DIP Episode 125 - USMLE Step 2CK Rapid Review Series 6 (IM)

Okay, welcome. My name is Divine. I am a resident and this will be episode 125 of the Divine Intervention Podcast. In this podcast, I'll be continuing my rapid review series for the USML Step 2 CK exam. This will be series 6 and I'm going to be focusing strictly on internal medicine with this podcast because again, internal medicine is the bulk of the exam. So let's get going. Okay, so let's assume you get a question about a patient and this patient, you know, over the last three days, they've been having like mental status changes. Let's say it's like maybe like a young person or something, like mental status changes, they've been having, you know, they've, I don't know, they're just kind of weird, like they're, they're close acquaintances, like, this is, this is not him, right? Like mental status changes, the person is kind of like, up-tunded and the person is not an alcoholic, right? And then they show you like, they tell you okay that you obtain like a CSF studies, right? And in that CSF study, you see like a ton of red blood cells. What are you thinking about? I really, really hope that under those circumstances, you're thinking about her piece, right? Like HSV and Sephalitis, right? So remember, HSV, right? It likes to cause, like, classically on NBM is it presents in multiple different ways, right? So it can present us like, and Sephalitis, or meningitis, and a newborn, right?

And again, classically, when you do CSF studies, you notice that they're very high levels of red blood cells in the CSF, although you kind of want to be careful there, right? So HSV, the problem will be more like, oh, over the past 24 hours, over the past, I don't know like 48 hours, this person has been out of it, versus a subarachnoid hemorrhage that can also present in a somewhat, I mean, I've seen NBM questions at the right in very similar ways where the person has like a subarachnoid hemorrhage and become with no core rigidity, right? Don't be tricked. A person that has a subarachnoid hemorrhage, it'll be something that probably started like two or three hours ago, right? It will look like meningitis, but it started two or three hours ago. That'll be the clue that, you know what, maybe this is not, maybe this is not necessarily meningitis, right? Because again, HSV and subarachnoid hemorrhage, those are two high-ill things. In fact, there are probably the two, like, only two things, other than a, like a bloody CSF tap that can cause elevated red blood cells from a lumbar, puncture on an NBM exam. So those are sort of kind of high-ill things you want to keep at the back of your mind for tests, okay? And remember that HSV, right? What does some other classic things HSV can do, right? So HSV, right, can cause like encephalitis in the, in the temporal lobes.

So if, again, if you're describing a person that has encephalitis and they come with like a seizure presentation, right? Or they have issues in the temporal lobes, so they show you like something, like anything that relates in any way shape or form to the temporal lobe or an NBM exam, that should really get you thinking about temporal lobe at encephalitis from HSV, okay? Now, remember another high-ill temporal lobe relationship you want to keep in mind for example is that most seizures, right? Most seizures start in the temporal lobe, okay? So on EEG, there are specific patterns that neurologists can actually identify, not sure them, oh, yeah, this seizure is coming from the temporal lobe, okay? So that's something else you want to keep at the back of your mind. And then remember that the medial temporal lobe, okay? If you have like increasing trachranial pressure from, I don't know, like a brain bleed or something, and you have high intracranial pressures, as pressure is building up, the medial part of your temporal lobe known as the ancus can hurt you, right? That's the thing that's known as the trans-tentorial herniation, and that can compress crinion or three, right? So those people will have like classically, they'll have like a down and out eye, right?

Because when you compress crinion or three, you'll essentially have function left with, I mean, like you'll essentially have the remaining crinioners that innervide the extracurricular muscles of the eye, acting on a post, right? So for example, those people will have like a down and out eye. So why does the down and out eye happen? Remember, essentially every extracurricular muscle is innervide by criniol-3 with the exception of superior bleak, which is done by criniol-4, that's your trachranial nerve, and lateral rectus, which is done by the abducent's nerve, which is crinion-6. So if the abducent's nerve is working on a post, the presence I would deviate out, right? Because your lateral rectus muscle AB ducts the eye, right? And then the eye will go down because remember the superior bleak muscle, its job is to depress the eye, right? The eyelid, I mean the eye bone, right? So those people's eyes are depressed, right? So that's why their eyes are down and out. And they will also classically have a blown pupil, right? The reason they have that blown pupil is, again, remember that crinion-3, right? Through this whole business with the edinja-s-4 nucleus, carries the fibers, like the parasympathetic fibers that deal with your eye, right? And remember your parasympathetic system causes meiosis. So if, again, you've compressed crinion-3 and you've knocked out its parasympathetic function, then the sympathetic function to the eye will act on a post.

And if that sympathetic function is acting on a post, you'll have a mitriasis, okay? So those are classic findings in a trans-tentoral herniation. And another thing you may find in a trans-tentoral herniation is the person who have like Ipsilateral upper motor neuron symptoms, because there is this thing known as a kernel-hands phenomenon where when you have like a trans-tentoral herniation, you'll compress, you compress the, like the midbrain. And when you compress the midbrain, like there is some, this is something that I can not necessarily explain right now is something I'll probably explain in a different podcast, maybe more for people that are taking a step one. But basically, you can compress the contralateral cerebral peduncle. And if you compress the contralateral cerebral peduncle, remember cerebral peduncles are found in the midbrain, right? So let's say you have like a herniation of your left temporal lobe, right? A trans-tentoral herniation of your left temporal lobe. You will compress your right cerebral peduncle. When you compress your right cerebral peduncle, remember that your cerebral peduncle has a lot of your cortical spinal tract fibers. So if you're compressing those, remember your cortical spinal tract dequeusetes at the level of the medallary pyramids, right?

So those fibers in the right cerebral peduncle, they will cross to the left side at the level of the medallary pyramids, and then they will go and innervate muscles on the left side of the body, right? So you'll notice that the person will have opamuronuron symptoms that are epsilonateral to the side where they have the on-call herniation. That is something that is floridly high you to know for NBM exams. Okay, so again, I know I sort of started on her piece, but I kind of ended at a trans-tentoral herniation. But again, this review is designed to be integrative. And then what if you get a question about a person that works in a prison or like a TSA agent or a person that has what is it called? A person that I don't know like is like an ivy drug user of some sort, and then they tell you that this person, you know, over the past two weeks, they've been losing weight, they've been having night sweats, they've been, they've been having like hemoptuses and all that stuff. And then let's say they show you like some kind of chest extra or some CT scan, some kind of lung imaging. And you're finding like hyalur adenopathy and you're finding like white around like the one of the upper lobes, like a cavitory lesion potentially in the upper lobes. What are you thinking about? I really hope you're thinking about TB, okay, TB, right? So remember TB, right? Again, if you're a person that works in like a public environment, right?

So like, oh, a person that works with prisoners or a person that works at an airport, for example, right? Or a person that has risky behaviors that could give them HIV, like being an ivy drug user, those are all things that can essentially have, those are all things that have associations with TB on NV Me exams, right? And again, if a person has TB, right, how do you make the diagnosis, right? Usually on an NV Me, the first thing you do is you do like, I mean, obviously, if a person has like the classic symptoms, like the, what is it called? The hemoptuses might sweat, weight loss. And you have a very high-sauce, especially when it's an immigrant, remember, immigrants also get TB quite frequently on NV Me exams. If you see all those things, right? Usually you want to like get the sputum and do like cereal acid fast stints, right? But let's assume like, oh, on an NV Me exam, you suspect it like an an outpatient or whatever, you can do like a TB skin test, right? You can do a TB skin test, you will find the inspiration and hopefully you remember like the intuitive values, right, for different people, right? So like, if your inspiration is more than 15 millimeters, you have TB. It doesn't matter what you have, whether you're healthy on healthy or whatever, it doesn't matter. You have TB for sure. But if you're like HIV patient or like an IV drug user, the cutoff for those people is five millimeters, okay? It's five millimeters.

And then if, for example, you're a healthcare worker, right? So like your resident, your physician or whatever, then the cutoff value is 10 millimeters, okay? So those are all things you kind of need to keep at the back of your mind. And if you have a positive PPD skin test, what is always your next step? You want to make sure you go ahead and get a chest X-ray, right? Because if you see active lesions on a chest X-ray, that tells you you have like raging bad TB, right? Like active TB that needs to be treated or if you have a negative chest X-ray, that tells you that you have latent TB, right? And how do we treat latent TB? We treat latent TB with isoniasid for how many months? For nine months, right? Treat it with isoniasid for nine months. And in addition to that, what's the vitamin you try to supplement? I really hope you're telling me vitamin B6, right? Remember vitamin B6 is also known as pyridoxin or pyridoxophosphate. So by giving that vitamin, you prevent the neuropathy that is associated with a person taking isoniasid. Because remember, isoniasid depletes your levels of vitamin B6. And if you deplete vitamin B6, there are certain high-yield enzymes in the body that stop working. One classic one is glutamate decarboxylase. Remember glutamate decarboxylase? Converts glutamate to GABA. So if and it uses vitamin B6 as a cofactor. So if you deplete B6 because you're taking isoniasid and you decide to not listen to your your physician, right?

You deplete your B6 glutamate decarboxylase doesn't work. So you have decreased conversion of glutamate to GABA, okay? So your glutamate will build up and with that in mind, you will have seizures, right? Because remember glutamate is an excitatory neurotransmitter versus GABA that is an inhibitory neurotransmitter. Now another enzyme that may not necessarily work as well is elicinthase, right? So delta amino levelinica sedacinthase. Remember that is the rate limiting enzyme. I mean many people know it as alas. That is the rate limiting enzyme in the synthesis of hym, okay? So remember that enzyme uses vitamin B6 as a cofactor. It's like it takes B6 as a cofactor and then maries, succino-coe and glycine and then boom, you have this happy marriage and you make a delta amino levelinica sed. So if again you're taking isoniasid without listening to your physician, your B6 pool is depleted, right? You won't be able to make him and you'll get a acetyroblastic anemia, okay? That's actually the mechanism behind acetyroblastic anemia being something that happens in people that take isoniasid. And then kind of as a throwback to step one that can show us like a bizarre question on NVME exams. Remember that isoniasid can cause drug induced lupus, right? So don't forget that association with your antihistona antibodies. And then you also kind of want to keep at the back of your mind that isoniasid, right?

Like you can get like it has this relationship with like the slow and fast acid later business. So they may present it to you as a bimodal curve on an NVME exam, okay? Like people that metabolize isoniasid differently. They're slow acid later, they're fast acid later, right? And again, if a person has lethal TB nine months of isoniasid plus vitamin B6, if a person has active TB, right? You'll treat them for six months. But the first two months you give them the right regimen, right? So the right regimen is like right fan pin, right? Isoniasid, pyrazinamide and ethanbuton, right? And then again you also take vitamin B6. And again, it's kind of high you to know some key things with those drugs. We'll try to talk about those. Remember you use ripe for two months and then you use rye for four months, right? So the first two months of your six months of therapy, you use the right regimen plus vitamin B6. And then the last four months you use rye, so rye fan pin and isoniasid plus B6 for the remaining four months to make up six months total. Now, the thing is, so that's for active TB versus lethal TB, where it's nine months of isoniasid plus vitamin B6. Now here's the deal. Rye fan pin, what's what are the key toxicities with rye fan pin? Well, I hope you're telling me like a hepato toxicity, right? Remember, rye fan pin is basically more, essentially all the TB drugs for the most part if you want to remember fewer things. Most of the TB drugs are hepato toxic.

So rye fan pin is hepato toxic and remember it also causes like orange secretions, orange tears, orange vaginal fluid, orange urine and all that crap, right? And then you should remember that rye fan pin on MBM is can actually be used to treat leprosy, right? Leprosy, there's like, it's almost like triple therapy for leprosy. You can remember with the nomonic DRC, right? So the D stands for Dapsum, the r stands for rye fan pin and then the C stands for Clophazemine. Okay, those are those three drugs I used to treat the mycobacterium leprosy. And then remember if a person is a close contact of some dude or some lady that has a nice sermon in Giddis, right? If you're a close contact, you can profile likes that close contact person with rye fan pin. Remember, there are three drugs you can use on that those circumstances. You can use rye fan pin or you can use safe triaxone or you can use super floxacin, right? But I mean, you've heard me say this at Nosem and multiple podcasts. The preferred agent is rye fan pin. However, if it's a patient that is pregnant, right? Remember, rye fan pin is a teradogen and remember that super floxacin is also a teradogen, right? It can cause like tendon problems in the fetus. So under those circumstances, if you have a pregnant patient, the drug of choice for close contact preferixis for nice sermon in Giddis is a safe triaxone. Remember, safe triaxone is a third generation of cephalospory. Now, isoniasid, right? I already talked about it.

Isoniasid is nephrotoxic, right? I mean, it's neurotoxics or neurotoxic that peripheral neuropathy. And it's also hepato toxic. And again, I've sort of talked about the neurotoxicity with the seizures, right? And an easy way to remember that maybe like divine, this is so much detail. How do I remember all this? Just remember many people know the symbol of for isoniasid. It's I-N-H, right? So remember that I mean isoniasid, the N meaning neurotoxic and the H meaning hepato toxic. So isoniasid is neurotoxic and hepato toxic. And then remember, pierazinamide, I'm just going to let that go. They don't really test the side effects of those. And then a thambutal, remember, it can cause vision problems, right? It can cause like a certain kind of a color blindness, okay? So those are things to keep in mind. And then before I sign off here with TB, remember, TB can also cause problems in the vertebral bodies, right? That's what's known as POTS disease, right? And if they tell you that a person has meningitis and they have enhancement at the base of the brain, very high your enhancement, at the base of the brain, also think about TB under those circumstances, right? And remember that if a person has TB, right? TB will cause if you're looking at like CSF in a person that has TB, the CSF studies of a person that has TB, right? You'll see like elevations in the the persons like lymphocytes, okay? Even if TB is a bacterial infection, you have a response with lymphocytes.

So you have like an velet lymphocytes, an velet protein, decreased glucose, the works, okay? And you have high CSF opening pressures. Those are very high your things to know, right? And remember, having a negative TB skin test does not rule out TB, right? Having a negative TB skin test does not rule out TB. Remember, people, there are certain people that can have false negative TB skin tests, right? So people with sarcoidosis, for example, can have false negative TB skin tests. People with HIV, can have false negative TB skin tests. People that are on steroids, people that are immunosuppressed, they can have false negative TB skin tests. So if you have the right clinical suspicion on an MDME or even in the real world, and the TB skin test is negative, that absolutely positively does not rule out TB, okay? That's a very high your thing you want to keep in mind for the MDME exams. Okay, now what if you get a question about a person that has, let's say, let's see, kind of question, can I make up here? Okay, so what if you get a question about a patient? And this patient, they tell you that they have these like, sores, under their, like their armpits, right? So like, I guess I shouldn't use the word armpit, I'm a physician. So let me use the more appropriate medical term, axilla, right? So a person has sores and all that crap under their axilla, right? And it's like a chronic problem. It hurts those things hurt a ton. What's your diagnosis? That is what?

That's hydrodynamitis superativa, right? That's hydrodynamitis superativa. And what is the kind of gland that is inflamed in hydrodynamitis superativa? Those are your epocrine glands, okay? Again, very high you to know those, those are epocrine glands. Contrast this with your sebaceous glands, right? That are inflamed in acne, okay? And remember those hydrodynamitis is really no good treatment, right? Those people really need to, that's why you see hydrodynamitis show up a lot on surgery shelf exams. It's a surgical problem. It's something that you fix by literally chopping out all those, all those abscesses and stuff. So surgical treatment is what you do for hydrodynamitis superativa. Okay, now what if you get a question about a patient, you know, let's say they are obtundate, like they have some risk factor that we make them obtundate. So let's say they have alcoholics, for example, right? Or let's say it's like an old person falls down, cannot get up. And then you tell you that this person's creatinine is now very high. What are you thinking about? I really hope you're thinking about a ruptum, right? ruptomyolosis. Again, if you notice, I've probably mentioned the diagnosis ruptomyolosis in like maybe like 10 or 15 different podcasts that I've made over the life of my website. The reason I say it is ruptomyolosis shows pretty much any notable NV Me based exam that you ever take. And for whatever bizarre reason, people still get rubbed, or questions wrong all the time.

So rubbed though is very high yield. It would just be a person that has some risk factor for being obtundate. Alcoholic, it's almost always an alcoholic on NV Me's. But it can be a person that again, old person falls down, cannot get up. Or it can be a person that just run a marathon, right? Or it can be a person that has like a injury from trauma. Those things all cause ruptomyolosis, right? Well, why you're worried with ruptomyol? The reason you're worried with ruptomyol is that it can torture kidneys, right? It can be a cause of AT&T. It can cause acute blood and crosses. And usually in an NV Me question, the person has ruptomyol, right? Classically, they will show you that, oh, when you look at this person's urine, you see like three or four plus blood, like some ridiculous amounts of blood on dipstick, on dipstick, right? But when you do my crispy, like, man, I'm seeing only one or two red blood cells. What's up with that? If you see that, right? So like, urine that is positive for blood by dipstick, but is negative for red blood cells. When you see that on microscopy, or you see like very few red blood cells on microscopy, that's pathonomonic for ruptomyolosis on an NV Me exam. Okay? And again, how do you treat ruptomyol? Right? You fluids, fluids, fluids. Give people a crap ton of fluids. I mean, these people can get up to like a liter of like normal ceiling every four hours. Okay?

To tell you how bad ruptomyol can be, you're trying to wash out that myoglobin from the urinary tract. And then remember that ruptol, right? Or your friends at the NV Me, occasionally love to test some electrolyte abnormalities that you may find in a patient with ruptol, right? So those people could have like hypocaucinia. Remember, those dead muscles can sequester that calcium. So that can present us like a prolonged cutie interval in an NV Me question. Those people can also get hyperkalemia. Remember, your sodium potassium ATP is pump puts three sodiums outside of cells and puts two potassiums into cells, right? So potassium is primarily an intracellular ion. So if your muscle cells explode, they release their cells into the surroundings that can cause a hyperkalemia. Or can remember that can manifest on an EKG as like picked T-wave, so topic T-waves, white carous complexes. If the cake continues to rise, right? They will have like the sine wave EKG. And then after that, they will work into like isisterly, right? Like a flatline. So hopefully remember from my medicine reviews where I talk about, oh, doing things like calcium glucone, right, to stabilize the myocardium, or doing things like insulin with glucose, right? To lower the apotassium, or doing things like a butyl, better to agonist, to help with lowering the apotassium, or inducing an alkylosis, right?

Like given sodium by carbon, remember, if you induce an alkylosis that will pull hydrogen out of the ions out of cells, and potassium will go in reverse, right? Or you can do things like diuresis with ferozomite. Remember ferozomite is a loop diuretic, loops cause hypochylemia as a side effect. So that can help you give those patients fluids, and then you diurest them at the same time with ferozomite. That will help them get rid of, get rid of that excess potassium. And then another thing you can do is you can give Kx, remember Kx, make K, exit out of your body, okay? So those are all things you can do for for hypochylemia, again, very high eotein, on exams. And then remember there is another, there is a drug overdose that can present as white QRS complexes on an envy and me. What drug overdose am I going after here? Kind of looks like hyperchylemia. Think about a like cyclist, let's assume it's a cyclist question. That will be a TCA, right? That will be a tricyclic antidepressant. Okay, good. So, so I guess let's go ahead and move on. So let me maybe talk about one more case, cause I want to keep this on there 30 minutes. Let's see. I guess what if you get a question about, I'll make this an easy question because it's like a big general concept I want to talk about. So what if you get a question about a person that you know has a pretty, you know, significant allergy history, right?

And then they tell you that they have like, you know, episodic like wheezing and all that crap. What are you thinking about? That's asthma, right? Asthma is what type of hypersensitivity reaction? It's a type one hypersensitivity reaction, right? And remember your type one hypersensitivity reactions. Basically the thing that happens is you get that first exposure to like some antigen and then your body is like, ooh, okay, your antigen presenting cells like your B cells microphygies, they pick that up, they presented to T cells, you have this whole weirdness with class switching that happens. So maybe like interlooking for sort of like hot sway and your class switch from like IGM to IGE, right? And then that IGE just lies in weight on the surfaces of like your xenophiles, your muscles and stuff like that. And then when you have the second exposure to the antigen, right? That antigen binds to those IG Es. You have cross linking of the constant regions and boom, everything gets bad, right? You begin to have like whizzing and all that crap, right? So that's the pathophysiology behind type one hypersensitivity reactions. Those things arise, they are meditated by IGE, muscles and your xenophiles, okay? And classic examples of those things that things like asthma, right? Asthma is a classic one, allergies, right? Any kind of allergy, right? Even like on medicine and BN is for whatever is in the love, like allergic bronchopomoneary aspergillosis, right?

Those things can all present as a type one hypersensitivity reactions. Another thing that can also remember, I love your bronchopomoneary aspergillosis, right? You may see like a fungus ball in the lung. In fact, sometimes those fungus balls look like lung cancer. So usually you want to like biopsy those things, right? Just to make sure that it's not cancer because you don't have like some crystal ball that tells you, oh, you know what? This is a fungus ball. This is aspergillosis. No, you really can make that chorus. So you still need to biopsy those things. And then, so that's something you want to keep at the back of your mind on exams. And then if you're thinking about like a type two hypersensitivity reaction, right? So you're thinking about making antibody. So it's like B cell meditated, antibody meditated. You're making antibodies against fixed antigens, like, like you're almost always making antibodies against like a cell type in your body. So take for example, if you make antibodies against your red blood cells, so like an autoimmune hemolytic anemia, that's an example of a type two hypersensitivity reaction. Or if you make antibodies against like GP2 B3 A, like an ITP, that's an example of a type two hypersensitivity reaction. Notice you're making antibodies against cells, okay? Or if you make antibodies against like your your follicular cells, right? Like antibodies like stimulating antibodies against like the follicular cells of your thyroid gland, right?

Like the TSH receptor, Graves disease, that's an example of a type two hypersensitivity reaction. Now, type three, right? Those are your antigen antibody complexes, right? So, classically, you're thinking about things like, um, uh, command of I think you're thinking about things like, like the nephritic syndrome, right? Like post-traptococcal, post-infectious glomerulina fritis, right? You form an antigen antibody complex, I kind of think of it as like two people partner of together, they show up somewhere, the red havoc, right? So same thing here. Antigen antibody complex, they go like they show up in places like your joints, your kidneys and stuff like that. And then remember, that antibody part, especially like if it's like IgM or IgG, those things can activate the classic complement cascade. So you have all this inflammation and then you destroy stuff, okay? Those are your type three hypersensitivity reactions. And then you type four hypersensitivity reactions, right? Those are classically things like, um, um, those are things like, I mean, it's called like your delayed type hypersensitivity reaction. So like contact dermatitis, poison ivy, right? The delayed TB skin test, right? Those are all examples of type four hypersensitivity reactions. And those for the most part are mediated by like your T cells and macrophages, okay? It's a delayed type hypersensitivity reaction, right? So again, those are all like key, high-yield examples.

Those are, so those are all examples of your hypersensitivity reactions, right? So again, keep those things at the back of your mind. I mean, like, I mean, another weird one that you love to test on NBM is it's like, say for example, a person has like a hypersensitivity pneumonitis, right? That's actually an example of a type three hypersensitivity reaction, right? So if for example you get a question about a person that has like, you know, like has birds or is a farmer, like a, like you probably remember this as like bird fancier as long, right? Those things can, because think about it, you're making antibodies against like a particular antigen. The antigen is the stuff, the organic whatever that you inhale, right? Like bird poop, bird's equations, whatever, okay? Hyper-sensitivity pneumonitis is an example of a type three hypersensitivity reaction. It arises in the setting of like an antigen antibody complex, right? And I remember, hopefully I really, really do hope that you remember that those are hypersensitivity pneumonitis are associated with like a thermophilic atinomysites, okay? That's a very high yield factor, you want to lock in your brain for NV Me exams, right? And I mean, you can also, I mean, you can arise from like many people are like used to like, oh, I'm exposed to a bird or whatever, I mean a barn or whatever. And this causes hypersensitivity pneumonitis. That's not the only thing that can cause it, right?

It can happen in a question that almost looks like legionella, right? So they may describe a person that is like close to like a warm spring or a hot tub or something, right? And then they tell you that this person seems to have like episodic symptoms. It's like, oh, they have exposure to this thing, they come back, they have like this thing that writes for like a couple of days, like they're like, ah, I have cough, I have wheezing, you listen to their lungs, you're hearing like what looks like almost like a fibroidic lung disease. If you see those things, also think about hypersensitivity pneumonitis, okay, because the thing is they will have exposure to something and then they will have like episodic lung symptoms. That's the thing that will lead you towards, um, hypersensitivity pneumonitis as your diagnosis on an NV Me. And I don't know since I mentioned the word hot tub. So hot tub seems to be a hot topic, these, these on NV Me exams, right? So the thing is basically there are three things that you can test with hot tops on an NV Me. One is hypersensitivity pneumonitis, right? Like again, exposure to hot tops, episodic, very high of notice, I keep saying episodic, episodic, episodic. I'm not saying it because I love to see the word episodic, I'm saying it because it's very high to know for examples. Episodic symptoms think about hypersensitivity pneumonitis, think about your thermophilic actinomycetes.

But another thing that may present in the context of a hot tub is something called hot tub lung, right? So classically, this would be a question about a person. It's usually like a female on NV Me's and they will tell you that if I'd like just me and they just have like chronic, like low level infection for like three weeks, like low level lung infection for like three weeks and maybe they begin to be even exposed to like hot tops. If you see that think about like Mac, like micro bacterial bacterium, avium, intracellularity or like the micro bacterial avium complex, those things are associated with hot tops and they tend to cause like long standing pulmonary infection. And the thing is it's almost always in a female and here is one telltale sign that you are likely dealing with hot tub lung from micro bacterial, avium on an exam. They will classically put it in a patient that is not immunocompromised, okay? Yes, you can shop in patients with HIV, but that would not be the, that would usually not be the patient demographic. You would see on an NV Me exam. And then the final thing that relates to hot tops on NV Me is if you see a person that uses hot tops a lot and they have a rash, right? That's hot top folliculitis, right? That's, you should really be thinking about pseudomonas on that those are circumstances. So hot top folliculitis think about pseudomonas. And really, how do you treat hot top lung from my micro bacterium, avium, interesting lary? You give a macro lead, okay?

You give a macro lead. Remember, macro leads can prolong the acute interval, right? And remember that erythromycin, right? The macro lead, it's a motylene receptor agonist, right? So it can cause diarrhea as a side effect. You can actually use that side effect in the treatment of a diabetica gastroparesis, right? And remember that if you exposed to erythromycin in the first few weeks of life, that can increase your risk of hypertrophic, a pyloric stenosis, right? Where you see like a newborn, maybe like a firstborn male, who knows? With like non-bilias vomiden and like a papaboma in the epigastra, right? Those are the classic ways those things are present. So I feel like I have to, I have more things to say, but let's just go ahead and stop here. Again, this is supposed to be a rapid review. So I do hope you get a lot from this podcast as I do whenever I end every podcast. I do offer one or one tutoring for all the USMLA exams. Step one, two CK, two CK, step three. I've done this with thousands and thousands of people that have been very successful. And then if you're a college student and you need tutoring for like physics, Gen CAM, O-CAM, Bio CAM, histology, physiology, I do offer tutoring for all those things. And then if you're also like a medicine resident and you're preparing for like your internal medicine, in training exam or the internal medicine board exams, I do offer tutoring for those.

And then if you're a college student applying to a medical school, so like an AMCAZAP or a med student applying to residency, like an ERAS app, so like personal statements, preparing applications and all that stuff, I do offer like one on one advising for that. Again, I've worked with tons of people. And most of the people I worked with this past admission cycle, most of them actually matched at their first choices. Pretty much everyone I worked with matched into the specialty of their choosing. And I mean right now I'm working with tons of people that are applying with this current ERAS cycle. So if you need help with any of those things, reach out to me there through the website or you can send me a personal email to you can send an email to divine intervention podcasts, podcasts with an S at the end at gmail.com. So I wish you all the very best, have a wonderful rest of your day, God bless you, and I'll see you in the next podcast. Thank you.

"Down and out" eye, blown pupil (mydriasis), and ipsilateral upper motor neuron deficits.

Cranial Nerve VI (Abducens). If CN VI is compromised, the eye cannot abduct fully, leading to diplopia/strabismus.

R = Rifampin, I = Isoniazid, P = Pyrazinamide, E = Ethambutol.

Isoniazid depletes B6, which is necessary for the enzyme glutamate decarboxylase (GABA synthesis) and ALA synthase (heme synthesis).

Type I hypersensitivity reaction, mediated by IgE antibodies.

Microbacterium avium complex (MAC).

Healthy/Healthy: >15 mm; IV Drug User/HIV: 5 mm; Healthcare Worker: 10 mm.

Nine months of Isoniazid (INH).

Hepatotoxicity and neurotoxicity (seizures due to B6 depletion).

Positive dipstick blood, but few or no red blood cells seen on microscopy.

Type III hypersensitivity reaction.

Preferred: Rifampin (RIPE). Alternative for pregnancy: Ceftriaxone (safe triaxone) because rifampin/ceftriaxone are teratogens.

Healthy/Healthy: >15 mm; IV Drug User/HIV: 5 mm; Healthcare Worker: 10 mm.

Nine months of Isoniazid (INH).

Hepatotoxicity and neurotoxicity (seizures due to B6 depletion).

Positive dipstick blood, but few or no red blood cells seen on microscopy.

Type III hypersensitivity reaction.

Preferred: Rifampin (RIPE). Alternative for pregnancy: Ceftriaxone (safe triaxone) because rifampin/ceftriaxone are teratogens.