I think kind of mirroring the organization we had in the physiology, we'll start with liver diseases first. So cirrhosis usually is defined as a replacement of liver by fibrosis and scarred due to chronic injury. And it implies there's some kind of level of irreversible damage that compromises the daily activities that the liver is supposed to perform. You might hear people discuss compensated versus decompensated cirrhosis. Actually, people with compensated cirrhosis said they still have some reserve where they may be mostly asymptomatic versus the decompensated where whatever damage has been accumulated is so that the liver can no longer perform its daily functions. And we'll talk a little bit more about what that looks like in the next slide. Cirrhosis is usually a permanent condition. Cirrhosis or just the scarring itself is sometimes something that can regress on biopsy or imaging if the appropriate cause is detected and treated early enough on. So this is a very lengthy list of possible causes of chronic liver disease that can possibly lead to liver cirrhosis. It's by no means exhaustive, but it's some of the most common. As we discussed this morning, the liver has a multitude of different functions and a lot of these signs and symptoms are related to any compromise of that function. Our little cirrhotic man on the right-hand side, these are a lot of physical exam findings that we can see. Anxiety or altered mental status follows a very specific pattern in the chronic liver disease patient. Jaundice, that is sometimes some obvious symptoms, either yellowing of the whites of the eyes called scleral ichthyrus or the yellowing of the skin, which can actually be quite dramatic. Results from sort of disruption of the management of bilirubin. The other stuff, spider angiomatas and gynecomastia. Spider angiomatas look like little red snowflakes on the skin. And gynecomastia, this is the liver plays a critical role in management of hormones as well as we discussed this morning. We know there's some difficulty in processing and inactivation of estrogen. That's why we see some of those results. Ascites, this is related to lack of the ability to produce certain proteins. I think I briefly touched on albumin this morning, which is not the only protein that regulates the amount of fluid in various compartments of the body, but is the one we most frequently talk about in this context. Lower extremity edema is not another manifestation of when fluids are not in the right amount in the right compartments where they should be. We highlight a few specific complications of cirrhosis because that is where most of our chronic management is focused on GI bleeding from esophageal varices. It's probably the most life-threatening manifestation. You can also get varices elsewhere in the body, but esophageal varices when they rupture can cause pretty dramatic exsanguination. We've talked extensively about upper endoscopy and banding today. Confusion and hepatic encephalopathy and finally swelling. There is a fourth. There is hepatocellular carcinoma. People with liver cirrhosis are at risk for developing liver cancer, and there will be a separate slide dedicated to that later on. In the past, liver biopsy was the only tool we had. It still remains the gold standard for diagnosis of cirrhosis, sending a sample of the liver to the pathologist. It does have its pros and cons. The liver is a very vascular organ, and there is a risk of bleeding, putting a needle into any organ that's filled with blood. There are significant risks and benefits. The other sampling error, the liver is a large organ, as we discussed, and it's possible to miss certain portions where there's fibrosis or cirrhosis just because it's not completely homogenously distributed. Now in the past 10 years or so, we've really had a lot more tools to help gather information in a noninvasive manner about whether someone has either had significant fibrosis or scarring to the liver or even reached the cirrhosis stage. Maybe later on the panel, some of my colleagues can speak to this as well, but there are some proprietary blood tests that we can send to give an estimation of fibrosis, which I don't personally use in practice, and some things like Aprescor and Fib4, which use a combination of readily available labs that we might routinely get in a liver patient to give an estimation. Elastography, particularly FibroScan, is a particularly useful tool in measuring fibrosis. ARFI and these 2D shear wave elastography, shear wave elastography basically implies that the technology gives a standardized ultrasound signal to the target tissue, which in this case is the liver, and what it receives in response, it sort of measures the resistance of that tissue, and based on each proprietary type of elastography, it'll give an estimation of how much scarring or whether someone has reached cirrhosis. So these first, the FibroScan, ARFI, 2D shear wave elastography, they're all a type of elastography. I think FibroScan's really taken over because it is a separate apparatus. It is something that a hepatologist can keep in their office and just do as an in-clinic testing. You don't necessarily have to go to a radiology department, get the test, wait for the interpretation from the radiologist, so on and so forth. I think MR elastography is not available at all centers, but it is a really helpful elastography mode on MRI that we sometimes use as a tiebreaker if we get equivocal results from any of these modalities and we really need to figure out what's going on before progressing to something as invasive as a liver biopsy, for example. Little focus on esophageal varices. Thinking back about the pathophysiology, as you recall, we may have mentioned that the liver performs a lot of the filtration of toxins and metabolism of medication. In the most general sense, the way I describe to people, if you think of the liver as a filter or a sponge, when it is healthy and compliant and flexible, it can perform its duties and the blood goes through fairly easily. But if we have continued insults or we continue to abuse it and develop scarring and fibrosis, you know that scarring, fibrosis in itself makes it stiff, the organ can potentially contract and get smaller. So it produces a sort of back pressure or portal hypertension in the veins that feed it. And the pressure has to go somewhere. So usually it fills these, in the simplest form, these varicosities. So as you can see, it's a pretty common complication in patients with cirrhosis. Not everybody has bleeding, but when it does start, they are high risk for having repeat bleeds and other complications. It's torrential bleeding. I think the first time I encountered a serious active bleed, the endoscopist, it was a medical student, was just covered with blood. So in its most severe forms, it can definitely kill someone. Management includes, in the acute setting, when there is an active bleeding, things like endoscopic ligation, or as Dr. Seuss mentioned earlier today, injection of certain sclerotic agents. That's not done so much anymore. I'm not sure if it's a manufacturing issue or people just feel that banding is a better treatment. But in some areas, you can still find it as a rescue therapy. TIPS or transjugular intrahepatic portosystemic shunt. This is probably the most definitive therapy for someone who has had a repeat esophageal variceal bleeds or variceal bleeds from other locations that are not as easy to treat. It is usually done by interventional radiology. And it involves placing a shunt or a connection in between the portal vein and the hepatic pain, sort of releasing that pressure and bypassing the cirrhotic liver. Why don't we do it right off the bat? That bypass effect has its pros and cons as well that are sort of outside the scope of this talk. In terms of medical therapy, we know that certain medications or beta blockers, such as propranolol, toprolol, and there is some data on carvedilol, can sort of medically reduce the pressure in that portal hypertensive system and help prevent further bleeds, even if somebody already has varices. Ascites is probably the most common manifestation of third spacing or fluid that's going into places that it doesn't belong. There is an accumulation of the fluid in the abdomen. Just from a symptomatic standpoint, patients often don't feel well just having a lot of fluid. They can feel significant distention, discomfort. It can keep them from eating in severe cases. It can really put pressure on the thoracic cavity, keep them from breathing. And also, it's unsightly. Nobody wants to walk around looking like they're pregnant, essentially. Mainstays of management are a low-sodium diet, diuretics to try and encourage the kidney to get rid of that excess fluid. Again, we've talked about TIPS and its role in bleeding, and it also has a role in refractory ascites, where people are not able to control the fluid in their abdomen despite following the diet, despite following the diuretics. And the other is actually basically physical drainage or paracentesis. So we may consider TIPS in a patient who is coming for paracentesis and large-volume removal of 5 to 10 liters of fluid every single week or even multiple times a week. Other than just having symptoms and it being unsightly, we do know in liver patients that there can be a translocation of the bacteria inside our gut into that fluid, causing something called spontaneous bacterial peritonitis. The symptoms of that can sometimes be very subtle. I think the classic symptoms are abdominal pain, fevers, and chills, but sometimes, as you see in older patients or patients who just are immunosuppressed, it can be a form in just not feeling well or altered mental status, and it can cause significant morbidity and death in a very short period of time if it's not managed appropriately. So hepatic encephalopathy, brain dysfunction caused by liver cirrhosis or portosystemic shunting. We say portosystemic shunting. There are some people who don't have cirrhosis or scarring or damage to the liver itself, but they may have anomalous connections in their circulation around the liver for whatever reason, whether they're born with it or it's a complication for a different procedure, and have encephalopathy for that reason. This can range from very subtle to sort of irritability, a reversal of sleep-wake cycle to something to further progression of someone being just overtly confused, not knowing who they are or where they are, to a coma and being completely unresponsive. So we use these kind of tools. It is a clinical diagnosis, and we have to have a high index of suspicion when someone is not acting as they usually are. A lot of times, we talk to patients' family or friends, people who are familiar with their baseline to get an idea of any changes in their usual behavior. There's a lot of focus on serum ammonia and encephalopathy, and people will sometimes check it, even serially, if a liver patient is in the hospital. They're often elevated, but it's not always a direct correlation, and trending it doesn't necessarily imply anything about that patient's altered mental status or liver disease. Encephalopathy can just be a sign of the liver tuckering out and not able to really perform its functions, but it can also be triggered by things such as infection, something as simple as being dehydrated in the setting of also having decompensated liver disease or medications that can cause a healthy patient to be drowsy or sleepy, can really tip people over the edge if they have cirrhosis or a condition that predisposes them to encephalopathy. HDC, or hepatocellular carcinoma, still one of the top five most common GI cancers and cancers in general in the world. It can happen in the presence or the absence of cirrhosis. We have a few slides later on some focus of different causes of chronic liver disease, and we'll talk a little bit more about that. The five-year survival is about 20%. People tend to do better if there is just a focal tumor or they do not have underlying liver cirrhosis or other liver disease. Increased risk factors, hepatitis B, and we mentioned that cirrhosis, hepatocellular carcinoma, is considered one of the complications of having cirrhosis. If someone has a condition where they're at risk for hepatocellular carcinoma, usually that means establishing long-term care with a hepatologist and having some kind of cross-sectional imaging, whether that's ultrasound or a triple-phase CT every six months to a year and trending of AFP. The gold standard for treatment is liver transplant, but not everybody has the resources or the availability or even wants to go through the lengthy process of getting a liver transplant. So surgical resection is one option, though we know that there's high risk of it coming back or recurrence, even if the surgical resection is complete and, in theory, curative. And then we have embolization or ablation procedures. Ablation is usually radiofrequency and involves using a probe to focally burn away using some kind of energy. Embolization, this is down to the unique blood flow to the liver where they can go through the portal vein and selectively clot off that portion of vessel that's feeding the tumor either through a chemical agent or just a bland bead to clot off that area. In cases where patients have metastatic hepatocellular carcinoma or they're not a candidate for surgery or other therapies, we have had significant advances in chemotherapy and immunotherapy, so people are able to live longer and longer with this condition. Liver transplant, it is a great treatment for patients with decompensated liver failure. It is, as I mentioned before, considered the best treatment if somebody has liver cancer. Acute fulminant liver failure for other reasons, this is most commonly seen in the inpatient setting. Patients who have had sort of acute fulminant liver failure from Tylenol and alcohol or some kind of toxic exposure is one of the examples. There are some other indications that are not listed here. Happy to answer questions about that later if needed. Organs are allocated based on a Mel's sodium score. This is a proprietary, well, not proprietary, but it was an algorithm that was designed by Mayo Clinic and it uses a combination of readily available lab markers to give a score and it was found to be an excellent predictor of survival in people with liver cirrhosis. So, they use that to determine who is the sickest and who should get an organ if it's compatible with that person first. Most of the time, the vast majority of the liver donors are from diseased donors. Living donor is actually a minority in the U.S., although in selected centers, they can screen a relative or someone who's compatible to see if they're an appropriate donor. People do particularly well with a one-year survival of almost 100%. There are a lot of people waiting for organs and stewardship of organs is definitely a hot topic. Next we'll talk a little bit about some of the common causes of chronic liver disease that were listed on that earlier slide. Alcohol is one of the number one causes of chronic liver disease. Alcoholic hepatitis can be diagnosed if someone has significant alcohol history jaundice within the past eight weeks and consumption thresholds listed here, it varies based on men or women and unfortunately, women are more susceptible to alcoholic hepatitis at lower amounts of alcohol than men. Treatment is primarily to stop drinking and supportive management of any complications that may arise. Chronic associated liver disease is interesting in that it's one of the few chronic liver diseases where people can have the complications of bleeding esophageal varices, ascites and encephalopathy and they may not actually have cirrhosis. So it's one of the few opportunities where you can really counsel those patients that if you just stop, there's a possibility that things will regress and heal itself and go back to normal. In severe cases of alcoholic hepatitis, there is another algorithm that we work, complex calculation that everybody goes online to use because it's not something you can do with pen and paper. And what we know, Madri is the name of the creator, Madri Discombinant Function or MDF. We know that it's greater than 32 or MELD is greater than 20. But giving them steroid therapy for about 30 days does improve outcomes and survival. We have additional scores to kind of do a progress check along the way, such as the LEAL score where we can reevaluate at about the seven-day mark to see if the steroids are working or not because as we know, steroids have their pros and cons. If someone is not able to get prednisone therapy for whatever reason or they're a non-responder, liver transplant referral is indicated. In the past, requirements for alcohol-associated liver disease were quite strict. But as our understanding of alcohol-related disease expands, that has been changing based on the liver transplant center. And finally, sometimes in very sad cases, if they're not eligible for transplant and there are no other options in palliative care. Non-alcoholic fatty liver disease, I think probably everyone's heard about it now in Western countries. It's really come to the forefront and becoming a more common cause of chronic liver disease. In the end of 2023, actually the AASLD and some of the international liver disease societies decided that they want to make a shift from calling it non-alcoholic fatty liver disease to actually calling it MAFLD or MASH. So they're changing it to metabolic dysfunction-associated liver disease. Obviously, nothing changes overnight, but in the next year or two, you may see the terminology start to change. There's a multitude of reasons why they decided to change the terminology, but there is some stigma attached to the fatty part. They really wanted to put the focus on steatosis, that is fat in the liver, and the steatohepatitis, that associated inflammation of the liver. So this kind of disease is not just about having fat on the liver, but associated inflammation of that fat on the liver that causes chronic inflammation, which can lead to scarring and finally cirrhosis. It is associated with metabolic diseases such as diabetes, obesity, high cholesterol. In the past, part of the diagnostic criteria was that there was a lack of significant contribution to alcohol, but we often counsel people to avoid alcohol just to avoid any possible patient-controlled contributors to progression of liver disease. And we know that diet and exercise and even a modest weight loss of five to 10% of total body weight can make a huge difference. So we really made huge advances in hepatitis C, I think, over the past 20 years. In the past, it was one of the number one causes of liver cirrhosis. There's still millions of people worldwide that do have hepatitis C and may not necessarily know they have it. And for that reason, the CDC usually recommends a non-one-time testing, even as an adult, to screen for this condition. Since I've been in training, we've had multiple direct acting antiretrovirals that are available to patients even with chronic kidney disease or other comorbidities. And they have really excellent cure rates. So we've really seen this as a cause of liver cirrhosis to really start to decrease. Hepatitis B is most common worldwide. It's less of an issue, I think, in developed countries because there is a practice of vaccinating for hepatitis B at birth. But it does continue to be endemic in parts of Africa and Southeastern Asia. Relatively speaking, it is more highly infectious than something like hepatitis C or HIV. And it is transmitted through blood and bodily fluids, as well as vertical transmission from mother to child. We do see it more commonly in immigrant populations. Prevention, as we mentioned, we don't see it so much in the United States anymore because there is that practice of vaccination in women who are giving birth that know that they have hepatitis B. If they are able to get good obstetric care, there are methods to prevent and significantly reduce the possibility of them passing it down to their child, including immunoglobulin treatment. Mainstay of antiviral treatment are these two, Entacavir and Tenofovir. Most of the time, I said, therapies cannot cure infection. Therapies cannot cure infection, but can prevent progression and lower risk of liver cancer. I would say that's fairly accurate for people who have chronic hepatitis B, that these antivirals help decrease viral load, decrease the repeated insult to their liver and ongoing inflammation. But most people are not curable. There are some people for their immune system in combination with medication that are able to clear the infection, but those are rare and actually quite unusual. I don't think we've had extensive conversation about biologic therapy, but it is a type of therapy for inflammatory bowel disease or sometimes various cancers. Basically, a medication with significant immunosuppressant effect. We do want to check for hepatitis B because not everybody knows that they have it. Or even if someone was exposed in the past, what we know about this virus is it does continue to have some dormancy in the nerves in the body. And if somebody is significantly immunosuppressed, it can reactivate. And that reactivation response can be quite dramatic and cause significant injury or even acute liver failure to the patient. So some of the medications, rituximab, anthracycline, and specifically NGI, TNF-alpha inhibitors are certain medications we use in inflammatory bowel disease. So this is our official recommendation if someone's discovered to have hepatitis B and need these medications. It's not the end of the world. It is something that we can manage with antivirals. I think we have primary sclerosing cholangitis. I think this is a good transition because following up, we will talk more about biliary diseases. But it is a condition where interventional endoscopy and hepatologists do tend to co-manage because there are some overlapping components. PIC involves the inflammation, fibrosis, and stricturing of the bile ducts. It doesn't involve the inflammation and stricturing of the bile ducts. It does involve the large bile ducts and now we know it can involve the peripheral or small bile ducts as well. So it is something that we can see on imaging. It is associated with inflammatory bowel disease. We know that patients with PSC that we routinely should look for ulcerative colitis because it is commonly found. The opposite is not as true, but about five to 10% of people with ulcerative colitis may also have PSC. Crohn's disease has also been associated with PSC. So it's not just ulcerative colitis, although that is the classic manifestation. Complications, I think the most feared one is probably progression of stricturing fibrosis of not just the ducts, but also the liver tissue itself leading to liver cirrhosis. There is an increased risk of cholangiocarcinoma or cancer of the bile ducts. The increased risk of colorectal cancer associated with ulcerative colitis. And we know that there is some change in the bile secreted by patients with PSC that further increases their risk of colorectal cancer. It's ending cholangitis or infection of the bile ducts of itself can happen as a result of the narrowing in the ducts, although it's much rarer for it to happen if we've never instrumented them by doing an ERCP or poking them or contaminating that system. There's a special protocolized MRI called MRCP that gives a fairly good look at the ducts. Usually we can obtain our diagnosis with a combination of that MRI and clinical signs and symptoms. Management, if somebody has the isolated biliary stricture that's causing liver enzyme abnormalities, giving them issues, or we have a high concern that this is actually cancer, then ERCP may be indicated to sample, treat, dilate, so on and so forth. So next we'll talk a little bit about gallstones. It is probably the most common disorder impacting the bile ducts, the gallbladder. Tons of people come to my clinic every day asking about gallstones, gallbladder-related issues. Probably up to 20% of people have gallstones in their gallbladder, and they may not necessarily know it. If it's a low burden and it remains in the gallbladder, usually it doesn't cause problems, hence why people aren't aware of it. It usually comes to our attention if somebody has pain for another reason or if gallstones start to escape and get impacted elsewhere and cause problems. They're formed from bile precipitates. I think in the U.S. the most prominent is probably cholesterol stones. If any of you are from the West Coast or work where there's a large Pacific Islander Asian population, you may see more pigment stones from pyogenic cholangitis, just related to a specific parasite exposure that they have called clonorchis. So as we mentioned, most people are asymptomatic. The stone burden isn't large and they just sit in the gallbladder. Nothing really happens. Biliary colic is the official term for what people feel if the gallstone is impacted either in the gallbladder neck or the cystic duct or further downstream in the bile duct. If we think back to how our process of our digestion works, if you recall that the gallbladder kind of collects bile as we're fasting, and when we eat at the right time, CCK stimulates the gallbladder to contract and kind of push with all its might to push that bile out downstream into the common dial duct and mix with the food that we've eaten. So you can speculate if there's something stuck or there's some downstream pathology that's probably gonna hurt and not feel very well. So the classic is sort of right upper quadrant carapy abdominal pain, 30 minutes to an hour after eating. Obviously, not everybody presents in the same way, but most people do have symptoms like this. So diagnosis of just gallstones in the gallbladder, the most common test is probably ultrasound. It's a good screening test. It is external, so we do have limitations of body habitus, bowel gas, depending on how much someone's eaten that day. And here we have a classic image of a gallstone in the gallbladder. You see that it's echogenic, which means it's bright, and it has a, do you see that triangular-shaped dark portion that associated shadowing that's pathognomonic or pretty much indicates that it's a stone of some kind? Other diagnostic tools include CTs, which can also show stones, MRIs. People will get those imaging studies for other reasons, and they'll frequently say, oh, you have some stones in the gallbladder. So the next pathology is acute cholecystitis or inflammation of the gallbladder, most commonly from infection, if the stone is impacted in the cystic duct and bile cannot get out. I think as we previously mentioned, the digestive tract is not a sterile place. If any of you guys are outdoorsy or just, we know that, well, it's much safer to drink water from a flowing stream versus a stale water. A flowing stream versus a stagnant puddle for bacteria has had time to ferment and grow and multiply. Symptoms involves sometimes acute right upper quadrant abdominal pain. People can have fevers, elevated white blood cell count. We talked about abdominal ultrasound and computed tomography. If you talk to your surgeons, you can talk about this later, but there are certain specific signs and symptoms. And we sometimes also associate it with gallbladder wall thickening on imaging and presence of fluid from inflammation on imaging. The mainstay is removal of the gallbladder with cholecystectomy. Some supportive treatments while they're waiting for that surgery or to sort of calm down the inflammation and bridge them include antibiotics and IV fluids. For those people who are not candidates for cholecystectomy, they can have a percutaneous drainage tube from IR and we are making more advances in endoscopy and endoscopic treatment. So this is just a diagram showing cholecystectomy. Depending on the anatomy of the patient, usually the surgeon will try to just leave a cystic stump, but there are certain times when they're not able to because of blood vessels or body habitus for whatever reason, and they may cut closer to the sac portion of the gallbladder. Cholodocal lithiasis, say that 10 times fast. This is probably what we most encounter or what we say is in our wheelhouse as an interventional endoscopist when there's a stone confirmed to be in the common bile duct either the best and tests for viewing the biliary tree in this area, there's a lot of stuff there. It's probably a MRCP or endoscopic ultrasound, but if you're lucky enough to see it on CT or ultrasound or the ASG itself produces a series, a set criteria based on the endoscopic ultrasound indirect measures such as liver enzymes, symptoms to determine whether someone's at high risk or not for having cholodocal lithiasis. You can use that criteria to make the diagnosis. Cholangitis is infection arising from an obstructed bile duct because cholodocal lithiasis and gallstone related issues are most common. That's probably the most common cause, but it can arise from multiple other reasons. Charcot's triad is considered sort of the clinical symptoms associated with cholangitis, right-sided abdominal pain, jaundice, fever, altered mental status. Not everybody presents this way, but if it's on your test, just pick it. It's what we have in medical school as well. Cholangitis is considered a GI emergency. What we know from our studies is usually we have about 24 hours to get to it if somebody is having symptoms, significant symptoms, hemodynamic instability, but most people are able to be bridged over and they recover with supportive therapy and antibiotics. Treatment, once you confirm there is a stone, it has to come out. So we've talked a little bit in brief about ERCP. So all the way over to your left, that is a endoscopic image of the major papilla. In the middle, we have a schematic of our side-viewing scope or jodinoscope. I kind of liken it to driving, but if your windshield is opaque and you can only look out your left side window. It's structured this way in particular because we're more able to access the valve or the major papilla on the side. It's not straight in front of us. And the elevator helps adjust the angle of our tools and give us leverage. And finally, the cholangiogram. This patient has an intact gallbladder and you can see it filling with contrast. Sphincterotomy, we need some room to introduce our tools and to pull out a stone. So that implies using either an electrocauter-enhanced wire above the sphincterotome, as you hear on the right-hand side, or a needle knife to just make a controlled incision. And then here we have a very, very dilated system. So it's just very big. And then a stone in the distal duct. Next, we'll move on to pancreatitis. Since we've just discussed sphincterotomy, ERCP has potential complications of bleeding at the site of sphincterotomy, but there's also about a 5% to 10% risk of something called acute pancreatitis, just because of the closeness of the main pancreatic duct at the major papilla to the bile duct. We know it comes out of the same exit and it is possible to accidentally instrument a pancreas or irritate it. So that is just one of the many causes of pancreatitis or acute pancreatitis specifically. In a broad sense, pancreatitis just means inflammation of the pancreas. Acute episodes, we'll talk about in a second, and chronic in more detail. They're actually quite different in signs and symptoms than the implications. You don't necessarily have to, acute pancreatitis doesn't necessarily lead to chronic pancreatitis, though it can, and people can have chronic pancreatitis without ever having acute pancreatitis. So acute pancreatitis is an isolated episode of acute inflammation. In the past, we largely attributed it to an accidental activation of the digestive enzymes of the pancreas within the gland itself, damaging it. We know that it's more complex than that now. It can range from mild severity to something that will put you in the ICU to even death. It's associated with severe onset abdominal pain in the center of your abdomen going all the way through your back. I've had people tell me it's worse than giving birth to a child without epidural. I think we're a little short on time, so I'll try to move on a little more quickly. But as we mentioned, there's a broad range of signs and symptoms, and people can die from complications of this. Gallstones and alcohol are the number one biggest causes, but we have another list here. Diagnosis is based on three criteria. You have to have the symptoms that we described before. Lipase or amylase greater than two to three, the upper limit of normal. Leps vary very much in what the upper limit of normal is, so the number can range broadly. And then either appropriate imaging findings. Two out of the three is diagnostic criteria. Treatment is mostly supportive. Unfortunately, we don't have good tools once it's started. We just have to get people through the acute inflammation and manage any of the complications thereafter. Gallstone pancreatitis is one of the few causes where there may be a role for ERCP as an obstructing stone. It does have to come out at some point. Chronic pancreatitis implies that there's some kind of long-term scarring and injury to the pancreas, either from repeated isolated episodes or insults like repeat acute pancreatitis. Or like I mentioned before, you don't have to have acute pancreatitis to get chronic pancreatitis. Or if you, for example, someone who's an alcoholic and chronically injuring their pancreas, they can have chronic pancreatitis and be unable to perform those main exocrine and endocrine functions that we discussed. Some science, this is by no means like every single diagnostic criteria, but things like atrophy or if the gland looks shrunken or if there's calcifications or a very dilated or torturous main pancreatic duct are some clues on imaging that this person may have chronic pancreatitis. Treatment, we need to stop whatever it is that's causing it, even if it's not alcohol-related. We usually recommend that people stop drinking just to prevent any further progression. Smoking is the other patient-controlled factor that can significantly impact pancreatic health long-term. If somebody has exocrine pancreatic insufficiency, then we replace them. Not everybody has over symptoms such as abdominal pain. The clinical presentation is very variable, but if somebody does have pain or weight loss or difficulty eating, then our management would be adjusted accordingly to manage those symptoms. Pancreatic cancer, we'll discuss because it is such a high morbidity, mortality cancer. The main type that we usually think of when we think of pancreatic cancer is adenocarcinoma, which has the worst prognosis. Neuroendocrine tumor, and there are some rare tumors that are sort of outside of the scope of this talk, but their behavior varies based on the pathology. There's a 6% five-year survival for pancreatic cancer. We just don't have great curative treatments for it right now. And diagnosis can be kind of challenging because the organ is so close to the back. Risk factors include having chronic pancreatitis if someone's a smoker, family history. And then symptoms, these often don't appear until the tumor has significantly progressed just because of the location. Painless jaundice is one of the most common symptoms that we see in patients. Painless jaundice is one of the big red flags. Endoscopic ultrasound is the mainstay for diagnosis of pancreatic cancer. Usually our role in GI is to diagnose and perform any palliative treatments. If people get complications from pancreatic cancer as it progresses. Standard of care treatment is right now chemotherapy before surgery. If someone is a surgical candidate or palliative chemotherapy alone. And finally, the last few slides are on managing biliary obstruction. This is mostly relevant to tumors in the head of the pancreas just because of anatomical reasons that it can cause obstruction, jaundice. We usually place a stent or a prosthesis to help relieve that pressure. One, because of symptoms, people can get intractable itching or pruritus just from the bilirubin buildup in their skin. Second, people don't like to look yellow. It's an extremely obvious manifestation to just a random person walking by that they're ill and it is a quality of life issue. And finally, to facilitate chemotherapy.

liver diseases

cirrhosis

hepatocellular carcinoma

liver transplantation

diagnostic tools

non-alcoholic fatty liver disease

hepatitis

pancreatitis