DIP Episode 202 - USMLE Step 2CK Rapid Review Series 30

Okay, welcome. My name is Divine. I am a resident. This is episode 202 of the Divine intervention podcast and this podcast will be Contina Rapid Review series for the US Family Step 2 CK exam. This is going to be Rapid Review No. 30. So what if you get a question about a newborn? And it's really that this newborn has like a very tiny head. So the word we use on an exam for that is microcephaly. And then they tell you that this child you know has been having like seizures on and off has like maybe has like you know like facial defects. And then they tell you that this child maybe his mom delivered him or while she was pregnant she maybe traveled to like some maybe like traveled to Brazil or you know some kind of foreign country. And then they tell you that all that the obtained image of the child's brain and they notice that the cerebral cortex is very thin. If you see that what should you be thinking about? I hope you think about Zika right? So Zika believe it or not actually shows up on the US MLE's. So it's one of those weird things you want to keep out the back of your mind right? So it's I feel like the tested more on step one but it's beginning to make it to step to CK territory. So essentially the thing that happens in Zika right is you know you kind of get exposed to the virus as a mom and then that virus is able to cross the placenta and then it causes problems in the fetus.

And the thing is Zika the virus loves to infect cells that ultimately give rights to neurons that you'll find in the central nervous system. So if you infect those cells and destroy them then the neurons that we find in the CNS they will not develop properly and many of them will just not work or they will just die off right? So that's what happens when a person has Zika right? So the classic presentation and in the exam you'll put some kind of international relationship in the QSTEM that's one. So mom may be you know like maybe like an eight worker or something right? And then they'll tell you that she delivers a child. This child will have microcephaly right? So you have a small head who have like facial defects right? The child can have seizures the child can have like eye problems right? And then in the brain the classic thing you're looking for is they'll have like a very thin cerebral cortex that's very important right? And then you even have calcifications in the brain but the thing is they brain calcifications are spread throughout the brain that is in sharp contra distinction to congenital toxoplasmosis where they have I mean they'll have intracranial calcifications but toxoplasmosis causes other problems besides just the intracranial calcifications you will not see the cortical thinning you will not necessarily see the seizures right? And then CMV also causes calcifications in the brain but the CMV calcifications are almost always peri ventricular right?

So again in toxop so again let me let me back track here. So Zika is intracranial calcifications with microcephaly with a thin cortex on imaging with seizures okay with seizures and then they can also have like the eye defects the facial defects and mom would have traveled to some kind of foreign country. Now for toxoplasmosis you also have intracranial calcifications but those kids will have hydrocephalus so instead of having microcephaly they'll probably have like a big brain right? And then they will also have like choral retinitis right? And usually they'll tell you that maybe mom rears cuts at home or something right? Or maybe she eats some undercooked meat at some function or whatever right? And then CMV right? CMV they will have like the blueberry muffin rash they'll have calcifications with the calcifications is very high you know those calcifications are peri ventricular they are around the ventricles okay? So they'll have peri ventricular calcifications they'll have the blueberry muffin rash they'll have here in loss so CMV can cause a sensoroneuro here in loss in a newborn right? Again that's very high you to know that right? And then syphilis I guess in some talking I guess I might as well go ahead and talk about this right? So some of the other things that are congenital infections the classic one is like syphilis if you see syphilis in a newborn right? You'll see the kid with snuffles that's very high you to know snuffles snuffles snuffles right?

And those things don't touch them with your hands if not you're you're gonna essentially give yourself syphilis those like the ryanorea essentially is tingling a ton of spirulchites right?

So that's how again that usually presents usually presents on exams and then if they want to test like congenital HIV on an MBM exam they'll give you a question about like a newborn you know maybe mom has HIV or maybe mom is an IV drug user or is like a sex worker and then this newborn seems to be having all these recurring infections and chronic diarrhea if you see that you want to use absolutely want to think about congenital HIV on an MBM exam so that's the classic way that that tends to that's the classic way that tends to present so something to keep at the back of your mind and then what if they give you a question about a patient you know this patient has a history of like diabetes has a history of like high blood pressure maybe smokes and then this patient to tell you that oh like for the last 20 minutes he cannot move his right arm or his right leg right like he has muscle strength that's like one over five in the upper extremities and and one over five in the lower extremities both on the same side if you see that what you want to think about well I hope you're thinking about some kind of like because use notice and let's say maybe they tell you in the queue saying that oh this person doesn't have any sensory abnormalities well if you see that right this person has like a pure motor problem right a pure motor problem I talked about this in the neuro podcast but this is one of those things that bears repetition but essentially the thing that happens is when a person has that those kinds of pyramidal strokes you want to think about a problem at the level of the internal capsule right most specifically at the level of the posterior limb of the internal capsule and the thing is when it's almost think of it as the classic we will present is you'll present as like almost like a surgical stroke what I mean by surgical stroke right so you know if you hear them use i

f you hear like the military use the word surgical that means is like very exquisite very specific if you notice you're like man this person has a stroke with these things you have just pure motor symptoms on one side upper lower extremities then you know that it cannot be a cortical problem right you have to be a sub cortical problem right you have to be at the level of the posterior limb of the internal capsule and usually the inciting agent there is where you have like a rupture right like a shackle bushard microorganism of the linticular striad arteries right and remember the biggest risk factor for those kinds of strokes is hypertension really for all kinds of strokes in general we have hypertension as the biggest risk factor again please don't confuse this with smoking being the biggest risk factor for a more cardiomy infraction and hypertension being the biggest risk factor for uric dissection and smoking being the biggest risk factor for triple A and smoking being the biggest risk factor for peripheral arterial disease okay just make sure you can link up all those cardiovascular slash blood vessel related risk factors they love to test those things on nbm exams so again linticular striad artery and again you have like a pulmonary parisis again if you also see a person that has like a again almost like a surgical just purely sensory stroke again think about problem at the level of the posterior limb of the internal capsule and that's usually again it's sub cortical right that will probably be something the otestin neurology shelf it's sub cortical right so again it just involves it doesn't involve the cortex because if you have a cortical problem you have to have like a pretty large MC stroke for you to have in fact let me put it this way to you when people have cortical strokes they really have upper and lower extremity problems right because if you think abou

t if you're just if you're looking at that from the perspective of the homonculus right remember that the lower extremities are in the middle in the anterior cerebral artery territory and then the lower extremities are on the all the way on the other I mean the upper extremities are all the way on the other side in MC territory right so you have to have a pretty big global stroke to have like upper and lower extremity symptoms with this cortical problem right so if you see like a pure like upper lower extremities pure motor problems or pure sensory problems think about a sub cortical problem it's a bizzal ganglia problem like again somewhere around the posterior limb of the internal capsule it can also be around like the coronary dea and all that stuff but think mostly in terms of the posterior limb of the internal capsule and then the transfusion reactions again I hope that's something people understand I don't know for whatever reason people don't seem to care much about this when you're studying for exams but you then it then ends up hampering your score pretty significantly I don't get it to this DIY people never seem to focus and like you know try to actually learn the transfusion reactions it's very high you to know it shows up all the time on tests right so just one of those things that you're essentially hurting yourself if you don't know right so I'm just gonna run through them real quick here right so and I killed him or the transfusion reaction is the first big one the thing that happens is a clerical error right so you're giving type B blood to a person that has type A blood that's bad right because the person that has type A blood is making anti-B antibodies right so you have preformed antibodies right and just as you're studying the transfusion the person begins to have flank pain and hematuria that's the classic presentation flank pain and hematuria if

you see that think about an acute hemolytic transfusion reaction right and remember it is a type of type 2 hypersensitivity reaction and usually the way you treat those people is you give them fluids and obviously you can establish the diagnosis by doing a comstest okay you do like a direct comstest now if they give you a question about a person that you know has a history of like recurrent upper respiratory infections and then this person gets a blood transfusion and immediately wants the transfusion starts the person starts to have strider, it's has to have a lot of airway problems if you see that I would hope you're thinking about an anaphylactic transfusion reaction right this person likely has an Ig deficiency remember Ig is the guardian of your mucosa so if you have Ig deficiency you're pretty supposed to get in recurrent respiratory infections and recurrent gastrointestinal infections and those people right when you give them a blood transfusion because think about it if you're deficient in Ig well your body will then begin to think that Ig itself is a foreign molecule so your body can actually go ahead and make antibodies against it right and if you know you have that first because usually these people don't have the anaphylactic reaction with the first blood transfusion you know they get it they get the first blood transfusion and then you know you have that first exposure to the blood transfusion you see Ig in that in that blood transfusion you then make antibodies against it you then do this whole class switching business right so since we're dealing with Ig in this case you'll be interlooking for that helps with the class switching so you know you have that class switching and then that Ig goes and settles itself on the surface of a mast cell and then your synafil and then the next time you get a blood transfusion you get the Ig A binding to the Ig E that

recognizes the Ig as a foreign molecule you have cross-link in you degranulate those mast cells and those your synafil and they get into big trouble real quick right so that's an anaphylactic transfusion reaction and that's actually an example of a type type 1 hypersensitivity reaction again it's an anaphylactic response so it's a type 1 hypersensitivity another classic transfusion reaction is the febrile non-humolitic transfusion reaction so just be a person that and if a person I guess let me talk about the Ig deficiency the anaphylactic transfusion reaction treat that with epinephrine right because remember epinephrine is a very powerful beta to agonist so by being a powerful beta to agonist you know you open up the person's airways and you know prevent them from certain death essentially and then if you're looking at the febrile non-humolitic transfusion reaction the classic presentation will just be a person that you know gets a blood transfusion they're fine for the most part and then you know afterwards they have chills they have fevers but they will not be hemodynamicly unstable everything will just be fine usually for those people just give them a sedum enough and just give them like a fever reducer the mechanism or pathophysiology behind that is you essentially just have cytokines from the white blood cells in the stored blood that are causing those issues right so you know that's pretty much that's pretty much it there are you doing to do anything special for those folks and then another classic one that you see on an exam is they give you a question about a patient and this patient has like hematuria has like you know relatively mild symptoms and they'll tell you that oh comstis is actually positive and this person you know got a blood transfusion like two or three days ago if you see that then you want to think about a delayed hemolytic transfusion reacti

on it's literally the way I think about it is the pathophysiology is essentially the same as an acute hemolytic transfusion reaction but the thing that happens is that one they tend to have less severe symptoms and two it tends to happen a few days after they get the blood transfusion right so that is the key difference between an acute hemolytic transfusion reaction and a delayed hemolytic transfusion reaction those will both have a positive comstest right and then if they give you a question about a patient and you know this patient gets like a large volume blood transfusion like like 15 units of blood or something like that and then the person begins to bleed like pretty severely if you see that then you want to think about like a dilution of thrombocytopenia that has happened from that blood transfusion right the thing is when you're transfusing people with blood you cannot just give people blood willy nilly right remember many things in the blood people tend to think of those things in terms of absolute numbers the truth is your blood usually does not care about the absolute numbers of something it's the actual concentration that ends up making a huge difference right so the thing is even if you give a person like you know like 20 units of blood right without giving platelets yes you may say oh but this person had enough platelets to start with no they do but because you've introduced that much extra blood you need platelets to essentially keep that blood in check right so the thing is when you give people a large volume blood transfusion and then you forget to give them platelets you're setting yourself up for you know pretty pretty bad disaster right so under those circumstances that's what's causing the person's problem you give a person like a super large blood transfusion that will just dilute out your platelet count and that can cause a lot of problems righ

t and then if they give you a question about a person that gets you know like a large volume blood transfusion and in this person is having like you know like shortness of breath it tells you that oh you hear crackles when you've scooted along so you hear that both bases and then you'll get like chest x ray or chest ct and you see like infiltrates like diffusing infiltrates everywhere but you know the person's like pulmonary capillary which pressure is fine if you see that or you know any other like marker of cardiac function if it's okay then under those circumstances you want to think about something called trolley right so transfusion related acute lung injury to be perfectly honest with you let me give you a simple way to understand this I think of it as ARGS from a blood transfusion okay if you think about it that way you probably be fine for purposes of the NV Me exams right so if you notice when I was giving out the vignette I said that the pulmonary capillary which pressure is fine the thing is the pulmonary capillary which pressure is a proxy for left-atrial pressure right so if the PCWP is fine that means this person's pulmonary edema style symptoms you're seeing is non cardiogenic in etiology right because the thing is your friends at the NV Me one thing they will try to trick you with this they can also give you a question about a person that you know gets a blood transfusion person has shortness of breath crackles when you listen to the lungs they have like infiltrates everywhere on chest imaging right and then they'll tell you that the pulmonary capillary which pressure is elevated right or they'll tell you that the central veno spray I'll say for the most part PCWP will be elevated right if you see that then that's a different kind of transition reaction that's actually something known as taco right so like a transfusion associated seculatory overload oka

y transmission associated seculatory overload basically people that you know have like heart failure or you know usually heart failure folks you know they can get into trouble if you give them like again big-time blood transfusions their hearts may not be able to handle those kinds of volumes right so they will have like pulmonary edema but it'll be from a cardiogenic etiology right so if you see like pulmonary edema and they seem to have like cardiac markers out of whack in the setting of a recent blood transfusion think about transfusion associated seculatory overload but if you notice that I work cardiac markers do I mean right so again things like pulmonary capillary which pressure central veno pressure which is a proxy for editor pressure BMP right remember if a person has like a CHF exacerbation the beam will be will be real high right and sometimes the beam will put that the person has like a new S3 heart sound remember S3 is usually indicative of like volume overload right with regards to the heart right so those are transfusion reactions they are very again it's just one of those things you know if you don't learn it you're gonna pay a price on your exam I mean if you're willing to be that price that's fine but I suspect that most people taking step to seek a probably not very you know willing to pay those kinds of prices because that just gives you less margin for air with regards to your test so just you know something to keep keep at the back of your mind and then one quick thing I want to review here I want to go ahead and review the trinocryl thyroid pidosodders again these things tend to be very pervasive on the USM a.m.

exam right but people tend to get these wrong right so let me maybe start with the easiest you know many people seem to recognize this pretty well right so what if they give you a question about like a 42 year old computer science professor beginning to do like inappropriate things at work inappropriate things at home puts a lot of stuff in his mouth and then the tell you that is that data age of 50 from like some weird stuff right under unusual circumstances if you see that I would hope you're thinking about hunting ten disease right so remember hunting ten disease has porosomal dominant inheritance right and don't forget it's the C.A.G.

trinocryl thyroid pete and because it's a trinocryl thyroid pete the solder right or it's a lot of the more dominant the solder you tend to have this principle of like anticipation like occurring right so anticipation is where like you know family passes the genetic disease down to like like the offspring right but the offspring seems to begin to begin to like they essentially begin to express symptoms at a much younger age right so it's like oh that died at 50 but this person sees 42 years old beginning to have troubles right because once you start expressing signs and symptoms of hunting tins they're probably going to be dead within like two or three years right so it's a terrible disease there's something you never wish on anyone so again if you have a family history of hunting ten disease you know it's probably not about I get to get some kind of genetic testing so you don't pass it along to offspring so hunting tins again or the Zomodominant and Heritins genetic principle anticipation C.A.G.

trinocryl thyroid pete they'll have like a lot of movement problems and I mean when they start exhibiting symptoms you can try treating them with a dopamine antagonist like Hallopere doll or you can treat them with like a V-matting inhibitor like tetrabenazine right but those things just is just kicking the problem down the road the the person is gonna die for sure it's just a matter of time right just a matter of time those drugs if I'm not mistaken I don't think that should do anything to survival they just reduce your symptoms but the person is still gonna die right so not the best situation to be in and then what if they give you a question about like a 23-year old guy and you tell you that this guy has like you know goes to see his physician for like a regular doctor's appointment and this person is having trouble the physician is having trouble releasing his grip from the patient right and then they tell you that oh this guy is 23 but he's bald right if you see that what are you thinking about well I would hope you're thinking about my attorney dystrophy right so my attorney dystrophy the classic presentation is early bald in in a young guy right I mean there are some young guys that get bald I'm not gonna make fun of anyone but there's you know some popular basketball players that especially on the team I support that you know we have those kinds of things but yeah let's just let that go because I'm a Laker finished probably not be trashy living a podcast so but we'll talk about that later so essentially if a person is bald right early you know early bald in physician is having trouble releasing his hand grip from the patient that's my attorney dystrophy you may also see there's a newborn that is hypotonic at birth in fact the mbm is beginning to love this presentation because when you're like hmm newborn with hypotonia but I thought people that have my attorne

y dystrophy are hypotonic yes they are hypotonic but they are hypotonic later in life not at birth at birth they are hypotonic that's a very high-yield thing to know right so what is the relevant triadentry of that repeats with myotonic dystrophy it's a CTG right so again haunting things will see a G my attorney dystrophy CTG the CTG triadentry of that repeats but one other thing your friends at the mbm expect you to know is that it adorizes from a dm pk gene mutation so d as in dog m as in mom and then pk right so dm pk gene mutation and again that's the classic we present on exams now what if they give you a question about about like a new like a child you know that has like a taxiia has to visit the orthopedic surgeon or ton has like deep problems has like scoliosis and then they tell you that oh they have like high arching feet so they need to wear like specially feet at shoes if you see that what are you thinking about that high arching feet by the way is known as best cave us right so if you see that what are you thinking about well I would really hope you're thinking about Friedrich's taxiia right now the thing is you may say why does the mbm e care about Friedrich's a taxiia well let me tell you why the reason your friends at the mbm e care about Friedrich's a taxiia is because it has some very unique properties compared to the other training fluid type repeat disorders it has definitely has some very unique properties compared to the other training fluid type repeat disorders right so what are those unique properties one is that it is not inherited in an orzo more dominant fashion it is inherited in an orzo more recessive fashion I'll say that again Friedrich's a taxiia is inherited in an orzo more recessive fashion okay that's one snuffle there and then the next snuffle there is the training fluid type repeat is a little atypical right because many people ha

ve tend to like oh if it's a training fluid type repeat the first letter in the training fluid type repeat must be a c well that is not the case with Friedrich's a taxiia Friedrich's a taxiia the training fluid type repeat believe it or not is g a a okay very high on it is g a a right so that's the classic presentation on exams it has orzo more recessive inheritance and it has a g a a training fluid type repeat and the thing is usually one of I will say probably one of the most common causes of death in these kids is hypertrophic cardiomyopathy although they don't die as kids usually die as adults you know usually around the age of like 30s like late 30s early 40s usually die of like a hypertrophic cardiomyopathy right and then the last training fluid type repeat the sort of I'll talk about I guess I can talk about it again in the context of a vignette what if they give you a question about a child you know like a boy right so obviously this will be a boy so it will be a boy that you know has like really bad intellectual disability this boy may have like other them related symptoms and you know they'll have like a long face they'll have like big ears they'll have like big testicles right so like the five dollar worth for that is macro or kid is him right if you see that or they may even have like the murmur of like my trovaugh prolapse if you see that what disorder are you thinking about I would really hope you're thinking about fragile X syndrome right fragile X syndrome I remember fragile X syndrome again it's unique in the sense that it's it's actually inherited in an X linked dominant fashion okay and the training fluid type repeat here is CGG okay CGG it's a CGG training fluid type repeat and one thing that happens here is that you want to make sure you know that it's actually associated with and with like and like the gene so you know like the way like my electr

onic dystrophy was associated with a DNP key gene mutation well unfortunately your friends at the mbm also expected to know the gene that's all screwed up in a kid with fragile X syndrome that gene happens to the F to be the FMR1 gene okay the FMR1 gene right so again that's kind of like the big thing you want to keep on the back of your mind with these tests right and sometimes they occasionally ask about the mechanism behind like some findings right so like for example like morphine you're like oh morphine they have fibrillium problems well here's the thing people that have fragile X when they have that training fluid repeat they begin to have like hyper methylation right so you may say divine this sounds a lot like step one further well we show the best as you take step two the thing is this is something I think I've not maybe said enough in my podcast many people don't seem to realize this but the truth is the learning objectives that the mbme uses for step one is the exact same series of learning objectives they use for step two and the thing is the USML is step two CK exam has kind of undergone a shift over the last couple of months they now focus quite heavily on you being able to understand pathophysiology right so because you see this common complaint from people that take the test they'll see you know I would define I was reading the question as I read the question I knew exactly what they were tested but then I was reading the answer and it was not what I expected right usually those answers are usually like sentences like you know one sentence where they're essentially throwing like different kinds of pathophysiologies for different diseases and then you need to pick out the right one the thing is fragile X syndrome is a great example of that kind of question because the thing is it's clinically relevant for starters that's one but another kind of nice thi

ng there is the mechanism behind the disease makes perfect sense because it's a throwback to cell biology from step one right so think about it when you met the late genes what happens to gene expression it goes down right so the thing is people that have fragile X syndrome they have symptoms because certain genes on the X chromosome that are supposed to be expressed do not get expressed right so it's a hypermethylation problem and the thing that causes the hypermethylation is when you have that FMR1 gene mutation and you have those CGG trinucrylthide repeats and again please do not forget that people that have fragile X it tends to have an association with autism and like all the autism related are the soldiers again these are things they all test so again let's run through this trinucrylthide repeats haunting disease is a CAG trinucrylthide repeats myotonic this and that's autosomodominant inheritance myotonic dystrophy is a CTG trinucrylthide repeat and it's also autosomodominant inheritance like content tense fridrixate taxia is a GAA trinucrylthide repeat and it's inherited in an autosomod recessive fashion and then fragile X syndrome is inherited in an X-linked dominant fashion and the trinucrylthide repeat is CGG okay the only other X-linked dominant the soldier that you need to know for purposes of the US Emily exams is outport syndrome outport syndrome is it's a trinucrylthide repeat but it's also inherited in an X-linked dominant fashion remember the classic triad there is can see can be can hear high C right so can see they'll have eye problems can be they'll have an fridrix syndrome style presentation and then can hear high C they'll have problems they'll have problems in the in the ears right so they'll have like like hearing loss and again you'll see it in multiple family members right in fact a very good test-ticking strategy for purposes of the US Emil

y exams I use this at least I'll say yeah actually I still use this to this day to eliminate answers or do not on US Emily exams thank god I'm well passed those tests but basically the thing that happens is if you notice that multiple family members seem to be having the same problem in an NV Me question right then it would make sense to eliminate all the answers that are not genetic sounding right because if multiple family members are having a problem that's essentially the NV Me telling you that this is a genetic disorder you need to pay attention to this right so again just a useful test-ticking strategy to keep at the back of your mind for exams now real quick let's look at the let's look at the like some rescue agents for some problems that you may see on tests right so if a person has a set of menophaned toxicity how do we treat a set of menophaned toxicity well I hope you're telling me in a cell system right remember if a person overdoses or a set of menophan you know you'll make all these three NEPQI right it's like N-A-C-DL-P-Benzo-Queen-O-N-E-Mino something like that basically people calling NAP-K-N-E-P-Q-I so that NEPQI it's a powerful oxidant right so you can cause free radical damage to your liver and then you get like hepatic macrosis so you know to kind of leave that off you try to regenerate the glutathione system by giving N-A-C-DL-C-DL-C-DL-C-DL-C-DL-C-DL-C-DL essentially provides of hydro groups to replenish your glutathione right so again high-o thing to know for exams and then what if they give you a question about a person that gets like a long like you know they've been getting like a nitro-procide infusion for days and in this person has like a lactic acid dosage, altered mental status becomes comatose if you see that I hope you're thinking about cyanide poisoning right remember cyanide I mean nitro-procide so they can set this up as a hypertens

ive emergency or hypertensive urgency question I remember nitro-procide is used to treat hypertensive emergency or urgency but the problem with nitro-procide is it contains a ton of cyanode groups right so it can cause a pretty nasty cyanide poisoning and remember that cyanide right it binds to hemoglobin right and when it binds to hemoglobin it essentially actually so let me explain this actually because again this is something that has classically misunderstood by medical students so maybe let me backtrack here for a bit so the thing is cyanide you may see define is it because like is cyanide bad because it binds to hemoglobin no cyanide is not bad because it binds to hemoglobin in fact your cyanide toxicity is certainly not from it binding to hemoglobin right many people tend to confuse that with carbon monoxide carbon monoxide binds to hemoglobin makes it unable to bind oxygen but cyanide does not do anything to your hemoglobin cyanide kills one of the complexes of your electron transport chain if you kill one of those complexes your non-stickin and pretty certain it's complex for if you kill complex for then you're not gonna have oxidative phosphorylation happening right so obviously you're not gonna be able to make adequate amounts of ATP from glucose breakdown right from like yeah from the breakdown of glucose right so if that doesn't happen right you obviously switch into anaerobic metabolism like glycolysis for example and what is the outgrowth of glycolysis it's lactic acid right so it should make sense that people that have cyanide poisoning get a lactic acidosis this is a high you'll think to know for example right so how do you treat that cyanide problem well the thing is cyanide because if you think if you look at hemoglobin our bodies hemoglobin our bodies hemoglobin contains iron in the two plus form in the ferrous form Fe2 plus right the thing is cyan

ide does not bind iron in the two plus form or at least it doesn't bind it appreciably but if you look at iron in the three plus form right ferric iron right that ferric iron bind cyanide really really really really right so the thing is you could be like oh divine well is there some magic way we could convert a lot of the Fe2 plus in our body to Fe3 plus and then bind that cyanide and get rid of it well it so happens that there is a way that that can happen right because again if you go back to college chemistry Fe2 plus has an oxidation number of plus two Fe3 plus has an oxidation number of plus three right so that means ferric iron right is more oxidized than ferrous iron so if you give an oxidizing agent like emol nitrate okay emol nitrate will convert the Fe2 plus Fe3 plus that Fe3 plus will bind the cyanide and then after you bind the cyanide then you then give sodium thylosolvite you form thylosanide and then you essentially pee and pop out the cyanide ciphly okay so essentially you are inducing a methemoglobin emium remember methemoglobin is hemoglobin that contains iron in the three plus form so you induce a methemoglobin emium with emol nitrate you bind up the cyanide you give sodium thylosolvite to form a complex iron and then you pee and pop it out ciphly now another thing you may occasionally see on MDM exams as treatment for for cyanide poisoning is hydroxyl cobalamin that's like a vitamin B12 derivative in fact to be honest with you if I were writing an exam question on cyanide poisoning instead of putting hydroxyl cobalamin I'll put like vitamin B12 derivative as an answer right again that's a classic thing the MDM does to people right they will take what you know and just either describe it or ask you for the mechanism behind it or give you like a different word that you're not familiar with right and you've probably heard me refer to some of my buddi

es as laminated calcifications that's a classic thing the MDM tends to do to people on exams now what if I they give you a question about like a child you know mom has a lot of bottles out the child maybe consumes like a newborn maybe not a newborn you're not that dexterious but you know like a little child couple months old and this child is now having like like bloody stones bloody MSS lactic acid doses this child is just not doing well you know becoming him with dynamicly unstable I hope you're thinking about like iron poisoning on that those circumstances remember iron is super toxic to the GI tract right especially when you take a ton at once right and the thing is usually you can actually a pretty easy way to diagnose iron toxicity is just to throw that child you do like a baby gram you know babies they're like tiny right so the it's almost like they're swallowed up by the extra machine and you just go baby gram and you see things that are radio peak right because there are very few things that you can swallow that you see on imaging right but if you see clearly on imaging it's probably a metal like iron right that's a classic way that tends to show up on exams and you can kill that iron with like deferoxamine right or deferoxerox right so you can use deferoxamine or deferoxerox please don't confuse deferoxamine deferoxerox with dexeroxamine dexeroxamine is also an ion killiter what it is used to treat or I mean prevent the dilated cardiomyopathy that can happen with toxicity of the anti-cancer agents doxorobsin and donor rubsin okay so don't mix those things up and then obviously for person over doses on an opioid you want to give them like an aloxone I don't give now trexone before the now trexone kicks in on your patient with long dead you know that's probably not a probably not a good outcome right and then for person has like methemoglobinemia where you wan

t to give methylene blue for that if a person has organophosphate because methemoglobinemia right it's when you have a ton of iron a ton of hemoglobin so you have a lot of hemoglobin containing iron in the three plus form right hemoglobin with iron we can remember a ferric iron cannot bind oxygen it binds to an eye great but it doesn't bind oxygen right that's why if you're really plugged back to biochemistry there's like one of those steps in glycolysis that involves the production of any pH that any pH is actually actively used in red blood cells to activate an enzyme known as methemoglobin or I guess as a cofactor for an enzyme known as methemoglobin reductase and methemoglobin reductase's job is to literally use the reducing power of any pH to convert Fe3 plus to Fe2 plus so if that happens you know you have Fe2 plus the ferrous form of iron that is able to carry oxygen right so again hemoglobin that has iron in the two plus form so if you have hem that contains globin and iron in the two plus form that's hemoglobin but on the flip side if you have hem that contains globin and iron in the three plus form that is methemoglobin right so if a person has methemoglobinemia so it usually be a person that's taking I don't know like you know like person going to an African country getting malaria perfect access maybe they get like primal queen as a pathologist ising agent so I can cause like a methemoglobin emia or like dapson so they can give you a question about a person being treated for like numocystis, zerovetsinomonia or getting like PCP perphylaxis right at that magic city for count of 200 or less right those things are pathologsydysine agents and those can cause those kinds of problems right so again that's something higher to know for exams and then if a person has carbon monoxide poison obviously treat those people like hyperbarica oxygen if a person has lithium

toxicity usually would thatize especially the acutelycein tomatic having seizures and all that badness you know you can go ahead and thatize out that thatize out that lithium what other things I want to say you know I feel like this podcast has gone on for long enough it's almost like 40 minutes I'll just go ahead and stop here so you know as I do at the end of every podcast again I do offer one on one tutoring and large group tutoring for many exams step one two CK two CES step three brick clinical medical exams 30th shelf exams if you're medicine resident I tutor to the internal medicine in treating exam the internal medicine board exam if you're a college student I tutor Gen CAM, OCAM physics bio-cam, histology, physiology if you have you know like a relative that needs to learn from any of those things you don't feel free to reach out to me and then I do these booster courses it's 10 hours for step two CK step three it's 20 hours for step one where I in a rapid fire format using clinical vignettes I reveal like the most knows for those tests again I've done it with many people they found it to be really helpful and then if you're a college student applying to med school so like an Amcass application or med student applying to residences or like an ERAS application I do offer like one on one coaching one on one advice in for the for like these things right so like editing personal statements editing applications, more interviews, rec letters again I do all those things I've done it with tons of people most of the people I've worked with they've much that they're one of their essentially most people have worked you know actually much at their first choice with regards to residency and again like I said I have admissions committee experience like a top two med school I actually have like one year's worth of admissions a community experience so again if you need help

with any of those things feel free to reach out to me and then yeah that's pretty much it and then I do like this big super comprehensive USMELY courses but again I need a group of five to seven people I need a location and I would need like a two to three week period so if you need to turn for any of those things you have that group just let me know reach out to me through the website or you send me an email at divineintervention podcast with an s at the end at gmail.com so have a wonderful rest of your day thank you god bless you i'll see you in episode 203 I believe okay bye for now

Microcephaly, thin cerebral cortex, and facial defects; mother usually traveled to a foreign country.

Toxoplasmosis (Mom often eats undercooked meat).

Peri-ventricular calcifications, blueberry muffin rash, and sensoroneuropathy.

The posterior limb of the internal capsule (suggesting a lacunar/surgical stroke).

Acute occurs immediately; Delayed occurs days after transfusion. Both have positive Coombs test.

Induce methemoglobinemia using sodium nitrite (oxidizing agent) to convert $\text{Fe}^{2+}$ to $\text{Fe}^{3+}$, followed by sodium thiosulfate to detoxify the iron complex.

It has a GAA trinucleotide repeat, is inherited in an autosomal recessive fashion, and often presents with pes cavus/high-arched feet.

Zika virus (Look for foreign travel history).

CMV $\rightarrow$ Peri-ventricular; Toxoplasma $\rightarrow$ Diffuse/Intracranial, often associated with hydrocephalus.

Anaphylactic Transfusion Reaction; Treat with Epinephrine.

Normal Pulmonary Capillary Wedge Pressure (PCWP). This points toward TRALI (Transfusion Related Acute Lung Injury).

Fragile X Syndrome.

Metabolic acidosis/lactic acid; Treat with N-acetylcysteine (NAC) to regenerate glutathione.

Iron poisoning. Treatment is Deferoxamine.

Zika virus (Look for foreign travel history).

CMV $\rightarrow$ Peri-ventricular; Toxoplasma $\rightarrow$ Diffuse/Intracranial, often associated with hydrocephalus.

Anaphylactic Transfusion Reaction; Treat with Epinephrine.

Normal Pulmonary Capillary Wedge Pressure (PCWP). This points toward TRALI (Transfusion Related Acute Lung Injury).

Fragile X Syndrome.

Metabolic acidosis/lactic acid; Treat with N-acetylcysteine (NAC) to regenerate glutathione.

Iron poisoning. Treatment is Deferoxamine.