what's up Ninja nerds in this video today we're going to be talking about Mal absorption this is part of our clinical medicine section if you guys like this video it makes sense it helps you to really smash your exams please support us and some of the ways that you can do that is by hitting that like button commenting down in the comment section and subscribing also do yourself a favor and I really mean this you'll gain a lot of understanding from from these topics if you go down in the description box below click on the link that goes to our website there you'll find great notes that I think will augment your learning illustrations that'll help you to go quickly and recap on the topic and maybe follow along on top of that quiz questions that'll test your knowledge and much more so go check that out on the website and become a member all right let's talk a little bit about malabsorption so we're talking about Mal absorption there's actually two different types of processes so malabsorption in itself is a very specific pathophysiological process but it can be very very similar to another pathophysiological process and that's called Mal digestion so I want us to have just a basic understanding of the pathophysiological differences between the two then once we do that we'll talk about what are the particular causes of malabsorption and what are the particular causes of Mal digestion okay so let's focus on the first one and that's malabsorption so what I'm doing here is I'm taking a piece of the small intestine so this could be dadum Jenum illium and I'm zooming in on it what I want you guys to understand is what's happening in malabsorption the primary process here is here we have the mucosa so these are the anas sites these are responsible for helping to aid in digestion but also allow for absorption do you see what's interesting about this one in comparison to this one the mucos is damaged so that's one really big difference between these two is you have what's called mucosal injury and if you have mucosal injury you're going to have mucosal dysfunction and so you have to think about what's the big concept here if the mucosa is injured the anas sites are injured am I going to be able to take things like nutrients let's say for example here I have some type of nutrient of some sort it's a macronutrient maybe this is a fat maybe this is a carbohydrate maybe this is a protein and here I have enzymes but these enzymes they're working normally so enzyme function is going to be intact all right so this is actually going to be normal so we'll put that this is actually okay there this is normal function here for the enzymes there's no injury here there's no problematic issue between these two so with that being said I take this big molecule here and I'll have it kind of metabolized or digested if you will by these enzymes and so they'll take these big big molecules here and they'll break them up properly into their smaller little kind of like building blocks like monosaccharides or fatty acids or amino acids so this process will occur properly they'll have the enzymes metabolizing these and digesting them into smaller little building blocks which will help it easier to be allowing for absorption but if the mucosa is injured if you don't have proper inas sites are you going to be able to absorb these nutrients no and so the problem that occurs here is is that these nutrients are not going to be getting absorbed and so what ends up happening is is you lose tons of things you increase your fat loss you increase your carbohydrate loss you increase your protein loss you increase micronutrient loss so you're going to lose a lot of different things fat loss protein loss carb loss and micronutrients and there's a bunch of different types of things for this one as well that we'll go into in the complication section but I think this is the big concept is that there is not going to be proper absorption so with this being said if you have decreasing absorption what's the primary mechanism behind the decreasing absorption of these nutrients it is going to be mucosal injury but the enzymes that are aiding in the digestive process are completely fine those aren't the problem before we go down and talk about the complic the actual causes of this malabsorptive process let's talk about the differences now comparing these two between malabsorption and Mal digestion same thing I have a piece of the small intestine dadum Jenum ilium whichever one I'm zooming in on it right have these big molecules again this could be a couple different things this could be fat this could be large proteins this could be carbohydrates whatever it is they're supposed to interact with these enzymes but what if these enzymes don't allow for this interaction so now these enzymes for some particular reason maybe it's an enzyme or something else that helps aiding in the digestive process if that's not occurring if we're not allowing for this to occur we're inhibiting the proper digestion of these M macronutrients so now you won't be forming some of these smaller molecules so you're going to get these big big big molecules can you absorb these things across these mucosal cells no so the problem with this is not necessarily A mucosal injury the mucosa is intact right so here we have a mucosa that is intact it's normal if you will we can even use that terminology that or that kind of eror that we showed over there that it's normal there's no problem with that the problem though that exists is there is some type of enzyme dysfunction or deficiency and that is the problem this is the issue here that there's decreasing number of these enzymes or there's dysfunction of these enzymes whatever it may be you're not allowing for good digestion if I have decreased digestion of these big molecules the issue is is that I can't absorb these big suckers that's the problem so this process won't occur has nothing to do with the mucosal cells it's because I can't kind of digest these big monsters here and that's the big process here so decreasing digestion will still lead to what do we say here it'll still lead to decreased absorption it's just a slightly different mechanism that's what I want you guys to understand so they're kind of similar and they're concept but they're different true pathophysiological mechanisms okay now if I'm not absorbing these particular things a lot of this stuff same concept I'm going to lose lots of fats I'm going to lose lots of proteins potentially I'm going to lose carbs potentially and another thing I could lose is micronutrients or you know so I may lose a lot of micronutrients now we'll talk about this because it's very interesting in this process it's slightly selective so not all of these things are being lost right so it's not always going to be fat loss protein loss carbohydrate loss mic nutrient loss it depends upon the enzyme that's dysfunctional what if the enzyme only helps in breaking down carbohydrates well then you're only going to lose carbs what if you have a bunch of enzymes that metabolizes everything well then you will lose all of these micronutrients and macronutrients and so that's a really important thing to be able to remember sometimes it could be partial malabsorption which is could be in the scenario of where you're only missing a very specific enzyme that digests carbs or Global Mal absorption which could be in the scenario that I'm not digesting all of my macronutrients and we'll talk about the comparisons there in a second now that we have a comparison to differentiate these two what I want to do now is I want to talk about what are the causes of malabsorptive physiology due to mucosal injury then we'll talk about what are the causes of Mal digestion pathophysiology due to enzyme or digestive dysfunction all right my friends so one of the causes of malabsorption which causes mu coal injury is celiac disease celiac disease is really interesting it's also kind of kind of like an Intero uh sensitive like it's a it's a Gluten Sensitive interop ofy and so there's a specific molecule it's called gluten so we see this in wheat Rye grain barley anything that contains that kind of substance and what happens is within the gluten there's a special type of like small protein here called gadin and gliadin for some some reason is like super immunogenic in certain people and so what happens is is this gliadin molecule can cross the mucosa and when it crosses the mucosa it comes into contact with some reason for certain types of antigen presenting cells find it like super amog genic and they'll phagocytose it and express it on an mhc2 molecule so here they'll Express a piece of that protein on this mhc2 which is in this red color it'll then go and take that to a t- helper so has a t- cell receptor which will click on it and bind it this t- helper cell once activated will then release a bunch of different types of cyto kindes so many different types they're not super pertinent here but these cyto will then go and stimulate this plasma cell and this plasma cell is really where everything starts to kind of go wrong the plasma cell will start secreting a bunch of different types of antibodies and these antibodies unfortunately were geared towards this gliadin but they'll unfortunately go and create a very significant amog enic reaction that'll cause mucosal damage and so whenever these are produced they're produced against the gadin which is in the gut unfortunately but that'll also lead to just inadvertent injury to the mucosa and so end up with all this like massive mucosal injury and inflammation the question is is what are these specific antib bodies because they're helpful diagnostically a lot of them are IGA antibodies because you produce IG antibodies and usually mucosal surfaces respiratory tract genital urinary tract and GI and so there's What's called the tissue transglutaminase antibody which is an IGA subtype you also have the deaminated gadin peptide which is an IGA subtype and the endom mical antibody IGA subtype these are going to be the really important types of antibodies that are produced that will go and cause mucosal injury and if you cause mucosal injury what do you think is the overall result especially if this affects your small intestine you're going to lead to decreased absorption of particular nutrients and so this is the concept that actually develops within this and I think this is the really really important point to take away and again usually it's gluten is the trigger with Whipples and tropical sprew these are much less common malabsorptive kind of causes Whipples is actually due to a really weird type of bacterial pathogen so let's say here I have this weird pathogen okay and this weird pathogen likes to cause potential injury okay and usually uh the particular pathogen that we see with this one is called t whip all right and it's tro ferma whip now this particular pathogen what it does is is it actually kind of causes direct injury causes direct injury to these patients mucosa so when it injures their mucosa it'll lead to decreased absorptive capacity the reason why patients experience lots of this troper wholly is not really understood we don't really have a reason as to why this guy is the particular problem but what we know is is that this potentially happens and this nasty bacteria can cause mucosal injury the other one that we may have a little bit more of an understanding of just because it's a little bit more understanding and kind kind of we have a epidemiological factor to it is there's other particular situations where PE people who live in the tropics or go in kind of experience lots of the tropical life they have much much higher loads or bacterial o overgrowth of nasty pathogens called eoli or klebsiella and these are naturally kind of part of our GI Flora but if you overgrow these really really nasty bugs they can cause mucosal injury all right the question is is why is there this bacterial overgrowth the concept behind this one tends to be that people who live in the tropics for some reason increase experiences of bacterial overgrowth which causes mucosal injury whereas TR traera whip which causes Whipples disease is not usually a patient who's living in the tropics so I think the big thing to ask ask the patient is do they have any sensitivity that they know of to gluten have they been living in the tropics or have they visited the tropics recently because then you can kind of narrow a lot of things down you can say it's probably celiacs if it's gluten sensitivity it could be potentially tropical sprew if they've been living in the tropics or experienced a lot of time in the tropics and if it's not those then I can start to say it could be Whipples disease now with that being said the overall concept is that these patients experience lots of mucosal injury and we'll talk about some of the other unfortunate complications that these guys experience we'll go into more detail of that a little bit later all right so we have an understanding the causes of malabsorption what about the causes to Mal digestion this one's relatively interesting you know patients who can have what's called pancreatic insufficiency usually there's some type of damage to the pancreas and this is usually like fibrosis or calcification something that kind of like really leads to a decreased capacity of the pancreas now you have to know that the pancreas makes a bunch of different enzymes it makes proteases right so what's one enzyme that it may make it may make these enzymes called called proteases and what do you think proteases do they break down proteins it may make amoles which break down carbohydrates it may make lipases which break down lipids but if you have a disease where you're producing little amounts of amasis little amounts of proteases and little amounts of lipases are you going to be able to properly metabolize these big big molecules these big macronutrients no and so this process becomes impaired and you won't be able to allow for these to be properly digested and you can't absorb these big big molecules that's why they develop a decrease in this absorption because of Mal digestion but what's causing the pancreas not to produce these enzymes the primary causes are usually chronic pancreatitis and so if a patient has chronic pancreatitis look for a chronic alcohol use that could be one really really big common cause another one could be in a patient who's a little bit younger and has a history of pulmonary frequent pulmonary infections maybe when they were little they had what's called moonium aspiration and you definitely want to think oh now they're having problems with Mal absorption think about cystic fibrosis so these are two potential causes that can lead to pancreatic dysfunction and lead to chronic chronic fibrosis damage of the pancreas and then decreased enzymatic production this patient will experience Global malabsorption these patients will all experience Global malabsorption these other two though do not experience Global malabsorption meaning that they don't lose proteins fats carbohydrates and micronutrients all of them they only lose some of those nutrients I'll explain which ones they are but remember global global global malabsorption this next one's called bile acid deficiency it's pretty simple you're not making or at least in some way shape or form getting bile acids into where into the small intestine bile is really important because what it does it takes it it doesn't really help in what we call digestion per se but let's say here we have these big fat globules all right so this is big fat globules these guys what bile salts are supposed to do or bile acids are supposed to do which is these little guys right here that I'm drawing in green is these bile acids are supposed to bind with the fat globules and help to emulsify so take big fat globules and turn them into small little fatty droplets and so if it does this process let's say here it's going to take these fat globules and they're going to interact with these bile acids what the bile acid should do is is they'll bind with the fat globules which I'll draw here in the mouth of these guys here's these big fat globules it should break it down into small small little fatty droplets you want to know why because now lipases which are produced by the pancreas should be able to go in there and rip those fats up into fatty acids and Aid in the absorption so it's not really an enzyme problem per se it's a emulsification problem so in these patients they don't allow for this process to occur there's no issue with there's no problem with being able to take the flat fat globules and turn them into small fatty droplets so there's decreased fat droplets and then because of that you're not going to be able to go and digest these by lipases then you won't absorb them So eventually Downstream you're not going to be able to absorb these bad boys the question that arise is what's causing the bile acids not to be pushed into the small intestine well one is it could be any kind of liver or biliary dysfunction so some of the things to think about is could it be therosis therosis is whenever you have liver disease right particularly irreversible and what happens is this could be leading to decreased production of bile because you know the liver makes bile and so if your liver is dysfunctional are you going to be able to make bile no and so this process is impaired so think about sorosis the other thing is what if I have a stone stuck right here in the common bile duct wouldn't that be a potential cause yeah so any type of bilary obstruction because now I can't get the bile out so I want you to think about sorosis I want you to think about biliary obstruction and the last one I think that would be important is bile acids are supposed to actually be after they're done with their function they're supposed to be absorbed via the ilium and then they eventually go back to the liver right so they'll be recycled and what they'll do is they'll eventually come back here to the liver what if the ilium is diseased or reected or have a disease that causes massive inflammation of that area and destroys it well then am I going to be able to use this interop patic circulation to absorb them and bring them back no and I'll lose them in my poop and I'll never be able to continue to regenerate them as fast what's a disease that causes ilal inflammation primarily Crohn's disease and so in patients who have some type of ilal disease and I think the best example of this is in the scenario of Crohn's Disease these patients won't be able to absorb the actual bile acids because they have an ilal disease that affects their their absorptive process so that's a really really big one as well the big thing to remember though with bile acid deficiency is they're only losing fats in their stool they're not absorbing fats so this is a example of what's called a partial mal absorption I'm going to write that down next to it this is an example of a partial partial malabsorption all the other ones are Global the last one that I want to tell you about is lactose intolerance it's another type of partial and this one it was only fats only fats and then Associated things from the fats like fat soluble vitamins in lactose intolerance it's also partial but the only thing that you are losing that you have losing here is carbohydrates so let's say here I have the small intestine and here's a big carbohydrate and it's particularly carbohydrates get broken down and eventually to what's called lactose and so lactose is present within a lot of milk kinds of containing products we have an enzyme here it's called lactase so here's this one little enzyme here it's called lactase what happens is is patients have dysfunction or decreasing numbers of these lactates and what happens is if you can't have this process what's supposed to occur here is lactase is supposed to take lactose and break it down into smaller little sugars so that they can easily be absorbed but if this process doesn't occur you aren't able to absorb the actual smaller sugar molecules because this process is inhibited so what ends up happening is is these patients lose tons of carbohydrates in their stool all right so they'll end up with tons and tons of carbohydrates in their stool so this is why this is primarily only an example of partial malabsorption the question is why is there a decrease or dysfunction in the lactase enzyme why we don't really have a great answer what's potentially suspected as the cause of this decreasing lactase is it could be genetic that could be one particular cause but often times what we think is that it's acquired so it's usually after a patient has like a a bout of gastroenteritis I think this is relatively common if they have a really really terrible bout of gastroenteritis what happens is you destroy a lot of these small intestine you inflame it and you destroy some of those lactase enzymes and then what happens is you might not be able to completely regenerate enough of those lactase enzymes so I think it's really important that lactase lactose intolerance is due to lactase deficiency which could be genetic not too common though or it could be acquired and I think one of the most common causes of the acquired states of decreasing lactase is injury to the small intestine from a really terrible bout of gastro entis all right so with that being said we've talked about malabsorption and we talked more specifically about the differences in the pathophysiology between the true definition of malabsorption and Mal digestion question understanding really the difference between which one is the mucosa that's actually injured which ones the mucosa is intact which ones the luminal enzymes are actually the not the problem which one the luminal enzymes or digestive products are the problem we talked about the causes of malabsorption which is all globally you're losing proteins carbs fats and micronutrients and then we talked about the Mal digestive causes with pancreatic against deficiency being the only GL Global malabsorptive cause and then bio acid deficiency and lactose intolerance being the only examples of partial malabsorption where you're losing only fat and only carbohydrates now let's talk about the way these patients present and the complications that arise all right my friends so when a patient has malabsorption right whether the malabsorption is truly due to a mucosal injury right which we really would consider malabsorption uh in the scenario of celiacs or tropical spal Whipples or if it's Mal digestion due to decreased luminal enzymes or B acids and you aren't able to digest particular things so that you can absorb them but either way you're not absorbing things it's just the difference in pathophysiology when these patients present because of not absorbing proper nutrients they can present with various complications and you have to be able to pick these up it's usually related to each particular type of nutrients that it's not absorbed so I think the big thing to remember is what if the patient doesn't absorb proteins so that's a one big one right so a decrease in protein absorption so protein is important for that thickness right you want to get that mass and if you you don't absorb proteins one of the big particular problems here that can start to arise is that the muscles really need those proteins and amino acids to be able to build up large proteins in the muscles and so without that protein you're going to start leading to one particular problem which is muscle wasting and so the muscles will definitely start to have increased muscle wasting so it'll start to atrophy you'll start to experience some weakness but the other thing is is that the muscles carry a lot of weight on our overall kind of frame and so one of the big things that can start to happen is that these patients will start to experience a pretty great degree of weight loss and so whenever you see these patients watch out for significant weight loss in the scenario of increased muscle wasting the next thing that I want you guys to think about is that not only is there a problem with not absorbing proteins which we would only see in global malabsorption there's also a decrease in the absorption of carbohydr rates now when we talk about carbohydrates that are lost and they're not being absorbed actually in this case decreased carbohydrate absorption we should really just say you're losing a lot of them but you're not absorbing enough of them so whenever we have decreased carbohydrate absorption one of the big Concepts to understand here is that carbohydrates when they're not absorbed they stay within the bowel right so let's say say that I keep these carbohydrates here sitting in the bowel one of the big things that carbohydrates do is they're osmotically active and what they'll do is they'll Yank A lot of water into the bowel all right they're super osmotically active and so now I'm going to represent this as this blue color that we already have here it's going to yank a ton of water into the bowel as I pull lots of water into the bowel two things potentially happen one is I'm going to end up with a lot of water that I'm not going to have the ability to absorb and that's going to lead to diarrhea so you're going to lead to diarrhea and this diarrhea is why it's because of decreased amount of absorption but the primary problem here is that you're having a lot of water pulled into the Lumen due to what the carbohydrates being the particular problem here so again lots of water is being pulled into Lumen as LS of lots of water is being pulled into Lumen you're then going to stimulate a very nasty watery diarrhea the other thing is is that whenever you have lots of water it distends the bowel so then you're also going to get a lot of distension you're going to distend the bowel from all that water that distension is then going to precipitate abdominal pain so these patients will also have a lot of abdominal pain a lot of this distension so watch out for abdominal pain and distension but the last one is that carbohydrates are really a source of being destroyed by bacteria we naturally have some bacteria that are present within this actual gut and let's say that these bacteria take and break down these carbohydrates when they break down these carbohydrates they'll Pro produce a lot of gas and so if there's an increase in gas production that's going to also cause more distension and worse in the abdominal pain but you know what else this is going to do it's going to cause you to little toots toots so you're going to end up with a lot of flatulence and so that's another potential complication here is lots of flatulence so I think that's one really really big thing to watch out for is does a patient have increasing diarrhea do they have increasing abdominal pain and increasing flatulence this is all because of decreased carbohydrate absorption pulling water into the bowel causing increasing distension lots of bacteria break down the actual carbohydrates produce lots of gas and increase flatulence so again just to remember here what are these like little maroon things here these are bacteria in the bowel and these can also help in aiding this process so carbohydrate absorption not occurring protein absorption not occurring what else could be a problem the next one is fat so fat not being absorbed is is another really big problem and so whenever there's decreased fat absorption what do we see here one of the big things is that if you don't absorb fat a lot of the fat ends up in the stool and if you have lots of fat in the stool so a lot of what we call fecal fat fecal fat is uh pretty nasty in the sense that it causes your stools to become super greasy and foul smelling and whenever you have these patients come in the often tell you that they're having these really greasy and very foul smelling stools and this is often classic of what we referred to as Storia so I want you to watch out for a patient who comes in with increasing weight loss muscle wasting diarrhea maybe some intermittent abdominal pain with lots of flatulence and greasy foul smelling stools these are all suggestive of potentially Global malabsorption the other problem that makes it even worse is that whenever you don't absorb fat so decrease fat absorption right so we haven't absorbed proteins carbohydrates fats another scenario is we have decreased fat absorption same thing here's the difference though you know what else gets absorbed with fat vitamins do you know which types of vitamins get absorbed with fat fat soluable vitamins and so what happen happens is these patients get deficiencies and a bunch of different vitamins what are those vitamins so you'll end up with a decreased absorption of vitamin A and if you don't absorb vitamin A this will lead to some particular presentations you'll have decreased absorption of vitamin D you'll have decreased absorption of vitamin E and you'll have a decreased absorption of of vitamin K and so this is one of the really really profound complications that you have to be watching out for which makes things a little bit more complicated sadly but if you have decreased vitamin A this really affects the eye and often times the most common presentation is this really affects some of the uh particular structures in the the actual retina that control our ability to see things during the night and so what happens is this leads to night blindness so if a patient says that they're having really really difficulty and being able to see things at night definitely think about a vitamin A deficiency the other one is vitamin D deficiency so in a vitamin D deficiency this is important in being able to control calcium so when patients who have low vitamin D they often times have low calcium and that low calcium because they're not absorbing the calcium will then drive the bones that'll stimulate the bones to say oh calcium's low if the calcium is low I need to to rip calcium from the bone and so as you start kind of chewing and chewing and chewing calcium from the bone the Bones start getting weaker and this can cause rickets in a younger patient or osteomalacia and an older patient all right or an adult age the other thing is that vitamin E can also be deficient this controls normal nerve function and red blood cell activity and so whenever there's less amounts of this the nerves don't kind of send signals properly and the red blood cells lice and pop open and we don't really know the exact mechanism of this concept but we do see that these patients developing increased uh uh incidences of neuropathy and increased incidences of hemolytic anemia I think the biggest one that you'll probably be related to or tested to on the exam is going to be related to this one vitamin K is really important and utilized by the liver there's an enzyme called vitamin K epoxide reductase and so there's this kind of circular reaction we'll talk about this more in Pharmacology but this helps him being able to Aid in the synthesis of procoagulants these procoagulant are going to be a bunch of different factors factors 2 factors 7 factors 9 factors 10 and there's even protein CS antithrombin 3 there's a bunch of these suckers what ends up happening though is if you have decreased vitamin K this enzyme is dysfunctional you don't synthesize all of these proteins these more particularly these are procoagulant and if you don't have enough procoagulant you can't stop you won't be able to induce a clot you should per se so procoagulants you want to stimulate a clot if you don't have them they can't stimulate a clot so you'll bleed and often times the most common presentation for these patients is bleeding and this could be in the form of GI bleeding this could be in the form of mucocutaneous bleeding so it's really important to look for that okay so fat malabsorption can lead to a lot of scary complications we can see this one in global Mal absorption but we can also see in the partial type due to bile acid deficiency because that affects fats the last thing and probably a really interesting one is that the small intestine is really important for micro nutrient absorption so this includes things like B12 uh folate as well as iron and if you don't absorb these These are super super important whoopsie and being able to tell the bone marrow they kind of help the signal and help with the development to tell the bone marrow hey produce red blood cells if we have less of these the bone marrow will no longer have the micronutrients it needs to be able to synthesize red blood cells and so these patients will have decreasing number of red blood cells what do we call that anemia and so often times you can see how malabsorption can cause a pleora of complications they going to be relatively difficult to identify I think the easiest way to remember it is what would be the protein absorp of kind of defects the carbohydrate the fat and the micronutrient think about about that in a patient who's definitely potentially presenting with a malabsorptive syndrome to finish this off I think it can be a lot I know it's kind of complicated to go through a lot of this and you're like dang I feel like I'm still kind of struggling a little bit it's okay I think one of the big things to remember here is a lot of these patients will present in one of two camps and I just want you to be able to remember these Global malabsorption is it's all of them okay so I'll represent them color coordinated you're not absorbing fats you're not absorbing proteins you're not absorbing what do we use this as black carbohydrates and you're not absorbing micronutrients all of these things are not occurring okay so if I were to represent this in that color coordinated fashion all of these are not being absorbed okay so this is what we call Global malabsorption so these patients will experience everything above which diseases cause global malabsorption anything that damages the mucosa and anything that leads to all the enzymes that metabolize these things being deficient so I would see this in Celiac I would see this in tropical sprew I would see this in Whipples and I would see this in what we I'm going to abbreviate we also call this exocrine pancreatic of insufficient so e p i ex pancreatic insufficiency all of these are mucosal injury this is the one where you don't produce any of the enzymes to digest all of these things okay partial malabsorption is it's only a few of these so for example in bile acid deficiency what are you not absorbing fats because you can't emulsify them and then Aid them to be kind of broken down by lipases and so you don't absorb fats very well in lactose intolerance what do you not kind of metabolize or digest carbohydrates particularly lactose and so you can't absorb carbohydrates but there's no problem with protein there's no problem with micronutrients of any sort and so that's the big difference this one pertains to bile acid deficiency and so it'll only present with features of of fat malabsorption diera and fat soluble vitamin deficiencies this one which is lactose intolerance will primarily present with lots of diarrhea flatulence and abdominal pain that's the big difference between these two now we've kind of gone through here and we've kind of developed a I'd say a pretty good understanding now of a patient having Mal absorption versus Mal digestion the differences microscopically between the two is really important here why well one of the reasons why is we can actually start off by determining is it Mal digestion or mal absorption based off getting what's called a dyos test we have them inest a tablet that contains dylos Now dylos does not require any metabolis you know it doesn't require any digestive enzymes essentially you can take it and it can get readily absorbed but the only way it can be readily absorbed is if the mucosa is properly intact to allow for the absorption so if a patient has a intact mucosa it'll get easily absorbed across the mucosa therefore or the amount of zylos in their serum or the amount that they scret onto the urine will be pretty good it'll be elevated or at least in some degree have a elevated level of dylos more than usual what that tells me is that the mucos is intact the enzymes again don't even matter it doesn't matter if you know I don't have any enzymes or not if the mucose is intact which tells me that it's either xrm pancreatic insufficiency bile acid deficiency or lactose intolerance again that will come right across the G because it's intact so that's Mal digestion in the other scenario if the mucos is damaged they have loss of the micro Villi brush B enzymes there's injury and they can't properly absorb the dyos it won't get into the bloodstream therefore the Ser serum levels will be low and therefore the amount their urine that they excrete will be low and that would indicate it's a malabsorptive process something like Celiac something like tropical sprew Whipples and that's very helpful so right away I've already differentiated these based upon the concept of the microscopic level kind of function now let's go down the Mal digested armarm I know there's exm pancreatic insufficiency and lactose intolerance really so what I want to know is is there fecal fat because I told you right away lactose intolerance is only going to be partial that means that there will only be carbohydrate loss so if the feal Fat's not really there it's low not really any feal fat or very low amounts it's it would be lactose and to and if it's really high it's exr pancreatic in sufficiency oh okay cool well if I know that the veal Fat's really high that's likely okay pancreatic ins efficiency there's another enzyme that I can test for especially in patients with chronic pancreatitis or cystic fibrosis if there's a very declined pancreatic function there's an enzyme that the pancreas releases into the stool called fecal elastase and if the pancreas is damaged it won't release the fecal elastase so if they have high fecal fat and a low feal elastase I have exocrine pancreatic insufficiency and that would be super helpful another reason why this is helpful if I tested the fal fat and it's positive and the feal El last taste was normal it could be indicative of something called bile acid deficiency it's important to remember that if the fecal fat is also positive it does indicate that there's probably a malabsorptive syndrome that's going on more specifically celiacs Whipples tropical sprew and that helps me along with this process but if the fecal Fat's negative then I suspect that it's probably lactose intolerance I can confirm that by doing a hydrogen breath test I'll have them consume some type of tablet usually when they they consume this they'll produce because they're having a lot of the lactose staying with inside of their git they'll metabolize it and they'll produce a lot of gases and one of those may be hydrogen if there's heavy amounts of hydrogen that's being detected in the breath that probably means that they have lactose intolerance and they're having lots of lactose in their G that the bacteria are metabolizing and producing lots of gases as a result now let's go down the malabsorptive limb so I already know high feal fat low FAL elastase pancreatic insufficiency high feal fat normal feal elastase probably bioid deficiency no feal fat high amounts of hydrogen detected in the breath on the hydrogen breath test lactose intolerance if I have low serum levels of Z xylos or I just test and they have a high feal fat could be malabsorption malabsorption I don't know if it's celiacs tropical sprew or Whipples what I do know is that in Celiac disease there is some specific antibodies trans trans tissue transglutaminase di deaminated glid imp peptide and endom myal antibodies and they have to be present at least some of them to diagnose celiac disease so if I have a tissue transglutaminase oh baby it's likely that they have Celiac but let's say that it came back negative or inconclusive I could get other ones like the DPG the DGP better in kids but if I get the anti-endomysial antibody and that's positive I've confirmed that it's likely the patient has celiac disease another thing that adds to the support of celiacs disease is that oftentimes they have something called dermatitis herpet foris which is this like weird skin lesion that's usually indicative of them so if I were to see a positive tissue transglutaminase a positive anti-endomysial antibody or a positive DGP and dermatitis or pedop foris I definitely likely have Celia ex disease here I could if I want to go down the limb and say I could get a biopsy to truly confirm and diagnose the presence of celiac disease and I would see that there would be a lot of knocking out of the Villi a lot of cryp hyperplasia and a lot of problems where the micro vilard like knocked down but it's not absolutely necessary but it would confirm the diagnosis if these antibodies come back negative at least all of them let's say I started off with this one it was negative that doesn't mean that it couldn't still be celiacs but if I get the DGP in the anti-endomysial and those are both negative it's pretty good idea pretty confident that it's not celiacs and then again do they have any dermatitis or P foris if they don't have that that probably means it's probably Whipples or tropical sprew often times history is going to be the key thing here another that could be helpful here is do they have any other neurological issues cardiac issues joint issues the reason why is if they have any cardiac instability a lot of arthralgias myalgias and the neurological like disorders this could be indicative of Whipples I think the big thing is also tropical sprew it's within the name have they had any recent travel to Tropical areas such as the Caribbean India Asia that could also suggest this either way usually the most diagnostic kind of confirmatory test for these would be a biopsy now if you did obtain a biopsy I think one of the interesting things is that sometimes you may see these periodic shift macro fages and these are relatively helpful and they kind of help with adding to the diagnosis here particularly of patients having something like Whipples disease all right so that covers the diagnosis now let's move into the next step here which is the treatment of Mal absorption and Mal digestive disorders so in a patient who we kind of diagnose has pancreatic insufficiency maybe we determine that based upon the presence of fecal fat a low feal elastase and elevated dyos on their urine or serum testing I definitely think that this would also be supportive if they have an underlying history of chronic pancreatitis maybe evident on Imaging and on top of that maybe a diagnosed history of cystic fibrosis if they do it's important to remember that they're you're not going to be able to kind of fix what they have the damage has already been done often times you just have to replace replace the enzymes that they're missing so you're going to have to give them pancreatic enzyme replacement so you're going to give them pancreatic lipase amas and proteases so they can ensure that those things are getting digested and properly absorbed lactose intolerance is often about avoiding lactose containing foods um but if you can't do that or you don't want to do that you often times can try to replace the lactase enzyme often times prior to consuming a meal that's rich in lactose again another option is avoid lactose in general celiacs disease is often times again avoiding the trigger which is usually gluten if you avoid gluten they should have an improvement in their symptoms they should have less diarrhea less malabsorption and again this is usually going to be the thing that we see as a benefit to these patients lastly Whipples disease is usually due to an infection the triph triera whipy and so once you diagnose these patients which is usually based upon the presence of neuro joint cardiac involvement along with negative Ser negative testing on their you know antibodies such as the TTG the DP dgb as well as the EMA antibodies that are seen in celiacs if that's negative neuro joint cardiac involvement and periodic shift macras that are present on their biopsy it's Whipples and you're going to treat these patients with antibiotics often times you start off with seph triaxone then you'll extend them for at least a year with Baum which is trimethoprim sulfamethoxazol the last one's tropical sprew again this one is usually some type of underlying infection maybe eoli maybe klebsiella of some sort either way with these patients they're going to require antibiotics and often times it's tetracyclin the last thing to remember is for these patients you can try your best to treat the underlying disease but they may miss some of the nutrients the micronutrients such as B12 folate and iron so if the patient is developing anemia due to the problems it's important yes give them the pancreatic enzyme replacement put them on a gluten-free diet treat them with antibiotics but don't let their anemia hang around replace those vitamins as needed or the micronutrients as needed give them fola and b12 replacement if they have anemia give them iron replacement if they have anemia and again give them fat soluble vitamins if they're developing things like night blindness if they're developing things like hypocalcemia if they're developing complications such as bleeding replace those in combination with treating their underlying plus all right my friends that covers Mal absorption and Mal digestion I really hope it made sense I hope that you guys enjoyed it and as always until next time [Music]