DIP Episode 126 - USMLE Step 2CK Rapid Review Series 7 (IM)

Okay, welcome to episode 126 of the Divine Intervention Podcast. My name is Divine. I am a resident and I'll be continuing the Rapid Review series for the USMLS step 2 exam and I'll be focusing on internal medicine again. Remember it's like 50% of the exam. So it probably makes sense that I should continue along those lines. Okay, so what if you get a question this is a pseudo-peat question but it relates to adults. So let's talk about it. So what if you get a question about you know like a newborn you know it's been examined by like a met student in a nursery and then you tell you that physical exam or you can guess from the scopic exam reveal some lukokuria. So this kid has like a white reflex. Now what is the kind of connective tissue malignancy you would maybe expect in this child in the future? I hope you're thinking about those osteosarcoma. So if you see a newborn with a white reflex right I really hope you're thinking about like retinoblastoma. Remember it arises if you have the RBG mutation. Remember RBN is a tumor suppressor gene right? So retinoblastoma RBG mutation and those people have a pretty high risk of getting like osteosarcoma in the future right? That's a classically tested a NBM relationship right? Then again you want to know the other things that can cause osteosarcoma right?

So you want to remember that Pajet's disease right has an association with osteosarcoma because remember if a person has Pajets excuse me they tend to have like a like a hypervascular bone marrow right?

Those things can predispose them to get in an osteosarcoma and then there is this fancy drug that's used to treat osteoporosis terryparatide it's like a PTH analog remember if you give PTH in a pulsatile fashion it actually encourages bone to build up but if you give PTH in a continuous fashion it encourages bone resorption so if you gave terryparatide in a pulsatile fashion if you really think about it you're effectively giving someone a growth factor you're essentially giving a bone growth factor so that can certainly increase that person's risk of a osteosarcoma okay and remember I don't osteosarcoma don't forget your classic like codmins triangle your sombus pattern and all that crap and remember that osteosarcoma loves to metastasize to the lungs okay that's a high-ealth thing you want to remember also what's the I guess will be getting my lignancy that loves to metastasize to the lungs that's for your carcinoma right so keep that at the back of your mind okay now what if you get a question about like a 55-year-old guy you know he comes to his PCP's complain of like pain whenever he walks two blocks and then he says you know when he rests or when he shops at Walmart the pain goes away or gets better what are you thinking about that's pineal stenosis right that's pineal stenosis and actually this is a tricky tricky question that your friends at the mbme can throw an exam what is the most common location in the spine of spinal stenosis it's actually the cervical spine okay that's actually a high-ealt factor you want to keep in mind okay now what if you get a question about like a 23-year-old female let's say she comes to the ED she has like severe joint pain that you know he started at her left elbow the weak prior and then she now tells you that now she has been in her right knee right and then they tell you that oh on physical exam they find like red vesicle lesi

ons on the skin and let's assume maybe she has like some kind of like vaginal discharge and they ask what's your next best step in treatment what do you want to give this person well I hope you want to give them like like a combination of like sef triaxone plus is ithromycin or sef triaxone plus doxycycline right because this person likely has gonococular thritis remember gonococcus loves to cause a migratory arthritis on mbme exams right so if you're treating gonorrhea you also want to concomitantly cover concomitantly cover what's the name of this bug chlamydia right and again remember chlamydia doesn't gramstine right so the classic chlamydia mbme question will be a question where a person has a vaginal discharge you draw a gramstine you don't see anything because remember chlamydia actually stains with the game's a stain it doesn't stain it doesn't gramstine basically okay so if you see a person that has like discharge you suspect like an STI where you're not seen any bugs that is like the more that is that the classic common presentation of chlamydia on mbme exams and I guess if you really want to stretch your thinking here little there are some other high-eal things that love to cause migratory arthritis right line disease loves to cause a migratory arthritis okay and a rheumatic fever rheumatic fever also loves migratory arthritis as a as a presentation so that's something you want to keep at the back of your mind okay now what if you get a question about like you know an 89 year old guy you bring him to the ED from like I don't know like a nursing home and the nurses at the nursing like the nurse or whatever staff that comes with him to the hospital says that you know for the past two days he's gonna be an out of it right and then they tell you that oh they check his vital signs and his temperature is 103 so he's like super febral his blood pressures like 90 o

ver 65 his heart rate is 107 beats per minute so let's say he's like tacky cardiac his respiratory it is like 32 and then they give you some labs right you check a CBC the white count is I don't know like I don't like 95 thousand right that should be a red flag right there the white count is like 95 thousand his hematocritus like 15% so think about it for persons hematocritus 15% what's the ahimo globin it's five right remember your hematocrit divided by three is your hemoglobin and then let's say it's bleeding count is 37000 so he's like profoundly thrombocytopenic right and his physical exam is notable for fullness let's say they tell you that oh there is fullness or tenderness on palpation of the left and right upper quadrants and then they tell you that you know for the last like year he has had like six pneumococcal infections or something crazy like that right obviously you're gonna give this person breast-peck antibiotics but what do you think this person has what do you think this person has I really really really hope that you're thinking about CLA okay basically if you get like really you shouldn't you should never give this wrong guy name being ever because they presented essentially this same way every single time if you get a question about a person that is super old get in recurrent infections and they're like you know white blood cell count is like crazy high so it's like higher than you'd expect with an infection right like you see their white blood cell count being like 90 thousand 80 thousand 70 thousand some crazy high white count in a person that is old and then you notice that every other thing is low their hematocrit is low their platelet count is low you really want to think about CLL okay really want to think about CLL right and remember CLL again it you're not gonna see CLL in a young person and an MBM right it's gonna be an old person with re

current infections and you see divine but this doesn't make sense if their white count is that high if it's like 95 thousand like I said for this question how do you get in all these infections right the thing is yeah they have all these B cells that are proliferating like crazy but the problem is those B cells either don't make antibodies or the make antibodies they don't work okay so actually having CLL is an immunodeficiency problem in and of itself and again they tend to get recurrent bacterial infections like pneumococcal pneumonia and all that crap right and for purposes of the USML is there are two kind of like weird things you want to keep in mind with regards to CLL right to remember that it tends to be like CD5 positive on exams right and remember that if you look on histology what particular type of cell would you see it's almost like a cell that looks like it was splattered on a surface what is that cell type called that's a smudge cell okay that's a smudge cell that's something you absolutely want to keep in mind for your for your test okay now what if you get a question about you know like a 44-year-old guy you know comes to his PCP comes for his animal physical and you know let's see this guy is kind of worried about losing his job because he has been caught falling asleep a lot at work right and they give you some vitals right they tell you like his blood pressure is like 145 or 85 his arteries like 87 bits per minute his respiratory is like 16 right they give you a white count you know 75 hundred on normal his amount of credit is like 48% right so it's like his hemoglobin is like 16 that's kind of high and his BMI is 32 right and then the tell you that you know you give him like the influenza vaccine as always and then you're referring to like a sleep I don't know like like to sleep specialist for polysomnogram right what kind of electrolyte abnormali

ties would you expect in this person what kind of a lecturer abnormalities we expect in this person what kind of a lecturer abnormality expecting this person what kind of acid-based problems would you see in this person would you see a respiratory acid dose or respiratory alkalosis when I hope you're seeing respiratory acid dose is because what does this person have you see a person that is falling asleep a lot during the day and they're obese right so they likely have and they they snore and all that crap they likely have either OSA right or obesity high-pove ventilation syndrome right so those people will have a respiratory acidosis because they are chronic CO2 retainers now what will be true of the person's bicarb you'll be high right because this is a chronic problem so I would imagine that the person's kidneys have responded appropriately so they will have a metabolic alkalosis because they will retain bicarb to counteract the pH lowering effects of the respiratory acidosis okay so they will have like a compensated metabolic alkalosis at the same time remember you will also find similar labs in a person that has COPD right and if you notice in the question I talked about how I talked about how the person's hematocryg was kind of sort of kind of on the high side remember if you are chronically hypoxic right so if you're a COPD or you have obstructive sleep apnea or you have obesity hypobicity high-pove ventilation syndrome right you're chronically hypoxic so your body is like you know what I kind of need oxygen from somewhere right so your body will say you know let's make more hemoglobin right so that I can have more oxygen carriers in my body right so those people get like a reactive polycyphemia okay so you can find in a COPD or in an OSA person in an OHS person in a person that has basically any condition that's associated with a chronic hypoxia and what will

be true of the levels of Epo in this kind of person yeah Epo levels will be high right because the chronic hypoxia triggers the production of Epo from the kidneys right and then if they have those high levels of Epo then they will make a ton of hemoglobin okay so that's why the hematocrit goes up remember Epo if you if you have like chronic kidney disease right you can have like a neuromocytic anemia because if your kidneys are dead then you're not making Epo you're not making Epo you're gonna get a normal acidic anemia right now I just said that this person these people have high hematocrit but their Epo levels are fine I mean sorry their Epo levels are elevated what will be true what disease do you think localize these two person having elevated hematocrit and they have normal or low levels of Epo what am I thinking about there I hope you're telling me police I theme you there right remember those people tend to have like a rodeo appearance on NV Me exams right so RUWDY so like a rodeo appearance and they have this thin known as aquagenic preridus that's a high-youth thin you want to keep in mind right so those people when they're taken after they take like a shower they just eat shaton right if you see that think about police a themia vera remember it arises from a person having like a jack-to-mutee right remember those my low proliferative yeah those my low proliferative problems most of them in general have an association with a jack-to-mutee like a police athermia vera essential thrombocytemia those all have associations with with a jack-to-mutee so that's something you definitely want to keep at the back of your mind and then remember there are certain cancers that can make Epo in a panheoplastic fashion right so remember hepatocellular carcinoma right can make Epo in a panheoplastic fashion again don't forget the association of HCC with AFP of a phylo protein a

s a tumor marker right and then you can also see what's the I guess the tumor that's associated with a person having let's say they have like brain hemangioblastomas right so they have like hemangioblastomas in the brain or they have like bilateral renal cell carcinomas right what are you thinking about there I'll be thinking about VHL right when hippo lend out I remember that condition is a chromosome 3 defect they tend to get hemangioblastomas in the brain they tend to get bilateral renal cell carcinomas and those hemangioblastomas can produce Epo as a panheoplastic phenomenon so if you see a person that has a brain tumor classic leads in the posterior forza so like in the cerebellum and then they have like a an elevated hematocrit you really want to think about hemangioblastomas on mbmi exams and remember renal cell carcinoma in and of itself can also produce Epo in a panheoplastic fashion right and I mean like the original question was about obstructive sleep happening how do you treat os a right I hope you're thinking about like CPAP right those people need like CPAP they need to lose some weight right there are some people believe it or not that their os is cured by losing weight and then if they really wanted to mess with your head on an exam this would probably be more of like a surgery question on on the usml is you do this procedure called you will know palato faringo plastic so you will know palato faringo plastic okay you basically call out some of the tissue that you have in there in your in your throat okay and that sort of relieves the airway obstruction and remember right there is such a thing as obstructive sleep apnea right and there is such a thing as central sleep apnea as well right remember central sleep apnea is just from people having a decreased respiratory drive all right so central sleep apnea how do you how is central sleep apnea treated so

central sleep apnea is actually treated with acetyzolomide okay it's treated with acetyzolomide right so here the high old things you want to keep at the back of your mind with that right so if a person because and again no one really knows why that works but I have a good teleologic explanation for why that may be the case right so let me explain how right so think about you but basically has central sleep apnea right they don't have much of a respiratory drive so that's a problem so because they don't have much of a respiratory drive you can try to do something that can spurs up their respiratory drives right so think about it what kind of acid base anomaly will your body respond to by hyperventilating think about it will it be a respiratory acidosis respiratory acolysis those obviously don't make any sense so let's go to metabolic will a metabolic acidosis or metabolic alkalosis increase your respiratory drive what do you think I really hope you're saying a metabolic acidosis right because think about it if you have a metabolic acidosis and your pH goes down right what kind of acid base problem will your body come up with to try to compensate for that obviously your body will try to hyperventilate right because if you have a metabolic acidosis the way you respond to that is with a respiratory alkalosis and in a respiratory alkalosis the way you achieve that goal is by hyperventilating right basically your respiratory rate increases so if you think about it if a person has central sleep apnea they have like no respiratory drive you know you could give them a sedalzolomide remember sedalzolomide is a carbonic and hydrism inhibitor so when it inhibits carbonic and hydrism you basically waste bicarb in the urine right remember that's kind of like type 2 RTA physiology right there right so the waste bicarb in the urine if the waste bicarb in the urine right they get a

metabolic acidosis they get a non anion got metabolic acidosis more specifically and non anion got metabolic acidosis arising from an RTA a type 2 RTA because that problem is at the proximal tubio because remember a sedalzolomide inhibits a carbonic and hydrism at the level of the proximal convoluted tubio so you pee bicarb in your urine you get a metabolic acidosis you what it tries to compensate for the respiratory alkalosis so that speeds up your respiratory drive so personally I think that is like the mechanism that makes the most sense for why a sedalzolomide works pretty well for a central sleep apnea right but I've not really found any good explanation online but that's the explanation that I kind of came up with in my mind that seems to make sense to me okay and then just before I round off with this acidosolomide business what's the other condition on mbmi exams that may be treated with acidosolomide there's actually many so I hope you're telling me I I H so idiopathic intracranial hypertension right so the tumor cerebride remember carbonic and hydrism involved in the progression of CSF so if you inhibited it you make less CSF I can reduce some of the intracranial pressures in people that have pseudo tumor cerebride right and then remember you can also use a sedalzolomide to treat just elevated intracranial pressures in general right and you can also use a sedalomide to treat glaucoma all right glaucoma because again remember acosumer in your eye you do need carb carbonic anhydrase in making some of that acosumer so if you inhibited carbonic anhydrase you won't make acosumer I mean you make less acosumer right and you'll relieve the symptoms of glaucoma right and then I mean if you go to Colorado something weird you go to Colorado some place with like pretty high elevation right remember as you go higher what happens to the oxygen tension in the in the atmosp

here it goes down right so if it goes down you become hypoxic if you become hypoxic you what is like you know what I sort of kind of need oxygen right so you begin to hyperventilate so that you can bring oxygen in right if you hyperventilate you get a respiratory alkalosis and if you get a respiratory alkalosis your body is like like you feel like crap so your body is like okay let me try to fix this by counter-balancing the respiratory alkalosis so your body says let me try to go into a metabolic acidotic state but your body is kind of slow to do that you can speed that process along with a sedalzolomide again because you dump by carb in the urine so you will create that metabolic acidosis for you are really fast and then this is an evil question that your friends on the mbm can throw on step 2ck or step 3 believe it or not so as a sedalzolomide right remember you're probably used to this that oh most diuretics cause metabolic alkalosis and hypochylemia like your lute diuretics your thazide diuretics those all cause metabolic alkalosis and hypochylemia but there is a diuretic that has the weird combination of metabolic acidosis by virtue of the weight works plus hypochylemia if you see that combination you really want to think about your carbonic and hydrace inhibitors like a sedalzolomide okay just because of the weight works it causes a metabolic acidosis already explain that process but in addition to that a sedalzolomide is it's a diuretic in and of itself and if you take a diuretic you become volume down if you become volume down excuse me you don't perfuse your afrin arterial as well so you rev up the activity of your renein and juteinsin our dose urine system right so if our dose urine is all revved up you waste potassium in the at the level of the principle cell of the distal nephra right so you get a hypochylemia with that and then don't forget that if you w

ant to go on the other end of the spectrum they are certain diuretics that are associated with like metabolic acidosis right and hypochylemia right those will be like your key sparing diuretics your potassium sparing diuretics like like a spurnolactone or a plerino okay so again those are all high-yield things you want to keep at the back of your mind for exams okay so let me maybe go over one more scenario and then I'll call it call it a day right so let's assume you'll get a question you know 62 year old guy you know comes in he says or he's lost like 15 pounds over the last two months it's not a good sign right probably thinking about cancer here and then they tell you that you know on physical exam you know he looks caquette he has temporal wasting and he quit smoking six months ago right and then let's say prior to that he had smoked two packs of cigarettes a day for 37 years right so that's like a 74-pack year smoking history that's bad right and then they tell you that you know on chest x-ray they see like a speculated cavitary lesion in the I don't know like left-operate loop of the long let's take that and then let's say you do a bronchoscopy with biopsy and when you send the specimen to like a pathologist the report back and see that oh you're seeing like dysplastic cells that look on differentiated and they're a keratin positive very high yield they're a keratin positive what kind of cancer are you thinking about on that these circumstances I really hope you are thinking about squamous cell cancer of the lungs okay squamous cell cancer of the lungs remember if you ever see anything that's keratin positive on an NVME exam it's a squamous cell cancer of somewhere okay if you're finding it in the lung well guess what a squamous cell cancer of the lungs okay now remember that there are certain high yield things you want to keep at the back of your mind with the

se lung cancers right they're kind of high yield is one of those things where you're like if you don't know like going into your stictus decay exam you're kind of asking for it right you know it's gonna show up right so you better know this right so this is like Florida high yield right so remember your squamous cell cancer of the lung right what is it classically associated with what panoplasmic problem well I hope you're thinking about hypercalcemia right remember your squamous cell lung cancers they can produce PT HRP right so like perthyride hormone a related peptide in a panoplasmic fashion right so those can cause hypercalcemia right so stones bones groans psychic overtones or like a short cutie interval on an EKG remember hypercalcemia causes a short cutie interval on an EKG right so that's the thing you want to keep at the back of your mind there now what is the lung cancer that may present on an NVME as a person that has you know like skin hyperpigmentation they have hyponitrine or they may have like cushionoid features or they may have like difficulty rising from a chair or like difficulty climbing stairs so they have like proximal muscle weakness what kind of lung cancer am I talking about here I really hope you're telling me small cell lung cancer remember small cell lung cancer it's a kind of neuroinducrate tumor and you never do surgery for small cell lung cancer it's considered to be metastatic at diagnosis right remember there are three high-yield panoplasmic phenomena you want to keep at the back of your mind on exams with small cell lung cancer right the first one you want to keep in mind is SIDH right so that can be a cause of a uvolymic hyposmolar hyponitrine right so those people have like bad bad bad hyponitrine right so they'll have like a low-serimus molarity but you have a higher in osmolarity right if you see that think about SIDH and then th

e way you treat that obviously is with water water is fluid restriction right and then remember small cell lung cancer can also make an ACTH right so a topic ACTH so remember that's the one that will not suppress with the administration of high dose dexamethosone so they can get cushionoid features with that right and then remember that small cell lung cancer you can actually make auto antibodies against the pristine uptake voltage-gated calcium channels that you'll find out the neuromuscular junction right so that can be like a classic teletyl presentation of a lumbar it in myostenic syndrome right lumbar it in myostenic syndrome remember this is the one that classically presents as like proximal muscle weakness right and it's the one that improves with use right so it's like muscle weakness that improves with use right so I remember my astenographies is the one that works in with use right so my stenographies works in with use lumbar it in gets better with use right and there is a gets better with use right if you think about it the more you use that muscle the more you recruit calcium to that voltage-gated channel and those calcium ions can outcompete those nasty antibodies so the muscle contraction will improve okay so if you see that think about lumbar it in and lumbar it in generally on mbms tends to affect more of the appendicular skeleton so like it tends to cause mostly like arm and leg symptoms arm and leg symptoms versus like myostenographies that usually on mbms causes more ballpark symptoms so they will have like toses difficulty swallowing and all that stuff okay and the thing is your friends at the mbms know that everyone has memorized gets better with use lumbar it in gets worse with use myastenographies so the thing is they are beginning to deem precise that on tests and they are beginning to give nerve stimulation results to see if you can put that t

ogether with lumbar it in or myastenographies right it's just basically another way of saying what you know they're just using slightly different terms right so if you think about it I just told you that myastenographies gets worse with use right so if you keep stimulating those people's nerves with if you keep stimulating those people's muscles in like like a nerfs team test right they will have a response that gets worse and worse and worse right that is a decremental response right so if you see decremental responses with repetitive nerfs stimulation that is myastenographies on your mbms exam on the other hand if you see an incremental response so a response is getting better an incremental response of muscles with repetitive nerve stimulation you want to think about lumbar it in myastenic syndrome on that those circumstances okay and then the last thing I will say right I get some last quick things again I want to hopefully keep this on the 30 minutes I feel like I almost never reveal that premise but anyhow so key things you want to keep at the back of your mind remember that lung cancer right I mean any malignancy right usually is a sort of like exudative effusions right so that's a factor you want to keep in mind and then remember that people can also have like a pancus tumor right remember that's a kind of lung cancer you can have a pancus tumor right so you can basically mess up your sympathetic chain right so you can get like an Ipsilateral Hona syndrome right so like toses myosis and and hydroces right and then remember they can give you a question about a person that is like a long-time smoker and in detail you that over like a four week period he has started having like diffuse really bad nasty joint pain right if you see that I really hope you're thinking about hypertrophic pulmonary osteopathy right your next step in management for those people is to ge

t some kind of chest imaging either like a chest CT or chest X-ray because that has a very strong association with with lung cancer and I mean obviously if a person has like a lung cancer like a scrimal cell and you want to go for surgical resection before you take those people for surgery this is something they love to ask this is a surgery style question they love to ask on the US MLE's you want to make sure you perform like like some PF Ts right because you want to sort of know what your lung function looks like because you want to like check their FVV1 because think about it if you reset the person's lung person's lungs and you have like very minimal FVV1 at the end then they won't make it out of surgery right so for person has like a really bad FVV1 that is essentially a contraindication to any kind of longer section surgery okay so I think I'm gonna go ahead and stop here this is right at the 30-minute mark and again as I say with every of my podcasts I'd offer one on one tutoring for all the US MLE exams step one two CK two CST step three the preclinical exams in med school the 30-ish off exams offered tutoring for those and then if you're a college student by some chance and you're listening to this or you know a college student that needs to do in like general chemistry organic chemistry physics physiology histology biochem I do offer tutoring for all those things and then if your college student applying to med school so like an Amcass app or med student applying to residency so like an era's application I do offer like one on one advice in and consulting for those so like personal statement writing mock interviews application prep rec letters all that stuff I do have experience working with tons and tons of people on those and I mean pretty much everyone I've worked with has matched into a has matched right so I guess take that for what you will and then if

you need tutoring for like the internal medicine in training exam or the ABIM in internal medicine board exams I do offer one on one tutoring for those as well so reach out to me either through the website or you can send me an email at divine intervention podcasts so podcasts with an S at the end and gmail.com so I do hope you'll find this podcast to be useful I will see you in the next podcast have a wonderful night rest and God bless you thank you

The cervical spine.

Osteosarcoma (due to RBG mutation).

Squamous cell carcinoma.

Ceftriaxone plus Doxycycline (or Azithromycin).

Lambert-Eaton Myasthenic Syndrome (LEMS) or Myasthenia Gravis.

Smudge cells.

Carbonic Anhydrase Inhibitors (e.g., Acetazolamide).

1) SIADH (low serum sodium/high urine osmolality), 2) ACTH production (does not suppress with high-dose dexamethasone), and 3) Lambert-Eaton Myasthenic Syndrome (LEMS).

It inhibits carbonic anhydrase, causing bicarbonate wasting in the urine. This leads to a metabolic acidosis, which helps stimulate respiratory drive. It treats Central Sleep Apnea (CSA) and Idiopathic Intracranial Hypertension (IIH).

Pain with walking/extension that improves with rest/flexion; most common in the cervical spine.

Elevated hematocrit (polycythemia) due to reactive erythropoiesis, accompanied by elevated EPO levels from the kidneys.

Myasthenia Gravis worsens with use; LEMS improves with use.

1) Reactive/Secondary (e.g., COPD, OSA), 2) Primary Polycythemia Vera (PV), or 3) Malignancy (e.g., HCC, Renal Cell Carcinoma).

1) SIADH (low serum sodium/high urine osmolality), 2) ACTH production (does not suppress with high-dose dexamethasone), and 3) Lambert-Eaton Myasthenic Syndrome (LEMS).

It inhibits carbonic anhydrase, causing bicarbonate wasting in the urine. This leads to a metabolic acidosis, which helps stimulate respiratory drive. It treats Central Sleep Apnea (CSA) and Idiopathic Intracranial Hypertension (IIH).

Pain with walking/extension that improves with rest/flexion; most common in the cervical spine.

Elevated hematocrit (polycythemia) due to reactive erythropoiesis, accompanied by elevated EPO levels from the kidneys.

Myasthenia Gravis worsens with use; LEMS improves with use.

1) Reactive/Secondary (e.g., COPD, OSA), 2) Primary Polycythemia Vera (PV), or 3) Malignancy (e.g., HCC, Renal Cell Carcinoma).