DIP Episode 141 - USMLE Step 2CK Rapid Review Series 13 (IM)

Okay, welcome. My name is Divine. I am a resident and this is the 141st episode of the Divine Intervention Podcast. And in this podcast, I'll be continuing our rapid review series for the USM list of juicy KXM. And this will be focused on internal medicine. This is I think series 13 from Lama's speaking. So just jump right into it. So what if you get a question about a 40-year-old female, you know, BMI is like 40, comes in with like, like pain in her, like opera of demand, at temperatures like 1.02, as she has a positive morphine sign, what are you thinking about? Well, I'll hope you're saying that she has a, a cure calluses status, right? Remember for a cure calluses status, what's your first step in diagnosis? You get a right-upocordren ultrasound, right? And then after that, let's assume the right-upocordren ultrasound is negative. What do you go for next? You should go for a high-discount. A high-discount is a nuclear medicine test. Essentially, if you don't see the gallbladder at like 90 minutes, after you've like, given morphine, that tells you that the person, that that has a very high sensitive sensitivity for acute or calluses status. And obviously, acute calluses status, right? You treat it like a laperoscopic or calluses tectomy. But there are a few variations that you want to be aware of. Or I guess some of the high-yield factors you want to be aware of.

The first thing you want to keep in mind is, if a person has a cure calluses status, but they tell you that the classic image in finding, right? The right-upocordren ultrasound is like the pericolacistic fluid, the gallbladder wall thickness, I think like three millimeters is the cut off. And again, they will have like a sonographic morphine sign. That's the big one. No, the thing is on the NBM is if they tell you that, oh, they see all these signs like the pericolacistic fluid, thick and gallbladder wall. But they add something to the descriptor and see that the runeotian obstructing stone. But you see all these, you know, classic signs of acute calluses status, especially in a patient that, you know, is like on TPN or the patient is on, what is it called? So the patient is on TPN or the patient is like super seeking the ICU. Under those circumstances, you want to think about an ecalculeus acolysis status. And under those circumstances, you absolutely do not want to do a colisestectomy. You want to go ahead and do something called a percutaneous acolysis stastomy, okay? Those are things that are, that's like a weird variation. You don't do a colisestectomy. They will try to trick you by putting in colisestectomy. Don't choose that option. It's associated with like increased morbidity and mortality in those patients that have ecalculeus acolysis status. And then another weird variation, you may see on exams, right?

They may describe a person that, you tell you that, how do I put this? They may describe a person that, you know, may have like an obstructing stone in the cystic duct or whatever. But they tell you that, oh, you also see like dilation of like the intrahepatic bowel ducts. And that's something that's usually tested on like surgery shelves. But again, it's something I can see them throwing you on step to see. It's called like meridseys syndrome. Basically the thing that happens is you have like a dilithic cystic duct or an inflamed cystic duct that's compressing on the hepatic duct. So that causes like, you can essentially see like a conjugated hyperbular renemia where you have like dilation of the intrahepatic bowel ducts. Now, what if they give you a question about a patient that has like redical corduropanetane, has fever, they tell you that this patient has sclerolicturus, this patient is altered and the blood pressure is 80 over 48. What are you thinking about? I hope you're telling me, sending colonjitis, right? And obviously your next step in management on the those circumstances is to get an ERCP and ERCP is diagnostic and therapeutic. And then what if they give you a question about a patient that just recently had like a repair of their spleen because they were in trauma and then this patient has like referred, like they had like a surgical repair of the spleen from like a motor vehicle accident.

And then the tell you that this patient has like a referred pain to the left shoulder and this patient has like fevers. I hope you're thinking about a sub-frenic abscess under those circumstances. Obviously, you want to drain the abscess and that should hopefully fix whatever is going on. And then what if you get a question about a patient that just recently got treated for like a cute pancreatitis and then they tell you that own image or like on endoscopy or whatever. They find like isolated gastric viruses. Under those circumstances, I really want you thinking about like a spleenic vein thrombosis, right? Remember, venous thromb... like weird venous thrombosis are like high autonofers step two. Like the big ones where I spleenic vein thrombosis with like a cute pancreatitis, you want to know that one. Renovine thrombosis with nephrodite syndrome classically. You see that with a membranous nephrodite, you want to know that one. And then hepatic vein thrombosis, right? We both carry syndrome kind of like a woman on OCP's or you see it like in a patient with a police nightmare. Now, what if a patient has like, you know, like knowing a big gastric pain and they've been on chronic treatment for osteoarthritis? What would that patient have? That would be a peptic ulcer disease, right? That would be a peptic ulcer disease.

And then if a patient has like a big gastric pain, you know, radiating to the back and let's assume it's like an alcoholic or a patient with sickle cell, right? Obviously, you want to think about like a cute pancreatitis on the other circumstances. So, other high-youthines, I guess I'll see with that is remember that there are certain drugs that can be associated with pancreatitis, especially like the HIV drugs, right? Like Stavidin and Didadocin, those are ones they expect you to know for the exam. And then another high-youthine sort of circulating your memories, you may see pancreatitis with some of these diabetes drugs like the JLP one, I'm going to send the DPP four inhibitors. And then again, like basically I'm just using this to sort of walk you through like some high-youthiopathologies. Actually, let me go ahead and see this then, right? So there's this thing called like IgG4-releafed pancreatitis, like an autoimmune pancreatitis. It's kind of like a weird thing you want to stock at the back of your mind because the occasionally tested in the context of like retroperitoneal fibrosis, like the pancreas is I think on imaging looks like like a sausage or something like that, almost like a longitudinal ball of poop. If you see that, you think about autoimmune pancreatitis. Those IgG4-releafed disease are kind of high-youthoneal, you can cause like renal disease, pancreas disease, and stuff like that.

And then again, if a patient has like parromblic opine progressing to the right lower quarter and what are you thinking about, right? That's a pain to say this, right? And then if a patient has like flank kind of like radiating to the growing and this patient also has hematuria, what do those people have? Those people have like nephrolithiasis, right? They have like a renal calculus. And then when if you get a question about like a twin three-year-old female, she has like severe at low quadrant pain and she uses condomsin consistently, what are you thinking about? That's an ectopic pregnancy, right? And then what if you get a question about like a 15-year-old female, you know, she's had like, you know, like a simple ovarian cyst like five centimeters that was detected like six, seven weeks ago at a pelvic exam. And then she has like this sodium onset severe abdominal pain. That's ovarian torsion, right? That's ovarian torsion. The thing is you want to be able to differentiate ovarian torsion from like a ruptured something like a ruptured cyst. The thing is if they want to you or your friends at the end of the month, they want you thinking about a ruptured cyst, they will see something about like free fluid in the peritoneal cavity. If you see the free fluid on imaging, if you tell you that explicitly, you know that something has ruptured. If you don't tell you that, you know that nothing ruptured. Okay, it's just a torsion of whatever structure.

Now, what if they give you a question about a patient that has like cervical motion tenderness, at next cell tenderness and vaginal discharge? I hope you're thinking about PID, right? Provekin inflammatory disease. Remember that this thing can ultimately involve like the hepatic capsule, right? That's what's called like the feed's here, a feed's here, credit syndrome, right? And remember the big bugs that cause this problem, chlamydia gonorrhea. So obviously, want to give like, septiaxone is it thromacinol like septiaxone or plus a doxycycline? And these people, right? Probably like in the few weeks or like early months after they have like the PID, it probably doesn't make any sense to give those, like you know, like if these people are seeking contraceptive options, maybe an IUD is not the smartest thing on those circumstances. And then what if you get a question about like left low cordon pain in an idiot female with fever? That's diverticulitis, right? Remember diverticulitis? You make the diagnosis with like a CT scan with contrast. You do not want to do a colonoscopy in the acute phase, but you need to do it like weeks later just to make sure they don't have a colon cancer. And then what if you get a question about like left low cordon pain, idiot male? And then they tell you that he has like air bubbles or like poop in his urine. That's a coloe vesicle fistula. Believe it or not, that's something your friends are the inbeving love to test.

Basically they formed like a fistula between like the like sigmoid colo and whatever and their bladder, right? So they have that communication from all the inflammation of a diverticulitis. And then this one is just something that you either know you don't. But what if they give you a question about like you know like some patient chemo and it has like a thickensic on abdominal CT scan? That's something called typhlytis. It's just something like TYPHI, no TYPHLITIS. It's just something you know unfortunately you want to commit to memory. It's just like a very severe form of a mechrotizing intercalitis. Now what let's walk through I get like some bleeding disorders. Some bleeding disorders. If for example a patient has hemolytic urebic syndrome, we'll be sure of the applitlets. The applitlets will be low, right? Those people have like thrombocytopenia. Remember like the triad, right? Like microindropatic hemolytic anemia, thrombocytopenia like right now failure. So and these people usually have like like E. coli 157, he's seven business going on or like some kind of like shiga toxin crap going on, right? So the applitlet count will be low if the applitlet count is low, the ablittentime will be high, right? For the most part the apetian pTT should be normal. Now what if you have a patient that has hemophilia, A or hemophilia B? What should be trove the applitlet count? It should be normal, right? How about the ablittentime? It should be normal as well. How about the apetite?

It should be normal, very good. But how about the apetite? It should be increased, very good. Remember hemophilia A and B, they are both inherited in an excellent recessive fashion. So should not show up in a girl on an envy and me. And remember that hemophilia is a factor eight, right? Remember A sounds like eight and then hemophilia B is a factor nine deficiency, right? Like B9, like B9. And then the ablittentime disease will be trove the pleitlet count. It will be low, right? I mean it will be normal, sorry. Will be trove the bleeding time will be elevated, right? Remember it's a qualitative ablittlet defect, right? When we're brain disease literally means you have a deficiency of one willy-bran factor, right? And the pT should be normal and the pT should be elevated, right? Because remember, when willy-bran factor is a protecting group for factor eight, right? So if you have a willy-bran factor deficiency, you'll have like, like, diminished survival of factor eight in the circulation, right? So those people's pT will go up. Because the half life of a factor eight goes down, right? And remember the restucity and co-factor as a something that we pop up on your tests is just something that tells you that a person has like some kind of a problem with like the first step in primary hemostasis, right? That step that involves like GP1 B9 and ablittentime factor.

So if a person has like deficiency of ablittentime factors, so like EG like ablittentime disease or a person has brana-solisi, in the way they have a deficiency of GP1 B, those people will have an abnormal or restucity and a co-factor as a. And then if a patient is in DIC, who would expect DIC is bad, right? The pT will go down, they're consuming pT lets, the ablittentime will go because the apelite count is low, their coagulation factors are all down, so the apetitipitit will both be elevated. Basically, if you see every like level screwed up, always think about DIC. And then if a patient is on war frame, we'll be trove their apelite count on the ablittentime. Those should be normal, right? But if we should be trove their pT and their pT, we should both be elevated. So here's the thing, right? Everyone says, oh, if a person has, it's a question, people get a lot of people get wrong on the end means, if a person is on war frame, we follow with a pT, so that means the pT should be all, should be the only thing that that could not be further from the throat, so I remember. War frame inhibits a vitamin key, peroxide reduftes. So you have issues like gamma coboxyletin, factors 279 and 10 ampertensionus. The thing is, factors like 2, like factor 7 find, that's like the extrinsic coagulation cascade, so the pT goes up. But actually remember that factor 10, right? And like factor 2, they sort of like are common to both pathways. So those people's pT also goes up.

Same deal also goes like heprin. Heprin also will cause innovations in your pT and pT. Okay, don't say, oh, we follow heprin with pT, so the pT must be normal. No, that is not true. The pT and the pT go up if you're using heprin or war frame, right? And remember the way you reverse heprin in, like predominant sulfate, the way you reverse war frame is with a four factor PCC, right? So like the four factor per thrombin complex concentrate, I think that's the thing that's called like a key center in hospitals if a mom is seeking. And then if you're an aspirin, right, what should we throw your pT? It should be normal, right? What should we throw your bleeding time? It should be increased because aspirin, right, knocks out a cox, right? So your pT lets the aroma, but they don't work right. And then your pT pT should be normal. And then if a person has like liver disease, you're not making coagulation factor, so the pT pT should be elevated. Your pT leg comb bleeding time is kind of variable. That's kind of all over the place. If you have like a spline omega, you have a thrombocytopenia, right? Because you have sequestion platelets in the liver, but that's a different story. Okay, now what if you get a question about, what if you get a question about, so let me make this like an NBM style question. So let's assume you have like a 45-year-old female, you know, she's HIV positive, she comes to a PCP, you know, for like routine full-up.

And then on physical exam, you notice that she has like bilateral pDL and a period of it all a dima. And then you're told that breath sounds at decrease in both long fields bilaterally, and there's kind of like doneness to precaution. And then they give you some vitals like the blood pressure is like 130 over 90, hot really 70 beats per minute, respiratory is 14 breaths per minute, temperatures 98.6, you know, white count 6700, so that's kind of normal. He might have quit his 41%, so hemoglobin is like, you know, almost 14, so that's kind of okay. PT is like 10 seconds, PT is 20 seconds. And then they tell you that she has no recent history of like an upper respiratory infection. And your analysis, they tell you it's notable for like four plus proteineria. And then you're told that an upright chest x-ray or like a P-lateral chest x-ray shows like bilateral blonding of the cost of any kind goals. If, and then this question says there are some diseases of this fluid who most likely reveal what. So let me give you some options. Option A says an LDH of 500. Option B says a pH that's less than 7.1. Option C says like a fluid LDH that is 80% of serum LDH. Option D says fluid protein that is 40% of serum protein. And then option E says an abundance of polymorphine nucleolucleusides and gram positive diplococci. Or let you think about those for a second. What do you think the answer is? I would hope you're saying that the best answer is like option D.

So in this case, you know like fluid protein that's like 40% of serum protein. So again let's kind of break this down. This patient has HIV. This patient because they have four plus proteineria tells you that they likely have nephotic syndrome. Four plus proteineria is essentially like a surrogate means for your friends on the mbim to tell you that a person has more than three and a half grams of protein in the air in 24 hours. And because this person is HIV positive, they likely have like FSGS. So like focal segmental or glomerulus paralysis. Remember that nephotic syndrome right it decreases conchoric pressure. It kind of tags along with this central construct that if you have anything that increases hydrostatic pressure or decreases on cortic pressure, that thing will be a cause of a transudidiv pleural effusion. Okay. So other things that can cause a transudidiv pleural effusion, I think like CHF or like a PE. For the remember PE can cause both transudidiv and exudidiv pleural effusions. And then don't forget that cirrhosis right because you're a hypoproteinemic I will like mostly from like the low up human right. So cirrhosis can also cause a nephotic syndrome. And again it's like flurryly hyal to no light criteria right. And it's kind of easier to remember. It's like fluid like pure fluid protein to serum protein less the ratio less than 0.5. If you take the ratio of like the pure free the LDL, the serum LDL should be less than 0.6.

And then the LDL should be like less than to third try to less than 0.67, the upper limit of normal of a serum LDL. Basically if you've already any of any one of these roles, the fluid is like exudidiv, essentially have like an exudidiv effusion. And the big things you want to think about there are things like malignancy, you know like a PE, ARG, as a sort of deal. And really the easy way to again like I said to remember the causes of a transudidiv effusions just think about processes that decrease on cortic pressure right. So like cirrhosis causes less albumin. Nephotic syndrome your PN Lbumin out in the urine right. Many trees disease you're losing protein in the in the GI tract. It's like a protein and losing antheropathy right. Or anything that increases hydrostatic pressure again like like CHF or PE. Those are all things that will cause transudidiv effusion on exams. Now let me again ask another like Stip 2 CK style question. So what if you have like a 55 year old guy, you know he develops like progressive dysmia like two days after emergency surgery for type A uric dissection. And then so this most tell you that this guy probably had like a pretty you know pretty bad hospital course. And then they tell you that on ABG you'll find like a pH of 7.47. His PCO2 is 34. His P little AO2 so that like his arterial oxygen tension is 58 right. So it's kind of hypoxic. And then his CVP right so his central venous pressure which is like a proxy for redicule pressure is like 8.

And the tell you that is pulmonary capillary which pressure is 14. That's important to know. And then his BMP is 97 right. So like he's a B type of natural edic peptide is 97. And then they tell you that on the quotation of the chest you'll find like bilateral crackles. And then they make sure your chest x-ray that we have like this butt wound appearance. I'll encourage you to look this up. And then they say what is the most likely mechanism behind this patient's dysmia. And then you get like five answer choices right. And then option A says like left ventricular systolic dysfunction right. And then option B says increased systemic vascular resistance. And option C says like pulmonary edema from impaired biocardial contractility. And then option D says increased permeability of pulmonary vasculature. And then option E says consolidate processes from like an intraparincumal lung infection. If you see that what you think the red answer here is. Again I will encourage you whenever you get an MBMI question of micodagnosus first. It makes your life so much easier. This person has ARDS right. This person has ARDS. So the red answer here should be like kind of like option D right. Like increased pulmonary vasculopermiability. The big thing I kind of wanted to point out with this question is you want to be able to differentiate between like a cardiogenic and non cardiogenic pulmonary edema right. Non cardiogenic pulmonary edema is essentially like ARDS.

ARDS is like the big because on USMELY exams. You want to be able to associate that with like a normal pulmonary capillary wedge pressure okay. I remember the PCWP is indicative of the left-itre pressure right. If the PCWP is less than 18 that's the magic number you want to remember. If it's less than 18 that tells you that you're dealing with a non cardiogenic pulmonary edema most likely ARDS on exams right. And again they'll have like a normal BNP telling you that the heart is functioning just fine. And really ARDS and Acoustem they'll kind of disguise it as like you know like a super sick ICU patient who has like neon septis near really bad hypoxia kind of like a few days after admission. They'll have like a P little A02 to FIO to ratio that's usually less than 200 right. And then they'll show you like a chest X-3 that has like this bad wing appearance or like essentially like a wide-out long just look at you'll find look up a picture online or an image online of like ARDS chest X-ray. It's pretty striking is something you want to actually be able to recognize on exams right. Really the way you treat this is kind of like supportive care. I mean obviously the patient will be on event right. The big thing I want to do is high-peep low tidal volumes right. You want to essentially use a long protective strategies in fixing the patients are problem. Although the mortality of ARDS is pretty bad is like 40% or some high number.

Although it's been decreasing in recent years with these are long protective strategies have been used. Now let's I guess run through some quicker scenarios with like like diarrhea. Yeah let's run through some quick scenarios with diarrhea. So what if they give you a question about a patient that you know has watery diarrhea and they recently like returned from a trip to Mexico. That's E-Tech right. In teratoxigenica equal like remember it's like travelers diarrhea, montezomas or venges. What if you get a question about a patient that has like watery diarrhea with like rice water stoves. That's vibrio color right. Basically this will look like a crap ton of fluid. You can give like tetracycline. You can give a micro lid and remember that those people you need to rehydrate them with a salt sugar solution right. Basically like oral rehydration of therapy. And then what if you get a question about like watery diarrhea like a hiker or like a camper or you may describe a person that has like IJ deficiency or like Brutanzica Maglublinemia. Think about like a Giardia Lambella okay. Remember Giardia excreta with metronides all. And then what if you see like watery diarrhea and a cruise ship. That's like the neurovirus right. Or like no alqueiris. What if you see like watery diarrhea and infant right. That's rotavirus right. That's rotavirus. Remember it's a single stranded uh no no no no no. I was thinking about parverb been 19. Parverb been 19 is the single stranded uh gieni virus.

It's just one of those rare things you still want to retain in your mind for step 2ck. But rotavirus um you don't it's actually vaccine preventable but you don't want to give that vaccine to people that have a histroventure perception or mechols that are particular or um there's one more syndrome or like Hinoxion line pepper. You want to avoid the um the rotavirus vaccine in those are three populations of all people. And then what if you see like watery diarrhea and eat space shunt. That's cryptosporidium right. Don't choose cryptococcus in the heat of an exam. Choose a cryptosporidium parverb um remember it's acid fast. So they may say like oh examination of the stool shows acid fast osis. You can pretty much stop reading the question if you see that that's cryptosporidium parverb. Really the way you treat that is like with uh there's this drug called a paromomycin. Both another drug you can also use is something called an nitazoxanide. Okay it works pretty well for those purposes. And then what if you get a question about a patient that has like bloodied diarrhea after like consuming beef. That's like shigel right. Remember ehec enter hemorrhagic coli uh Campulo bacteria geninine can also cause those um and then actually I will say one thing with Campulo bacteria geninine it's actually the most common cause of blood it there in the US. Okay and don't forget the association with like Guiomba is syndrome right. Guiomba is syndrome like symmetrical is sending paralysis.

Uh remember you treat that like you know plasma phrases or like IVIG and uh remember that if you check the CSF of those people you'll find a ton of protein where you're like oh crap all this protein why am I saying like one or two white blood cells. That's the thing called the classic abumino cytological dissociation. And remember that um Guiomba is syndrome uh Guiomba is syndrome. Don't only think about your like GI infection you can also say your like respiratory infections and stuff like that. And then um what if they describe a patient that has diarrhea after you know getting like anti-biotics of any sort right. That's cdif right. I remember cdif it's the toxin that screen um so the screen that patient over. And um cdif first line is actually like vancomycin right before it used to be metronidazole. Right to me here like in my super old podcast metronidazole but no that's no longer first like these days first line is uh is a vancomycin. And then what if a patient has like diarrhea like bloody diarrhea and they have like you know like right right low quadrant and detail that this patient has um um like has caused you pork recently right.

I hope you think about like your senior um most specifically your senior in tereocolytica right is the thing that causes like the like the pseudope and the side is um and then what if they give you a question about a patient that has like bloody diarrhea and they have like a liver abscess um I hope you're thinking about like e histolyrica so like intamibah histolyrica.

I remember that's classic you treat out like patronidazole um if they have like a liver abscess you want to like inject something called ayudoquinol um into the abscess it sort of kills off everything there um and um what if a patient has like bloody diarrhea and they have like low platelets low hemoglobin and elevated creatinine that's uh H.U.S right that's him only uremix syndrome right so you're thinking about like ihek like enter hemagic colanderous circumstances all like shigella right and remember shigella you just need like less than actually like a little under tenor microbes to cause like a really bad maceration infection and then what if a patient has like diarrhea and there isn't like consumed oysters or seafood what are you thinking about that's like vibriol parachymolytica right um what if they tell you about a person that has like you know like very bad like morbidity mortality the consumer oysters and they have a history of like cirrhosis or some like liver pathology think about vibriol bonificus okay think about vibriol bonificus it has like this association like bad morbidity and mortality in people that have like uh some kind of like liver pathology and then um if they give you a question about a patient that it's not a diarrhea thing but if a patient like you know swam in fresh water and then they die quickly like three four days later think about this bogan like lyria fallorite that's like a weird thing your friends at the mbm the mbmiocaicinalia love to test right and then if you see like diarrhea and like a ton of vomiting after consuming like reheated like rice or like fried rice or you see like some kind of Asian restaurant fried rice and then the patient has like permanent like diarrhea and vomiting think about um um bacillus serious right uh it has a toxin i think known as like serylite that causes like the permanent vomiting you'll find uh y

ou'll find with it um i know i've certainly had a b-serious uh before i literally ate fried rice so there was my germ fried rice but whoof the thing is terrible i like essentially like throw up for like three D-strizzles or a terrible thing to have it's not ideal i'll tell you i'll tell you that okay no what if a person has like diarrhea like two hours after consuming like potato salad or like at a picnic that's that for you right usually it's more vomiting less diarrhea um so i think yeah i think i should maybe stop there with regards to um these are diarrhea causes and then uh let me do one more question and then we'll call it a day right so again another mbmistile question so what did they tell you you know have a 44 year old guy brings his five year olds on to the emergency room um and this four year old son you know has like a four he's show of like profuse sweating this son is rolling has watery diarrhea and they tell you that oh this kid has never had these symptoms before he has been home for the past week you know can explore in the house and they give you some vitals right you get like a blood pressure it's like 89 over 58 heart rate is like 33 beats per minute temperature is like you know 99.1 so not too high and the respiratory rate is 8 right notice this kid is pretty cardiac this kid is a little hypertensive and then they tell you that physical exam is notable for like diffuse wheezing in all long fields and this kid has like bilateral populary construction and they tell you that this kid's mom has like a three year history of like deplopia and the sathre that is worse by the end of the day that's a hint and then they tell you that he's that notice the pill bottle on the floor the child's playroom but cannot remember the name of the medication of course they'll never remember the name of the medication on NB Ms and then they ask what is the next best step

in the management of this patient so I'll give you five options option a let's say atropine right option b let's say in our tracks on therapy option c let's say phyzo stigma option d let's say intramuscular administration of flomazinal and then for option e let's assume it's a nebulized up pilot carping so what are you thinking about here right or what do you think the best answer is think about it for a second maybe pause the podcast and try to figure out the answer the answer here is a right so this is atropine right I mean essentially this patient's mom has like my austenia gravis and if you think about it right the way you treat my austenia gravis is with like an acetylcholinesis inhibitor like pyridol stigma you remember you get rid of my austenia with pyridol stigma right basically by giving the acetylcholinesis inhibitor that bumps up levels of acetylcholina than your musculoskeletal junction right because remember my austenia gravis is where you make like autoantibodies against the nicotinic acetylcholina receptor at the neuromuscular junction it's the thing that you know kind of like worsens with you so the hotel you that all person has like a decremental response with repetitive stimulation that's my austenia gravis right so this kid probably you know swallow one of those pills and it's kind of like getting like symptoms of colonergic excess or like bradycardia the kid is drooling the kid has diarrhea the kid is sweating so really your right step is to try to administer something that essentially like blocks those are colonergic receptors right so things like atropine for example phyzo I guess to kind of discuss the other answers remember phyzo stigma is used to treat my austenia grav no it's used to treat like an atropine overdose right you fix an atropine overdose with phyzo stigma because atropine right it is described like I think like a gym sandwich st

yle question you give phyzo stigma because phyzo stigma is again it's an acetylcholinesis inhibitor so bump of the levels of acetylcholine so you can essentially like bump bump off the atropine from the muskernic receptors phyomazenia already used to reverse like benzodiazepine or like in benzodia zepine overdose although you can also use it to reverse like the z drugs that I use when somnia so drugs like zopidem zaloplone zopiclon those z drugs you can reverse their deleterous effects with with phyomazenia and then in a lot so now tracks on you can use those to treat opioid dependence I mean to reverse opioid overdose although the one you really should choose on exemptions and aloxone do not treat do not choose on our tracks on now tracks on is used more for like opioid dependence it can also be used to help with like smoking cessation and then pylocarpine is like a colonergic agonist right it's easy to treat like glaucoma you can use it also treat chrogrins right because phybinamus granic agonist will prove like sort of aid in the production of saliva right so you can give it to patients with like chrogrins syndrome and you may see put define this patient had like pinpoint pupils like the population of the person right the thing is pinpoint pupils yes that can be opioid overdose but those people have like constipation right not diarrhea right remember like drugs like lopera might it's an opioid it's like kind of like the active ingredient like an imodium right is used for diarrhea causes constipation as a it causes constipation because I mean it causes constipation that's why use it for diarrhea because you're taking advantage of the constipation is the side effect and I guess to go ahead and stop remember that lopera might it can also use it treat like ibs like d so like ibs would like a diarrhea component that ibs with a diarrhea component essentially treat it wit

h something that causes constipation so like lopera might which is a synthetic opioid you can use a tricyclic and tady present remember that has like anti-colonogenic activity um so that will help there um but for ibs with like constipation you give something that causes diarrhea so you can give like you know like a stool softener you can give this drug a cordal lubey prostone that pops up quite a bit on mbim examples it's like a correctional activator so chloride will come into the lumen water of folus you get like a secretory diarrhea so sort of help with the constipation of symptoms of of uh of uh ibs uh c right well remember in ibs they won't have they won't have any physical exam abnormalities they will not have any lab uh abnormalities so that's a big thing you want to keep at the back of your mind so i guess i'll go ahead and stop here uh i hope you get something from this podcast again as i said at the end of every podcast i tutor a lot of things step one two two cs step three medicine and training the exam ibi-im board exam um college physics gen cam ocham bio cam histology physiology and then if you're like a preclinicomets to the nitrilo the preclinicle exams if you're a third year medicine i tutor the shelf exams um and then i do this longitudinal tutoring thing that i can have been sort of mentioning in a recent podcast um i've done it for quite a while um i essentially tutor you all through like your first years of med school and then tutoring you uh tutor you during your step one dedicated period of your studying now thirty i tutor you for all your shelf exams and then i tutor you during your step two ck dedicated period basically when i work with these people i meet them for like two to three hours every week and then um i infuse like so say for example like the preclinicle uh student i infuse step one knowledge with each of your preclinicle blocks so

that when you hit your dedicated period you're like super ready for step one same thing with like those uh third year shelf students i sort of like again prepare them avidly for steps two ck through like the third years so that again when they hit the a step two ck dedicated period they're like super super ready for the exams i'll do like teaching with the mbm questions and i'll also teach you like testicin strategy so again it's worked out uh extremely well for people that i have i have done this longitudinal tutoring with and then if you're uh met you in a plane for like ear ask like residency i'd offer like one on one advice and i'm consulting for that um if you're if you're college student applying to like med school again same deal advising consulting like personal statement writing editing application mock interviews letters of recommendation stuff like that i'd offer all those things again if you're an international medical graduate i work with a lot of international medical graduates i'll feel free to reach out to me i'll be more than happy to point you in the right direction with these things uh essentially every international medical graduate i've worked with has matched right and most of them have marched into like their first choices so again i have a lot of experience if you didn't any of these things uh reach out to me through the website or send out an email divine intervention podcasts with an s at the end at gmail.com so i do hope you have a wonderful day god bless you i'll see you in the next podcast thank you

Right upper quadrant ultrasound (RUQ US). If negative, proceed to a high-discount (nuclear medicine scan).

Cholecystectomy. Instead, perform a percutaneous cholecystostomy.

Obstructing stone in the cystic duct combined with dilation of the intrahepatic bile ducts.

Diverticulitis. Diagnosis requires CT scan with contrast; colonoscopy should be delayed until the acute phase passes.

Platelet count, bleeding time, $\text{aPTT}$, and PT should all be normal. The $\text{aPTT}$ is prolonged due to factor deficiency.

Guillain-Barré Syndrome (GBS).

Non-cardiogenic (ARDS) typically presents with a normal $\text{BNP}$ and low PCWP ($<18 \text{ mm Hg}$). Cardiogenic failure is associated with elevated PCWP.

Fluid Protein / Serum Protein ratio $< 0.5$. (Also, Fluid LDH/Serum LDH ratio $< 0.6$).

Cirrhosis (low oncotic pressure), Nephrotic Syndrome (protein loss in urine), and Heart Failure (increased hydrostatic pressure).

Fluctuating weakness, often worsening with activity or end of day; positive decremental response on repetitive nerve stimulation.

Acetylcholinesterase inhibitors (e.g., Pyridostigmine).

$\text{PT}$, bleeding time, and platelet count are normal; only the $\text{aPTT}$ is prolonged.

Shigella (or EHEC/Campylobacter). Remember that Campylobacter jejuni is the most common cause of bloody diarrhea in the US.

Acid-fast oocysts. Treatment involves Paromomycin or Nitazoxanide.

Fluid Protein / Serum Protein ratio $< 0.5$. (Also, Fluid LDH/Serum LDH ratio $< 0.6$).

Cirrhosis (low oncotic pressure), Nephrotic Syndrome (protein loss in urine), and Heart Failure (increased hydrostatic pressure).

Fluctuating weakness, often worsening with activity or end of day; positive decremental response on repetitive nerve stimulation.

Acetylcholinesterase inhibitors (e.g., Pyridostigmine).

$\text{PT}$, bleeding time, and platelet count are normal; only the $\text{aPTT}$ is prolonged.

Shigella (or EHEC/Campylobacter). Remember that Campylobacter jejuni is the most common cause of bloody diarrhea in the US.

Acid-fast oocysts. Treatment involves Paromomycin or Nitazoxanide.