DIP Episode 616 - USMLE Step 2/3 Rapid Review Series 127 (More Basic Sciences)

Alright, welcome to episode 616 of the Divine Intervention Podcasts. Into this podcast we're going to be continuing the Rapid Review series for Step 2 CK and Step 3. And this is going to be series 127. You may notice from the last Rapid Review, I did talk about a lot of basic sciences that are relevant to Step 2 and Step 3. I'm going to be doing the exact same thing with this podcast. The thing is Step 2 and Step 3. These days they really do fall in a lot of step 1 information. So I want to show you what really matters and how to make these integrations as you prep for your exams. So please do not completely ignore basic sciences. I'm not saying go back and review all of our state for Step 1. But don't ignore basic sciences. That'd be a huge mistake. Step 1 material is hugely integrated into Step 2 a lot of these days. So you've noticed this many times, you see people struggle with your Step 1 study and then they just magically believe that Step 2 will be very different. No, chances are if you've struggled studying for Step 1, you'll also probably, especially if you've not fixed those foundational issues you have, you probably also struggle as you study for Step 2. So just kind of make sure you're laying the right foundations. What if they give you a question about a five-year-old girl and they tell you that she's brought to the emergency room by her parents because she has had a lot of seizures over the last two weeks.

That she has been completely in a very significant headaches. And then they tell you that brain imaging is obtained and is positive for a brain mass. And then you're asked anatomically which of the following locations is most likely or whatever. If you see something like that, pick the answer that talks about the cerebellum. Pick the answer that talks about the cerebellum. The thing is this child has some kind of pediatric brain tumor. And again in this case, it's probably going to be some kind of, either like a pilositic astrocytoma, which is the most common primary pediatric brain tumor or like a medalloblastoma, something of that nature. The thing is pilositic astrocytomas are very, very common in kids. And when they happen, they usually are going to shop in the cerebellum. They're usually going to shop in the cerebellum. So be careful about that. So make sure you anatomically know where some brain tumors love to pop up. Cerebellum is where we tend to see things like pilositic astrocytomas, things like medalloblastomas, things like hemangioblastomas, those tend to shop in the cerebellum. Now in terms of the ventricular system, if you're looking at the ventricles, the ventricles are where we tend to find ependymomas. Ependymomas love to obstruct CSF flow. And then if you're talking about cerebellum convexities, like around the dura and things like that, you want to think about things like meningiomas. Meningiomas love to grow around cerebellum convexities.

They like to grow by meninges. That's why they're called meningiomas. And then remember the frontal lobe that will ligodendroglyomas love to grow. Frontal frontal frontal lobe, ligodendroglyomas, they love to grow around the frontal lobe. And then around the corpus calossum, crossing from one cerebellum cortex to the other, typically you want to think about glioblastoma motifomi. Glioblastoma motifomi loves those anatomical regions. And then if we're thinking in terms of around the pituitary gland, around the optic chiasm, you want to think about pituitary adenoma. Remember the most common pituitary adenoma is going to be a prolactinoma. But also you want to think about a craniofaringioma. Creniofaringiomas, they can compress the optic chiasm and they can cause problems. They can cause like bytemporal hemie and opsy. And then if you see a person that has a pineyloma, a pineyloma is going to be just above the superior collectulus. It's going to be superior to the superior collectulus. That's a nice way to kind of remember that. So please make sure you actually know these stains. These anatomical locations of these brain tumors. These are classic test questions. The things you're basically going to get wrong if you don't study it and if you don't know it. All right. Now, I think I want to take a quick tour through the cranio nerves. I think it's kind of helpful to know how the key things they love to focus on for cranio nerves with the USME Li step 2, CKN step 3 exams.

You can know everything about cranio nerves as you did for like step 1 or when you were doing your basic science coursework like knowing the terigo palatin, fossa and all those things. No, right. There's no one has time for that. But there's some key critical things I think you want to know about each cranio nerve. So let's go through the key high yield ones. So cranio nerve number one. The big thing I want to know here is what is common syndrome, common syndrome, right? Common syndrome, right? Remember, common syndrome is a neuronal migration defect. So if your neurons don't migrate properly, right? You're going to have issues with smell because cranio one doesn't migrate properly. But also these people also have a high pool, good autotropic high pool, good autism, right? So because cranio one, the olfactory nerve and your GNRH producing neurons, they kind of migrate together in uterus, right? So if they don't in on barology, so if they don't migrate together, they will end up at the wrongs. If they end up, if they don't migrate, then they can do their thing, right? I just like to think of it this way, right? Like for me, I'm probably useful in a hospital, right? Like, you know, nothing or talk about medicine, you know, thank God. So I can be helpful there, right? But if you take me to like, to like a cockpit of a plane, I am like completely useless. If you want to migrate me back to the hospital, right? Because that's where I'm going to be helpful for people, right?

So don't forget common syndrome, GNRH producing neurons, cranio, no, factory nerve, they don't migrate, right? So they have an osmium, but in addition to that, they have an infertility, right? So and it's again a hypogonadotropic hypogonadizen because they're not making GNRH, right? So their GNRH is low, their FSH and LH is low. So their gonad is not going to be stimulated, right? So they're going to have low levels of their sex steroids, right? Now, cranio nerve number two, the key thing I want to know about this is the afferent popularity defects, right? Afferent popularity defects, you know? So because remember cranio two is the afferent part of the popularity light reflex, right? So they are certain classic disorders. They love to test on the USM Ds like you see like a painful vision loss in an MS patient, right? You think of optic neuritis or you see a person that has had a recent MI or, you know, they have AFIP and they have this painless vision loss, right? I think it has a central retinal artery occlusion, right? Those things can cause an afferent popularity defect, right? And then don't forget that you can have tumors of the optic nerve, optic gliomas, right? Optic gliomas in people that have neurofibromatosis, right? People that have neurofibromatosis. So just kind of keep that at the back of your mind as you study for your exams, right? And then remember that cranio nerve number two is the only cranio nerve that is derived from the central nervous system.

All your cranio nerves with the exception of cranio two are derived from the peripheral nervous system. So two is derived from the central nervous system, right? It's derived from the from the diencephalon. So if a person has a central demilinating defect like multiple sclerosis, it should make sense that cranio two is the one that should be affected on those circumstances, right? And remember, when a person has an afferent popularity defect, right? When you shine light in the affected eye, both pupils will not constrict, right? Because literally light is not coming in, right? So there's no instruction given to cranio three, which is the efferent part of the reflex to cause both pupils to constrict. Right? Now let's go to cranio nerve number three, right? So remember cranio one is the olfactory nerve, cranio two is the optic nerve, cranio three is going to be the oculumodonerv, right? The oculumodonerv, right? So remember the big thing to know about the oculumodonerv number one is that is the efferent part of the popularity light reflex, right? Is the efferent part of the popular life light reflex. So you may have an efferent popularity defect when you have this, right? And if you have an efferent popularity defect, it literally doesn't matter what eye you shine light into. You just notice that the eye that has the cranio three that's not working will always not constrict, right?

Will always not constrict because that constriction of the pupil is under the control of the parasympathetic fibers from the oculumodonerv, right? And then it's also high you to know that if you have uncle herniation, if you have uncle herniation, right? You can also begin to compress cranio nerve three, right? So you have that blown pupil, right? You have that blown, blown pupil basically, right? And also if you have a midbrain stroke, a midbrain stroke will absolutely positively destroy a cranio nerve number number three, right? Remember, sometimes we call that Weber syndrome, right? And then cranio four is the trochlear nerve, super low yield nerves, we're going to skip that. All right. Now cranio five, that's the trigeminal nerve. I remember the trigeminal nerve. The big things to know for step two, step three is that it controls pain and temperature in the face, right? Pain and temperature in the face, right? It also does some stuff with the tongue, but we're not going to go into the details of that. That's more of a step one further, right? But it controls pain and temperature in the face, right? And don't forget trigeminal neurology, trigeminal neurology, right? You know, where these people will have like this fleeting, you know, sodium onset, lancinidine pain in the distribution of the trigeminal nerve, right? Remember, typically I'm going to manage that with carbamase, a pain, which as we know, can cause things like SIDH, and it can also cause the granuloseitis.

All right. And generally, if you have a lateral brain stem stroke, if you have a lateral brain stem stroke, you will damage cranio five. Those cranio five fibers decrease first through the lateral brain stem, right? So that's why a classic signature with a lateral brain stem stroke is that you have pain and temperature loss on the face. That's Ipsilateral to where you have the stroke. All right. Now let's go to cranio nerve number six. cranio nerve number six is the abducent nerve, right? The abducent nerve, right? So what are the key things to know about the abducent nerve first step, two step three? Well, it's going to get damaged in a medial pontean stroke, in a medial pontean stroke. It's in the middle of the pons, right? So if you have a medial pontean stroke, so like an issue of the paramedian pontean artery, that will infarct cranio nerve number six, right? And also, another way they can test cranio six on your exams is you've got to notice that the person cannot AB docked, AB like abs, AB, A and B, A as in upper B as in boy, you cannot abduct the eye on horizontal conjugate gaze, right? Remember, horizontal conjugate gaze is where you keep your head fixed. And then you move your finger on object and you try to follow your truck, you know, follow that object with your eyes, right? So the abducent nerve supplies the lateral rectus muscle, which helps with ab abduction of the eye.

If you cannot abduct the eye on horizontal conjugate gaze, you want to think about an abducent nerve lesion, right? Now, contrast this with being unable to AD ducts the eye on horizontal conjugate gaze, AD ducts the eye on horizontal conjugate gaze. That can be a medial rectus palsy, so that can be a cranio three defect, because the medial rectus, which does A Dduction of the eye is controlled by the oculum of the nerve. But another thing that can also cause impaired abduction, A Dduction of the eye on horizontal conjugate gaze is if you have a problem with the medial longitudinal fascicular, if you have an interneucleopthamoplisiac. So one question I think some of you may have is divine. How do I differentiate interneucleopthamoplisiac, as the cause of an A Dduction, like stagmas on horizontal conjugate gaze, from an oculum of the nerve, you know, medial rectus defect. Well, the thing is if a person has interneucleopthamoplisiac, they are still going to have normal accommodation. Accommodation is something that is under the control of cranio three, right? It's not under the control of the medial longitudinal fascicular. So if you see a person that has an adduction, nice stagmas, or impaired A Dduction on horizontal conjugate gaze, and you test the accommodation and it's still fine, they have interneucleopthamoplisiac. They don't have a cranio three palsy.

If the person has impaired A Dduction on horizontal conjugate gaze, but they also have impaired accommodation, that's a cranio three defect. All right. And then also I guess another thing I want to say is that if you have a medial pontine stroke, you also have contralateral corticospinal tract signs. So you're going to have like upper motor neuron problems that are contralateral to the to the to the lesion in a medial pontine stroke. Because remember the fibers of the corticospinal tracts, they're running the medial brain stem, they're running the medial brain stem, and then they cross at the medial ary pyramids, right? So that's why you get contralateral findings. All right. Now how about cranio seven? Cranio seven is going to be called the facial nerve, the facial nerve, right? Now remember the key thing you want to know about the facial nerve is that you're going to get it, you know, bells palsy, right? You have Ipsilateral oper and lower facial paralysis. Ipsilateral oper and lower facial paralysis, right? This with an MC stroke that will affect the contralateral lower face, right? And will also affect the contralateral oper extremity. Because remember the MC the middle cerebral artery supplies your upper extremities and your face, your contralateral oper extremities and your face, right? But in this case, if it's a MC stroke, it's the contralateral lower face that will be affected. Why? Because the upper face has dual innervation, right?

But again, if you have a peripheral, you know, you know, issue, right? Your lower nerve issue, cranio seven issue, right? That's going to be a lateral point in stroke. That's going to be an AIK stroke and an anterior inferior cerebral artery stroke. You're going to have Ipsilateral oper and lower facial paralysis because you basically infarcted the actual cranio seven nucleus, right? Right? And don't forget the causes of bells palsy, right? Like Lyme disease can cause bilateral bells palsy. I don't forget acoustic aromas, you know, things of that of that nature. Right? Now let's go to cranio nerve number eight. Cranio eight is the vestibulococlear nerve, the vestibulococlear nerve, right? So remember, people that have a cranio eight issues, right? You know, bilateral acoustic neuromas. Don't forget that in NF2, right? Remember, those acoustic neuromas, I was kind of talking about anatomical locations or brain tumors. Those things tend to be at the cerebellaral pontine angle. That's very high yield to know for your exams. Cerebellaral pontine angle, right? So if you damage, you can have those bilateral acoustic neuromas, right? And then I think it's also pretty high yield to know for your exams. The drugs that are auto toxic, right? The drugs that can damage cranio nerve number eight, right? So like for example, don't forget your amino glycosides, right? So things like gentamysin, tobra-mysin, right? They can damage your cranio eight.

Don't forget your lube diuretics, especially if a cranic acid, right? Super, super, super auto-toxic. And then don't forget vancomycin, right? Vancomycin is also auto toxic. And then don't forget your platinum agents like cisplatin. cisplatin is also auto-toxic, right? And then if we look at cranial nerves nine and ten, I'm gonna group them both actually together, right? So cranial nine is the glossopharyngeal nerve. cranial ten is the vagus nerve, right? So these two nerves, they kind of do the same thing. But the key thing I just want you to understand here is people are gonna have like swallowing issues when these nerves are messed up, right? And these nerves are classically gonna be messed up when you have a lateral medallary stroke. You have like Wallenberg syndrome. These are pica, pica, pica, strog, pica, pica, pica, strog. So you're gonna have issues with swallowing, you don't take sensation in the posterior third of the tongue and all those fun things. All right, so I guess not fun for the person going through them, right? So and then cranial number 11 is the spinal accessory nerve, super low yield, so we're gonna skip that. But let's go to cranial 12. Right? cranial 12 is the hypoglossal nerve, the hypoglossal nerve, right? This one controls your tongue muscles. Remember whenever you mess up the tongue muscles, your tongue is gonna deviate towards the side of the lesion. You're gonna basically lick your wounds. That's a nice, the monique to remember that, right?

That's gonna be from a medallary stroke, right? So if you see a medallary stroke, if you see a medallary stroke, think of, especially initially the anterior spinal artery, right? That's gonna damage cranial 12. You're gonna have like tongue muscle paralysis, right? And you're gonna have a contralateral corticospinal tract issues as well. Because again, as I've said, in medial brainstem strokes, let me summarize this, in medial brainstem strokes, you usually have contralateral corticospinal tract issues because the corticospinal tract as it descends through the brainstem, travels in the medial brainstem, right? Travels in the medial brainstem. Now, contrast this with lateral brainstem strokes, where you're gonna have a lot of sensory problems, right? You're gonna have contralateral sensory problems on your body, because again, many of those sensory pathways, they travel in the lateral brainstem, they travel in the lateral brainstem, okay? Especially the fibers that control pin and temperature, especially the fibers that control pin and temperature. Again, these cranial nerves that kind of work through, I would not ignore these stains. These things actually very, very high up to know for your exams. All right, now the next thing I wanna discuss here, what if they give you a question about a patient that has been taken, has a histro of like, like, what's the name of this thing you're thinking about? So let's say this is a person that has a Turner syndrome, right?

The person has Turner syndrome. And then you're told that this person has a histro of chronic UT Is, you know, recurring UT Is. So this person has been on pharmacotherapy, on chronic pharmacotherapy. And then now over the last two to three months, this person has been having like, worsening shortness or breath. They won't tell you that this person has like, jogula venous distension. And you notice that this person, you don't hear any crackles in the lungs, or if you don't hear any crackles in the lungs, right? And you're told that again, this person has been on chronic pharmacotherapy as UTI perphylaxis, you know, to prevent like renal scarring, right? So what am I trying to get out here? This person having pulmonary hypertension, right? Pulmonary hypertension. This person with Turner syndrome has pulmonary hypertension. So let's kind of integrate the story and it's like, gee, divine, how do you get to a pulmonary hypertension with this? Well, there's a way to get here, right? So first things first, this person has Turner syndrome. We know that Turner syndrome is 45 XO. Okay, now let's look at the kidneys and the urinary system. What are the kidneys slash urinary system issues you can have with Turner syndrome? Well, you can have this thing called horseshoe kidney, right? Where the inferior pores of the kidneys are fused, so you then get stuck on the inferior mesenteric artery, right? So those people can have recurring UT Is.

The thing is, if you keep having all these UT Is, it's gonna cause scarring, fibrosis, and damage to your kidneys and urinal collecting system, right? So because they keep getting these UT Is, getting these UT Is, right? The inflammation from those UT Is, damaging the kidneys, damaging the collecting system. So your body is like, gee, this is not good, right? So what you can do as a, you know, some of these people is that they can take antibiotic prophylaxis, right? So let's say for example, they happen to take something like nitroferent towing as UTI prophylaxis. They take nitroferent towing. Nitroferent towing, many resources don't cover this, but it's actually pretty important to know for you exams. It can cause pulmonary fibrosis. It can cause a restrictive pattern of lung disease. And if that happens, that can cause pulmonary hypertension, right? That can cause pulmonary hypertension. One classic presentation of pulmonary hypertension on the USMEL exams is that a person is going to have a GVD, right? They're going to have like heart failure signs, but you won't hear crackles in the lungs, right? Because the problem is basically like with pulmonary arteries and things like that. All right. But now that we've kind of talked about this nitroferent towing association, what are some other causes of pulmonary hypertension? You want to know for you exams. Well, you also want to know idiopathic pulmonary arterial hypertension, right?

It's going to be classically being in young females on your test. That's a really good BMPR2 mutation, BMPR2 mutation, right? When you have that BMPR2 mutation, that's going to cause you to have a hyperplasia of the small muscle of your pulmonary arteries, right? So that's going to cause that right heart failure, right? And then don't forget also, if a person has a, you know, corpomonalis from things like COPD, for example, cystic fibrosis, right? I remember corpomonalis, a term we used to define a right heart failure because of a pulmonary issue, right? Because remember, the most important cause of right heart failure is left heart failure. But whenever you have a right heart failure from a pulmonary cause, that's called corpomonalis, that's called corpomonalis, right? That can certainly cause cause problems, right? And then don't forget your drugs that can cause pulmonary hypertension, right? Because they can cause pulmonary fibrosis. So things like bleomysin, things like methyltricsit, things like amyoteroine, right? Things like nitrofyrantoin, right? You should certainly know those for you exams, right? They can cause pulmonary fibrosis that can cause a pulmonary hypertension. Don't forget icy-manger syndrome, right? So you see a person developing pulmonary hypertension after they've had a VSD for a long time, right? Because remember, when you start off with a VSD, it usually starts off as an as an a-sia-notic defect, right?

So blood is flowing from the left side of the heart to the right side of the heart, across that VSD, right? Because the left side of the heart has higher pressures. But over time, right? Remember, your pulmonary system, your right heart is not built for 100-in-dose, all that excess blood, right? So as that blood keeps flowing to the right side of the heart, over time you develop pulmonary hypertension. And then the right side of the heart pressures will exceed the left side of the heart pressures. And then blood will now start flowing across that VSD from the right side of the heart to the left side of the heart, right? That case, you've developed pulmonary hypertension. That's actually pretty deadly. We call that icy-manger syndrome, right? icy-manger syndrome can cause pulmonary hypertension, right? And then don't forget that diffuse sclerosis, right? The diffuse sclerosis can also cause pulmonary, basically like any kind of scleroderma can actually cause pulmonary hypertension, right? Both the diffuse sclerosis, right? Because those people can get fibrolyclone disease, which can lead to pulmonary hypertension. Or people that have crecleroderma, when you have crecleroderma, you directly fight brosial pulmonary arteries. And then that leads to pulmonary hypertension. People that have crecleroderma, they don't usually have fibrolyclone disease, but they directly fight brosial pulmonary arteries, right?

And then don't forget that sclerodosis can also cause pulmonary hypertension, because sclerodosis can cause restrictive lung disease, right? And then don't forget that idiopathic pulmonary fibrosis, IPF, right? That's classically going to be an old guy, usually in like his 60s or older under USML Es, right? And it's going to have like, Bisila predominant fibrosis. You're going to hear like these fine crackles kind of sounds like velcro. Uh, actually had a patient pretty recently that had this, um, um, IPF, right? IPF, IPF, IPF, right? It's Bisila predominant. I remember another Bisila predominant thing that can cause restrictive lung disease and pulmonary hypertension is that's best stosis, right? On like most other pneumoconiosis, because remember, your pneumoconiosis, your pneumoconiosis can all lead to pulmonary hypertension, right? You can all lead to pulmonary hypertension, but, um, most pneumoconiosis, they affect the IPF, AP Cs of the lungs, the top of the lungs versus, uh, as best stosis that tends to affect the base of the lungs, right? That anatomical distinction is pretty high, you to know for your, for your exams. All right. Now, what if they give you a question about a patient and they tell you that this patient, um, you know, uh, you know, had a renal transplant a few months ago, and has been on a immunosuppression, has been doing pretty well, but that he has been noticing, uh, like a disfigurement in his, in his mouth, right?

And then they show you a picture on the exams and you notice that the gums have like these abnormal growth patterns. Uh, what, what should you be thinking about on your exams? I would really hope you're saying, ooh, divine. This sounds a lot like a gingival hyperplasia with, uh, with cyclosporing, right? Remember, cyclosporing is an immunosuppression, right? We, we use it as, uh, immunosuppression in people that have had, people that have had a transplant, right? So cyclosporing can absolutely cause gingival, uh, hyperplasia, right? So if they show you a picture and you see like just an abnormal growth of a person's, uh, gums, you really want to think about the gingival issues caused by cyclosporing. Now, is there another drug that can cause a kind of similar issues with the gingiver? I'd hope you're thinking about fanny, what fanny to win, fanny to win, fanny to win, fanny to win, fanny to win. All right. Now, what if they give you, uh, question on your exams and they give you a pedigree, right? Like a genetic pedigree. And you notice that in this pedigree, you have a woman and all her kids seem to, uh, so you have a woman that's affected with a disorder. And then all her kids, uh, seem to have that same problem. Uh, and they ask you about the pattern of inheritance, right? And then they put all these answers or the Zomo dominant or the Zomo recessive yada yada yada. Uh, you want to pick the answer that says mitochondrial inheritance.

You want to pick the answer that says mitochondrial inheritance, right? Remember, uh, these mitochondrial disorders, uh, the, the tend to be passed on from mom to all her offspring. Why is that? Because you get all your mitochondria from mom. Um, you don't get any mitochondria from that, right? And these mitochondrial disorders, right? There, there's a bunch that they love to test on the exams. They, they have all these very exotic names, right? So they have like one is called a melas. Uh, I think it's like metabolic and my mitochondria is a phyloopathy, uh, with lactic acidosis and a stroke like episodes that's melas, M-E-L-E-S. There's another one called Merf, um, you know, the R-R-F. I believe stands for ragged red fibers, um, Merf, M-E-R-R-F. And then there's another one called L-H-O-N, uh, Libre Hereditri optic neuropathy, right? The key things to know about these mitochondrial disorders is the number one. They are associated with ragged red fibers, right? So they can either show you a photo of ragged red fibers, so that's something I want to be able to register in your mind for your exams. Or they can tell you that, oh, they did a muscle biopsy and they saw ragged red fibers, right? They saw ragged red fibers, right? And many times these people that have these disorders, they tend to have lactic acidosis, right? Because you may be wondering, divine, why is it that when I, when a person has a mitochondrial disorder, they tend to have lactic acidosis.

It's actually not like a random thing. The thing is, if you remember, your mitochondria is like the energy powerhouse of the cell, right? So what exactly does the mitochondria do? The mitochondria, um, it does oxidative phosphorylation, helps you generate ATP, right? But if you have a mitochondrial disorder and your mitochondria is not working, you cannot do oxidative phosphorylation. If you cannot do oxidative phosphorylation, you have to depend on glycolysis as your cellular source of energy. If glycolysis is your cellular source of energy, let me ask you this, what is the end product of glycolysis? The end product of glycolysis is lactic acid, right? Because that pyruvate, you remember pyruvate can be converted by LDH, by lactic dehydrogenase to lactic acid, right? So those people, they are depending more on glycolysis for energy, that's why they have that lactic acidosis, okay? It's actually pretty high up to no, those things for your, for your exams. All right, now what if they give you a question about a patient? And they tell you that this patient has, you know, this patient, you know, when they were born, they tell you that they were born with like limb issues, right? And they tell you that this child was like drooling with breastfeeding. And then they ask you which of the following diagnostic tests or screening tests should be performed in this child after stabilization?

I would really hope you're picking the answer that talks about to get like an echocardiogram and to get like a renal ultrasound, right? So what does this child have? This child has a vector, right? This child has a vector issue, right? This child has a vector issue. The thing is, these vector disorders, the way they love to test them on the USML is that they will give you a vector of finding in the Q stem, like one or two of those. And then the right answer will be another vector of finding, right? But let's kind of dig into this. So what in the world do I mean by vector? Well, the V stands for vertebral problems, the A stands for anal problems, the C stands for cardiac problems, right? That's why you're going to be getting an echocardiogram. And then the T stands for a T E fist shell with a syphagyletrija. That's why the child was a drooling, right? Because remember, the syphagos basically ends in a blind pouch, right? So if they try to breastfeed, like, where's the breast milk going to go? Right? And then the R stands for renal problems, and then the L stands for limb defects, right? So those renal problems, because think about it of all those organs that are messed up, which ones are going to have the most dangerous consequences for the child? It's going to be the kidneys and the heart, right? Those organs are kind of important, right? So it makes sense that you should get an echocardiogram, but you should also get a renal ultrasound in that circumstance, okay?

That's pretty high yield to know for your exams. And then what if they give you a question about a patient? And this patient has like showering syndrome. And then you're asked which of the following pharmacotherapies is indicated in this patient? Well, I would really hope that you're thinking of things like artificial tears, right? Because they have dry eyes. But also you want to consider a mascarinic agonist like pylocarpin, pylocarpin, pylocarpin, pylocarpin, pylocarpin, right? Pylocarpin is a mascarinic agonist. It's going to help them, like, you know, it's going to stimulate their glands to like mix stuff, okay? So they don't have that dry mouth. They don't have that dry mouth. All right. Now, what if they give you a question about a patient that is placed on an acenhibitor, right? An acenhibitor. And then you're asked what is, and they give you like our questions, right? And they say, oh, which of the following is the effect on, like, preload and afterload? This is the last thing I think I'm going to talk about today. But remember, acenhibitors, right? They're diuretics literally, right? So they basically make you lose fluid. If you're losing fluid from the body because they're diuretics, that's obviously going to reduce your preload, right? That's obviously, obviously, obviously going to do what is going to reduce your preload. That's pretty high yield to know for your exams. Okay, that's number one.

Number two is that they're going to reduce your afterload as well, because they are very potent visual dilators. Why the potent visual dilators? Actually, for two reasons. Number one is that an acenhibitor decreases the conversion of angeotencing one to angeotencing two. Angeotencing two is a very, very potent visual constructor. So if you're inhibiting ACE, you're not going to be making angeotencing two. You're not going to be making a visual constructor. So you're going to get visual dilation. As you dilate your systemic vessels, that's going to reduce your afterload, right? Now, another thing that also explains the reduction in afterload with acenhibitors is that by taking an acenhibitor, your levels of bradykining in the body are going to rise. Remember, bradykining is what causes that dry cough with acenhibitors, right? And bradykining is broken down by ACE. So if you're taking an acenhibitor, your bradykining is going to rise. But this is one thing that many resources basically don't cover, but it's actually very, very high yield to know for the USML exams. Bradykining is actually a very good visual dilator. It's actually a very good visual dilator. So that actually explains part of the blood pressure lower in effect of acenhibitors. Because of that rise in bradykining, you pretty much have a rise in a visual dilator and a drop in a visual constructor. In this case, the visual dilator is bradykining. In this case, the visual constructor is angeotencing two, right?

That explains the blood, that explains part of the blood pressure lower in effect, associated with ACE inhibitors. Right. So thank you for joining me in this podcast. Again, I hope you find this podcast to be helpful. Again, if you love the way I teach, you love the way I integrate basic sciences. You love the way I teach material. I think you really love my classes. I'm actually today, I have a 20-hour step, two-step three-class that's starting over Zoom. Many people have taken these classes and done really well. I literally have literally had emails from people that took this class very recently, like within the last, like I'll say, like, probably like six to eight weeks. And these people have gotten like 250's on the exams, 260's on the exams. And they're like, divine, I never had scores this high in any of my practice tests. What I did this well on my test. Right. So the class is four hours every day from Monday to day to Friday. Right. Many people have taken those classes, found them to be extremely helpful. Right. So shoot me an email if you're interested. I can give you some more information. And then in the month of August, I have a test-taking strategy class for step one to three, a bio-statistic class for step one to three, that's four hours long. And then I have a social sciences, ethics, quality improvement, and healthcare systems class. That's five hours long, that's for step one to three.

And then I also have a last minute review for step two and step three that is three hours long. Again, many people have taken these classes, found them to be extremely helpful. Right. And then I also offer one or one tutoring for the USML and Conlex exams. And I also help with ERAS applications, you know, mock interviews, personal statements, editing these things, and kind of preparing your application really well, so that you can have very good impact with your residency application cycle. And then I have this podcast on Apple Google and Spotify, so check those out. I also have a You Tube channel where I post the videos that I make. And then finally, I have another website titled divineinterventionlifelessons.com. Divineinterventionlifelessons.com. Basically every week, I post like one or two podcasts. I'm pretty sure I have like 352 episodes on there right now. Where, you know, from a biblical perspective, I address a life lesson. Or I kind of break down script or really break down the Bible. So if you're interested, you can check that out. Divineinterventionlifelessons.com. There's an Apple podcast associated with that, called the Divine Intervention Life Lessons Podcast. So thank you for listening to me today. I will see you God willing episode 613, I believe. No, no, no, no, 613, I've gone past 613, 617, right? So have a wonderful day. God bless you and I'll bye for now. Thank you.

Failure of olfactory nerve (CN I) and GNRH-producing neurons to migrate properly, leading to anosmia and hypogonadotropic hypogonadism.

Cranial Nerve II (Optic Nerve). All others are peripheral.

When shining light into the affected eye, both pupils will fail to constrict because the signal from the optic nerve cannot reach the midbrain.

A lateral brainstem stroke (affecting CN V fibers). The sensory pathways for pain/temperature travel in the lateral brainstem.

Aminoglycosides (e.g., gentamicin), Loop diuretics, and Vancomycin.

Ipsilateral CN VI palsy (due to location) AND contralateral corticospinal tract signs (because the tracts run medially).

The cerebellar convexities.

Trigeminal Nerve (CN V).

Because the mitochondria are failing to perform oxidative phosphorylation, forcing the cell to rely on glycolysis, which produces lactic acid.

INO causes impaired adduction/gaze deficits but preserves accommodation; CN III palsy affects both pupil constriction and gaze.

Eisenmenger Syndrome (or "Eisenmanger's").

Gingival hyperplasia.

Internuclear ophthalmoplegia (INO).

The cerebellar convexities.

Trigeminal Nerve (CN V).

Because the mitochondria are failing to perform oxidative phosphorylation, forcing the cell to rely on glycolysis, which produces lactic acid.

INO causes impaired adduction/gaze deficits but preserves accommodation; CN III palsy affects both pupil constriction and gaze.

Eisenmenger Syndrome (or "Eisenmanger's").

Gingival hyperplasia.

Internuclear ophthalmoplegia (INO).