And it's a pleasure to be back to talk to you about evaluation of abnormal liver tests. So I'm changing the title up a little bit. And you will find that this is as much a linguistic lesson as it is a medical lesson. And there's a great reason for that. I think it's important to be precise. And the reason to be precise is so that we always know that we are all talking about the same thing. If we're not talking about the same thing communication suffers, and if we make mistakes as a result of that as clinicians, we can hurt people. So I think it's important to be precise. We use our words. And it's also important for you to understand how to use tests, so that rather than making you a pattern reader. I'd like for you to understand what each liver test represents physiologically. And then you'll be all set, you'll have the tools, and then you can study the patterns and the workup, knowing full well what each one of these tests means, and what it is useful in representing to you and the care of your patients so here we go. Alright so again I have no disclosures. The objectives of this talk are the following to define liver tests to describe and categorize different types of liver tests to discuss the implications of the abnormalities of specific liver tests to learn the disorders associated with liver test abnormalities, and to determine how to work up patients with liver test abnormalities. So let's start with some polling questions for the first one, a LT, which stands for alanine amino transfer race is a, a liver function test. Be a liver injury test. See a colostatic liver enzyme or D, a liver synthetic test only one is correct. Which one is it. And that is excellent. And I understand the discrepancy in the answers here so let's go through them one by one. 92% of you, that's the highest percentage identified correctly that a LT is a liver injury test. Okay. AST alkaline phosphatase sometimes GGT and five prime nucleotides are frequently referred to as liver function tests. Now I know that that you know that that is a vernacular term so to speak, people say yeah they're all liver function tests, but technically, a which are amino transfer races, do not reflect the function of the liver. They reflect injury of the liver and we'll talk about that in a bit. So those of you who said a liver injury test you are corrected is that. So as a ST. That's a giveaway. And for those of you who answered a almost as many. I understand why and it's okay and I'm glad that you did answer it that way because we're going to change that and you're going to teach others, the difference between a liver function test and a liver injury test. Now while a LT may well be elevated and colostatic liver diseases. It is a liver injury test and not a colostatic liver enzyme. It is not a liver synthetic test. There are others that are liver synthetic tests and we'll go over that in a moment as well. All right, so alkaline phosphatase often abbreviated a LP. Which one of these is correct only one is correct alkaline phosphatase a is specific to the liver. B is specific to the bile duct. See can rise, only in bile duct obstruction, or D can rise in any colostatic process. So alkaline is correct, only one is right. So alkaline phosphatase is not specific to the liver alkaline phosphatase is made in a number of tissues. Another prominent one is bone, and sometimes when an elk fossils elevated you need to differentiate whether the source of the elevated alkaline phosphatase is liver or bone so alkaline phosphatase is not specific to the liver so a is incorrect, as most of you cited. It is not specific to the bile duct either. It. Like we just said can come from bone and other tissues, and so it's not specific to any one tissue. It can rise in bile duct obstruction but it doesn't rise, only in bile duct obstruction, it can really rise in any sort of colostatic process, whether that's bile duct obstruction or obstructed cannula like your lie, or disrupted bile transport at the hepatocyte membrane, or, quite frankly. As we said earlier from other tissues not directly from the liver, or the bile duct so. correct which leaves you with D, it can rise in any colostatic process, regardless of where in the line of, of bile, getting from the liver to the intestine. The disruption and the flow results. Okay, let's move on the third one Billy Rubin, a is a colostatic liver enzyme. B is a breakdown product of hemoglobin C is an amino transfer a CD is a liver synthetic test only one of these is correct. Which one is it. Okay, so let's go through them one by one. Billy Rubin is not an enzyme. Okay, most enzymes. And with the suffix ace Billy Rubin is a molecule or a chemical if you want to think about it that way. It is not a protein that is folded in a specific way that has a catalyst function. So it is not an enzyme at all. So, while it may be an indicator of colostasis, it is not an enzyme, and that's why that trick answer is wrong. Correct. As the majority of you noted, it is indeed a breakdown product of hemoglobin, your red blood cells remember live around three months. At that point, they send us and they break down and the hemoglobin pigment. As it breaks down one of the products of that breakdown is indeed Billy Rubin, and is excreted in the bile. So we know that Billy Rubin isn't any kind of an enzyme and an amino transfer ACE is in fact a type of enzyme, it is a liver enzyme. In fact, it is a, they are liver injury tests and Billy Rubin doesn't fall into that category. It is not a test of liver synthesis liver does not synthesize Billy Rubin Billy Rubin is a breakdown product of hemoglobin, the liver does synthesize other things, including albumin and other proteins that are involved in the coagulation cascade. And so, while Billy Rubin is is transported through the liver cell and down the biliary system. It certainly isn't a liver synthetic test so there we go. So let's move on now to question for gamma gt, also known as GGT or GGTP gamma glutamyl transfer ACE or trans peptidase either is correct, and five prime nucleotide days, a are used primarily to detect liver injury their liver injury test or is it be a liver enzyme used to help determine the source of elevated alkaline phosphatase level or see are always ordered together with alkaline phosphatase always or D are liver synthetic tests, which one is correct. Excellent. So, gamma gt is not a liver injury test delivery injury tests are a ST and a lt, otherwise known as the amino transfer races. So gamma gt is a liver enzymes used to help determine the source of alkaline phosphatase elevation. And that is correct. The alkaline phosphatase is elevated and you're not sure if that's coming from the liver or from bone for example, you can either fractionate the phosphatase into the bone proportion, or the air and or the liver proportion. Those proportions are called fraction so liver fraction or bone fraction, or you can simply add on a GGT or a five prime nucleotide days depending on what your lab likes to perform and provide for you. If either of those are elevated concomitantly with the outposts, it highly suggests that the source of the alkaline phosphatase abnormal elevation is liver rather than bone because GGT and five prime don't come from bone. None of you chose, always. Good job. And then these aren't liver synthetic tests, the liver synthetic tests are albumin and PT, I nr. Okay, great job. Okay, so moving on from polling questions. Much as I mentioned back during my earlier talk yesterday. As the liver enzymes. They are more than numbers. But remember they are just a tool in your clinical workup and management of liver disease, and they are tools to help direct the rest of your workup. So that when you look at the liver tests, they give you some clue as to what the underlying differential diagnosis is what potential liver disorders can have that pattern of liver test abnormalities, which will then direct what additional testing blood tests or imaging or endoscopy or some combination of those will be most yielding in your subsequent workup. So the liver tests can give you and their patterns of abnormality can give you some clues into whether there might be a viral hepatitis underlying those abnormalities or non alcoholic steatohepatitis or fatty liver disease, or whether there might be hepatitis or even cirrhosis, due to alcohol for example, or autoimmune hepatitis, or a couple of other autoimmune disorders. Some autoimmune disorders that cause liver disease such as PBC which is primary biliary cirrhosis, or PSC which is primary sclerosing cholangitis which is associated with inflammatory bowel disease which Erica was just educating you about a few minutes ago. Other disorders that might clue you in, in terms of what might be causing liver enzyme and liver test abnormalities. So acute fatty liver of pregnancy, and hemolysis elevated liver enzymes and low platelet or help syndrome. Those two occur in pregnancy. So if the patient isn't pregnant and those aren't on the potential differential diagnosis help as you may recollect is highly associated with preeclampsia and as part of the pre eclampsic sort of disease category or drug induced liver injury, called Dilly by many just so it's less of a mouthful alpha one anti trips and deficiency. You may recall that this is a genetic disorder, primarily in patients of European extraction, and actually more probably known to the public as a lung disorder because the lack of adequate alpha one anti trips and results in early COPD you may recollect, and particularly in patients who smoke on top of that. But alpha one anti trips and deficiency can also result in a situation in the liver, where it becomes a protein storage disease where abnormal alpha one anti trips and protein folds abnormally, and can't be gotten rid of by the hepatocyte. And then the liver cell gets sick as a result of the inability to get rid of that abnormal protein, which then accumulates and causes damage to the liver cell, and that can result in in cirrhosis and require a liver transplant acute biliary obstruction might might be something that you are clued into by certain patterns of abnormal liver tests in the setting of the correct clinical presentation the right symptoms and signs and chronic biliary obstruction not just acute but chronic biliary obstruction, such secondary sclerosin cholangitis or secondary biliary cirrhosis can be things that come out of your investigation that started with abnormal liver tests. So what can they tell us liver tests when abnormal can tell us about liver injury, or they can signal us that there may be problems with liver function. And so if there is a problem with liver function, you might have an issue with the ability to synthesize proteins that are normally synthesized by the liver. Some important proteins are those that include serum proteins like albumin. So, if the liver is sick, so to speak, it may not produce enough albumin, and that may result in a lower than normal serum albumin level. And a sick hepatocyte may also not produce other proteins in normal amounts, such as clotting proteins like factor seven. So if enough factor seven is not synthesized, then the extrinsic and common pathways of the coagulation cascade will be disrupted. And the PT and I and R will be elevated. So there are your liver synthetic tests albumin and PT and R, as well as liver function disruption resulting in the hepatocyte the liver cell, having difficulty conjugating and transporting bilirubin out of the hepatocyte into the bile can and therefore ultimately to the bile duct. Remember, from your cell physiology class that trans conjugation and transportation of bile across the hepatocyte membrane is a highly energy consuming process. So if the hepatocyte is sick, it's going to have trouble doing that heavy lifting, and the bilirubin may not be conjugated and or may not be actively transported across the hepatocyte cell membrane. I'm going to slice and dice liver tests for you here so that you don't get these things mixed up and you understand the terminology properly, so that you're able to both communicate and understand precisely. ALT is aspartate amino transferase, ALT is alanine amino transferase. ALP is alkaline phosphatase sometimes nicknamed ALK-phos. This is again not an enzyme but a hemoglobin breakdown product is nicknamed Billy, and can be fractionated into a total bilirubin, or a direct fraction, or an indirect fraction. This is GGT, or gamma GT, or gamma GTP, they all mean the same thing. This is gamma glutamyl trans peptidase, or some will say gamma glutamyl transferase, it's all the same thing, it's all a GGT. There is five prime nucleotidase. Right. And remember GGT, and five prime nucleotidase we mentioned earlier, are tie breakers. When you have an elevated ALK-phos, and you're not sure whether it's truly coming from liver and bile duct, and might be coming from bone. You can either fractionate that ALK-phos into a bone versus liver fraction or simply order a GGT or a five prime nucleotidase. And if those are elevated, if one or the other of these or both are elevated in the setting of an elevated ALK-phos, that helps you determine with confidence that your elevated ALK-phos level is coming from liver disease. And so, PILN is a liver test, and PTINR is a liver test, and those test liver function, essentially indirectly, because if the liver is unhealthy, the liver cell has trouble producing these two types of proteins. Disruption of proper protein synthesis is a suggestion that liver function is not normal, because the liver is ill. AST and ALT are aminotransferases, and they are liver injury tests. ALK-phos, gamma GTP, and five prime nucleotidase are cholestatic liver enzymes. They're all enzymes. They all end in ace. Billy Rubin can also be a clue about cholestasis, but it is not an enzyme. Okay, let's keep going with the nomenclature and categories. So, the most all-encompassing term for all of these tests that we are describing is liver tests. Liver tests is general and all-encompassing, and every one of the tests that I mentioned in the previous slide falls under the overall umbrella category of liver test. Liver injury tests, or LITs, are AST and ALT. Why? Because AST and ALT are produced by the hepatocyte, and they are stored in the hepatocyte. So, when the liver cell is irritated, poked, if you will, and it is injured, then it will release these stored enzymes, the LITs, the AST and the ALT, out into the bloodstream, and they can be measured almost right away. And because they are released upon liver irritation or liver injury very quickly, and they can be because they are made and stored in the hepatocyte, they rise very quickly and are great tests for determining liver injury. But they don't tell you how well the hepatocyte is functioning, whether it's firing on all eight cylinders or not. That depends on your determining whether the liver is synthesizing proteins properly or not. So, the liver synthetic function tests that are commonly available are albumin and PTINR. Liver enzymes, it has to basically end in ACE. Liver enzymes include AST and ALT, which are the aminotransferases. It also includes GGT and 5' nucleotidase because they are enzymes as well, and they are liver enzymes, but they are not aminotransferases, and they are not liver injury tests. Liver function tests, that term should be really reserved for the liver synthetic tests. PTINR and albumin should be what you would consider to be technically the liver function tests, and that's why I starred them. So, going back and reviewing again because this is so doggone important. The liver injury tests are the aminotransferases, AST and ALT. The liver function tests are albumin and PTINR. The liver enzymes are AST, ALT, ALGFOS, GGT, and 5'-Nucleotidase. They are enzymes. They are protein catalysts. And the liver function tests are the liver synthetic function tests, albumin and PTINR, because they depend on a healthy liver cell to produce these proteins, these serum proteins. And then bilirubin can fall into this category because like we were suggesting earlier, conjugation and transport of bilirubin is energy consuming, and so requires a healthy hepatocyte to do the heavy lifting, to conjugate and transport bilirubin from the hepatocyte to the biliary system. So other ways to categorize and subcategorize, I know this seems complex, but if you follow me here, you can make this simple and precise. The cholestatic liver tests, ALTFOS, GGT, 5'-Nucleotidase, and bilirubin can rise in any cholestatic process. The cholestatic liver enzymes, however, bilirubin is not an enzyme, so it's ALGFOS, GGT, and 5'-Nucleotidase. So in summary, the liver enzymes include the aminotransferases, which are liver injury tests, AST and ALT, cholestatic and the cholestatic liver enzymes, which are ALGFOS, GGT, and 5'-Nucleotidase. Liver chemistries include liver synthetic chemistries and bilirubin. The liver synthetic chemistries are albumin and PTINR, neither one of those are enzymes, and bilirubin, which can be fractionated into total and direct. Now, misnomers and confusion. Let's knock this out immediately, okay? I mentioned earlier LFTs, that term is highly misused and abused. AST and ALT are liver injury tests. They reflect liver injury. They don't reflect liver function. So they are liver injury tests, don't refer to them as liver function tests, right? Liver function tests are PT and INR, and from a transport standpoint, bilirubin. Liver enzymes can also be misused. Bilirubin is not an enzyme, right? Although it can reflect the transport function of the liver, so it's a liver function test of sorts, it isn't an enzyme. So while sometimes people include bilirubin in their term liver enzymes, or include it in the category of LFTs, it actually is neither. Finally, transaminase and transaminitis. You'll hear those terms batted around left and right, even by hepatologists who are the liver specialists. Those are not real terms. They are non-existent terms, somebody made them up. So don't use transaminase, it's aminotransferase. And don't say somebody has a transaminitis, say elevated aminotransferases, that's the proper term. And so you've heard it, that's the deal, and that is the truth, and nothing but the truth, okay? Now let's move on to patterns of abnormality. Liver injury and liver function compromise. With liver injury, AST and ALT, which again are the LITs, the liver injury tests, the aminotransferases, are elevated out of proportion to alkaline phosphatase, which is a cholestatic liver enzyme. So in liver injury, the liver injury tests are elevated typically out of proportion to the cholestatic enzyme alkaline phosphatase. Now with liver function compromise, as we mentioned earlier, the albumin might be low because of reduced synthetic function due to reduced protein synthesis by the hepatocyte because it's ill, and or, typically and, the PTINR might be elevated because the clotting protein synthetic function of the liver is also disrupted in hepatocyte illness. The bilirubin might also be elevated because of reduced uptake or transport of bilirubin because conjugation and transport of bilirubin is heavy lifting, energy requiring work on the part of the hepatocyte. And if the hepatocyte is sick, it may not be able to do the heavy lifting. What about cholestasis? Cholestasis means a diminishment in conveyance of bile. Chole is bile, stasis is low flow, low flow of bile. And that's not just in the big bile ducts that you can see, that's at the microscopic level, including the canaliculi. So cholestasis can be indicated by cholestatic enzyme elevations or bilirubin rise out of proportion to liver injury tests, for example. So in the setting of cholestasis, the ALKFOS may be elevated out of proportion to the aminotransferases. Now that doesn't mean that the ALKFOS will go up first. The aminotransferases may actually spike first in cholestasis and then the ALKFOS will follow. Why? Because AST and ALT, as I told you, are produced by the hepatocyte and stored in the hepatocyte. So they are ready to eat. They are already prepackaged and ready to eat. They're kind of like a prepared ramen or a frozen dinner or whatever. They're already there and you poke the hepatocyte and out it comes. ALKFOS, on the other hand, has to be synthesized by the cholangiocyte, the bile duct cell has to make that stuff. So you have to be obstructed for a little while before that's going to be elevated. But ultimately, ALKFOS will be elevated out of proportion to what you would expect compared to the AST and the ALT. In cholestasis, the GGT and the five prime nucleotidase will be elevated, just like the ALKFOS. The bilirubin will, much like ALKFOS, rise later than the aminotransferases and will actually rise later than alkaline phosphatase because the bile duct's got to be obstructed for a while before the bilirubin is going to leach backward up through the sinusoid back into the bloodstream. Okay. And then ALT and AST typically rise before the ALKFOS or the bilirubin, because again, ALKFOS has to be synthesized in cholestasis, whereas AST and ALT are already stored in the hepatocyte. And bilirubin is going to follow. So the pattern in cholestasis is AST and ALT will typically rise first, followed by ALKFOS, and then finally the bilirubin will rise. However, the proportion is such that the cholestatic enzymes will be proportionately higher than the AST and the ALT in general, not all the time, but in general. Okay. Now, GGT and five prime nucleotidase, we said before, help you ascertain whether the source of ALKFOS elevation is liver or bone. I'm trying to hammer this into our brain. So if it's too repetitive, I'm sorry, but for the benefit of those who are new to this, I really want to make sure you get it. Other common patterns of abnormality, ultra high liver enzyme elevation suggest ischemic injury. Very high liver injury tests suggest acute hepatitis. Very high liver injury tests with elevated PTINR and the presence of encephalopathy could signal acute liver failure. This is all in general, okay? Moderate elevations of aminotransferases with AST, ALT ratio two to one or greater in the right setting that suggests alcohol to be the etiology, two to one alcohol. Okay, in general, this isn't always going to be the case, but I'm giving you some pearls here. And usually moderate elevations of aminotransferases with ALT greater than AST, typically rising before ALT or before ALKFOS and bilirubin are suggestive of biliary obstruction. Now remember that history and physical exam come first, right? So presumably this is what prompted you to order the liver tests in the first place. So a good history and physical exam will do wonders to help you nail what to do next and to even give you a decent differential diagnosis before you even get the liver test results back. History and symptoms provide you a lot of direction, right? The patient's gonna tell you what's wrong if you listen well. And gosh, if they're encephalopathic, they may not make much sense. And that may be a huge clue. Acuity versus chronicity can narrow your workup. Past medical history, pregnancy, right? Help, acute fatty liver, pregnancy. You don't get that if you're not pregnant. Medications, right? Drug-induced liver injury. If you're not on any medications and never took any, it ain't gonna be that. Social history, genetic stuff, family history, same thing. Social history, drugs, alcohol, what other toxins? You know, what do you do at work? Oh, you work in a chemical plant? Allergies, intolerances, all that stuff. Work history, toxin exposure, travel history, drug and substance abuse, illicit or not, over-the-counter. All that stuff that you already know, don't forget to use that for potential liver disease too. So what do you ask or what do you look for in history? Pain or not? Pain would suggest gallstone-related obstruction. Not always, but many times, including cholangitis or cholecystitis, or maybe not biliary, acute hepatitis. How about pruritus, which is itching, right? Pruritus, dark urine, weight loss, easy bruisability, right? PTINR elevation, synthetic dysfunction, or low platelets. Low platelets, weight loss, new medications, alcohol, drugs, transfusions in the past, in the distant past, occupational exposures, risks for viral hepatitis, such as travel. You know, you're not gonna get happy around here. Pregnancy, underlying autoimmune disorders. You know, have one autoimmune disorder, that makes another one more likely. You have ulcerative colitis, might have PSC. If you don't have inflammatory bowel disease, much less likely to have PSC, for example. Diabetes could be related to fatty liver disease. Confusion, neuropsychiatric symptoms, better, you know, think about Wilson's disease, for example. What about the physical examination? That was history. Now for physical exam, jaundice or scleral icterus. You know, you can, especially under lights like this, fluorescent, you can usually detect that at a billy as low as three. Or if you're used to looking at it, maybe even a tad lower. Evidence of pruritus, cholestasis, ascites, or other portal hypertensive stigmata, such as abdominal distension or bulging flanks, shifting dullness, splenomegaly, right? Your left upper quadrant abdominal exam. Venous collaterals, look for portal hypertension. Ascites with jaundice, is it cirrhosis or maybe metastatic disease? An enlarged liver, a tender liver edge, is that hepatitis? You feel a mass in the liver, is that hepatocellular carcinoma or metastatic disease? Right upper quadrant tenderness, or even more specific, a Murphy's sign. You have cholangitis or do you have cholecystitis? Remember Charcot's triad. Working up these LFT or liver test or liver synthetic dysfunction test or amino transferase abnormalities, right? You can call them whatever you want, just be precise. But regardless of which is elevated, it's ultimately gonna be a pattern that's gonna help direct your workup. So if the AST and the ALT are elevated out of proportion to cholestatic tests, that's what we call a hepatocellular pattern or a hepatocellular injury or hepatitis pattern. That's a big clue. History is going to direct potential etiologies too. For example, often start with viral serologies if appropriate if you think that there's a hepatitis, a liver injury elevation kind of pattern. Elicit an alcohol history and possibly get an alcohol level or an acetaminophen level. And onto autoimmune markers, immunoglobulins, if you think alcohol might be an issue or autoimmune disorders or cirrhosis. Iron studies, if you think there might be a risk of hemochromatosis because of demographic or genetic factors. Alpha-1 antitrypsin levels, like we talked about, if they're low or you fractionate them and you get a ZZ pattern or an MZ pattern. Genetic tests, urine copper, if you think that there might be Wilson's disease or maybe ultrasound with Doppler's of the hepatic or porta hepatis vessels, if you think somebody may have vascular occlusion related to the liver. Cholestatic tests out of proportion to AST and ALT, we said earlier, was a cholestatic liver test abnormality pattern. There you'll probably usually start with non-invasive imaging to exclude biliary obstruction, typically an ultrasound, which may be followed by an MRI if needed, because the MRI is gonna be more sensitive and more specific. You might need a liver biopsy depending on what you find with the above workup. I think it's always helpful to go through cases to sort of tie all this knowledge together. So let's go for case one here. So here's a 64-year-old man who was witnessed collapsing while walking for exercise in a city park. EMS was nearby and found him to be pulseless and V-fib when they found him. He was immediately resuscitated and transported to the hospital and blood work drawn on admission demonstrates an AST of 2,800, an ALT of 3,000, an alkaline phosphatase of only 150, a bilirubin of 1.4, which is slightly elevated, and an albumin of 3.9, which is kind of low normal. The liver enzyme abnormalities are most consistent with, and remember the aminotransferases were elevated out of proportion to ALKFOS and bilirubin. Is it A, acute viral hepatitis C? Is it B, acute cholangitis from an obstructing bile duct stone? Is it C, ischemic hepatopathy, otherwise known as shock liver? Is it D, veno-occlusive disease? Or is it E, acute alcohol hepatitis? Which one's correct? So it is ischemic hepatopathy or shock liver. This patient doesn't have any history suggestive of viral hepatitis. Acute viral hepatitis C is not that common and the presentation would not be one of walking in the park and having V-fib all of a sudden. Acute cholangitis from an obstructing bile duct stone also doesn't present with that kind of a liver enzyme pattern. What you saw was a highly liver injury type of pattern, not a cholestatic one, which is what you would see with biliary obstruction. It's not veno-occlusive disease. I didn't give you any history of the patient having had a stem cell transplant or a radiation to the liver area anytime recently. And there isn't an alcohol history associated with this. And the aminotransferases look nothing like a two to one elevation ratio and they're way too high for alcohol hepatitis. So the management here includes which are the following? Viral hepatitis serologies, B, ERCP, C, treating the underlying cardiac condition, supportive ICU care, D, liver biopsy, or E, alcohol cessation and behavioral modification. Which one would it be? This one of course is easy. I'm giving it to you. It's treating the underlying cardiac condition in supportive ICU care. So the V-fib related in an ischemic hit to the liver and you saw a shock liver, highly aminotransferase skewed elevation of a liver test pattern, okay? Case two, a 32 year old woman presents with right upper abdominal pain and chills. She's experienced this intermittently over the past two months. She says that she drinks a beer or a glass of wine on most evenings but denies any drug uses on no prescription meds and has taken only acetaminophen for her pain. And her urine has been clear. She's never had surgery. Her weight is stable. She has a three month old daughter and an adopted two year old son. She works in a liquor store and bartends on occasion. The exam reveals a temp of 38 stable vitals, mild right upper quadrant abdominal tenderness with a negative Murphy's sign. She doesn't look particularly ill, but she appears tired. She started exercising again. Blood work demonstrates the following. The AST is 103. The ALT is 135. The ALFAS is 198. Total bilirubin is mildly elevated at 1.9. Albumin is normal at 4.3. INR is stone cold normal at 1.0. And the white count is mildly elevated with a left shift. The liver enzyme abnormalities are most consistent with A, acute viral hepatitis C, B, early acute cholangitis from an obstructing bile duct stone, C, acute hepatitis from alcohol, D, HELP syndrome, or E, acute fatty liver of pregnancy. Which one is it? Only one is correct. Early acute cholangitis from an obstructing bile duct stone is correct. The liver enzyme pattern does not suggest acute viral hepatitis C. It's mildly cholestatic. It doesn't suggest acute, the history doesn't suggest acute hepatitis from alcohol. She only has an occasional drink here or there. I threw in the bartending thing just to try to fool you, but that's not what this is because the AST to ALT ratio is not consistent with alcohol. And so the history and the enzyme elevation pattern is incorrect for acute alcohol hepatitis. It's not HELP or AFLP because while she recently delivered a baby, she's not pregnant. So if you're not pregnant, you don't get HELP or AFLP, okay? In fact, delivering the baby is the treatment. So the best management here includes A, viral hepatitis serologies, B, empiric antibiotics and a liver biopsy, C, empiric antibiotics and urgent ERCP, D, empiric antibiotics, right upper quadrant abdominal ultrasound and surgical consultation, or E, alcohol cessation and behavioral modification. It's D, viral hepatitis serologies is obviously wrong. Empiric antibiotics and a liver biopsy. This patient doesn't need a liver biopsy. She has biliary obstruction. Empiric antibiotics and urgent ERCP is incorrect because this patient has mild cholangitis. So if you consult your Tokyo guidelines 2018, this patient has mild cholangitis. She needs a surgical consultation along with right upper quadrant ultrasound and empiric antibiotics. And this isn't alcohol disease, okay? Do we have time for case three or should I transition? Sarah, what would you like to do? Can you give one more case? I think if we can go to the Q&A and maybe we can come back to these that are final one if we have time. Perfect. All right, I'm gonna flip through the last case here and then I'm gonna wrap it up. Your practice pearls, most liver test abnormalities require workup. History and physical exam can narrow and focus the direction of the workup, acute versus chronic, hepatocellular versus cold static, viral versus toxic, autoimmune travel, et cetera. Patterns of liver enzyme abnormality combined with clinical presentation direct the next steps in testing whether laboratory imaging or endoscopic. Understanding what each liver assay tests for and how it reflects liver injury or liver function is key to interpreting the nature of the underlying pathology and how to investigate and manage going forward. And finally, additional investigation typically involves a combination of viral serologies, autoimmune markers, immunoglobulins, metabolic enzyme assays, iron studies, genetic tests and imaging. Thank you very much.

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