DIP Episode 120 - USMLE Step 2CK Rapid Review Series 4 (IM/Peds)

Okay, welcome. This is the 120th episode of the Divine Intervention Podcast. My name is Divine. I am an R1 Reelger resident, I guess PGOI2. And to the I will be continuing my Rapid Review Series for the USM Listep 1. And I will be this will be series, I mean sorry for the USM Listep 2 CK and this will be series 4. And our focus on a broad range of subjects but again I will try to hit internal medicine pretty hard. So let's go ahead and begin. Right, so what if you get a question about like an 80-year-old person that you know is losing their way like coming back from a store and they forget to turn off the stove and the MMS is like 20 over 30 what are you thinking about? Right, that is clearly Alzheimer's right. So those people have Alzheimer's and remember in Alzheimer's right what is the neurotransmitter that is classically low? That'll be a pseudo-coaling right. And unfortunately your friends at the MBM, they love to test your ability to integrate neurological disease with neuro and atomic relationships right. So the thing is in Alzheimer's there's low levels of acetylcholine. The thing is if that's all you needed to know everyone will cross step two right but unfortunately that's not the case. So they cannot take things a step further right. So remember that acetylcholine is meeting the BISO nucleus of my nerd right. So when a person has this dysfunction of the BISO nucleus of my nerd they will have symptoms of Alzheimer's disease right.

And another way they also love to test it on the exam is remember that the rate limiting enzyme in the synthesis of acetylcholine is an enzyme known as colina acetyl transferase right. So if you have dysfunction of that enzyme right you again that will increase the presence risk of like an acetylcholine deficiency and Alzheimer's right. And then don't forget right that kids with kids with Down syndrome right. They tend to get early on set Alzheimer's because they have tried SOMI 21 so they have too much of the pre-sendling gene if you may right. So if you know right of the bat that deficiency of acetylcholine is kind of like involved in many of the symptoms in Alzheimer's or at least in the path of physiology you then ask yourself okay so how do I treat Alzheimer's right. So obviously you want to do something that involves bumping up your levels of acetylcholine right. So you want to do something like an acetylcholinesteris inhibitor and those acetylcholinesteris inhibitors that I use for Alzheimer's you do actually need to know them specifically right. There's three of them like a DRG right. So the one is a Donepesial right. And then the next one is a gallantamine and then the next one is a rivestigmin. They have all acetylcholinesteris inhibitors that I used in the treatment of Alzheimer's. Okay now what if you get a question about a kid you know let's assume it's a kid that so this will be a piece focused stem I guess.

What if you get a kid that has the children that occasionally this kid has episodes where he cries and he becomes sad not it.

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s cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries cries I think I used this numonic ash to remember like in order of like decreasing life expectancy right so if they have like so the A stands for Argentina the S stands for syncopy and then the H stands for Hart failure if a person with a diodesis has Hart failure symptoms the mortality within a year is I think like 50% of some crazy high number okay so that's a high you thing to know and then if you see a person in the a 50's with a diodesis right you want to think about a bicospediotic valve right that's pretty classic for for a diodesis the no system and remember people that tend to get

bicospediotic valve early people that have like toner syndrome right like toner syndrome remember toner syndrome has some other high-yod associations in addition to the bicospediotic valve they have like congenital lymphedema right so those are cystic hygromis and then remember that they can also have a partition of the yoda right so if they give you a down syndrome having sorry a ton of syndrome patient that has hypertension in the upper extremities and hypertension in the lower extremities think about a partition of the yoda right and then remember those people they also have like a hyper gonadotropic hypogonadism right because they don't have a gonadotropic hypogonadism right and then remember that they can also have horseshoe kidney right so again if they describe it according to T Is in a lady that is like fall for them some inches tall right think about horseshoe kidney right because remember those toner syndrome kids tend to be pretty pretty tiny right tend to be like short right so think about like horseshoe kidney with the inferpals of the kidney fuse they're stock on dead in fear of the entire recovery right again these are all integrations you need to that's the thing like I tell people this tell all the people I tear this doing well on these mbm exams is not about how much did you memorize of course like you need to have a good memory to do well on this to be honest actually you don't need a great memory you just need an okay memory the thing that is important is being able to one be a good test sticker and then to just be able to integrate concepts amongst multiple fields that's why do these rapid review series it's really like literally from requests like divine how do I pull this together that's why I love to do these kinds of podcasts okay so back to the world right so I just talked about a Yodic stenosis now what if you get a question right about a pe

rson that has that has they have like bounding pulses they have this a dastolic murmur that is heard best that the left-low external border and then you notice that they have blood pressure is like 150 over 50 right so they have like a super white pulse pressure what number are you thinking about I really hope you're thinking about the Yodic regurgitation right and fuck limited the strict frame bm's if you ever see a white pulse pressure on an mbm exam your next thinking step is am I dealing with a kid or an adult it's an adult it's very likely going to be very critical to the right answer it's a kid it's very likely going to be patent doctor satiriosus that is the right answer the thing is the Yodic regurg and patent doctor satiriosus those things tend to have fairly similar like he more dynamic consequences if you really think about it again that's something for not not something I'm going to be discussing in a rapid review lecture but it's just one of those things you want to keep at the back of your mind for example again I promise you take these mkms take your real exam you see that all these things I'm saying are true right and then what is the congenital heart condition that's classically associated with people with morphins right so people of morphins tend to get what mitrovol prolapse right and I hope you remember the path of this buzzword for my trova of prolapse right that'll be a mix some of those degeneration right mix some others degeneration and then they also can get like erotic dissection right and remember in the erotic dissection the bus phrase you want to remember is like a cystic medionic crosses ok cystic medionic crosses or cystic medionic degeneration they love to test those for whatever bizarre reason on mbms right so remember morphin syndrome with those right and then also remember like those other connective tissue diseases like urn as downl

oads right those things can be associated like erotic dissection as well erotic valve problems also if a person has a kilo sin spawned a lightest it has an association with erotic problems right and then also don't forget right if a person has syphilis remember syphilis loves to torch the viso viso viso of your erotic arch that can also cause an erotic dis right and then what if you get a question about a person that has that has like you know they're an immigrant from a developing country and you hear a dastolic murmur with an opening snap at the apex right what are you thinking about there right I hope you're thinking about again mitro stenosis right mitro stenosis so white did I mention the term immigrant well I mentioned that term because they likely had an operator infection that was likely from strip pyogenes right so group E strip and then it was likely not treated and then they got mitro stenosis from that right so remember that mitro stenosis the biggest risk factor for mitro stenosis is rheumatic fever right that's how you to know for example and then remember that mitro stenosis itself is the biggest risk factor for a fifth again they love to test these risk factors on step two seeking on step three right and then remember that your biggest risk factor right for like for like um myocardial infarction for triply smoking right and then your biggest risk factor for strokes and voyotidisection is hypertension right these are things you should have on your fingertips as you prepare for these exams now what if you get a question about a patient that um has a continuous machine like murmur like this you hear this murmur throw the cardiac cycle what are you thinking about right that's pretty easy that's a bit into dr satiriosus and then remember people that have a history of like carstenoid syndrome right remember doesn't cause any problems if it's in the bowel rig

ht because the liver has the ability to metabolize a carstenoid but remember again carstenoid is a tumor that makes aerotonic right pretty much right so remember that in carstenoid um you need mitro to the liver to begin to have like systemic problems right so when you have those mitro liver um the liver right or release the serotonin from the carstenoid a tumor and then that will begin to cause a lot of like right-sided heart lesions right and the way remember the right-sided heart problems is like with the nomonic tips right so like try cosperine sufficiency and pomonic stenosis right so those people have those kinds of uh symptoms uh the reason you don't get left heart problems with carstenoid is again the lungs has the ability to to metabolize that as serotonin right remember the lungs in addition to helping with like oxygenative function and all that crap your lungs actually pretty solid metabolic organs right I mean like your angiotensin converting enzyme but you think it's found it's found in the lungs right it's found in the endothelium of the capillaries of the lungs right so um your lungs have the ability to work on a serotonin and uh you do need to remember the right and again I apologize if this podcast seems kind of random I'm literally like about to go to bed it's almost 11 30 I'm literally about to go to bed I'm just sitting on my bed just uh uh saying outstep to seek your related things before I sign off and uh go and sleep but basically um um people with carcinoid right so remember one of the breakdown uh things from uh serotonin is something called 5hechi AA right so remember that if a person has carcinoid you screen first by uh checking uh levels of like you observe elevated levels of 5hechi AA in the serum or in the urine right and the thing is right one nifty way your friends at the endgame you actually love to test that 5hechi is in the context o

f depression right so we know that people that are depressed right if you remember like the monoamine theory of depression those people tend to have low levels of serotonin or epinephrine and dopamine right so the thing is if a person is depressed they probably have low levels of serotonin metabolites in the SCSF for example like what 5hechi AA okay so that's a very nice way they can test that factoid on mbmi exams right so those are I guess the kind of like the cardiac things I want to um actually let me say one more thing about um carcinoid syndrome right so the thing is carcinoid syndrome right you're basically making a ton of serotonin the problem there is serotonin ultimately comes from triptofan right I mean another info serotonin is 5hechi 5hechi Droxy triptofan right so if you're burning up all your triptofan in making serotonin there is some other high-yoda amino acid you're not making like myocene right if you're not making niacene that's a problem right because you can get a pelagra with that right so you get like the four d's the dermatitis the diarrhea the dimension then the bad D that is death right so that's one way they can integrate carcinoid syndrome with uh pelagra right with like a niacene remember niacene if I'm not mistaken it's vitamin B3 okay uh so again those are all high your things to know there okay so let me maybe talk about one more topic and then integrate a few more things and then I'll sign off for the day let's see what can I talk about um okay so what if you get a question about a patient that um let's see so what if you get a question about a patient that over the last three months he has been feeling really tired like just feeling super fatigued he has been losing a ton of weight um he has been having like skin hyperpigmentation um and then you get some laps right and then you notice you're like man your CBC looks terrible you're l

ike man this person you'll see no field count is like 15% and then you look at their BMP you notice the sodium is like 123 their potassium is like 6.5 what are all those things leaning towards I really really hope you're seeing adicence disease right adicence disease right so adicence disease another name is primary adrenaline and sufficientcy right remember adicence disease it's basically an autoimmune problem where you destroy like the you essentially destroy the adrenals right so your adrenal cortex is gone right so your zone of glomerulosa will not work so you're no longer making an outdoster your zone of fasciculata will not work so you're no longer making cortisol and your zone of particular is also not work so you're no longer making sex steroids although that's maybe not the most important consideration in the world where you won't be making things like GGS anymore right so let's sort of revisit that right so the thing is adicence disease right so you see all these things I posed in the Q step right we have hyponitrymia because remember when you have an outdoster in deficiency remember our doster on right so if you go way back to step one you remember like the distal nephrine that has like the collecting duct with the principal cells remember on the urine side of the principal cells you have this inic channel that reabsorbed sodium that's on the activity of our doster right and then as sodium is being reabsorbed you create a negative charge on the urine side that draws out potassium through I believe a channel known as the romky channel right and then you waste potassium in the urine so our doster is to reabsorbed sodium waste potassium right easy enough right so if a person has an outdoster in deficiency basically they have adicence disease they will have hyponitrymia because they are not reabsorbed in that sodium and they will have hyperchilemia because they

are not wasting potassium that's one thing next thing is those people tend to get a metabolic acid dose because if you really think about it outdoster if you scale a little further down in the in the distal nephrine where you have those alpha-intercalidate cells those alpha-intercalidate cells right on the urine surface they have a proton that literally just dumps protons into the urine right so the problem is if you again if you have an outdoster in the efficiency you will not be able to dump those protons in the urine right and if you don't dump those protons in the urine you retain them right and the thing is if you want to sort of take this thought to a logical conclusion those people the metabolic acid doses they have is a non-anion gap metabolic acid doses right and taking this even a step further remember that non-anion gap metabolic acid doses right it I mean it's literally arising from a high-poil to sterone state right so that's literally a type 4 renal tuberculosis that you go there right so remember anything that causes a high-poil to sterone state will cause a type 4 RT right so again that's a high up we to sort of put adicence disease together with with um your non-anion gap metabolic acid doses right and then remember right people with adicence disease they have this eosinophilia right so remember you definitely like this is one of those things where you'll be doing yourself a huge disservice if you take step 2ck without knowing this you absolutely positively need to know the differential diagnosis for eosinophilia it just shows up 12 on the internal medicine shelf exams on the surgery shelf exams on the endgames for step 2ck on the real exam for many people right and that differential is something called DN I kind of bore this for many different sources and then I've progressively expanded it as a time as going on but probably the more complete one is

DN quadruple acp right so all those that stand for the D stands for drugs right the N stands for new plasm the first A stands for like adicence disease the second A stands for acute interstitial nephritis remember that with the tread of a fever rush and the eosinophilia the third A stands for allergies right the fourth A stands for asthma right and then the so DN quadruple acp the C stands for collagen vascular disease so you're autoimmune crap like tulip, sclerodermal and all that and then the P4 parasites right so the thing is if people have adicence disease maybe like divine why do they have eosinophilia well here's the thing the thing is steroids glucocorticoids basically because of eosinophils right so the thing is if you have glucocorticoid deficiency because your zona fasciculata is all knocked out with adicence disease well your eosinophils will persist for a longer time in the serum because they're not just gonna die they're not gonna like die before their time pretty much right so you have an eosinophilia with that okay if you ever see a CBC odocinophilia that should be a gimmick question and an NV Me because they essentially telling you the answer once you know that differential chances are you will get to the right answer right so how do we diagnose adicence disease right classically on NV Me is what you will do is you will do something called an act stimulation test right because if you think about it if you give act H right if your adrenal glands don't work right your cortisol levels will not rise right your cortisol levels will not rise so failure of your cortisol to elevate with act H administration is pretty good with regards to diagnosing adicence disease and obviously if you want to treat adicence disease you need to replace them in a localicoid they are missing with the fluidocortisone and then you need to replace the glucocorticoid they are missing

okay and again remember you have sodium and potassium problems when you have primary adrenaline insufficiency if you had secondary adrenaline insufficiency so let's say for example you have like some reason why you're I don't know like she has syndrome of some weird crap where you're not making it so you're not stimulating the adrenal glands you're not gonna have sodium and potassium problems right because remember your sodium and potassium balance is maintained primarily by our duster right and our duster and is under the control of the renein and juteins in our duster and system so if your adrenal gland itself is not all screwed up then that's not a problem at all that that is literally not a problem right because the renein and juteins in system sort of starts kicks off in the kidneys the adrenal gland is right there it's not a huge issue so you will get like the your synophilia and all the other weird crap but you won't have like the you won't necessarily have the hyponitremia or the hyperchilemia right because again your drostronis alive and well the reason you get those problems in primary adrenaline insufficiency is like literally and juteins in two has no sites to act on because the adrenal gland is essentially gone right so on this whole topic of primary adrenaline insufficiency right so why do they have the skin hyperpigmentation right clearly they have that because remember there's this agent known as pomc or pro opiomelano quartine right that is a precursor to acth and msh right and so an msh right is melanocytes stimulant so if you're making a ton of it because there's no negative feedback from the adrenal gland because you're not making cortisol you'll be making msh at the same time you stimulate your melanocytes and you get a you get a skin hyperpigmentation and some other weird high your things you want to know there right so remember the term pro opio

melano quartine right that should kind of tell you what pomc gives rise to so if by some wear chance you're taking step one or you're taking step three in the future and you're listening to the spot cast because believe it or not on step three and also on step two ck to a very large extent they test these basic science thingies every now and then right so what does pro opiomelano quartine stand for so pro let me just bring down the term pro so precursor opiom so some kind of opioid-related thingy melano melano right something that relates to melanocytes like msh quartine like cortisol like a tropin for cortisol like acth right so the thing is the three derivatives of pomc actually acth msh and also an endogenous opioid known as as beta endorphine okay beta endorphine that is one of those weird high your things that you probably need to know for step one but again you mean it may show up as an incidental loma on step two ck or step three all right so let's break down those products a little bit right so probably the big one I should focus on is ect right so ect it's already talked about how you can use it to diagnose to diagnose primary genomics of insufficiency but remember ect also has another use in the pediatric population right so if they were to give you a question about a patient that has I don't know like hypopigmented macros on the skin intellectual disability and they have like a renal mass or like a renal angioma or lipoma or they have like a cardiac mass like a cardiac aryptomaioma I would hope on that those circumstances that you're thinking about tuberous chlorosis right so remember kids with tuberous chlorosis especially they're less than a year old on mbms they tend to have this as seizure syndrome known as an infantile spasms and what I mean for infantile spasms is a west syndrome right remember that that seizure disorder right as like generalize seizu

res classically on an eeg you'll find like your classic hapsaridmia you actually treat that with act h okay so that's kind of like a nice act relationship you want to tie together on on your exams okay so I think um that's all I'm gonna say with this podcast it's already 30 minutes long that's right around where I want these are rapid review series to fall around and again as I always do for every podcast I do offer I guess at the end of every podcast I don't if I want to want you to read for many exams so step one to CK to CS step three internal medicine board exams internal medicine in training exam right your pre clinical med school exams your 30-year shelf exams and then if you have like a college buddy that is needs tutoring like physics gen cam o-cam physiology histology biochemistry I do offer tutoring for all those things right then if your college student applying to med school so like an amcass app or uh med school that applying to residency so like an iris app I do offer one on one like advising and consulting for those um again I've been on the admissions committee of like a top two med school for like a year and I've also worked with hundreds of people through the iris process and again pretty much everyone I've worked with as much that usually are their first at their first choice so take that for what you will so if you need any of these services uh reach out to me through the website or you can email me personally at uh divine intervention podcasts with an s of e and gmail.com or just email me through the website so have a wonderful rest of the day um I guess a rest of the night uh and I will see you in the next podcast god bless you thank you

Acetylcholine.

Donepezil, Galantamine, and Rivastigmine (DGR).

Hyponatremia, Hyperkalemia, and Non-anion gap metabolic acidosis.

A wide pulse pressure with bounding peripheral pulses.

ACTH, MSH, and $\beta$-endorphin.

Bicuspid aortic valve, Patent Ductus Arteriosus, cystic hygromas, and horseshoe kidney.

Acetylcholinesterase (or Choline acetyltransferase).

Drugs, New Parasites, Addison's disease, Acute interstitial nephritis, Allergies, Asthma, Collagen vascular disease, and Parasites.

5-HIAA (5-hydroxyindoleacetic acid).

Primary AI causes Na+/K+ issues because aldosterone deficiency is the main problem; Secondary AI does not cause these imbalances because the RAAS system remains intact.

Marfan syndrome or Ehlers-Danlos syndrome.

Hyponatremia, Hyperkalemia, and Non-anion gap metabolic acidosis.

Acetylcholinesterase (or Choline acetyltransferase).

Drugs, New Parasites, Addison's disease, Acute interstitial nephritis, Allergies, Asthma, Collagen vascular disease, and Parasites.

5-HIAA (5-hydroxyindoleacetic acid).

Primary AI causes Na+/K+ issues because aldosterone deficiency is the main problem; Secondary AI does not cause these imbalances because the RAAS system remains intact.

Marfan syndrome or Ehlers-Danlos syndrome.

Hyponatremia, Hyperkalemia, and Non-anion gap metabolic acidosis.