Blood Groups Overview

[Music] hi and welcome back to the bloodbank guy video podcast my name is Joe Chaffin for the next hour or so I'm going to be your tour guide through uh an overall kind of big picture look at the blood groups there is a lot of information to cover in this lecture and uh not a lot of time to do it so I'm going to go fairly quickly just warning you right up front um as always I need to let you know that this is being recorded in December 2011 as a result I am uh I've made this as up to-date as possible at that date but depending on when you're listening to this uh new information may or may not have come out uh as I said it's December 2011 and we are in Colorado so this is as I look out my window to the right well you're not in Colorado maybe I'm in Colorado as I look out my window to the right this is what I'm seeing um and uh it's a little depressing uh but what's even more depressing is if when I turn back to my left and look at what I'm going to be staring at for the next hour or so and that's this so I'll do my best to uh lecture against a wall uh with with some some degree of entertainment for you I hope anyway over the next hour or so this is what we're going to do um first thing you should know is that there is a handout available uh please go and get it pause the pause the presentation right now if you don't already have the handout because you will need it um I think it'll be useful to you go to www.bb.com 3 you'll know that this is this is kind of a variant of what I called bloodbank one uh at the Osler course and in in fact if you look at the bottom left of the slide here um the reference uh on many of the slides as we go through today will tell you exactly where we are in that blood bank one handout this is the first uh of a series of at least three probably four imoh hematology lectures excuse me after after this one I'll record pre-transfusion testing and then we'll do most likely a two-part series on antibody identification it's designed to kind of take you from the ground up where obviously in that short time we can't cover everything but we're going to cover as much as we can today we're going to do the background and basics of of the blood groups um it's in some degree of detail but not as much detail as you will hear in the pre-transfusion testing podcast uh which is as I said going to be recorded next so we'll just kind of skim over that then we'll go specifically through the blood systems uh specifically looking at what I call the enzyme classification I'll explain that to you in just a little while basically categorizing the blood systems by the blood system/ blood groups by their reaction uh with proteolytic enzymes and then we'll hit some miscellaneous groups at the end as I said that'll take about an hour or so probably a little over I apologize in advance if I talk quickly but there is a lot to cover so let's get started um as far as the background that we start with the basic reactions in blood banking certainly the most basic reaction in blood banking is uation um and you see here on the the right side of the of the screen uh an example of red cells being GL glutin by IGG antibodies on the top and migm antibodies on the bottom certainly migm is much better at doing that than IGG IGM antibodies tend to react in lower temperatures IGG antibodies tend to react in warmer temperatures and that's some of the difference between warm antibodies and cold antibodies that we'll talk about in just a little while there are three classic phases of of testing in particular testing that's done in a test tube that you should be well aware of and well familiar with and those three phases as you see here on the slide are the immediate spin phase the 37 degree phase and the IAT or anti-human globuline phase also known as the kums phase basically what those are designed to do is it's it's a testing pattern designed to determine um the presence of antibodies that may be what we call clinically significant meaning that they have the capability to cause hemolytic transfusion reactions or hemolytic disease of the fetus and newborn uh in general the the antibodies that are most significant are those that react either at 37° and or at the IAT phase specifically the IAT phase that's certainly the most important phase uh you see at the top of the screen on the right an example of a negative tube test on the left and a strongly positive tube test on the right um there are certainly alternatives to tube testing in fact the majority of of Laboratories in the United States now use alternatives to tube testing including gel testing or solid phase testing and again you'll hear more about this in the pre-transfusion testing lecture but this is just an example of gel testing uh with a very strong positive on the left side of the image and a complete negative on the right side of the image if you're not familiar with gel again we'll discuss that further in the next lecture solid face testing on the other hand um is uh my personal favorite in terms of of these types of testing I I have a long background in solid phas testing um and solid phas testing is is different than gel in that you're doing the test in a in a very small little micro well and it's it's a little confusing again more on this in the pre-transfusion testing lecture but if you look at the the images here if you look at these these two uh two close-up views of Wells at the bottom left of the of the slide you'll see that a positive actually is a diffuse carpet of those indicator red cells and a negative is a pellet at the bottom of the tube and that may be a little confusing to those of you that haven't seen solid phase before again if that's not clear to you we'll we'll hit that more in the pre-transfusion testing lecture it's important that you understand the indirect anog globulin test uh the IAT is designed to detect the presence of antibody antigen interaction that occurs in vitro in our example here on the slide it's antibody antigen interaction that occurs in a test tube so for example when uh antibodies are present and the corresponding antigen is present on the surface of red cells that interaction occurs in the test tube you get coating of the cells but not necessarily A glutin that happens commonly with IGG antibodies then you go on you wash away any Unbound antibodies add anti-human globulin shown as little blue y's or antibodies here on this slide and those uen by binding to the antibodies themselves lots of different ways to do the IAT and that's a very simple look at it the DAT on the other hand uh simply looks for the presence of that same sort of interaction in other words antibodies binding to Red cells that occurs in Vivo in other words in the body so you pull the pull the red cells off you do a washing step to wash away any Unbound antibodies and again you add the anti-human glob and get utenation as you see there dosage is an important term for you to understand um we're going to mention it a couple times as we go through the different blood groups so let me just hit it here quickly um imagine that we have a a fake blood group called the zy blood group and in that zy blood group um you have obviously two different alals you have the Z alil and the Y alil so if the individual on the top of this slide is homozygous for the z ant sorry the Z Gene and they in other words their genotype is z Z and they you react their red cells with antiz uh and you get a strong reaction okay we're making this up by the way this is not based on reality but this is how dosage works on the other hand the person on the bottom has the zy genotype in other words they are heterozygous or have only a quote unquote single dose for the Z antigen um if their red cells reacts weaker with antiz as you can see the one plus reaction at the bottom of the slide then that antibody by definition antiz shows dosage um this is fairly common in in regular blood group antigens in real life the kid Duffy RH and MNS uh systems have a tendency to have antibodies which show substantial amounts of dosage um and again we'll talk about that a little bit as we go on through the different groups let's take a quick look at proteolytic enzymes I mentioned that earlier that we're going to take we're going to Define our blood groups based on their reaction with proteolytic enzymes confuses people a little bit so I'll hit it here a little and and a little more in the pre-transfusion testing section with enzymes basically you take enzymes that cleave proteins such as fisin and pepan for example what they do is they may they may change the way that antibodies bind to uh to Red cells and may increase or decrease the amount of utenation that you get and that occurs as a result of either direct manipulation of the antigens or as manipulations manipulation of the environment around the antigens let me just kind of show you how this works so let's exam imagine that this is the surface of a red cell um and if you look at the surface of a red cell there's a lot of proteins sticking up off the surface this is just an example of glycophorin a for example there's about a million glycophorin a antigens sticking up from the surface of a red cell okay if that's the case um glycophorin a carries several antigens including the M antigen so here we have the M antigen sitting on a gly for a well you throw in a proteolytic enzyme this is a glycoprotein on the surface you throw in a proteolytic enzyme and our friend the little Pac-Man comes in and does its thing and actually Cleaves some of these proteins you lose some of them and guess what happens to your M expression you get a decreased amount of M antigen expression that seems pretty obvious right so that's a direct manipulation a direct decrease of the amount of antigen and you would expect an anti-m to react weaker after that s after that sort of a treatment uh on the other hand that same glycoprotein or glycophorin a um since it's present in such a a large quantity on the surface of the red cells it has a tendency to mask some of the antigens that bind or that are present closer to the surface of the red cells and one example of that are RH antigens this is just a schematic obviously of of how um glycophorin a uh waves far above the surface and the and the RH antigens are found closer to the surface so an antibody against RH can come along try to bind but be blocked by that glyc ofor a now obviously this is just a a an example or a schematic because as you well know RH antibodies bind fairly well to RH antigens however if you do the same thing and you throw in a proteolitic enzyme and that proteolytic enzyme goes and Cleaves some of those uh glycophorin a molecules well guess what happens we've cleared the forest a little bit and that antibody has more access to the surface of the the RH antigens that are closer to the surface Sur of the red cells and that can lead to and in fact does with RH lead to Stronger binding uh of the RH antigens RH antibodies I should say so that leads me to the enzyme classification and this is what we're going to use in just a minute to go through the different blood groups basically you throw in protic enzymes with uh antigens and antib red cell antigens and antibodies and you can either enhance their effect decrease their effect or basically leave them unaffected and these are the main groups that we're going to talk about in just a few minutes but before we get to that let's talk about a couple of other things neutralizing substances which are which inhibit antibody activity against red cells I can explain this by showing it to you easier imagine that you have antia you put it in a test tube with group a rbc's well you know what you're going to get you're going to get a glutation group a uh antibodies bind to group a uh red cells very fairly nicely okay but what would happen if before you did that you threw in soluble uh group a in other or group a antigen in other words it's just floating free you mix that with your antia and then add that to the mixture that contains uh group a rbc's you get you actually get neutralization you get the the all the binding sites of that antia being taken up so that in the end you end up with unag glutin uh red cells so that's neutralization and Ne there's a lot of weird neutralizing substances you see them here on the slide my favorites for the P blood group The HED cyst fluid and pigeon egg white stuff which is just craziness but again uh that's that's not something we're going to take a lot of time to talk about today we'll talk about some of these as we go through the the different blood groups you should also know about lectins lectins are basically um plant derived or seed derived substances which act like antibodies basically um you throw in doose boros lectin for example and at the concentrations that we use in blood banking it will uate cells that are group a blood group A1 but not cells that are blood group A2 and you see see further examples here on here on this slide lectin are are especially useful when you're working up polyagglutination and you see a couple of those that are used towards the bottom for T and TN uh type red cells and and again uh that's deeper than we intend to go in this lecture general characteristics of antigens and antibodies well blood group antigens are present on red cells but not necessarily exclusively and they are targeted by an aloe antibody in other words an antibody against someone else's Red Cell antigens that's the definition of of a blood group antigen there's over 325 of these suckers out there and many of them are gathered into blood group systems that we'll talk about today which are genetically linked blood group antigens there's there are 30 according to the uh International Society for blood transfusion or the isbt and we'll show those 30 on these two slides we're not going to talk about all of them but we're going to talk about a lot of them most of them on this first slide and some of them on this second slide this is just to give you an IDE give you an idea of how many are out there further the the the general characteristics of blood group antibodies um include categorization as clinically significant and insignificant significance means that they cause hemolytic transfusion reactions or hemolytic disease of the fetus and newborn warm reactive as I said before those that react best at IAT um cold reactive are those that react best at room temperature or below or below 37 degrees um and there are some characteristics that are classic for warm reactive and cold reactive antibodies in general warm reactive antibodies are primarily IGM colds are usually I sorry warms are IGG colds are usually IGM warms usually require exposure through pregnancy or transfusion whereas colds are generally naturally occurring meaning pregnancy or transfusion doesn't have to happen uh warms usually do cause hemolytic disease of the fetus and newborn or have that potential whereas colds usually don't uh same thing with hemolytic transfusion reactions and the same thing with clinical significance or insignificance now you notice there's an asterisk by the bottom botom three uh entries on the right under the cold antibodies and and that's because um some of these antibodies are exceptions to the rule um in particular the antibodies are the big exception to the rule antibodies are primarily as we'll talk about uh they have a large quantity of IG um they're primarily cold reactive they react best at colder temperatures but they obviously are very significant because they react very well at warm temperatures all right so let's now that we've done that let's hit the specific blood group systems we're going to talk first about the related systems under the enhanced enzyme enhanced blood groups meaning you use protolytic enzymes antibody and antigen interactions get stronger with these blood group systems and so the related groups are uh Lewis big ey and P and we'll hit those one by one and then we'll hit RH and kid all right so in order to understand you have to understand a little bit of biochemistry there's two basic types of chains on which uh antigens are built and those are called creatively the type one and the type two chains the type one and type two chains uh really differ in a couple things first they differ in how the terminal galactose is bound to the terminal subterminal anoco galactosamine not super important for you to remember that specific detail whether it's galactose aneto galactosamine but remember that last residue is important in terms of how it binds and then the quote unquote group in other words what's going on with the rest of the chain well let's talk first about the type one chain um the in the type one chain you have a couple of things going on first that that last residue is bound to the subterminal in aeto galactosamine with a beta 13 linkage okay great but more importantly from our perspective is that the R Group um in other words the majority of the chain is primarily glycoprotein and those chains are primarily found in secretions now they're also present with on the surface of red cells to an extent but here's how I want you to think of it I want you to think of it as primarily glycoproteins some glycolipids but primarily glycoproteins in secretions as being type one chains type two chains on the other hand have a different linkage they have a beta4 linkage there and they are primarily found on red cell membranes so they're primarily glycolipid um okay so type one chains glycoproteins in secretions also somewhat in plasma but glycoproteins secretions primarily type two chains on red cell membranes and primarily glycolipid that distinction will become important in just a second um when we're talking about type one chains in order for a type one chain to do anything in the blood group system the first thing that has to happen is you have to have the action of a particular Gene product that gene is called the secretor gene or the SE Gene also known as fut 2 fut2 fut stands for fucos transferase so that Gene makes an enzyme that adds fucose to type one chains right there at the terminal galactose 80% of us are capable of doing this that means that 80% of us are so-called secretors when that happens you have just made an antigen which is known as H antigen very important to understand H this is a type what we call a type one H meaning it's occurring on a type one chain on the other hand on a type 2 Chain an enzyme which is made by the H Gene does exactly the same thing so that enzyme causes uh the addition of of a fucose onto that terminal galactose just about everybody can do that and what we've made when we do that is Type 2 H you have to have H H is required for a or b anen formation and and from the point of either a type one H chain on the left or a type two H chain on the right from there you can go on and add one additional sugar to that terminal galactose and end up with either A or B antigen so um again let me show you how this works for for the blood group a those individuals have a gene which which is the a gene and that a gene uh makes a anoco galactosamine transferase as a result an aneto galactosamine gets added onto that terminal galactose and you have blood group a on the other hand for blood group b the the B Gene product is a galacto seal transferase so a galactose gets added onto to the other galactose and you have blood group b that's all the difference between blood group a and blood group b now I'm showing this on a type two chain but the truth is it happens the same way for a type one chain or a type two chain so so you can make group A or B antigens in secretions with type one chains or on the surface of red cells with type two chains AO antigens have a very specific characteristic in that when we do what I just showed you on the last slide when we make uh either a or B antigen that chain no longer carries H antigen specificity in other words the more A or B you make the less H you have remaining that leaves you with a relative amount of H antigen that'll make more sense in just a minute where blood group O has the most H and blood group a1b has the least H uh AO antigens are coded for by by three different genes on chromosome 9 the a the B and the OG Gene the O Gene doesn't actually do anything A and B do what I've already showed you and note that the genes don't code for the antigens themselves they code for an enzyme which makes the antigen the antigens are there fairly early about 6 weeks uh estimated gational Age and and they come to adult Levels by age four and they're also found on a multitude of other uh areas of other places aside from just on the red cells including platelets and endothelial cells Etc antibodies appear only after four months after the baby's born um and they don't get to adult levels until about age 10 and over the course of time in the very elderly those antibodies can fade probably not as much as we used to think but they can fade over time the antibodies do differ by by blood group and this is so big important for you to recognize this um everyone agrees that blood group A and B carry IGM antibodies in other words the anti-b that a group a person has and the anti-a that a group b person has will be IGM they are naturally occurring they don't um they don't Ross the placenta they are they're classic IGM antibodies on the other hand there's some disagreement with blood group O uh but the current version of the technical manual describes it this way basically they say that that anti-a and anti-b in a blood group O person is primarily IGG rather than IGM and in addition people with that are blood group O have an an additional antibody called anti-a comma B now anti-a comma B is clearly IGG I don't think anyone disagrees with that and it can't be separated into the individual parts and that leads to a scenario where people that are blood group O moms in particular that are blood group O haveo antibodies that can cross the placenta and cause some damage to the baby and we'll talk about that in just a moment um types by race we're not going to spend any time on this other than just make sure that you recognize that this order that I show you here on the left o a b AB that's pretty much true across most racial boundaries um you see four racial boundaries listed here and and that that order stands uh stands in place for for all of them um there are differences in relative percentages obviously but just remember it that way and you'll be in good shape uh the genotypes we've already talked about individ individuals who are who get two o genes will be blood group O and uh individuals who get two a genes as well as an A and an O Gene are group a same thing with b and if you get an A and A B Gene you are group a AB all right let's talk a little bit about the specific blood groups uh in the blood group system blood group O first is the most common blood group across all racial lines we've already mentioned that the antigen on its surface is only the H antigen remember if you don't make a or b you're left with h um you can tell a blood group O by using ulx eurobus lectin ulx reacts against cells that have a lot of H so not just blood group O but obviously it would react against blood group O we've already talked about the antibodies and as a result of the IGG component of those antibodies the blood group O gives you the most common but a usually fairly mild form of hemolytic disease of the newborn I I you may wonder what that little icon is there after hdfn that's a little flashlight and I that's because I call this fact a flashlight in the eyes it's so important that it should be reflexed to you I should be able to shine a flashlight in your eyes and say what's the most common form of hdfn and you'd spit out immediately group O mom group A or B baby so that that's you'll see this kind of scattered throughout this lecture but that's what I'm going for with that group a is the second most common you see the percentages there they have a antigen and H antigen in some proportion more on that in a second and they have a naturally occurring IGM antib that reacts against obviously Group B cells now there are two subgroups of a that you need to be aware of they are group A1 and group A2 and you can basically divide everyone whose blood group a into A1 and A2 it's not completely true there are some much less common less than 1% uh additional subgroups but roughly 80% are A1 and roughly 20% are A2 um now in terms of excuse me in terms of how these how these blood groups differ well basically the the big difference is that blood group A1 has five times more a antigen on its surface than blood group A2 does so if you look at the bottom of the slide here I put together a fabulous fabulous animation just so that you can see what I mean by that uh isn't that good yeah lots more a on a group A1 than on a group A2 um so think about that for a second though what does that mean in terms of relative amounts of H and if you think back for a second you remember the more a you make the less H you have so an A1 Red Cell will have less H than an A2 red cell that would seem fairly obvious okay there are also some so there's a big quantity ative difference but there are also some qualitative differences as well there are some differences in the biochemical composition of the a chains on on an A2 cell um and of of even greater importance individuals who are blood group A2 can form antibodies against blood group A1 in other words an anti- A1 and you see the percentages there on the slide up to 25% of people who are A2 B can form an anti A1 but fortunately that antibody is usually clinically insignificant unless it reacts all all the way up uh at body temperatures blood group B on the other hand is not all that exciting I'm sorry for those of you that are blood group b you have kind of a boring blood group uh it has b or H and B and H antigens um it has an an IGM anti-a and there are some subgroups there but they're really not exciting and they're really not common so we won't talk about them blood group AB on the other hand is the least frequent of all blood groups across all racial lines um roughly 4% in Caucasians and African-Americans they have the A and the B antigens and hardly any H at all and remember we talked about that relative proportion individuals who are group AB can actually be further classified into subgroup a1b or A2B depending on what their a is and so if an individual is blood group a1b they would have hardly any H at all they'd have somewhat more H if they have if they blood group A to B um people who carry both antigens would not carry either antibody obviously so no antibodies as a result that these folks are designated as the quote unquote universal recipient we do testing testing in the blood bank uh all the time and and it's important for you to have a good handle on it fortunately this is not difficult to understand there's several different names that that this testing goes by but the the on the left side of of the table here the cell testing um also known commonly as serum testing or I'm sorry also known commonly as forward grouping that's what I'm trying to say so cell grouping or forward grouping basically takes the patients red cells or the person you're trying to test takes their red cells reacts it with reagent anti-a and reagent antib and that gives you whether or not they that tells you whether or not they have what either of those antigens on their surface um in for the serum testing the serum grouping or the reverse grouping as it's commonly known or the back typing is another name that blood Bankers call it you take the p patient serum or plasma and reacted against reagent red cells A1 cells and B cells and so obviously on the top line if you've got someone whose's blood group a you would expect their cells to have to react with the reagent anti-a if they're blood group b you would expect their antib to react against the group b reagent red cells and you see that's how that works notice the fact that for each and every blood group as you go down the as you go down this table the reactions are opposite in other words the cell grouping or the forward reactions are opposite from the from the serum reactions you have positive negative negative positive for blood group a for blood group b you have negative positive positive negative if you don't have that uh inverse relationship or that opposite relationship for every for every test that you're doing then by definition you have what's called an discrepancy AO discrepancies are a lecture in and of themselves and we've got we clearly don't have time to go through that but just recognize that you can have issues either with the antigens or with the antibodies you can have missing antigens in subgroups or or uh transfusion or transplant for example you can have antigens that are there that shouldn't be and there's a wide variety of reasons for that as well you can also have antibody problems where you have you don't have antibodies that you should have uh imuno deficient patients for example or in different subgroups or in transfusion or you can have unexpected antibodies antibodies that shouldn't be there that are um and a lot of reasons for that as well overriding all of that is technical problems obviously if you do the if you do the testing wrong you can completely screw up everything for most of these blood groups I'll talk about just a couple of things that are kind of odd and strange just so you'll have an idea of some of the things that are that are important to know just not only for trivial purposes but if you're going to take an exam these things tend to get focused on um for one of the one of the discrepancies that doesn't happen all that often but it's fairly famous on examinations is the acquired B phenotype that's a scenario where blood group A1 red cells come into contact with inic gram negative organisms in other words bacteria from the gastrointestinal tract that happens with colon cancer gastrointestinal obstruction or sepsis and they present with an Avo discrepancy that looks kind of like this where you have a strong reaction with anti-a on the forward grouping uh a weaker reaction with antib but you would interpret that forward grouping as a and just a straightforward uh group a in interpretation on the reverse grouping well that's a fairly classic uh appearance for acquired B and again discrepancies are are a lot uh there's they're big Topic in and of themselves but when you see something like this the one reaction that's out of place is that weak one to two plus reaction with antib um so that's where you would focus your energy knowing the clinical history you would go uh you would go fairly quickly to to acquired B this is not the only thing it can be obviously but here's how acquired B works that uh terminal an aceto galactosamine for blood group a gets damaged by excuse me gets damaged by those inter gr negative bacteria and you end up with a free floating acetal group or the uh the uh acetal group comes off and you're left with uh not quite galactose but something that uh something that looks kind of like galactose and close enough that our reagent antibodies will react but uh but it's not really a Group B that's why it's called an acquired b um there's a lot of ways to resolve it including acidifying the serum um Auto incubating in other words if you mix this person's own antib with this reagent or sorry with this acquired B you're not going to get any reaction because it isn't really uh a true Group B you can also use a different form of monoclonal antib in your typing that doesn't recognize acquired B and go from there there's also um The Bombay Fen type in the blood group system is one of the weirdos Bombay phenotype is the O phenotype basically these individuals have no h antigen no a antigen and no B antigen because they have neither the H gene or the SE Gene the two genes that I talked about at the beginning that make H antigen so that's their genotype you see on the second line there sorry the third line down little H little H and uh little SE little SE they have a strong anti-a remember anti-a occurs when you're you get it when you don't have a antigen same thing with antib but in addition their big problem is that they get antih basically that means that they while they look like blood group O on your basic testing they have an antibody that will react against basically every other red cell that carries any H at all so the only way you can transfuse them appropriately is to use blood from another Bombay donor another H negative donor parab Bombay is similar it's just that those folks are secretors so they have a smaller amount of uh of uh H antigen present and in in their secretions and to some extent in their plasma uh less of an issue but they still need H negative blood okay so let's move on to the Lewis system um and remember this is part Lewis is part of the family it's related to the Lewis gene or the Le gene is called uh also known as fut 3 and as a result of that you should know kind of what it does it's a fucos transferase the distinction is the Lewis Gene product only acts on type one chains and it adds the fucose not to that terminal galactose but to the subterminal an aceto galactosamine when you do that you've just made an antigen which is known as Lewis a now don't get confused there's no such thing as a Lewis a gene and a Lewis B Gene there's just one gene it's the Lewis Gene and it does this it makes Lewis a in order to make different Lewis antigens you have to have the action of some other genes well we already know about something else that acts on type one chains and that's the SE gene or the secretor gene uh the secretor gene as we know throws a fucose onto the terminal galactose on a type 1 chain to make type 1 H as we've already talked about um so if that happens in addition to the Lewis Gene doing its Duty and putting on uh a fucose on the subterminal galactose then that combination the presence of both of those fucoses gives you not only H antigen activity but also LS B activity okay so remember Lewis B is formed through the the interaction of both the SE Gene product and the Lewis Gene product so both occur again don't get confused you can have H activity and Lewis activity at the same time you can't do that with blood group A or B but you can do it with Lewis okay so let me show you kind of graphically how this goes let's imagine the life of a type one chain um that's sitting there with nothing being done to it you've seen you've seen this up close before so imagine this type one chain and it has a couple of things that can happen first either the ls Gene product can act on it first or the SE Gene the secretor gene product can act on it first let's just imagine that the ls Gene product acts on it first okay if that happens then we make LS a and you know what you've seen that before the fucose gets added to the subterminal in aceto galactosamine what actually happens in real life is that things stop right there it that particular chain is not going to go on and and have the SE Gene product act on it it's just as a result of steric interactions and it's again more complicated than what I'm telling you but if you if the chain goes down that pathway it doesn't do anything other than Lou a fortunately the SE or the secretor gene product is better than the Lewis Gene product and faster so most of these type one chains are going to go down the pathway on the right which is the SE Gene pathway the secretor gene pathway and be be changed into type 1 H after that happens if a person for example is blood group a then that particular chain can have the a gene product act on it or the leis Gene product act on it if the a gene acts on it then it goes from type 1 H into a if the leis Gene product acts on it then it still retains its H activity but it's also LS b as we've talked about before and that's the pathway that most of these type 1 chains go down now in addition that that Gene product or sorry that chain can also undergo uh leis activity so it's absolutely possible to get a chain with both Le B activity and blood group a or blood group b activity depending on what they the individual is genetically okay so um why are we even talking about this as a as a blood group or as a system because as you as you know we've already described type one chains as occurring um in secretions and not on red cells and that's absolutely true but I also mentioned that type 1 chains do float free in plasma and as a result these antigens can kind of stick onto the red cells or absorb onto the red cells Lewis B is much better at doing this than lwis a so as a result if you look at the bottom uh the bottom of the slide on the left you'll see that in floating around in secretions uh sorry in the plasma you can have a lot of Lis B usually not much LS a remember the the secretor gene product usually acts on type one chains first so you usually will get lwis B rather than just LS a um then Lewis B is better than lwis a at absorbing onto the surface of the red cells so this is kind of how it looks um with the image on the right you have red cells that look like they're Lis a negative B positive but the reality is that there is LS a around in other words if you think about it it's not possible to make Lewis B without having the ability to make LS a right you can't do LS B without having some LS a around that's important in and we'll describe that in just a second so when it comes to antigens and antibodies there are three different possibilities that you see there for Lewis phenotype the most common one by far is Lewis a negative B positive um 22% of African-Americans are Lewis a negative B negative though uh versus only 6% of whites and the antibodies to to Lewis uh against leis antigens are they're cold reactive and as opposed to antibodies that are IGM and cold reactive these are not significant they are IGM generally insignificant they're only seen for the most part in people or leis a negative B negative for reasons that we've already talked about remember if you make if you're if you look like your Lewis a negative B positive on your red cells you still have LS a around so you're not going to make an anti-sa um the antibodies themselves are insignificant as I said hemolytic transfusion reactions are rare um and hemolytic disease of the newborn is not seen because these antibodies are IGM and can't cross the placenta and those conversions of type one chains that I mentioned to you before only have happen after the time of birth couple weird things about about Lewis is that antigens do decrease during pregnancy and these patients can go from Lewis a negative B positive to all of a sudden being Lewis a negative B negative and in fact can make antibodies in those scenarios fortunately that's usually not a big deal um children can have variable type as the type lewiis types I should say as their chains are converting um and there's a couple of facts down at the bottom about uh attachment of different infectious organisms uh through the Lewis B chain all right a couple things on on the eye system remember this is also part of the family we have the ab we've talked about and H we've talked about um Lewis and now we're talking about big ey uh these are related to the blood group system they are in fact type two chains um there are two antigens in the eye system big eye and little eye big eye attends to occur in adults and while little eye predominates in in children and basically the difference between big eye and little eye is not so much related to a specific sequence of uh residues on a chain but it's more the three-dimensional structure of the chain older people have greater branching of their chains and let me just show you that so you have a type two type two chains that's kind of sitting there doing nothing but as and that's how babies type two chains are but as you get older those chains get more complex and you start branching and the more those chains Branch the more you get complexity to the chain and the more complexity you get the more uh the antigen present is Big ey rather than than little eye and that brings me to my f one of my favorite illustrations about the the eye blood group system and that's that big eye tends to occur in big people while little eye occurs in little people shouldn't be too terribly hard for you to remember I hope um here's a couple of other things a couple of flashlights in the eyes when it comes to this system uh it the first is that auto anti-big eye is classically associated with micoplasma pneumonia in older patients especially um it's also the antibody that's usually the Target in in cold of gluten disease uh or cold um cold reactive uh autoimmune hemolytic anemias um Auto anti-le ey on the other hand is is classically associated with infectious mononucleosis especially in younger children um that and that would certainly make sense based on what we know uh the P blood group system or the P system is absolutely my favorite system not because uh I have any special attachment to it not because I've seen antibodies more than the others I just think there's so much weirdness in this system it makes me laugh P system is based on AO related chains there's only one antigen in the P system and it's not the P antigen that really hardly makes any sense at all it's actually P1 there are a couple of other related antigens the p and the PK antigens that help Define the overall P system type um and you see that on the the fourth row down most people are phenotype P sub one meaning they carry uh the p P antigen the P1 antigen but lack the PK antigen rarely some people can lack all three of those antigens and and have acute hemolytic transfusion reactions and spontaneous abortions as a result when that antibody occurs the p uh antigen is the receptor for parvo virus b19 easy to remember um the antibodies against the P1 antigens are are cold insignificant MMS no big deal they they are seen in Greater frequency in people who who are associated with birds bird handlers and especially in those with HED cyst disease and and that should help you remember what we talked about before is that some of these antibodies can be neutralized with the use with the use of pigeon egg uh excuse me pigeon egg fluid from pigeon eggs I can't talk and as well as from highed cyst fluid there is another association with a p blood group system that you should know about and that's the association with paroxysmal cold hemoglobin area or PCH PCH is a basic um IGG that reacts against uh P antigens and that biphasic IGG is known as the doni lon Steiner biphasic hemalin uh basically what happens is that IGG binds to Red cells at cold temperatures and when the red cells are warmed then the red cells are hemal and obviously the antibody dissociates that's why it's basic uh it used to be seen in association with with syphilis and now it's seen commonly in association with viral infections in children all right so that's everything from the family let's move on and talk about the RH system I promise things will go faster from here on out the RH system uh was defined in terms of the terminology by uh doct Fisher and race in England uh basically they defined two different or sorry five different antigens the Big D and then uh two pairs of small of of other antigens Big C and little C Big E and little e in the Fisher eras terminology RH positive simply means D positive um and Rh negative is described as having a little D but there really is no such thing as a little D antigen more on that in a minute uh Dr vener on the other hand uh described what's known as the rhhr terminology and he gave different names for those five main antigens but really those are not important for us in blood banking now hardly anybody even remembers them uh and very few people use them some do but very few uh but his main contribution was that he believed that the RH genes were inherited as a group one from each one hype from each parent and let me show you how how he described this his terminology is still used though his his understanding of the actual genetics was not quite correct he believed that basically there were three these three genes um or these three alals that you got as a group from from each parent uh or a so-called hype that you either got a big D or a little d uh a Big C or a little c and a Big E or a little e uh from each parent that hype came and uh and in concert with the other parents hype would give you your overall RH genotype now what I would like you to do when you look at this and you see this terminology dce um I would like for you to think of the C position as position one and the E position as position two that'll become clearer exactly why I want you to think of that in just a minute but for now just fix that in your brain the C is is one the E is two and you that's alphabetical so you can remember that okay so anyway so you got one hype from one parent one hype from the other parent and your overall uh RH genotype and resulting RH phenotype was based on this combination now we know now that he wasn't Dr vener wasn't quite right there are actually two genes that give you your Rh genotype and that's the rhd Gene and the rhce gene in the RH with the rhd gene again you get a Big D or the lack of big d whether that's a mutation or whatever and then in the for the rhce gene you have the possibility of four different Al uh and those Al include Big C little e little C Big E uh little C little e and little and big c big e you can see those on the right side of the slide there so the genetic wheel spins and in position one you get either a Big C or a little C uh in position two you get a little Big E or a little e again keep that in mind more on that in just a second again uh the hype theory is certainly true you get one of those from your parent from one parent one of those from the other parent in the end that determines what your Rh genotype is okay so now we have to do something that's not necessarily fun but you got to Dr vener put specific abbreviations to these Hypes um and you got to know them it's it's just all there is to it whether you're working in a blood bank or whether you're taking an exam about blood banking you got to know know these what these abbreviations stand for and fortunately they're pretty easy and let me show you how to do this okay there are eight different abbreviations you see them listed here on the slide in the The Big Box in the middle big R1 big R2 big r0 big RZ and then little RP Prime little r double Prime little r and little r y okay the great news is that the first thing that you have to remember which is whether or not these have a big D or a little D is simple because if it's a big r it's a big D if it's a little r it's Little D no problem so it's it's really easy to generate that first uh that first uh memory slot which is whether it's a big D or Little D okay no sweat right well so now we have to figure out what goes in the next spot and that's uh in those spots you're going to have and you see these four listed on the bottom of the slide either a big the AL with a big c and little e the one with a little C biggie Etc so how do you determine that well the easiest way to determine that is to to take a look um at each of these rows and I've written these I've written these in in these rows for specific reasons big R1 and little r prime or one prime carry the same rhce Al in other words in position one you have a capital letter position one as you recall from before is the C position so as a result if you have little sorry big R1 or little r one prime or little r Prime then The Big C little e goes there right that's not too terribly hard let's move down to the next one big R2 or little r double Prime well take a guess position two is the one that's capitalized and you can see that the next one on the list the one where Big E where e is capitalized and C is not uh is the little C Big E and you can kind of see where we're going this with this uh R zero or just plain little r with nothing means that neither one is capitalized so you get the little C little e and then finally our r z or any letter RZ or little r y will give you both being capitalized or Big C uh Big E okay so that's that's what we're left with and this is absolutely a flashlight in the eyes you got to know this terminology you got to know uh how these abbreviations work fortunately there are only four of these that actually occur with any great degree of frequency um in in our population and those four are big R1 big R2 big r0 and little r those those make up over 97% of of people that you'll see it's important um for reasons of test taking primarily but also somewhat in real life to have an idea of the relative frequencies of those four uh in both African-Americans and Caucasians and there's a couple of rules your handout talks about this as in terms of how to do this it's pretty simple um take a few minutes to to do this after I do it and you'll see it's not a big deal so Big R zero is always the most frequent in African-Americans and the least frequent of those four in Caucasians little r always comes second and now you have two slots to fill for both and big R1 always comes before big R2 um so with that you're left with this relative order of frequency of of the main four or the big four RH Hypes um again that as we go through um you'll see some questions on the bloodbank guy website that talk about how to how this is used itiz we don't have a lot of time to go over that today so we're just going to continue on okay we're uh the the RH antibodies I should say that they are exposure requiring warm reacting Iggs exactly the opposite of of antibodies um and they are certainly the D antigen in particular is the most immunogenic non-abo antigen that we have that we have out there uh we used to believe that as many as 85% of Rh negative people or D negative people would make an anti-d when they were exposed to a single unit of D positive rbc's recently though that number has dropped pretty substantially in hospitalized patients patients that are in that situation are primarily patients that are losing a lot of blood that have a lot going on and they are much less likely than what we thought before roughly 20 to 30% of them will make an anti-d which is still pretty substantial these antibodies are significant they cause hemolytic transfusion reactions usually extravascular ones um and they caused the classic prototypical hemic disease of the fetus and newborn you can also get hemolytic disease with anti-al C but the other RH antibodies are are fairly it's hemolytic disease is fairly mild now please note that I've only talked about in the r system I've only talked about the five main antigens and antibodies against those five main antigens there are 50 RH antigens out there and I haven't talked about uh about a lot of the any of the other ones at this point um again not enough time to do that that'll be a separate lecture weird stuff in in the art system include the fact that D negative is not just you don't have a d there's a lot of weird stuff that that goes on and depends on depending on your race you can have you can be d d negative for a variety of reasion reasons Caucasians usually are D negative because they've deleted the gene entirely African-Americans on the other hand have a pseudo Gene a gene that just doesn't do anything um and Asians on the other hand have they have rhd there but it's just in activated so again lots of different reasons to be D negative it and we describe it as Little D but there's as I said before there's no such thing as Little D and there's a lot more to it than that there are several variants of D that you should be aware of um I mentioned weak D and partial D here I'm not going to talk about Dell or D illusion um that's again a topic for another day but let's talk about weak D and partial D because people confuse this a lot with weak d That's a scenario where uh where an individual really is D positive um however they have they they have a normal D externally fairly normal D antigen however they're quantitatively less uh their their reactions are are less strong I'm sorry with anti-d so those individuals as you see on the bottom of the screen here they can have a situation where when you test their red cells for uh the presence or absence of D you throw in anti-d and in most situations now people who are really dep positive that's just going to give you a direct utenation you're going to get a positive reaction however people who are weak d by definition get coding of their red cells but not utenation and in order to see that utenation you have to do what's called the weak D test which is basically just an indirect antiglobulin test you see at the bottom of the screen you have coated uh dep positive coated red cells you add anti-human globulin you get visible utenation does not happen very often at all and there's a wide variety of reasons that it can can occur including mutations including uh the so-called C and trans where you have the the a Big C little e Al opposite the uh rhd alal um functionally though what this comes down to is that the only people who really need that weak D test or the IAT for someone who appears to be D negative are blood donors um if you're a blood donor and you test as D negative we are required to do a weak D test on you to make sure you're not really dep positive for that because it has the potential if your blood went to someone else of immunizing them um it's done very uncommonly for D negative recipients on the other hand primarily because it just very do very uh it's very uncommon nowadays because of the the strength of our the strength of our antibodies that we have in addition if you do the weak D test on someone who appears D negative you may actually inadvertently harm uh harmed a recipient because you might pick up a partial D in other words someone who's partial D who shouldn't be called dep positive as a recipient more on that in a second may be called dep positive um finally the the the only people who really do need weak D testing in a hospital transfusion service are D negative babies with d negative moms um basically that's going to give you an idea whether or not you need to give that Mom rhig whether the baby really is dep positive but otherwise the testing is good enough that you really don't need uh to do to do the the weak D testing for partial D on the other hand partial D is confusing to people basically with partial D you're lacking certain portions of the D antigen or certain epitopes antibody binding sites on the exterior part of the of the Red Cell um week D does tend to have some deletions and lacking certain epitopes but it's usually on the interior part of the Red Cell so it's it's less it's less of an issue externally um so if you lack those epitopes and you're exposed to excuse me D positive red cells then you can develop antibodies against the part of the D antigen that you lack if you if you have partial D um so when these individuals are recipients it really actually is important for them to get D negative blood and the current forms of anti-d the most common ones that are used actually will call the most common forms of partial D recipients D negative and that's exactly what you want that's the reason that doing weak D testing can actually harm you in those situations um D negative moms who have partial d uh actually need rhig prophylaxis because if you're partial D excuse me if you're partial D and you're a mom and you're exposed to baby's D positive red cells you can form as I said antibodies against the portions that you lack differentiating weak D from partial D can be really really hard to be honest it it can require absolutely can require genetic testing in fact usually does to be completely sure so if you're not sure be as conservative as you can if someone might be partial D treat them that way and avoid exposing them unnecessarily okay so a lot on family and Rh but we're going to move fairly quickly through the rest the kid the kid system is the last of the enzyme enhanced blood groups uh there are two main antigens in the kid system jka and jkb a is somewhat more common than b and that's unusual in most blood group systems uh the the B is more common than the a but that's neither here nor there um the kid system has is famous for having antibodies that are that require exposure they're warm reacting they're usually IGG but they may have an migm component in fact 50% of kid antibodies will fix compliment that shows you that those that's probably the proportion that has an mm component because IGG doesn't usually fix compliment they have marked dosage the the big F the two big famous things about kid antibodies are that they have Mark dosage in other words that they can easily react completely negative against a heterozygous heterozygously expressed kid antigen and react very strongly with a homozygous kid antigen and they have variable expression over time in other words the antibody can form it can be obvious and then as time goes by it can completely disappear and that's why uh kid antibodies are famous for causing delayed hemolytic transfusion reactions as well a lot of famous stuff for kid right anyway these reactions are usually anamnestic in other words they they have an antibody it goes away as far as we can tell um usually happens when someone is transfused at a different facility or if if was never if they were never tested after they developed the kid antibody they we don't know that they have that antibody they're reexposed coincidentally the antibody comes back and it causes a severe intravascular form of hemolytic trans transfusion reaction um the as far as hemolytic disease the newborn that's usually not an issue primarily because it's difficult for kid antibodies to react against heterozygous Expressions which when you think about it that's what it would have to be all right so we've done the enzyme enhanced systems let's do the enzyme decreased systems and and finally we'll finish up with the unaffected ones the in the decrease systems you have the M&S the Duffy and the Lutheran systems and we'll start with M&S M&S we talked about this a little bit before when we were talking about enzymes MNS antigens are carried on glycoproteins which are known as glycophorin there are two of them the glycophorin A and the glycophorin B chains and glycophorin a carries M and N whereas glycophorin B carries big S little s and a an and a very important antigen known as U more on that in a second so here's just a quick schematic of of a red cell membrane you've got a glycophorin glycophorin a um here that we're showing which is a trans membrane glycoprotein um the the the last five amino acids on a glycophorin a chain are what distinguishes a glycophorin a that has M activity from a glycophorin a that has n activity and you see those here the the exact order is not really important for you to memorize but you see position one and position five are the only differences okay um on the other hand glycophorin B excuse me glycophorin B is also transmembrane it's a little shorter there's only one uh amino acid difference between glycophorin B that has s activity big S from glycophorin B that has little s activity either form of glycophorin B also carries down near the surface uh activity for the U antigen U pretty much stands for Universal so you can imagine that it's very very high frequency in the M&S system uh the free the amount of uh M antigen roughly equal is equivalent to the amount of n antigen or the number of people that are M positive is equivalent to those that are n positive I should say little s is more frequent than than big S and very important that that only about two% of African-Americans completely lack big S little s and U that's never seen in Caucasians why why is that a big deal well it's primarily a big deal because of the fact pardon me that those individuals tend to be the ones that completely lack glycophorin B the big S little s thing is not that big a deal but if you make an antibody against something that stands for you Universal you're going to have a potential problem um okay so uh there's also eltin viaga that that acts on uh group N positive red cells the antibodies from these s from these two different groups are actually somewhat different in other words when you think about the MNS system you you can kind of divide that down the middle in other words you have the M and N antibodies and then you have the big S and little s antibodies and they're almost completely different anti-m and anti-n tend to be naturally occurring whereas big S little s and U antibodies require exposure um anti-ms are IGM and anti- NS but that's easy to remember right anti-m is IGM uh whereas anti- bigs little snu tend to be IGG um the m&n antibodies are usually insignificant whereas the big S little snu antibodies are very significant and do cause serious potential problems if they're present um the Duffy system which is the second of the enzyme decreased blood group systems have two main antigens including FY and fyb um coming from the corresponding genes the individuals that lack both uh Duffy a and Duffy B FY and FIB that's seen in 68% of African-Americans very rare in Caucasians and it's usually do uh to to what's known as the fyfy genotype and you notice that doesn't include either the FY or fyb genes it's actually a separate Gene and they have no Duffy antigens whatsoever um again that Gene is seen very rarely in Caucasians but it's seen in in over two-thirds of African-Americans the antibodies really when you think of Duffy with the exception of the enzyme activity you should think of kid because those two groups have very very similar antibodies they have marked dosage just like kid they have variable expression in other words they can disappear over time just like kid and for that same reason they can cause delayed hemolytic transfusion reactions also just like kid though the severity uh tends to be somewhat less than with kid um kid antibody induced delayed htrs uh the weird stuff about the about the Duffy system includes the the malaria resistance thing and this is this is so important big flashlight in the eyes people who are Duffy a negative B negative FY a negative B negative are resistant to both plasmodium viac and plasmodium nisi infection and that's probably because the the regular Duffy glycoprotein which is not seen in people with the fyfy genotype is the receptor for those plasmodium marites so without those uh significant resistance to to to different forms of malaria all right um the last blood group system within the enzyme decreased groups is Lutheran I don't have a lot to say about Lutheran it's not hugely important uh the two main antigens Lutheran a and Lutheran B Lua and LU Lutheran B is the one that's high frequency Lutheran a is not uh the antigens are destroyed by some en some enzymes but not all and it's they're definitely destroyed uh by by sulfur reagents like dtt dio3 atol the antibodies are IGG except sometimes you can get an IG with anti-an a um they cause mild hemolytic transfusion reactions at worst and really are not known to cause hemolytic disease of the fetus and newborn okay that's enough of that let's let's move on to the to the enzyme Una affected systems and we'll spend most of our time here on Kell a little bit on Diego and Colton so you you use protolytic enzymes on on these red cells and they don't and it doesn't have any effect um with the Kel system two main antigens multiple other antigens but the two main antigens are Big K and little K Big K is also known as K1 little K is also known as K2 just about everybody you when they talk about Big K they'll call it Kell um that's technically not correct but everybody pretty much knows what you mean better to say Big K or K1 either way but um the the Big K antigen is seen in 9% of caucasians and 2% of African-Americans so it's moderately low frequency the little K on the other hand is seen in just about everyone and if you look at the a couple of the other antigens in the system the jsb and JSA kpb and kPa they are very similar in that the B is high frequency uh the a is low frequency uh so they kind of correspond KX on the other hand is an antigen that's closely closely attached to the Kel antigens on the on the red cell surface even though it has the name KX it's not technically part of the Kel system but it's certainly certainly related and you'll see in just a second it's it's important in several significant uh significant situations with related to the Kel system Kel antibodies um anti-big K and anti- little K are very very similar they just differ in frequency basically um Big K is a very immunogenic antigen after d it's the next most immunogenic antigens so non-abo antigens so people who are who are Big K negative and get exposed to Big K are very likely to develop an antibody that antibody is usually an IGG which is exposure requiring uh and warm obviously it can cause severe hemolytic transfusion reactions it can cause severe hemolytic disease of the fetus and newborn though it's not really hemolytic it's a bit of of a misnomer basically anti-big K will bind to precursor red cells and suppress them from even forming mature red cells okay so anti- little K does very similar things it's just very uncommon because just about everybody has uh little K A couple of strange things in the in the Kel system include the the Kel null phenotype or k Subzero basically these people have no Kel antigens at all and have a paradoxical increase in KX and not usually important there but what is important is that they develop an antibody which is known as anti-k or Kel Universal which reacts against virtually everyone's red cells except other Kell null people uh the the classic favorite of people who write exam questions is the McLoud syndrome or the McLoud phenotype McLoud is defined by the absence of the KX antigen so that that antigen that sits right next to the Kel um the Kel structures on the surface of the red cells that antigen is gone as a result you have a decrease in Kel antigens you have membrane instability which leads to acanthocytes and a canotic hemolytic anemia and the famous association with xlink chronic granulomatous disease now cgd um important disease that you should that you should be aware of um basically it's a lack of nadph oxidase and individuals with cgd will develop excuse me will develop infection with catalyze positive organisms like staff for stacus for example um so anyway that's that that borders on microbiology and and I might get sick if I start talking about micros so let's move on that's it for for for Kell let's talk about Diego and Colton for just a second the Diego system has uh has some antigens that are distinctly different they live on an an anian exchanger protein known as Band 3 there's the Diego A dia and dib pair um which is L basically low and high frequency and the right a and right b or w a WB pair which are ALS the same thing B is high frequency and the a is low frequency the antibodies uh for Dia and dib are both capable of severe hemolytic disease but not much in the way of hemolytic transfusion reactions uh with with WR and WB those antibodies are are W is usually naturally occurring it can cause significant disease but it's not seen all that often um it can cause hemolytic transfusion reactions and hemolytic disease of the newborn whereas antiw WRB because remember WRB is is very high frequency the antibody is commonly seen as an auto antibody the colon system which is the last in the enzyme unaffected group actually is a misnomer from the beginning um Colton was actually written on the original test tube as celton and someone misread it or someone wrote it badly and and the the the system has gone by by an incorrect name for a lot of years uh doubtful it's going to get changed back I don't think it will anyway that there are two antithetical antigens the co COA and the co pair um it's unusual in that it's the opposite of what normally happens COA is extremely high frequency Almost 100% whereas Co is extremely is well it's not extremely low but it's lower frequency about 10% the antibodies are usually IG um both of them can be significant primarily in terms of causing severe hemolytic disease of the newborn uh but not all that commonly seen a couple of different uh systems that I should mention before we go away uh include dck YT XG and Vel uh Vel is actually not a system it's an antigen more on that in a second D brck has a pair DOA and do as well as five additional uh antigens that are in the Dom Brock system and you see them listed there uh both of the both DOA and OB are common um and and the antibodies while they can cause uh acute hemolytic transfusion reactions as well as delayed hemolytic transfusion reactions so they're significant but they don't cause hemolytic disease of the fetus and newborn the YT system used to be called the cartrite system these are antigens present on an enzyme uh known as acetyl colon esterase which is primarily seen in in uh neural tissue why it's on red cells nobody's really sure uh yta is extremely high frequency YT is much lower frequency um the antibody against yta can cause problems but the antibody against ytb usually doesn't cause problems XG is an is a system that you will see on every single uh blood antibody identification panel that you that you look at uh however the antibodies are usually not an issue at all uh it's called XG because the because the antigen is excuse me the gene coding for this antigen is present on the X chromosome so 89% of females carry the antigen 2third of males carry the antigen as well um and as I said despite the fact that the antigen is there it really doesn't cause problems let's finish with Vel Vel is an antigen that does cause substantial issues uh when it's seen fortunately it's rare the antibody is rarely seen um I I think I said that poorly it's it's an antigen that the antibody against it causes substantial problems but it's rarely seen because the an the antigen is so high frequency it's not part of any system the antibodies though um they do cause problems because they're an IGG and IGM mix they can look fairly weak but despite the fact that they look fairly weak they can cause very very serious problems severe hemolytic transfusion reactions severe hemolytic disease of the newborn they can be Auto antibodies they can be Alo antibodies the Alo antibodies are the ones that we usually worry about and and uh and deal with most of the time in addition because these these antibodies have a very broad thermal thermal range they can react at room temperatures and can cause problems with serum grouping anyway bottom line with Vel is that if someone is Vel negative um and has a an antiel they really need Vel negative blood um and that may that may be an issue sometimes most Blood Centers and certainly rare donor Registries have access to to substantial numbers at this point of Vel negative blood so it usually doesn't cause tons of problems once the antibody is finally identified okay well have I beaten you to death so to quote Wesley from The Princess Bride you wish you mean you wish to surrender to me very well I accept so uh thanks for thanks so much for hanging around I know this has been a bit of a long haul um I very much appreciate you you taking the time to download this please give me feedback both directly and on the website and through iTunes if you're watching this through iTunes um and we'll finish out with a disclaimer but thank you very much the pre-transfusion testing and antibody ID podcasts are coming um they may be already there by the time you hear this go check them [Music] [Music] out [Music]

Channel: BloodBankGuy

Views: 349,574

Keywords: immunohematology, Chaffin, blood, ABO, Rh, blood groups, Blood Bank Guy, Kell

Id: ogr90JOvsI4

Length: 74min 38sec (4478 seconds)

Published: Sat Oct 20 2012