DIP Episode 316 - USMLE Step 2CK Rapid Review Series 58

Okay welcome my name is divine this is episode 316 of the Divine intervention podcasts and in this podcast I am going to be continuing our rapid review series for the USML step 2 CK exactly really this all the stuff I make for step 2 CK is pretty much for step 3 and this will be series 58 again for the list into this as much as you can listen to basically the more you listen to the more you understand the better your scores will be that's kind of like the way things things work right again these USML is again it's just about again you have to you know putting efforts to do well but let's just jump right into it so what did they give you a question about a patient?

they tell you that this patient has a history of hypertension and they see that oh over the last the patient was placed on a new anti-hypertensive drug about three four weeks ago and then this patient has been noticing a low libido has been noticing like low libido and let's see they tell you that his sexual desire seems to have dropped that is having trouble achieving directions with his wife and things of that nature or this would be a same question in a woman since she started taking this anti-hypertensive as sexual desire has gone down and they tell you that oh she's having these bilateral discharges from her breast right and one thing your friends at the MBME want to do to you I can almost promise you that you put an answer choice that says bitter blocker right because many people know that bitter blocker call sexual dysfunction but one thing right that many of us know is that on MBME exams you want to look at all the information you're given not just some of the information you're given so this person yes they have this sexual dysfunction but you seem to have a little more than that right breast discharge blah blah blah blah blah if you see stuff like this I hope you're saying huh this person looks like they have hyper-prolactinemia if you see hyper-prolactinemia in the setting of a person taking some kind of anti-hypertensive right or something to help them for their a-fib or things of that nature I'll say this drug is used more for its cardio active properties unless so for its blood pressure lower in properties right I will hope you're thinking about a calcium channel blocker like Vera Pamell right remember Vera Pamell has the ability to cause hyper-prolactinemia because this hyper-prolactinemia and prolactin one of the things it does is that it shuts down the production of G and R H so if you produce less G and R H then you produce less FSH and LH and then y

ou produce less estrogen right you produce less Hormus or productive hormones and if you make less in the way of reproductive hormones right you essentially have in some kind of hypo-gonautotropic hypo-gonadysm so that's why these people have poor sexual desire remember calcium channel blockers just as a drug class in general it pretty high-youtu understand for the USML exams they are some classic side effects they love to graft with those so we've talked about the hyper-prolactinemia Vera Pamell but remember calcium channel blockers as well can cause constipation because remember you need calcium for smooth muscle to contract so if for example a person is taking a calcium channel blocker maybe you're blocking the calcium channels of the smooth muscle that we find in the GI tract unfortunately that will prevent the person's GI tract from propelling food along and the person can have constipation right so they will have like you can literally almost get like a small bowel of obstruction presentation especially in a person that is already susceptible let's see if had prior abdominal surgery or let's say they are taking opioids for some pain chronic pain syndrome or things of that nature they have like diabetic neuropathy for those people calcium channel blockers like you know I generally know the smartest idea because those things can cause constipation can really really make their situation really bad and then remember calcium channel blockers especially the dihydroperidine calcium channel blockers right and where they have the ability to cause peripheral edema because those drugs remember they are powerful viso-diilators but they specifically viso-di-lit pre-capillary arterios remember those arterios I mean literally look at the name pre-capillary arterios right it's an arterial bed that lies before capillary if you dilute those pre-capillary arterios if you think abo

ut it more blood will flow to the capillaries and if more blood flows to the capillaries now will increase the hydrostatic pressure within those capillaries that will cause more fluid extroversition within those capillaries and if you have more fluid extroversition then you're going to have peripheral edema so it would make sense that if you wanted to treat that condition of severs in many different podcasts the smart thing typically to do is to say you know what what if I can dilute the vessels that are distal to those capillaries right aka venials if you can dilute those venials then you would draw fluid from those capillaries and you reduce the hydrostatic pressures in those capillaries and you'll reduce fluid extroversition in those capillaries that's exactly how is inhibitors work that's exactly how is inhibitors work is inhibitors the dilute post capillary venials and that will bring fluid away from those capillaries that reduce the hydrostatic pressures within those capillaries now cause less fluid extroversition within those capillaries in fact as a general concept is inhibitors they love to dilute blood vessels that come the I mean the dilute arterios as well but I think a key principle to keep in mind that you can make lots of integrations with is that is inhibitors we have this wonderful ability to dilute blood vessels that come distal to capillaries for example I've talked about this is inhibitor business with dilute post capillary venials right those venials that come right after capillaries we find systemically but if we're looking at the kidneys the efferent arterial remember in the kidneys we have an arterial portal system the efferent arterial is an arterial that literally comes distal to the glomerular capillaries is inhibitors preferentially dilute that and again if you think about it you essentially by doing that decreasing the hydrostatic pressure

s within the glomerular capillaries this whole concept of high of hyperfiltration injury people that are diabetics you can essentially like slow down the rate of decline of those people's kidneys by giving is inhibitors because remember in diabetes you have this non-insemotic like oscillation of the efferent arterial prevention when that happens that's almost like a visual construction of the efferent arterial so if you constrict the efferent arterial because the glomerular capillaries are proximal to it fluid is going to back up into those glomerular capillaries so the hydrostatic pressures in those glomerular capillaries will go up right and over time if your glomerular capillary pressures are chronically elevated that will cause something caused a called a hyperfiltration injury to those glomerular capillaries so the way to cut that down is to dilute those efferent arterials and that's where is inhibitors coming to play remember the primary physiology there is that angiotensin 2 is a very powerful constrictor of the efferent arterials so by giving an is inhibitor you'll inhibit the conversion of angiotensin 1 to angiotensin 2 so you have less angiotensin 2 so you have less constriction of the efferent arterials right and we know that our friends at the MBME on step 2 CK step 3 you're beginning to bring all these USML step 1 like questions so if they give you a question and ask oh what is the primary side of action of anala pral or lysinoprall when you have these are ACE inhibitors I hope you're seeing oh divine this is going to be in the pulmonary capillaries right it's going to be in the lungs don't make them because you know people like ACE ACE inhibitor ACE inhibitor almost be kidding kidding kidding kidding kidding you guys don't get me wrong it's sort of kind of does some stuff in the kidneys but the primary side of action is in the pulmonary capillaries remem

ber the pulmonary capillaries they are very those endophilia cells that lie your pulmonary capillaries the extremely metabolically active right they are the other cells that express angiotensin converting enzyme right that helps you convert angiotensin 1 to angiotensin 2 in fact remember your pulmonary capillaries they have the ability to metabolize serotonin that's why when a person has carcinoid syndrome back that excess serotonin yes no problem will torch the right side of the person's heart but it won't torch the left side of the person's heart why because that's serotonin as it makes it way through the pulmonary capillaries if I'm not mistaken I believe the pulmonary capillaries I think have like monamine oxidies or some enzyme that can really help with breaking down serotonin just one of those weird things again weird integrations you kind of want to keep at the back of your mind for for exams now what if they give you a question about a person right again you know the MDM is they love this thing about risk factors most common cause of stuff so what if they give you a question about a person that has they say oh that we have what is they give you some question about a person that you know has prostate cancer right and then the then maybe talk about a research studio whatever and then they say they are trying to quantify the most common clinical presentation of prostate cancer like let me ask you this what is the most common clinical presentation like if a person comes to the line lights let's say they are presented to the physician and they are ultimately diagnosed with prostate cancer what is the most likely presentation what is the most likely clinical presentation I really hope you're saying bon pinho bon pinho this is very high you to know bon pinho is the most common very high most common clinical presentation of prostate cancer is the most common clinical

presentation of prostate cancer the reason that's the most common presentation is prostate cancer right remember it likes to go through that but the vertebral plexus right so it likes to make us the size to like the bones especially to the spine to like the vertebral column right so that can ultimately cause problems so many times we see an old guy with bone pain on an embankment exam besides Pages disease of the bone we should diagnose with a bone scan one of the first things you want to think about is prostate cancer and guess what you also diagnose prostate cancer made to the bone with a bone scan right so that's why you get a bone scan to settle between those two different pathologies if you see like hot spots everywhere around the body right always like the fuse then you're thinking more along the lines of prostate cancer that has metastasized to the bone but if you see like very localized very dense hot spot right pretty classic in radiology then you're thinking more along the lines of Pages disease of the bone now again going along the same lines of this business of our friends at the MVME bringing questions from step one to step two CK what would you expect to be true of the cardiac output the systemic vascular resistance the pulmonary capillary wedge pressure the central venous pressure and a person that has a PE person that has a pulmonary embolus well if you think about it the thing is because for me I love when I'm talking about things to talk about how the MVME will also try to confuse you so the way your friends at the MVME will try to confuse you is they will give you the standard values or the standard arrows for cardiogenic shock because typically if a if a person has a very big pulmonary embolus they're going to cardiogenic shock but guess what the values you getting these different pressures for a person that has a cardiogenic shock from a PE is ver

y different for the kinds of values you get for cardiogenic shock for a person that has like like a myocardial infarction or cardiac tampon not for example right so I think one thing that would be helpful is to first talk about the standard things you get in a person that has cardiogenic shock and then after that talk about the standard things you get like the differences you get in a person that has a PE so think about this for a person has cardiogenic shock let's see they have like a big left main coronary artery infarction well obviously the first thing that will happen in those folks is that your heart will stop working well if your heart is not working your cardiac output is not going to be good at all right because your heart is literally not pumping with blood because cardiac myocytes have died so those people's cardiac output will be low if your cardiac output is low well your blood pressure is going to be really low so your body is going to be like okay well let's try to see if we can prop up those persons blood pressure so we can supply the very important organs so what happens you have visual construction so you have an increase in your systemic vascular resistance whenever there's cardiogenic shock and again because the heart is not working it's not pumping out blood then things are going to begin to back up in the heart for example blood will back up inside the left itch right so your pulmonary capillary wedge pressure will be elevated remember your left itch or pressure your any your pulmonary capillary wedge pressure is a surrogate for your left itch or pressure and also blood will back all the way into the pulmonary vascular tree and then back up all the way into the right side of the heart right including the right itch right so your central vino's pressure will be up remember your central vino's pressure is a surrogate for right itch or pressure well

why is that maybe like the way why do they call it central vino's pressure well think about it where do pretty much all the veins must in 100% of them but let's say like 99.5% of all the veins in your body with the exception of like the pulmonary vein and maybe like the thabesian veins where do they all drain into well they're draining to the right itch right so essentially the right itch is the central hub for drainage of all your veins in the body so that's why the right itch or pressures are called central vino's pressures so because fluid is backing up in the right itch in a person that has a hygienic shock then that person's central vino's pressure is going to be elevated right so again if a person has a hygienic shock the a cardiac output is going to be low the systemic vascular resistance is going to be high their PCWP which is a you know the pulmonary capillary wedge pressure which is a surrogate for left itch or pressure it's going to be high as well and your CVP right the central vino's pressure which is a surrogate for right itch or pressure will also be high as well but on the flip side if a person has a pulmonary embolus again is always important to look at where the problem is a person that has a pulmonary embolus has an occlusion of a pulmonary artery I'll say that again a person that has a pulmonary embolus has an occlusion of a pulmonary artery so if the pulmonary artery is occluded what side of the heart is going to be facing those symptoms I'll really hope you're saying oh divine is going to be the right side of the heart so pressures are going to be elevated just on the right side of the heart pressures are going to be elevated just on the right side of the heart so guess what the central vino's pressure or the right itch or pressure in a person with a PE will be elevated but the PCWP the pulmonary capillary wedge pressure which is the left itch o

r pressure will be normal or even decreased in these kinds of people because again blood is like venus return for the left heart remember the venus return for the left heart is from the pulmonary vein when if the pulmonary artery is all clogged up then there is no blood flowing from the pulmonary artery to the pulmonary capillary is the pulmonary vein so there is not much of any blood reaching the left itch so the person's left itch or pressures or the pulmonary capillary wedge pressures will be decreased so because the venus return for the left heart is decreased then that means the cardiac output for the left heart which again pumps blood out to the rest of the body through the other will be decreased as well so those people's cardiac output will be low and guess what because the cardiac output is low and the blood pressure is low then your systemic vascular resistance is going to be increased so again try to prop up your blood pressures so again in guardian variety vanilla cardiogenic shock caused by most other things your cardiac output is going to be low your systemic vascular resistance is going to be high your PCWP which is your left itch or pressure and your CVP which is your ready-trow pressure will both be high but if your presi-hast cardiogenic shock as a result of a PE the central venus pressure which is the ready-trow pressure will be high the PCWP which is the left itch or pressure will be low the cardiac output will be low and the systemic vascular resistance will be high so again I know you may be like wow divine you're harping so much on this but again you can already begin to see why a lot of people will potentially get that strong on an exam and again you don't have to be one of these people right if you just understand if you notice something like this is not something that you have to on key or anything just something you don't understand because

it makes perfect sense if you really think about it and then one other thing I want to talk about there are these newborn blood element disorders that people often confuse on Indian exams and it really breaks my heart when people do this because it's something that is pretty straightforward although it's very easy to confuse right so what if they give you a question about like nine month old child and this child they tell you that for the last three four months this child has been having fatigue this child looks has power has like a second more or say no say so say no see around the mouth right and then they tell you that they give you some labs I noticed that this child's hemoglobin is like two it's like really low but then you notice that this child's white blood cell count is normal and this child's split leg count is normal so this child literally has a pure etsyl a pleasure if you see that what do you want to think about well let me tell you first one thing your friends at the end of your trip you with you'll try to trick you with giving you like you'll give it like power be 19 or something weird like that right but the thing is the child will not have any history in the question of a hemoglobin apathy in fact in the question they will not give you any hemoglobin electrophoresis result what do you know that people that are taking these exams in the heat of the moment they begin to manufacture all this information that is not there right they begin to create their own information so they will create they will create the schema in their mind even if it's not printed in the question or that this person must have a hemoglobin apathy so this must be an anemia crisis in a present that go probably 19 they will not even give you any antecedent history of power be 19 but again they know that people take these exams very emotionally and then you fall into those traps right

so if you see a pure etsyl a pleasure with a normal white blood cell count with a normal split leg count in a child that is very young right usually these kids are gonna be less than like three years old on exams if you see this I would really hope you're thinking about diamond black fun and anemia I would really hope you're thinking about that one black fun andemia many times the mcv in these people is gonna be high it's gonna be like more than a hundred they are usually gonna have some kind of macroscopic anemia so these people have a pure etsyl a pleasure for the most part it's a mutation in like ribosomo proteins that's why they have all those problems right so they have issues yes they've synthesized the DNA but then they are having all these problems making protein so it has somewhat like a similar pathophysiology to what happens in people that have B2 O fully deficiency but it's a little down down the line right is not at the DNA level it's more the RNA level right because essentially that DNA you're not getting any gene product from it because you've essentially hijacked that ribosomo portion of things and going from mRNA to proteins so these people have a macrositic anemia and you have a pure etsyl a pleasure again that's a diamond black fun andemia so what are some common things that people unfortunately conflict diamond black fun that black fun anemia with well one thing that people often conflict this with is another syndrome that has diamond in the name is called shwakman diamond syndrome right shwakman diamond syndrome so again remember diamond black fun anemia it's your red blood cells that are low every other thing is normal but in shwakman diamond syndrome it's your white blood cells that are low those people have a look opinion but the red blood cell count is completely fine and the athlete's count is completely fine that's how you differentiate diam

ond black fun anemia from shwakman diamond syndrome and then to compare this to fanconia anemia fanconia anemia these people have a pancylopenia everything is completely low the athlete let's say low the white blood cell count is low the red blood cell count is low the hemoglobin hemoglocure everything is low right so again don't conflict diamond black fun anemia where people have just their red blood cells being low with shwakman diamond syndrome where people have just their white blood cells being low with fanconia anemia where people have all their blood elements white blood cells red blood cells play let's all be in low and also in a plastic anemia present that has a plastic anemia that name the mbm uses is to its advantage because it's a misnomer when a present has an a plastic anemia it's actually all their blood elements that are low it's actually all their blood elements that are low it's not just their red blood cells that's by what the name says a plastic anemia does not mean that just your red blood red blood cells are low everything is low your red blood cells your white blood cells are your platelets so again very high you to keep that at the back of your mind for for exams now what if they give you a question about a patient to tell you that it's like a 32-year-old female and have bm is like 37 and the tell you that she has all these very painful red lesions that sometimes give out posts under armpit that you know under axel limit is armpit you know where medical professionals here anyway but under her axel that be keep recurring recurring recurring first things first what do you want to think about in terms of the diagnosis when I was really hoping you're saying oh divine sounds like this person has a hydrodynamic a super active right and classically people that have hydrodynamic super active are people that are unhealthy on in-beaming exams it's really

going to be a person that is obese right it's going to be a person that is diabetic remember obese people that have a bm i more than 30 there will be a lot of these persons going to be a diabetic person right the thing is for people that have hydrodynamic super active are you having all these problems you need to unfortunately and you know it's recurring it's reaffecting the quality of life the smart thing to do an in-beaming exams is to actually reset this tissue that's causing all these problems right as you can imagine that's not the easiest being most being free surgery in the world right but you're going to be resetting those the tissue right you're going to be resetting those glands that are causing the problem remember when people have hydrodynamic super active it's a problem with ipocrine sweat glands right ipocrine sweat glands so you're going to essentially reset those ipocrine sweat glands and that usually has a pretty good pretty good effect on on visa people and then one other thing I want to mention I think I'm going to try to break this down to under 25 minutes today is this whole concept of urine specific gravity right so that's something that many people seem to mess up on exams right because the mbmi right like the like to put things that illustrate classic concepts that many people know but then they just describe the putting the informats that people are not used to right especially people that don't understand people that don't understand path of this so remember urine specific gravity is basically like a surrogate for how concentrated your urine is if you really dig that back down to like college physics specific gravity is basically a measure of relative density the magic number you want to remember here is 1.012 if your urine specific gravity is greater than 1.012 if it's much greater than 1.012 it tells you that this person's urine is concent

rated it essentially tells you that huh this person is dehydrated on an mbmi exam because before you're into be concentrated that means your body is trying to keep as much fluid as possible although that's also something you would find in a person that has SIDH right so in an mbmi question they can literally give you a person that has hyponitremia and then they won't give you any urinous molality they're just telling you that oh the urine specific gravity is 1.0125 which is much higher than 1.012 that tells you that huh this person's urine of molarity is pretty high but they're just giving you surrogate information like really like the recent mbmi exams one of the reasons that it's like so challenging for people is the mbmi is writing an exam of surrogates what do I mean by surrogates is the same concepts that they've always tested well they've added quite a bit of new things but and again if you want to know what those new things are check out the reddit article I wrote on the R step 2 sub I wrote a pretty detailed article on how to approach the more recent mbmi exams but that's a different discussion but essentially they give you all these surrogates same classic concepts they are still testing but they're just putting it in a different term from what most people are used to right they're putting it in terms that require understanding not just plain memorization don't get me wrong do you need to memorize those things yes but you need to understand them as well absolutely the newer mbmi exams have like almost no buzzwords whatsoever in fact if you see a buzzword you should be thanking God it should be really happy right so that's something I will just encourage you to keep in mind urine specific gravity is a surrogate for persons urine or molarity so if the number is much greater than 1.012 means the person's urine is concentrated is something you find in a person th

at is dehydrated or a person that has SIDH if the urine specific gravity is really low less is like 1.006 right that means the person's urine is very dilute that's something you're gonna find in a person that is dumping a ton of water in the urine so say for example it can be a person that has psychogenic polydipsia although remember psychogenic polydipsia those people have high ponytail and a low urine specific gravity or it can be a person that has diabetes in sypitus remembering diabetes in sypitus in each has no effect either making no ed each that's central diabetes in sypitus or you're making ed each and ed each is not able to work on its receptor maybe because you're taking lithium for bipolar disorder or you're taking the mechalocycline for some bizarre reason I don't know why a doctor prescribed the mechalocycline to you or you have hypercalcemia right these white people that have hypercalcemia they typically present with volume depletion right because they are like very very stranded on on EDH activity hypercalcemia causes and unfortunate diabetes in sypitus so people that have diabetes in sypitus they will have a low urine specific gravity but they will have that in the setting of hypermetrymia to be honest with you lose a great mbmi questions right there so if you see a person that has hyponychrymia with a low urine specific gravity and you want to be thinking about psychogenic polydipsia because those people are drinking so much water that they diluting the serum if your serum is dilute that will suppress ed each secretion and then they'll make your urine dilute because you're not keeping water from your urine but then for prescribing as diabetes in sypitus ed each is not working so they're losing a ton of water in the urine so the urine specific gravity is low but because they're losing so much free water the serum is becoming more and more concentrated

so those people have hypermetrymia so hyponychrymia in the setting of a low urine specific gravity is equal to psychogenic polydipsia on your exam hypermetrymia in the setting of a low urine specific gravity is equal to diabetes in sypitus on your test so I think I'm gonna go ahead and pause here as I do at the end of every session again I do offer one or one two during four many exams step one step two CK step three preclinical med school exams 30 a show of exams and if you're seeking tutoring with me I would say it's usually wise to book the sessions about the month in advance that is how far out my tutoring schedule tends to fill up and then I also offer these 20-hour review courses for step two CK step three they're very comprehensive we cover medicine neuro bio stats ethics peds surgery psych OB-GYN those changes from last year November of 2020 again many people have taken these courses and they've done proceeded to do really well on the exam so if that's something you're interested in the course actually starts in about two hours from now but then we also have another course taking place next month between the 17th to the 19th of June I'm kind of compressing is still gonna be the same amount of time it's just it's gonna be more hours per day so if interested in any of those just shoot me an email through the website and I will give you some more guidance I actually designed the June course to essentially try to accommodate people that have like rough schedule so it's gonna be like the test taking strategy scores will be like from 3 to 5 30 pm pacific standard time on June 17th and then the 20-hour course will be 10 hours each day on June 18th and 19th so that's kind of like a Friday and Saturday so you don't have to miss much of your rotations or whatever if you're in a rotation or something of that nature so and then I also have a You Tube channel the Vine inter

vention USM any podcasts and videos if you subscribe to that that's where I put all my videos and then I also have this podcast on Apple podcasts on Google podcasts on Spotify so if you subscribe if you you know if you subscribe on those podcasts apps then you will get basically like any time I make a new podcast or automatically upload to your feed although remember for those podcasts apps is the most recent 150 podcasts there's really not much I can do about that it's like a Word Press role that I've tried many work around it's pretty much not worked so if you want every episode from episode one you need to go on the website to find those things so thank you for listening to this podcast I hope you find it to be helpful again the stuff I discussed today extremely extremely high notes so have a wonderful rest of your day God bless you and thank you

The pulmonary capillaries.

Calcium Channel Blockers (e.g., Verapamil).

Bone pain/metastasis to the vertebral column.

Both will be elevated (PCWP $\uparrow$, CVP $\uparrow$).

PCWP (left heart) will be low/normal because venous return from the pulmonary vein is compromised.

DBA involves only red blood cell deficiency; SDS involves primarily white blood cell deficiency.

The threshold for concentrated versus dilute urine.

They induce hyperprolactinemia, which suppresses GnRH $\rightarrow$ decreased FSH/LH $\rightarrow$ hypogonadism.

Diamond-Blackfan Anemia.

SDS affects primarily neutrophils/WB Cs; FA causes pancytopenia (all three lines low).

Psychogenic polydipsia (excessive free water intake diluting the serum and suppressing ADH).

The PCWP will be low/normal because venous return to the left heart via the pulmonary vein is restricted.

Aplastic Anemia; it's a misnomer because it means all blood elements (RB Cs, WB Cs, Platelets) are low, not just RB Cs.

They induce hyperprolactinemia, which suppresses GnRH $\rightarrow$ decreased FSH/LH $\rightarrow$ hypogonadism.

Diamond-Blackfan Anemia.

SDS affects primarily neutrophils/WB Cs; FA causes pancytopenia (all three lines low).

Psychogenic polydipsia (excessive free water intake diluting the serum and suppressing ADH).

The PCWP will be low/normal because venous return to the left heart via the pulmonary vein is restricted.

Aplastic Anemia; it's a misnomer because it means all blood elements (RB Cs, WB Cs, Platelets) are low, not just RB Cs.