DIP Episode 160 - USMLE Step 1 Rapid Review Series 10

Okay, welcome. My name is Devine. I'm a resident. This is a episode 160 of the Divine Intervention Podcast. This podcast I'm going to be containing the Rapid Review series, but this is for the US and the Step One Exam. This is series 10. And this podcast to be honest is not going to have any particular like, oh, I'm focusing on G.I. or whatever. I want to try to integrate like multiple disciplines in this podcast. So it's going to be like a freestyle kind of podcast. So what did they give you a question about a patient? And this patient, you know, they tell you that this patient was recently given a, you know, came in for surgery and got like a succinocholine and the notice during the course of the case, this patient is getting like superhyperturmic and has like diffuse muscle rigidity. What's your diagnosis? I hope on that circumstances, you're thinking about something more along the lines of malignant hypothermia, right? Remember malignant hypothermia? It arises classically, the classic presentation is a person will be exposed to like a succinocholine or they'll be exposed to halothane, right? Like the inhaled anaesthetics like halothane and then they get like, you know, like this profound muscle rigidity and all that stuff. And they're typically hypothermic, okay? They will try to confuse you on your exam and put your leptic malignant syndrome as an answer choice. Don't fall for that because NMS, guess what?

You need exposure to a neuroleptic to have neuroleptic malignant syndrome, right? So if a person, you know, recently started on like haloparydol, omidoclopromide for like diabetic gastro parisis when you think like that, then yes, you can elects to do one of those things. And remember that malignant hypothermia, right? It's actually inherited in an autosomal dominant fashion. It classically arises from mutations in the ryanodinoreceptor. That's the more common. So R-Y-E-N-O-D-I-N-E. So commonly I raise from mutations like in the ryanodinoreceptor occasionally. That's more common. And then in some situations, you may also see where people have like mutations in the bihydroperidine receptor. And really the way you treat malignant hypothermia, right? You can, I mean, you can give a dantroline. Remember dantroline is a calcium channel blocker. It's essentially a ryanodin receptor antagonist. So it prevents the release of calcium from the sacroplasmiparticular. And then since I kind of talked about succinocholine, you should also please not forget, right? Like succinocholine, right? Remember, there are two types of, if you want to, you know, into bait someone, you know, you need to like paralyze, you need to, you know, knock them out first. And then you paralyze them with a muscle relaxant, like a neuromuscular blocking agent. So the thing is the neuromuscular blocking agents, before into two categories, right?

So, and I've talked about this ad nauseam in my, in my neuro-pharmacology podcasts, like weep, they're one of like the earliest podcasts on this website. Just again, use the search feature on the website. You can find these podcasts pretty easily. And also I also break things down like by tags. So I guess that's another thing you can do. But basically right, the depolarizing your muscle blocking agents, right? Like the way I think about them is that they activate the nicotinic acetylcholine receptor. But in the key bits activated for long, at some point the receptor just burns out. That's why typically people when they get succinocholine, they tend to have like fasciculations. I kind of talked about that again in my prior in the neuro-pharmacology podcast. And remember that succinocholine, right? It's actually broken down by an enzyme known as a pseudo-colonesteris, right? So it's broken down by pseudo-colonesteris. So if a person, for example, or it has like decreased activity of pseudo-colonesteris, then that can potentially cause, that can potentially cause an issue with them, you know, being wind off that succinocholine. That's another very high-off thing that commonly comes up on the USMLA exams. And then what if they give you a question about a patient that has, you know, like a guy that's like six foot, five inches tall. And this guy has been having marital problems because he's not able to have kids with his wife.

And the tell you that on physical exam, this guy has gynecomastia. And this guy has like a tiny, like you know, like a micro penis, very small testicles. What's your diagnosis? Well, I hope you're thinking about client-felture syndrome, right? So client-felture syndrome, classic presentation, right? Tall guy, infertility, poorly developed secondary sexual characteristics, gynecomastia, micro penis, micro testicles, right? Does the classic presentation on Indian being exams? I remember these guys, you may actually want to strongly consider getting an orchietomy at some point, because with their testes, they actually have a pretty high risk of getting a germ cell tumors. Another group with these like reproductive style issues where you know, you need to don't get to me sooner or other than later, are people that have angiogenic sensitivity syndrome, you need to get rid of those, get rid of those testicles they have, because that can very easily give rise to like again, like a gonadu blastuma. Same thing also kind of applies to patients with a history of tonic syndrome. And client-felture syndrome, really, the way you treat it when those people get older, like in puberty or whatever, you can actually give them testosterone to sort of help them develop secondary sexual characteristics as appropriate. And the reason this person has gynecomastia, the way I think about it is the body tries to maintain like a testosterone, estrogen, resuminous sense.

So whenever you have something that makes one hormone higher, relative to the other, you will get like effects from that hormone, right? So if for example, the person has a client-felture, remember, client-felture is like 47xxy and you make the diagnosis with a charyotipin, right? That's a pretty easy one there. Don't get that wrong, I'm going to test. But basically the thing that happens is, you know, because the testicles don't really work as well, right? So they only get an off-testosterone. So they have a relative excess of estrogen, right? So that's why they have the gynecomastia. And then one next thing I want to talk about here is, what if they give you a question about a person that is you know like an albino, right? And they ask for like the enzyme deficiency that's giving rise to that person's albinism. What do you think it is? Well, I would really, really hope you're thinking about like a tyrosine oxidase deficiency, right? Tyrosine oxidase deficiency. The thing is for purposes of the USMLA exams, right? You definitely want to know that dopamine pathway. There's just way too many pathologies that arise along that pathway that you'll be doing yourself, you know, pretty, pretty decent disservice if you don't know it. So it's one of those things I would highly, highly recommend that you know for exams. So I mean obviously you want to know that this whole pathway starts with phenolalanine, right? And you know that phenolalanine, right?

It's converted to a tyrosine by the enzyme known as a phenolalanine hydroxylase, right? So phenolalanine hydroxylase is the enzyme that converts phenolalanine to tyrosine, right? And remember that if you have a deficiency of pH, right? The person will have the person who have pQ, the uppq, but again, the thing is your friends at the MBM realize that everyone has memorized that. So they're beginning to reach out to other things with the pQ, right? So what are the other things? The thing is if you really think about it, phenolalanine hydroxylase uses a pH for tetrahydrobiobtering as a cofactor. So if you have a mutation in the enzyme that regenerates that cofactor, it's known as a tetrahydrobiobtering, like pH for reductase, then you'll also have like a phenol type of pQ, but they will have like, they won't have like the pH deficiency, they just have a deficiency of the cofactor. So that's something that certainly pops up on exams you definitely want to know. And then remember that tyrosine, you can use tyrosine oxidies to convert it to melamine, right? So if you have a tyrosine oxidies deficiency, obviously you'll be an albino. And remember that albinism, right? If you see albinism in the context of like low platelets and eczema, right? Actually whoops, I take that back, I make it a wrong relationship here. If you see albinism in the context of like an amino deficiency, I'm really hoping to think about like Chiria Kigashi.

The other thing I was thinking about that I almost mentioned, if you see like low platelets, eczema, right? That's another skin condition. And you notice that a person has like, you know, like, like problems with like recurring viral and fungal infections. I want you to think about a whiskotodric syndrome. Remember that's that's an excellent disorder. So it would not be in a girl on an embankment exam, it would be in a boy. Okay? So those are two high-youth things to know. And then that tyrosine, right? Obviously tyrosine hydroxylis can convert the tyrosine to like dopa. Remember that pH 4, right? Stetrahydrobiocteryn is also the co-factor there. And then that dopa, you can convert it to, you can convert it to dopamine, right? You can convert the dopa to dopamine. And the clinical relevance there is with Parkinson's drugs, right? So you've probably heard of the Parkinson's drug, Carbidopa, Livo Dopa, right? So the thing is Carbidopa is a, you know, is a dopa analogue. Livo Dopa is also a dopa analogue. But the thing is you want that Livo Dopa to go into the brain and be converted by an enzyme known as dopa dicarboxylis to dopamine, right? So that you want the effect in the brain because that's where you have all the issues in Parkinson's. But problem is there is also dopa dicarboxylis in the periphery, right? So you need to present like almost like a sacrificial drug in this case, Carbidopa.

So that Carbidopa will be metabolized by the peripheral dopa dicarboxylis so that Livo Dopa can make it to the CNS and then be converted by the CNS dopa dicarboxylis into Carbidopa, I mean into dopamine, right? And then that can, that can, you know, help relieve the symptoms of Parkinson's disease. Dopa dicarboxylis, remember it uses vitamin B6 as a cofactor. Don't forget that vitamin B6 is a pyridoxyl phosphate. Again, that's another reason why when a person is taking an isoniasid, you really do need to supplement vitamin B6, right? If you don't supplement by the vitamin B6, you're putting that, as a patient or you as a physician, you're putting that patient a lot of trouble. And then dopamine, right? There are many things that break up, metabolize dopamine, so things like a caracol or methyl transferase, right? So COMT, it brings down dopamine into like inactive stuff, right? So there are drugs like intacapone and tocapone, right? So intacapone and tocapone, they work by inhibiting compt, when you inhibit compt, dopamine will persist for longer and you can use those to treat a Parkinson's disease. And other things that breaks down dopamine is a monamine oxidize B, so M-A-O-B, right? Remember that's inhibited by drugs like cell-H-L-N under-astagely. So if you inhibited monamine oxidize B, again, dopamine will persist for long and again you have, you have, so dopamine will persist for long and you can again hopefully relieve the symptoms of Parkinson's disease.

And then I get some other things to keep in mind, so dopamine, right? It can be acted on by this enzyme, dopamine beta hydroxylase, that can convert it to like Norepinephrine. And then Norepinephrine can be converted to a pennephrine by this enzyme known as many people call it like PNMT, it's like, if I'm not mistaken, it's like phenyl, come on, divine thing. I believe it's phenyl ethylnolamine N-method transfer, it's yeah, PNMT, I think that's right, so because PNMT adds, excuse me, you essentially add in a methyl group to Norepinephrine to make it into epinephrine, so you need PNMT for that, and remember you need a methyl donor, right? And the classic methyl donor is S-adenocel methionine, right? So that, remember, when Sam gives its methyl group off, it becomes almost system. So you can already see again why your friends at the NBME really, really like the spathway, because there are many biochem concepts you can integrate here. And another thing is, you always hear that, oh, glucocorticoids have a permissive effect on this empathetic nervous system, well guess what, one of the ways they have a permissive effect on this empathetic nervous system is by activating PNMT, right? Cortisol is a direct activator of PNMT, so that's just something you want to keep at the back of your mind for tests.

So again, really this tyrosine dopamine, whatever pathway is very high, you know, you'll be doing yourself a very big disservice if you don't know that, if you don't know that stuff as you are preparing for, for your USML is the one exam. And then, what if they give you a question about a patient that has, you know, like two days ago, they came into the hospital and they tell you that this person has, this person, you know, came in with no co-rigidity and severe headache, very high fevers, and let's say it's a college student that lives in a dorm, whatever, and then they say, what's your diagnosis, right? Obviously, you know this person has meningitis. meningitis, remember, it's vaccine preventable, right? There's a meningococcal vaccine, they're supposed to get it at the age of 12 before you start college, right? So that's a high your thing to know for exams. Another high your thing to know is that what if they then give you a question and they tell you that, oh, you know, this person, you know, was doing okay from a meningitis perspective, but then you notice one morning, the patient is like profoundly hypotensive and the patient becomes like comatose and they tell you that despite the administration of multiple pressers, this patient's blood pressure is still like 50 over 30 or some very low number. What are you thinking about on that those circumstances? I would really hope you're thinking about on what a house of phrygixin syndrome, right?

What a house phrygixin syndrome, remember, when a patient has an insure meningitis, remember an insure meningitis can involve the adrenal gland and then that can cause a something called a what a house phrygixin syndrome. And the thing is your friends at the MBM, you know that every human being has memorized, oh, an insure meningitis, what a house phrygixin syndrome, right? You know every human being has memorized that. So they don't really go after that anymore. They go after more like the primary, originally in sufficiency that essentially happens when a person has a when a person has a what a house phrygixin syndrome, right? Because essentially it's it's almost like you're getting an adicence disease style presentation from an infectious cause, right? So essentially they can ask you they can give you like a question with a lot of hours and then you need to figure out what happens to things like I don't know like sodium, potassium, yada yada yada in the setting of what a house phrygixin syndrome. Very high you'll to know that these people's sodium will be low, right? Because again, if the adrenal gland is been destroyed by the an isure meningitis, right? Then you won't have local corticose like cortisol, you won't have mineral corticose like our doster. So if you don't have our doster and on board, you lose the ability to reabsorb sodium at the level of the principles that are of the connecting duct.

So if that happens, you'll become hypoinitremic because you are also not reabsorb sodium at the level of the principles that are of the connecting duct. You'll also lose the ability to dump potassium in your urine. So those people will actually be hyper-chiliic, right? And then if people have because the adrenal glands, right? I know work into it. I'm no longer making cortisone. Those people will get if you if you check the levels of acth, the acth will actually be invaded, right? Because there's no negative feedback from cortisone. If you wanted to say, oh, let me test this people for this primary adrenaline insufficiency. If you give a person with an isridial stress sensing from you, give them like ACTH or like an ACTH analog, they would not have, basically, the accordisone will fail to rise with ACTH augmentation, right? Telling you that, oh, this person's problem likely lies at the level of the adrenal gland. And then remember, these people, they will also have a metabolic acidosis, right? Because again, remember, one of the jobs about dostroin is to increase the activity of that proton pump that is found at the alpha-intercalitate cell of the distal near front. So if our dostroin is not around, that proton pump doesn't work. You don't dump protons in your urine, so you retain protons. So you develop like a metabolic acidosis with that.

And that metabolic acidosis, to be honest, if you really wanted to stretch your thinking a little more, that will be non-anion-gap metabolic acidosis. And if you want that, you stretch your thinking even some more, that will be a type 4 RTA. Remember, type 4 RTA is arising in the setting of high both augmentation and dostroin states, like what happens in the setting of primary adrenalin sufficiency. Another thing they could also test, right? They could ask you for like a CBCF normality that arises in the setting of what a house rejects in syndrome. Obviously, right? Those people's eocenofil counts to go up. Because remember, right? Glucocorticoids cause epoptosis of eocenofil. So whenever you have primary adrenalin sufficiency and you're no longer able to make glucocorticoids, you have less epoptosis of eocenofil. So your eocenofil count will rise. So you have signs and symptoms of... You essentially have hyper eocenofilia detected on CBC. Again, that's a high-yield thing to know. So I think that's what I'm going to say about a what a house rejects in syndrome. And I think I'm going to go ahead and move on. Now, what if they give you a question about kid? You know that the experience notice that his head has been swelling for the last couple of months. And they tell you that this kid is at the 99th percentile for head circumference. And they tell you that this kid seems to be having like visual difficulty. And then they tell you that the obtain imaging of the kid's brain.

And they notice that they see like this calcified mass in the brain. What's your diagnosis? Well, I would really, really, really hope that you're seeing that this person has a craniofarin juma, right? Again, some pathologists call this and adamantinomatos, a craniofarin juma. But craniofarin juma, it's very high yield to know that those things are associated with... You want to know the embryologic origin. It's just something that your friends at the MBMD love to test quite a bit. Those craniofarin juma's they derive from raffky spout, right? They derive from raffky spout. I guess some other weird high yield like embryological boss phrases that your friends at the MBMD want you to know, right? Is for example, they can give you a question about a kid. Newborn has like profound respiratory difficulty at birth. And they tell you that this kid, like the perform imaging of the chest, and they notice that you have seen a GI force in the thoracic cavity. If you see that, I would really hope you're thinking about like a diaphragmatic cavernia, right? That's right, remember the diaphragm, right? It divides your thoracic cavity from your abdominal cavity. So they may ask for the embryologic pathophysiology behind a diaphragmatic cavernia. The thing you really should think about is you should think about it as problems with like the develop and I've said this in like many podcasts in the past, but again, repetition always helps.

It arises from issues with the development of something called the pleuroparital nerve membrane. Again, that's the thing. Try to understand things and you won't have to memorize much, right? So how do I remember that it's pleuroparital nerve membrane? Well, think about it. Just literally look at the name pleuroparitoneal, right? So that means you have some kind of membrane that is separating the pleurokavity from the peritoneal cavity, which is effectively what the diaphragm does, right? So when you have problems with the development of the pleuroparital nerve membrane, then that person can have a diaphragmatic hurl. Because the membrane that's supposed to separate the thoracic cavity from the abdominal cavity does not exist. So those are again all high-yield things to keep at the back of your mind. Now, what if they give you a question about a patient that has been having a, you know, pretty, let's say it's like a patient from a developing, okay, you know, let's not use developing country. Patient from a developed country, let's say this patient went to like, went like on a missionary trip somewhere and then you know came back with like really bad diarrhea, like really bad watery diarrhea and they're like profoundly volume depleted and the tell you that this person on exam, they have like skin tinting and all that, yada yada yada, and then they ask him for the mechanism behind the person's diarrhea.

The thing is your friends on the end being at the end in the mirror, they love to test mechanisms behind the diurel diseases on tests. I don't know for them. Actually, it's actually a nice thing to know because it helps you group things un-mogically so you know what you're treating. But basically this person likely has a secretory diarrhea, right? And you again, you should hopefully know that this person has a diarrhea from a cholera, right? Remember, the cholera toxin is essentially like an adenylid cyclisyne and of itself. So it converts ATP to cyclic AMP and that increases the secretion of chloride through the CFTR channel, right? If you secret more chloride water will follow alongside and you get a secretory diarrhea with that. The thing is literally, with the mechanisms of diarrhea can literally make up maybe like 10 or 20 different MDME style questions, right? I mean, like think about it, right? What if they give you a question about a patient that is, you know, has a, you know, was recently started on a drug for diabetes and they have like really bad like diarrhea, right? Then you may want to think about an osmotic diarrhea. So the mechanism here will be a smoses, right? So an osmotic diarrhea, remember, there are certain drugs that are used to treat diabetes. They work by preventing the reabsorption of glucose in the GI tract. So they are brush-border drugs, right?

So drugs like Acarboz and Miglital, they inhibit this brush-border enzyme known as alpha-glucosides and believe it or not, your friends at the MDME can actually ask for the location of this enzyme. You want to go ahead and pick the answer that says microv-ly or says brush-border, okay? So drugs like Acarboz and Miglital, right? They inhibit alpha-glucosides and when inhibiting alpha-glucosides, you prevent the reabsorption of glucose in the distal nephron because you're essentially preventing the breakdown of dyssaccharides to monosaccharides. Remember, dyssaccharides are not able to be reabsorbed, but monosaccharides can. So if you inhibit a dyssaccharide, like alpha-glucosides, so again, on your examine, instead of putting alpha-glucosides and as an answer choice, they can actually put dyssaccharides. If you inhibit alpha-glucosides, you don't break down dyssaccharides to monosaccharides, you prevent glucose reabsorption. Those agents sting the GI tract, the extract water, and then you have an osmotic diarrhea with that. I mean, another thing that can cause an osmotic diarrhea, right? You can give you a young person that you know has been having like a lot of like bloating and abdominal pain with an diarrhea that are coupled to like the consumption of meals. It'll be like a teenager or it can be like an Asian person or an African person. If you see that, right? You obviously want to think about a lactase right?

So this person has like lactose intolerance that's essentially causing the symptoms. Very high youth thing to keep at the back of your mind. Remember, if you have a deficiency of lactase, again, you have a deficiency of a dyssaccharide. If you have a deficiency of a dyssaccharide, you don't be able to break down lactose into glucose and galactose. And guess what? If you can do that, well, you're in trouble. You don't be able to deal with lactose and you can deal with lactose, then obviously you have issues with... You have my absorption issues, right? The lactose is then your GI tract flow. It will attract a fluid and then you get an osmotic diarrhea with that. And remember, right? Kids that have a history of essential galactoseemia. Remember, that's when you have like a galactose 1.4-speed-eredeal transfer is deficiency. Those kids, they cannot get breast milk, right? Because breast milk again contains lactose, right? So you don't want that. So again, just how you think to keep at the back of your mind there. And then, secretory diarrhea, I already talked about cholera, right? So again, developing country, germ from a stream, yada yada, losing like a Kryptonofluid. Remember, if a president has cholera diarrhea, your treatment is to give the president something called oral rehydration therapy, right?

He essentially give like a solution, like a sugar water, like a salt sugar solution, because the salt sugar solution, right, will promote the reabsorption of that glucose, right? And salt and water, right? Because when a president has cholera, right, most of the transporters in the GI tract are knocked out. But the sodium glucose linked transporter, most specifically the SGLT1 transporter, is still functional. So look at the name of the transporter, sodium glucose linked transporter, right? Sodium glucose linked transporter. So that means it's a transporter that links sodium and glucose reabsorption. So by supplying a salt sugar solution, right? You will increase the reabsorption of stuff through that SGLT1 transporter. And that will help with, uh, at least trying to maintain a hydration, at least however you can, in the setting of a cholera diarrhea. Although those people also probably need like, you know, very good IV fluids. Now, um, remember, right, this, uh, they, you know, this gives you like a non-specific question about a patient that, you know, traveled like out of the controversy, traveled to like Mexico and they come back and they have like, you know, like a mild water diarrhea. Um, I hope you're thinking about like a teratoxogenic like, right, eat tech. Remember, sometimes it's known as a, want to zoom as revenge. Remember, eat tech, right, has two toxins, right?

Like it has a heat stable toxin that activates, uh, guanelose that activates, uh, guanelose cyclists and then it has like a heat libel toxin that activates adenolose cyclists, right? So you have an increase in cyclic AMP in the presence of the heat libel toxin and you have an increase, uh, uh, an increase in cyclic GMP with stable toxin, right? The heat stable of the heat libel toxins, again, as I mentioned. So that's, that's a big thing when you keep in mind again. If you activate adenolose cyclists, again, you have a secretory that I know with that. Um, and I mean, I just mentioned a few seconds ago about the SGLT1 transporter. Well, hopefully remember that if there is an SGLT1 transporter, well, guess what? There is also an SGLT2 transporter, right? Those are the SGLT2 transporters. You find them at the level of the proximal convoluted tubio. Remember that those transporters are inhibited by drugs like a cannagly flossing or a dipagly flossing or impagly flossing, right? Those are your SGLT2 inhibitors that are used for the treatment of, uh, diabetes and melatres because you're essentially preventing the reabsorption of glucose at the level of the, uh, the proximal convoluted tubio. Remember that's where you actually reabsorb, um, 100% of the glucose that gets into your urine. And then another secretory diarrhea question, right? Be kind again, easily give you a question about a patient, you know, that has a history of like MEN1 syndrome.

And then they tell you that this person has been having, you know, pretty bad, uh, watery diarrhea for like months and months and months. And then they give you like all these labs and notice that the presence chloride, um, is like, uh, 90, right? So it's pretty low, like pretty low. And then they give you like the, uh, BMP, you see that the presence potassium is like three, right? So the person has hypochylenia. I would really hope on that those circumstances, you're thinking about a, a Vipoma. Sometimes a Vipoma is known as WDHA syndrome, right? So that's essentially like, uh, like watery diarrhea, hypochylenia and eclohedra. That's why they have the local right on, uh, on labs, right? So I remember that, uh, uh, visual active so Vipoma, right? It means like an OMA, so a mass as secrets VIP, visual active intestinal peptide. The thing is, Vip, uh, VIP, right? The hormone, right, increases GI mortality. It increases rocks through the GI tract. So that can again cause like a secretory diarrhea, right? With a Vipoma, the contested in the context of the MN1 syndrome. Again, I hope that you remember that MN1, right? Has a mixture of problems with the parathyroid, right? So they can get hypercalcemia, they get pancreatic neuroendocrine tumors like Vipomas, insolendomas, uh, gastronoma. Remember, insolendomas will present with weepostryide, gastronomas will present with the context of the Zolange elicit syndrome.

Remember, you're glucanagonomas with the necrolidic migratory arithema, right? So those are all presentations. Um, so, uh, so like I said, MN1, parathyroid problems, pancreatic problems, and you can also get pituitary adenomates, right? So like, like a prolactinoma, for example, or a growth hormone secretina tumor. So those are all things that can present there. And please don't forget, right? That MN1, it's in herithidin and or zomodominant fashion, right? And um, the mutation is in the meningi, okay? So that's again a high-yield thing to keep in mind. And then, so I've kind of talked about like the areas that, you know, can happen from a small size, can happen from secretion. There's others, but these are, you know, the big, high-yield ones. There are also those that can arise from my absorption, right? So, like, for example, if a person is taking an early stat, right? So if a person is taking early stat, um, only stat, right? There's a drug that used to treat, um, does used to help people with last-rembered, it's an inhibitor of lipase. Well, if you can inhibit lipase, you'll prevent the conversion of triglycerides to monoysil glycerol and two-three-fadi acids. Well, the thing is, you cannot directly reabsorb triglycerides, right? So you essentially causing like, my absorption in a sense, right? So that can cause a, like, a malabsorptive-style diarrhea, ciliac disease, right? Same issue, right? You have like, uh, destruction, right?

Like autoimmune destruction of like your brush border, right? In your GI tract, right? Those things can all cause, uh, those things can all cause problems with a malabsorption, and you can get diarrhea with that. Although remember, ciliac disease also tends to be associated with like a rash, especially on extensive surfaces. That's the thing called a dermatitis or pre-informus, right? That's a high-yield thing you want to keep at the back of your mind. And remember that people that have a history of ciliac disease, ciliac disease has really has a very nice association with like IG deficiency. So that's something you want to, you don't want to commit to memory. Another thing you want to commit to memory with ciliac disease is that they can ultimately develop something called an enteric associated t cell lymphoma. So EATL and enteric associated t cell lymphoma. That is something that is not in many study resources, but it shows up quite prominently on the USMG exams. So it's one of those things you sort of kind of want to keep at the back of your mind. Remember, right? People that have ciliac disease, they tend to have antibodies against like gliadine or anti-indomacial antibody, so ENDO, MY, SIA, L antibody, and then they also have antibodies against tissue transglutamines. And then remember, people that also have ciliac disease, right? They tend to have like very low weight on end beam exams.

If a person has, you know, like they are overweight or obese, they can have ciliac disease on an end beam exam. That's just for tests. Now another thing that can cause malabsorbed tube diarrhea, things like tropical spru, right? And actually, I think that I guess to mention this remember, ciliac disease, right? You obviously treat ciliac disease by, you know, restricting gluten in the diet or eliminating gluten from the diet, right? Cystify bropsis again is another thing that can cause malabsorbed type of stalled diarrhea, right? Because in CF, right? Remember chromosome 7, you have problems with, you know, the CFTR transporter, right? So, you are not your intestinal contents get like gong thump, that's one. But really, it was a thing that really causes the diarrhea. The thing is, they also gong cup like they are pancreatic ducts, right? So like lipase is not released. Well, if lipase is not released, it's almost like, it's essentially like, you have like a generate disease that will press like all your stuff. You don't have any activity of lipase because it just doesn't make its way to the GI tract. So if it doesn't make its way to the GI tract, you're kind of in trouble there, right? Because you, again, you have a Fat Malabsorption and then you run into issues. And remember that when you have Fat Malabsorption, right?

One other thing that can happen is, you can also have like my blindness from like vitamin E deficiency or like secondary hyperparapathy and radysine from like vitamin D deficiency, or you can have like A-taxia because your spinal cerebellar tracks don't work well, or you can also have like A-kanthusitis, right? If you look at a red blood cell smear, because you have a vitamin E deficiency, or you can have bleeding because you have a vitamin K deficiency. Because the thing is whenever you have a Fat Malabsorption, you're also going to have a Fat Solvable Vitamin Malabsorption, okay? So again, those are all higher things to keep in mind. And then there are certain GI motility disorders, so this can be like a motility cause of diarrhea, right? So if for example, a person is taking a, you know, a person has like a history of diabetes and then they have like, you know, constipation that is alternated with diarrhea. I really hope one of those circumstances that you are thinking about a diabetic gastroparesis that can actually be a cause of diarrhea because they essentially have like an autonomic neuropathy of the GI tracks, right? So the hyperglycemia is kind of like a mess of their, messed of their messed of their neurons that constitute like the plexite that we find in the GI tract. Also, drugs like, I mean, think about it, why do people get diarrhea, right? When they take a microlitre, right?

So remember, microlitres can cause diarrhea, so there'll be a motility style cause of diarrhea, because remember your microlitres drugs like aerithromicin, for example, aerithromicin is a motiline receptor agonist, right? So by being a motiline receptor agonist, it actually promotes GI motility, so again, those are things you want to keep in mind. I mean, for pressing has, and remember that, actually, maybe it's sort of taken, in fact, because I know this has gone on for more than 30 minutes, I'm going to round up probably within the next two minutes. Well, they're just too high-yielding to judge integrations I want to throw in here, right? So one thing I want to maybe mention here, they can give you a question about a patient, you know, that has like, you know, like a histrop like diabetic gastroperises, and then they tell you that, oh, you're staturing person with a clot permide, and then they start describing like extra pyramidal-style symptoms, right? That is a very nice way your friends at the MBME can integrate GI with psych, right? So that's one thing you want to keep in mind, like, they've done this, it's like a time-honored, like MBME trick, it reduces all the time, where they will give you a question about a person, has a histrop diabetic gastrop perises, you set the patient a metoclopromide, many people forget that metoclopromide is a dopamine receptor antagonist, right?

So it can certainly cause the extra pyramidal side effects that you observe with the regular good old-fashioned anti-psychotics, like a hallow periodo, so that's something you want to keep at the back of your mind. And then the last integration I think I want to mention here, remember, chronic diarrhea can also arise in a person, this will be more of like a secretory diarrhea, but it can arise in the setting of a crash-in-late syndrome, right? Remember your crash-in-late syndrome, you have a tumor usually like in the appendix or summary and a small intestine, producing a crap ton of serotonin, when you produce all that serotonin, then you can then ultimately run into trouble, right? And remember, the way you, the classic presentation of, of, come on, divine think, the classic presentation of, of crash-in-late arthritis, like the person will have like a, like diarrhea, you'll have like flushing and you'll have like right-sided heart legions, because remember the lungs, right?

Have the ability to break down serotonin, so it's only the right side of the heart-own-city effects, and usually the right-sided heart problems you get at things like a tricospitary gorge and like pomonic stenosis, there's this nice, pomonic that exists out there, it's called like tips, that's a way to remember the right-sided, pomonic pathologies that arise in the setting of crash-in-late syndrome, so things like tricospitian sufficiency and pomonic stenosis, remember whenever you detail that a valve is insufficient, is the same thing as a valveular regurg, so that's something to keep at the back of your mind, and then one other thing I guess I'll go ahead and see is, remember if a person has a history of crash-in-late syndrome, right? You'll also have, sorry, I know I said I'll take an extra two minutes, oops, sorry about that, again, but I promise I'm gonna be done very soon, but whenever a person has crash-in-late syndrome, right? Again, all these ideas as I'm speaking, just more, I guess you'll just keep dropping into my head, and they are all you assembly worthy, so sorry, I just don't want to, I just want to, you know, give you, I guess, the best bank for your buck with this podcast, so my apology, so if a person has crash-in-late syndrome, remember they can also get like, they can also get, what's this condition called, Pelagra, right? Because remember, whenever you have high levels of serotonin, remember serotonin, another name for serotonin is 5 HT, right?

So like 5 HT drug seechreptophan, so it converts, so essentially serotonin is at the rate of triptophan. Well, problem is triptophan is also used to make my insane, so if you have like this weird tumor, right? That's making you like, consume all your, essentially make you consume all your, consume all your triptophan to make serotonin, right? Then you have less feedstock available to make my insane, and obviously that causes a lot of problems, right? So that's just something you want to keep in mind, so they can get like the three, actually it's more like 40s of Pelagra, we have like the diarrhea, the dermatitis, the dementia, the death, the death is, oh, I mean, obviously that's not an ideal outcome, right? So that's something you want to watch out for, and another thing that can cause, you know, like that problem, right? Easy for person has like, you know, like, what's this thing called? Like, heart note disease, right? So heart note disease, we have trouble reabsorbing like neutral amino acids at the level of the, at the level of the proximal convoluted tubular, and also in the GI tract, right? So if you have those problems, right? Well, you won't be able to reabsop triptophan, well, if you can't reabsop triptophan, you have a whole new set of problems on your hands, right? So you can't reabsolving triptophan, can't make niacin, and then you obviously have the 40s of Pelagra. And then remember, the way you diagnose carcinol syndrome, right?

It's obviously you check the persons urine, and you notice that you'll have elevated levels of the substance of 5 HIA, because remember, 5 HIA is a derivative of serotonin, right? So the levels of 5 HIA in your urine mirror the levels of serotonin in your body. So whenever you have carcinolid syndrome, the levels of 5 HIA in your urine will go up. Now, one of the things I'll go ahead and mention, because the thing is your friends at the MBM again, people say all the new USML exams are so hard, bloody, bloody, bloody, bloody, bloody, they're essentially just taking again the things you know, and just, you know, texting a slightly different light, right? So the thing is your friends at the MBM, they can actually ask you, like a novel question, would be, what would be trove the levels of 5 HIA in the urine of a person that has depression? Well, for a person who's depressed, if you remember I don't know, it's called like the, is it called a colamine hypothesis of depression, where, oh, depression is a little low levels of serotonin, or epinephrine and dopamine. Obviously, if a person has depression, they should have low levels of serotonin. So if they have low levels of serotonin, they should have low levels of 5 HIA in the urine. So that's the way they can tick some of the knowledge you need from carcinolid syndrome and infuse it in a psychiatry question.

I mean, that's, believe it or not, that is something that your friends at the MBM again, they've been doing over the last three, four months on exams. So just something to keep at the back of your mind. So I think I'm going to go ahead and stop here. This rapid review has gone on for too long, but as I do at the end of every podcast, I do offer one or one to learn from any exams. Step one, step two, CK, step three, step two, CS. If you're a met student, you're pre-clinical exams, you're, if you're a 30-metre student, you're shelf exams. If you're a medicine resident, like the IBI M board exams, the internal medicine, and treating exam, offer tutoring for all those things. And then if you have like a college buddy, you know, that needs tutoring for like Gen CAM, O-CAM, Physics, Bio CAM, Histology, Physiology, offer tutoring for all that. And then there's this thing I've been talking about recently, like longitudinal tutoring, where if you're a met student, a tutor, you're like your first or second year tutor for your block exams, or if you're a 30-year tutor for your shelf exams, but at the same time, a tutor for your upcoming USMMD exam, everyone I've done this with, it'd been like wildly successful on their tests. So if that's something I'm interested in, reach out to me, it's something that works really, really well for people. Again, I've done it with a select number of people over the last couple of months, but it's worked extremely well for those people.

So if you're interested in that, just let me know. And also there's this buster USMD course, I also offer where for step two seconds, step three, it's 10 hours, for step one, it's 20 hours, where again, like in that time frame, I review a lot of the high-yield concepts that you'll see tested on the exam. So again, if that's something I'm interested in, I feel free to reach out to me, you can either reach out to me through the website or you can send me an email at Divine Intervention, podcasts with an SADN at gmail.com. So have a wonderful rest of your day, I'll see you in the next podcast. God bless you. Thank you.

Succinylcholine or inhaled anesthetics like halothane.

Pseudocholinesterase.

Relative excess of estrogen due to impaired testicular function.

Tyrosine oxidase deficiency.

Carbidopa/Levodopa (Carbidopa prevents peripheral breakdown of L-DOPA).

Cortisol levels fail to rise, indicating the problem lies at the adrenal gland level.

Cholera (cAMP) and ETEC/Heat stable toxin (cGMP).

VI Poma (secretion of Vasoactive Intestinal Peptide, which increases GI motility).

Phenylalanine hydroxylase (PAH); Tetrahydrobiopterin ($\text{BH}_4$).

Osmotic diarrhea; Undigested disaccharide (lactose) remains in the lumen, drawing water.

Phenylalanine $\rightarrow$ Tyrosine $\rightarrow$ DOPA $\rightarrow$ Dopamine.

SGLT2 transporter.

Watery diarrhea, hypochylenia, and elevated fecal fat/malabsorption signs.

Anti-tissue transglutaminase IgA (tTG-IgA).

Diarrhea, flushing, and right-sided heart lesions (e.g., tricuspid regurgitation).

Phenylalanine hydroxylase (PAH); Tetrahydrobiopterin ($\text{BH}_4$).

Osmotic diarrhea; Undigested disaccharide (lactose) remains in the lumen, drawing water.

Phenylalanine $\rightarrow$ Tyrosine $\rightarrow$ DOPA $\rightarrow$ Dopamine.

SGLT2 transporter.

Watery diarrhea, hypochylenia, and elevated fecal fat/malabsorption signs.

Anti-tissue transglutaminase IgA (tTG-IgA).

Diarrhea, flushing, and right-sided heart lesions (e.g., tricuspid regurgitation).