9 ABSITE_Pancreas_edited

All right. Welcome back to behind the nice ab site review topic today is pancreas. So as always, we'll start with the anatomy and let's go with the vascular supply. So Kevin arterial supply to the pancreas. Walk us through it. Yes. We'll split it into the three main parts of the pancreas, head, body, and tail. The head is supplied by the pancreatic echo duodenal arteries. And so you have the superior and the inferior. The superior comes off the gastro duodenal artery and the inferior comes off the SMA. Now let's go to the body. So you have you have the greater inferior and dorsal arteries that branch off the splenic artery. The splenic artery runs just superior to the pancreas and it generally kind of has a curly Q pattern throughout the superior aspect of the pancreas. And then we'll go to the tail. The splenic artery feeds the tail of the pancreas through its gastro papilloic and caudal pancreatic arteries. Okay, how about the venous vasculature? Yeah, so you have your splenic vein which kind of runs directly posterior to the pancreas. And that's the, the main outflow and then the

SMV converges of the splenic vein behind the pancreatic neck to form the portal vein. Okay. So John one pearl when it comes to anatomy of the pancreas is the congenital variant of a pancreatic divism. You may see this sometimes on the test. What is pancreatic divism? How do you diagnose it and how do you treat it? Yeah, this is the failed fusion of the pancreatic ducts at eight weeks gestation. The majority of the pancreas is drained by the Dr. Santorini via the minor papilla, specifically in pancreativism. The majority of patients will be asymptomatic, while a small subset will develop pancreatitis or other idiopathic postprandial pancreobiliary symptoms. We diagnosed it with an MRCP with a secretin test. And the treatment is ERCP with sphincteroplasty of the minor papilla. Yeah. So in most cases that's going to be asymptomatic, but for those symptomatic patients, yeah, that's, that's the, what you do to work it up and then tell you treated at ERCP, sphincteroplasty of the minor papilla. So let's move on to acute

pancreatitis. Most common causes are alcohol and gallstones. Kevin, how do we approach, we talked a little bit about this in the Bout of Biliary, but how do we approach gallstone pancreatitis? Yeah, so you need to make sure the duct is clear, whether ERCP versus IOC followed by cholecystectomy during the same admission. Yeah, so these have a high rate of recurrence, which is the reason for the recommendation for cholecystectomy during that same admission. Most of the stones will pass, so it's rare to need an ERCP. Because the stones will pass but certainly need to evaluate that duct in, in some way, either MRCP or an IOC drainer, lap coli, and if there's, you know, persistent blockage, then you'll need that ERCP. Pancreatitis can result in a pseudocyst, so, so John, what can you tell us about pseudocysts? Yeah, most of these will resolve spontaneously, and we typically manage these expectantly for at least six weeks, and ideally up to three months. Because we want to develop a mature wall of the Pseudocyst. We do consider

intervention if it's greater than 6 centimeters or symptomatic, so it compresses symptoms around that area, so unable to eat, without pain, or oral intolerance. It's often associated with a pancreatic duct abnormality, and it will need an ERCP or an MRCP prior to intervention. We would attempt endoscopic pancreatic stenting to address the duct abnormality. Okay, so how about if a patient comes in with, you know, persistent abdominal pain, PO intolerance, they have nausea, vomiting, and other symptoms after an episode of pancreatitis what would you need to do? We typically get a CT scan to confirm contained fluid collection, and then we would also consider imaging of the pancreatic duct through MRCP. There's something called the revised Atlanta classification. So it helps us distinguish these different types of peripancreatic fluid collections versus Pseudocyst, walled off necrosis How does that, how's that all parsed out? So you can divide it into two parts, so non

necrotizing and necrotizing and there's also a timeline associated with it So less than four weeks or greater than four weeks. So in non necrotizing fluid collection that's less than four weeks old We call that an acute peripancreatic fluid collection. A non necrotizing fluid collection that's greater than four weeks old, then we call that a pseudocyst. If it's a necrotizing collection that's less than four weeks old, we call that an acute necrotic collection. And if it's greater than four weeks old and it's a necrotizing infection, then we call it a walled off necrosis. So yeah, our goal with these patients is to really convert this into a chronic problem. So we don't want to intervene on those acute peripancreatic fluid collections or those acute necrotic collections. But if we can get those patients to a point where the the pseudocyst or the walled off necrosis is well developed, with a well developed wall, then we have some options if they're symptomatic and do need intervention and typically your options are endoscopic, so endoscopic transluminal

drainage. That's kind of becoming the standard versus a laparoscopic versus an open cis gastronomy. So John, when you were walking through the revised Atlanta classification, you broke, you broke it down, this pancreatitis between non necrotizing and necrotizing. So let's talk a little bit more about necrotizing pancreatitis. These patients can be very sick. They have severe pancreatitis. And you see necrotic portions or non vascularized portions of the pancreas under CT scan. So, a question that often comes up is, these patients are sick and, and necrotizing pancreatitis, do, do they need antibiotics? Yeah, really only if they have signs of infection do they need antibiotics. And what's, like, what signs are you looking for? Yeah, so clinically you'd see, you know, the patient be febrile, they would have leukocytosis. On imaging, you'd be concerned if there would be gas within the fluid collection. And in, in this situation, before you start antibiotics, if they're, of course, if they're sick, you're going to start antibiotics immediately,

but you'd also want to consider doing image guided fine needle aspiration to confirm the growth of organisms and you also get a culture of the organisms. Yeah. So I would agree with that. If the patient's really sick. And, and you suspect it. A lot of times you'll empirically start an antibiotics, but of course you can do an f and a to, you know, confirm that. What, when you talk about antibiotics, which antibiotic is usually the go-to that is good penetrance of the pancreas. Yeah. Imipenem is the best for this. Okay. Okay, John? So when I was a resident, we talked a lot about necrotizing pancreatitis and pancreatic necrosectomies. Which were very morbid procedures. So there's been a trend to more minimally invasive approaches to necrotizing pancreatitis. What is that? And tell me a little bit more about it. Yeah. So now most of these types of problems are approached with a step up approach and it's basically an algorithm for infected pancreatic necrosis that entails starting with the least invasive intervention and escalating as necessary. So, first thing would be, you know, admit the patient, put them in the

ICU, resuscitation, nutritious supportive care. And then additionally would be the antibiotics and then consider percutaneous drainage of these areas. And when that drainage drops because of this area, this, these fluid collections tend to get very thick and it's hard to drain them, then we upsize the drains. And this is to allow more and more drainage and we continue to advance our aggressiveness as time goes on. And the last kind of step of the step up approach would be a video assisted retroperitoneal drainage. So, what are some of the reasons that we would, you know, step up to an operative intervention? That would be failure of conservative management and and non operative interventions for infection. So if the patient continues to deteriorate, or things aren't going in the right direction, or if they're stalling, we would step it up. Additionally, if they had symptomatic sterile necrosis, and this one might be evident by PO intolerance, nausea, chronic low grade fevers, and lethargy. And then lastly, symptomatic Waldorf necrosis,

same kind of deal, you would have PO intolerance, abdominal pain, would be reason to continue to step up the your interventions. Yeah, and you know, like I said, historically open pancreatic necrosectomies were were done and then, and they tend to be very morbid with a high mortality. So there's been a trend to, to, you know, try and treat these patients non operatively and, and really, you know, to go from least to more invasive as slowly as possible in these patients and delay operative intervention for as long as possible, ideally at least four to six weeks. Okay. Thank you. In order to allow for medical and nutritional optimization and for that that fluid collection to, to really mature. All right, so that's our acute pancreatitis or necrotizing pancreatitis. Now, what about chronic pancreatitis? What are what are some causes of chronic pancreatitis, Kevin? Yeah, so long standing alcohol abuse, biliary tract disease, autoimmune or sometimes idiopathic. Okay, and what do we see with autoimmune pancreatitis? Yeah, they have

the increased IgG4 Plasma cells. Okay. And, and what do, how do patients present with chronic pancreatitis? Yeah, they'll have persistent abdominal pain, weight loss, pancreatic insufficiency, which results in malabsorption, ssa, and diabetes. And they'll have a history of more bouts of pancreatitis in the past. Okay. How do we image these patients and what do we see on imaging? Yeah, CT is really helpful here. It can help demonstrate that there's fibrosis, atrophy, and calcifications of the pancreas. Yeah, okay. And so we know chronic pancreatitis it's a recurring theme. Chronic inflammation increases the risk for malignancy. So chronic pancreatitis does increase the risk of pancreatic cancer. So, John, we'll go to you now. So, what are some management options for chronic pancreatitis? Let's start with non operative management. Yeah, so non operatively, management, obviously not drinking alcohol. And pancreatic enzyme replacement would be good options. Okay, perfect. Yeah, so it's, it's symptom

control, trying to replace those pancreatic enzymes, reverse any known causes of the pancreatitis. Now, let's say Kevin, what, what are some operative? options for chronic pancreatitis. I was like, they're not great ones, but what, what are some? Yeah, I've never been involved in these cases, but two main categories for the operative pancreatitis. You want to either decompress the obstructed ductal system or you want to resect the disease tissue. Okay. So yeah, there's a variety of operations available, but the, you know, the specific ones for chronic pancreatitis management for the ab side would be, you know, the, the pusto, the, the beggar procedure and the fry procedure. And what's a pustote procedure? Yeah, this is the one that kind of sticks out to me most commonly, at least from what I can tell, is the longitudinal pancreatic jejunostomy. Perfect. Longitudinal pancreatic jejunostomy. The beggar procedure? So this one, you resect the pancreatic head up to the wall of the duodenum with either an end to end or side to side pancreatic jejunostomy.

So this is a duodenum preserving pancreatic head resection. Okay, and the fray procedure? So this is a lateral longitudinal pancreatic oogygenostomy with an excavation of the pancreatic head. So you core out the head of the pancreas, but avoid pancreatic transection that is required with the bager procedure. Okay, great. So, which procedure we choose really depends on the disease morphology, and this actually is pretty high yield and testable for the ab side. So like, Kevin, let's say we have a dilated pancreatic duct over six millimeters and the pancreatic head looks normal. So which procedure would you choose there? Yeah, in this situation, you do the Poustou, also known as the longitudinal pancreatic jejunostomy. Right. So normal pancreatic head, dilated pancreatic duct, Poustou procedure. So what if we have, you know, dominant disease in the pancreatic head? Let's what are your options there? So it kind of depends on whether you have duct dilation or not. Without duct dilation, the Baeger procedure is the better

one. With duct dilation, the Frey procedure. Okay, so let's just remind people again what the Baeger procedure is. So now we're dominant disease in the pancreatic head. Without duct dilation, you're doing the bigger procedure, which is... So it's the resection of the pancreatic head up to the wall of the duodenum with an either end to end or side to side pancreatic ojiginosomy. Okay, so a duodenum preserving pancreatic head resection. So now with duct dilation. It's a dominant disease in the head of the pancreas. Duct dilation, you said you do the fray procedure, so what is that? That's the lateral longitudinal pancreatic ojiginosomy with an excavation of the pancreatic head. Okay, so you core out the, the head of the pancreas, but avoid the pancreatic transection. Okay. So what about distal pancreatic duct stricture and you have a normal pancreatic head, whatcha gonna do there? So in this situation, it lends itself to a distal pancreatectomy. Okay. And then sometimes we hear about this thing called minimal change, chronic pancreatitis. What, what's, what's the deal there? Yeah, so this is also known as the small duct chronic pancreatitis. And, and in this situation,

resection and or drainage will not help. So you really have two options. You can do the innervation operation. Or, this is one of the few situations that they recommend a total pancreatectomy. Okay, what's an important contraindication for, for, for that? Yeah, if there's any evidence of neoplasm with malignant potential. Such as? PNET or IPMN. Okay, good, good. Okay, so, John, let's go back to you. Let's start, let's go over some cystic neoplasms of the pancreas. So, very high yield, these will always show up in one form or another. So a lot of these are found incidentally abdominal imaging, say you, when you're trauma patients and they, on their pan scan, they see a cystic neoplasm in the pancreas and what's further workup. Yeah. Like you said, a CT is going to find these usually off the, usually first, and then we would further work them up with the MRCP to really get a better characterization of the cystic neoplasm and its relationship to the duct anatomy. Endoscopic ultrasound can also be used to better characterize the cysts and allows

for aspiration and for fluid analysis of what's in the cyst. Okay, so what's our differential? So there's three main types of cystic neoplasms of the pancreas. So you have serous cyst adenoma, you have mucinous cystic neoplasm, Or you have neoplasms. Okay, so let's, let's tackle those and kind of unpack those a little bit. So, with serous cystadenoma, first off, is that a benign or a malignant thing? It's benign. Okay. So, you mentioned we'd get an EOS and we'd get a fluid aspiration. So, if we did a cyst fluid analysis of a serous cystadenoma, what would you see? You would have low CEA and low amylase. Okay. Low CEA low amylase and ace cystadenoma. Would you see any mucin? No. Okay. What other distinct characteristics would you, would you see? So you may see it's positive for periodic acid shift staining. Okay. And what's the, so we, let's say we diagnose it with our EUS, what's the management of a cist? Adenoma.

So we resect these if they're symptomatic. Oh, or greater than four centimeters, or if they grow on surveillance studies going forward. Sure, okay, so they're benign, so as long as they're stable and they're, you know, small and there are no worrisome features, you can leave them alone unless they're symptomatic. So, the other thing you said was a mucinous cystic neoplasm. So, benign or malignant? They have malignant potential. Okay, they're they're have malignant potential. It's a good way to put that So, what would you see on the fluid analysis for a mucin a cystic neoplasm? You have potentially high levels of CEA but low amylase levels Okay, so high CEA low amylase and that's again in contrast to serous adenoma, which had low CEA and low amylase Is, is there a mucin? It's in the name, so there's mucin, right? Yes. Okay. And what else would you see that's a distinct characteristic on that analysis? Yeah, on histology, you might see ovarian type stroma, which I've seen come up on a test before. Absolutely, ovarian type stroma. So, management of mucinous cystic neoplasms of the pancreas? Yeah, we

want to resect all mucinous cystic neoplasms, especially in patients that are surgically fit. Okay, great. So the last one that you mentioned there was the introductal papillary mucinous neoplasm, IPMN. Benign or malignant? Malignant potential. Okay, so, that's cyst fluid analysis. You'd have increased CEA and also increased amylase, right? Both CEA and amylase are increased. Is there mucin? Yes. Okay. Now we're going to, the management of IPM ends is a little more convoluted than serious cyst adenomas and mystic cystic neoplasm. So we're going to. Do a little bit of a deeper dive on IPMNs. So a lot depends on how they're classified. So Kevin, What's the different types of IPMNs we might encounter? Yeah, so you have the main duct IPMN, you have the nix duct IPMN, and you have the branch duct IPMN. Okay, so let's let's address those kind of one by one. So what can you tell me about main duct IPMN. Yeah, so you'll have diffuse or segmental

dilation of the main pancreatic duct greater than or equal to 5 millimeters. Okay, and what, so these are a little bit higher risk of malignancy the main duct IPMNs, so they have higher risk of malignancy. As you say, diffuse segmental or segmental dilation of the main duct over 5 millimeters. There is something we talked about that's a pathopneumonic finding that you would see on, on endoscopy. Do you know what I'm getting at? Yeah, that's the patchless fish mouth with mucin secretions on endoscopic visualization of the ampulla. Perfect. Okay. And management? This, they require surgical resection. Yeah, because of that risk of malignancy, main duct IPM ends, surgical resection. So Jason, I know you have a slightly different opinion than what some of the techs say, so what do you think it looks like on endoscopic visualization of the ampulla? Oh yeah, so we've actually been in arguments about this. I've always said it's a fish eye, and John says it's a fish mouth. We've looked at pictures, I still think it looks like a fish eye, he thinks it looks like a fish mouth. Interestingly, we

found publications of NIH funded studies that call it both either a fish eye or fish mouth, so I don't know. You, everybody should Google it and make your own assessment of whether it looks like a fish mouth or a fish eye. Alright John, so the next classification of IPMN is that mixed type IPMN. What, what does that mean? Yeah, so that's a pancreatic cyst associated with main pancreatic duct dilation. It's a combination of branched duct and main duct IPMNs. Okay, so there is a main duct component, right? So, it's reasonable to think that that also has a higher risk of malignancy. So, what's the management of those mixed type IPMNs? So, they do have a higher risk of malignancy. So, the management is surgical resection. Okay, great. So, finally let's talk about branched duct IPMN. So, how do we define a branched duct IPMN, Kevin? Is this a pancreatic cyst with a greater than five millimeter in diameter that communicates with the main pancreatic duct? Okay. So this has a lower risk. So there's no main duct components of the

branch duct. IPM has had a lower risk of malignancy, which makes the management a little bit more complicated. So there are multiple guidelines that help guide management. The most. popular and cited one is the Foucault consensus guidelines. So, we already talked about the, the role of endoscopic ultrasound and and cyst aspiration for those that are concerning, have concerning features on CT or MRI. So, John, how, how do we manage these, these branch ducts, IPMNs? Yeah, the decision to resect these is based on the cyst characteristics. And you also gotta take into account the patient's fitness for surgery and risk tolerance. Okay, so let's say we have a surgically fit patient. What are an indication for, for resection for a branched adduct IPMN? So this is a high risk stigmata. It's an enhancing myrtle nodule greater than five millimeters. A main pancreatic duct greater than 10 millimeters or obstructive jaundice. Okay, so if you have those high risk stigmata against enhancing murial nodule

over 5 millimeters, main duct over 10 millimeters or obstructive jaundice, that's an indication for resection in a branch duct IPMN. Now what are worrisome features and, and, and what do we do with those? That's where you have a cyst size greater than 3 centimeters. It's thickened or it has an enhancing cyst wall. It also may also have an enhancing neural nodule less than five millimeters, lymphadenopathy, a main pancreatic duct five to nine millimeters, or an abrupt change in main pancreatic duct size with atrophy of the distal pancreas, and also a cyst growth rate of greater than five millimeters over two years and acute pancreatitis caused by the cyst. Sure. And of course, also if you have any suspicious FNA cytology results. So those are considered worrisome features. So there's high risk stigmata and there's worrisome features. So high risk stigmata is a clear indication for surgery. You would want to consider resection in the presence of any of those worrisome features. So in the absence of those things, you can typically survey these.

But for the test, if you have any of those stigmata or the worrisome features, the recommendation would be resection. So one way to help memorize these is that you can. Narrow down the differential diagnosis based on age. So the popular way of memorizing, so a daughter has solid pseudopopular tumor, a mother has mucinous cystic neoplasm, and a grandmother has serocyst adenoma. It's just based off of age. Okay, great. So let's move on then. We're moving away from our cystic neoplasms and let's now go into neuro endocrine tumors of the pancreas, peanuts and other very tested neoplasm of the pancreas. So, you know, these comprise one to 2 percent of pancreatic neoplasms are frequently non functional. They can also secrete a variety of bioactive peptides to include gastrin, glucagon, somatostatin, insulin, VIP. That result in characteristic clinical presentations. So Kevin, what let's first talk about

Non functional peanuts tell me a little bit about their malignant potential their most common location The symptoms and the management of a non functional peanut Yeah, so they're most commonly malignant 60 to 90 percent are malignant the most common location to find these is in the head of the pancreas they're typically asymptomatic. Most are discovered late and are large at the time of diagnosis with high metastases. And patients with local regional disease can undergo resection for these. Okay. Now let's go through our functional PNETs. Let's, John, let's start with insulinoma. Tell me everything you know about insulinomas. It's the most common functional PNET. Benign is the most common, 90 percent of these are benign. The most common location within the pancreas is throughout the whole thing. The most common bioactive peptide is insulin secreted by the beta cells. The symptoms you would see with an insuloma is called the Whipple Triad. So you have fasting,

hypoglycemia, and you might have neuroglycopenic symptoms, such as confusion, combative seizures, visual changes, and loss of consciousness. And all these symptoms are relieved with the administration of glucose. Yeah, you'll see, they'll give you that patient on the exam, the Whipple Triad, and then they'll have the relief of symptoms with glucose. As you said, these are benign, they're found throughout the pancreas. How do you, how do you work them up? It's a biochemical diagnosis and you can confirm with tests. If these criteria are met, We can then perform localization studies. So, the biochemical criteria are symptoms with plasma glucose less than 55, insulin greater than 18, C peptide greater than 0. 6, pro insulin greater than 5, beta hydroxybutyrate less than 2. 7, And an increase in plasma glucose of at least 25 after administration of glucagon. Okay. I wouldn't spend a lot of time committing all those specific numbers to memory, but certainly

the clinical presentation of that Whipple triad is something you're likely to see on the exam. You talked about localization studies. What are those? Yeah, most people would start with triphasic CT or MRI. You can also do an endoscopic ultrasound. If you're unable to localize off those modalities, you can do a selective intra arterial calcium injection with hepatic venous sampling for insulin. Perfect. What about you know, for a lot of these or that we're gonna talk about, we'll, we'll hear about a, a somatostatin scan. Can you do that with the insulinoma? It is not effective for insulinoma, right? So this is the one you cannot, that is not effective. So somatostatin scan not good for an insulinoma. How about management of an insulinoma? So, it depends on the location within the pancreas or suspicion for malignancy, and also if there's other tumors around. If you're suspicious for malignancy, this requires a formal resection. Solitary, benign appearing tumors can be true with enucleation if they're

less than two centimeters in size and greater than two millimeters away from the main pancreatic duct. Right. Yeah. So small solitary ones, enucleation insufficient for malignancy or, you know, multifocal, you know, large, involving pancreas, back duct, all those things need formal resection. Okay. Great. So next one we're gonna tackle is gastronoma. So Kevin, all those things we talked about, their malignant potential, where are they, how do they act, how do they present, gastronoma, go. Yeah, I keep getting the malignant ones. Gastronoma is mostly malignant, 60 90%. But you will find these in the gastronoma triangle, so The triangle is the junction of the cystic duct and the common bile duct, the junction of the second and third portions of the duodenum, and the junctions of the head and neck of the body of the pancreas. And so we have a good picture of this in the book if you need to see this. The bioactive peptide that you'll find with this is obviously gastrin which stimulates acid secretion from parietal cells. The typical symptoms these patients will have will be abdominal pain, diarrhea, and weight loss in the

presence of peptic ulcerative disease. Okay. Yeah, exactly. Abdominal pain, diarrhea, and weight loss. Diarrhea with excess gastrin. That comes up frequently, I've seen. What about workup? So with this, you'll see an elevated fasting serum gastrin level and the setting of a low gastric pH or high basal acid output. You want to make sure you stop PPIs or H2 blockers in patients for at least two weeks prior to testing gastrin levels as these medications will raise gastrin levels. And if the fasting gastrin level is greater than 1, 000, This is diagnostic. If the fasting gastrin level is less than a thousand, but still elevated, you need to do a secretin stimulation test. A gastronomal will have a paradoxical effect. From Secretin Administration, the gastrin level increased greater than 200 with Secretin is diagnostic. Yeah, and those are important numbers to remember, because those are the ones you might actually see. So, gastrin over 1000, that's diagnostic, you're done, you've made the diagnosis. If it's less than 1000, you do that secretin stimulation test, and you should see a rise of over 200 with that test.

Okay, we've made the diagnosis, now we need to find it. So what are our localization studies? Yeah, I would definitely stick with secr how do you say it? Secretin. Secretin rather than my secretin. Okay. Back to localization studies. Triphasic CT or MRI. And also this is one of the ones that somatostatin receptor scintigraphy works. And then, of course, endoscopic ultrasound is helpful for this. This is one of the ones that a selective intra arterial calcium injection with hepatic venous sampling for gastrin is helpful. And if you're unable to localize any of the above tests exploration with the following maneuvers can be helpful, such as an intraoperative ultrasound, transduodenal palpation, Intraoperative upper endoscopy with transduodenal illumination and then ADU autotomy with palpation. Yeah, and I've seen this show up before where you can't find it in your, you, you, the, the keys are that you look in your gastro triangle and those intraoperative maneuvers that you just mentioned specifically that intraoperative upper EGD with the transduodenal illumination appears to be a, a, a favorite in my experience.

Now, how about management? So if you have a tumor in the duodenal mucosa, you can do enucleation and periduodenal lymph node dissection. If the tumor is in the head of the pancreas, for non invasive tumors less than 5 cm, you can do enucleation with periduodenal lymph node dissection. If it's greater than five centimeters or invasive, you need to do a Whipple. Now, if the tumor is not in the head, but in the body or tailored pancreas, you need to do a distal pancreatectomy. And they should always do a prophylactic cholecystectomy due to the possible need for prolonged somatostatin therapy. Yeah, great. And that's a good thing to remember for, for any of these, or where you're going to have. adjuvant somatostatin therapy that you need to do that prophylactic cholecystectomy. Okay, John, back to you. Now we're on to glucagonoma. So glucagonoma, malignant potential, where is it located? How does it act? Yeah, so these are mostly malignant, about 90 percent of them are malignant. The most common location within the pancreas is in the tail of the pancreas. The peptide that you want to worry about with this one is glucagon. It

acts on hepatocytes and adipose tissue to increase gluconeogenesis. The symptoms related to glucagoma are the four D's, dermatitis, diabetes, depression, and DVT. It has a characteristic skin rash, the necrolytic migratory erythema. DVTs are caused by a factor X like antigen secreted by the tumor. The workup with this you will find, within the workup, you will find glucose intolerance. And you'd have fasting glucagon levels between 1, 000 and 5, 000. There are some localization studies we can use to track down glucanomas. So, like most of them, you do a triphasic CT or MRI. You can track these down with somatostatin receptor scintography. Endoscopic ultrasound is also a good option. And you can do selective visceral angiography. We manage glucanomas with resection of, resection with regional lymphadenectomy. Plus a cholecystectomy. All right, Kevin, same deal. Somatostatinoma. What's the malignancy

rates? Where is it located? What's the bioactive peptides? Yeah, so, I just keep getting the malignant ones, so the somatostatinoma is mostly malignant. It's mostly located within the head of the pancreas, but it can also be found in the duodenum. The bioactive peptide is, believe it or not, somatostatin. Broad spectrum of inhibitory activity within the GI tract. So it's kind of the stop sign for everything in the GI tract. The symptoms with this are cholecystitis, diabetes mellitus, malabsorption and steatorrhea. The localization studies are very similar to what you've heard recently. Triphasic the somatostatin receptor scintigraphy, The endoscopic ultrasound and then the selector of arteriography management with this is resection of the regional lymphagnectomy and Cholecystectomy just like the last one no enucleation due to the high malignant potential so both this and glucagonoma They're too highly malignant. You cannot do an enucleation Okay, John, how about a VIP Noma? So these are mostly

malignant the most common location within the pancreas or throughout the pancreas body or tail . They have also have extra pancreatic locations such as the adrenal retroperitoneum mediastinum. The bioactive peptide, obviously is VIP. This is a neuropeptide that stimulates secretion of fluids and electrolytes into the lumen. It also inhibits gastric acid secretion. The symptoms are the WDHA syndrome, watery diarrhea, hypokalemia, and a clerid. The workup is elevated fasting VIP levels with diarrhea. We can localize these, similar to the other ones, using triphasic CT or MRI. You can also use the somatosentin receptor scintography endoscopic ultrasound, as well as selective arteriography. We manage VIPomas with resection with regional lymphadenectomy and cholecystectomy. We also cannot

enucleate these due to the high malignant potential similar to the last two. Great, great review. So let's do some just some word associations. Okay, so some most commons. Okay, so most common pancreatic tumor? Non functional peanut. Non functional peanut. How about most common functional peanut? Insulinoma. Yes, you have to be careful the way they ask you. So they may ask you, you know, what's the most common neuroendocrine tumor and the answer is non functional, but they ask you what's the most common functional neuroendocrine tumor of the pancreas, it's insulinoma. Be very careful with the wording of that question. How about the most common tumor associated with an MEN1 syndrome? Yeah, so that is kind of all peanuts. It can be functional or non functional. Okay, great. And if it is a functional one with MEN? I think that's gastronoma. Yeah, correct. Okay. So, let's move on now to pancreatic adenocarcinoma. John, what are some risk factors for pancreatic

adenocarcinoma? Yeah, very similar to most cancers. So, cigarette smoking, heavy alcohol use. chronic pancreatitis, obesity, exposure, and also exposure to chemicals and heavy metals. Okay. Okay. How do we image these? So pancreatic protocol CT or MRI is the best way to see a pancreatic endocarcinoma. And before we get there, I guess, how do, how do these patients present? So the classic presentation is painless jaundice. Perfect. Okay. So yeah, as you mentioned these get worked out with a pancreatic protocol CT or MRI. And you also want to complete your staging with a CT of the chest and pelvis in addition to the abdomen. What about John, what about the role of staging laparoscopy? Yeah, it's quite controversial. I did this in the institution I trained. It's used routinely by some, selected by others, but usually only in patients at high risk for disseminated disease such as borderline resectable, high CA 19 9s, tumors greater than 3 centimeters, or large regional nodes. So what's the role of

biopsy with a suspected pancreatic adenocarcinoma? Yeah, so these tumors don't need pathologic diagnosis before resection. But it is required prior to initiation of any chemotherapy such as neoadjuvant or definitive chemotherapy for unresectable tumors Right. So if you're gonna if neoadjuvant therapy is indicated Obviously your medical oncologist is going to want tissue before initiating that therapy But if you're going straight to resection then a biopsy is not is not absolutely necessary Okay, you know we mentioned that these patients present with painless jaundice. So do they need stents for biliary drainage? Or what is the role of biliary drainage, Kevin? Yes. So there's no effect on survival, but it is associated with increased wound infection rates, surprisingly. So you can consider drainage only if the patient presents with significant pruritus, cholangitis, and or coagulopathy. Okay. What about for patients? Yeah. So I'll agree with you. People are trying to avoid stents if possible,

but if patients have parietis, if they have coagulopathy, severely elevated bilirubin, they may need preoperative drainage. So what if your patient is, you know, is a jaundice and they need neoadjuvant therapy, would you drain them? Yeah. In that situation, I would drain them. Okay. What kind of stent? So you use a self expanding metal stent are preferred because they're easy to place without dilation. They have longer patency rates than plastic stents and they do not interfere with the resection. Okay, so John, let's get into now the management or the treatment of of a diagnosed pancreatic adenocarcinoma. So how do we assess a resectability? So yeah, like you said primary surgery is the option for pancreatic adenocarcinoma. We must determine the involvement of both the artery and the vein in these. So, walking through the major blood vessels in the area. For the superior mesenteric artery, for it to be resectable, it can have no contact with the tumor. For it to be borderline, it's less than 180 degrees contact, and locally advanced would be considered greater than 180 degrees

contact. For the celiac artery, for it to be resectable, is no contact with the tumor. And the same deal, borderline is less than 180, locally advanced is greater than 180. For the common hepatic artery, once again, no contact with the tumor to be considered resectable. But borderline is contact without extension to the celiac artery or the common hepatic artery bifurcation. Locally advanced is contact with extension to the celiac artery. or the common hepatic artery bifurcation. Regarding venous involvement for the portal vein in the SMV, for it to be resectable is less than 180 degrees of contact without contour irregularity of the vein. For borderline resectability is greater than 180 degrees of contact or with contact irregularity amenable to resection and reconstruction and locally advanced is greater than 100 degrees of contact. With contour irregularity, not amenable

to resection reconstruction. Obviously these are all surgeon dependent and some surgeons will be more aggressive than others. Yeah. So I think a way of kind of generalizing that, when you think about pancreatic adenocarcinoma is in order for it to be resectable, you have to have no contact with those named main arteries. Borderline is going to be less than 180 degree contact with those, with those arteries. And with regard to the veins for resectable less than 180 for, and borderline would be greater than that, but you can reconstruct those veins as part of the resection. And for those borderlines and locally advanced, those patients are gonna get neoadjuvant therapy and we may be able to convert them to more resectable disease. Now, obviously any distant metastasis will make this disease unrespectable and those patients need definitive chemotherapy. But let's say if respectable respectable John, so what do we do for let's, it's going to depend on where the tumor is located. So for distal respectable tumors, what's the surgery? Yeah. So this is distal

pancreatectomy and splenectomy in these patients. You always combine the two. Yeah, unfortunately these tumors typically present late because the patients still present with obstructive jaundice and then the distal tumors, and so usually are too advanced at the time of diagnosis for resection. But if so, yeah, distal pancreatectomy and splenectomy. And now, now Kevin, what about a pancreatic adenocarcinoma at the head of the pancreas? So this is your classic pancreatic pancreaticoduodenectomy or a Whipple? Yeah. And, and, and like we mentioned before, you know, assess the relationship to those blood vessels, but just keep in mind that the portal vein or the superior mesenteric vein can be resected and reconstructed as part of the resection in order to obtain an R0 resection. Okay. Let's talk a little bit about adjuvant therapy. So recurrence rates are, everybody knows that this is a very. Morbid disease and recurrence rates are high. So every, everyone gets adjuvant therapy. So, John, what is, what is the typical adjuvant therapy for pancreatic adenocarcinoma? Yeah. The, the common one is folfirinox, it's folinic

acid, fluoro, uracil, ran tecan and oxaliplatin. Okay, great. So that wraps up pancreatic adenocarcinoma. Now let's, let's finish it out with some quick hits. So Kevin, we'll go to you. You have a patient with a history of multiple episodes of pancreatitis. Who's now presenting with hematemesis. What's the diagnosis and what's the management? So this is gastric varices from a splenic vein thrombosis. The treatment is a splenectomy. Absolutely nailed it. Okay, so John, you have a patient who presents with multiple branch duct IPMNs on imaging. There are multiple small benign appearing cysts throughout the proximal pancreatic body and a larger dominant one more distally with worrisome features. What do you do with this? Yeah, you want to target the distal lesion. It's okay to leave the smaller ones behind. But they will need surveillance. Right. Don't do a total pancreatectomy or anything crazy. Just go after the one with the worrisome features and survey the rest. Kevin 48 year old patient incidentally diagnosed with a two centimeter branch duct IPMN on abdominal CT patient has microcytic anemia noted on

laboratory workup. What other workup does the patient need? Yeah. So surprisingly this patient actually needs a colonoscopy. IPMN patients have a higher incidence of extra pancreatic malignancies. Yeah. Great. So yeah, don't forget that association. John, what are, what syndromes are associated with peanuts? Yeah. If I want to test, you'd be thinking of MEN1. That's usually multiple peanuts. It can be functional or non functional. They need routine screening with a fasting gastrin, glucagon, VIP, insulin, and chromogranin A levels, as well as yearly imaging. Perfect. Okay. Kevin, what's the most common pancreatic neuroendocrine tumor? Non functional tumors. Right. Non functional. Okay. And, and we said what's the most common functional neuroendocrine tumor? Insulinoma. Insulinoma. Okay. Perfect. John, a patient presents with episodes of fasting, hypoglycemia and dizziness that resolves with glucose administration. The patient's C peptide is low. What's the diagnosis? Yeah, I'm not seeing this come up before. It's exogenous

insulin administration. Exactly. So they're trying to lead you down the path of insulinoma, but the key is that C peptide which is, which is low in this patient. Okay. Kevin medical management of a functional neuroendocrine tumors of the pancreas, of the pancreas. Octreotide, except for insulinomas. Yeah, so octreotide not with insulinomas, and that helps you kind of remember. That What, what scan doesn't work for an insulinoma? Somatostatin A somatostatin scan. Perfect. Okay. John, most common gene mutation associated with hereditary pancreatitis. This is your PR SS one gene. Yep. Another one of those annoying genes that they, people like to ask for whatever reason of a PRSs one is associated with hereditary pancreatitis. Kevin somatic mutations associated with pancreatic adenocarcinoma. So those are your KRAS, your TP53, your CDK N2A, and your SMAD4. Yep, KRAS, TP53, CDK N2A, SMAD4. Most commonly ones tested

there are KRAS. That's the one, if I had to remember just one, that's the one I remember. Okay John biomarkers associated with the pancreatic adenocarcinoma? There are a few, but the most commonly tested one is CA 19 9. Yeah, CA 19 9 is the common one that kind of everybody knows and, and, and tests for. Okay. So, Kevin, so during a Whipple procedure for pancreatic adenocarcinoma, you find a clinically positive lymph node outside of the field of resection. Should you, A, you should leave it alone. Should you perform a regional lymphadenectomy or should you sample the node, but not perform a complete regional lymphadenectomy? So, I'm going to go sample the node, but not perform the complete regional lymphadenectomy. Okay, why did you say that? So it's because nodal metastasis are a marker of systemic disease and removal is unlikely to alter overall survival. So outside of a clinical trial, a regional lymphadenectomy should not be performed during a Whipple. Perfect, you nailed it. Okay, so that's our, our Pinker's review for the ab site. Everybody, thank you for listening.