Okay, today we will finish our discussion about clients with gastrointestinal disorders and be covering Tim chapters 46 and 47 and also briefly be talking about some of the peeds in chapter 38. So constipation and diarrhea will not be covered on this test because that was covered in fundamentals. However, we are going to talk about laxatives and antid-diarals. So laxatives of course are used for constipation to help patients poop. Laxatives all end with the same function by helping the patients have a bowel movement but they all work in slightly different ways. Bulk producing laxatives your psyllium husk which is found in metamucil is a very fibrous fiber what and it causes the stools to bulk up therefore making it easier to pass that stool. Emollient laxatives like mineral oil soften the stool much like stool softeners will also soften the stool like duck docusate. They don't force the body to go they just make it easier to go since it loosens the stools. Hyperosmotic drugs such as lactose lactose is a form of sugar that the body cannot digest. So, it helps the body poop that way, but it also pulls water into the intestines, which again makes it easier for the patient to evacuate their bowels. Irritant or stimulant laxatives do just that. They irritate or stimulate the intestines or intestinal lining. Viscodal and senna are examples of those. Saline laxatives also pull water into the intestine and make it easier for the patient to go to the bathroom. Ball evacuants just do exactly that. They cause the patient to have to go to the bathroom rather quickly. That's your polyethylene glycol marax or go lightly which we use for colon prep specifically with colonoscopies. So uses straightforward constipation or any other disease process that causes constipation like irritable bowel syndrome. Lactolo specifically is used to prevent hpatic encphylopathy in patients with cerosis of the liver because not only is it pulling water into the intestine but also ammonia. So it's helping the body get rid of ammonia as well as helping the body poop. Common side effects whenever we give laxatives we worry about make you know causing the opposite effect like now they're going to the bathroom too much so diarrhea and then also other GI upset nausea bloating and flatus laxatives should only be used shortterm because chronic use can lead to dependence. your body gets used to you taking the laxative every day and then if it's abruptly stopped uh the body has a hard time going to the bathroom without it. So if patients do need to be on laxative long term and some of them do they should be monitored by a provider. All right, antid-diarral. So, low paramide, dipoxilate, bismouth, and probiotics. Probiotics work a little differently because those kind of help with the natural digestive process because that helps restore the good bacteria in the gut, which is really essential for health having a healthy GI system and also having um regular bowel movements. The other medications listed on there, they can work one of two ways. They slow the absorption of water into the intestines. So, because now that there's less water in the intestines, that means that the stool is going to harden up. They can also slow down paristalsis. So, the stool isn't going through the body so quickly. common side effects, dry skin, mucous membranes, and then also constipation if too much is taken. We want to encourage the patient to drink a lot of fluids to again avoid constipation and stay hydrated if they are having diarrhea. Hence why we need to give them an antid-diarral. And then of course we worry again about making the um stool too hard. So we want to assess for impaction or obstruction. All right. So irritable bowel syndrome. Irritable bowel syndrome is a functional motility disorder. So essentially what that means is that the intestines move at their own pace. So they're either moving too fast or too slow. They're not moving consistently. Women are more affected than men. Young are more likely to be diagnosed and there is a genetic tendency to irritable bowel syndrome. So this is a picture of the colon and you can see this picture is representing the spasming of the colon which is common with irritable bowel syndrome. No, I just skipped over. Okay. So, irritable bowel syndrome signs and symptoms. So, most commonly reported with irritable bowel syndrome is chronic constipation with bouts of diarrhea. So, that is again that irregular motility of the bowel pattern. Also, belching and flatulence can occur but there's no changes in weight or metabolism. Another thing that sets irritable bowel syndrome apart from other disease processes of the lower GI tract is that there's an absence of a detectable disease. So essentially when every other lower GI disease process is rolled out like Crohn's or ulcerative colitis, there's really not any disease process going on. That is how we characterize irritable bowel syndrome. So that's important to remember when someone is diagnosed with irritable bowel syndrome. It means that there's no other disease present. They just have usually these bouts of chronic constipation with diarrhea. Diagnostic and test findings for irritable bowel syndrome. Again, we are using barerium enema and colonoscopy uh to rule out other disease processes. Medical management for irritable bowel syndrome is mainly going to be lifestyle changes. high-fiber diet, um doing a food diary to kind of track what makes their bowels feel worse or better. And then antiolinarics which block the parasympathetic response or the rest and digest response can also be given such as um diclo cyclamine which again slows down the bowels and can prevent this bastic colon. Again is what we see with irritable bowel syndrome. Okay. So, inflammatory bowel disease is very different from irritable bowel syndrome. Inflammatory bowel disease is a chronic disease that is autoimmune that results from the immune system attacking the bowel. It does not resolve without medical intervention. So, that's important to note. Medical intervention needs to be done in order for it to get better. Crohn's disease and ulcerative colitis are the most common types of inflammatory bowel disease. So, I'm going to use this infographic and use this infographic to study when you're studying the difference between ulcerative colitis and Crohn's disease because I'm going to talk about them at the same time because they're very similar, but they also have characteristics that make them different from each other. So location of inflammation, ulcerative colitis is going to be large intestine and colon. Okay? So when you think ulcerative colitis, think of like it's targeting the large intestine and the colon. Crohn's disease can be anywhere in the GI tract. It mainly occurs um in the ilium, but it can be found anywhere in the GI tract. So pattern of inflammation, Crohn's disease has like this very patchy inflammation where they'll kind of feel inflamed all through their GI tract where they'll just have a continuous pain usually where their large intestine or colon is located when you have ulcerative colitis. So ulcerative colitis 2 they'll typically feel pain in their left lower abdomen whereas Crohn's disease they'll feel pain in the lower right abdomen. Another thing about where the inflammatory process affects. So with ulcerative colitis it's it's just the inner lining or mucosal lining of of the abdomen. Um, Crohn's disease penetrates several layers. So, it's not just the inner lining. It can actually go even all the way through the abdomen. So, Crohn's disease tunnels more through the digestive tract where ulcerative colitis will just eat away at that first layer. Bleeding is very common with ulcerative colitis. Bleeding is very uncommon with Crohn's disease. So you can see the different types of inflammatory bowel disease right here. Right here on the left, ulcerative colitis. That's where I t what I talked about earlier where it's just affecting um the colon and the rectum where you can see irritable bowel disease is more dispersed. Um mainly patients will experience croins disease in that illiam area. So Crohn's and ulcerative colitis are diagnosed the same way. Stool cultures, CBC to check for anemia, barerium enema and colonoscopy. Surgical management, Crohn's disease. um surgical management doesn't alter it the progression or reoccurrence. So if they go in and let's say like fix any tunneling or ulceration that occurs with Crohn's disease that is just a temporary fix the Crohn's will can come back and erode the same area. Where as with ulcers of um colitis, if they fix or surgically fix a certain area affected, specifically through the ilioanal pullth through anos um stomosis, where they essentially make a new pouch to get rid of that area that was ulcerated by the colitis. So they kind of like join they cut out the bad part of the bowel and then join the healthy portions to make a new pouch. Ulceritis ulcerative colitis will not go back and now affect that new pouch area they created after the surgery is performed. All right. So, amino siliates, an example of this is sulfazine. It's used for Crohn's and ulcerative colitis. So, it's a topical anti-in it has a topical anti-inflammatory effect in the bowel. You take the medication orally but then when it is secreted into the intestines it has this topical anti-inflammatory effect. Common side effects headache, abdominal pain and nausea. Nursing considerations. If somebody has an allergy to aspirin um they will probably have a cross sensitivity to this medication as well. Labs should also be monitored if the patient has renal failure. Other medications used for inflammatory bowel disease, supplementary vitamins and minerals because they have absorption issues because of the different ulcerations. anti-inflammatory corticore steroids such as predazone. And then since um inflammatory bowel disease is an autoimmune disease, immune modulating agents and biologic agents can also help in preventing flare-ups. There's nothing you can do to cure Crohn's or ulcerative colitis. We're just managing it. Okay. Appendicitis. So, inflammation of the veraform appendix. So, that is the technical medical name of what we know as the appendix. Its full name is the veraform appendix. So, obstruction happens to the sphincter of the appendix leading to enlargement. Um, this is most common in adolescence and young adults. So usually that sphincter gets obstructed by inflammation or disease process or even fecal material. Okay. When that sphincter becomes obstructed, at first the patient will develop very generalized abdominal pain, but then later on that pain will be very specific to Mc Bernie's point where that's where the pain is coming from. That's where the patient will complain of the most pain. Mc Bernie's point is between the umbilicus and the iliac crest, the right iliac crest because McBernie's point is found in the right lower quadrant. So that is very specific to appendicitis. So it's important to know where Mc Bernie's point is. They might also have other symptoms such as rebound tenderness, fever, nausea, vomiting, lumbar pain, and dysura can also occur if there's a lot of inflammation and the appendix inflamed appendix is pushing on the back or the bladder. If the appendix ruptures, so this is a later symptom, that's when the patient might develop paralytic ilas. So if the appendic ruptures or there's a perforation in the ilas, this paralytic ilas can occur. So this is like when the patient will then feel abdominal pain throughout their whole abdomen and then they'll also be absent of bowel sounds. And that is because that ilas is now not working like it should. It's paralyzed. Why it's called a paralytic ilas. So we know that when you don't hear bowel movements and paristalsis is no longer working that that is a different emergency in itself. Young children may act restless or irritable. They might have a slight fever or rapid p pulse. A lot of times in young children, the appendix ruptures before they're diagnosed with appendicitis diagnosis, diagnostic tests and finding. So luccoytosis would occur specifically an increase in the neutrfils which shows a bacterial infection and then a CT or a sono would show the appendicitis. That's what's going on. Medical management, antibiotics, surgical management, appendecttomy. So, nursing care involving an epidetomy, um, giving IV fluids, monitoring pain, making sure that the patient takes it easy because after their appendix is removed, a lot of times the patients will have a fast recovery where they start feeling very good, very quickly, but we still want them to take it easy. Um, we want to make sure that we avoid palpating the stomach if we're worried a patient has appendixitis because we don't want to risk rupturing the appendix. Geriatric considerations. Sometimes geriatric patients can have non-typical symptoms. So maybe they'll have some nausea and vomiting and a slight fever, but they won't necessarily have abdominal pain or that Mc Bernie's point pain. So we have to do some more investigating if we look into appendicitis on a geriatric patient. All right, diverticula. So we're going to specifically talk about diverticula of the intestines. You can get diverticula um in your esophagus, too, but we're just going to be talking about diverticula of the intestines. So that's when you get sacks or pouches that herniate or go through the mucosa, a weakened area and out into the intestine. So you get these I think I have a picture. You get these little out pouches and issues arise arise when fecal material starts going into that diverticula because then it stays there and then inflammation and infection can occur. So diverticulosis is when you have the diverticula but you're asymptomatic. There's no inflammation or infection. Diverticulitis is when you have inflamed diverticula. So that is more serious to have diverticulitis. You're at greatest risk factor for developing um diverticulitis. if you have a low fiber intake because again fiber helps move everything through the bowels and also if you have chronic constipation because again when you're constipated the stool sits in the bowel and can push on the intestinal wall and weaken it and cause those diverticuli. So chronic constipation is a huge risk factor for developing um diverticulosis or diverticulitis. And then there's possible a hereditary component to it. Some patients might just have weakened intestinal lining. So again, I mentioned it's that feal m bacteria, that fecal material that gets into that diverticula which causes the inflammation. So signs and symptoms, they'll have constipation that alternates with diarrhea. They'll also have flatulence, pain, tenderness in the left lower quadrant. They might have maroon stools, so blood in their stools or stools that look like current jelly. So basically stools that have blood clots in them. diagnostic test. Um, a CT, a barerium, enema, a colonoscopy can all let us know if somebody has diverticulitis or diverticulosis. Medical management. So, high-fiber diet is going to be the most important because again, fiber is going to kind of help clean out those diverticula and get the stool out of there. So they either need to be consuming 20 to 35 grams of fiber a day or taking a lot of bulk forming laxatives such as Metamucil. So again, somebody that has diverticulus or diverticulitis would probably be on a laxative for like the rest of their life, the bulk forming laxative because they need to make sure that they get 20 to 35 grams of fiber a day. Just to give you an idea, an apple has 4.4 4 gram of fiber in it. So if somebody wanted to get that fiber naturally, they would have to eat like at least five apples a day. And we know the majority of our clients are not going to eat five apples a day because if they did that in the first place, they probably wouldn't have ended up with diverticulosis or diverticulitis in the first place. Surgical management, we only worry about like if they have a perforation. If there's a perforation, they'll have to go in and do a bowel resection. And sometimes um that will result in a colonos a colonostomy as well. Colostomy. Sorry, I couldn't think of the word. But that is less common. Okay, moving into chapter 47. So our dis disorders of our accessory structures. So we're going to start with disorders of the liver. So jaundice is a symptom not a disease. We know that jaundice occurs when Billy Rubin builds up in the body. So normal Billy Rubin levels and the Billy Rubin is building up in the body because of liver disease primarily cerosis of the liver. Normal Billy Rubin levels 0.2 to 1.3 we start seeing jaundice if Billy Rubin levels get above 2.5. So the easiest places to see jaundice, you can get jaundice all over your body, but the easiest places to assess jaundice are um the scalera and the palms. You can also look on the gums too or hard pallet, but most of the time the easiest places to assess jaundice are the palms and the scalera or the white of the eye. So what is exactly happening to this Billy ribbon where it is building up in the blood? It it mainly is happening because the liver is not functioning properly. So it's not excreting the Billy Rubin properly. So when we talk about Billy Rubin, your body has two types of Billy Rubin at it in it going on at all the time. So you have direct or conjugated which circulates freely. Okay. So conjugated means that it has been processed by the liver. Indirect is unconjugated which means it has not been processed by the liver yet. So indirect or unconjugated there's no direct way to calculate that. We're not going to get into testing like when will my direct what do I need when will when would I suspect direct Billy Rubin to increase versus indirect. But you can determine disease processes too based on direct and indirect and the levels that there are in the body. What you need to know for the test is that when you have an increase of Billy Rubin greater than 2.5, that is when you're going to see jaundice. And again, that Billy Rubin is occurring because the liver is not processing it. Billy Rubin is a byproduct from hemoglobin when it gets broken down. So now let's talk about cerosis. So this is a chronic degenerative liver disorder caused by generalized cellular damage. So cerosis means that there's just damage to all the cells throughout the whole liver. And this really becomes an issue when the cells become so damaged that they don't regenerate anymore and then start forming scar tissue which then becomes fibroids which then becomes not functional. So basically patients with very serious cerosis means that the majority of their liver is now taken up by scar tissue and we all know that scar tissue is not functional tissue. So the prognosis of how well someone will do with cerosis because it's irreversible is based on many factors basically like medication compliance, how advanced it is, how advanced their liver disease is by the time they're diagnosed, and just their willingness to be compliant. in most cases. So, cerosis the majority of the time is caused by alcohol. Okay, that's pretty common knowledge. We all know that alcohol is bad for the liver. The more alcohol we drink, the more our liver has to work. The more it works, the harder it works, the more likely we are to damage cells and cause that scar tissue. So again, liver cells are irreversibly damaged and become non-functioning and when that happens um our body our body has a hard time then absorbing fats. We get portal hypertension, esophageal variases, acites and hpatic encphylopathy. So there are a lot of complications that occur due to having cerosis of the liver. I also just want I know that I talked about the majority of the time cerosis is caused by alcohol. So alcoholic cerosis but nash you might also see which is non-alcoholic stoep hepat hepatitis or nash as it's called. This is like a fatty liver disease that causes cerosis. So this has to do with more of like diabetes, elevated cholesterol or coronary artery disease. So you might also see cerosis fairly commonly and it's related to nash and that's not alcoholrelated. So signs and symptoms of cerosis they're categorized as compensated versus decompensated. You don't need to memorize the difference between compensated and decompensated. just know this is how the symptoms are classified. So as liver failure progresses or cerosis gets worse, you'll see more decompensated signs and symptoms. diagnostic tests and findings. So a liver biopsy will reveal the hpatic fibrosis that we talked about that occurs when cells are damaged and can no longer regenerate. Um they can do Billy Rubin levels. They can look at liver enzymes. So we would expect the A, ALT, ALP, GGGT to be elevated, low red blood cells, low platelets and albumin would also be decreased. So remember that living liver also helps with clotting. So we would see decreases again in the platelets and um you would also develop anemia. So red blood cells would also go down. And albumin we know has to do with protein in the plasma that helps maintain that intervascular pressure. So we see a lot of that third spacing where they have fluid going into the their abdomen when you have cerosis of the liver. So no cure exists. The goal is to prevent um deterioration and to keep it from getting worse. Medical management. Um high protein diet, low sodium, calorie dense frequent meals. We also want to eliminate alcohol because again the majority of time cerosis is caused by alcohol. And then lactolose is also really important in the management of cerosis. So it is a laxative that patients will usually take lactolose three times a day because again that is how ammonia is leaving their body since their liver can no longer break down ammonia and when it builds up in the body it becomes very dangerous which we'll talk about here in a moment. So they need to be taking lactolose three times a day because they need to be having about at least three bowel movements a day. So lactolose is really important. All right. So let's talk about some of the complications that occur when a patient has cerosis of the liver. So first one is going to be portal hypertension. So that scarred tissue in the liver compresses the portal vein which causes blood to back up into the rest of the body into the portal system which which is a very specific circula uh circulatory system that involves like the esophagus, the intestines, the pancreas. So, as you can see here, when that blood starts to back up into the portal system, it causes um congestion or edema. So then you start seeing things like um esophageal and gastric variouses, spleenomegaly and um you can also see hemorrhoids. So symptoms of portal hypertension, GI bleeding, ascites, decreased platelets, treatment, again we want to reduce the fluid volume and venus pressure. So again with that portal hypertension that occurs that blood backing up causes this esophageal verices which is this dilated bulging esophageal veins and these are especially vulnerable to bleeding. So if these rupture the patient can bleed to death. So they'll get esophageal bleeding treatment. Um they can do injection scalerotherapy which is just a procedure where they take a tiny needle and inject a solution into the vein and then it kind of like causes the vein to be reabsorbed into the body. So it stops the bleeding. And then they can also do um verical banding where they will basically just put rubber bands around the veins to close them off. Okay, ascites is that collection of fluid in the peritineal cavity and this can also lead to hpatino syndrome where then when the fluid starts backing up into the peritineal cavity it causes the kidneys to shut down too. It's kind of a phenomenon they don't understand entirely why it triggers the body to do that. So again, ascites is coming from the portal hypertension, but it is also being made worse by the low album in the body because we know that that albumin 2 helps hold the fluid in the intervascular space. So symptoms excessive and massing abdominal swelling treatment paracentesis. So they can actually go in to the peritineal cavity and pull out fluid with a needle. We can give diuretics. We can do also do a low sodium diet. So that question on the bottom that's really important for nurses. How does a nurse assess ascites is improving? Then that's when we measure abdominal girth. So we would expect if a sites improving the abdominal girth would get less. So their waist would get smaller because that means that the swelling is going down. It's important too when you measure abdominal girth that everybody is measuring from the same place. So usually we measure uh we use the umbilicus as a guide. Okay. Hypatic encphylopathy. So if that ammonia builds up in the bloodstream, it is toxic and it can cause um central nervous system symptoms and again that's directly related to increase in serum ammonia levels. So you're going to see disorientation, drowsiness, confusion. So if you have a patient and they start getting very confused and they have a history of cerosis and they're not acting right, definitely want to check an ammonia level on them. This is another reason why they need to be taking their lactolosis scheduled which compliance with lactose is difficult at times because it gives patients diarrhea. So they don't want to take it. But it is so important to prevent hpatic and syphilopathy. So education is key. All right, moving on from cerosis, hepatitis. So hepatitis just means inflammation of the liver. It can be acute or chronic. Most common cause is a virus. Here are different types A, B, C, D, and E. So we're going to run through how each is transmitted. So A and E are transmitted via the oral fecal route. So A and E come from contaminated food or you know contamination of feces that then gets ingested through the mouth. So A and E oral fecal root. B and C are transmitted through blood or sexual contact. and D occurs secondary in people that are infected with hepatitis B. So D is something that can all you can get a a second form of hepatitis if you have hepatitis B. And then G is kind of like the catchall. It's doesn't behave like any of the other hepatitises. We see it more in patients after a blood transfusion is when we see hepatitis G. It's not that common. All right. Assessment findings, signs and symptoms for all type. They follow these um they follow these four phases. So incubation phase, asymptomatic but the patient is infectious. Pormal phase is when they develop nausea, vomiting, anorexia, fever, malaise and then the symptoms start. Um ectctor phase is when symptoms peak and then um postric phase is when symptoms start to subside and liver function returns to normal. So you don't need to memorize what occurs in all of these phases, but this is the pattern that hepatitis follows. diagnostics, viral antibodies, PT, PTT, and liver function studies. And again, these kind of like let us know what type of hepatitis it is and then also if the hepatitis is flared up or if it has gone away. So medical management and nursing care, we are managing the symptoms. So this includes bed rest, eating a balanced diet, IV fluids, supplemental vitamins. There are new treatments that have been developed specifically for B and C such as recumbent interferon um and antivirals that are force the virus into admission. So B and C are with you for life, but these new drugs basically force the virus into um remission. So it's at very low, sometimes indetectable levels. So there's been a lot of breakthroughs in how we treat hepatitis B and C. worst case scenario that it causes permanent liver damage again where the patient will need a liver transplant. We all know how hard it is to get organ transplants right gallbladder. So choleathiasis and choleiccyitis. So choleathiasis stones in the gallbladder. Um and then choleaccyitis inflammation or infection of the gallbladder. You can have acute or chronic. And then usually if you have one, you have the other. They almost always coexist together. Advanced age is a risk factor and being female. So signs and symptoms belching nausea and that right upper quadrant pain that you get with um choleosis or choleiccyitis is called biliary collic. that's specific to your gallbladder is that biliary collic diagnostic test and findings CT ultrasound and ERCP. All right. Medical management, making the patient MO diet modification. So again, best is like we're going to make them mo and then if it's acute, it might resolve on its own or they might just have a flare up. So then we can start them back slowly on like a low residual diet and then analesics for pain. In severe cases, we might have to put an NG tube down for um abdominant for decompression. And we use NG's a lot after um you have a choicesctomy to decompress the stomach and to help everything heal. Surgical manage fit. You could do a lithotripsy or again we we talked about lithotripsy when we talked about breaking up um uriteral lithiosis or stones of the urinary tract. That's using sound waves. And then there's um a laparoscopic choicesctomy which is the preferred way because there's less incisions or there's an open choleicasectomy where again they make an incision and open the patient up more. On the next slide I have a picture of the differences between them. So lower left that's supposed to be your lap choleacyctomy. A right open coliscasectomy where they actually retract the skin and the muscle apart and get down to the organ. Okay. Acute pancreatitis can be mild to severe and it can be fatal. if mild should have normal function with six months of onset. So it when with acute pancreatitis the pancreatic enzymes get backed up into the pancreas for whatever reason something is causing an obstruction and this causes the pancreas to autodigest or which means that the pancreas starts to digest itself or break down itself. So that's kind of a scary notion. And then causes again vary widely for what causes acute pancreatitis. A lot of times it's alcoholrelated. It could also be related to metabolic disorders, trauma, infection, hereditary factors, um refeeding after prolonged fasting or anorexia. And then sometimes it just develops idiopathically like we don't know why. So severe to mild upper abdominal pain and the pain gets worse after eating. Stratera which is fatty or foamy bowel movements. Diagnostic tests and findings amalase lipase are going to be greater than 200 and then liver function tests will also be elevated. CT scan and ultrasound can also be completed. Medical management and nursing care making the patient NPO controlling the pain usually improvement will occur within one week. However, it can turn into chronic pancreatitis. So this is prolonged or progressive pancreatitis. Alcohol is the cause in most cases. 20% no particular case is found. So pancreas hardens and function is destroyed. So in chronic pancreatitis we have loss of function. Signs and symptoms. severe present with weight loss and extreme pain. Diagnostic tests and findings are going to be same as acute pancreatitis. Um medical management stop drinking alcohol can usually help improve the pain. Um NSAIDs and opiate analesics can be used for pain control. And then also a lot of times we'll have to replace the pancreatic enzyme. So the patient will have to end up taking like um pancreatace and insulin management because another thing with acute and chronic pancreatitis we know that the pancreas has those endocrine functions of controlling blood glucose levels. When the pancreas is inflamed, it's not producing insulin like they should. So patients glucose levels will become very high with acute and chronic pancreatitis. So they're very sensitive to large amounts of glucose. So and in chronic pancreatitis, a lot of times they'll end up needing to replace that pancreatic enzyme, but also they'll need insulin as well. In severe cases, um partial or total pancreatctomy will need to be done for chronic pancreatitis. Okay. So to review, these are some things that you should be able to know for the test. So this is a good review. What is jaundice and how and what lab should be assessed? That should be what is jaundice and what lab should be assessed. Then we have what are the characteristics of irritable bowel disease? What lab findings reflect pancreatitis? What causes acute versus chronic pancreatitis? What is the medication sul sulcazine used for? What are the nursing considerations when administering this drug? What are the complications associated with cerosis of the liver? So how does the nurse assess these complications? So by complications, this is like yourites, your portal hypertension, esophageal varies, hpatic and sephylopathy. You should know all about those complications and then how the nurse should assess for them. How do you prevent hepatitis A and E? So those are our oral fecal root hepatitis. So what would you do to prevent that? How does the nurse care for patient after choleiccasectomy? When would the nurse administer lactose? What are the main differences between Crohn's and ulcerative colitis? And for that, use that infographic that's going to help you understand the differences between Crohn's and ulcerative colitis for the test. Give an example of a stimulant, saline, and vulforming laxative. What are nursing considerations when administering laxatives? What are the signs and symptoms of appendicitis? And then what are the risk factors for developing diverticulosis/diverticulitis? So again, go through these review questions and then I will be available for questions before the test as well. Make sure you go through your notes and we from Monday as well and please reach out to me if you have any questions.