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- [00:00]
Annie Geary
Foreign.
- [00:07]
Podcast Host 1
Podcast where we explore how PAs contribute to healthcare and the practice of medicine. Today we are joined by Annie Geary, Assistant professor at Butler University and GI and Hepatology PA at Hendricks Regional Health, as we discuss her review of Metabolic Dysfunction Associated Steatotic Liver Disease, or mastle. Much easier to say. And listeners, don't forget you can now earn CME by listening to the podcast. To receive your CME credit and access your certificate, you just listen to the podcast, then complete the post test and evaluation in AAPA's learning central@cme.aapa.org before we jump into talking about hepatology, Annie, we'd love to learn more about you. Can you tell us more about your journey? What led you to both academics and hepatology?
- [00:54]
Annie Geary
Well, first I want to say thank you so much for having me on here. I'm excited to talk about my subspecialty and talk about this topic that means so much to me as far as how I got started. I graduated from PA School at Butler University, which is actually the school I currently teach at, in 2015. Early on I really wanted to talk to patients about difficult topics. I always have found that that's something that I excelled in and I enjoy talking about sensitive topics to patients who are maybe having trouble talking about those things. Initially I thought I'd do that in women's health. There was no job in that in 2015, and so I kind of traded what I thought was my dream job with pelvic pain and painful menses to switching to talking to patients about weight loss and diarrhea and abdominal pain. And it really kind of was a natural fit for me. And so I've stayed in that field for the last 10 years. The switch from working as a PA clinically to then academia worked kind of organically for me. I started out just taking students as a preceptor, really enjoyed teaching on the job, and then eventually transitioned to kind of flipping that. So now I teach as my main job and still practice medicine one day a week. So that's kind of been the process for me and I've always practiced in GI and now I get the opportunity to teach that to future PAs. So it's a really rewarding career and I'm glad I'm doing it.
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Podcast Host 1
That's awesome. Thank you for sharing. So, a little bit of background for our listeners. Formerly known as non Alcoholic fatty liver disease, or NAFLD, metabolic dysfunction associated liver disease, or MASLD, affects nearly 30% of the global population. This increasingly prevalent condition is associated with multiple comorbidities and has been identified as a significant public health risk. Complications of MASVID include decompensated cirrhosis and hepatocellular carcinoma. We as PAs play an important role in early detection and management.
- [02:53]
Podcast Host 2
Okay, let's get started with a case. We have Mr. Smith, who is a 56 year old male who presents to the primary care office for an annual physical. He notes that he feels fatigued, which he attributes to stress, and comments that he feels that he's gaining weight no matter what he tries to. On exam, his blood pressure is 142 over 94, heart rate 99, BMI is 42, and you note central adipoxy. You elect to get a baseline set of lab and find that his glucose is 130, ALP125, AST, AD, ALT82, total bilirubin 1.1. And the cholesterol panel is abnormal. With his total cholesterol of 270 and triglyceride level of 200, his platelet count is 200. So, Ann, what are some aspects of this case that jump out to you and how would you begin to discuss metabolic liver disease with this patient?
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Annie Geary
Sure. So let's get started. Mr. Smith sounds a lot like patients that we all see on a regular basis. Right? Someone in their mid-50s who has a clear metabolic risk profile. Right. He's got some central obesity, hypertension, dyslipidemia. He's got an elevated fasting glucose at 130. So when I hear kind of this profile of Mr. Smith, I'm already thinking about metabolic syndrome in this patient. And I'm thinking about this even before I hear his liver enzymes. So I'm highly suspicious that Mr. Smith has metabolic risk factors that make him prone to having mastle even if his liver enzymes weren't told to be. Once I hear his liver enzymes and kind of the way I teach this is, I can't help but put on my academic hat as an educator. I really teach interpreting liver enzymes as an analogy between a house and the pipes in your house. So with Mr. Smith, he's got a mild elevation in his AST and his ALT. Those are his transaminases. Right. And so those two values are really talking about the house of the liver. So the cells specifically of the liver. If we have a problem with our house, like our real house at home, maybe we have an older house or we've got, you know, peeling paint, or we've got floors that need redone, there may also be some problems with the pipes in Our house. Right. Because if we're not taking care of our house, we're probably not taking care of the plumbing. So sometimes when you have elevations in AST and alt, and the problem is a house, the liver cells, you might see some mild elevations in alk phos. It's not true for Mr. Smith. He just has an elevation as AST and ALT. When we see elevations in ALK fos and not as much elevation in AST and ALT, I think about that as we've got a problem with the pipes of the liver. Right. The biliary tree. But just like in our house, if you had a burst pipe in your home, your flooring is going to get ruined. And so you're going to see in a patient who has a problem with something with their pipes, something that's hepatobiliary. They may also have elevations in their AST and alt. In this patient's case, it is a pretty obvious hepatocellular pattern. We've got an issue here with the cells of his liver. In addition, with his normal alkaline phosphatase and his normal whole bilirubin. I'm really not necessarily as concerned that we've got anything more going on than just a problem with that. Something with the cells of the liver. He's got all the risk factors for Mastle. Right. He is a clear picture of metabolic risk profile. But we still need to ask this patient about his alcohol use. We still need to ask this patient about his viral hepatitis risk factors. Just because he has a metabolic profile doesn't mean he also doesn't drink and doesn't mean he also hasn't had an exposure to hepatitis B or hepatitis C. So I'm still going to ask those questions when I see him for the first time. In addition, I'm going to consider secondary causes for Mr. Smith. He mentioned he's mildly fatigued. He's had a little bit of unintentional weight gain, maybe his thyroid is hypoactive. He's got hypothyroidism. So I'm probably going to get a TSH at some point during this patient's early visits with me because hypothyroidism alone can cause elevation and transaminases. Regardless of if there's a secondary cause going on for this patient, he's got every risk factor that makes me think about metabolic liver disease. And so I'm going to go ahead in the first visit with him, talk about that, and kind of start the conversation. And so I almost always start the conversation about Metabolic related liver disease by talking actually about alcohol. So pretty common way this goes with patients is I say, I'm actually concerned that you may have some underlying liver disease. And they almost always will say, I don't drink. And I say, I know it's not from alcohol. So I kind of start out by using something that most patients are going to associate liver disease with and kind of stop that stigma right away. Liver disease isn't just from alcohol use. And so I talk, kind of using that pattern. I talk about how fat can be toxic to the liver just like alcohol. And so kind of going from there. Talk about how one of the first places that our body gains fat is actually the liver. But thankfully it's one of the first places that we will lose steatosis. And so losing about 3 to 5% of somebody's total body weight, just a small amount, although that's harder to. Harder done than said. Right. But even just a small amount of weight loss can be a meaningful reduction in fatty infiltrate in the liver. And so I kind of start the conversation talking about alcohol, explaining that that's not the only thing that can cause this, and then talking about how that fatty infiltrate in the liver is potentially the cause of the liver enzyme elevation and kind of moving on from there about how we can treat that even early on, before we know how much fibrosis they have or any of those additional things by just talking about weight reduction.
- [08:54]
Podcast Host 2
That's awesome. I felt like I already, I'm already learning a lot. And I really like that analogy that you use about the house and the pipes. We use that a lot in heart disease as well, describing different types, you know, vessel, you know, coronary artery disease versus if it's a valve issue. So I really like that analogy. I could relate.
- [09:13]
Annie Geary
Yeah.
- [09:14]
Podcast Host 2
And about the weight loss in metabolic syndrome. So we were, Kim and I were saying we are on our metabolic street right now. Our next podcast, we're not going to say what it is about, but it's going to involve that as well. So I like how you talked about weight loss in muscle. So that's. That's really awesome. We mentioned earlier that in 2020 there was a name change. I remember it used to be called Nash and now the medical community moved away from Nash. At some point it was nafld. And all of a sudden recently it's masled. I know a lot of people are getting confused with all those names, name changes. And can you tell us a little bit more about that? Why those changes?
- [09:56]
Annie Geary
Absolutely. It sounds like Alphabet soup, right? But I'll try and kind of explain the process and the thought process behind it because agree with the name change. So nafld, Non alcoholic Fatty Liver disease was what we originally called this condition that was metabolic associated liver disease. But NAFLD really defined the disease by what it wasn't, right? Non Alcoholic Fatty Liver disease. And so we're starting the terminology to describe a disease process by something that it's not. And so we've really flipped the way we think about this disease process and defining the name of the disease would with the actual driving factor of the disease, which is metabolic dysfunction. So switching from non alcoholic to metabolic dysfunction really kind of changes the thought process of avoiding what it's not and talking about what it truly is. I also think it's great for reduction of stigma. So when it comes with kind of two words, and non alcoholic fatty liver disease, that initially put on a stigma for patients with that diagnosis. The first one is alcohol, right? So we're removing non alcoholic or the talk of alcohol at all in the disease, which I think is helpful. And then we're also removing the word fatty. So we're actually talking about it scientifically. We're removing words that have a stigma related to them. And so I think that's another important reason that the name has changed and why I honestly support it. It also allows us for the introduction of a new disease process, although the disease process itself is not new at all. But there was no term for it, which was very difficult. If you, if, if you can imagine a, a disease that's pretty common that doesn't have a term. So that allows us to have met ald. So that's metabolic Associated Alcoholic Liver disease. So it allows us to give somebody a diagnosis who has metabolic syndrome, but also drinks a moderate amount of alcohol, its own condition. And so I think that's very important because it was really difficult to talk about NAFLD and alcohol use at the same time. Like we've got a condition that says non alcoholic, but this patient drinks on a daily basis. What does that mean? And so now we're able to get rid of that thought process entirely and have met ALD as its own additional kind of vein of this liver disease process, we've also changed how we define this disease. And so in the past it was simply do they have steatosis or do they have steatohepatitis? Like do they just have fatty infiltrate in the liver or do they have inflammation and fat in the liver? And so now we're able to define mass sold as kind of the uber arching term and then classify somebody's severity of their mass sold based on how much fibrosis they have in the liver. So how much scarring they have in the liver. Which allows us four different options. F0 to. I guess that's five. F0 to F4 fibrosis and not simply fat. Fat and inflammation. And at some point, when do we call it cirrhosis? So lots of talk about the Alphabet soup, but I think massold is the right name and I think that one is going to stick.
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Podcast Host 2
I totally agree. And I was going to mention, I was, I was wondering if it was because you removed the stigma and it helps also when you want to get treatment for those type of diseases when you remove those labels and stigma to it. So as you describe in your article, muscle D is driven by an increase in fat storage in adipose tissue and ectopic fat accumulation, which promotes inflammation and insulin resistance. Furthermore, an inflammatory response in visceral fat leads to lipolysis. Thinking back to Mr. Smith case, what physical and lab findings should we look for when evaluating patients with muscle D?
- [13:47]
Annie Geary
That's a great question because the answer is probably you're not going to see too much abnormal. And I think that's why it's so at risk for getting, getting missed. So in somebody with metabolic associated steatotic liver disease mast on physical exam, you're probably just going to see the findings that go along with metabolic disease. Right. So central obesity and increased waist circumference that in my practice I see on, you know, multiple patients a day, if not everyone, you might see some additional evidence on vitals of some underlying hypertension which goes along with that metabolic profile. Potentially they'll have hepatomegaly on physical exam. Although not everybody with fatty infiltrate in the liver is going to have an enlarged liver. And if somebody has a significant waist circumference, they probably are going to have, for you as the clinician, are probably going to have a difficult time feeling their liver even if it is enlarged on physical exam. So the exam itself may be very normal initially in the disease process. Late findings and things that I'm definitely going to look for on any patient who I know has underlying mast or any patient that has abnormal liver enzymes that I'm working up the first time are going to be assessing for sequela of cirrhosis. So things like jaundice, do they have evidence of ascites? Do they have some lower extremity edema? Are there spider and angiomas on their skin? Do they have trouble sleeping? Are they having feeling sleepy throughout the day? That kind of goes along with early signs of hepatic encephalopathy. Those are things I'll look for to at least assess for concern for underlying cirrhosis. But your standard patient just with metabolic associated liver disease is not going to have any abnormal physical exam findings that don't differ in any way from what we see with any other patient with metabolic syndrome. The labs themselves are oftentimes completely normal. In fact, our diabetic population are the one that's ones that are most likely to have entirely normal liver enzymes when they have mast. And that's really interesting because they are the patients who are more likely to have it. In fact, the guidelines from endocrinology have recently included assessing for MAST for these patients, even from an endocrinology standpoint when they're getting their regular visits for their diabetes. So labs might be normal, you might see elevations in AST and alt, you might see a falling platelet count. That's going to be more significant. If they have some underlying fibrosis and we're starting to see a change in the function of the liver, you might see a rising bilirubin. I always joke with students and I'm sure they don't find it funny because they're my students, but I always joke with my students that the only liver enzymes of the hepatic function panel that tell you anything about function is actually the bilirubin. So your alos, your ASD and ALT don't tell you anything about liver function, but the bilirubin does. Right. So if that's increasing, that probably means we might be seeing a decline in the synthetic function of the liver. An elevation in the INR might show us that there's a decline in the synthetic function of the liver. And imaging alone may just have some incidental findings of steam steatosis, which, you know, if you've practiced medicine for any amount of time, you're seeing a lot of incidental steatosis on ultrasounds and CTs all the time. So, so labs and physical exam all may be completely normal. And that's why this is so easy to, to not think about when you're seeing your patients in family practice eye opening.
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Podcast Host 1
So we are all very efficient optimal PAs and we've identified some risk factors in Mr. Smith's case for MASLD, we should probably get some additional testing. What are non invasive tests that primary care providers and other clinicians should consider?
- [17:31]
Annie Geary
Absolutely. So I think the big key here is non Invasive. We don't want to be biopsying every patient who has incidental findings of steatosis on their, you know, ultrasound. They had for something else. Right. So the most important thing we want to do when we have a patient in front of us that has some risk factors for mast is to risk factors, stratify them. The way that we've determined is probably best to do this is a simple calculation. It's called a fibrosis four index score. The fib four score. It's a great score because it uses four things we probably already have in our patient's chart. So it's the age, your AST and your ALT and your platelet count. It doesn't diagnose mastle, but it allows us to estimate the fibrotic risk within that patient's liver and really allows us to risk stratify. Is this somebody who can be followed in primary care, or is this somebody who needs to kind of be escalated to maybe seeing somebody in hepatology or in a GI office? The scoring system is pretty easy. If the score is less than 1.3 in somebody age 35 to 65, it's really unlikely that they have scarring in the liver. We can talk about weight loss. We can treat their metabolic risk factors with all the other things we do for that, those risk factors. And they don't need any special treatment based on the fact that they may have some underlying fat infiltrate in the liver. However, if that score is above 2.67, and it's amazing when you look at the patient, all their labs are in the normal range. But then you calculate the score, it's amazing how often the score is over 2.67 with normal labs. That's actually concerning for advanced fibrosis. And that's somebody who's going to need either a referral to a gastroenterology practice or if you're capable of ordering that this in primary care, you could order additional testing with elastography. Caveats to the fib four over the age of 65 or under the age of 35 test isn't quite as validated. So we kind of have to think about that. When we order the testing. We've actually changed the cutoff to over 2 as the low risk score in patients over the age of 65, because with that age that the value is going to be falsely elevated. And so kind of in summary, that fib4 is a great way to triage patients and then kind of restratify them.
- [19:48]
Podcast Host 1
The FIB4 is really simple and Easy to use. So we took our, you know, our patients lab values as age, ast, ALT and platelet count and just plugged it into an online calculator. And even at my institution, I just put. There's a little calculator inside the emr, which makes it so easy. So we put in the calculator, and then we can see that Mr. Smith's Fib 4 is 2.46. What does the score indicate and what should be the next steps?
- [20:12]
Annie Geary
2.46 is going to put Mr. Smith in that indeterminate range. And so it's not low enough to reassure our patient. It's not high enough to really suspect advanced fibrosis. But what it really tells us is we can't stop here. We've got to know a little bit more about our patient to determine is he at risk for having scarring? Do we need to consider potential treatments for MAST for this patient, or is he going to be okay to continue working on typical risk modification, weight loss, et cetera? And so the best thing to do next for a patient with an indeterminate range fib 4 score is some secondary risk assessment. So the best way to do that is some sort of liver stiffness measurement testing. There's several options out there, but the two that are kind of most common are transient elastography. So that's a Fibro Scan or Mr. Elastography, which is a specialized MRI that's not necessarily at every institution. But those two tests are kind of ones that we see most often utilized at that as that secondary way of looking at fibrosis before we have to kind of get an actual biopsy to prove if there's scarring in the liver. And so in interpreting lastography, it gives us a elevated versus low amount of stiffness, if you will, essentially telling us how much fibrosis is in a patient's liver. It's a great way of kind of risk stratifying them without putting them through something that has any additional risks like. Like a biopsy would.
- [21:47]
Podcast Host 1
So with all that we have found so far, has Mr. Smith met the diagnostic criteria for MASLD and are there abnormal transaminous levels? Are they required to have this diagnosis?
- [21:57]
Annie Geary
It's a great question. I get this a lot with students. So absolutely, Mr. Smith has met criteria to get a diagnosis of mast. So the criteria to diagnose mast only requires hepatic steatosis, which you can get from imaging. If he'd had a prior liver biopsy, histology would do that, or by definition, a, a strong clinical Suspicion actually counts for this. So whether he's had imaging or not, he's got a strong clinical suspicion for hepatic steatosis based on his multiple kind of his clinical picture in general. He's also got to have at least one or more cardiometabolic risk factor. He's got a whole host of them. Right. So he's got obesity with central adiposity, he's got hypertension, dyslipidemia to elevated glucose elevate, AST and ALT for him. And so he's got every type of suspicion that he's got underlying mast. And so he meets criteria. The only other caveat to criteria is being able to, to exclude another primary liver disease process and so on. My patients who are presenting and I suspect they have underlying mastle, I still am going to ask all of the questions to risk stratify whether or not they have underlying viral hepatitis and most of the time I'm going to go ahead and get a chronic hepatitis panel to ensure they don't have underlying hepatitis B or hepatitis C. That's kind of making this a complex picture for him. But yes, at this point he, he meets the criteria for underlying mastle. The second part of your question about the abnormal liver enzymes, absolutely not required. In fact, normal liver enzymes are very common in somebody who has mastle. I'm going to reiterate it because it's so important to me. Diabetics are way more likely to have normal liver enzymes even though they have every other risk factor. They just don't seem to amount as high of an AST and ALT response. And so they can have absolutely normal liver enzymes and have underlying muscle.
- [23:56]
Podcast Host 1
Great.
- [23:57]
Podcast Host 2
So much information here. As with many conditions, lifestyle interventions are usually the foundation of the management of muscles. In your article you mentioned that weight loss of 3 to 5% total body weight reduction can improve keatosis. You also shared that exercise independent of weight loss also helps to improve clinical outcomes in addition to lifestyle. What are other treatment options that we have now for Marcel?
- [24:24]
Annie Geary
Yeah, so great question. And this is kind of where the field is most exciting right now because we finally have treatment which we didn't have even a few years ago. First line therapy is still lifestyle modification. So exercising. We actually a lot of times recommend a Mediterranean style diet, maybe with some underlying calorie restriction if the patients need that. In addition, a small amount of weight loss often improves steatosis. So that special area there is somewhere between 3 to 5% weight loss and then optimizing all the comorbidities is still going to be really important. So if you've got underlying diabetes, we got to get that A1C under control. Got underlying hypertension, we got to get that under control. Right. So we've got to have this kind of multidisciplinary approach for these patients. But now we have pharmacotherapy, which we didn't have in the past. So the, the initial drug that was approved for masal was actually approved in 2024, and that's Resmetirom. And this drug is a thyroid hormone receptor beta beta agonist. It is specifically for non cirrhotic mash patients with F2 to F3 fibrosis. So once you have a diagnosis of cirrhosis, you're not a candidate for this treatment. But the idea is this drug will hopefully keep patients who don't have cirrhosis yet from developing underlying cirrhosis in the future. It's a fantastic drug. It targets that underlying inflammation and inflammation is what's leading the scarring, which is then leading to cirrhosis. And so it's a great option to kind of keep these patients from developing this severe disease process that can really affect their quality of life. We always recommend it with lifestyle modifications and we can even give the drug without a liver biopsy. So if that transient elastography demonstrates F2 to F3 fibrosis, we're able to prescribe it without putting them through any underlying invasive testing. A second drug has been approved for the diagnosis of Bassold. It is also for F2 to F3 fibrosis. This is semaglutide. So this drug is. Is known to a lot of us for diabetes. I do want to highlight that it is the highest dose that's approved. So patients with diabetes who are on semaglutide at the diabetes dose, that's not actually the. The dose that has been studied and proven to help improve the fibrosis. And so it's just a note that some people haven't noticed. And so I kind of want to highlight that, that it's gotta be the 2.4 milligram dosage to be used for mastle. We also are going to encourage weight loss with this one and that one also can help encourage weight loss. And so it has that dual metabolic hepatic benefit effect that is a fabulous option for patients as well. I think the most important thing to highlight with treatment is early treatment matters. Let's touch these patients before they have cirrhosis and prevent them from having that underlying disease process which is going to significantly improve their Long term quality of life. We can do that.
- [27:26]
Podcast Host 2
Great. Yes. I was wondering if that's what something you guys were doing in practice and started since the new indication using the GLP1s. If a patient is started on resmetirom, what monitoring should they receive and are there interactions also with other medications?
- [27:47]
Annie Geary
Absolutely. So I think there's kind of two focuses I want to have here. So safety of the medication and then we're also going to talk about kind of the treatment response because we've got to monitor really for both of those. How are they doing on the drug itself and what's the safety profile for starting the medication and then are they getting a response from the medication? So as far as safety monitoring, I always check their AST and ALT at about 12 weeks into treatment. We do sometimes see that a mild elevation even above what they had before of AST and ALT can occur early on. It's very transient and so a lot of times I'm going to continue to treat through that, but it's something I'm going to check pretty early on. I also am going to check a baseline thyroid function. It's honestly not because their thyroid not functioning appropriately will affect the medication even though it works within the thyroid receptor. It's actually because optimizing treatment of underlying thyroid disease is going to improve the overall outcome on resmetirom. So. So we always check a TSH at baseline as well. And then I typically, as far as assessing for treatment response, I typically am going to reassess liver stiffness most of the time with a non invasive fibrosis assessment of some sort of transient elastography or FibroScan at about 12 months to see if we are getting a good response from the medication in these patients. There are a few drug interactions that I probably want to highlight. Most of these are mild but worth mentioning. So the key pathway we have to think about is the CYP2C8 pathway. One of the big ones that does this is GEM fibrozil, which not very many, many patients are on. But since we do sometimes see patients on that with really high triglycerides who have metabolic syndrome, it's worth noting that that's one that we would need to avoid with this medication. And then we do need a dose adjustment with our moderate inhibitors. And the big moderate inhibitor of the CYP2C8 pathway is going to be your clopidogrel. So we'd reduce the resmetirom dose by about 20 milligrams for these patients. They still get a great response to medication. But because they're on that underlying clopidogrel, we got to reduce their risk. Their resmetirom dose, the last and final thing would be statins. So resmetirom can increase the statin level. And so we actually have max doses of our statins that we have for patients who are on resmetirom. Simvastatin, the max is 20 milligrams a day. Atorvastatin, the max is 40 milligrams a day. And so if you kind of the key takeaway here is if your patient's on a statin, double check their dose before you start them on the medication. And then, you know, we gotta review our labs thoughtfully and assess for a treatment response at about a year.
- [30:37]
Podcast Host 2
Great. So we know that muscle increases the risk of hepatocellular carcinoma. Which patients should receive screening for that type of cancer and how often should they be screened?
- [30:49]
Annie Geary
That's a great question. So the people who need screen for hepatocellular carcinoma are patients who have cirrhosis of the liver. So we absolutely must screen any patient with cirrhosis who we think would be a candidate for treatment of hepatocellular carcinoma regardless really of the cause. So they could have mashed cirrhosis. So cirrhosis from metabolic associated liver disease or a cirrhosis related to alcohol, or cirrhosis related to primary ability cirrhosis. It doesn't matter necessarily the cause of their cirrhosis. But all cirrhotic patients should be surveilled for hepatocellular carcinoma. We typically recommend imaging every six months. The form of imaging that's on the glide lines are going to be an ultrasound. The caveat to that is that sometimes can be a test that's not a great test for those patients of ours who have metabolic syndrome and significant central obesity. So sometimes other imaging like a CT or an MRI might be better. In a patient that we can't get a good look at the liver with an ultrasound. And then the second testing we do every six months is an alpha feta protein, that's a tumor marker for liver disease that we would do every six months on patients with cirrhosis. Those with advanced fibrosis, it's not recommended that we do overall screening for hcc. So unless they have a true diagnosis of cirrhosis, if they have F2, F3 fibrosis, we really don't recommend any additional screening for HCC.
- [32:19]
Podcast Host 1
Annie, thank you so much. This has been a very comprehensive review of mass vault. I have learned a lot. Before we wrap up, do you have any final thoughts to share with our audience?
- [32:30]
Annie Geary
First of all, I really enjoyed being on here. This has been fun. I love talking about my favorite thing, liver disease. But in addition, I guess my big takeaway would be that MAST is common and it's quiet. Patients that are sitting in front of you for all sorts of other reasons. Maybe they're coming in for acid reflux or you're seeing them for their copd. But if they're sitting in front of you and you know they have at least one additional metabolic risk factor, this is something that you're you could pick up a lot and really help your patients. So these patients feel fine. They might have normal liver enzymes, but they they may have underlying liver disease and we want to catch them before they present due to a complication of cirrhosis like esophageal variceal bleeding or ascites or hepatocellular carcinoma. Right. And so be curious about your patients. If you suspect they have risk factors for MAST, go ahead and calculate a FIB4. It's a really fast test on labs you already have in the chart and allows you to risk stratify them very easily. So start the conversation with your patients early about weight loss and getting them to the appropriate people. If you don't feel comfortable kind of doing it in the primary care setting, I think is my big takeaway from this talk.
- [33:45]
Podcast Host 1
Common and quiet. What a good description and quite a call to action. So thank you and to our listeners, thank you for joining us. Before you go, don't forget that the podcast is associated with cme. To receive your CME credit and access your certificate, just listen to the podcast. Then complete the post test and evaluation in AAPA's Learning Central at cme. Aapa. Org. Until next time.