Acute Pancreatitis

now let's talk about acute pancreatitis so let's first Orange out ourselves with a diagram that I've drawn up here we have the stomach and we know the stomach leads into via the pyloric sphincter of the duodenum which is the first part of the small intestines you can see the duodenum curves and within the curvature of the duodenum that's where our pancreas sits now we have the head of the pancreas the body of the pancreas and then the tail of the pancreas which sits on the surface of the Splane that's what this little guys here this plane now we've also drawn up the liver in the gallbladder because we need to have a look at the ducts associated with the pancreas and also the ducts that are coming from the gallbladder and liver going to the pancreas as well so you've got your hepatic ducts and your cystic duct and then what you've got is the common all of it coming together for the common bile duct so the common bile duct so let's label that now the common bile duct the common bile duct is going to come together with the pancreatic duct and when they come together they form the ampulla of the pancreas or the pancreatic ampulla which then turns into this area here which is the sphincter of Oddi and this is where whatever has been released from the liver and gallbladder and also what's being released from the pancreas he's going to enter the duodenum the question is what's being released from the liver and gallbladder and what's being released from the pancreas well you should know first of all that bile is going to be released from the liver and gallbladder and squirt it into the duodenum why because bile emulsifies fats you're gonna have big globules of fats coming through from the stomach because when you eat a burger for example your mouth or your saliva glands don't produce much lipase this is the enzyme that breaks down fats your stomach does an either which means by the time that fat gets to your small intestines or the duodenum it hasn't really been broken down so it's in these big fat globules we need to break that down first we need to be able to emulsify it to turn it into smaller more manageable pieces of fat that's what bile does it's like detergent it emulsifies it the other thing that happens is that you can see I've drawn these little groups of cells in the pancreas and these groups of cells are called a cenar cells now what a cenar cells do is they release the pancreatic juices what are pancreatic juices pancreatic juices include the enzymes so the molecular scissors that can break down the proteins fats and carbohydrates so this includes proteases amylases and lipase --is proteases break down proteins amylase breaks down carbohydrates lipase breaks down fats now if we look at the protease that have been produced by the pancreatic that are produced by the ACE inner cells within the pancreatic juice these are going to be enzymes such as trypsinogen and chymotrypsin adjure and as you can see they end in OGE and now what that means is when you see the suffix OG en it means that it's the stored and inactive form of that particular molecule so when they're released so when these proteases trypsinogen and Carmo trypsinogen are released from the a sauna cells into these ducts and then squirted from the pancreatic duct through the pancreatic ampulla and into the duodenum they are inactive which means they can't break proteins down so how do they break proteins down well they break proteins down because you've got a group of cells here lining the walls of the duodenum called entero endocrine cells now these inteiro endocrine cells release something called inteiro kinase and what in Tarot kinase does is in Tarot kinase comes along and it chops off this OGE n of trypsin in Tara car nose chops off the OG en of trypsin which means we now of trypsinogen and now what we have is trypsin trypsin is now the active form of this protease and what it cannot do is cleave off the OG en of chymotrypsinogen which means we then have karma trypsin now what we have are some activated protein proteases that can break down the proteins here in the duodenum the whole reason why we have to go through this step here on this stepwise process is because if we release trips in itself and karma trypsin itself inside the pancreas it's going to digest auto digest the pancreas itself now if this happens and we get auto digestion of the pancreas due to the enzymes released by the pancreas this can result in an inflammatory event that can cause tissue damage and other localized complications this is the definition of acute pancreatitis so I'll say that again acute pancreatitis is when you have the auto digestion of the pancreas by pancreatic enzymes that result in inflammation and inflammatory cascades that can further result in tissue damage of the pancreas and also tissue damage of other localized areas that is acute pancreatitis now what we need to talk about are the causes of acute pancreatitis meaning how do we get these enzymes activated and destroying this tissue in the pancreas now if we have a look at the incidence of acute pancreatitis especially within Western countries so that's a look at the incidence what you'll find is it's around about 5 to 50 people per 100,000 are affected with acute pancreatitis now that's quite a large number five in every 105 to 50 in every 100,000 people and what you'll probably also find is that the mild cases of acute pancreatitis actually go unreported as well so this number may actually be even higher if we look at the mortality so the rate of death well the rate of death is usually between 5 to 10 percent of individuals with acute pancreatitis die from it but if it's severe so you can have mild you can have moderately severe and you can have severe if you have a severe case that mortality rate can even be upwards of about 30% so this is something that really needs to be looked at and addressed very quickly what about when we have a look at what's causing remember I said to you that when we look at what's causing acute pancreatitis we're going to have the release of these enzymes it's going to break down the pancreas itself now what can cause this well two main things one is a sana cell degeneration and the other thing so remember if the ACE and ourselves are degenerating they're going to be just releasing their enzymes within the tissue itself and these enzymes can be activated and break the tissue down or it can be due to ductal obstructions now what do I mean by ductal obstructions well what if for example the pancreatic duct was blocked so what if there was something here blocking the pancreatic duct or what if something was blocking the ampulla of the pancreas or what if something was blocking the sphincter of Oddi at the pancreas well all these things would result in a backlog or increased accumulation of these pancreatic enzymes upstream of the blockage which means they will accumulate increase their likelihood of being activated and then again Auto digestion of the pancreas itself so these are the two most common causes of acute pancreatitis but we need to know what actually causes those things to occur the two most common causes of acute pancreatitis that causes again a sauna so degeneration and ductal obstruction includes for a sauna so degeneration it's alcohol and for ductal obstruction it's gall stones now gall stones are also known as cholelithiasis okay I'll call it off ices so these are gall stones now gall stones let's first have a look at the gall stones and the ductal obstruction we know that gall stones are going to be produced by the gall bladder liver produces bile stores it in the gall bladder and if you have an abundance of cholesterol within this gall bladder it can promote the formation of gall stones these Kali Lilith Isis so these gall stones can block any aspect of these ducts so they can block the cystic duct for example they can block the bile duct but think about it if you're a blood bath cystic or bile duct it's not really going to affect the release of the pancreatic juices so that means that large gall stones have less of an effect on pancreas on acute pancreatitis than the smaller gall stones so for example usually it's gall stones less than five millimeters in diameter that are more commonly associated with acute pancreatitis and the reason being is so that it can go down here and block at least the pancreatic duct or the ampulla or the sphincter for gall stones this is the most common cause of acute pancreatitis so for gall stones it's between 40 and 70 percent of acute pancreatitis cases are due to gall stones when we look at alcohol it's between 25 to 35 percent of cases and due to alcohol but in actual fact if you were to break it up into males and females the most common cause for men alcohol most common cause for females or women gall stones okay so again two most common causes of acute pancreatitis gall stones between 40 and 70 percent of all acute pancreatitis cases but the most common cause for women and alcohol between 25 and 35 percent of all cases but also the most common cause for men so we spoke about gall stones being less than five millimeters in diameter blocking now not everyone with gall stones will develop acute pancreatitis in actual fact less than seven percent of people with gall stones will develop acute pancreatitis and this has to do with a number of different unknown causes but I think one of the reasons being the size of the gall stone let's look at alcohol now how does alcohol result in a sauna cell degeneration well we know that the liver being the major site of alcohol or ethanol metabolism the pancreas also metabolizes ethanol as well and what alcohol can actually do is a couple of things if I were to just write it down here alcohol can one increase pancreatic juice secretion pancreatic juice secretion but what it can also do is increase the viscosity of the pancreatic juice now this viscosity increased amount and increased viscosity can lead to stone formation so pancreatic stone formation but also protein plugs and this protein plugs and stone formation can block these pancreatic ducts or the smaller duct dolls okay what else can alcohol actually do what alcohol can actually increase the amount of fatty acids in the a sinner cells and if you increase the amount of fatty acids in the a sinner cells it increases what's called fatty acid degeneration and can result in one necrosis and two oxidative stress so you can say oxidative stress which can result in necrosis and necrosis can therefore result in scarring and fibrosis now if you have scarring and fibrosis the scarring can block up these ductal zand ducts as well okay so these are some of the major causes or effects of alcohol nap it's also been shown that alcohol in this process of increasing fatty acids resulting in fatty acid degeneration also promotes inflammation and cytokines from being released and therefore results in an inflammatory cascade there's also another hypothesis that because people abused alcohol now what you'll find is that binging and alcohol is in a very common cause of acute pancreatitis but long-term use of alcohol is associated with it now how well is a theory out there stating that over time alcohol abuse can result in sub clinical damage of the pancreas leading to scarring over time and then these scars can form these ductal blockages and then that will present as acute pancreatitis so again these are the two most common causes they're not the only cause not the only cause of acute pancreatitis what's the third most common cause of acute pancreatitis well it's something called hyper triglyceride emia hyper triglyceride emia so let's just say gall stones are number one alcohol is number two number three is hyper triglyphs so ready Mia triglyceride D Mia and the hypertriglyceridemia is an increase or an abundance of triglycerides and what they usually state with in the literature is greater than a thousand milligrams per deciliter however some studies are now suggesting that this needs to be higher even upwards of two thousand milligrams per deciliter so I assume that this will continually be updated as well now how does hypertriglyceridemia results in this process well the thought is similar to alcohol in that sense that it promotes the abundance of fatty acid degeneration or something called lipo toxicity which can result in oxidative stress inflammation necrosis and then fibrosis so this is hyper triglyceride emia the third most common cause what about the fourth most common cause well what you can have is something called endoscopic retrograde kali angio pancreatic rafi endoscopic retrograde cholangiopancreatography what is this a-c-p well basically it's putting a scope down and endoscope down with a radioactive dye or a labelled dye and what you can do is view these ducts of this system why would you want to view these ducts well you can have a look for gall stones you can never look for strictures or scarring you could have look for cancers or tumors now how can the endoscopic retrograde cholangiopancreatography results in acute pancreatitis well the thought is that it can be due to direct damage from the equipment itself so meaning maybe the endoscope has directly damaged the ourselves or maybe the radiographic diner's also damaged the a sauna cells again resulting in a release of the pancreatic juices and the auto degradation from those pancreatic juices of the pancreatic tissue itself so these are four most common gall stones alcohol hypertriglyceridemia and endoscopic retrograde cholangiopancreatography they're not the only causes but the most common causes if you want to know less common causes things such as drugs things such as infections direct damage so trauma genetic diseases with genetic aberrations and even scorpion toxin well scorpion venom had a scorpion venom result in acute pancreatitis while scorpion venom seems to tell the ice on the cells to increase the amount of pancreatic juices it releases and then it tells the sphincter of Oddi to close up which means it accumulates here or there's pancreatic enzymes and auto digests the tissue okay so these are the different causes what we need now need to have a look at is the clinical presentation and the clinical criteria now one of these clinical presentation clinical criteria what am i referring to well usually the patient needs two out of three of these criteria in order to be diagnosed with acute pancreatitis so what are these criteria well one is abdominal pain now this abdominal pain can be epigastric or right upper quadrant or can even radiate to the back number two biochemical evidence now what I mean by biochemical evidence we need some sort of biochemical readout there's going to be indicative of acute pancreatitis this includes elevated serum or elevated what I should say is elevated pancreatic enzymes such as amylase and lipase greater than three times their normal amount that's the biochemical evidence elevated pancreatic enzymes amylase and lipase greater than three times we're in the serum elevated serum pancreatic enzymes okay what's the third well this is radiological evidence we need some view to have a look radiological evidence we need a view to have a look and see whether so sonic sonic graphically for example have a look and see what's going on so we need to tick two of these three boxes in order for it to be counted as acute pancreatitis now you can also break acute pancreatitis up into various classifications so what are the classifications of acute pancreatitis so classifications include mild moderately severe and severe how do they differ okay so for mild what you're going to find is it usually resolves within one week and there's also no organ failure and no local complications I'll talk about what that means in a sec when it comes to moderately severe well moderately severe is associated with transient organ failure transient organ failure being less than 48 hours but still really no local complications well maybe some local complications let's say some local complications and then for severe we have ongoing organ failure so this is greater than 48 hours and we have local complications so the classification can be mild moderately severe and moderate and severe mild usually results within a week no local complications no organ failure moderately severe transient organ failure less than 48 hours and some local complications and then for severe its ongoing organ failure greater than 48 hours and various local complications so what we need to talk about or what am i referring to when I say local complications alright so local complications include the following it can include an accumulation of pancreatic or peri pancreatic fluid so let's write this down local complications local complications include pancreatic well Perry you know what we could do let's write it under here because since these are complications of what's happening here let's write them down we can have a sauna cell degeneration ductal obstruction and what's going to have is when the ACE and a cell's did generate it's going to result in trypsinogen right and trypsinogen is going to turn into trypsin ductal obstruction and trypsin trypsin with a staff of obstruction is going to result in a breakdown as well of tissue breakdown and this tissue breakdown is going to also be associated with these local complications such as local complications going to include pancreatic perry pancreatic so perry means near or around fluid accumulation necrosis so death that tissue something called pseudo cysts and hemorrhage pancreatic pancreatic fluid accumulation necrosis cirrhosis and hemorrhage these pancreatic perry pancreatic fluid accumulations are happening near or around or within the pancreatic tissue itself and can be observed by radiological imaging necrosis is going to be tissue death this is going to be death due to secondary inflammatory events and also direct tissue destruction pseudo cysts when you've got with these with the pancreas you've got these cysts that are forming on the walls of the pancreas and you'll find that the walls of the system selves aren't made up of epithelia like most cysts they're actually made up of fibrous or granular tissue hence have been called pseudo cysts and then hemorrhage again bleeding due to the destruction of the tissue as well so these are the most common local complications now what do you need to do when it comes to treatment though well when you look at treatment for acute pancreatitis you need to treat the underlying cause of this particular Aysen a cell degeneration or ductal obstruction you also need to make sure that fluids are being placed within the patient so that they don't have go into shock or you know have hypovolemia or blood pressure issues recoup electrolytes for example they may potentially have sepsis or bacterial infections due to some of the damage so maybe antibiotics what else do you need basically pain relief as well because there's going to be a lot of pain associated with the acute pancreatitis this could include analgesics maybe morphine but remember that morphine can constrict smooth muscle and so may potentially constrict the sphincter of Oddi potentially could make things worse so maybe other forms of analgesic and that's basically the some of the treatment options not all the treatment options but some associated with acute pancreatitis so hopefully that helps and made sense

Channel: Dr Matt & Dr Mike

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Length: 26min 57sec (1617 seconds)

Published: Wed Aug 08 2018