DIP Episode 503 - LFTs and The USMLEs

Welcome, this is Divine, this is episode 503 of the Divine Intervention Podcasts. Into this podcast I'm going to be addressing the topic I like to title, the USM Lis and LF Ts. The USM Lis and LF Ts. This podcast is very, very high yield because LF Ts show up on pretty much every single USML exam. So today my goal is to talk you through the LF Ts, talk you through some weird factoids that again you will not see many resources or you will not see emphasized in many things or you will not even focus on it as you're studying for your USM Lis. But the ends of being extremely important for you exam. So I'm going to examine these things and I really hope that as you listen I pray that you get a lot from it and you know not just that but you're going to see us integrate a lot of concepts, talk about a bunch of diseases and just some clues right that may guide you in one way or the other. Because again at the end of the day is not profitable to just know LF Ts. The thing is you may know all the LF Ts in the world but if you don't know certain associations then it's not going to be very profitable for you on your exam. So let's go ahead and begin. So first things first right let me just maybe establish some kind of a foundation and then we'll start hitting some questions. But the first thing I think you want to keep in mind is there are certain classic LF Ts. So what are the key LF Ts? Well, we know we know we have the AST right?

The the Aspartate Amino Transferries we know the LFT, Allenina Amino Transferries. And we also know that there is bilirubin right both direct and indirect bilirubin. And we know that then there is those that are associated with problems with your biliric tract especially your bowel duct. So things like GGT, Gamma Glutamol Transferries and 5-Premiumucleotides right? So again the key labs right? LT, AST, Alcforce. Alcforce is a big one, bilirubin is a big one. And then if you want to specifically test for bowel duct injury you want to look at things like GGT, Gamma Glutamol Transferries and 5-Premiumucleotides. Although remember Gamma Glutamol Transferries is not associated only with bowel duct injury, it's also associated with alcoholism. And one thing I just want to throw out there is that LT and AST they're going to be they're not going to work as well. Honestly every transaminis will not work as well if you have B6 problems. So you can see how they can through an isoniasid connection there. Like many people always wonder, man, divine wise isoniasid hepato toxic. Well you have your reason right there. They're transaminases. So isoniasid is hepato toxic because it affects the function of transaminases. Transaminases which sometimes we call amino transferases, they use B6 as a cofactor. So remember isoniasid inhibits the activation of B6 so you are not able to form active B6. So it's going to cause like a B6 deficiency, like a functional B6 deficiency.

So that can make your transaminases no work right. That's why again isoniasid can be hepato toxic because again, AST and LT obviously pretty important enzymes for the liver. Now one other thing to keep at the back of your mind as you study for your exam is that one thing they love to test. They love love love to test this on exams. They love to ask, oh, what are some labs that are indicative of the synthetic function of the liver. I promise you this thing I'm saying is very, very high you'll know for your exams. Like, oh, what are labs that, oh, if the abnormal kind of tells you that delivers synthetic function, you'll be messed up. I want you to think of two big ones. Number one, think of your album. Right. That's a very liable indicator of a person's liver status. If your albuming is not good, you probably have issues with your liver. Right. Because albuming is literally made in the liver. But the one that they test more commonly and the one that people don't keep in mind as often is the PTINR. Right. PTINR. PTINR. PTINR is probably the most classic one they test on the exams as a test that reflects liver synthetic function. Now, one of the foundation I want to establish is that there are two general patterns of liver disease. Right. There are two general patterns of liver disease. There's the hepato cellular pattern and there's the colistatic pattern. That is like the very first foundation you want to establish in one of the first foundations.

You want to establish in your head. You want to be able to say that, oh, wait, what pattern of liver disease am I dealing with? That is like a very good approach to many LFT problems. Just ask yourself, what pattern of liver disease am I dealing with? Right. So say for example, if you're dealing with a hepato cellular pattern, you're going to notice that the LT and the AST will be elevated. The LT and the AST will be elevated. Now, one fancy, schmancy thing that our friends at the USML is going through on an exam is the conascu. Between LT and AST, which one is more specific for liver disease? Oh, I know someone may be like, divine. Come on, they're both released by the liver. Okay, but remember, specificity means that this is a lab that is most strongly associated with liver damage. There is literally nothing else in the body or fewer things in the body that can give you those kinds of labs. I'm going to tell you that right now it's ALT. It's actually pretty high to know that for your exams. It's going to be ALT because you may see it divine wise AST not as specific for liver disease. Well, the thing is AST is not only released from the liver. AST is also released by the heart. So if your heart is being damaged, you better believe your AST is going to skyrocket. Your skeletal muscles, basically your strided muscle, your cardiac muscle, your skeletal muscles. In addition to your liver, they all release AST. But ALT is mostly produced in the liver. Don't get me wrong.

Are there other tissues that make ALT? Yes, there are. But the liver is kind of like the crown prince in terms of releasing ALT. So ALT is more specific for diagnosis in liver disease. ALT is more specific for diagnosis in liver disease. And again, another association I'll show you if you know is that for persons in alcoholic, the AS Ts, their AST and ALT will both be elevated. But the AST is going to be quite a bit higher than the ALT. Now many people learn this from, oh, if you have alcoholism, your AST is going to be double your ALT. No, don't use that role. Just all you should go with on your exam is that your AST will be higher than your ALT. Live it at that. Because again, our friends at the MBM is right. Again, they know med students. They always want these clean questions. So of course, they're going to give you an AST question where the AST is precisely not double the ALT. And in Cp, they're like, oh, it's not double. So I'm going to let that go. No, don't let it go. Okay. Right. So AST, ALT, those are the things we see with the Hepatocelular injury. But if we have a polystatic pattern of liver disease, if we have polystatic injury, the classic thing you're going to see is that the alcohol force is going to be elevated. You're going to see an elvision in your serum, alkaline phosphatase. Right. And many times you're also going to see an elevation in your bilirubin, especially your direct bilirubin, especially your direct bilirubin. Right.

You're going to see an increase in your direct bilirubin. Okay. You're going to see an increase in your direct bilirubin. Now, I'm not the thing I guess I will also see since we've talked about direct bilirubin. But again, I have a bilirubin podcast. You should check that out. I can't remember exactly what podcast it is, but I think it's in the 200s, maybe episode 257. Simply as you define my podcast, just literally go on Google and just type in a divine intervention on bilirubin podcast. Right. So I really spend time drilling deep on bilirubin. So I'm not going to spend much time on bilirubin today. But you know, I just talked about how if you have a polystatic pattern of liver disease, where things are not flowing well in the liver or where there is an obstruction to bio-flowing the liver. Right. Your outforce is going to go up. Your dribbly rubin is going to go up. Well, what are the just as a broad, broad, broad picture? What are the things that are going to elevate your indirect bilirubin? You don't want to get a bilirubin. Well, think of some situation where you're overproducing bilirubin. Say for example, you have a hemolytic anemia. Right. So say for example, you have like a hairidigestripsitis, or hairidiotraliptocytosis, or g6pd deficiency, or sickle cell disease. All those things are going to raise your indirect bilirubin. Right.

Another thing that can raise your indirect bilirubin is if you have problems with conjugation of bilirubin, if you have impaired conjugation. Right. Many times we're going to see this with congenital problems, right, like the ober syndrome. That's a congenital issue where you have like a mild deficiency of UDPGT. UDPGLUCO-RCA-SELT-TRANS-FRA, which is the enzyme that helps us conjugate bilirubin. Remember, you can also see this with curriculum and heart syndrome. That's like a more severe deficiency of UDPGT. Right. And you may also notice like many newborns that have jaundice, most times they have indirect type of bilirubinemia. Because honestly, newborns, these two things I said that go along with an elevation in indirect bilirubin, we tend to find them in newborns. First things first, newborns tend to have polycythemia. Right. Because in utero, right, they don't use their lungs, the body kind of thinks of it as a state of hypoxia, relative hypoxia. So they make a tunnel equal, so they have polycythemia. And also if you think about it, in utero, the primary kind of hemoglobin that exists is hemoglobin F. Hemoglobin F has a left shifted, oxyhemoglobin saturation curve. So because it has that kind of curve, it's not very big on releasing oxygen to tissues. Tissues tend to be more hypoxic when you're in utero. So, and again, think about it, you only get an oxygen from mom through some placenta. Right. So tissues tend to be hypoxic in utero. That's going to trigger the kidneys.

Remember, it's the kidneys that make epo to make a rethropoetine. That's going to cause polycythemia. So when a newborn is born, then they have a ton of hemoglobin. And then you may think that, oh, okay, they're going to deal with this quickly. But no, right. They have all that high hematocrate. And you know, they're going to stop breaking, breaking, breaking those things down so that they look more like adults in terms of their hematocrate. But the only problem is that little kids, they have like very little UDPGT activity. UDPGT does not become adult levels for a while after you're born. So, you know, they have this high hematocrate, high hemoglobin. But then you also have this nasty issue of having like, in fact, I think as a newborn, if a mom is speaking, if I remember this correctly, I think I read this here as a go that as a newborn, you probably have like 1% of adult UDPGT activity. So you kind of have like a double one here, right? You have like too much hemoglobin because of your epo issues in uter. But then you have 1% adult activity, 1% of the adult activity of UDPGT. Well, that's not those two things together are going to cause you to have a neurobi. High hemoglobin, right? That's why we see, most times when we see a newborn with John this, most times he's going to be from indiretipar, milirubinemia. But again, I don't want to keep our festering too much on that.

But again, we said whenever you have a colistolic pattern of liver disease, your conjugate hemoglobin is going to go up, right? And again, many people always ask me, divine, what is the specific level we should keep in mind? See, I don't have any specific level in mind. Okay? I don't. Here's what I'm going to tell you. Usually on your exams, or at least if you're thinking in terms of your age, at least if you're thinking in terms of bilirubin, there are three kinds of bilirubin. There's total bilirubin, which is the combination of your indirect and your durability. There's your indirect bilirubin, and then there's your direct bilirubin. Basically, the kind of hyperbilirubinemia you have will be judged by the fraction of your bilirubin that is more than 50%. So if, for example, you have a total bilirubin of 10, and your indirect bilirubin is 6, your direct bilirubin is 4. Well, your indirect bilirubin is 60% of the total. So that means you have an indirect hyperbilirubinemia. If you see, so that's the predominant. That's the predominant. So, I mean, if you check the USM editable of values, the dribbilirubin of 4 is probably high. But again, the predominant hyperbilirubinemia with this example I gave is indirect hyperbilirubinemia. Another classic example I'm going to give, so let's say a person has, again, a total bilirubin of 12. But the indirect bilirubin is 4, and the dribbilirubin is 8. Well, that dribbilirubin is 67% of the total.

So that person has predominantly direct hyperbilirubinemia. And again, remember, whenever you have this polystyrene pattern of liver disease, additional dribbilirubin going up, being more than 50% of the total, you're going to have an increase in your alkaline phosphatise, as I've said. Again, this topic I'm discussing today, I know it's kind of dense. So you're going to hear me repeat myself a few times. I'm just trying to get in a few reps for you with repetition before the podcast is over. That's actually a pretty powerful way to teach. If you're a person that loves teaching, I'm going to encourage you, repeat yourself a few times as you teach. I'm just going to help your audience remember those things, especially those things that you repeat. OK, but going on, right? So you're going to see an elevation in the alkaline phosphatise. But again, remember, it's not only polystyrene liver disease, obstructive liver disease that elevates your outfoss. If you have a metabolic bone disease, your outfoss is going to be elevated. Believe it or not, outfoss is made from bone, is made from your intestine, is made from the placenta, is made from many other organs. So outfoss does not have this specific thing to fill with the liver. It just does not. So if you see an elevated outfoss level, and you're like, man, is this elevated outfoss level of liver origin? Confirm it. Confirm it by checking in, sounds like GGT, gamma glutamil transfer is or 5-prem nucleotides.

That 5-prem nucleotides is not something here. Many resources is not something to see many resources, but it's pretty important to know for your USMLE. And again, just to reiterate, whenever a person has issues with liver synthetic function, always think of a decrease in albuming, and always think of an elevation in their PT or INR. And an embedded PT INR is very, very helpful on the USMLE. You see how I've said this like three times now. It's important to know for your exams. It's a very good window into like, hmm, how's my liver synthetic function? Although remember, there are other things that can raise your PT INR, right? Like if you're taking a waffle ring, or if you're taking a happer ring, those things can both raise your PT INR, right? Because they both affect factor too. So even if we follow happer and with PT, it's still going to raise your INR. Even if you follow waffle ring with just PT, again, it's going to raise both of them raise your PT INR. But remember, if you have a vitamin K deficiency, your PT INR is also going to go up, maybe like, hmm, divine. What's the mechanism there? Well, the mechanism there is that remember, vitamin K supports an enzyme, it's like a cofactor for an enzyme known as vitamin K, boxy reducties. What does vitamin K boxy reducties do? Well, it gamma caboxylites, that's an activation step. It gamma caboxylites factors 279 and 10, and protein C and N.

So if you cannot gamma caboxylite factors 279 and 10, then those chlorine factors are not going to be activated. They're not going to participate in your calculation cascade. So your calculation cascade is going to take much longer, right? So your PT INR is going to be elevated, right? And also think about it if you have like some kind of malabsorbed tip disorder, especially a disorder where you have fat malabsorption, but if you have fat malabsorption, you're not going to be able to reabsorb fat soluble vitamins, like vitamin K. Remember, your fat soluble vitamins are vitamins A, D, E, and K. There's this adec, no money, right? So A, D, E, and K. So if you have like Celiac disease, for example, right? Or let's say you have like EBITDA lipoproteinemia, that's not really a malabsorbed tip problem, because you can reabsorb the fat and fat soluble vitamins well, but because you have a microsomal transfer protein problem, those things are pretty much stuck in the enterocytes. So they get into the enterocytes, but they don't get into the bloodstream, right? That's what we call EBITDA lipoproteinemia. That can also cause you to have a vitamin K deficiency. That's going to cause you to have a vitamin K deficiency. Okay, so now that I've kind of laid a foundation, another kind of laid a foundation, let me just again walk you through some general thoughts, right on hepatocellular.

Again, I'm trying to do this in some repetitions format to really help you remember certain things, right? But again, let's just walk through some of these, let's walk through these two patterns again, when we're going to walk through them from a somewhat different perspective, basically the rest of this podcast, I want to divide in three sections. I'm going to talk about the hepatocellular pattern of liver disease. Again, but in a somewhat different context, I'm going to add some more details, a colistatic pattern of liver disease, in some more context, that's the second thing I'm going to do. And then I'm going to do a lightning round at the end, why just review some key liver diseases and talk about what maybe some clues in the queue stem that it's this liver disease and what you may see lab wise, right? Again, hepatocellular pattern, remember the key feature, as we've said, before we start out lightning round is that your EST, your ELT is going to be elevated out of proportion to your ALC force, right? And again, whenever you're thinking of hepatocellular patterns, look at the queue stem that you're getting, right? There are many drugs that damage the liver, right? Like for example, think of a sedamin of fenn, I mean think of sorry, think of aspirin and rice syndrome, right? But a sedamin of fenn, believe it or not, is also hepato toxic, right? Because of this, any PQI business, right? It's one of the most common drugs that's used to commit suicide, unfortunately, right?

And again, as I mentioned the words you said, please med students, physicians, take care of yourselves, right? Mental health care is importantly health care in the lives of health care practitioners, right? But remember there are many drugs, right? Asprin, right? As sedamin of fenn, don't forget isoniasid, we've talked about the relationship there, right? Fampine is also hepato toxic, a methyl trexic, which is used for rheumatoid arthritis, right? So if you see a person that is on therapy for RA, and the LFT is a op-think of methyl trexic toxicity, right? Vapuricacic is a multibalyzer, it is profoundly hepato toxic, right? Look at the person, do they drink, right? If the person has an alcoholic history, right? Think of that as the cause of the hepatocellular injury, right? And also diabetes, diabetes can torture persons liver. Even being obese, I'm sure you've heard of non-alcoholic fatty liver disease, right? That can cause a hepatocellular pattern of injury, right? And again, don't forget your viral hepatitis, right? Your hep A, your hep B, your hep C, right? Don't forget your hep E in pregnant women. You see like this big, big, big LFT elevation in a pregnant woman, as she has eaten stuff recently. Think about hepatitis E. Remember it has a pretty nasty mortality in pregnant women, right? And again, remember, certain just drugs of abuse can torture persons liver, right? Don't forget that, right? Don't forget things like well-sensed disease, right?

And your seroloplasmic business that can cause a hepatocellular pattern of liver injury, right? So you can just kind of keep these things at the back of your mind. Remember, certain viruses can go after your liver, right? Like your EBV, CMV, those things can certainly go after your liver, right? And again, please don't forget your non-alcoholic fatty liver disease. Any time you're going to diagnose that by getting a CT scan of the liver, okay? So that's the first part. Again, you see I'm adding some more liars, right? If you look at the colistatic pattern of liver disease, again, what is the big, big, big thing you're going to see? Your out force is going to be elevated out of proportion to your ALT and your ESD, right? And one important thing I would say that's kind of helpful on the USMEL exams honestly, to look at when a person has a colistatic pattern of liver disease is try to ask yourself in the question. Did you tell you if the bowel docks are dilated or not, right? The bowel docks, you know, like the common bowel docks are like your main docks, your main bowel docks are lead, dilated or not. Here's the thing. If you're not dilated, then you want to think about some problem within the liver parankoma itself. Let us say that again, if you notice that your biliric tree, right, like your main bowel docks, your common bowel docks is not dilated, then think of some problem that is going on within the liver itself, within the liver itself, right?

So like for example, primary biliric colonjitis, most two, remember that's where you have inflammation, right? Remember you have these antimicryl antibodies, you have inflammation of your intra hepatic bowel docks, right? Usually for people that have PVC, they are common bowel docks, they are very large bowel docks are not going to be distended on your exam, right? It's more of an intra hepatic problem. The problem is inside the liver. It's a colistatic problem, but it's inside the liver. Remember, there are two kinds of colistices in the liver. There's intra hepatic colistices that's happening within the liver parankoma, and then there's extra hepatic colistices, something that's happening more around the portal system area, your main bowel docks, your common bowel docks area, right? Those big, big docks, those are more of the extra hepatic docks. Those ones are torched more in primary sclerosin colonjitis, but PVC torches more of your intra hepatic, you know, your bowel kind of liqueoline and all those things, right? And also hepatic cellulocarsinoma is one of these sneaky things that can also cause a colistatic pattern of liver disease. I remember you're going to see an elevation in the alpha fetal protein. Okay, I think one thing that may be helpful for the sake of time, let's just go straight to the lightning round. Again, before I go into the lightning round, again, I have a bunch of courses coming up this week for the USME Ls.

If you're taking step one step two, step three, I have three classes this week that can help you have a testic in strategy class on Thursday evening. I have a four hour biostatistics class on Friday evening and I have a five hour social sciences quality improvement health care systems ethics class, you know, communication skills professionalism class taking place on Saturday. These classes are for step one, just the three, they are all over zoom tons of people have taking them funding to extremely helpful. These classes are not lectures, we have tons of scenarios like the five hour class on Saturday. We have like 200 of their about scenarios that review that touches on many parts of ethics, health care systems quality improvements and things like that. And then next week, starting on Monday, we're having it on Monday Tuesday Thursday and Friday. I have a 20 hour step two step three course. If you're interested in these courses, just shoot me an email and give you some more information. Again, many people have taking these courses, they found it to be helpful. And if you love the way explained things, you've loved the way I use clinical scenarios, you love the way I integrate things across many different disciplines, then you're going to find these courses to be profoundly helpful. Okay, now let's do the quick lightning round. Okay. So what if they give you a question about a person that has eaten something recently, right?

You know, has that seen like the kind of relevant exposure and you see this big elevation in the AST and ALT, right? What you know, the ability is not that much elevated. If you see this on you and this is something that has happened over just a few days, I mean, notice that they have John days, they have a right or pro-cordant pain. I really, really hope you're thinking about some kind of a cute viral hepatitis. I hope you're thinking about some kind of a cute viral hepatitis. Okay. Now what if they give you a question about a person that just suffered among your cardio-infarction? And you notice that this person is AST and ALT is like crazy, crazy, crazy elevated. And then they tell you that all like two, three days after the event, the AS Ts and the AL Ts have normalized, right? So the person's results have rapidly resolved. If you see that, what should you be thinking about? I really hope you're thinking about shock lever. Shock lever. They can call this shock lever on your exam or they can call this is skinny hepatitis, is skinny hepatitis. When you have like systemic hypotension, that can cause like very big time damage to a lot of your hepatocytes. Right? Well the key feature is you're going to see the person, they have a history that they were hypotensive. And they notice that this person's lever function tests that were super abnormal, the rapidly resolved. Within a few hours, within a few days, they start normalizing very, very quickly. Okay.

And then what if they give you a question about a patient? And they tell you that this patient has received a blood transfusion in the past or the patient was an IV drug user or the patient was a sex worker. Right? Well the patient was born without proper newborn vaccinations or whatever. And you notice that they're AL Ts and they're AS Ts are high. I'll see most of the ALT. If you see that I want you to think about some kind of chronic viral hepatitis. Right? Chronic viral hepatitis. Okay. What if they give you a question about a patient? This patient does not drink, does not do drugs, but this person is very obese. This person has a history of diabetes. This person has a history of metabolic syndrome. And again, you notice that they are AST, LT, LVD. And again, most of the ALT. If you see this, I want you to think of non-acoholic fatty liver disease, non-acoholic fatty liver disease. Remember, there are two types of that disease. There is NASH. There is a non-acoholic stiato hepatitis, which is worse. And then there is the non-acoholic fatty liver, which is not good, but not as bad as a NASH. Okay. What if they give you a question about a person? You know that they have weariness or they have course or coughs. Right? Or the person you have like a megaloblastic anemia. Right? And you know, they are alcoholics. Right? And you notice that again, the AST is higher than the ALT. I want you to think of alcoholic hepatitis.

Again, remember, now, alcoholic hepatitis, you're going to have an innovation in your GGT, your gamma glutamol transferase. Okay. Now, what if they give you a question about a person that has a positive, a positive A&E, and they have a positive, anti-bodies against positive anti-sputusual antibodies. I notice that the AST and ALT are profoundly elevated. I want you to think of autoimmune hepatitis. I really want you to think about autoimmune hepatitis. Okay. Now, what if they give you a question about a person that has an innovation in their indribelyurabid? And they have these neuropsych symptoms. You know, they have like a type 2 RTA. Right? They have like a normal anion, they have metabolic acidosis, they have neuropsych symptoms, they have like, you know, sometimes abdominal pain. If you see this, I want you to think of well-sense disease, well-sense disease. Remember, these people, it's an auto-sumorescessive disorder in a gene known as ATP7 B. Are you going to see an increase in their indribelyurabid? The AST ALT is going to be up. And again, because of copper deposition in many organs, right? Like in the bizoganglia, it's mainly in the putamen. That's how you to know for your exams. In the putamen, right? You can have lots and lots and lots of problems. So you're going to see a lot of neuropsych symptoms, right? You're going to see renal tuberculosis because this thing can torture persons a proximal convoluted tubule. So they're going to get a proximal RTA.

They're going to get many problems. They can get like joint problems. They can get hypopetritoryzm. They can get hypothelamine dysfunction and things like that. Right? Because again, copper can use that same fentine reaction. That's in fentine reaction that's used by iron to cause problems. Okay, now what if they give you a question about a person, you know that you know, you use youngest right, like in their 40s and they already have in, unless they're smokers and they're having like long disease, you see like long hyperinflation on chest x-ray. I don't know. I really hope you're saying, oh divine. This person probably has an awful lot of antitripsina deficiency. Remember, people that have a lot of same disease, are they going to have low levels of serum copper and they're going to have low levels of seroloplasmic. That's important to know for your exams. Remember, seroloplasmic is like the transport protein for copper in the body. It's kind of like the transferring, just like transferring needs to iron. Transferring is the transport protein for iron in the blood. Seroloplasmic is the transport protein for copper in the blood strip. Okay. Now, what if they give you a question about a person that has diabetes, right? They have erectile dysfunction, they have like a restrictive cardiomyopathy. And you see the afraid thing is really elevated. They have like a high hematocrytor whatever. Then think of hemochromatosis.

Hemochromatosis can cause a, can cause a person to have abnormal LF Ts. Right? And then again, they give you a woman middle-aged has jaundice. Right? Her outfoss is super, super elevated. She has a lot of parietas, it's a chronic issue. And you see positive and time out of control antibodies. Obviously, that's going to be primary bilionary, serosis. Now, what if they give you a question about a person that has inflammatory bowel disease? Inflammatory bowel disease, and you notice that their outfoss is super, super elevated, is elevated out of proportion to the AST and ELT. Then I want you to think of primary sclerosine colonjitis. Remember, there you're damaging both the intra and the extra-operipate bowel dots. Contrast that with PBC where you're damaging only the intra-operipate bowel dots. Okay. And then, you know, if a person has like sodium onset, you know, severe, right, or pro-corporate pain, and you notice again that the outfoss is elevated, right? And the dribbler means elevated. You know, they probably have, unless you have like fever, they have jaundice. Right? That's probably going to be sending colonjitis. Right? They have a stone that's occluding the common bowel doctor. Remember, the big difference between sending colonjitis and colidocolethiasis, because it's the same pathophys. Colidocolethiasis, you have a stone that's obstructing the common bowel doctor. Isendic colonjitis, you also have a stone that's obstructing the common bowel doctor.

But the big difference between those two is that isendic colonjitis and infection has happened. Colidocolethiasis, no infection has happened. Okay. And then, what if they give you a question about a person they've been losing weight for months, they have malice, they have an lymphadenopathy, they have fever's, night sweats, weight loss, they have a paromegaly, think of some kind of lymphoma. Right? Remember, many of these hematologic malignancies, they love to torch the liver and the spleen. Why? Well, think about it. You'll live around your spleen as sites of extra medallary, hematopoesis, they're sites of extra medallary, hematopoesis. Right? Because remember, blood and, you know, it's not only made in your bone marrow, you can also make it in your liver, you can also make it in your spleen. Right? You can also make it in your liver, you can also make it in your spleen. So there's something you want to keep at the back of your mind. And many times, when people have lymphomas that go after the liver, you're going to see more of a colistatic pattern of liver disease. You're going to see big, big, big innovations in the Alco FOS. That's a very high olfactory to know for your exams. Remember, there are certain malignancies like pancreatic cancer or colisocarsinoma that can also cause that colistatic pattern of liver disease, cause that colistatic pattern of liver disease. Okay. I think I want to go ahead and stop here.

But again, I promise you this podcast is very, very high on stuff to know for your exams. But again, I offer one or one tutoring for all the USML exams, pre-clean cool med school exams, 30-ish-off exams. I also tutor for complex, the due exam, I tutor for all the complex exams. The only thing I don't tutor is the OMM, OMM. I don't tutor to that stuff. I just want to make that clear, because some people in the past have told me that the word OMM in your mouth, with your accent, sounds like women. No, I tutor men and women. Okay. It's just OMM. I don't tutor to. Okay. So hopefully that's kind of clear. And then again, I have the review courses. I have a separate podcast on that you can listen to. You can just read me an email. I can give you some more detail on the review courses. I have this 100 hour course that's coming up in May. It's a very big course, very high level course. I'm mostly making that attendance, but very, very high-yield, very comprehensive course for the USM Ls. And then finally, I have these podcasts on Apple Google and Spotify. I have a You Tube channel you can check out. And then I have another website called divineinterventionlifelessens.com. divineinterventionlifelessens.com. On that website, every week I post like two life lessons. We have about 245 episodes right now. And there's actually an Apple podcast as well with that called the divine intervention life lessons podcast.

From a biblical perspective every week, I post two podcasts usually on Friday and Sundays, that from the Bible, again, addresses a life lesson. Again, many people have listened to those and found it to be supremely helpful. Okay, so I'm going to see you in the next podcast. Have a wonderful rest of your day. I'll see you in episode 504, I guess. God bless you and bye for now. Thank you.

ALT (Alanine Aminotransferase). While AST can be elevated by muscle damage (heart, skeletal), ALT is predominantly produced in the liver, making it more specific.

Alkaline Phosphatase (ALP) and Direct Bilirubin. This indicates impaired bile flow (cholestasis).

AST > ALT. The ratio of AST to ALT will be greater than 1, though it should not necessarily be exactly double.

Vitamin K deficiency. Vitamin K is essential for the gamma-carboxylation of clotting factors II, VII, IX, and X.

Copper deposition, particularly in the putamen. This condition also presents with low serum copper levels.

Anti-mitochondrial antibodies (AMA). PBC is an intrahepatic cholestatic process.

Cholestatic pattern.

Albumin (low) and PT/INR (prolonged).

UDP-glucuronosyltransferase (UDPGT) deficiency.

Gamma-glutamyl transferase (GGT).

Neurological symptoms, low serum copper, and basal ganglia deposition of copper.

Primary Biliary Cholangitis (PBC).

Cholestatic pattern.

Albumin (low) and PT/INR (prolonged).

UDP-glucuronosyltransferase (UDPGT) deficiency.

Gamma-glutamyl transferase (GGT).

Neurological symptoms, low serum copper, and basal ganglia deposition of copper.

Primary Biliary Cholangitis (PBC).