Acute Kidney Injury / Acute Renal Failure Explained Clearly – Remastered

By Adem Lewis / in , , , , , , , , , , , , , , , , , /

okay so welcome to another MedCram lecture we’re going to talk about acute renal failure and for that when we sort of bring up our chem seven again we talked about this before you remember you’ll see this a lot it’s standard we have sodium you’ve got potassium you’ve got chloride you’ve got the bicarb and we could talk about the B UN the creatinine okay so that’s this third column bu when should we refer to as the B you I never call it the bun it stands for the blood urea nitrogen okay blood urea nitrogen and the C R is simply creatinine okay so blood urea nitrogen and creatinine so these things have to do with acute renal failure but let’s get into a little bit about what they are and where they came from and as you know when you’re talking about energy you remember something from biochemistry called the Krebs cycle Krebs cycle okay and it goes around and around and you remember what went into it first there’s this thing called acetyl co a okay and it was basically two carbons when it to ask Toa and what came out of Krebs cycle ATP you know you had these reducing agents nadh fadh2 they went into a electron transport chain down the electron transport chain and you got ATP okay so basically you need to have two carbon units to get into this Krebs cycle well let’s talk about what are the three different types of energy sources in the body there’s three types we know that there’s carbs okay and carbs are usually six carbon chains and six carbon chains get broken down into two times three carbon chains and then remember one of these carbons comes off in the form of co2 during glycolysis and then you’ve got a two carbon chain and boom you’re ready to enter Krebs cycle the other one is fats or lipids okay you remember that it had the carboxylic and on it and you had a bunch of these carbons that went off it was 16 carbons then it’s palm mathilde koay and then remember beta-oxidation it chops these thing in – guess what – carbon units you’re able to enter into Krebs cycle well the last energy group is you guessed it proteins proteins if you recall is a collection or a string of amino acids which have the backbone of n C C and then you have another n c c well you would have protease is that are chopping up these proteins they’re chopping them up into these NCC units these are amino acids how do you get these NCC s to C C’s well you basically chop off this n group and then boom you’ve got C C’s going in and you can make ATP the problem is is that there’s these ends that are left behind so what are these ends these ends are something called ammonia or nh3 okay so we got to get rid of these NH 3 groups well these NH 3 groups ammonia as what it’s known as okay ammonia is toxic to the body it’s toxic to the brain if you have too much of it it can cause hepatic encephalopathy so the body’s got to do something about it somehow to get rid of it and that’s where we talk about the BU n ok so clear the screen here we’ve got nh3 which is ammonia and nh3 goes to the liver okay here’s my picture of the liver so it goes into the liver and what comes out is something that looks like this C double bond o wooden to the nh3 or NH 2 on one side and an NH 2 on the other this is urea okay you are e a it goes into the blood then you get blood urea nitrogen so the nitrogen is now compounded this is not as toxic so this is really nice to have because you can excrete this through the kidney so again ammonia goes to the liver and then gets made into your wreath through something called the areia cycle which we won’t get into and then you get this bu n now bu n blood urea nitrogen goes to the kidney okay there’s my little picture of the kidney and it goes out and that’s how you get rid of be went so we know how that happens now let’s talk a little bit about bu and remember a first point is this it’s made in the liver okay and there are a couple of things that have absolutely nothing to do with the kidneys that could increase the amount of bu n that you measure in the blood first of all let’s talk about burns so burns is a catabolic state what do you what do you think is gonna happen when you have a burn burns are gonna cause you to have more protein breakdown as we already know more protein breakdown is going to give you more ammonia all right what about steroids again steroids induces a catabolic state accountable like state is going to give you more breakdown of proteins that’s gonna give you more ammonia livers gonna make more urea what about certain antibiotics tetracycline okay so here is tetra SCI clean burns can do it and steroids catabolic state okay all of these things can do it let’s think about something else let’s say you’ve got liver problems now in liver problems or liver failure or cirrhosis you can get esophageal varices esophageal varices is basically situation where blood is trying to get back to the heart through the liver the livers dysfunctional and because of that the blood has to find an alternative route back to the heart and one of those ways is through the esophagus so these tiny veins which are normally built only to take so much blood become engorged and so these veins can burst and high mortality high mortality associated with this so you’ve got bleeding what is bleeding bleeding into the into the digestive tract well when that happens you’ve got these red blood cells okay red blood cells are full of globin globin is a protein you digest down all this protein guess what you’re gonna get you’re gonna get ammonia well you already have liver failure so you’re not making this urea and so what’s get a skyrocket your ammonia levels going to skyrocket and that’s why we see in patients with liver failure who have bleeding hijole bleeding they get hepatic encephalopathy and in fact that’s how you can tell they’re having a patek encephalopathy now let’s say that they have a GI bleeding and it’s not due to liver failure if their livers working just fine you won’t see a buildup of ammonia but in fact the liver will take that ammonia and guess what you’re gonna have an increase in you’re gonna have an increase in the B um so you can have an increase in your bu n if you have GI bleeding and your liver is working what are some things that could cause your bu n to be decrease so all of these things cause your bu n to go up okay what are some things that could cause your bu n to go down well the obvious thing is this your livers not working because if your livers not working you’re not gonna make bu n and so liver failure I see this all the time patients come in with liver failure and I’ll look on the chem-7 and their bu n is pretty low sometimes it’s really even undetectable okay so we’ve talked about bu and let’s review that again it’s synthesized in the liver things that increase it that have nothing to do with the kidney would be fever catabolic state GI bleeding tetracyclines all sorts of things things that decrease that would be liver failure because it can’t make the BU n okay with all those things in mind let’s talk about what we’re talking about today which is kidney failure so I’m gonna draw a nephron here’s my little stylized nephron okay this is remember the kidney works kind of like you should clean out your closet you take everything out of a closet everything and then you put back just the stuff that you want to keep and everything else gets thrown away so here’s the nephron and here is the blood supply so you have the afferent arteriole going in and the efferent this is a bunch of capillaries and what you have is you’ve got flow of fluid into Bowman’s capsule or the glomerulus and things go down and basically everything that you want to keep gets reabsorbed and what get what is left gets dumped out into the toilet okay but remember stuff that you want to keep gets reabsorbed and most of the stuff that gets reabsorbed gets read absorbed right here at something we call the proximal convoluted tubule probably 70% of the stuff that gets reabsorbed gets reabsorbed here at the proximal convoluted tubule so about 70% of stuff here in the proximal combo to it gets reabsorbed and so really there’s two things that you’ve got to be aware of that effect the serum concentration of things in the serum so if things here are being reabsorbed back into the serum and those two things are is the GFR the glomerular filtration rate what is the rate at which stuff is being filtered into Bowman’s capsule if you’ve got acute renal failure this is going to be reduced and therefore if less for instance if less B UN is being filtered into Bowman’s capsule you’re gonna have an increase in your B UN outside that goes for just about anything that’s being filtered the less filtration rate the greater that accumulation is going to be in the serum because it’s just not being filtered but there’s an extra added thing here with bu in and that is is that once it gets filtered if this GFR or this glomerular filtration rate is low it’s going to go along here some more slowly and if it goes along here more slowly it’s more likely to be a reabsorbed because B UN is specifically reabsorbed here at the proximal convoluted tubule so there are in fact two reasons why the B UN would go up in a low GFR situation number one it’s because it’s not being filtered at the same rate and the stuff that is being filtered is more likely to be reabsorbed that’s going to become very important later on now this is a contra distinction to something called creatinine we’ll talk about creatinine cratan basically comes from muscle but specifically creatinine is also filtered here at Bowman’s capsule but it is not reabsorbed it just keeps going through and right on out in fact there are areas here where creatinine is actually actively secreted okay so what does that mean that means that if there is a low glomerular filtration rate that’s a reason why creatinine is going to go up but it’s not going to have the other reason to go up because it’s not being actively reabsorbed in fact it’s being secreted and so creatinine only goes up for one reason in a low GFR state that’s the major difference there between creatinine and the B UN let’s talk a little bit about creatinine what is creatinine okay creatinine again and the chem-7 is this area down here and where does it come from it comes from muscles so muscle breakdown is going to give you creatinine that’s just a natural byproduct so the more muscle you have the higher your correcting is going to be normally and the less muscle you have the less your Kratt name is going to be and typically you need to see a reduction in your GFR by at least 50 percent before you see an increase in your creatinine so what are some non renal things that could increase Kratt knee and things that have absolutely nothing to do with the GFR well as we talked about remember there are areas here in the nephron specifically where creatinine is secreted if you could take a inhibitor of that and block it you would block the secretion of cranny that would increase your serum concentration of creatinine and there are a couple of drugs that do that one of them is called cimetidine tagamet it’s an h2 blocker and the other one is an antibiotic called trimethoprim okay so you’ll see an increase in crowding for that what about decreased cracking what could cause a decrease in creatinine we talked about profound muscle wasting so low muscles so if you don’t have any muscles that would cause you’re creating to go down and that would be a reason for your Kratt need to be low okay so to review remember bu and is synthesized in the liver it is both reabsorbed it is filtered and reabsorbed the creatinine is filtered and secreted it is not really so if there is a slowdown in filtration the BU n is going to be increased because of lack of filtration and also because of reabsorption the cratan is only going to be increased because of lack of filtration therefore you’re going to see a larger bu n increase than you would creatinine in a low flow state all right that does it for part 1 join me for part 2

6 thoughts on “Acute Kidney Injury / Acute Renal Failure Explained Clearly – Remastered

  1. You don't get hepatic encephalopathy because of esophageal varices. They are separate results of liver failure.

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