DIP Episode 628 - USMLE Step 2/3 Rapid Review Series 131

All right welcome my name is divine this is episode 628 of the divine intervention podcasts and into this podcast we're going to be continuing the rapid review series for the US Emily step 2 CK and step 3 exams this is going to be series 131 all right so what if they give you a question about a patient and they tell you that this patient you know is a 32 year old male and you're told that he has a history of Hashimoto's thyroiditis and he's currently on level thyroxin therapy and then you're told that you know for the last six months he has been having a lot of vomiting after meals there is a lot of post-proneal vomiting and that he feels full very very early and then you know you're told that he has a lot of abdominal pain and that when he is you know that he you know he has been having like some minor weight loss over the last two three months and then they ask you which of the following represents the most appropriate next best step in management I would really hope you're picking the answer that says to check this person's a1c you're like what divine okay this is 2026 but you're like what are you doing here okay so let's gonna talk through this right this stuff is actually pretty high yield to know for your exams right so the first thing I think we're gonna start off with is that it's important to know this principle with the USML exams whenever they're testing an autoimmune disease they will almost always give you a pass medical history of another autoimmune disease I'm gonna say that again when the USML is are testing an autoimmune disease like almost guarantee they'll give you not always put a lot of the time they'll give you a pass medical history of another autoimmune disease so what other autoimmune disease does this person have this person potentially has type 1 diabetes right because we see this person has a history of Hashimoto's which is an autoimmune di

sease where you damage the thyroid glands right anti-thyro peroxidase or anti-thyro globulin antibodies right so it behooves us that this person may actually have another autoimmune disease like type 1 diabetes remember in type 1 diabetes you can have anti insulin antibodies you can have anti-i-let polypeptide antibodies you can have anti-gluidamiducroboxylase antibodies right so what is going on with this person's diabetes that is causing them to vomit after the eat not want to eat losing minor amounts of weight feeling for early right if you see something like this you want to think about gastroperaces right you want to think about what diabetic gastroperaces whatever you see a person that's a diabetic and they have a lot of GI problems think of diabetic gastroperaces think of diabetic gastroperaces right so again they feel full early they have a version to food they have abdominal pain right they eat and boom very very quickly they feel very very full really really fast whenever you see something like this I absolutely positively want you to think about diabetic gastroperaces so now the big question is how are we gonna diagnose this well you can do a gastric emptying study right remember diabetes can cause neuropathy right so these people essentially have like a neuropathy of the stomach and when you have that neuropathy right when you have that neuropathy when you have that neuropathy right when you have that neuropathy right you're gonna have issues with peristalsis in your GI tract right so in fact sometimes on the exams I think I was kind of telling people this recently I wrote on my classes that the USM is these days they don't give straight answers right they're gonna give you a derivative answers right so why put gastroperaces as an answer to a gastroperaces question where they can just put reduced GI tract peristalsis or something like that right many times

these days on the USM exams most of the answers that they throw out there are answers that are pathophysiological answers they relate in some way shape or form pathophysiology wise to the pathology that they are referring to in the question stem right so this person has gastroperaces and you're gonna do a gastric emptying study again it's like a paralysis like neuropathy of the person's GI tract so how are we going to manage this person's neuropathy well typically to diagnose it first you're gonna do a gastric emptying study right because things are gonna take longer to empty through the GI tract right so the gastric emptying study is gonna be abnormal they're gonna have a longer latency of gastric emptying it's gonna take a much longer time for the stomach to empty but it is also high you to know that hey how are we gonna manage this well the first line treatment is gonna be a pro-kinetic agent like meadow clopromide you're gonna use what meadow clopromide remember how those meadow clopromide work meadow clopromide is a D2 receptor blocker it's a dopamine receptor antagonist he pretty much works like an anti-psychotic right but by doing that it's actually gonna promote GI mortality right but there are some offshoot points that are friends at the MBM is love to integrate right they love to integrate they love to integrate into this thing right and one of the off-should things they love to integrate into this is a person that is being treated for gastroparesis and then you notice that this person is now having these abnormal tongue movements well obviously want to think about tardy dyskinesia it's gonna be a person that has taken the meadow clopromide for a long period of time right they have tardy dyskinesia because again remember meadow clopromide effectively works in fact is not effectively it is essentially an anti-psychotic it just happens to be a purpose for the

management of that get diabetic gastroparesis right so they can have like tardy dyskinesia they can even give you a neuropsychmalignant syndrome question in a person that has diabetic gastroparesis right so they give you again a person that has managed diabetic gastroparesis and the person has very high body temperatures very high fever's right the person has like severe muscle pain and you're told that the person's urine is red when you see something like that think of neuropsychmalignant syndrome so maybe one drink divine why would this person have red urine again the person has red urine because they've started having a rupto myolises right neuropsychmalignant syndrome remember they're gonna have high fever's they gonna have muscle rigidity their muscles can start breaking down right and as your muscles break down you begin to have rupto myolises right and that can cause your creatinine to rise so they can ask you a question about hey this person's creatinine is like two point something what's the mechanism behind this person's whatever right you want to pick the ruptomylosis answer of the acute kidney injury answer or the acute tubular necrosis answer right and again the urine is red because you're seeing myoglobin not hemoglobin right you're seeing what you're seeing myoglobin not hemoglobin right they can even ask you you know they can even give you a question about a person that has NMS and then they show you an EKG and then you see topic T waves or you notice that the presence QRS is really wide and then they ask you which of the following is the most likely mechanism behind the observed EKG findings well I'll really hope you're picking the answer that says electrolyte abnormality right well what's the electrolyte abnormality in this case is going to be hyper kelimia because again remember potassium is primarily an intracellular ion right so as a cell as a lo

t of cells explode you're gonna release a lot of potassium into the bloodstream and that potassium that is releasing to the blood stream can cause hyper kelimia right so that person believe it or not you may get a question on the person that has your elliptic malignant syndrome and they give you EKG findings and then your next step on your exams is actually to give them IV calcium glucone to stabilize that myocardium to stabilize that myocardium again I know some people may be uncomfortable with this method of review where it's like I'm calling across concept to concept concept to concept concept to concept but from being completely honest with you this is how the USM is layered their questions these days right so the thing is you want to go through this mental discomfort in your learning so that when you see those kinds of things on your exams you're more apt to pick up on those things right so just keep this at the back of your mind right so again we started this whole journey right let's backtrack our story with diabetic astro parisis with the first lactropen B-menoclopromide and then saying that metoclopromide is a D2 antagonist right so because it's a D2 blocker it pretty much gives you everything that you can get from an anti-psychotic where you can get tired of dyskinesia you can get your elliptic malignant syndrome you can get Parkinsonism you can get many of these things right and remember if a person is a metoclopromide and they develop like a small bowel obstruction it's not a very good idea to keep them on that bed of clopromide you should probably go ahead and discontinue that metoclopromide why because it's a pro-kinetic agent you really should not be taking a pro-kinetic agent when you have a small bowel obstruction because that can increase your risk or bowel rupture and that can be very bad for the patient right in fact they can give you a question ab

out a person that you know is a metoclopromide and the person has been on a you know is a person is a metoclopromide and then for the last two days the person has been vomiting blah blah blah blah right and they'll tell you that they are symptoms of previously well controlled and then now they seem to have all this vomiting you know you know they have like this abdominal bleeding on all these stains and then they give you a chest radiograph and you notice free on that diaphragm they can ask or which of the following represents the most appropriate next best step in management you want to go ahead and do exploratory laparotomy okay you want to go ahead and do what exploratory laparotomy because the person has developed bowel rupture the rupture the viscous so that person is going to need X lap okay so going back to gastroparesis what did we say was first line treatment we said it was going to be metoclopromide but what's going to be the second line treatment for diabetic gastroparesis the second line treatment is erythromycin right erythromycin so why would you say erythromycin well the thing is erythromycin is a motillin receptor agonist it's a motillin receptor agonist it literally stimulates the motillin receptor whenever you stimulate the motillin receptor whenever you stimulate the motillin receptor that's going to encourage GI tract motility and as you have that GI tract motility that's going to be helpful so you may wonder like divine I mean like you've just told me a lot of bad things about me to clopromide like you've told me about how it causes NMS causes tardy disk condition all these things why would we pick that over a benign macrolid like erythromycin well let me explain something well the thing is there's this phenomenon unfortunately known as takifi laxas that are preached with erythromycin right so it's going to help your symptoms of diabetic gastropar

esis really fast but after a while you lose the effect of it after a while you lose the effect of it right so you almost need like some kind of drug free holiday well that's drug free holiday issues do not apply with metoclopromide so that's why metoclopromide is preferred right is preferred over erythromycin right but erythromycin works really well right and hopefully this thing that I've told you that oh erythromycin is a motillin receptor agonist this helps you understand why macrolids can cause diarrhea as a side effect it's actually a very common side effect of of macrolids right because the stimulate motillin receptors the increased GI tract motility and that can certainly increase your risk of having diarrhea okay increase your risk of having diarrhea all right now what if they give you a question about a patient and you're told that this patient has had gastric bypass you know like two years ago and that this patient was lost to follow up this person has not followed up with her physician for the last you know six months or whatever right and you you're told in the history that this person has been having very heavy periods and then you're told that this person has been having a lot of sleep problems that in fact she has been caught sleeping on the job multiple times she's been having a lot of sleep problems right and you you're told that you know she just she notices that when she goes to bed she has this uncomfortable urge right to to move her legs right when she goes to bed and then they ask you which of the following is the most appropriate next best step in management well I would really hope you're picking the answer that says to check serum ferritin so again I know some of you are like divine come on check serum ferritin what in the world are you thinking here okay so let's let's put it all together let's make integrations because that's supposed to be

your job on the exams your job on the exams is to make integrations right so what does this patient have this patient has restless legs same from restless this costless case right this person has restless legs syndrome but how did she get there from gastric bypass okay let's layer the story so number one she had gastric bypass remember when people have gastric bypass they literally bypass portions of the big portions of the stomach you pretty much connect the stomach like early stomach to distal small intestine that's the connection you make there's all these other permutations but that's the basic idea the basic gist you want to know for your exams right you connect the proximal stomach to the distal small intestine so think about it you're pretty much bypassing pretty huge sections of the small intestine right pretty huge sections of the small intestine like the duodenum and like the jajunum and if you think about it where do we reabsorb iron in the GI tract we reabsorb it in the duodenum right so it behooves us that a person that has had gastric bypass because they have literally bypassed sections of the small intestine that help with iron reabsorption like the duodenum those people can develop iron deficiency anemia right this is why close follow-up is extremely important in a person that has got in gastric bypass right in fact sometimes they can make you assembly questions with the ask which of the following is one of the key determinants of the patient of the patient's risk of developing complications from this procedure aka gastric bypass it's actually close follow-up with the physician that's actually a prognosis question believe it or not that they can repurpose and throw on your exams right so these people need to number one follow-up with their physicians and number two they need to take a ton of supplements into take a lot of multivitamines because again b

ecause of the way their GI especially for the early parts you know first few months first few years after they get that bypass right you know because over time the GI truck lanes to adapt in some way shape or form but early it's not right so they are not reabsorbing iron so they can absolutely positively develop iron deficiency anemia right and that iron deficiency anemia has led to this person's restless legs syndrome right has led to this person's restless legs syndrome remember restless legs syndrome has a very very strong association with iron deficiency especially giving the other risk that I give in this question of oh the person has been having very heavy mancy's well that's a very nice rapid way to develop iron deficiency anemia right that's a very very nice rapid way to develop iron deficiency anemia very very nice rapid way to develop iron deficiency anemia right so the person number one is like they have a double warming number one they are not reabsorbing iron in the lumen of the GI truck because again the duodenum has been bypassed because they go gastro bypass but number two they're losing a lot of blood right because they're menstruating right so that's potentiating the iron deficiency right so that iron deficiency has led to this person's restless legs syndrome so how are we gonna treat this oh why we checking the fairytale we remember fairytale is a measure of your iron stores right fairytale is a measure of your iron stores it's a measure of what of your iron stores so whenever your iron is low whenever you have iron deficiency anemia your fairytale is going to be low right your fairytale is going to be low so this person is not gonna get the classic restless legs syndrome therapy that we're used to giving people right this person should probably go ahead and get supplemental iron okay the person should get supplemental iron the person should get sup

plemental iron and that's gonna be more than enough to take care of her restless legs syndrome symptoms okay so keep this at the back of your mind for your exams now there's this thing I just want to say is just one of these constructs that our friends at the ambient is love to introduce on exams to see if you can make certain integrations with iron right so the thing is there are certain conditions that seem to improve when you've lost blood there are certain conditions that seem to improve when you've lost blood on the US Emily exam so let's gonna collect them to get around through them right so number one for example we'll be a person that has a porphyryocutinia tarda right whenever you see a person that you know they seem to have like this chronic skin rash this chronic skin bruising right this you know strange color of the urine discoloration of the urine and they tell you that their symptoms have improved you know you know improved temporary after they lost a lot of blood you want to think about porphyryocutinia tarda well how does that work exactly well if you think about it porphyryocutinia tarda is a disease it's a it's a defect in the enzyme euro the euro porphyry nogin decarboxylis euro porphyry nogin decarboxylis is an enzyme that you can be deficient in and then that can cause you to have a PCT right porphyryocutinia tarda it's one of those those are porphyrys right it's one of those porphyrys where they're gonna have skin issues right that's why it's called porphyryocutinia excuse me excuse me right so porphyryocutinia cutinia is ready to fix the skin porphyryocutinia tarda right so they have a lot of cutinia's manifestations and they may have a discoloration right so why is it that bleeding may help these people's symptoms get better well bleeding helps these people symptoms get better if you think about the treatment of PCT if you think about the treat

ment of porphyryocutinia tarda one of the primary treatments is to do phlobotomy when you do phlobotomy right when you do phlobotomy you're gonna create an iron deficiency whenever you have a mild iron deficiency it's actually going to increase the activity of urod so whatever uro porphyrynogen decarboxylis you have hanging around works better works better when you have an iron deficiency okay when you have an iron deficiency so if this person is bleeding all this person is having you know pretty heavy mancy's it makes sense that their symptoms will improve and remember whenever a person has porphyryocutinia tarda those people have to be screened for hepatitis C right there's a very strong gastronomy between HFC and having porphyryocutinia tarda right now what's another disorder that improves with bleeding and stuff well I want you to think hopefully of polycythemia vera right in fact this is why women tend to present with symptoms of polycythemia vera later in life versus men that tend to present with symptoms of polycythemia vera earlier in life in fact let me tell you something amazing here our friends at the NBM Es they can literally make a bio-statistic question of this you notice that wow they give you like some cross-sectional study or whatever or some kind of research study that talks about the and the thing that they're studying is the incidence or the prevalence of polycythemia vera and you notice that for the men they seem to have it like studying in their 40s you know you see like this they'll give you like some graph and you see the incidence kind of increasing studying the 40s but then you see for women you see the incidence kind of studying the 50s and then they'll see which of the following biological mechanisms right or which of the following pathophysiological mechanisms on the lies the observed graph findings well I would really really hope you're pi

cking the answer that talks about right like a woman's menstrual cycle or whatever right because if you're a woman and you have men's ears you you're pretty much getting an auto-flip bottomy every single month when you have your periods right you're losing some blood that is reducing some iron that's gonna help your symptoms of polycythemia vera right because remember in polycythemia vera you have a jaqtum mutation and then you have excess hematocrit right so you can have all these issues right you can have all these problems with headaches blurry vision blah blah blah blah blah right but women don't have this at least until they hit menopause and then that hack that they have of auto-flip bottomy every month with losing blood you know through their main sees they don't have that anymore right and then they start having symptoms so keep that at the back of your mind for you exams in fact the USML is one of their so fun fact about the USML is these days one of their favorite kinds of questions is to integrate bio statistics with like another subject right I like to call them sometimes like internal medicine bio statistics questions I am bio questions right it's an I am question but it's usually bio statistics right so they're trying to see if you can simultaneously apply pathophysiological knowledge from like internal medicine or pizza whatever and then they bring in bio stats with it right so it's just something I want to keep at the back of your mind for for exams okay so again I think we're kind of coming up on the 20-minute mark so I think this is probably a good place to stop again study this material right again the USML is they love love love love love to test these things and if you love the way I teach you love the way I make integrations you're gonna absolutely love my classes in the month of February I have a study enough I have a 25-hour step one class good

for people taking step one or people taking step two step three with bad basic science foundations right and then I have a 20-hour step two class that's first step two and step three and then I have a last-minute review that is also for step two and step three and then for step one to step three you know besides the 25-hour step one class I have a test taking strategy class that's two and a half hours long have a biostatistic class that's four hours long and I have a social sciences quality improvement hospital medicine review ethics review that is five hours long again many people have taken these classes and found them to be extremely helpful so if you're interested they're all held over zoom their life classes shoot me an email and I'll give you some more information and then I also offer one-on-one tutoring and I also help with ERAS applications mock interviews personal statements recommendation letters and things of that nature so thank you for listening to today you can check out this podcast on divine intervention podcasts.com there's also this podcast on Apple Google Apple podcast Google podcast and Spotify and then I also have You Tube channel where I post the videos that I make and then have on the website called divine intervention life lessons.com divine intervention life lessons.com many of you know I'm a Christ follower I'm a Christian so every week I make like one or two podcasts where from a biblical perspective address a life lesson divine intervention life lessons.com is actually an Apple podcast there called the divine intervention life lessons podcast so thank you for listening to me today I will see you God willing in episode 629 have a wonderful day God bless you and bye for now thank you

Early satiety, postprandial vomiting, abdominal pain, and minor weight loss.

It is a D2 (dopamine) receptor antagonist/blocker.

Tardive dyskinesia, Neuroleptic Malignant Syndrome (NMS), and Parkinsonism.

Myoglobin (muscle breakdown product), not hemoglobin.

It measures total body iron stores. Low levels indicate depletion.

Gastric bypass surgery.

Prokinetic agents, such as metoclopramide (though second-line may be erythromycin).

Because it increases the risk of bowel rupture.

Iron deficiency stimulates the activity of uroporphyrinogen decarboxylase (UROD), accelerating porphyrin breakdown.

Hyperkalemia (due to massive cell lysis/rhabdomyolysis).

Low serum ferritin.

Erythromycin; increased GI motility leading to diarrhea (due to tachyphylaxis).

Prokinetic agents, such as metoclopramide (though second-line may be erythromycin).

Because it increases the risk of bowel rupture.

Iron deficiency stimulates the activity of uroporphyrinogen decarboxylase (UROD), accelerating porphyrin breakdown.

Hyperkalemia (due to massive cell lysis/rhabdomyolysis).

Low serum ferritin.

Erythromycin; increased GI motility leading to diarrhea (due to tachyphylaxis).