DIP Episode 199 - USMLE Step 2CK Rapid Review Series 29

Okay, welcome. My name is Divine. I'm a resident. This is episode 199 of the Divine Intervention Podcast. In today's podcast, I'm going to be continuing the rapid review series for the USM list of two CK exam. And this podcast is going to be relatively short and sweet. Although again, I feel like I've said that many times and then all these ideas keep popping in my head. And then ends up being long. But you know, try to be as a succinct as possible. So what if they give you a question about a patient, you know, and this is series 29, I believe, of the rapid review step to CK series. So these series 29, right? So what if they give you a question about a patient and you know, they tell you that this patient, you know, had some kind of problem that kept them in the hospital and they interpreted mechanically ventilated. What is the best kind of nutrition you'd want to explore for those kinds of people? Well, I would hope you're thinking of pursuing internal nutrition, right? Internal nutrition is much better than TPN, right? Basically, if a person's balls can move, right? You know, just go ahead and use their balls, right? So because the thing is, if you use a person's balls, there are certain things that that buys you. One thing that buys you is that it gives you the ability to, you know, keep your GI tract online so it keeps working. And there's also a lower risk of infection. I mean, think about it.

How many people have ever seen have an infection from like a feeding tube, right? But TPN, you know, usually is a problem. On TPN, you can give it through like a central line or you can give it through a peripheral line. Now, like, originally, maybe go with a central line. Although, again, TPN through a central line has a pretty high risk of infection, right? Like central line associated with bloodstream infections, right? So that's one very high thing. You want to keep at the back of your mind on tests, right? So again, internal nutrition is preferred, especially through a feeding tube. If that's not an option, right? Then you can give TPN or TPN, you typically give it through a central line. And it's actually very high, you know, for purposes of exams that TPN is associated with a very high risk of selenium deficiency. This was one of those weird bizarre things you never think about for exams. And then it ends up being in a very high, right? So TPN, selenium deficiency. And then another weird deficiency that can arise on the absurd circumstances on an endemic exam or a complex exam is they can give you a question about a person that has well-sensed disease. And then they tell you that, oh, this person is getting, this person is getting, you know, like a copriculator, you know, like triantine or like penicillamine. And then they tell you that this person has dysguzia and this person has alopecia and is having like impaired wound healing.

If you see that think about a zinc deficiency, the thing is when people have well-sensed disease, right? When people have well-sensed disease, they are not able to take, you essentially treat them with cop, like a copriculator, right? You give them a copriculator. Now the problem with those copriculators is they also have their, especially like triantine. So TRI, EN, TIN, triantine, it's a very powerful killer of zinc as well, right? So they can actually give you a nifty zinc deficiency question. And a person that has a history of well-sensed disease that's being treated, right? So again, very high-yield thing to keep at the back of your mind, for exams. And then don't forget, right? If people have a history of well-sensed disease, you cannot give them the copriode. That's one high-yield thing to know. And if people also have a history of like really bad bleeding, you also cannot give them the copriode. If people have a history of like forgetting to take the amends, you don't want to give them any kind of oral contraceptive option, right? If a person is postpartum, you don't want to give them any kind of estrogen-containing contraceptive option because they will reduce the amount of protein in their milk supply, right?

And then if a person has a history of, you know, the person doesn't want to get in with it and they want to return to fertility real quick, you don't want to give them like the implanted a medroxy-progesterone thingy that you put in the, put in the person's, like those medroxy-progesterone injections, yeah, those are not, you know, those are typically not not very ideal things for those things. And as a person has a history of osteoporosis as well, those injectable medroxy-progesterones, right? They are not good. So, history of osteoporosis doesn't want to gain weight, wants to return to fertility real quick, don't give the injectable medroxy-progesterone or whatever. And then if a person has a history of breast cancer, right? Basically, the only option is a copriode. You cannot give, because remember, many breast cancers are ERPR positive, right? So you don't want to give them anything that, like, even the myrina is not ideal in those people, right? And then if a person has a history of endometrial cancer again, you don't want to give them on a post-destrogen, that's probably a bad idea, probably gets sued if you did that. And then if a person has, if a person has like a recent history of a PID, or like some kind of like infection of the urinary, like of the, you know, like the pelvic vaginal tract, right? You don't want to give those people like an IUD, right? Because again, they can kind of run into trouble with those, right?

And then remember, the only means of contraception that associated with decreased risk of transmitted anesthi is if you abstain, that gives you like 100 percent protection, or if you, you know, use condoms, which does not give you 100 percent protection. So again, those are Ohio things to know for the purposes of exams. And then one of the weird Ohio things to keep in mind is if they give you a question about a person that gets like a prosthetic valve, right? One thing your friends at the MBM have studied, you know, kind of getting interested in these days is they'll ask you questions about a person having like endocraditis after getting a prosthetic valve, right? After getting a prosthetic valve, right? So the thing is, you want to be able to divide that by early or elite, right? So early prosthetic valve endocraditis, so you may say, oh, divine, okay, what in the world tells me that it's an early prosthetic valve endocraditis? It's 60 days. But person has endocraditis after you put in a prosthetic valve, like within the 60 day, day, day, cutoff of the surgery, the most common cause of endocraditis in those folks would be stuffy bedermitas, okay? Or be stuffy bedermitas. If it's more than 60 days, right? Then think about stuff for us, okay? I'll say that again. Early prosthetic valve endocraditis is less than 60 days after surgery. Late prosthetic valve endocraditis is more than 60 days after surgery.

So the first one you want to think about within less than 60 days, think of stuffy bedermitas, it's greater than 60 days, think about stuff for us, okay? Very high you to know that, okay? Very, very, very high you to know that. And then if they give you an usual situation where it's more than 12 months after they got the surgery, then the thing you want to strongly consider in your exam is strep viridance, strep viridance, almost think of it as causing like a super elite prosthetic valve endocraditis. And don't forget that if a person gets a prosthetic valve, they need anti-qualgulation for life, okay? They need anti-qualgulation for life usually with warframe, okay? In fact, many surgeons make people sign contracts with that, you know, if the valve thrombosis and the diobastroclusonthin, you know, it's like surgeon is kind of like not at fault for anything. So that's the disadvantage of a prosthetic valve over like a bioprostetic valve. But the thing is the bioprostetic valves, yeah, you don't need anti-qualgulation for those, but you don't last as long, right? So it's kind of like a trade-off there. Okay, so what if you get a question about like a newborn, you know, that has like either like a clicky hip or they can tell you that oh, this newborn has like a leg length discrepancy. And then they can tell you that you may see like a probable step off around the hip joints, what are you thinking about?

Well, I hope you're thinking about like developmental disclosure of the hip. How do you make the diagnosis, right? I mean, you can again, you can make the diagnosis, you can do like, there are some physical exam maneuvers, you could you could pursue. And sometimes you can even try to reduce the hip yourself, but you know, if those things are not working out so well, because usually those maneuvers actually don't work very well, you know, you can go ahead and make the diagnosis with like an ultrasound. Ultrasounds are very good. Don't pick MR Is, MR Is are very expensive, right? You probably need to set it the kid to make that happen. So you know, it's probably not a smart idea. And then you can put that kid in a public harness. Okay, public harness is like a weird device that you know, they kind of look like, it's kind of bizarre. Look, look up a picture of it online. You see what I mean? So you can do an ultrasound of the hip. But if the kid is more than six months old, right? Things that kind of, as if it was, if I'd a little better. So the public harness may not be the best idea. So typically under those circumstances, you actually try to do like some kind of surgical reduction. And then after you do the surgical reduction, you then consider doing like a, like a spiker cast of the kids hip. And that will usually resolve things within a couple of weeks to month. And then what if they give you a question about a patient?

And this is like good for like a question ready, show you like a video on the exam and you didn't have to decipher what's going on there. Basically, what if they give you a question about a patient? And this patient kind of like walks up using his, using his, like his hands walks up his knees. And they tell you that, oh, that his calves look kind of enlarged. And it's a boy. What are you thinking about on the little circumstances? Well, I really hope you're thinking about the shape of muscular dystrophy, right? Remember, the shape is what are some key high-yield things you want to keep at the back of your mind? Well, the key high-yield things you want to keep at the back of your mind is that first, it's inherited in an ex-linked recessive fashion. That's one. So it will not be in a girl on a test. It will be in a boy. Right? And then remember that these kids, right, they have mutations in dystrophy, right? So they have like no dystrophy, right? So usually many of these kids usually die like in their 20s. You know, if they live real long, they get the best care and everything, you know, they can live to 30, but really kids with the sheins, they die, they die relatively quickly. So that's a high-yield thing to know. And then there's a close causing of the sheins that you want to keep at the back of your mind. It's called beckers, muscular dystrophy. Some key things you want to be able to differentiate.

Yes, beckers is inherited in an ex-linked recessive fashion, but unlike the sheins where they have no dystrophy, kids with beckers, they do have some dystrophy, right? So the onset of symptoms is typically different. So usually kids with beckers, they tend to have the onset of symptoms when they hit like, you know, like pretty early in life, but kids with beckers, they usually don't have an onset of symptoms up until about like, you know, like 14, 15 years of age. So that's something high to know for example. And then beckers, again, they can live to like their 50s or their abouts before they pass away unfortunately. And then you should also remember that kids with, they can easily give you a question and they will ask, well, how do you treat beckers or the sheins muscular dystrophy? There's really no good treatment. Well, those people need like very good nutritional support, right? So you want to give them like very high calorie diets. You want to consider, you know, like physical therapy. You want to consider giving them corticosteroids, especially when they have like very severe symptoms that can help. And then another weird thing you want to keep at the back of your mind is that people that have beckers or the sheins, actually the most common cause of death in those people is a dilated cardiomyopathy. Okay, dilated cardiomyopathy is very high. You know, the most common causes of the sheins and beckers, muscular dystrophy on Indian exams.

And then the final thing I will say is if they give you like a doshains muscular dystrophy like presentation in a girl on your test. Again, like I said, don't pick doshains, don't pick beckers. One thing you want to pick is something called LG MD, like a limb girdle muscular dystrophy. It basically presents almost identically to the muscular dystrophies. But it can, it's inherited in like an orozomo recessive or orozomo dominant fashion. So most likely you ask about like, oh, orozomo inheritance on a test because there's like a type one, there's a type two, but you don't need to go that deep in terms of details. But basically, it's inherited in a orozomo dominant one orozomo recessive fashion. Again, that's a high yield thing to keep at the back of your mind for example. And then what if they give you a question about a patient, you know, maybe this patient just came from South America. And then they tell you that for the past two months, this patient has required like multiple pillows to be able to sleep comfortably at home. And this person has like, you know, like three plus pitting edema to the ankle, I mean, to the thighs on both in both lower extremities. And, you know, maybe they don't give you that many more hints. What should you be thinking about on those circumstances? Well, I'll really hope that you're thinking about chagas like a type one orozomo cruziate, right? Remember, T cruziate can cause a lot of big problems, right?

They have three big problems that it tends to cause, it can cause a dilether cardiomyopathy, right? That's very high yield to know, right? And then it can cause them so they can get big hearts, they can also get big esophagus. Remember, it has a very strong association with ecalija, right? It has a very strong association with ecalija, right? So, and if you see a South American with ecalija, think about a type of ozomer cruziate, right? So don't forget about that. And then it can also cause like a toxic mega colon, right? So like a big esophagus, right? Because it can destroy the outbacks flex side that you find so they can get, sorry, I already talked about the esophagus problems. It can destroy the the my interior flexes, so like the outbacks and my is the split side. Most specifically, an in-be-em-examptus, the outbacks flex side, like in the distal colon, and that can cause like herchproms disease, right? And if you get herchproms disease, that can certainly give rise to, like a toxic mega colon. And please don't forget your other causes of a toxic mega colon, an in-be-em-examptus, right? Remember, C-DeF, right? Especially if they give you a question about a person that has C-DeF and they show you like an image and the transverse colon is more than like six centimeters in diameter that's bad, right? Or the person has like rebound, guardian, like abdominal rigidity, and all that crap, that's toxic mega colon. And then don't forget that all three of collides, right?

It's also as you do a toxic mega colon on exams. Again, they will show you big transverse colon more than six centimeters. The person will have signs and symptoms of period tonight is those people need a emergent surgery, right? That's a surgical emergency, right? You can die, you can die relatively quickly, right? So you do not, you certainly do not want that. And then one other bizarre thing that can cause toxic mega colon on exams is if a person has like scleroderma and they have like bacterial overgrowth, that can ultimately lead to a toxic mega colon as well. Those are all, again, high-yield things that your friends at the MBM love to test on exams. And then the way you treat T-Crosia, right? Because it's like a protozoan, right? You know, you can treat, it kind of works like the worms, right? So remember worms are bendy, so you can treat them with bendersoles, right? So you can use a drug like Bensnida-Zol, Bensnida-Zol, so B-E-N-Z, N-I-D-A-Z-O-L-E, Bensnida-Zol is actually the first line medication for the treatment of a tri-ponusromacruziae. And then if you don't see that as an answer choice, you can pick a drug known as my 40-mox. My 40-mox is spelled N-I-F-U-R-T-I-M-O-X. I'll spell that again. N-I-F-U-R-T-I-M-O-X, my 40-mox, my 40-mox is the second line drug for treating sugar disease from tri-ponusromacruziae.

Now, what if they give you a question about a patient that has a history of bipolar disorder, and in this patient starts having tremors, maybe this patient has seizures and all that badness, and I don't know, maybe they also have like, you know, like really bad hypo-neutriniac, no, really bad hypo-neutriniac. What are you thinking about on little circumstances? Well, I hope you're thinking about lithium toxicity. Remember, lithium can cause many problems, right? So lithium can cause like nephrogenic diabetes and sypedus. I've said this that not many, many podcasts. This is probably the most, the concept I've talked the most about across my different podcasts because it's just high over. It's just one of those things you know you're going to see it on an exact, right? So lithium can cause nephrogenic di because again, remember, it uses that in X-channel, now we find that the level of the principle cell of the collecting duct to go and scrub the second messenger signaling cascade of ED. So you can cause nephrogenic di and remember, you treat that with an in-ech channel blocker like a milleride or triamtering. I've talked about the mechanism and the reasoning behind that I've known them. So I'm going to move on. And then remember that lithium can also cause hypo-thyroidism, right? So before you start a personal lithium, you typically want to go ahead and check like their TSE, try just to make sure that they have adequate thyroid function.

And then remember that lithium can also cause like Epstein's anomaly where you almost like have like, it basically causes a right heart failure. You have like this, the buzzword is like, it's realization of the right ventricle. That's something high out to know. And then the most common toxicity of lithium is the tremors. But lithium can also cause seizures, especially when you have lithium at like super therapeutic levels, it can cause seizures, right? So because it can cause seizures, if a person is seizing from lithium use, one thing you should strongly consider doing is going ahead and like, you know, like, put in, there's this thing they call the Gambro. It's done at turning the ICU. Basically, it's like a dialysis catheter. And then you try to get like emergent dialysis done. You insert the Gambro in like a central vein, like in the like one of the jogging veins. You actually works, works works, works pretty well. But yes, for a person is like seizing and all that real badness from lithium toxicity, you know, you should strongly consider dializing those people to get rid of the toxicolithium. And since I talked about hypernitrinia, this idea just kind of came into my mind. It's something that again, your friends at the MM seem to care about relatively recently. But the thing is, come on, I think, this drug that is used to promote like contractions like oxytocin. Oxytocin can actually cause like hypernitrinic seizures. So that's one thing you need to watch out for.

It's just a throwback to a step one concept, right? So because remember, EDH and oxytocin, I think they differ by like two amino acids. And they come from the same general area in the hypothalamus. Remember the superoptic nucleus of the hypothalamus mix EDH, the parvin trigolonylus of the hypothalamus mix oxytocin. But there's actually a lot of research that actually shows that some cells in the superoptic nuclei of the hypothalamus also make oxytocin, right? So the thing is, if you give a person, EDH works by basically making you reclaim a like re-resorbital ton of water, through binding to like the viso-pressing vitro receptors and then you, you know, stick all those acroporines at the level of the principle cell of the collecting duct, right? So the thing is, if a person gets like a prolonged oxytocin infusion, that can certainly cause like a hypernitrinic seizure, right? Because that oxytocin is essentially taking the place of EDH, right? So because it's taking the place of EDH, those people can run into significant problems with hypernitrinin. That is something you absolutely want to commit to memory for in-beam exams. It's a very common concept that shows up all the time on tests, right? So again, that is something super, super high you, you want to make sure that you know, because again, like I said, oxytocin can act like EDH. So let me even talk about one of those look, another look, like molecule, a stalk was shown, you see on a test, right?

So remember that cortisol, right, has partial activity on mineralocorticoid receptors. So usually when people have cushion syndrome, right? They will have like many of the labs that you would expect in a person that has primary hyperodosterone syndrome. So you know, they'll be hypertensive, they'll have like a hypochylemia, they'll have a metabolic alkylosis and all that stuff, right? So that's something to watch out for. Another area you may see those kinds of symptoms is if a person has like 11 beta hydroxylase deficiency, remember in 11 beta hydroxylase deficiency, one key thing that builds up is that's one of the causes of the congenital adrenal hyperplegia. One key thing that builds up is something known as 11 deoxycocortico sterone. The thing with it, 11 deoxycocortico sterone is that it has partial agonist activity on mineralocorticoid receptors, right? So under those circumstances, you can actually see people get again, hypochylemia, metabolic alkylosis and hypertension, under those circumstances. Now, what did they give you a question about a patient that you know, gets like a vascular procedure, right? Like a recent vascular procedure, maybe like a central line was inserted or something. And then this patient starts having shortness of breath, has like juggler venous distension, they tell you that, oh, you're scooting the person's lungs. And on one side, you don't hear any breath sounds and blah, blah, blah, blah, the patient's gasping for air.

If you see that, what should you think about? Well, I would really, really, really, really hope. You're thinking more along the lines of like like a pneumothorax, right? Like probably like a tension pneumothorax. And if a person has an attention pneumo because they've probably punctured the lung in the process of doing those vascular procedures, remember if a person has an tension pneumothorax, you want to consider doing like a needle decompression. Although one thing your friends at the MME can do to these, instead of calling the needle decompression, they can just give it another name. Remember needle decompression can also be known as a needle for a constant, okay? needle for a costomy, right? So that's one thing you can absolutely do, absolutely do on an exam, right? So again, something to keep, something to keep at the back of your mind. And then, if a person has like just like a regular mothorax, you can insert a chest tube, right? But again, instead of putting the name chest tube, they can put like the term tube for a costomy on your exam, okay? So remember needle decompression can also be called needle for a costomy. Chest tube is meant can also be called tube for a costomy. You do a needle for a costomy when a person has an attention pneumothorax. And then one of the against complication that can arise when you're doing vascular procedures is a person can get like an air embolus, right?

The person can get an air embolus and nothing can actually kill people relatively quickly. It's almost kind of like the pathophysiology very similar, like deletious effects as like a person that has like a son's disease, for example, like the bends where you know like gases can precipitate in a blood vessel and can kill them relatively quickly. So the thing usually do under those circumstances is that if a person, if you suspect an air embolus, usually they will give you a question and the person's lungs will sound fine, right? To basically tell you that it's not a new of thorax. And basically those kinds of situations, the thing you absolutely want to think about on your test is just to consider giving those, you know, telling those people to turn to the left lateral, the cubitose position. When deturning the left lateral, the cubitose position, the thing that happens is we essentially take an advantage of the effects of gravity so that the air does not go to the right side of the heart and then doesn't ultimately settle and go to like the pulmonary arteries and then cause like a nasty nasty PE, right? So you don't want that right. So you know, you tell the person lie on your left side. So that's like the left lateral cubitose position. And they also put them in like Trindalemberg again to prevent the air embolus, essentially from getting to the right side of the heart too that they don't get into, they don't get into trouble.

And then this I think I may have mentioned a podcast or two, but I can't really remember so I'm just going to talk about it, right? So what are the two genetic mechanisms behind Down syndrome? What is probably the most common genetic mechanism on the line Down syndrome? Right? It's maternal non-destruction, right? That's why again, as women get up there and each, you know, they have a higher risk of having kids with Downs, right? And then what's the second, what is the second common mechanism that tends to show up on exams? Probably causes like less than 5% of cases of Downs. Well, that's a robot Sonia translocation, right? That's a robot Sonia translocation. The thing is these genetic mechanisms that on the lie certain genetic diseases or certain diseases, they are things your friends at the endemic kind of expect you to know, right? So you see the way we've kind of talked about how like Down syndrome you can have like the maternal non-destruction of the revertion in translocation for things like like prediably engolment syndrome. So I remember those associated with what is it called? Like uniparental, dicemigian, genetic imprinting kind of deal, right? So those are again all key things to keep at the back of your mind. And then Down syndrome, right? Let's not forget the associations, right? So remember they can have like cardiac problems like endocardioclucine defects. They can have a lot of GI problems, they can have like herchprung disease.

You can see like the billiards vomiting in a newborn like double bubble, do it not at resia. They could have like anula pancreas, right? That can also cause a small bowel obstruction like thingy, but that will not be in a newborn bowel like they'd be like in a kid that's you know kind of live where we're down syndrome. They can also have like ELL, right? Remember that the monocleofal down, right? So ELL is coming in kids with Downs. And remember that because they have three copies of chromosome 21, right? So they're like trisomy 21, you can make the diagnosis with like charyotipin, but another thing is they have like three copies of the amyloid precursor protein, right? So those kids have a very high risk of early onset, early onset Alzheimer's. So again, those are all important things you want to keep at the back of your mind on on tests. Okay. Now, and then when I put that idea, I actually just dropped in my mind with Downs, right? So don't forget your quad screen result with Down. I really love to test this all the time when exams. Basically, it's like they have like high levels of beta HCG and in HBIN A, right? And then every other thing is low like the AFP and there is fetal, is trial as low, right? And then the way I remember that is I just remember like high beta, like high, like HI beta, right? So high beta, right? So if you remember like high beta, you can remember that, oh beta HCG is high in HBIN A is high as well in those in those people.

And then AFP has trail those are low. So those are important to know. And then what is one other high-year thing? Yeah, at what syndrome, right? So try something 18. Basically, everything is low in those people. Yeah, Edwards is bad. Like they're pretty much everything in those people for the most part is low. You know, one of one things may be normal. But these if you see like three things that are low in the quad screen, that's Edwards syndrome, try something 18 on your exam. Try something 13, the results are all over the place so they don't test that on on exams. And then remember if you have any kind of neuro tube defect, right? Or you have like an abdominal wall defect like gastroskeces or on phallocel, right? That's like an abdominal wall defect. Those can all cause elevations and maternal seroma of a fetal protein. So again, key things to keep in mind for example. Now, to wrap up, right? So what are the two kinds of hernias that you don't watch and wait? What are the two kinds of hernias where you notice them, you fix them relatively quickly. And I'll hope you're thinking about like a pair of a gel hernia, right? And also a femoral hernia, right? Pyrus of a gel hernia is femoral hernias. Femoral hernias will not be in males. They'll be in females. Remember the F in femoral for the F in female, okay? So they'll shop in females on exams, right? And they'll be below the Inguino ligament. There will really be like medial to like the femoral vessels, right?

So whenever you see that, you know, you don't want to go ahead and consider surgery because those have a you know, pretty high risk of like incassaration and strangulation. And again, those are all things your friends at the NBME really care that you know for exams. Okay. Now, um, um, I think maybe I should go ahead and stop here. Um, oh, you know, let me give you like one last vineyard. Um, this one just kind of popped in my mind. So what did they give you a question about a person? Maybe this person, I don't know, saw an amadillo recently or farms like works with monkeys or it came from like a foreign country where they may have contact like strange animals. And then they have like like they have lots of sensation over like the tip of the nose or the tips of the fingers or they may have like these weird swellings on their faces, like the smurfing facial features. What bug are you thinking about on the other circumstances? I don't really hope you're thinking about an EPC, right? EPC, my co-back term, an EPC, uh, let's see, it's bad, right? But the thing is, it lost to affect like cold regions of a person's body, right? Cold regions of a person's body. And terms of treatment, don't forget like the way I remember it is like DRC, like demographic republic of Congo, that can help you remember like the way you treat it. And the treatment is after it for two years. So you may see how it's defined. What in the world is DRC? Whether the distance for DAPSON, right?

The R stands for IFAMPIN. And then the C stands for KLOFAZEMI. I'll say that again, DAPSON, RIFAMPIN and KLOFAZEMI, okay? For 24 months, right? So LEPRESY is something you don't want to get. So you know, if you see like a 9 banded armadillo, you know, it's probably not a good idea to like, oh, go chill, rub the amadillo. Maybe rubbing yourself with some good old LEPRESY as well, which is probably not an ideal thing. I mean LEPRESY treatment for two years, if you can, just don't get LEPRESY if you can avoid it. It's a bad thing to have. Okay, because you're going to have like permanent nerve damage that you know, you never recover. Okay. Now, and really the way you make the diagnosis, really for the most part, you just do like a biopsy and you should be fine. Like, you know, just find one of those areas that it's affected. Go a biopsy, you can usually like, you know, stain and find the micro-bacteria, LEPRESY. So yeah, I think I'm going to go ahead and stop here. As I do at the end of every podcast, basically if you need tutoring at your med school, I probably offer something that can help you out. So step one, step two CK, step two CS, step three preclinical med school exams, 30-ish-off exams. If you're a medicine resident, I need tutoring for like the intranine exam or the IBI-I-M board exam or your cholesterol exam, I need tutoring for like Gen-CAM, O-CAM, Physics, Bio-CAM, Histology, Physiology. I'd offer tutoring for all those stents, one on one, a large group.

And then I also do like these booster courses. It's like 20 hours for step one and it's 10 hours for step two CK, step three. They're like very rapid review courses. We talk about the most knows for these exams and pretty much everyone I've done those courses with, they have ended up doing extremely well on the exams. They found it to be very helpful. Like many people have recorded some pretty decent scoring quizzes from that and usually this course goes for like a week. Although I guess it kind of depends on your own timing, usually runs for like a week for the set number of hours as I mentioned. And they also do like large group sessions. In fact, this is something I plan to offer in the month of February, March, April and May. So February, March, April and May. Basically they're like detailed, comprehensive US Emily courses where you run for about 100 hours, you run over a couple of weeks. Probably you run for like a month or less. So if you have a group of seven people that need tutoring for the US Emily step one exam or step two CK or step three, if you can arrange a group again just reach out to me, you can either reach out to me through the website or you send me an email at Divine Intervention Podcasts with an SADN at gmail.com. Right, and I'll be happy to point you in the right direction. So that's one thing I offer.

And then the final thing I offer is if you know if you need like coaching for like if you're a matching applying to residency so like an era's application or or a collection applying to Met School so like an Amca's application, right? You can do you know like if you need like one on one coaching for like rec letters, personal statements, mock interviews, editing applications. Again I've worked with a lot of people, a lot of people have worked with me, they have much that they have much that they have first choices. So again if you need any of those things reach out to me. Probably make a podcast soon on like the different course offerings I have that's something that people have kind of asked me about. So have a wonderful rest of your day. I will see you next time. Good night. God bless you. Thank you. And actually one thing I shouldn't forget. My You Tube channel I'm going to be posting a lot of videos to that like over the next couple of days, two weeks. So please subscribe. It's called Divine Intervention Podcasts and Videos. I'd like to hit a thousand subscribers hopefully before the end of the month. I'm at almost like 670. So please subscribe, tell your friends, share that your Met Schools. Okay well I think that's I guess all I'll say. This is going for 32 minutes now. God bless you. I'll see you in episode 200.

Enteral nutrition via feeding tube, as it maintains gut integrity and has a lower risk of infection compared to TPN.

Selenium deficiency.

Chelating agents, specifically penicillamine and trientine.

Copper IUD (or other non-estrogen methods), as estrogen-containing options are contraindicated due to increased risk of recurrence in ER+/PR+ cancers.

Early is defined as within 60 days post-surgery; late is more than 60 days post-surgery.

Left lateral cubitus position (lying on the left side with the elbow flexed).

Maternal non-disjunction (most common) and Robertsonian translocation.

Cardiomyopathy (dilated cardiomyopathy) and megaesophagus/esophageal dilation.

Coprioxacobalsine is contraindicated in patients with active or history of severe gastrointestinal bleeding due to its potential for mucosal irritation and hemorrhage.

DMD typically leads to death in their 20s; BMD onset is often later (sometimes up to age 14-15), and they may have some residual muscle strength.

Clostridium difficile infection (C. diff) or severe colitis/inflammatory bowel disease, but also consider chronic opioid use or scleroderma with bacterial overgrowth.

DAPSON (Dapsone, Rifampin, Clofazimine) for 2 years.

Cardiomyopathy (dilated cardiomyopathy) and megaesophagus/esophageal dilation.

Coprioxacobalsine is contraindicated in patients with active or history of severe gastrointestinal bleeding due to its potential for mucosal irritation and hemorrhage.

DMD typically leads to death in their 20s; BMD onset is often later (sometimes up to age 14-15), and they may have some residual muscle strength.

Clostridium difficile infection (C. diff) or severe colitis/inflammatory bowel disease, but also consider chronic opioid use or scleroderma with bacterial overgrowth.

DAPSON (Dapsone, Rifampin, Clofazimine) for 2 years.