high levels of LH and the LH to FSC, which tends to be increased. Although remember, that's not part of the diagnostic criteria, right? But the thing with people that have PCOS is the never-of-illeged, right? Literally, another thing for PCOS is like an ovulation, right? So if you don't ovulate, well, you're not going to ever make a progesterone, right?

So the uterus is never going to be ready to properly take you off an implanted embryo, whatever, right? And also, you're literally, if you're not ovulating, you're literally not releasing eggs. It's not like the sperm can like do like this, uh, marry, go around and make it sweet to the, make it sweet to the ovaries, right? So, um, so in that case, right? Again, PCOS, remember, they'll have like an ovulation, they'll have signs of hypoindrogenism, right? And then they'll have polycystic ovaries on ultrasound. And remember, you just need to out of those three, you need to just basically check two of those three boxes and then the person is, uh, is good to go, right? Or what if they give you a question about a woman, they tell you that, um, she delivered a kid three years ago and that that delivery of that kid was complicated by, uh, you know, like very major blood loss. And after she stopped breastfeeding, she has been traveling her husband to have new kids and it's not working out. But if you see stuff like that, then I want you to think about she and Sandra, right? So just backtrack to her delivery, she delivered, she bled out a ton. Remember, when you're, when a woman is pregnant, she has like, it's like hormone central, just like a ton of hormone going around well, that woman's got to come from somewhere. In this case, it's the antirapitry. So the antirapitry gets huge during pregnancy, right?

So the thing that can happen with the antirapitry is, it can pretty much, um, it's very susceptible to ischemia because it's now very big, very vascular. So the person bleds out a lot in pregnancy, um, they can pretty much have an ischemic stroke of the antirapitry and how Cauchy hand syndrome, right? So those people will not be able to make FSH and LH, right? No FSH, no LH, right? Uh, but their January should technically be big enough, right? I mean, should be high because you're not getting FSH, you're not getting LH, so no estrogen, so there's no negative feedback, right? But, uh, the antirapitry is literally gone, so you're not going to be making any FSH or LH, right? So in that case, people that have shi-hand syndrome, right? The FSH and LH will be, we decreased, okay? The FSH and LH will be, will be decreased. And then remember, if they give you a question about a patient and they tell you that, you know, it's like a 17 year old girl, never had men sees, but they tell you some story about how she has like cyclical abdomen open at the end of every month. You want to think about an impetraid high men, right? You can even tell you that you see a blue bulge in the vagina when you do like a vaginal exam. One thing about impetraid high men sometimes, they call this like a transverse vaginal septum, but basically you treat that with surgery, you just do a cruise sheet incision and boom, you pop out all that old tissue and the woman should be fine, you pretty much cure her.

But one thing that I'll tell you that you're dealing with impetraid high men or transverse vaginal septum is that the FSH and LH will be normal, okay? The FSH and LH will be normal. Another thing you can also do to your own exam is they can tell you something about a woman that has had PID many times or multiple abortions with a ton of DN Cs, right? And then they tell you that, oh, she's now married trying to have kids having a lot of issues, well, you want to think about Ashwin syndrome, right? Remember, another name for Ashwin syndrome is uterine cynicky. Cynicky is S-Y-N-E, C-H-I-E, right? Sometimes they may even call it uterine adhesion disease, right? So they have a ton of adhesions in the uterus. Basically, when you keep scrubbing, scrubbing, like you do a ton of abortions, have a ton of PID, you keep scraping, scraping, scraping, the endometrial lining, well, unfortunately, at some point, you may go ahead and scrape the desidrabi salis, right? So those same cells that kind of support the uterus, the endometrial lining, so those are gone, well, doesn't matter how much estrogen you have, or how much fresh gestion you have, there's no stem cell to make those endometrial lining cells in the first place, so the presence kind of screwed. So those people actually, they're FSH, LH, estrogen, everything will be all normal, right? Because there's just no place for the estrogen projecting is around, but it's just not able to accomplish any ego, okay?

Not able to accomplish any ego. So just trying to like juggling my memory of there, any other, like high-altotherologies I have not mentioned with regards to causes of amenorrhea. Oh, we can give you a question about a woman, right? So tell your old female, tell you that she has a history of Prince Metal Angina, right? And then they tell you that she's, she was studying a new drug, right? And then now she's having an amenorrhea, right? Again, if you think of it, when people have Prince Metal Angina, again, remember these days it's called a variant, Angina, it's called variant Angina, that variant Angina. Essentially, you can treat it with a non-dihydroperidine calcium channel blocker, so something like Vera Pamell or Dealtyzen. Remember Vera Pamell is very, very excellent at causing hyper-producing email, but it causes an increased release of prolactin. So again, that will kill Gen RH, kill FSH, LH, kill estrogen, so you have a hypo-guernodotropic hypo-guernodotropic, right? And then remember that if you're breastfeeding, breastfeeding right doing for you to breastfeed, you literally need prolactin around. That hyper-locked in, at least for the first six months after you deliver, can really help with killing Gen RH, killing FSH LH, so you don't have any, you don't have any menceses.

It's almost like the body was designed to like, okay, you know, let's, let's try to not get pregnant again so that we can actually take care of this new baby that came like, you know, like six months ago. And then one thing I think I want to, one thing I think I want to mention here is, if a woman of her productive potential presents with him in area, always get a pregnancy test, right? Always, always get a pregnancy test, because remember, again, pregnancy is the most common cause of secondary menoria, okay? Pregnancy is the most common cause of secondary in menoria. Even if it's like a 14 year old kid, just get the pregnancy test. Even if you've never had menceses before, they may have had sex like when they were about to pop out their first eggs, okay? Just one of these weird bizarre things that your friends at the end being sort of kind of expect, expect you to know, okay? They expect you, they expect you to know, right? And again, some other like weird stuff that can cause amenoria for pressing has aromatase deficiency, right? Pressing that has aromatase deficiency, they won't be able to make estrogen from their endrogens, right? Remember, there's this two cell theory for how estrogen is meeting the ovaries, right? So the thicker cells will make testosterone. Remember the team, thicker 14 testosterone, right? So the thicker cells will make testosterone, but oh, there's no aromatase.

Oops, so because they have no aromatase, they're going to lose themselves and not be able to aromatize that testosterone to make estrogen, right? So if you're not making estrogen, yikes, those people, unfortunately, they're going to go ahead and have um, um, lower estrogen so their gene rHFSHLN will be elevated, right? So they will have a hyper gonadotropic hypo gonadism. Remember, they give you a person that has amenoria, can smell it, can smell a thing, right? You want to think about common syndrome, right? So common syndrome, those gene rHFSHLN will be low, your estrogen will be low, right? So you're going to have a hypo gonadotropic hypo gonadism, okay? Hypo gonadotropic hypo gonadism, okay? And then remember that, um, I think I've mentioned that already. Okay, so I think I pretty much talked about all the common causes. I mean, like, again, I will not be surprised if you get like, at least if you're taking a step one step, just a year, step three exam, like two or three questions from this, from this podcast, if not more, right? And if you're studying for your OBGYN SHOF exam, this is definitely a podcast you should, you know, sort of kind of listen to because you're going to get tons and tons and tons of amenoria questions on your exam. Um, and as I wrap up today, uh, please subscribe to the podcast. Again, I have this on Apple podcasts on Google podcasts and on Spotify and I have a You Tube channel, the Vine Intervention USM only podcast and videos.

So please subscribe to that. And then also if you want to get on my, you know, an notification whenever I, you know, make a podcast, uh, just sign up on the website, divineinterventionpodcast.com. And again, come on in, feel like, get from people you say, oh, divine, on Apple podcasts. I did not find episode two or three or whatever, right? Again, remember, it, I promised his layout of my hands, but Word Press has a role and is also kind of like, it's kind of a Word Press for you. Pretty much can get more than 150. Essentially, the most recent 150 podcasts will be the things that will show up on Apple podcasts, right? So basically, this is episode 278. So after this is uploaded, um, the first like if I'm doing my math correctly, so 150 minus 278 is one, 28, right? So you would not see the first 120 each to 100 and maybe 35 podcasts because there are some announcement podcasts of media along the way, right? And then I do offer one on one tutoring for the USM any exams. So step one, step two, see, step three, uh, pre-clinical, uh, uh, uh, exams, 30th-ish of exams offered to you during for all those things. And again, if you're medicine resident, actually tutor for the medicine boards and the medicine training exam. And again, I've worked with thousands of students. I've had very successful students. You can look up the testimonials on my website.

That's like a fraction of many of the very good testimonials I've had, even with the newer NBM exams that are a little more challenging for for people. So if you filled a step one exam, filled a step two exam, filled a step three exam, I have a lot of success stories of people have worked with that. I've filled the exam even multiple times. And then we work together and you know, thankfully to God, they ended up doing well. And then, as you saw, like maybe an hour or two ago, uploaded a podcast on on the course, I'm going to be offering from the six to the ninth of January. So I'm offering the NBM testing in strategies class. It's two and a half hours. And we'll basically teach you how to approach NBM questions. And then from the seventh to the ninth, the 10 hour course that I used to have before, I'm expanding it to be a 16 and a half hour course because I want to cover bio stats, I want to cover ethics, I want to cover those healthcare systems since that came in November 2020. And also there's a bunch of high yield like medicine, neuro, PEG surgery, OB-GYN, psych concepts that the NBM is beginning to care about these days that I also want to cover. So I'm expanding the course. So it's going to be three days from 11 AM to 4.30 PM, Mountain Standard Time on the seventh, the eighth and the ninth. The test against strategies courses from two to 4.30 PM, Mountain Standard Time on the sixth. So thank you for listening. I'll see you in the next podcast.

Have a wonderful week ahead and God bless you. Thank you.

Never having menstruated.

With secondary sex chars: wait until 16 years old; without them: diagnose at 14 years old.

Hypergonadotropic hypogonadism (High FSH/LH, Low Estrogen).

Androgen Insensitivity Syndrome (AIS).

Pregnancy.

Hyperprolactinemia (e.g., pituitary adenoma or medication side effect).

High LH to FSH ratio; signs of hypoestrogenism (due to lack of ovulation/progesterone).

Wait until 16 years old.

High FSH and high LH, but low estrogen (indicating primary ovarian failure).

Hyperprolactinemia (e.g., pituitary adenoma or dopamine antagonist use).

Low FSH/LH; normal estrogen. Estrogen is maintained because the patient has normal aromatase activity converting excess testosterone to estradiol.

Ovarian failure due to damage from radiation/chemo, removing negative feedback.

Low FSH and low LH (due to GnRH suppression).

Polycystic Ovary Syndrome (PCOS).

Wait until 16 years old.

High FSH and high LH, but low estrogen (indicating primary ovarian failure).

Hyperprolactinemia (e.g., pituitary adenoma or dopamine antagonist use).

Low FSH/LH; normal estrogen. Estrogen is maintained because the patient has normal aromatase activity converting excess testosterone to estradiol.

Ovarian failure due to damage from radiation/chemo, removing negative feedback.

Low FSH and low LH (due to GnRH suppression).

Polycystic Ovary Syndrome (PCOS).