Gastrointestinal - Liver Disorders

Hello, I am Professor Beth Pitman and today we're going to talk about the functions and some disorders of the liver. So just a quick little anatomy recall at the macro level, you have your liver which is connected to your small intestines as well as your pancreas via the biliary system. And that system consists of different ducts, you have a hepatic duct, a pancreatic duct, as well as your gallbladder. And the reason I'm pointing this out right now is because it is important to note that a problem in any one of these systems because they are connected by a one way pathway through the ductal system can really cause injury to another surrounding organs. So this is part of the GI system but they're the surrounding organs around the intestines. When we move to a micro level, it's important to note that there's a few things different about the liver than the other organs. One is that these hepatocytes, 80% of the liver is made up of these supporting cells called hepatocytes. They can regenerate themselves, which is a lovely thing if you think about it because one of the major roles of the liver is to detoxify the body and it's very highly vascularized. So it can become injured fairly easily. And so it's nice to note that this organ can, over time, if given rest, can regenerate those cells. A few things I'm going to point out here. A hepatic lobule is kind of like a hexagonal shape of an inner working system within the liver. And so each part of that system I would like to point out has an artery branch, venous branch, as well as a biliary duct. And so the reason I'm pointing this out is because again, the liver is very highly vascularized. It serves as the filtration system for all of the blood in the body. So it's going to be filtering lots of blood throughout the day, as well as separating things that could be toxic to the body and getting rid of those. So these cup-first cells here that I'd like to point out, they lay, they kind of sit in the middle of the filtration system. And they have baggasside-sidic activity. So if they see some sort of toxic substance, they sit there in the vessel and they eat and absorb and excrete those toxins. We have come up with a mnemonic to help you remember the functions of the liver. So here's my little Peter Griffin. You can see he's a little couple sheets to the wind. And so our mnemonic is PDSM. Peter drinks so much. And this is to help you remember all the functions of the liver because there are a ton of them. But these are the major functions. So PDR stands for produce. Your liver is responsible for producing many important substances in your body. And we're going to go through each one of these independently. D is for detox. So again, the liver is responsible for detoxifying the body as stands for store. And then m stands for metabolism. So let's go into each one of these a little bit more specifically. Again, p is produced. And under that I want you to think of ABCs again just because it's easy. So the a stands for albumin. And we know that albumin is a very important protein that is in the body. Proteins we know attract water. So if I have proteins in my vascular system, I'm going to be able to pull and hold fluid in the vessels. If I do not have any albumin in my vessels in my vascular, then I'm more able to lose fluid into the interstitial area. And I'm going to go through all of these. And then I'm going to go through all of these. So ammonia is a byproduct of protein metabolism. Ammonia is very, very toxic to the body. And it can cross the blood brain barrier. So if we again have a liver that is not functioning. And we're not able to process and rid the body of that ammonia. Then we have a build up in the body. This is presented in the patient as hepatic in cephalopathy. So in cephalopathy related to the liver. We're going to talk a lot about hepatic in cephalopathy later. So I'm not really going to go through all the signs and symptoms right now. But just know that if our liver isn't functioning, we're going to have a problem with our metabolism, specifically related to protein and ammonia, build up in the body. All right. So back to Peter drinks so much. Produced detox, store, and metabolize. If our friend Peter is in liver failure, let's think about which labs we're going to see changes in. So our first one is albumin. And we know that the liver produces albumin, which is a protein. So it's Peter is in liver failure. We're going to have decreased albumin levels. Billy Rubin. Hmm. Let's think about that. So if Billy Rubin. Goes to the liver to get processed and excreted. If Peter is in liver failure, then we're probably going to have increased Philly Rubin levels. last year all we talked about that being important for or metabial excretion metabolism. So cholesterol levels are going to go up. Our PT, PT, and INR, so our clotting times, again, are going to go up because we have decreased clotting factors. And then ammonia as well is going to go up. So we'll talk about disorders of the liver, the first one being jaundice. Now, I wanna point out, you can have jaundice, which is what we think of depicted here on the slide. So yellowish coloring of the skin and sclora, amicus membranes, all of that. But it can be its own diagnosis as well as being a part of the bigger picture. So for example, if we have someone in hepatitis or cirrhosis, so hepatitis is liver inflammation, cirrhosis is end-stage liver disease related to fibrosis scarring, all that stuff. Both of these scenarios, you could see jaundice in. So again, it can be its own independent diagnosis as well as seamless other things. So we're gonna talk about the different types and there is a chart in your book. I'm gonna go ahead and pause the recording right now just to make sure the table's correct for you guys. So cold type. Okay, so my suspicions were correct. It is not table 483. It is table 42. Oh no, 43, 3, sorry, 43, 3. So it's in your liver, belly, and pink chapter. But there is a chart in here talking about the different types of jaundice, chemo, lipid, hepatocelular, and obstructive. And it will be important for you to be able to differentiate these three. So we'll go ahead and talk about them in the next slides. The other two pictures I wanna point out to you is just a description of, you'll read a lot about tea colored urine or dark urine. So this would be urine with belly rubin in it. We see this oftentimes when we have an obstructive or hepatocelular disorder. And this is where the belly rubin can't get through the bile duct into the small intestine to turn the urine, or the urine. I'm sorry, the fecal matter brown. So it is the belly rubin that turns your stool dark. And if it's not going that way, it goes through the blood system and then eventually ends up in the urine. So the urine is getting darker here. And this is the corresponding stool without the belly rubin. So you can see in your book it was called clay colored stool, but here in Oklahoma, we've got red clay. So they can be a little confusing, but what they really mean is it's a very light colored stool. So again, dark urine, you think there's more belly rubin in the urine, light colored stool or clay colored stool. You know that the belly rubin is not reaching the small intestine, so you have a light stool. We'll talk about this as far as disease processes what you will see later. I just wanted to include the picture here so you know what we're talking about. All right, so here's our discussion about belly rubin. So belly rubin is a product of the breakdown of red blood cells, which is constantly happening in your body. We're getting breakdown of cells and formation of new ones. You have uncongiagated and conjugated. So the thing to think about here is that your liver is responsible of turning uncongiagated into conjugated belly rubin. So anything pre-liver is going to be uncongiagated or free belly rubin and then it will get processed in the liver to become conjugated. And it's the conjugation that makes it soluble so that it can then be excreted through the GI tract and some through the urine. So as we look at the types of jaundice, remember there's three types, hemolytic, hepatocelular and obstructive. You will be able to differentiate those based off of your levels of conjugated versus uncongiagated belly rubin. So let's take a look at it. For hemolytic jaundice, it sounds like just like what it is. So we've got our red blood cells that get broken apart so hemolysis and from that we get free belly rubin. So this is indirect uncongiagated belly rubin. And what happens here is we have red blood cells getting broken down frequently and the liver cannot keep up with it. So we see an increase in the uncongiagated belly rubin. So it's the belly rubin before the liver can process it. Things that cause this disorder, red blood soil abnormalities, if we have incompatible blood transfusion or a blood transfusion reaction, where we have lysis of those cells, you can see it, sickle disease, hemolytic diseases, we also see it in malaria. So again, hemolytic jaundice, breakdown of red blood cells before it reaches the liver. So we have an increase in that uncongiagated belly rubin because the liver can't keep up, it can't process it to turn it into conjugated. Our next one is hepatocellular jaundice. So here we have a problem within the hepato cells themselves, they're hepato sites. So we have a dysfunction in the liver, therefore the liver cannot take up, conjugate, or excrete the belly rubin. So here we have an increase in both. So we have an increase in uncongiagated belly rubin because the liver can't take it up and process it to turn it into conjugated. However, we also have an increase in conjugated belly rubin because the liver is not able to process it and excrete it. So with hepatocellular jaundice, which again, is a disorder to the actual liver itself, we have damage to the hepato sites. So the liver can't take up and process. We have an increase in conjugated and uncongiagated belly rubin. Things that cause this disorder, hepatitis, inflammation of the liver, cirrhosis, and stage liver disease, as well as types of liver cancer. So we have hepatocytes that are not able to function and do their job. With our final one, we have obstructive jaundice. The most common form of obstructive jaundice is depicted by our little diagram over here, where we have gallstones that move into and wedge or obstruct the biliary tree. Here, we have normal, uncongiagated because the liver, as you can see, is still working, still intact, fully functional. So the liver is able to grab all the uncongiagated biliary rubin and transfer it into conjugated. However, it cannot be then excreted because we have a blockage to the system. Remember, the biliary rubin is created in the liver, along the file, goes through the bile ducts, enters the small intestine, again, which makes the stool dark. And if it cannot enter here, we're gonna have high levels of conjugated because it's already been processed in the liver. However, it's not reaching the small bowel for excretion. Again, here's that little reminder, when we do have an obstruction because that biliary rubin cannot get into the small bowel, we're going to have light colored stool because, again, if the biliary rubin that makes stool that dark brownish color. Cause by gallstones, number one, risk factor. Also can be caused by tumor somewhere in the biliary tract or biliary strictures. So if we have the ducts that are becoming more narrow, we have fibrosis, any sort of stricture that happens there, it can block the biliary flow. So now we're gonna talk about hepatitis, and we're gonna talk about the different types of hepatitis. The main thing to know that hepatitis in and of itself is inflammation of the liver. It is typically mostly caused through a viral infection. So it is important to know the types that are common in the US, that's hepatitis A, B and C. It's also important for you guys to note how they are transmitted, as well as how they are prevented or treated. So hepatitis A is a fecal oral root, meaning that when we have a hepatitis outbreak, it is because people often have to have the disease, use the bathroom, don't wash their hands, and then it's transmitted that way. There is a vaccine for hep A, we'll talk about this in a minute. Hep B is blood, so it can be passed mother to baby, high-risk sexual activities, needles, that kind of stuff. There is a vaccine for hep B as well as some treatments. Hep C is one that is most likely to become chronic out of all of them. We'll talk about acute versus chronic in a minute. Hep C is also passed through the blood. Again, IB drug users, high-risk sexual activities. With Hep C, there is no vaccine. However, we've gotten really good with our medications and if a medication regimen is started at an appropriate time, meaning the patient is ready to commit to the drug regimen, it is 90% curable at this point. So that's a huge progression forward in the treatment of Hep C. If left untreated, Hep C is most likely to turn into chronic hepatitis as well as liver cancer, we see a long time. So it goes Hep C Serosis Liver Cancer. As far as the pathophysiology, this is again a virus that either directly invades the cells, the hepatocytes, or indirectly does by some mediated immune response. We've got two, I apologize for that. We've got two videos here for you to watch. They're both pretty good and I suggest you watch them on your own. But we'll go through a little bit of each of these viruses in a minute. So the total result, regardless of the infection type, is that you can have acute hepatitis and overall hepatocytes may become damaged and again can lead to liver dysfunction. So when we talk about acute hepatitis, we have inflammation of the liver, but it's usually for a short duration. Hepatitis A in particular is usually self-limited, it resolves on its own, the patient might become sick for a little bit, and then because the hepatocytes can regenerate, they will get better over time. If we have hepatitis that lasts longer than six months, that then falls under chronic hepatitis. Oftentimes this can be very insidious, meaning there aren't a lot of signs or symptoms, however we're having damage on a cellular level. And if left over time, so chronic inflammation leads to scarring and fibrosis, if left over time, then eventually we can result into cirrhosis and then as I said again, and stage liver disease with carcinoma. So of people with hepatitis C, again that's the one that usually goes to chronic. Hepatitis A, usually just to queue, usually self-limiting. Hepatitis B can be both. Some they resolve after they're acute infection, never have it again. Others with hepatitis C, most cases will turn chronic. So normal liver with Hep C infection, 50 to 80% become chronic of those 20 to 30% end up with end stage liver disease, which is called cirrhosis. And of that about one to four will end up with liver cancer. So here's a table in your book and again I'm going to point out that it's not 48, it is 43, 2 in your Lewis text. I will be sure to get all of these corrected by the time we go through the PowerPoint in class. So what do we do for a patient who has hepatitis? So their liver is inflamed, probably showing signs of not working, maybe they're some nausea vomiting. We tell them to rest again. Those hepatocytes can regenerate, so we make sure that they get adequate rest and nutrition. We absolutely tell them to avoid any sort of hepatotoxic drug. So this would be drugs in alcohol, absolutely number one, but also things like insets, any sort of medication that is known to be hepatotoxic, we're going to go ahead and pull them off with all of that. The other thing that's important from a public health standpoint is that we need to be sure that they're not spreading the disease to other people. So there's a good table in your book again, 43.9, where you can look at that. And it's important to know for each AB or C, which ways to help them ensure they don't transmit to others. So remember again, HEPA is fecal oral, whereas B and C are through blood. So you know how you go to the bathroom at a restaurant or really any kind of public place where they might be serving food or drinks. And you always see this, employees must wash hands before returning to work. Well, you can think hepatitis A for that because again, it's fecal oral. So it is mandated by the government and the CDC for any place that is serving handling food or drink that they have to hang this sign in their restroom. So that is a big one, hand washing for HEPA is huge. Nursing care, there is a vaccine, all kids around the age of one receive it. Also, any adults that are at risk for being exposed to hepatitis A should be given the vaccine. We talk a lot about personal and environmental hygiene. So HEPA, we do see increases in outbreaks in developing countries as well as I remember there maybe about 10 years ago, I'd have to look to see for sure, but there was a huge hepatitis A outbreak in California about a decade ago among the homeless populations. As you can imagine, it makes sense. If we have unsanitary living environments as well as inability to wash hands before we eat, you could see how that would lend itself to hepatitis A getting spread very easily. For healthcare workers, PPE is important anyone that's suspected to have HEPA, just be sure to protect yourself when you're dealing with any sort of fecal matter. Hand washing after bowel movements before eating is going to be kind of the standard education for people that have the virus. For HEPB, it's important to think about prevention versus exposure. So for prevention, there is a vaccine. Most people have born all of the students probably received this. I didn't when I was young because it wasn't standard care back then, but as soon as I got a job in the nursing field, I was given the HEPB vaccine and now it is recommended for all babies. It is a series of three injections, so you need to make sure that when you start this series, there's clear understanding that they will have to come back for injection to an injection three. For education for patients that are infected, we need to be sure not to share things like razors or toothbrushes and this might seem pretty common to us, but it is important not to just assume that people have access. People that might be struggling kind of paycheck to pay check, they might share razors, they might share toothbrushes. So it is important to not just assume that everybody has access to their own toiletries and things like that. Of course, sexual condoms for sexual incurs, intercourse, sorry, it's a Saturday, so I'm moving a little fast today. This includes both male and female condoms or dental dams, so make sure that you're familiar with that and able to educate your patients about that. If we do have one partner that is infected, we would recommend the other sexual partner to become vaccinated for that if they are not already. Using hand washing and gloves, of course, whenever touching blood. If a patient has become exposed to HEPB and we are aware of it, we still get them the vaccine after exposure. We would start the three-part vaccine. We can also give them passive immunity through the infusion of immunoglobulins of the antibody. So we would start immunoglobulin therapy as passive immunity for that patient. So if we know somebody has been exposed within a short amount of time a week to two weeks, we would go ahead and vaccinate that patient post-exposure as well as likely start immunoglobulin therapy. For HEPC, there is not a vaccine, so we can't prevent it. One of the mainstay treatments on again a public health standpoint is to identify people who might be at risk. Because HEPC, again, is the one that usually goes chronic, right? And the thing about HEPC is that it's very insidious. If they do not have symptoms during their acute infection component, it kind of sits almost dormant for about 10 years, 10 to 20 years, before we see signs of liver injury. So what happens here is that people may have been infected a long, long, long, long time ago, and I put this picture on here to jog your memory. The highest risk or the population that we see highest levels of HEPC in are the baby boomers. So we might see them today as you know 70-year-old person coming into your office sweet little old lady, but let's not forget that she would have been around 20 during the sex drugs in rock and roll era. So don't overlook patients who might be high risk for Hep C because what we need to do is we need to test them. And if they have it, get them on treatment because again, it is up to 90% curable, curable. So we need to see who's at risk test them so that we can prevent them from transmitting to other people because again, it's insidious. It sits for up to 20 years without any signs or symptoms. However, during that time, we could be passing it along to other people. So we screen people at risk. IV drug users, high risk sexual behaviors, baby boomers, which are identified as anyone born between 1945 and 1965. Anyone with a blood transfusion before 1992, because that is when we started testing for Hep C in blood donations or anytime somebody comes in and they have abnormal liver function tests. And that would be for Hep A, B or C. If we have a patient who has abnormal liver function tests, so I'm talking about AST, ALT, possibly alkyphosphate, we're going to go ahead and run some tests and see what's going on with the liver. We do screen now blood organ tissue donations so that we don't pass it along. Infection control measures, precautions, the same things like we talked about with Hep B, anything that could pass it along through the blood pathway. And then modifying high risk behaviors. So if we do have an IV drug user or high risk sexual behavior type patient, then we would educate and talk to them about modifying some of those risks. Again, high, high curable rate if we take the medicine according to how it's ordered or prescribed. So for cirrhosis, again, I've alluded to this a few times. This is end-stage liver disease. Here we have diffuse injury to multiple hepatocytes. We also have the inability of the hepatocytes to keep up to keep regenerating those cells. So the liver was not able to keep up with the diffuse injury here. So we have an overall dysfunction of the liver. What happens here when we have scarring and fibrosis is that the liver becomes very congested, if you will. It becomes thick and fibrolytic. So the cells itself cannot form the function. As well as the ability of the body to get the blood into, remember the liver is the filter. So if we can't, if we have a very dense congested liver, we can't get the blood into filter it through. So we have impeding vascularization and biliary flow. So what that means is we're going to have a back up of that fluid of that blood around the liver because it's not able to get through. Sanding with the biliary flow. If we have a liver, remember the ducts go through the organs. If we have a liver that's very congested, it can constrict on the bile ducts. So we have impedance of that flow. It will of course affect everything that the liver can do. So thinking back to heat or drink so much, we're going to have issues with production, excretion, storage, and metabolism. This is caused by chronic hepatitis C, which we've already talked about, Nash, which is non-alcoholic cirrhosis, as well as alcohol induced cirrhosis. So risk factors, excessive alcohol intake. Alcohol is hepatotoxic. One thing I will mention about this when we're talking about our patients, trying to at earlier phases, hopefully trying to get them to stop drinking or at least lower their alcohol content intake is to remember that because the cells can regenerate, we can have a circulation over of those hepatocytes in about five months. So if we can get our patient to stop their alcohol intake, you will see in about five months. I mean, you can start to see those levels, those liver enzymes trending down. But in about five months, if they have enough healthy liver left, we can really see improvements in the overall function of that liver. Chronic hepatitis and Nash, which we talked about the non-alcoholic fatty liver disease. So what happens is we have liver inflammation, which leads to necrosis. When we get to necrosis, obviously the cells aren't going to function. And then over time, we have scarring and fibrosis. And what happens here is we get liver failure when overall the liver can't perform its functions, hepatic encephalopathy ensues because we have a build up of that ammonia, the the liver can't rid the body of the ammonia. So we have a build up and then we have neurological deficits. Then that can lead to hepatic coma and eventually death. When we have the scarring portion, remember the thick congested part, we have a build up a backflow of that blood that cannot get into the liver to filter through the liver. So we get a portal vein hypertension. And we'll talk about that in a few slides and hopefully that will become pretty clear to you guys. Here's just another picture of what we talked about. Again, inflammation leads to necrosis, leads to scarring. And when we do have this, you're going to see different things through your patient profile. So when we have liver inflammation, the patient might feel pain. So right upper quadrant pain, they may have fever, they may not, it might be a slight fever. Naja vomiting and erexia. So we usually see some GI upset issues related to this as well as fatigue. From there, if we go to necrosis, again, you're not going to be able to see the things that the liver should normally do in a regular fashion. So here we might see some jaundice, those light colored stools, bleeding tendencies, dark urine. We're also going to see maybe some issues with the societies because we have decreased out human. We might have some hypoglycemic issues because again, the liver stores glucagon. Another thing is that your liver is highly involved in the endocrine system. So we might see a lot of sex characteristic things that are changing here. So for males, we might get gynecomastia, loss of body hair, testicular atrophy, spider angiomas, and palmer. Your athema, I have pictures of in a minute. And again, this is due to the metabolism. So so you have hormones produced in your body for multiple reasons. And your liver is the organ that will process and excrete those hormones from the body. If you have too many, if the liver can't do its job due to liver and acrocyst, then you're going to have a build-up of those hormones, which will present in multiple different ways. What else do we have? Eventually, liver failure and cephalopathy, coma and death. For fibrosis and scarring, we're going to have liver congestion, which presents as portal hyper tension. So the liver or the blood cells around the liver are going to have become overloaded essentially. And that fluid is going to back up into the system around the liver. I have pictures coming in a minute and I think it'll be more clear. So if we're dealing with that, we think of fluid. So we're going to see a sideys, edema, splino megalithe, varices. We're going to talk a lot about varices, hemorrhoids and then other abdominal veins become congested and big. Here's your lab values related to necrosis. Again, if the liver cells can't form their function, you're going to see increased AST, ALT, alfos, bilirubin, your bleeding times increase and your albiumin decreases. So I do have another chart that we'll talk about. Actually, it might be right. No, it's not next, but it's coming in a minute with your labs altogether on one page. All right, so here's some of the pictures of clinical manifestations, just to be sure we understand what they are. So early signs of cirrhosis. Again, nausea vomiting, GI issues, flatulence, you might be a little tired, weight loss, that pain to the right upper quadrant, which is described as dull pain, not a sharp pain. Late signs, we're going to see the more obvious thing. So I like to think of early signs as being like patient centered. It's what they feel. They're nauseous. They feel tired. They might feel pain. When we get to late symptoms, it's usually what we as clinicians can actually see on your patient. So jaundice, yellowing of the sclura or the skin, edema, whether it be via ascites in the abdominal cavity or through peripheral or dependent edema. We might see perperas. So here, these little speckily tiny dot, oh, I'm sorry. Perperas up here, there is a bigger sort of eraser shape like tiny bruises or this is petite guia. I'm sorry, I missed book there. Here's the tiny like pencil pinpoint bruising that we see here. Spider angiomas are these little things. We can see them anywhere on the body. Sometimes men like to get them around their nose, but you can see it takes on this little spider formation where it's like a star light, all these little veins stick out as well as Palmer, Irrathema, so redness of the palms. And again, these two here are because the body, the liver can no longer rid itself from excess hormone buildup. So that's how we see these. This one, Ascides, is obviously related to decrease albumin levels. Whereas these two bleeding disorders, or bruising disorders, are related to decrease and clotting factors. Again, all related to things that the liver should be able to do that no longer can manage those functions. Hepatic and suppolapathy, again, a buildup of ammonia, the liver can't get rid of ammonia. So we have a buildup of ammonia, which is toxic to the brain. And the patient can become confused, lethargic, but I have a picture here of what is called asterixins. Here is a simple thing you can have your patient do is to extend their arms straight out and then flex their wrists. And somebody that has hematocincephalopathy or a buildup of ammonia in their blood isn't going to be able to hold this. It will be like a flapping. Like they're not going to be able to fully extend or, yeah, extend those wrists back. Here's just another picture of all the systems that are involved. You can read through that. We've kind of talked about most of them already. Here is the other diagnostic page. I promised you that you would receive. So it's important to know everything that you might see as well as how it is associated to the liver. So of course, if we have liver dysfunction, our enzymes, AST, ALT and alphosph will go high. Protein is going to go low because we can no longer make that out of human. Billy Rubin, think about total Billy Rubin goes up, but even from there, you need to think about is it conjugated or un-conjugated? And I'm going to tell you one more time. Remember, un-conjugated is pre-liver. It's what comes through the blood. Remember, it comes from the breakdown of red blood cells. So we have un-conjugated, then it goes to the liver to get processed into conjugated and conjugated is what comes out and then is excreted. So if you have injury to the blood cells where you have a hemolytic jaundice, you're going to have high levels of un-conjugated Billy Rubin. If you have hepatocytes, hepatocelular jaundice, you're going to have increased levels of both. And if you have an obstructive issue, a post liver injury, you're going to have high levels of conjugated. So make sure you go through that and I'll probably even make a chart for you guys to understand that a little bit better. Colestral levels is actually going to go up. So I'm going to need to fix that because your your body is not able to metabolize the fat. So cholesterol levels will go up. Bleeding times go up because we have a decrease in clotting factor. The way we can diagnose somebody's cirrhosis is through an ultrasound, which specific to the liver is called a fiber scan. It will tell us the degree of fibrosis. So here if we're leaning towards some sort of cirrhosis, this would be a first step. However, true staging of the cirrhosis is only done through liver biopsy. So if we need to do that, this is for a true diagnosis of cirrhosis is only done through liver biopsy. So complications related to cirrhosis we're again going to talk about each one of these individually. We have portal hypertension, gastric and esophageal varices, ascites and hepatic insophilopathy. So for each of these, you need to know how it happens related to the liver, what it is, and what the treatments are. So you need to know all three of those things for all four of these complications and we'll go through each one. So again, portal hypertension is when you have a serotic liver, a congested full dense, unfunctioning liver that remember processes all of the volume for the body. So the blood can't even get into the liver. So it backs up into the vasculature around the liver. So we have a lot of vessels around the gut, the stomach, the esophagus, the small intestines. Some is going to back up into the spleen and then some is even just going to go into the peritoneal cavity. So we get because of the in-fee pressure that portal vein hyper-tension. So high pressured system in the portal veins around the liver. We're going to get fluid shifting to places, which is going to present itself as splenomegaly. So the spleen's going to get big. We have large collateral veins. So you can see all of this vasculature, all these veins around all of this. Normally it's pretty straight, maybe a little wiggly, maybe a little branchy. What we see here because of the hypertension, we see large tortuous, meaning they're moving a lot. They're becoming large and congested. They've got nowhere to go. So there's full and dense veins around the stomach and the esophagus. So how that presents is through esophageal and gastric varices. And these are so big and so congested. I was going to go to my other slide. Let me go to it real quick, just so you can see it. That you can actually see these on the inside. So a normal esophagus would just be a smooth, clean pink tube, right? If you were to stick a tube down there and look. Someone that has esophageal varices has these large tortuous. So these are the actual vessels and the veins that are completely congested and filled. And you can see them from the inside of the esophagus. This is abnormal. The problem with these is that they're very, very, very high risk for bleeding. Think about it. You're constantly swallowing food and it's rubbing up against the inside of your esophagus. So these can bleed very, very easily. This is the most life-threatening complication of cirrhosis. Because a high-pressured system, you get a perforation, you start bleeding. What's that patient going to do? When they bleed from here, it goes into the stomach. It's toxic. Your body doesn't like it. So you immediately start vomiting and out. At that point, we're worried about not only blood loss, but airway. And that's why bleeding esophageal varices or gastric varices, most commonly, there are esophageal varices that cause the issue, are the most life-threatening complications. So we'll talk about those in just a minute. I'm going to go back and get through our slides related to portal hypertension. The first one we'll talk about is ascites. So here, again, we have a serious fluid that goes into the peritoneal or abdominal cavity. And this is just pressure-based. We have portal hypertension, which is causing congestion and backflow of the vasculature system and of the fluid in the area around the liver and the gut. So that eventually moves into the peritoneal cavity. This is increased by the fact that our liver is no longer making elbuman. Remember, elbuman is a protein that stays in the blood vessels that helps pull and hold fluid into the vasculature. If we don't have any elbuman in there, then there's nothing holding that fluid in the blood. It's going into the peritoneal space. What else? What else? Decreased colloidal, onconic pressure. This is managed. If we have a patient with severe ascites, it can cause pain. It can cause issues with breathing because your diaphragm can't go down and your lungs can't fully expand. So we typically. I typically recommend low sodium for these patients, two grams a day or less. We might do diuretics at home. If they need to, and honestly lots of serotic patients come in pretty regularly for a paracentesis so that we can remove that fluid. When we do talk about a paracentesis, it's important that you know that it is an intermittent. So we go in, we tap the belly, we remove whatever fluid we're going to remove, and then we stop. It is not a continuous drain. For nursing care, it's important that we think about prepping the patient. So this is something that can usually be done at the bedside interventional radiology might come and do it. We have the patient completely empty their bladder before we start, and that should be fairly obvious to you because if the bladder is super extended or full, there's very high risk that we could puncture that the bladder. Oh, I'm sorry, that is that patient's in. Sorry, hold on. Okay, I apologize for that, I was clicking all sorts of weird buttons. Okay, and I apologize, the bladder is down here. This is their uterus up here. So, regardless, you need to make sure that the patient empties their bladder so that it's not at the front of the abdomen so that whoever's going to tap this belly does not hit their bladder. We do need informed consent for this procedure because there are of course risks associated just like everything else. We have the patient sitting up in a foulard's position and the easiest way to remember that is just based off of gravity, which will come so that all the fluid comes down to the bottom for easier removal. And then we're going to monitor. So, always when we talk about removing fluid from a patient, we need to keep in mind a hemodynamic stability. So, at any point, if you remove a large amount of fluid from the body, we expect all the other fluid in that system to shift. So, we would expect things like blood pressure to go down, maybe then the heart would go up to compensate, but you're just going to monitor for risks of high bovolemia. We also want to monitor the dressing for leakage or bleeding afterwards. Back to the esophageal varicides. So, again, we have these torturous, large congested veins around the lower esophagus as well as the stomach. They are very fragile due to the high pressured system around them. The most likely to bleed are the esophageal varicides because the esophagus just serves as a transport tube. And it constantly is swallowing that volus of food. So, it's very easy for those cells to become sloughed off and for these to rupture and bleed. Again, most life-threatening complications. Once they start bleeding, they're either going to immediately start vomiting or, well, they'll start vomiting, really, is what it is. The blood will go down to the stomach. The stomach will realize it. Eject all of that. When we do start vomiting, we're probably going to injure it even more. So, thinking of airway and blood loss as the most life-threatening things that we'll see, we need to manage that airway. And what we do as far as stopping the bleed, most commonly is we'll do an EGD esophagogastro duodna scoffey. So, it just means a scope and upper scope, where we can visualize those areas of bleeding and we can band clip, or, which is called a ligation of those areas. So, what they do is they actually stuck up the bleeding area, clip it with a band so it stops the bleeding. And then eventually that band causes an acrocysis, a little clot will form and it will fall off and get stooled off. So, that's the management of it. We can also, if it's a large bleeding, that we cannot control through endoscopy, we can put in a balloon tamponade. So, it's essentially what you think. We have a big tube that we can place in the nose, pass it all the way down into the stomach. And then we inflate the gastric balloon, which is in the stomach, which will stop at that sphincter. And then we inflate the esophageal balloon, which will put pressure on whatever part of the wall is bleeding to help control and stop that bleeding. As you can imagine, this is a very sort of tense situation when we put it in. The patient may or may not be intubated. The most important things when we think about these balloons, holding pressure on the internal walls of the esophagus, or yeah, the esophagus, is that it needs to stay in place. We do not want this to move at all, or we risk them bleeding again. You will see that the catheter itself has three different lumens. We have one to fill the gastric balloon, one for the esophageal balloon, and then the very last one that you can see is right down here at the bottom, is that we can still use it like a regular NG tube and aspirate fluid from the stomach. So this patient could also still be on low intermittent suctioning to decompress whatever's left in the stomach. Again, with that, we're always thinking airway first with the esophageal blades. Another procedure that we can do for somebody who has portal vein hypertension is a tips procedure. Tips stands for trans jugular, interhepatic, portus systemic shunt tips. Here, what we do is we are bypassing the liver. So we are creating an artificial shunt from essentially the portal vein, which is getting blood into them filter through the liver to the exit, which is the hepatic vein. So we're bypassing the entire filtration of the liver externally. What this is going to do is it helps to lower the pressure system in the portal vein. So that will help with things like varicies. It will help with ascites. However, it will make everything else worse. It will make the labs worse, because even if you have the patient in cirrhosis, it's pretty likely that maybe some parts of the liver are still working a little bit. But then when we go ahead and bypass the liver's ability to do the tiny little bit that it can, we're increasing all of those toxic things that the liver is not able to get rid of. So things like ammonia will be worse. Things like any sort of toxic substances will be worse. So we expect when we put a patient, or we have a tips procedure done on a patient, things like ammonia will be worse. The risk for hepatic and cephalopathy will be worse, because we are no longer allowing the liver to do much of any work at all. So as you can imagine, this is a last resort treatment. It's not going to solve their cirrhosis. It's not going to improve the function of the liver. What we're doing is we're buying time at that point, so that they don't die from bleeding varicies and their esophagus. Again, hepatic and cephalopathy, a buildup of ammonia, because the liver is no longer able to rid the body of it. It crosses that blood brain barrier. It is toxic. So we see this in our patient because they start to have changes in level of consciousness, maybe inappropriate behavior. As that ammonia level gets higher and higher and higher, there's different levels of hepatic and cephalopathy. Eventually, they will go into coma and they will die if we do not catch it and correct it. Other things was that as to rick this, where if you tell them to stand with their arms straight out and flex their wrists, they're not going to be able to hold that position. We can have a praxia, so we have impairments, either with speaking, formulating the articulation of words or writing. We also can have a thing called vector hepaticis, where we have a musty, sweet odor of the breath. It's weird people call it sweet, 'cause to me it's musty and nasty, but you might see that. This is where we have the ammonia actually coming out in the breath. How we treat hepatic and cephalopathy is we give our patient lactolose. Lactolose will bind to the ammonia in the gut and help them stool it out. It does have a laxative effect, so just now, if we give them high levels of lactolose, they're gonna have high levels of liquid stool that comes out and that's a good thing, because we. With that, we should start to see their ammonia levels take down. For management, we want to slow the progression. So much like hepatitis, we give them rest. We allow the liver to stay calm and hopefully regenerate if at all possible, some components of that liver. Remember, we're going to tell them absolutely no drinking, no drugs that are hepatotoxic, including NSAIDs and things like that. We do want them to have high calories, so high caloric intake because we want them to have good nutrients. We recommend about 3,000 calories a day. High in carbohydrates with moderate to low fat. Protein restriction is usually not recommended. Remember protein, the byproducts and breakdown of protein is ammonia. You might think that maybe they're a higher risk for ammonia if they eat high protein, but rarely do we tell them to decrease their protein intake. We would much rather regulate the ammonia through the lactolus. What else? So for acidities, again, I told you you need to know how all of these are related to the liver dysfunction as well as how we treat them. So with the sideys, again, sodium restriction, we may give them albumin in the vasculature, which will help pull the fluid back in and then a diuretic to diurese it out. That's usually the pathway you see. If you give diuretic and albumin, it's very important to give the albumin first and the diuretic second. If those are ineffective, of course, we would do a parasympae to remove the fluid. Non-selective beta blocker is a non-selective beta blocker. We want them on a non-selective because we don't want it to only be cardio. We want it to affect their portal system. So that's why it's non-selective. Non-selective beta blockers will hopefully decrease the pressure in that portal system and lead to management of the esophageal varices and a little bit will help with the acidities. If those are ineffective, we might also do that tips procedure and make sure you know what the tips procedure will help and what will it make worse. Asophageal varices, we can do banding. Last resort will do balloon tamponade. We can also replace their volume if we have high blood loss. We would give them pactyroid blood cells or normal saline or something like that. For hepatic encephalopathy, we'll give lactolose, possibly decrease protein intake, but just know that that really isn't standard of care recommendation. And again, your drug therapy book, it is 43, 14, not 48. So I will get all of those tables corrected. When we meet in class this week, we will go through the case study, but I'm not going to do it here because I'd rather do it with you one-on-one. So if you have any questions, of course, reach out to your faculty members. And I hope you guys have a wonderful rest of your day. See ya.