9 ABSITE_Pancreas_edited
[00:00:00] 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
[00:01:00] 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 [00:02:00] 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 [00:03:00] 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 [00:04:00] 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 [00:05:00]
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, [00:06:00] 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 [00:07:00] 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, [00:08:00] 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 [00:09:00] 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[00:10:00] 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.[00:11:00]

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 [00:12:00] 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,
[00:13:00] 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[00:14:00] 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. [00:15:00] 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 [00:16:00] 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 [00:17:00] 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 [00:18:00] 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 [00:19:00]
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 [00:20:00] 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.[00:21:00] 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 [00:22:00] 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, [00:23:00] 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 [00:24:00] 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 [00:25:00] 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 [00:26:00] 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. [00:27:00] 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.[00:28:00]

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[00:29:00] 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
[00:30:00] 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[00:31:00] 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 [00:32:00] 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 [00:33:00] 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 [00:34:00] 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,[00:35:00] 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[00:36:00]
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 [00:37:00] 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[00:38:00] 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 [00:39:00] 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 [00:40:00]
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 [00:41:00] 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 [00:42:00] 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.