DIP Episode 488 - USMLE Step 2/3 Rapid Review Series 105

Welcome my name is divine this is episode 488 of the Divine Intervention Podcasts into this podcast will be continuing the step-to-step through our pre-review series this will be series 105 let's begin what if they give you a question about a 71-year-old male and you're told that for the last three weeks he has had recurrent seizures or let's make him more realistic let's say for the last one week he has had recurrent seizures and you're also told that he has lost quite a bit of weight over this time period and you're told that he has skin hyperpigmentation what should you be thinking about and then let's say they give you a sodium and a sodium is like 124 or something really look like that what should you be thinking about well I really hope you're saying that oh divine is sounds like this guy has small cell lung cancer um again remember the US similarities are just about putting things together he'd be like oh come on divine like seriously man like how did you get to small cell lung cancer well how did I get there well let's explain number one this guy has um been having seizures and okay you see seizures what maybe the cause okay well he has no sodium so 124 is not great right it's just pretty bad so this person has hyponitremia you see you see skin hyperpigmentation um put it all together it's an older person right that skin hyperpigmentation should make you think of maybe this person has a lot of acth running around because acth is not meeting a vacuum right it's made from pomc together with msh so whenever your acth is high you can have high levels of msh dose to malitium melanocytes I can get skin hyperpigmentation right so it's pretty as a lung cancer pretty as small cell lung cancer now a common question I get from many students divine those small cell lung cancer the high acth is that associated with skin hyperpigmentation or not or the thing is honestly it

varies it honestly does vary so you can't leave any cogentry man say I beat my hands to my chest that oh this does not happen blah blah blah no no no you cannot so honestly all these people that stress out about oh wow if you have high acth as such those small cell lung cancer do you have skin hyperpigmentation or not it doesn't matter basically right they could have either or they could have either or they would literally have either or just want to throw that out out there right so it's pretty as small cell lung cancer right so remember small cell lung cancer what are some big things to know about it number one it loves to grow in the center of the lungs right it's not a peripheral mass although it could be peripheral on your exams that's why sometimes yeah certain things that many resources see are high yield but they're really not what do I mean by that or like certain classic associations people learn and they're really not that classic because I'm telling you our friends at the MD Ms they can totally write a step two or step three question where the person has small cell lung cancer and they present it as a peripheral mass right and a lot of the question we're telling you that this is small cell lung cancer right but you throw in that range that you know what this stuff is peripheral and some people once they see that wow this mass is peripheral yeah I got to be at no cost you know my cannot be small cell lung cancer they just ignore it and then they get the question wrong again please don't be in that camp don't be in that camp um don't be in that camp I'm just kind of encouraging you yes most times small cell lung cancer is going to be a central mass but every now and then it can be peripheral right so just don't be so rigid like that in your thinking on the exam sometimes it can really get you in a pretty decent amount of hot water if you know what I'm talking

talking about so small cell lung cancer again is one of these lung cancers that has the strongest association of parlioplastic syndrome right number one it produces it at EDH right so that can cause a high point of trimmer right because when you have a ton of EDE running around you're gonna soak up a lot of free water from your urine when you soak up all that free water from your urine you're gonna become high point trinic but what's gonna happen to your urinous molarity urinous molarity is gonna be pretty high again remember our friends at the end of the year means can take a lung cancer question and make a bunch of arrows out of it right so your sermons molarity will be low because you're sucking up more free water from your urine because you have high levels of EDH right EDH is just got anti-diarrytic hormone and then too you're gonna have a higher in osmolarity because all that free water that's being sucked up from your urine is gonna make your urine very very concentrated right and then on that weird bizarre question they can just kind of slide in there is oh what is trove your urinous reaction of urinous reaction of urinous reaction will also go up as well that's something you don't find in many resources but it's very very high to know for the USMN exams urinous reaction of urinous reaction of your urine will be high and the view of EDH is high well the thing is EDH many people think that oh oh that EDH does is that it helps your reabsorbed water that could not be further from the truth EDH believe it or not has a bunch of different functions number one is that it helps your reabsorbed water at the level of the principal cell of the collectin duct okay the exams number two EDH helps your reabsorbed urinous reaction but you may wonder like the vine is kind of a weird story like why would EDH want to help your reabsorbed urin like what's the point well think ab

out it for you to be able to reabsorbed all that water in your kidneys you need this also wonderful thing known as a medallery concentrating gradient I'm gonna say that again a medallery concentrating gradient now that medallery concentrating gradient for purposes of the USMN exams again there are more fine details here but they don't matter for your test but for purposes of the USMN exams number one half of EDH is created by ions what are those ions those ions are ions you'll largely get from the thick ascending lamp of the loop of Henley from the all you know let's not even worry about thick of thing just the ascending lamp of the loop of Henley right so where loop diuretics basically work that's when loop diuretics are such powerful diuretics because about half of the eye of the medallery concentrating gradient generated by ions that we get from that loop of Henley so if you block that loop of Henley with a loop diuretic you may notice that wow you've really depleted this person's medallery gradient and that just makes them not able to reabsorbed water so they lose a ton of fluid that's why loop diuretics are used in like CHF exacerbation or crazy things like that but the other half of that medallery concentrating gradient for purposes of the USMN exams is created by urea right because urea believe it or not is a very osmotic reactive substance it is a very osmotic reactive substance various motic reactive substance so EDH basically helps establish a medallery concentrating gradient so that makes things more ideal for reabsorption okay so that's the big thing there and then you may then wonder okay what's a third use for EDH?

well a third use for EDH and then we'll get back to the small cell lung cancer is that EDH is also a very powerful visopressor in fact literally another name for EDH is a visopressant I believe it or not EDH visopressant is used in um in a many different visopressant is used in many shock situations right like um in fact if people have certain kinds of a septic shock if you're giving them nor a beneficeren as the first line presser visopressant in some settings in some settings is used as a very good second line presser although some people also use a beneficeren as a second line presser in septic shock but that's a different conversation and then remember there is this situation where some people just don't make EDH right so say for example they have central diabetes and sepidus because they have like some kind of pituitary tumor or some kind of hypothelanic tumor if you're not able to make EDH then you'll not be able to hold onto free water those people can become hyper-metrivic again I know I'm going on this sidebar but I think discussing the functions of EDH is extremely high yield so I just want to go into that and I'll get back to the lung cancer case that's the benefit of these rapid reviews you can really integrate many things but basically for pressing has like central diabetes and sepidus for those people the defect is they can make EDH for whatever reason hypothelanic tumor so the thing that will happen in this case is if you give them an EDH channelon like decimal press and that's going to help them right and fact if you did the water deprivation test because that's one of the ways you can confirm that a person has diabetes in sepidus you deprive them of water when you deprive a person of water that person's hearing or similarity is supposed to shoot up like spotnik because basically you wonder like man this person has not drunk water for a long time so le

t's the body will be like wow let's try to hold onto water but if you have diabetes in sepidus for whatever is in bead central which is where is no mickey EDH or bead in a phirginic where they're not responding to EDH your urinal similarity will not rise as much as you would expect it will just rise up by a few points instead of going up multiple forward i'll tell you that oh man this person probably has diabetes in sepidus so you're like hmm okay which one do they have is it central or is it in a phirginic or the way you're going to tease those two apart is literally by giving an EDH channelon give this impressive when you give this impressive is going to help you tease those two conditions apart because if you give it this impressive fixes the problem then that tells you that oh but the small pressing deficiency and EDH deficiency was the original cause of the issue right so that will tell you that oh it's central diabetes in sepidus so if you notice that the person's urinal similarity normalizes with the administration that mean the person's urinal similarity rises appropriately okay rises appropriately rises appropriately with the administration of the small press that tells you that yes this is a central diabetes in sepidus what if it does not if it barely changes then that's the phirginic diabetes in sepidus where you start to start having to think about things like lithium, the cycliclyne, hypercalcine and all those things causing that nephirginic dion okay and then another use for EDH is that EDH basically can help you form pleatlethrombine all right and help you form pleatlethrombine how does it do that it does that by increasing the release of an olybron factor from wibon paladibadis okay helps you increase the release of an olybron factor from wibon paladibadis so if you increase the release of an olybron factor right you're going to promote primary hemosta

sis well where did that come in handy well let me come in handy when a person has an olybron disease remember if olybron disease you literally have a deficiency of have a deficiency of olybron factor so if you have that deficiency primary hemostasis is not going to work very well and think about it if primary hemostasis is not working well your bleeding time is going to be elevated and if your bleeding time is elevated then now tell you oh this is a primary pleatlethrombine disorder but what does mother clues that we tell you that oh this is when wibon disease well your pct is going to be elevated as well because factor 8 will have a shorter half life when you have an olybron disease because one of the jobs of olybron factor is to increase the half life of factor 8 but if you're short on olybron factor factor it will have a shorter half life so pct is going to go up and then also you're going to notice that you have an abnormal restocetinco factor as a the first step of primary hemostasis which involves GP1 B and olybron factor if there's anything wrong with that your restocetinco factor as you'll be abnormal let me podcast on this stuff so people that have an olybron disease on the USMV exams many of them have a partial little full deficiency so most of these people respond very very well to death more present because again they will encourage the release of olybron factor from these wibopaladi bodies now what is another use for EDH again that you may see on your exam another use for EDH may see on your exam believe it or not is in a child that is more than five years old that's pin on themselves that's not generally in your recess it's more of a second line measure for treating an alternative in your recess you can use the small pressing you can use the small pressing again this compressing being an EDH analog it will pretty much again help you soak up a lot of free

water from your urine if you do that in the child will not be pin on themselves as much at night now what is a very good follow-up question to that that they can slot on your exam one very brilliant full-on question they can throw in if I for the USMV exam will totally do stuff like this is and I would not be surprised if they totally do stuff like this is it just feels like a USMV question they give you a question about a child who was recently placed on pharmacotherapy for nocturnal in your recess and then they tell you that this child has generalized tonic clonic seizures and then they ask for your next best step they say oh the the child had generalized tonic learning seizures for like three minutes or whatever or something crazy like that and then you know they say that right now the child is not on that going any kind of seizure activity he's in the emergency room you see what's your next best step in management your next best step in money tends to get a to get some kind of B&P get some labs get a basic metabolic panel why because you're going to discover high-pony trimia that's an easy question they can test and I kid you not right and even like define how do you make that like yeah the thing is there's more pressing than ED channel work right so you suck it up all this forwarder from your urine that can make your sermons malarity really plummet that can cause high-pony trimia and that high-pony trimia can cause what seizures exactly can cause seizures although what is one other thing associated with no trinidad neuroses that make cause the child to have seizures what is one other thing as so you don't know trinidad neuroses and it cause the child to have seizures um TC toxicity TC toxicity that's why I love these rapid reviews you can really stretch your thinking if you if you apply yourself but yeah TC is because remember TC is a like in some situation secon

d or third-line mitigation as well for sure no trinidad neuroses although we try to know use that stuff because it just has a ton of side effects right sodium channel blockers we can like widen your cures cause all these nasty radmias um they have anti-colonurgic properties they can cause all those static hypertension yeah yeah yeah yeah but we can use them for no trinidad neuroses right now remember um these drugs are neurotoxic they are neuro neurotoxic so because they're neurotoxic they can certainly cause seizures so you see seizures um you see seizures you know USM person being treated for no trinidad neuroses I want to think about either hyponytraining or TC toxicity again oh they find how like differentiate well if they are testing TC toxicity they're going to give you an EKG there's no real EKG finding in hyponytraining so it doesn't make any sense to be testing this what person has the cause and then slap an EKG in the question no they slap an EKG in the question you're like oh I mean this cure is those in look those in look or they start giving you that the person has like a temperature of 101 it's like come on you're not going to get a fever from from having a from taking decimal pressing no right you're not going to get a fever from taking decimal pressing right is the anti-colonurgic toxicity of the TCA now cause that fever right so they are just many clues they can give you they can tell you that oh the person is tachycardic or the person has um my dry asses for example remember when you're in an anti-colonurgic toxicity when you're going to have my dry asses or you can toss in something about orthostatic hypotension which is certainly something you can see with TCA it's because they have anti alpha one properties that that and all the person is very sleepy right because they have anti-histamine properties right so these are all clues right so they're no

t just going to leave you hang it they're going to give you clues in the question that guide you in one direction versus the other if people walked into the US English without mindset they probably make fewer fewer mistakes honestly um just work with the clues you're given the question will contain a series of clues right the consequential container series of clues um to helping you pick out the right answer and that's why again I if I love the review courses I teach if you're interested in many of those I teach things and I say okay these are the classic clues they'll throw on the exam to go over this concept or these are the different variations of the same thing that you can use to test this concept I have a bunch of classes that you know Friday I have a separate podcast on that if you're interested just trip me an email or listen to the podcast on on that stuff okay so those are pretty much all the uses of EDH that you can see on your exam I'm just be very be very cognizant of that um again I know you need to seem like wow divide with study with small cell long cancer and again problems were going back to that but I'm glad we made all these EDH integrations because it's really difficult to take any US Emily exam literally it's really difficult to take any US Emily exam and not have an EDH related question in some way shape or form okay really really difficult so it's just one of those things it cuts across many many disciplines right even the reading and your dancing our those students system is related to EDH in some way how is that we'll think about it if you have higher reading and you know reading converts and your dancing no change on your dancing one no and your dancing one is converted to and your dancing to in the pulmonary capillary by ease and your dancing to goes to the hypothalamus and goes to release EDH right because it's release ED from the from the

supra optic nucleus of the hypothalamus so and your dancing to is a very powerful stimulator of EDH release rate just many things they can test with this with this stuff many many things please so just don't don't ignore it okay now going back to small cell lung cancer so we talked about the first part of your plastic syndrome that was EDH right now we had that big story right and then the ACTH right remember ACTH a topic ACTH production remember that's the one that does not suppress with high dose dexamethasol that's the thing you're gonna see with a person that has small cell lung cancer right so you can present that a skin hyperpigmentation that person may begin in weight they can even give you some electrolyte abnormalities because remember when you have a ton of ECTH well a ton of ECTH is going to go to the zona fasciculata of the adrenal cortex and it's going to cause it to spit out a ton of local corticotes in this case cortisol well cortisol leave it or not works like out of sterone to an extent um cortisol works like out of sterone to an extent so because it works like out of sterone to an extent you can meet you excrete a lot of potassium in your kidneys that can cause you to have hypochylineia you can meet you and you can express a lot of protons in your kidneys as well that can cause you to have a metabolic alkalosis so if they give you a question about a person that has a long mass right a long mass and they have hypochylineia and metabolic alkalosis you can pretty much stop reading the question is small cell lung cancer it's a topic ACTH production that's under way they may test it right because that's one thing you see a lot of people about the skin hyperpigmentation or no skin hyperpigmentation yeah can they test that on the exam fine but again really really to the test that what's a very classic way to test a topic ACTH production even this suppresse

s with high dose dexamethasone they still test it but i'm telling you a more inventive way friends at the mbmi's have found to test this information is you know what just give you a question about a person that has long cancer and they have hypochylineia and metabolic alkalosis let's see what these students think yeah yeah that's a perfectly good way to test it right so just kind of keep that at the back of your of your mic and then what's the third part of your plastic as you know small cell lung cancer the third part new plastic as you know small cell lung cancer is that the person well can have lumbarine etymisthenic syndrome lumbarine etymisthenic syndrome i feel like with each of these pyrnoplastics there's like a bunch of derivatives they can test lumbarine etym what do we know about it basically many people have memorized most of the weakness that in prison you so okay fine whatever great let's talk about why that's the case well in lumbarine etymisthenic remember you make urwan tibodies against the presynaptic vortish-gated calcium channel presynaptic vortish-gated calcium channel while i'm making this big fuss about presynaptic vortish-gated calcium channel because the thing is many people mess this up the usml is detest this in so many different ways they can say urwan tibodies against calcium channels all right or they can see urwan tibodies against vortish-gated channels they will they will intentionally meet the calcium or they can see urwan tibodies against presynaptic channels so just be ready for any of those things on your exams okay that's why you truly want to understand what you're just memorizing okay so we make urwan tibodies against those channels right calcium is not going to be able to come into the neuron and remember that presynaptic vortish-gated calcium channel calcium comes in through that and that causes vesicles that continue your trans

mitters to exo cytos neurotransmitter so if calcium can come in because you blocked the channel calyxotide cytos neurotransmitters especially acetylcholine then you won't have any neuromuscular transmission you're going to get weak but if you start using that muscle start using that muscle start using it using it well what would happen what I think that would happen is as you use that muscle use that muscle use that muscle you can recruit more calcium to that vortish-gated calcium channel and those calcium molecules can outcompete those nasty antibodies and then you have an improvement here in your muscular transmission okay so you're going to have that muscle weakness that improves with use with more use of the muscle you have more recruitment of calcium with more recruitment of calcium you have better competition against those nasty antibodies although again instead of saying oh most weakness that improves with use what is another fine way they can test it another fine way they can test is they can see it's and say this in a previous podcast an incremental response to repetitive nerve stimulation right an incremental response to repetitive nerve stimulation so as you keep stimulating with a nerve you get an incremental response that means oh the response is getting better the response is getting better and although we can also test this on your exam believe it or not is they can say oh you you have improved your muscular transmission with muscle challenge or something like that right if you just see that term improve your muscular transmission think of a person that has a Lamborghini TMI stenic syndrome okay think of a person that has a Lamborghini TMI stenic syndrome okay so I think I'm going to go ahead and pause here I think we've covered quite a bit today I think we've definitely covered quite a bit today this is a pretty pretty high-heeled stuff I'll pick up fr

om hearing the next in the next podcast so I do offer one to you for all the USMN exams step one step two step three complex one two and three and I guess I want to address something some people say oh divine doesn't you are women no that's not true I don't know maybe with my accent I may have sounded like what I said I don't do it to use O M M O M M I don't know how some people misconstrued that O M M sound like women I don't know it's kind of bizarre but yes I I don't do it to women it's something I've never studied it's something I have no idea about so I don't do it to that but pretty much every other thing I do for the most part and then I offer review courses for step one of a 25 hour course coming up in January and then I have a step two courses coming up next week actually although I have a bunch of courses that are first step one step two step three studying on Friday have a testic and strategy score Saturday I have a four hour bio statistics class and then on Monday next week I have five hour social sciences ethics, holiday improvement, healthcare systems, communications, professionalism class those are first step one of the way to step three.

I think many people have taking these courses and don't really well on the exam so if you're interested in any of them just honestly shoot me an email and I can give you some more information and please if you're expecting like lectures they don't come for the courses kind of a waste of your time these courses are all seem pretty much almost exclusively scenario based because that's just going to be a little more realistic to what you examine it's going to look like I'll teach you the concepts I'll teach you the path of faiths I'll make integrations but it's not going to be by will of like a standard lecture no no no no I don't believe in standard lectures that's not a good way to teach medicine just in general in my experience okay and then I have these podcasts on Apple, Google and Spotify and then I have a You Tube channel divine intervention you have seemingly podcasts and videos that's why I post the videos that I meet and then I have another website called divine intervention life lessons.com divine intervention life lessons.com many people say that oh divine I love many of the life lessons you're putting your podcast so you know many of you know I'm a Christian so I made a separate website where from a medical perspective I address a life lesson trying to put like two podcasts every week for the most part and we have more than 210 podcasts on there right now so I'll just check that out there's actually an Apple podcast as you know with that called the Divine Interventional Life Lessons Podcast.

Well thank you for listening to me today I will see you in the next podcast have a wonderful Wednesday wish you all the best video or admission cycle or bless your microphone now thank you

Seizures, weight loss, skin hyperpigmentation, and hyponatremia (e.g., Na 124).

It often produces high levels of ACTH, which stimulates melanocytes via the POMC pathway.

By increasing the release of anylorbin factor from Wibon Paladi bodies, promoting platelet function and hemostasis.

Hypochloremic metabolic alkalosis (due to mineralocorticoid effects).

1) Water reabsorption in collecting ducts; 2) Establishing medullary concentrating gradient (via urea/ions); 3) Vasopressor agent.

Central DI will show an appropriate rise in urine osmolality after DDAVP; Nephrogenic DI will not.

Skin hyperpigmentation, hyponatremia, and metabolic alkalosis/hypochloremia.

Urea (osmotic solute) and ions derived from the thick ascending limb of the Loop of Henle.

Presynaptic voltage-gated calcium channels.

Nephrogenic Diabetes Insipidus (DI).

Lithium, Cyclosporine, and Hypercalcemia.

Elevated bleeding time and elevated Prothrombin Time (PT) due to reduced half-life of Factor VIII.

The presence of specific EKG changes or signs like fever/mydriasis in TCA toxicity.

Skin hyperpigmentation, hyponatremia, and metabolic alkalosis/hypochloremia.

Urea (osmotic solute) and ions derived from the thick ascending limb of the Loop of Henle.

Presynaptic voltage-gated calcium channels.

Nephrogenic Diabetes Insipidus (DI).

Lithium, Cyclosporine, and Hypercalcemia.

Elevated bleeding time and elevated Prothrombin Time (PT) due to reduced half-life of Factor VIII.

The presence of specific EKG changes or signs like fever/mydriasis in TCA toxicity.