A couple of quick comments regarding excellent talks this morning, I actually love them. But regarding the clips, I think the biggest thing that we get called upon is just, even though they are non-ferromagnetic, meaning that they are MRI conditional, oftentimes we will get phone calls from radiologists saying it either leads to artifact or that there's a concern if somebody just had a bleed that that clip might move and disrupt the bleeding blood vessel or a closure. So just things to keep in mind as we're talking about clips, because some of those, I mean, you may work with companies that have a clip. So I'm going to talk about liver, gallbladder, pancreas, and some diseases within the GI, within the liver, gallbladder, pancreas. One of the things, earlier we asked, last five years, greatest innovation or greatest change in our practice, as I think of the liver and what has happened over the past decade. I mean, I was training at a time when, and I'm probably dating myself by saying this, but we're pegylated into furan and ribavirin, were the mainstay of treating hep C. And they had horrible side effects. They weren't greatly tolerated, but that was the best. And we were curing probably 50% of patients with hepatitis C. Now it's almost unheard of not to cure somebody of hepatitis C, 95% efficacy with some of the drugs that are available out in the market. So a lot has changed. And as even mentioned on one of the slides earlier, why isn't a spray on that slide? Because things evolve. Things evolve. Even if we reviewed these last year, things are progressing. It's all from that partnership with industry. So I'm really excited here to talk to you guys about, maybe less about the liver since I'm an advanced endoscopist, but I deal with what's inside, within the bile ducts and what's inside the liver. So what is cirrhosis? Cirrhosis is when the liver is replaced by fibrosis and chronic injury. So this is a diagram of the normal liver. This is when you start seeing some fibrosis and this is advanced. So where you see the patient has cirrhosis and possibly even a mass there, which is a cancer. This leads to loss of function in the liver. And for the most part, it's irreversible, but there are some studies and there's some things to suggest that if you catch it at an earlier stage, early cirrhosis, or maybe at a point where there is fibrosis, that the liver will be able to heal itself and revert back to or close to normal. And oftentimes we do see that in our patients who present with fatty liver disease. So what are the causes of cirrhosis? The most common, these two compete and fight for the top spot. Alcohol used to be believed to be the leader, but really what was called NAFLD, as of this year, this is, or even last year, it was changed. The term is no longer non-alcoholic fatty liver disease. It's MAFLD, metabolic associated fatty liver disease, and MASH, metabolic associated steatohepatitis. So that's just a change in terminology and it's relevant because it just reflects that it's not necessarily tied to alcohol or the absence of alcohol. It's more so related to some of what you're seeing here and dealing with, I'm like you, I can't deal with this thing, with this pointer. But dealing with the metabolic syndrome and obesity and the epidemic that we're seeing in our country. Hepatitis C was higher on the list. It's gone down because of the cures that we are, the cure rate that we have with some of the medications out there. Hepatitis B, still relevant, especially if somebody acquires it at birth. Primary biliary cholangitis, this used to be called primary biliary cirrhosis, but the term is, again, something that's changed over the past several years. PSC, autoimmune hepatitis, some hereditary conditions such as hereditary hemochromatosis, Wilson's disease, and alpha-1 antitrypsin are the most common causes of cirrhosis in our country. So what are some of the signs and how do these patients present? Some constitutional symptoms, some general fatigue, muscle wasting. You'll see the patients have developed encephalopathy, meaning confusion. Beyond this, you'll see yellowing of their eyes and yellowing of their skin at a more advanced stages. Spider angiomata, which are little red blood vessels that you'll also often see on the face and in skin. Gynecomastia, based on some of the hormones that are being produced. Splenomegaly, the spleen is enlarged, normally not palpable on physical examination, but somebody who's cirrhotic, now you could palpate the spleen. Anxieties, caput medusa, these blood vessels that are now more prominent than visible, and they start developing some swelling in the lower extremities. Patients can develop some complications associated to cirrhosis, including GI bleeding from varices, whether it's in the esophagus, the stomach, or in the rectum. Confusion related to the hepatic encephalopathy and the swelling that I had just mentioned. So how do we diagnose cirrhosis? A lot has to do with standard labs, initially where we're looking at platelets, we're looking at their liver function tests and liver enzymes, and some commercial assays. And basically what's happening here is you go from non-invasive to more invasive measures to be able to diagnose either fibrosis or somebody's making it towards cirrhosis. And that's where imaging really has changed over the past decade. And LSDography is probably the most common that you'll see in the offices of most hepatologists, or that they are referring patients to, to be able to get a sense of how much fat is detectable in the liver or how much scarring is seen there to suggest whether the patient is progressing towards cirrhosis. But the gold standard still remains to be a biopsy. So whether that's taken percutaneously, as seen here, transjugular by an interventional radiologist or by endoscopic ultrasound, which some advanced endoscopists are now performing, we do perform biopsies in order to diagnose cirrhosis and more so the cause. So sometimes we'll find that a patient has some changes in their liver enzymes and we can't really nail the cause. A liver biopsy would help us with what's being seen under the microscope. So what are gastroesophageal varices? Varices are when the blood is basically blood vessels. These veins are trying to find a alternate route rather than going through the liver secondary to the scarring and the fibrosis that's been presented there. And when a patient presents with hematemesis, bleeding, vomiting up blood, their risk of dying is close to 25% within that year. So the mortality rate is really high when somebody's gotten to that point where they're having an active bleed from a variceal hemorrhage. The risk of a patient who has esophageal varices of bleeding can be 10% to 15%. And that's why hepatologists do take or gastroenterologists and hepatologists take measures to treat patients when we identify that they do have varices. And that can include medications or esophageal band ligation. The other method that we can treat them are using interventional radiologists where they a shunt to decompress the flow from these varices into another portion, basically going from one portion of the blood flow to another to decompress the collaterals that have formed. So basically, what you're seeing here in this picture are varices in the esophagus. We call them columns of esophageal varices. We grade them as either being small or large, large being greater than 5 millimeters. In the past, they used to be graded based on how much you're seeing within the lumen based on insufflation of the esophagus. And then you have gastric varices, which could be also categorized into different types, whether they're in communication with the esophageal varices or whether or not they're isolated. Acides is when you have accumulation of fluid within the abdomen, but not within a particular organ. It's in the mesentery, so you have this fluid that's basically causing the abdomen to become more distended. This is the patient's belly button, begun from an innie to an outie. And that's just based on that fluid, that third spacing of fluid. How do we manage these patients? We manage them by putting them on a low-sodium diet, by diuretics, or by, again, creating a shunt. What that tips is, in order to be able to shunt some of that blood flow out of the portal system in order to decrease the ascites, to decrease the esophageal varices. One of the biggest risks when a patient has ascites is that that fluid becomes infected. And that's what SBP is, it's spontaneous bacterial peritonitis. And that also carries with it great morbidity and a high risk of mortality. So what is hepatic encephalopathy? That's when you have brain dysfunction caused by the shunting of blood, portosystemic shunting, and liver and or liver insufficiency. It can manifest either by somnolence, the patient complains of being more sleepy than usual, to being full-on confused and not knowing where they are, really almost to a comatose state, usually diagnosed in the setting of advanced liver disease. And one of the tests that is often checked is serum ammonia, which is often elevated, but it has to be drawn in and stored in the appropriate way in order to be a test. But we just use the spectrum of symptoms within the patient and the history of advanced liver disease to be able to make that diagnosis. And what we often do is when these patients present, we want to make sure that there isn't SBP or that there isn't an infection, correct electrolytes, avoid medications that are no longer being metabolized appropriately by the liver, avoid sedating medications, and also trying to get rid of those toxins, usually in the form of lactulose through the stool or rifaximin, which is an antibiotic. So one of the biggest complications with our patients who have cirrhosis is hepatocellular carcinoma, progressing to hepatocellular carcinoma. It's the fifth most common cause of cancer and the third leading cause of cancer death worldwide. And patients, when they have cirrhosis, they are at a much higher risk for developing hepatocellular carcinoma. That's why we do take, there was a question earlier about screening. These are the patients that we screen for hepatocellular carcinoma. Their five-year survival, once identified with one of these tumors, is 20%. But there are methods, such as surgical resection, where patients can survive after having been diagnosed with hepatocellular carcinoma. So what are some of the risk factors? They're at a higher risk if they have hepatitis B and just basically any cirrhosis for any cause. It's really rare or almost impossible to have it without any of those two risk factors to have a hepatocellular carcinoma. What do we do as far as screening or surveying these patients for it? Oftentimes we'll do a transabdominal ultrasound. Some will add an MRI every six months, alternating between one and the other, and checking an alpha-beta protein, which is elevated in these patients because the tumor itself can secrete this as a marker. Management, these patients are often sent for surgical resection. Sometimes if surgical resection is not on the table, then they'll, depending if they fit within the appropriate criteria, they could be sent to a transplant center for a liver transplantation, or they can be embolized percutaneously by an interventional radiologist, which would shrink the tumor or destroy the tumor. If it's not identified in an early stage, then chemotherapy or immunotherapy is the mainstay of treatment. Liver transplantation, a lot of our centers, our center is a busy liver transplant center. Often we're seeing patients come in for cirrhosis, hepatocellular carcinoma, or acute liver failure for many reasons, whether it's alcohol or whether it's drug-induced or viral. But these are the patients that are often referred for liver transplant. They're allocated based on this scoring system, the MEL score. And in 2021, there were close to 10,000 liver transplants in the U.S. Of those, close to 9,000 were from deceased donor, 569 were living donors, so that means a portion of the liver was transplanted to another human being in that. And those are for different causes, so for different indications. The one-year survival after a liver transplant is great. I mean, these patients have a close to a 92% survival rate after liver transplant. Had they not gotten the liver transplant, their chance of death was significantly high. On the waiting list in the United States, in 2021, I think the numbers are higher now, it's close to 11,000. So what are some other common liver diseases? We had talked about the alcohol-associated liver disease. And here's the spectrum. This can go from somebody having alcohol-related steatosis, going to alcoholic hepatitis, cirrhosis, and then this is where they're at a higher risk for developing complications from cirrhosis, including portal hypertension and or hepatocellular carcinoma. So what's alcoholic hepatitis? It's a constellation when a patient develops inflammation of the liver associated with consumption of alcohol. To be at risk, usually we talk about 40 grams of alcohol per day for females, 60 grams of alcohol per day for males. What does that translate? 40 grams is two drinks. So that's two glasses of wine. That's two shots of tequila. That's the equivalent. That's two 12-ounce bottles of beer, just so you can get a sense. So between two to three drinks for greater than six months would put you at a higher risk for this. How do we treat these patients? There's different medications, but the mainstay would be prednisolone, 40 milligrams daily for 28 days. And there's a calculation called the discriminant function score, or MELD, and based on that is how we decide which patients are going to be treated. And if these patients are really at a severe stage, sometimes they can actually go on to liver transplant. As I had mentioned early, non-alcoholic fatty liver disease is now MAFLD, metabolic-associated fatty liver disease. And again, it's this continuum where you go from steatosis to steatohepatitis. So it's no longer just identifying fat within the liver. It's also identifying fat and inflammation to fibrosis, which means scarring, to cirrhosis, then being put at a higher risk for portal hypertension or hepatocellular carcinoma. So in order to get this, you need to have cirrhosis. And really, this is where the world, worldwide, we're concerned based on the metabolic syndromes associated with liver disease, 32% of the world's population, higher here in the United States, with regards to developing complications associated to this. It's the most common liver disorder in the industrial nations associated with type 2 diabetes, obesity, and dyslipidemia. How do we treat this? Avoid alcohol, lose weight, even just 10% decrease in body weight. And at the moment, there really aren't any approved therapies. But I know that there are several studies going on as far as treatments. And one of the big ones is just losing weight. Hep C, as I had mentioned early on. This is one of the greatest things where 50% cure rate or sustained virological response to having patients close to 95% being cured with current antiviral therapies that are available. The WHO estimates 58 million chronic hep C infections worldwide and 1.5 million new infections each year worldwide, being the most common blood-borne infection in the United States with 2.4 million people. Also associated to increased use of drug use, intravenous drug use. Most people are unaware that they're infected. And in 2020, there were recommendations that anybody above the age of 18 without any risk factors should be tested at least once. And all pregnant women during every pregnancy should also be tested for hepatitis C. Regular testing should be performing those patients who are known to be IV drug users. If they're on hemodialysis or if they have risk factors. Direct acting antivirals, as I had mentioned, greater than 95% cure rate and recommended for all patients with acute or chronic hep C virus. Hepatitis B is the most common hepatitis worldwide with 2 billion people with evidence of past or present infection. WHO in 2015 had estimated that 257 million people living with hep B virus leading to greater than 887,000 deaths worldwide. Endemic in African Asia, most people, again, like hepatitis C are unaware that they are infected and in the U.S. it's highest in immigrant populations. Transmission can be vertical. Those are the patients that can progress to hepatocellular carcinoma without any knowledge of that they're even infected. That's the vertical transmission. It's transmitted sexually or bloodborne. It can be prevented. Healthcare workers in the United States are all vaccinated against the majority of vaccinated against hepatitis B and you can also give IVIG. Biotherapy is effective at preventing progression, but it doesn't cure the infection. So one of the things with the ibediologists that they are concerned that often many of the biologicals come with a warning about hepatitis B virus. Why does that happen? It's because of the concern for hepatitis B reactivation or a flare with certain risk factors. So if a patient is gonna start on a biological, they're tested to see if there's any evidence that they have had previous exposure to hepatitis B. And the risk of acute liver failure with risk of death is much greater in these patients with a reactivation risk of greater than 10%. So if you do identify somebody, you recommend hep B antiviral therapy while on biological treatment for six months after they discontinue it. So, and do you continue, I mean, if somebody is gonna be on it for lifelong, I'm assuming you just continue it while they're on therapy. PSC previously called, well, no, that was PVC, but PSC is inflammation fibrosis within the biliary tree. This is something that is oftentimes referred to an advanced endoscopist because you have these patients who have these tiny little strictures, you have these little beating, or you have this beating within the biliary tree, but then they can also develop what we call a dominant stricture. And the reason that it's important for us to take a look at these and follow them closely is because of that risk of progressing to cholangiocarcinoma cancer, the bile duct. This is higher in patients who have inflammatory bowel disease. Most of the patients who present with PSC, about 90% or greater than 90% of them have ulcerative colitis. And with those patients who have ulcerative colitis, five to 10% can progress to have PSC. Tricky to treat because oftentimes they'll present with these strictures, they're at a much higher risk of developing an infection in the biliary tree. And as I had mentioned, higher risk for cholangiocarcinoma and colorectal cancer. Usually diagnosed by MRCP, and they're sent to us for an ERCP when they have a stricture that needs to be treated, or if there's a concerning stricture that needs to be sampled for cancer. Galstone's most common disorder of the bile duct affecting 10 to 15% of the US population. They're formed from bile precipitates. There are two types you'll see on the right over here. You have cholesterol stones, which are formed from cholesterol deposits. And then you have pigment stones, which are most often related to hemolysis or stasis that lead to infection, that lead to these black or brown stones. How do most patients present who have stones? They usually don't have any symptoms, but those that do present with symptoms have biliary colic. And when you think of colic, you think of something that comes and goes, but it's actually not that. They'll often present with epigastric or right upper quadrant pain. It doesn't come and go. It lasts for at least 15 minutes at times, hours at a time. Patients who've had Galstone's as a predominant of their symptoms can probably set their alarm clock. 2 a.m. they present with this band-like pain or mostly right upper quadrant or epigastric pain that will subside. It's often after eating, a couple of hours after eating, where they'll present with these symptoms, but then it goes away. When it doesn't go away, then you're concerned that they might have itis. Itis meaning inflammation associated with an organ, so cholecystitis, which we'll show you in the next slide. Diagnosed typically by abdominal ultrasound. Sometimes you'll see it on a CT or MRI. That's done for another reason. Again, most often it's diagnosed asymptomatically. You know a patient has Galstone's. And if they do have Galstone's and they have no symptoms, then you don't do anything about it unless one of those Galstone's has made its way out of the gallbladder into the bile duct, and that's, we'll discuss in a minute. So what's acute cholecystitis? It's when there's inflammation of the gallbladder, and that's related to there being a blockage of the cystic duct. Remember I had mentioned earlier or told you earlier that the bile duct drains into the small intestine through the ampullae of water into the major papilla. Common hepatic duct, right hepatic duct, left hepatic duct, and the pancreas down here. What happens is a stone makes its way out of the gallbladder, gets stuck as it's making its way out, and that causes inflammation because this can no longer secrete into the small intestine. Sometimes those stones get stuck here. Sometimes as the stones are making their way out, they transiently block the pancreatic duct, and that's another entity called Galstone pancreatitis. What do patients present with? They'll present with severe right upper quadrant pain that doesn't go away, fever, and when they're evaluated, they're found to have an elevated white blood cell count. Diagnosed initially by an ultrasound, they'll have an ultrasound that'll show that the wall of the gallbladder is thickened. Sometimes you'll see fluid around the gallbladder and also can be seen by CT. As the ultrasonographer is putting the probe underneath the gallbladder, they'll have a Murphy sign. They'll have inspirational rest. It'll hurt when they palpate it with the probe, and these are all features that suggest that this person has achilles cystitis. How do we treat? Mainstay is antibiotics, removing the gallbladder. At times, if a patient's not a candidate for a cholecystectomy and they're not responding to antibiotics, sometimes percutaneously, a tube can be placed into the gallbladder. We can also place that endoscopically through the wall of the stomach or the duodenum. So this is what a diagram you had talked about. This isn't a Netter's, but we had talked about the Netter's-like images. Gallbladder sitting here under the liver, and once it's out, you'll see on fluoroscopy, if you see the clips, you'll see three clips cutting off the cystic duct, the artery, and the vein. So choledocholithiasis, as I had mentioned, that's when choledocho, meaning the bile duct lithiasis stones, is when one of those stones makes its way out of the gallbladder, doesn't block the cystic duct, but actually makes it into the bile duct and gets stuck here because it's trying to make its way out. As I had mentioned, it can transiently obstruct the pancreatic duct, but when this happens, that stone sometimes opens up the portal at the opening of the ampulla of water where enteric, meaning enteric content, or bacteria can make its way into a sterile environment, and that sterile environment now becomes infected, and that's when you have something called ascending cholangitis. That means that the bile duct is inflamed and infected. How do we, oops, how do we diagnose that? Patients present with Charcot's triad, which is right-sided abdominal pain, jaundice, and fever. When it's more severe, they actually will develop some altered mental status along with that. So what is the treatment? Get the stone out. And how do we do that? That's with an ERCP. So here's a view of the major papilla, and the major papilla has the ampulla of water, which is that opening into the bile duct. So the ERCP scope is this tube that you'll see here. So oftentimes you'll see either the scope is white on a cholangiogram. Sometimes you'll see it opposite, where the background is white and the scope is black. But what's happening here is you have the scope, you have contrast injected through the bile duct. Here you're seeing, well, you don't see a stone here, but you're seeing contrast make its way into the bile duct, into the cystic duct, and also filling the gallbladder. But what happens is you'll have the stone removed by cutting that muscle. This is a sphincterotomy. When we talk about cutting that sphincter, the biliary sphincter, sometimes you could also cut the pancreatic duct, which would be a pancreatic sphincterotomy, and that's to open up the door and to pull that balloon out. And you could pull that out with a balloon or a basket. Here's a cholangiogram where you could actually see this filling defect. So contrast is in the lumen, but there's a lack of contrast right there, and that's the outline of the stone. So moving on to the pancreas. Pancreatitis is inflammation in the pancreas. Comes in two forms, acute and chronic. Acute is when you have acute inflammation in the pancreas. Usually presents with sudden onset severe abdominal pain. Could be mild, it could be severe, and there's several different symptoms that present. So when the patient complains of pain radiating towards their back, worse with eating, the reason it radiates towards the back just has to do with the location of the pancreas and referred pain from the nerves that are being innervated in that area. Patients will have nausea, vomiting, usually self-limited and resolves in a few days. Severe is when you could have almost, when we describe an acute abdomen, the term refers to an abdomen that's almost a surgical abdomen. The patient's tender to palpation. There's some irritation in the peritoneal lining. The patient has fever, they can have shortness of breath in most severe cases. They can become confused and present in a shock-like comatose state. They may have multi-organ failure, which shock, meaning hypotension, often can be life-threatening and they can spend a lot of time in the hospital. What are the most common causes? The top two being gallstones and alcohol. There are about 30 causes of acute pancreatitis. The third probably being elevated triglycerides. And then we start looking for all of the others, whether the patient had a medication that's associated, whether they had a trauma. If you're ever in a hospital and somebody attending is pimping a student or a resident, they'll always ask about scorpion bites, probably the most rare form, but it's isolated to like one island in the Caribbean, I think it is, where that scorpion is. But an important one is ERCP. And ERCP itself carries about a 5%, 2% to 5% risk of pancreatitis. And oftentimes you'll hear us talking about measures which we take to minimize the severity of pancreatitis associated with ERCP. And for the same reasons, it has to do with passage of an instrument at that opening where the bile duct and the pancreatic duct share an opening, or cutting, or electrocortis, but that 2% to 5% is there. And we use methods such as rectal endomethasin, lactated ringers, and just aggressive IV hydration to minimize that risk. How do we diagnose it? You have to have two out of the three, meaning typical abdominal pain. You have to have elevated pancreatic enzymes in the blood and or imaging suggestive of pancreatitis. On this, this is a CT. Here you could see the pancreas. In this case, there is some peripancreatic stranding. In this case, you can't even see where the pancreas is. You also see some loops of bowel that are distended, just related to the severity of the pancreatitis. How do we treat it? Supportive care, nothing by mouth initially, although more and more studies are pointing towards early enteral nutrition if the patient's able to tolerate it, giving aggressive IV hydration, correct electrolyte abnormalities, and treating their pain. But no medications are shown to actually help acute pancreatitis in the acute setting. Removing the stone that's causing the obstruction if it is gallstone pancreatitis. And I'm just gonna fast forward through this because we're really out of time. Chronic pancreatitis is when there's been longstanding inflammation, most often associated to alcohol consumption and repeated bouts of pancreatitis. It's when you have damage to the normal structure of the pancreas and you have a loss of both exocrine and endocrine function. You really, in order to start having malabsorption, you need to lose probably greater than 90% of the exocrine function of the pancreas and also can lead to diabetes. How is it diagnosed? You'll see calcifications in the pancreas. You'll see strictures. When we do endoscopic ultrasound, you'll see some heterogeneity, meaning that the echo features of the pancreas are different. You'll see strands and the pancreatic duct may become dilated. How do we treat it? Avoid alcohol, smoking, cessation. Those patients who have chronic pancreatitis and smoke are at a significantly higher risk for pancreatic cancer. We treat their pain and give pancreatic enzyme replacement. If they have stones in the pancreatic duct, then endoscopically we can remove those stones or surgically we can bypass the pancreatic duct or remove those stones surgically. Lastly, we'll talk briefly about pancreatic cancer. It's a cancer originating from the pancreas and it's the third most common cause of cancer-related deaths in the United States. There are two types, the most common being adenocarcinoma with a smaller percentage, 5% being neuroendocrine tumors. The overall prognosis is less, it's five-year survival, 6%, and a lot of that has to do with the inability to diagnose these pancreatic cancers early. What are some of the risk factors? If there's a family history, age, smoking, smoking and chronic pancreatitis, alcohol, obesity, and diabetes. What are the symptoms? Painless jaundice. Why do we say painless jaundice? That means a patient presents with yelling of the eyes, yelling of the skin without any abdominal pain. That often suggests that the tumor is within the head of the pancreas and causing a blockage of the bile duct. So bile is no longer making its way out of the bile duct into the small intestine. So it goes back and systemically it'll cause icterus and jaundice. Unexplained weight loss. Itching, secondary to the bile salts accumulating, causing an irritation in the skin. Poor appetite. At times patients do present with abdominal pain. Oftentimes that abdominal pain is intractable, meaning that we can't really treat it effectively. Nausea, vomiting, oftentimes related to an outlet obstruction, as you had learned earlier. So how do we diagnosis? The mainstay is getting tissue. We do that by means of either percutaneous or endoscopic ultrasound, where in this case, again, a tumor in the head of the pancreas is sampled by means of an endoscopic ultrasound. A tiny little needle makes its way out of the scope and actually samples that tumor. And then you could see the cells which show that this is a pancreatic cancer. How do you treat? Surgery is the only hope for a cure. If not, chemotherapy, immunotherapy, studies ongoing now about using vaccines in the treatment of pancreatic cancer. Complications, biliary obstruction. That's why the patients present with jaundice. Oftentimes can be treated with a stent placed into the pancreatic duct. I'm sorry, into the bile duct. As you remember earlier, I had mentioned that part of the bile duct travels through the pancreas, the intrapancreatic portion of the bile duct. And we can treat that with a stent. As you can see here, that stent is now bypassing the tumor and allowing bile to flow through. This is a fluoroscopic image and this is an endoscopic image of that stent. Last thing, sometimes the pancreatic tumor can actually block the outlet of the stomach and you can place a stent into the small intestine, into the duodenum to also bypass that. So that's a lot. Any questions? Thanks for your attention. Lastly there with the bile duct stent placement, how do you choose metal versus plastic? Great question. Oftentimes, in the past, it was almost always plastic early on until we've become more comfortable with metal stents. And it goes even further. How do you decide between plastic? And if you decide metal, how you go from covered to uncovered or vice versa? It often depends on what's next. So let's say I see a patient and I sample the mass, but I'm not 100% certain it's a pancreatic cancer. Oftentimes I'll place a plastic stent first. And then that'll give me a good three months of patency to be able to drain that bile duct. If we know that that patient might be going for surgery within a short period of time, then again, we might choose a plastic stent over a metal stent. If we know at the time that this is most likely gonna be a pancreatic cancer, oftentimes we'll place a covered versus an uncovered metal stent, even if they're gonna go for surgery because that portion of the pancreas is gonna be removed with that Whipple procedure if it's in the head of the pancreas. Is Whipple the most common surgery in that case? Depends again on the location of the pancreas. So a Whipple surgery is when the pancreatic cancer is in the head of the pancreas. So yes, that would be the most common for a pancreatic head cancer. If it's in the tail of the pancreas, then it's a distal pancreatectomy. It really just depends where in the pancreas the mass is. Other questions? One more. Go for it. Okay, earlier you were talking about cirrhosis. And I was wondering if upon the onset of cirrhosis, is it detectable throughout the entire liver or does it normally present in one lobe before the others? Interesting question. It doesn't uniformly present across the liver. So at times there have been some who have advocated or not advocated, but had asked for biopsies of let's say the left lobe and the right lobe of the liver because it might be geographic. But when it's at that stage, that's probably more likely to be an early cirrhosis, less likely in later stages of cirrhosis. But remember, we're also looking at some of the other markers, including cirrhological evaluation that's gonna help us make that diagnosis in addition to the liver biopsy that would tell us that there is cirrhosis. So it might have patches that are less advanced than others. So that's why when a pathologist is looking at a liver biopsy, they need to have a certain number of what they call portal triads to be able to see that there is fibrosis and scarring across that to suggest that there is actually cirrhosis. And that probably opened up for 10 more questions, right? Any other questions? All right, thanks for your attention. Thank you.

liver conditions

pancreatic conditions

cirrhosis

gallstones

pancreatitis

pancreatic cancer

biliary obstruction