DIP Episode 577 - USMLE Step 2/3 Rapid Review Series 119

Welcome, my name is Divine. This is episode 577 of the Divine Intervention Podcast. In today's podcast, we're going to be continuing the Rapid Review series for the USMELIS Step 2, CKN Step 3 exams. This is going to be series 119. Let's begin. So what if they give you a question about a 25-year-old female? You're told that for the last three months, she has had a lot of weight gain and the described physical exam findings, they tell you that her blood pressure is 155 over 95. And you're told that her core MBMI is 32 kilograms per meter squared. And then you're also told that she has these appropriate streaks on her lower abdomen. And then you're asked for the most appropriate next, and they give you some labs. You notice that her potassium is low. You notice that her sodium is a little bit high or normal. And they notice that her bicarb is elevated. So what should you be thinking about here? I would really hope you're saying that Divine, this person has a Cushing Syndrome, right? This person has many of the classic findings. Like for example, you notice that this person has weight gain, right? Steroids cause a person to gain weight, right? It really boosts your appetite. If you even think about it, when people have a terminal sickness, many times they're giving steroids because steroids can improve the appetite. It doesn't improve survival, but it certainly improves their appetite.

And then we see that this person has hypertension because cortisol has our industrial-like properties. So if, for example, you take cortisol, cortisol works like our industrial in a sense. So it's going to increase sodium and watery absorption in the kidneys. That can increase a person's blood volume and that can raise your blood pressure. And that also explains why the person may have hypochylemia because if you remember one of the drops of our industrial is to make you excrete potassium in your kidneys. And if you excrete potassium, that's going to cause your potassium levels to drop in your serum. And then the metabolic alkalosis makes sense. The elevated bicarb makes sense because again, one of the drops of our dosturant is to make you excrete potassium into your urine. So that, I mean, not just potassium as we've said, but also hydrogen ions. So if you're getting rid of a lot of hydrogen ions, you'll be left with an increase in bicarb. So that's going to cause you to have a metabolic alkalosis. So let's say for this patient, you know, we check the labs, you know, we notice that, wow, the we do a low dose dexamethasone suppression test, which is one of the ways you can screen for cushions. And we notice that, ooh, okay, this person has, you know, you check their cortisol the next morning. So you give low dose dexamethasone the night before, check cortisol the next morning, it does not suppress.

And then you're like, ooh, okay, let's look at your 24 hour urine or record is always check and it's still elevated. Or we do the late night's ivory cortisol, we check and it's still elevated, right? All these things pretty much tell us that, hey, you got cushing syndrome, right? But after that, we need to then kind of figure out, is this ACTH dependent, or ACTH independent? Because remember, you can have cushing syndrome because you have too much ACTH, right? So from like small cell lung cancer or from cushing disease, remember, cushing disease is when you have a pituitary denoma that's making a ton of ACTH. Or turning, so those things will be causes of ACTH dependent, cushioning syndrome. The ACTH will be high. Or you can have cushioning syndrome because your adrenal cortex has just gone rogue. So it's just, you just have an adrenal adenoma or something that's making a lot of cortisol. And then that cortisol is negatively feeding back and shutting down the production of ACTH, right? So in that case, you will have cushioning symptoms, but the person's ACTH will be decreased because the extra cortisol coming from the adrenal cortex is suppressing ACTH production. So those are all things to know. So for this person, what's the next logical test you want to do? Since these initial tests we've talked about kind of give a positive screen for cushioning syndrome. Well, I hope you're saying, okay, divine, let's check the ACTH levels.

So let's assume you check the ACTH and the ACTH is low. What would then be your next step? Well, again, if the ACTH is low as I've described and explained already, it means that you probably have an adrenal adenoma that's causing you to have cushioning syndrome. So your adrenal glands again, you're making a ton of cortisol that's suppressing ACTH production. And because your ACTH production is suppressed, the value is low. So obviously the problem in this person is likely in the abdomen. So how do we image the adrenals? It was like one of the best imaging techniques for the adrenals. Well, I hope you're saying divine, we're going to do a CT of the abdomen and pelvis, right? Which you're going to do. And then you're going to find this adrenal adenoma. So you're like, oh, okay, I find this adrenal adenoma. So what do you do next? Well, you should remove the adrenal adenoma. Okay, so you remove it. But they then ask you a question on the exams, which of the following post-operative interventions will most likely decrease this patient's risk of the literal outcomes. And I would hope in those circumstances, you're going to pick the answer that says to give glucocorticoid therapy. I know so if you may be like, what? Divine, what are you talking about? Like this person had cortisol excess. We just literally yanked out the adrenal gland. The adrenal gland that was messed up.

And then you are telling me as a post-operative intervention, I should go ahead and give this person glucocorticoid therapy. How does that even make any sense at all? Well, let's explain how it makes sense. All right. Again, this is one of those things you can see on your USMLE exams and you're like, this is something that almost most people will get wrong. But you don't have to get it wrong because you're paying attention. So this person, let's again, like many things in life, if you work it out, it will make sense in your brain. This person had an adrenal adenoma. That was making a tonal cortisol. Okay. So they have one abnormal adrenal gland. The other adrenal gland that we'll imagine is working pretty fine. So this person made a lot of cortisol suppressed ACTH. Now that was not really a problem because this person had excess cortisol from the one working bad adrenal gland. That had the adrenal adenoma, not a big deal. But what can you tell me about stimulation of the adrenal cortex for the other adrenal gland that is normal? Well, that adrenal gland that is normal is not being stimulated because the ACTH has been suppressed by the elevated cortisol from the abnormal adrenal gland. So after you've removed the source of the crazy amounts of cortisol, aka the abnormal adrenal gland, then you're going to be in a state of adrenal insufficiency. You're going to be in a state of adrenal crisis because it's not like the ACTH will just rise immediately.

No, that process takes time. So the thing that can happen is that you will essentially have a big time suppression of the other adrenal cortex of the normal adrenal cortex. So once you've removed the abnormal adrenal, you're not making any cortisol. You're not making any out of the that's going to put you in some very, very, very, very big trouble, very, very, very big trouble. At least let me not extend my thoughts on the industrial. But for sure, you will not be making cortisol. For sure, you'll not be making cortisol. So these people, because they're not making cortisol, they're in a state of adrenal crisis. So those people are going to need a stressed dose of steroids to tidy them over. If not, they will be throwing to adrenal insufficiency and they will land in hot water, right? These kinds of people, they will be like profoundly hypotensive. They won't necessarily do very well at all. So just something I want to keep in mind. They're going to need a stressed dose of steroids. The thing is, I'm sure many of you are familiar with stressed dose of steroids from people that, hey, they've chronically taken cortical steroids. Maybe they have like asthma or whatever, or they have like gyrancylla, like, arthritis or whatever. Now, our friends at the NBM is they know that everybody that has the job description medical student probably knows that.

So why don't you just manufacture a person that has ACTH independent pushing syndrome as the source of crazy cortisol and then you do surgery. And they notice after surgery that they are crushing and burning from a hemodynamic perspective. So just make sure you understand this scenario I've just described. It kind of looks like a benign scenario, but I promise you it's not benign. It's actually very, very high yield to know for your exams. It is extremely high yield to know for your exams. So please, please, please, I'm begging you keep this at the back of your mind as you're preparing for your test. Now, one thing I want to mention here is what can help you physically exam wise differentiate an ACTH dependent pushing syndrome from an ACTH independent pushing syndrome. Because the thing is sometimes our friends at the NBM is they may give you a question and they will try to see if you can differentiate just based on physical exam findings. I will strongly encourage you to consider looking at the skin finding, right? If you see skin hyperpigmentation, you want to think about ACTH dependent pushing syndrome. But if you don't see skin hyperpigmentation, then I want you to think of ACTH independent pushing syndrome. Well, why does this make sense? Well, the thing is if you think about it, ACTH is made from an ancestral molecule known as POMC. POMC literally stands for pro opi, melanocortin, pro opi, melanocortin, right? So pro opi, right?

So opi gives this compound gives rise to better endorphin. Pro opi, melanoc, melanoc, giving rise to melanocystimulating hormone, cortin, cortin, giving rise to ACTH. So whenever you're making a ton of ACTH, you're going to make a lot of melanocytes stimulating hormone as well. And what does melanocytes stimulating hormone do? It literally stimulates melanocytes. I want you to stimulate melanocytes. That's going to cause you to have skin hyperpigmentation, skin hyperpigmentation. So if you really think about it in this wise, if a person has ACTH independent pushing syndrome, like an adrenaline, a denoma that's making a lot of cortisol, that adrenaline, the normal making cortisol is going to suppress ACTH production from the interpreter. If that happens, if that happens, then if you're not making ACTH, you will not be making a message. So you will not have skin hyperpigmentation. But if you have ACTH dependent pushing syndrome, for example, like in the setting of Cushing's disease, remembering Cushing's disease, that's where you have a picture of the denoma that's making a lot of ACTH. You will have skin hyperpigmentation. Because again, as you're making all that ACTH, you're going to make MSH. Right? So again, skin hyperpigmentation can be found in people with Cushing syndrome. I also see people that have Cushing syndrome and they will not have skin hyperpigmentation. Do you know that this same role can also apply to adrenaline sufficientcy? Maybe like what? Really? Yeah.

People can have adrenaline, insufficiency and have skin hyperpigmentation. People can also have adrenaline, insufficiency and not have skin hyperpigmentation. You may be like, divine, how's that possible? It is possible, again, like many things in life. If you work it out, it's going to stick in your brains. So think about it. If a person has Adescent's disease, if you have Adescent's disease, literally your adrenal cortex is messed up. Since your adrenal cortex is messed up, you will not be able to make our dosterone, you'll not be able to make cortisol, you'll not be able to make DGS. So because you're not making cortisol, there is no negative feedback at the level of the hypothalamus and the antirpatory. So you've been making a lot of corticotropin release in hormone, CRH, but you also be making a lot of ACTH. So all that ACTH that's been made, you better believe it's going to be made from POMC. So as POMC is making a lot of ACTH, you'll also make a lot of MSH. So you're absolutely positively going to have skin hyperpigmentation. But imagine a person that has like pitotropoplexi or a person that has shihan syndrome, you know, where the aturpatory doesn't work as well. If your aturpatory is not working well, then guess what? You will not make ACTH. And if you don't make ACTH, then you will not make MSH. But remember, since you're not making ACTH, you're not going to stimulate the adrenal cortex. So you will not be able to make cortisol.

So you're going to have signs of adrenal insufficiency. This would be a secondary adrenal insufficiency. But in this case, since you're not making ACTH, you'll not make MSH. And that's going to cause what that's going to cause you to have, that's going to cause you to have no skin hyperpigmentation. You will not have skin hyperpigmentation. Again, I don't know why you see me really trying to weight through and explain the pathophage behind all these cortisol and ACTH things. But I promise you, these things are not loyal by any stretch for your exams. These are things that you will definitely absolutely, positively need to make sure you know for your for your test. All right. So please just kind of keep that in mind. And the original situation I described of the pressing post stop having adrenaline insufficiency. Again, it's a very high yield scenario to know. Right? Again, all that cortisol from the bad adrenal suppress ACTH. And then that ACTH that suppresses means that the normal adrenal gland is not stimulated. And if the normal adrenal gland is not stimulated, guess what? It's going to atrophy. Right? The adrenal cortex in that case is going to atrophy. And if it atrophies, then again, atrophy is a process that takes a long time to resolve. So just something you want to keep at the back of your mind, for example. All right.

Now, what if they give you a question about a 37 year old male and you're being told that this man is being, you know, prepared for, you know, this man is going to obtain an elective in-winner, herniary pair. And then you're told that this man is currently a methyl trexeta pharmacotherapy. And that he has had multiple flares of his disease, of his joint disease. And, you know, he has had to take, you know, IV steroids a few times. And then they ask, again, which of the following preoperative interventions will most likely decrease the stress risk of the literary outcomes? Again, you know, this today's divine is going really ham on these pre-op interventions. They kind of like you to know about these pre-op interventions for you exams, right? So let's kind of discuss this case. So what's going on with this man? Well, this man probably has rheumatoid arthritis, right? Remember when you have rheumatoid arthritis, the first length of it is a demard, like methyl trexit, like methyl trexit, like what? Like methyl trexit. So, and this person has had a lot of, he appears a lot of exacerbations or flares of the arumatoid arthritis, you know, they've used a ton of steroids. And then this person is getting surgery for an in-winner, herniary pair. This surgery is probably going to be elective, right? It's not emergent. And let me ask you, this what kind of inguinar hernia should we expect in this person that is a 37-year-old male? Well, I hope you're seeing divine.

I expect this guy to have a direct inguinar hernia. Remember, directing inguinar hernia is a found in the older people. In directing inguinar hernia is a found more younger people, right? In younger people like kids, right? And remember, don't forget, bring, you can draw some anatomy forward on your exams, right? Remember, these directing inguinar herniars are found medial to the inferior epigastric vessels. But the indirect inguinar herniars are found lateral to the inferior epigastric vessels. So, they can literally tell you on your exams, you know, just to mess with your head a little bit, they can give an indirect inguinar hernia to a person that is an older man, right? Because yes, the fact that directing inguinar herniars are more common in older men does not necessarily mean that they cannot have indirect urniars. So, you can be one of those things where they will give you this question about like a 37-year-old male. And then they will tell you that a reducible bulge is found lateral to the inferior epigastric pulse, right? If you see that, don't rush head first and pick the answer choice that says directing inguinar herniars. Now, in that case, they've given you hard evidence, they've given you like, you can pound your fist to the table evidence that, hey, this is an indirect inguinar herniars, right? So, just be careful. Again, that's why you don't just want to go based off of heuristics as you're studying for your exams.

That's usually a pretty terrible way to take exams actually, right? You want to make sure you read the whole thing, you know? That's why all these new fungo the strategies of read the last sentence, skim through. I don't subscribe to any of those things. It doesn't make sense for the overwhelming majority of people that are studying for the exams, but I digress. I'm going to step away from that, right? So, this guy is having an inguinar herniary pair. Probably going to be directing inguinar herniars just because of his age. All right. So, what kind of preoperative assessment would you want to do? Well, I would hope that your picking the answer that says to do some kind of cervical x-ray. You know, why? Well, the thing is, people that have rheumatoid arthritis do not forget, these people are prime candidates for atlanto axial instability, right? Sometimes on exams, this thing is called C1 C2 sub-location. And the thing is, for these folks, if you manipulate their next extensively, you can get a life-threatening sub-location of C1 from C2. And that can cause like a cervical myelopathy, right? That can cause the person to have a spinal cord dysfunction at the cervical level, right? The thing is, atlanto axial instability don't mess around with it, don't joke with it because it can cause some very serious problems for people on in the real world and also on your exams.

So, we need to screen for that atlanto axial instability, that C1 C2 sub-location by going ahead and getting some kind of image of the neck, some kind of image of the neck. All right? So, along your exams, they want you to get a cervical x-ray, please. The USML is almost never want you doing CT to rule out, to like look at the neck, not a good idea, right? Generally, they want you doing a chest x-ray, a cervical x-ray, right? Or sometimes on exams, they can call it a cervical radiograph or something like that, right? Now, there's some other people that you miss hearing your exams to which this same advice of getting a cervical x-ray applies, or the answer to that is going to be an OES, like who? Or people that have Down syndrome, remember they can also have that atlanto axial instability. Another group you miss hearing your test are people that have ankylose in spine delitis. Those people can also absolutely positively have that C1, C2 sub-location. Something you definitely want to keep at the back of your mind for your test. Now, since we're talking about methyl-trexate, methyl-trexate is one of these weird but high-yield drugs that they love to test on the exam. So, what are some potential uses of methyl-trexates that you may see on your test? Already talked about one. Methyl-trexate is a D-Mart. It's basically a first-line D-Mart for managing rheumatoid arthritis. Remember, when you have R-A, you can use NSAI Ds. But NSAI Ds do not modify the course of your disease.

You want to go ahead and use methyl-trexate. So, how exactly does methyl-trexate work? Well, we know that methyl-trexate inhibits dihydrofolate, reductase. Dihydrofolid-reductase. Dihydrofolid-reductase. So, you pretty much prevents folid production, right? So, that can already begin to tell you that, ooh, this thing can really cause issues with cells that are rapidly dividing, like what? Well, like your bone marrow elements, right? So, methyl-trexate can certainly cause, because remember, it's basically an S-phase agent. Again, you may be like divine. There is no way on step two or step three, that they will ever test that methyl-trexate works in the S-phase. Man, you could not be more sadly mistaken. Remember, S-phase is the synthesis phase of cell division. It's the synthesis phase of cell division. Right? During that phase, you're making a lot of DNA. Let me tell you this. If you want to make DNA, you're going to need a lot of folid. If you want to converge deoxyardine monofosate to DTMP deoxythymidine monofosate, you absolutely need, you absolutely need folids to make that reaction happen. Okay? So, if you're lacking in folids, that reaction will not happen. And if that reaction does not happen, then you're going to have issues making DNA. Right? And this is part of why methyl-trexate is used as an anti-cancer agent, right? Because it pretty much prevents cell division. We know that many times cancer cells are very, very rapidly dividing.

So, do not forget that methyl-trexate can cause bone marrow suppression. And we can fix that or prevent that by giving the drug for lemic acid, for lemic acid. Another name for that as you may know, very well be aware of is locovoring. But again, a friend at the NBM is they know that all of you that have the job description medical student probably know about the term locovoring. Right? So, they're going to use folinic acid instead of you exams. Remember, folinic acid is not the same thing as folic acid. Okay? Please, not pick folic acid for locovoring. folic acid is not locovoring. For lemic, F-O-L-I-N-I-C, for lemic acid is locovoring. Okay? For lemic acid is locovoring. All right. I remember that methyl-trexate before I talk about the other uses is hepato toxic, right? And it's also auto toxic and sorry, hepato toxic and it can also cause a pulmonary fibrosis. Sorry, it is not auto toxic. It's hepato toxic and it can also cause some pulmonary fibrosis, right? So, there's something we want to keep at the back of your mind for exams. Now, what are some other uses for methyl-trexate on your exam? Well, if they give you a question about a person that has a flank mass and this person has a beta-HCG that is in the hundreds of thousands, right? That's probably a choreocorsidoma. Chlorocorsidomas are very, very, very sensitive to methyl-trexate on the exams. Well, what else can we use methyl-trexate for in the USML Es?

Well, you can use methyl-trexate for a topic pregnancies, right? Although it is rarely used. Most times for a topic pregnancies would rather go after like surgical interventions, the thinnest methyl-trexate, you can use it, but again, the criteria is just too much, right? So, usually you're not going to be able to use methyl-trexate for a topic, but when can you use it for a topic? So, you can use it for a topic if the beta-HCG is less than 5,000. So, that means that, wow, this beta-HCG has barely risen. Another one is if there is no evidence of phytochardic activity. Remember, if you go back to embryology, when those phytochardic activity usually starts, in utero, usually starts around week four. So, you can see that, man, if you have an ectopic, I mean, think about it before you even find out that you have an ectopic. Chances are a few weeks have gone by, right? So, the thing is, you're probably going to miss this window of opportunity for which you could give methyl-trexate. So, again, just one of these weird things that you kind of need to know for your exams. Again, I know some of the things I'm discussing today, they kind of sound weird, kind of sound bizarre, but I promise you, very high you to know these things for your exams. Now, let me ask you this, which of the following will most likely be elevated in a patient that has been on methyl-trexate therapy for a year? And then on your exams, they will give you a series of answers.

They can give you an answer that says, homocysteine, they can give you an answer that says methanol-malonic acid, and then they'll give you a bunch of other bogus answers. So, which one should you pick on you exam? I would hope you're saying, ooh, divine. I'm going to pick the answer that says, homocysteine is going to be elevated, right? Or they can actually make this an arrow question, where they will give you a bunch of arrows, they'll give you homocysteine levels, they'll give you methanol-malonic acid levels. Please pick the answer that says that your homocysteine is going to be elevated. Remember, folate deficiency, right? Whenever you're deficient in folate, and it's easy to get into folate deficiency because we only have about 10 to 12 weeks worth of folate in our buddies, that can cause you to have an increase in your homocysteine, right? That can cause you to have an increase in your homocysteine. But your methanol-malonic acid levels are actually completely fine when a person has folate deficiency, right? Remember, the enzyme methanol-malono-coemutees that we use in converting orching fatty acids and kind of throwing them into the TCE cycle. That enzyme uses B12 as a cofactor, but it doesn't use folate as a cofactor. So, the thing is, you will actually have a completely normal methanol-malonic acid level if you're fully deficient. But in B12 deficiency, your homocysteine and your methanol-malonic acid will both be elevated, okay?

That's a very critical way to differentiate fully deficiency from B12 deficiency. In fully deficiency, you're going to have just an increase in your homocysteine levels. You will not have an increase in your methanol-malonic acid levels. But in B12 deficiency, you have an increase in both your homocysteine and your methanol-malonic acid. Very high to know these things for exams. So, why is it that the homocysteine is elevated in this person that is taking methyl-tracksit? Well, we know that methyl-tracksit inhibits the production of folate by shutting down dihydro-folate reducties. So, can you see how they can take a methyl-tracksit question and transform it into a homocysteine question? Watch out! Again, some people may be like, may not have never seen this on an exam. See, the USMLE is what they do these days is that they take what you know and just extend it to a novel situation. So, it's not like that they're magically testing things you've never seen before or things you've never heard of before. They're just testing it in inventive ways that you may not necessarily be used to. So, just FYI, something you want to keep at the back of your mind as you prep for exams. So, you can already begin to see how they can extend the same story. To, for example, a person that is taking pyramid and sulfurizing, remember we tend to use that for toxoplasmosis, or a person that is taking trimethyramesophamethoxysone. Think about it.

Who do you think will be chronically taking TMP SMX on your exams? It can be a person that has a CD4 count on the 200 and we're trying to protect them against the mucicidrivetsi. It can be a person that has a CD4 count on their 100 and we're trying to protect them against toxoplasmosis. So, again, make sure you can make these links. I know it's frustrating. I know it's annoying. I cannot talk about this in a previous podcast that, oh, I think it was episode 576 that, oh, the vine is kind of jumping all over the place. Honestly, this is an intentional jumping all over the place because this is the way you're supposed to think and integrate through things on your exams. Just something you want to keep at the back of your mind as you're preparing for your test. All right. So, since this is a rapid review podcast, I'm going to go ahead and stop here. Again, after a bunch of review classes for step 1 to step 3, I actually have a 25-hour step 1 class starting today. So, if you're studying for step 1 or you're studying for step 2 or step 3, you have a poor basic science foundation or you failed step 1 or whatever, because again, a lot of basic sciences have been imported to step 2, step 3 these days. Shoot me an email and you can sign up for the class. The class is starting this evening. And then, you know, I have a 20-hour step 2 step 3 review. I have a last minute review for step 2, step 3. I have a bio-stats class, test-taking class, social science class.

Those are for step 1, all the way to step 3. And I have a 50-hour step 2 step 3 class taking place in the first two weeks of June. That's the only time that class is going to be held this year because it's a huge time commitment. But very high level class, I actually made a separate podcast where I talk about that class. And then, I also offer one or one tutoring for all the USML Es and complex exams. And then, I have this podcast on Apple, Google and Spotify. So, check those out. And then, also, check out my You Tube channel, Divine Intervention, USMLE, Podcasts and Videos, Divine Intervention, USMLE, Podcasts and Videos. That's why I post the videos that I make. And then, I also help with Euras applications, more interviews, personal statements and do all those things. And then, finally, I have another website called Divine Intervention Lifelessens.com. The Divine Intervention Lifelessens.com. There's actually an Apple podcast associated with that. It's called The Divine Intervention Life Lessons Podcast. Every week, I post like two or three podcasts where from a Biblical perspective, address a life lesson. So, just check that out again. Good number of people check that out every day. And they find it to be really helpful. All right. So, thank you for listening to me today. I will see you in episode 578. You know, have a wonderful day. God bless you and bye for now. Thank you.

Skin hyperpigmentation, due to co-secretion of Melanocyte Stimulating Hormone (MSH) from POMC.

ACTH-independent source, such as an adrenal adenoma.

Indirect inguinal hernia.

Folate (Folinic acid) deficiency.

Atlantoaxial instability (C1-C2 subluxation).

Folinic acid (Leucovorin), not folic acid.

POMC (Proopiomelanocortin).

Folinic acid is the active form used clinically for deficiency treatment; folic acid is the dietary vitamin.

Low (due to negative feedback from high cortisol).

ACTH-dependent Cushing syndrome (e.g., Cushing's disease).

Vitamin B12 deficiency.

Atlantoaxial instability.

POMC (Proopiomelanocortin).

Folinic acid is the active form used clinically for deficiency treatment; folic acid is the dietary vitamin.

Low (due to negative feedback from high cortisol).

ACTH-dependent Cushing syndrome (e.g., Cushing's disease).

Vitamin B12 deficiency.

Atlantoaxial instability.