Hepatobiliary 1

part of the reason we might see ascites is that increase in sodium retention and this happens because there is excess of renal sodium absorption because there is increased aldosterone production and decreased inactivation of that aldosterone. so we also have that sodium angle going on now the peritoneal cavity can hold up to ____ liters of fluid and there's some estimates that that they can hold even higher than that but that's a lot of fluid now they just said when the fluid shifts some of the protein goes with it too and the fluid in the peritoneal cavity can have one to two grams of protein per 100MLs of that fluid. So what you have on this side is __________ which is a procedure that drains the fluid but also along with that drain some of that protein and also increases the risk for peritonitis.

15 1/2 paracentesis

how do we treat how treat hepatitis from the MNT perspective? so nutritional care is the same for the different types of viral hepatitis as well as alcoholic hepatitis to some degree so the goal with MNT is to really spare the liver from further damage while really optimizing nutrients for the liver regeneration so if alcohol is involved that abstinence is required as far as calorie goals are concerned you want to think higher calories as in ______ calories per kilogram which may yes result in some individuals having to consume 3000 calories or more now as far as protein is concerned your module says 1 to 1.2 grams per kilogram per day now if you look in any other M NT book they'll all say ______ grams per kilogram per day so just keep in mind so this one to 1.5 is a new guideline that's been suggested

30 to 35 1 to 1.5

now in hepatitis one of the things that is fairly common that you might see some fat intolerance and so you might see that manifest itself as steatorrhea as it relates to the ineffectiveness of the bio salts and impaired intestinal absorption so steatorrhea so because of that fat may have to be adjusted in terms of amount so _____% is not really a restriction in any way but if you continue to have problems with fat intolerance then you can either go down to 30% or even a little bit lower or change to an MCT oil now. __________ is also often recommended because of the increased prothrombin times due to that decreased production of those clotting factors so generally vitamin K is given in water soluble form in addition to the other fat-soluble vitamins in order to really correct the ___________ times that are significantly impacted with that vitamin K with the vitamin K deficiency

30 to 40 vitamin K prothrombin

what then is the difference between acute hepatitis and chronic viral hepatitis so hepatitis becomes chronic when histological changes can be associated with the disease so in acute disease oftentimes the situation will resolve itself over a period of days maybe sometimes weeks even maybe sometimes will take months but if it doesn't progress and it stops right there then you can go back to a healthy liver but sometimes then it can progress to a chronic hepatitis. so acute hep B evolves into a chronic hepatitis in about 5% of cases and as many as ____% of cases of acute hepatitis C will evolve into chronic hepatitis C. there is a much higher risk of moving into that chronic stage. what are the symptoms of hepatitis we'll see things like jaundice anorexia fatigue nausea vomiting sometimes you'll see a fever not always but look at these symptoms besides a jaundiced look at the symptoms that the anorexia to fatigue the nausea it could be any general condition that could cause and so it becomes very difficult unless somebody has a very visible form of _________ to know that this viral hepatitis is going on so this diagram just shows the clinical course of hepatitis C and even though the natural course of hepatitis C varies slightly from person to person it generally does follow this progression

85 jaundice

bio salts are really what aid in the absorption of fatty acids and cholesterol and other lipids as well. because what do we need in order to absorb fat we need to be able to form those micelles which is accomplished by these bile salts allowing the micelles to be soluble in the chine so bio salt secretion is tightly regulated by enterohepatic circulation and once the bio salts enter the small intestine approximately ___% are then reabsorbed into the blood where they enter the portal blood and then are then returned back to the liver so there they can absorb back into the hepatic cells where they once again will be re secreted into the bile so this enterohepatic circulation occurs about two to three times per meal and ________ times before the salts are then excreted into the feces now what we lose in the stool then is replaced by new bile salts that the liver is continually producing

95 18 to 20

now folate too is activated in the liver to its active form and again if you don't have that conversion to the active form that folic acid then you essentially will see a folic acid deficiency which can then manifest itself as a macrocytic anemia you would see elevated homocysteine all of those things that you would expect with the folic acid deficiency. we know that macrocytic anemias are also seen with a ___ deficiency so why would there be a vitamin B12 deficiency in someone with liver disease because B12 is also stored in the liver. now in this last one which is really a big one to is a conversion of vitamin D to the active form or that first ____________ of the vitamin D and then it goes to the kidney for that second hydroxylation so that intermediate step is interfered with and therefore the production of vitamin D3 becomes much lower when we have any sort of liver disease

B12 hydroxylation

alkaline phosphatase and bilirubin can be used as indicators of ___________ which is when the flow of the bile is either blocked completely or reduced to a great degree and even small blockages will result in increases in this alkaline phosphatase and even bilirubin so they are good indicators that there might be something happening with the flow of the bile. we can also look at hepatic enzymes so the typical ones that you see that are drawn in the labs like the _________ which almost similar to the transaminase is what happens is these start to leak out into general circulation too when the liver cells are damaged or if they're not working appropriately so if you see elevated levels of ALT or AST again it can be an indicator that something's happening with the liver. which is when the flow of the bile is either blocked completely or reduced to a great degree and even small blockages will result in increases in this alkaline phosphatase and even bilirubin so they are good indicators that there might be something happening with the flow of the _____. we can also look at hepatic enzymes so the typical ones that you see that are drawn in the labs like the ALT in the AST which almost similar to the transaminase is what happens is these start to leak out into general circulation too when the liver cells are damaged or if they're not working appropriately so if you see elevated levels of ALT or AST again it can be an indicator that something's happening with the liver.

Cholestasis ALT and the AST bile

what are some of the diagnostic tests that we can use to identify how well the liver is functioning or how impaired it is? let's start with this first one this __________ so if you see altered prothrombin time or you see increased ammonia typically this is indicative of dysfunction of the metabolic processes of the liver so it alerts us right away that there might be something happening with the metabolic processes. So what we're seeing is that the clotting factors are not being made or that the ammonia is not being detoxified so again it alerts us that there's some sort of issue. now these transaminase can be really good indicators of _________ because when the liver cells start to die they leak these transaminase is out into circulation and specifically one of the tests that they use pretty often to determine whether cell necrosis is happening is looking at ____ this lactate dehydrogenase which again when you start to see this cell necrosis you start to see it leak out into general circulation so you would measure it with the lab test if it's elevated you would look further and see whether there is cell necrosis or something else happening with the liver.

PT2 and this NH4 cell necrosis LDH

this is just another way to look at alcohol metabolism you start with ethanol and you end up with _______________ on the other side

acetyl aldehyde and acetate

we could also start to look at cognitive abilities because generally cognitive abilities correspond to alterations in ________ levels disruption of certain amino acid profiles. the other thing that affects cognitive abilities are the vitamin D deficiencies we might see in someone with end stage liver disease or severe liver disease there might also be physical signs of muscle or fat loss because of the malabsorption that often accompanies some of these hepatobiliary conditions. you might see someone that has this parictis which is __________ ataxia this imbalance in the gait this polymer erythema and even muscle wasting so there's a lot there's a lot of physical findings that you would want to use in conjunction with the lab tests

ammonia itching all over

there's a lot of physical findings that are used along with the laboratory diagnostic tests. we can look at liver size and Histology but when something is going wrong you can see the changes in the color of the liver you can see changes in the fatty infiltration and the streaks in the liver maybe some nodular components would be visible when looking at the Histology. see if we can actually use scans and looking at the liver to tell us that something is going on. we can look at this whether it's very dark as a clay colored. what's happening to the urine the color of the urine as well fluid distribution. we should look at fluid distribution because with liver disease we tend to have a lot of fluid shifts and we might see edema of certain areas or we might see this ______ which is around the abdominal area or we may see this sort of _______ which is edema throughout the entire body. so it could be either or producing a lot of ascites with liver disease.

ascites anasarca

portal hypertension is not a physical finding per say but it leads to some of the physical findings that we'll be talking about so portal hypertension is most often the result of liver cirrhosis regardless of why the cirrhosis happened in the 1st place so when you have cirrhosis a lot of times you see portal hypertension but as liver function declines there are three major complications that can lead to mortality and morbidity one is portal hypertension the second is ______ in the third is ____________. when you have fatty liver or you have a sclerosed liver you generally will see this portal hypertension in conjunction with that.

ascites hepatic encephalopathy

now the onset of portal hypertension may not be associated with any specific symptoms. It can really help you identify that something is happening in the liver but some of the late stage symptoms would be that GI bleeding the ascites you might even encephalopathy reduced levels of clotting factors but usually the diagnosis of portal hypertension does not happen until the ______ develops because it's hard to know that this is actually happening. what can we actually do about it? there are some interventions like medications and even some dietary interventions which one of those would be a low sodium diet but more effective than that is a procedure that's called tips or this transjugular intrahepatic portosystemic shunt which is basically a stent that's implanted into the middle of the liver which helps to relieve some of that ________

ascites pressure

what ends up happening is that you have this increased pressure gradient so if someone has liver disease and ascites they most certainly will have portal hypertension which is high blood pressure in that hepatic portal system so this high blood pressure is in that whole entire hepatic portal system so that is composed of the portal vein and all of its branches and its tributaries so portal hypertension is then really defined as an elevation of hepatic venous pressure gradient. So what happens is that this pressure gradient can cause the blood to flow _________ and that causes the veins to enlarge so then what you have is some of these collateral veins and arteries which turned into what we call ______ which actually start to expand in increase in size particularly you'll see this happening in the esophagus but also can happen in the stomach as well.

backwards varices

now as the pressure increases or as the portal hypertension is prolonged those varices can rupture and bleed and there is a link between the rupture or bleeding from esophageal varices and hepatic encephalopathy when there is this bleeding or this hemorrhaging from the varices we've seen increased risk for encephalopathy now basically it's thought that the intestinal absorption of toxic substances generated from those _________ is what leads to elevated ammonia levels exacerbating or promoting that hepatic encephalopathy

blood proteins

the function of the Gallbladder is to ________________ the bile that's produced in the liver and it controls the delivery bile salt into the duodenum. when you have any disease or impairment in your gallbladder you are going to start to see lots of issues. these Gallbladder conditions are not uncommon they affect millions of people in a lot of suffering

concentrate store and excrete

so stool generally for those that are excreting too much bilirubin tend to be very ____ in nature and for those who are not excreting enough the stool tends to be very light colored or almost like a _____ colored stool so that is also another indicator we can use we can also look at other so do we see any changes with blood clotting are we seeing something like a portal hypertension so we can look at some of the physical signs and symptoms but we can also we can also use these biochemical measures which would be a little bit more definitive in telling us what's not only that there's something happening but what's happening. now these tests are not perfect, but they certainly can indicate what specific areas are being affected and how badly they are being affected

dark Gray

their eyes can be as yellow as this because bilirubin is an end product of red blood cell destruction sometimes you see jaundice because there is a significant __________ of those red blood cells. now if this happens you end up seeing a pretty rapid release of bilirubin into circulation and then you have what's termed a hemolytic jaundice that second reason you might see jaundice is due to an obstruction of the bile ducts or because of damage to those hepatocytes. so this ends up then resulting in an obstructive jaundice because even normal amounts of bilirubin are then prevented from being excreted into the GI tract and that's why you get the name obstructive jaundice. now when you look at labs usually, you'll see bilirubin levels less than ___ but if an abnormality exists you might see numbers even as high as five sometimes there's babies that have very high levels of bilirubin right after they're born and I've seen numbers up to 15

destruction 1.1

Now the liver is responsible for synthesis as well as the breakdown and clearance of hormones and also bilirubin. it also plays a large role in ____________ again primarily of drugs alcohol ammonia. also plays a role in the excretion of bilirubin and drugs and hormones and bile acids and cholesterol

detoxification

when we talk about the hepatobiliary system generally we are thinking about the liver but the hepatobiliary system it not only includes the liver but the accessory organs as well. all of those that are involved in the homeostatic processes. so as we can see from this picture the liver is in the right upper quadrant and it's placed strategically behind all of the other accessory organs that participate in the ______________ processes that really then allow the liver to be that central or key organ that's involved in homeostasis. now generally the liver is about 1200 to 1600 grams and it's about 2 to 2.5% of total body weight so it is one of the largest organs. you also notice that when the liver is healthy it is a very nice dark pink or brownish red color and again the other organs of the hepatobiliary system are the gallbladder the small intestine the biliary duct of the pancreas etc

digestion and absorption

sometimes there's so much ascites that we have to do this paracentesis but let's say we're worried about the risk for paracentesis or worried about the protein losses what else can we do well we can use _________ so you'll see that very commonly in anybody who has portal hypertension and/or ascites, we can use a low sodium diet and then we can use fluid restrictions but the problem with that is that you already have systemic ________ now add to that a fluid restriction or add to that even diuretics and you can easily throw someone into AKI if you're not careful. so the use of diuretics in fluid restrictions and lower sodium diets are done very slowly in an attempt to maintain fluid balance in all of the different compartments. basically what you need to know is by the time someone gets to cirrhosis you are more than likely going to progress down the line not always but progress down the line and can result in the portal hypertension and the ascites as well

diuretics dehydration

now as far as synthesis is concerned the key to this homeostasis and one of the biggest issues that is problematic for people with liver disease is the fact that a liver synthesizes so many different things. it synthesizes blood proteins so things like albumin pre albumin transferrin prothrombin it also produces hormones enzymes. now clearance is obviously a huge function of the liver we clear a lot of toxic substances through the liver one of which is bilirubin and detoxification of things like ______________ which are two of the primary substances that are detoxified by the liver and ones that can actually affect its function and alter the health of the hepatocytes.

drugs and alcohol

so it's really sort of this first half of the picture where MNT should be very aggressive and supportive of regeneration in this situation with these then repeated attacks and continued exposure though these two diagnosis of steatosis and hepatitis will then develop into cirrhosis and then you'll start to see this fibrosis you'll see this hyperplastic nodules here at this stage the amount of reversal becomes very compromised so if a liver is partially cirrhotic there may be some reversal but for the most part you want to catch someone early and be aggressive with nutrition interventions and nutrition support in order to really reverse that damage because again in these ______ stages you can go right back to that healthy liver

early

now the so the MEOS system is sometimes called the cytochrome P-450 and that takes place in the ___________ as opposed to the cytosol for the other one and also contributes to the oxidation of ethanol in the liver. this pathway is initiated with chronic alcohol consumption and also metabolizes ethanol to acetyl aldehyde when we have high concentrations of ethanol. and then we have a catalyst pathway which is this enzyme that's located in the __________ but this is really a minor pathway of alcohol metabolism except in a fasted state. So what are the products of oxidative metabolism of ethanol acetyl aldehyde but we also have _________ which is produced by the oxidation of the acetyl aldehyde. acetate itself is not an inert byproduct and it ends up increasing blood flow to the liver and it also depresses the central nervous system. it's also metabolized to acetyl CoA which is involved in lipid and cholesterol biosynthesis and there's this hypothesis that in cases of chronic alcohol intake that the brain then starts to use _________ rather than glucose as a source of energy

endoplasmic reticulum peroxisomes acetate acetate

a liver weighs about 2100 grams so normal liver is about 12 to 1600 grams so you can sort of see this overall increase in size. so there could be a lot of different lot of different reasons for this it could be due to hepatitis it could be due to malaria a biliary cirrhosis hemochromatosis Wilson's disease so there's a lot of etiologies of why we might see this hepatomegaly or this _________ but generally it's diagnosed through a medical history and a physical examination and then how we treat this depends obviously on what the cause is

enlarged liver

what do we know about the pancreas? it's a small organ it's located right behind the stomach it's also an accessory digestive gland so the pancreas is like this elongated tapered organ to function endocrine and exocrine and its exocrine function we're looking at digestion so the pancreas produces the _________ necessary for digestion. now when we talk about the pancreas were usually focused on its relationship with diabetes so we're usually focused on the endocrine function

enzymes

on the right is this enlarged sort of yellow liver. now some fat in our liver is normal but when fat starts to make up more than _______% of the organs weight that's when it can become quite concerning while the two main causes of fatty liver are alcoholic liver disease and nonalcoholic fatty liver disease you might also see this in an overweight or obese individual or even sometimes in _________ you'll see a fatty liver and it's termed acute fatty liver of pregnancy now individuals who have fatty liver can be asymptomatic for many years so they may have this fatty liver and they may not know but some of the common symptoms that you could see would be things like exhaustion feeling really tired loss of weight loss of appetite weakness nausea some of the cognitive impairments would like confusion poor judgment and even trouble concentrating

five to 10 pregnancy

now in this chronic hepatitis C the liver becomes more and more inflamed and more and more scarred over a period of years but the speed at which the information in the scoring takes place varies between people so a 3rd will develop severe liver scars will develop severe liver scarring and the liver will stop functioning normally within about 20 years or so another third take about 30 years for that cirrhosis to occur and in that remaining third remaining third though liver disease progress is very slowly does not really become a major problem during their lifetime. let's just go back to this acute hepatitis side of the flow chart for a second some patients with acute hepatitis will develop what we call this ___________ and this is very rare yes but it can be problematic so fulminant hepatitis is acute liver failure that's really complicated then by hepatic encephalopathy but in either case whether it takes the sub clinical course or more of an acute course you can end up with liver cirrhosis then we'll get into more about cirrhosis

fulminant hepatitis

it's important for the components of the bile to stay within a normal ratio otherwise cholesterol can precipitate out and form __________. the bile is secreted by the liver and it ends up in the Gallbladder where it's expelled from the Gallbladder into the common bile duct eventually into the small intestine where its entry is controlled by this sphincter of ODDI which has to be relaxed to allow the bile to flow into the duodenum. So what is bile doing in that intestinal tract? it acts as an __________ and it allows for the fat globules to be broken up.

gallstones emulsifier

now if you have lower blood sugars and you haven't eaten in a while and this is somebody who has liver disease it becomes very difficult to provide glucose in a steady state because of the impairment in glycogenolysis the release of glycogen and as well as the synthesis of glucose from pyruvate. now the liver's role in protein metabolism is probably the most important of its metabolic functions so the liver functions to deaminated amino acids which is a critical step before amino acids can actually be used for energy or be able to be converted into __________ so this deamination then produces ammonia which then our body must get rid of right via _______. the liver also produces many different transport proteins in blood clotting proteins.

glucose urea

as far as metabolism is concerned we're not only looking at the macromolecules but we're also looking at the micronutrients as well. now when we have someone with end stage liver disease there are many nutritional deficiencies that can occur as a result of that impaired liver function. so we have glucose regulation what happens is glucose rich blood enters the liver through the hepatic portal vein and the hepatocytes absorb a lot of that glucose and so then they store that glucose as ___________ and so we can use it for glycogenolysis if needed. so what's glycogenolysis that is the release of glucose into the bloodstream in order to maintain that fine range of glucose and we also have gluconeogenesis so ___% of gluconeogenesis occurs in the liver and only ____% occurs in the kidneys.

glycogen 90 10

In terms of synthesis what are we synthesizing in the liver for either export or use the liver synthesizes and stores approximately 100 grams of glycogen right via the ____________. it's also responsible for that gluconeogenesis synthesis of glucose from certain amino acid acids or lactate or glycerol and all these parts of the carbohydrate metabolism. the liver also plays a role in the production of the clotting factors as well as ____________ production so it's role in synthesis cannot in synthesis be trivialized. now obviously there is also the synthesis of bile and bile acids and cholesterol that takes place in the liver but the main point here is that the liver plays a role in synthesizing, so some of these things for use throughout the body but also for use within just the liver itself

glycogenesis red blood cell

we have the bile which drains into a large duct that is called the common hepatic duct which is then joined by the cystic duct from the Gallbladder so the bile salts then move from the liver and to the __________. now in the Gallbladder you have the bile that was secreted by the liver into the canicula so the Gallbladder contracts so all of that bile can be expelled and then moved along towards the common bile duct where then it can join with those ________. so the bile and the bile salts come together and they move towards a small intestine having to pass through this sphincter of oddi where then they eventually will flow into the duodenum and into the small intestine. in the __________ the majority of the bile salts will get reabsorbed by active transport and diffusion where then they will enter portal circulation so then they get absorbed and then they're reabsorbed by this _____________ and then they'll enter portal circulation where then they're going to go back into the liver as part of that enterohepatic circulation so then it starts all over again

hepatic duct bile salts small intestine active transport and diffusion

and there is a review of the literature and of the studies that really does support this higher amounts of protein because the thought before we don't want to get too much protein because it could precipitate _____________ but all of this newer literature the review is really saying that we can support these higher amounts of protein without precipitating hepatic encephalopathy or putting extra stress on the metabolic processes in any way. now when you think back to nutrition support our go to number was at ____ grams at a minimum right for protein now in liver diseases unless they're very compromised with hepatic encephalopathy you're going to push more towards the higher levels of proteins you're still going to push higher towards that like 1.5.

hepatic encephalopathy 1.2

so if you are at this stage how you can see that you can go back to a normal liver we abstain we reduce fat we reduce our weight sometimes will use metformin to improve insulin resistance and we try to get the triglycerides down the insulin resistance improved we try to get the glucose down lose the weight remove the alcohol whatever is causing it whether it's one of those things or all of the above so if you make changes what you have then will be this conversion back to this normal healthy liver but now let's say you don't stop the exposure to alcohol or those other toxic factors then that continued exposure is going to lead you to ______ where then we start to see the liver cell necrosis we start to see inflammation we see Mallory bodies and we start to see more fatty changes within the liver and again at this point with abstinence you can still go back to this normal liver.

hepatitis

hepatitis as you can probably tell from the name simply means inflammation of the liver and can result from a lot of different causes both infectious and non-infection. so infectious those viral bacterial fungal parasitic organisms and noninfectious could be alcohol drugs autoimmune diseases and even some metabolic diseases. according to the CDC there are four and a half million Americans that are currently living with chronic hepatitis and a lot of people don't even know that they have it so even more people probably don't even know that they have it and the most common causes for viral hepatitis in the USA ______________. so hepatitis a is generally transported through food through feces but generally as far as how it manifests itself it causes more of the acute flu like symptoms and generally is reversible doesn't really cause any long term damage whereas hepatitis B&C are contracted through ___________ and there's generally a much more rapid decline in liver function with the hepatitis B and hepatitis C when it comes to liver disease though we generally see hepatitis C as a major causative agent.

hepatitis a hepatitis B and hepatitis C semen saliva and blood

since our liver is so critical to metabolic processes and homeostasis we want to minimize any risk for any diseases or any dysfunction of the liver. what causes liver disease and how can we actually prevent it? so the three most common causes of liver disease are hepatitis viruses toxins primarily alcohol but not limited to alcohol lifestyle factors besides alcohol so namely fat consumption and obesity and then fatty liver as a result of that obesity and insulin resistance. the top three __________ mostly alcohol not only alcohol and then lifestyle factors like the fat consumption and obesity and knowing the cause of the liver disease is important and the liver functions pretty well until we've lost about ___% of the hepatocytes that's when we start to see a dramatic decline in liver function. the good thing about the liver too is that they can regenerate itself so if you determine what the cause of the liver disease is you can remove or minimize that because if you can remove it and minimize then you provide the liver with the opportunity to ________ itself with appropriate nutrition and then the removal of that etiologies. the diagnostic measures they're not perfect but they do help us diagnose what's going on and what the possible etiologies might be because if you look at all of these there's just so many different reasons why it can be

hepatitis viruses toxins 75 regenerate

so the endocrine function of the pancreas really occurs in those small clusters of cells that we know are the islets of Langerhans and then we know that the pancreatic cells also have three major types. each one is responsible for a different pancreatic product we have the Alpha cells which are making the Glucagon we have the beta cells which focus on diabetes and we have the Delta cells as well. now aside from insulin Glucagon and somatostatin there's a number of other _________ that are being made by the pancreas. those exocrine glands so they're producing a lot of enzymes. now when we think about digestion when food enters the stomach what happens in terms of the role of the pancreas so the pancreatic juices are released into a whole system of ducts that culminate in the main pancreatic duct so they're released they culminate they end up in this main pancreatic duct the pancreatic duct also then joins this common bile duct. they kind of all come together over here the common bile duct and pancreatic duct will kind of come together and then they form what we call over here this _____________ which is located in the first portion of the small intestine or the early part of through the duodenum and then you can see over this sphincter of ODDI

hormones ampulla of Vader

the progression of liver disease occurs regardless of the etiology so it doesn't matter what the etiology is this progression is going to be the same. let's start with this normal liver in the early stages you should note that liver disease can be corrected by _________. so we have this normal liver so we're going to start with this steatosis which is fat in the liver so let's say that we have exposure of alcohol to the liver and the fat starts to infiltrate into that liver and not only just exposure to the alcohol but anything that can be hepatotoxic so even exposure to high fat diet we start to see this fatty infiltration. so we start to see this to steatosis which is characterized by fatty change and by perivenular fibrosis. now usually when there is fatty liver there is a concomitant elevation of those __________ so you can generally even in a 16 year old that is morbidly obese you can see this just steatosis present and you will also see elevated liver function tests without having to do a biopsy. you can do an ultrasound here at this at this point and you would see a fatty liver.

intervention liver function tests

one of the things that we see very often when we see some disorder with this with the excretion is ___________. so why are we seeing this jaundice? jaundice this is a result of large amounts of bilirubin either conjugated or unconjugated in those extra cellular fluids. now if you've seen anyone with jaundice they have a very distinct yellow Hue to their skin and if it's severe enough you can see that yellow Hue it in their eyes as well and even in the inside of their mouth.

jaundice

esophageal varices are a direct result of portal hypertension. what happens is that when the pressure in the portal system that the differential in the pressure gradient causes that blood flow through the hepatic portal system to be redirected from the ______ into areas with lower venous pressure which means that collateral circulation then starts to develop in that lower esophagus in the abdominal wall the stomach and even sometimes in the rectum so these small vessels due to that excessive pressure from the portal hypertension causes sort of the blowing or the ballooning of the muscles in the esophagus.

liver

the function of the biliary system is to make move store and excrete bile and it's comprised of the Gallbladder the bile ducts and then certain cells inside the liver as well as the bile ducts that are outside of the liver. bile is an aqueous solution consisting of water electrolytes bile acids cholesterol phospholipids also contains as conjugated bilirubin and it's secreted by the ____. not all bile that's produced drains into one large duct from each lobe of the liver as well. bile is secreted continuously by the liver and enters the cuniculi to be drained and then eventually the bile makes its way to the Gallbladder. now between meals what happens bile stored in the _____________ but remember during meals what happens the bile is secreted into the duodenum to aid with the digestion and absorption of fat but it's also secreted to rid the body of the waste that is stored in the bile.

liver Gallbladder

we can also look at serum proteins and specifically we can look at albumen. now how we use this as a diagnostic measure seems fairly obvious since the _____ makes albumin if serum levels are low because the liver is isn't able to make the albumen then that's a pretty clear indicator that liver function is impaired. now we can start to look at other functions of the liver too to see if something is happening so for example we can start to look at hepatic excretion so we know that excretion takes place in the liver like excreting the bile salts excreting the bilirubin so we can measure serum levels or we can look at you know what's being excreted via the ____________.

liver urine and the stool

fulminant hepatitis is rare but it is very acute in terms of both onset and progression and it's very difficult to stop the progression once it starts so most often it's the result of viral hepatitis and so really the only way to prevent fulminant hepatitis is really to prevent that viral infection in the first place this is a critical illness situation where most people are admitted into the ICU and really for most people a __________ is the only lifesaving option. basically you have a liver that is lost its capacity to remove any of the serum ammonia there's also decreased insulin metabolism gluconeogenesis becomes impaired and so the treatment really depends on which viral hepatitis caused the fulminant condition in the first place usually this is not something that you would see though that in fulminant hepatitis because it has such a _____________ and progressive so quickly you really are going to have to start to treat this very individually and you have to determine what is that underlying cause.

liver transplant rapid onset

the liver is also the main organ for ethanol metabolism. alcohol or ethanol is very rapidly and completely absorbed by the GI tract even in conditions where someone might be Malabsorbing the alcohol is also not one of one of the nutrients that can be stored in the body so most of the alcohol has to be oxidized by the liver with only about 2 to 10% that's being eliminated by the __________ so most of it has to be oxidized by the liver. so the hepatocytes have three pathways by which ethanol can be metabolized they have the ADH pathway they have the microsomal ethanol oxidizing system and then we have the catalase pathway. the major pathway of oxidative metabolism in the liver of ethanol involves ____ which takes place in the cytosol of the cell so the metabolism of ethanol via the ADH produces acetyl aldehyde which is highly reactive and very toxic and can cause tissue damage and some research has shown that it actually might play a role in the addictive process as well. but really this process leaves liver cells in a state that where they are particularly vulnerable than to damage from the byproducts of ethanol metabolism so namely to damage from _____________ and those free radicals.

lungs or the kidney ADH acetyl aldehyde

excretion is another function when we when we think excretion we often think of the kidneys as an excretory organ because of its role obviously in excreting waste out of the body but the liver also excretes various _____________ into the portal system for excretion in other areas of the body

metabolites

when we have portal hypertension one of the consequences is this ascites this is a mild picture I have seen people with ascites so badly that their skin is actually starting to like crack open so what you see here is that fluid that's accumulating in the peritoneal cavity and really what you're seeing are shifts from the vascular system into that ________. So what you end up with is someone who has a dehydrated system so they're very dehydrated systemically in a very overfull peritoneal cavity. this is the most common complication of cirrhosis and again results from that portal hypertension and reduced ________ because the liver is unable to produce the albumin so we're seeing differences changes in that osmotic pressure and that increases the retention of sodium. So what you have going on to some degree is the fact that the liver is not producing the serum proteins and you have water then leaving the vascular system but when water goes somewhere what else goes with water even more _______. So what does that do that further exacerbates the ascites.

peritoneal cavity osmotic pressure protein

Now the liver is really is an essential storage site for a number of different nutrients vitamins and minerals that are obtained from blood passed passing through the hepatic portal system. we know glucose is stored as glycogen fatty acids are stored from the digested triglycerides we also see the fat soluble vitamins and B12 as well as iron and copper so I just talked about vitamin A&D but vitamins K and E are stored all are also stored in the liver. so again if we have someone with liver disease we could also very likely see deficiencies in vitamin K and E. now let's say someone has a vitamin K deficiency what might see something like a ______________. now what might we see with the vitamin E deficiency might see ________ something that we would typically expect to see. these repositories are there so we have a constant supply of these essential nutrients which of course then become jeopardized when there's liver disease or there's any sort of liver dysfunction

prolonged bleeding time hemolysis

Now important function of the liver is the breakdown of bilirubin but what actually is bilirubin? bilirubin is this brownish yellow substance that's found in bile it's produced when the liver breaks down old __________ but we really don't want a buildup of this bilirubin. So what happens is our body has a mechanism to remove it pretty quickly from the body through the stool and that's what actually gives the ______ it's like normal Brown color and when we think about bilirubin there's actually two types of bilirubin that we can find floating around in the blood. we have ____________ or sometimes it's also referred to as indirect bilirubin which is insoluble in water. So what happens is that this unconjugated bilirubin has to go to the liver where then it gets converted to the soluble or what we call the conjugative form so that it can actually be excreted out of the body.

red blood cells feces unconjugated

so once these varices develop so they are also at risk for rupturing and This is why you will see the GI bleeding or esophagus bleeding when you have a patient with liver disease it's because of this portal hypertension and those varices. now this pressure can also cause the ______ to become enlarged. why are we actually seeing this portal hypertension? the most common cause is ______ and it's because the vessels in the liver are blocked due to that cirrhosis so the blood can't flow through the liver and high pressure develops in that portal system

spleen cirrhosis

there are consequences or complications when it comes to prolonged ascites and the main aim of medical management of ascites is to prevent or minimize complications. now one of the common complications is a ___________ which would then be treated with antibiotics what you also might see in someone with this SBP is the administration of IV albumin as a preventive measure against the development of renal impairment and also just to improve overall survival rate. hepatorenal syndrome is not extremely common but it is seen in about 10 to 40% of patients that have ascites and cirrhosis so it's not very common and it is essentially the development of _________ in a patient with chronic liver disease and happens when there is ascites and there's portal hypertension. now what we know is that the Histology of the kidneys ________ so the Histology of the kidney is perfectly fine but that renal function declines because of vasoconstriction of the renal circulation and the systemic arterial are vasodilation resulting in reduced systemic vascular resistance and in arterial hypotension.

spontaneous bacterial peritonitis renal failure normal

the liver's function is primarily to maintain homeostasis. it does it primarily through the metabolism of nutrients so we know that protein carbs fat even alcohol are all metabolized in the liver and usually those processes are affected when liver function is impaired. what are some of these different functions? it is responsible for the metabolism of nutrients yes but it's also a ___________ for what from various macromolecules as well as vitamins and minerals and when there is impaired liver function you see issues with nutrient storage and in some situations and some diseases we might even see excessive storage. so things like excessive copper and sometimes excessive iron with some of these ________________.

storage unit inherited disorders

the liver is a major organ in the processing of dietary fat and the conversion of stored fat into products that can be readily used for energy. the liver is responsible for removing ______________ that are circulating after a meal and also responsible for storing the fat. now vitamin metabolism is also really important in order for the fat soluble vitamins to be used. activation has to occur and a lot of the activation of some of these vitamins and minerals takes place in the liver as do storage of some of these vitamins and minerals. now 3 examples are the conversion of carotene to the active version of _________ and what you'll often see in someone with advanced liver disease are symptoms of vitamin A deficiencies so things like night blindness that we often think about what the vitamin A deficiency.

triglycerides and fatty acids vitamin A

now because of the associated encephalopathy you will sometimes see the use of branching amino acids and medium chain triglycerides being used. what else can we do the most evidence based intervention that we have in the main thing to take home and in regards to this fulminant hepatitis is that we may be able to entertain these branched chain amino acids and MCTS in certain situations but that really isn't evidence based what we need to do is monitor carbohydrate metabolism we need to address the _________ because let's say the underline causes like a drug toxicity then you can counteract the damage of the drug you may be able to reverse some of the progression of that liver disease it's one of the hepatitis the viral hepatitis is then we can get rid of that too will try to treat that so the main thing is really to address the underlying cause

underlying cause

so the Histology of the kidney is normal So what that means is that if we can get rid of the vasoconstriction then kidney function should be restored and that's exactly what we see in a patient who's had a liver transplant so they may have had impaired renal function but they get that that transplant the liver transplant and then their kidneys start to work. now the hallmark of this hepatorenal syndrome is that renal ___________ although the so the pathogenesis really is not that well or is not well understood multiple mechanisms are probably involved and they include sort of this interplay between disturbances in systemic hemodynamics and the activation of the vasoconstrictor systems and a reduction in the activity of the vasodilator systems. so this chemo dynamic pattern of patients with HRS is characterized by an increased cardiac output a low arterial pressure and reduced systemic vascular resistance so this renal vasoconstriction occurs in the absence of reduced cardiac output and blood volume so it's happening even if cardiac output and blood volume are not actually reduced which is in contrast to most clinical conditions that are associated with that renal ____________

vasoconstriction hypo perfusion