so in today's video we're going to be covering anemia and anemia is a topic that absolutely sucks to learn you do need to be familiar with anemia and in real clinical practice you'll probably only see a few types of anemia in your life unless you're a hematologist oncologist however on u.s emily and complex anemia is high yield it's literally all over your exam the reason being is that anemia has so many different types right there's so many different types of microcytic and normocytic and macrocytic and blah blah blah blah blah it's nuts they love showing you pictures on your exam and making you infer from that picture what type of anemia we're talking about or what type of blood disorder we're talking about there are literally hundreds of ways they could get after this and that's why you need to know anemia cold so what are we going to cover today first we're going to start with the kind of overview slide that will show you the three different ways that we categorize anemia then we're going to talk about lab findings not all of these have really high yield lab findings but where i think it's pertinent is how you use the labs to differentiate one type of anemia from another so we'll cover what the labs are where appropriate we'll talk about all high yield clinical associations so some of these anemias are related to really really high yield diseases and i'll point those out as we go through the last thing that we're going to do today which i really love are just the pictures of the red blood cells and depending on what type of anemia or what type of blood disease we're talking about the red blood cell changes accordingly and you need to be familiar with the pictures because one of the board favorites is that all they'll do is show you a picture and then they'll ask you a question so you got to know what you're looking at so that's sort of the overview of today's lecture and with that said let's talk about how anemia is classified so first i want to start and just take a step back and kind of give a general definition of anemia so anemia is when there is a decreased or hypo functioning red blood cell or hemoglobin and in all of the cases of anemia regardless of whether we're talking about a low normal or high mcv anemia is pretty much going to present the same way it's going to just be constant chronic unexplained fatigue so if you see that that's your cue that we're talking about anemia now the way that anemia is classified is according to something called the mcv which stands for the mean corpuscular volume and when that mean corpuscular volume is below 80 it's considered low so let's first start by talking about the diseases that we're going to go through of course i'll go through these one at a time but again this is our overview slide so what you see here in this diagram is kind of the composition of hemoglobin and hemoglobin is broken into four subunits and in each of those subunits you have a heme group with an iron at the center so on the right you see kind of what that looks like chemically and then on the left you see the 3d representation so four heme groups and at the center of each of those heme groups are iron when all four of those subunits are bound together you have one hemoglobin molecule so that's what we're talking about now in a low mcv disease state any one of these components of hemoglobin can be messed up so in the case of iron deficiency anemia which is our first type of low mcv anemia we we lack iron so we lack that iron that sits at the center of the four heme groups in citroblastic anemia we have a problem with heme itself so heme production in the porphyrin pathway is going to be messed up and as such we're not going to have functioning hemoglobin because those four heme groups are are not being produced correctly and then in thalassemia we have a problem with the actual gene that codes for the heme so the problem with one of the alpha genes or one of the beta genes also included in the low mcv group is anemia of chronic disease i will touch on that again by itself but that doesn't really relate to that diagram that you just saw and anemia of chronic disease can actually be considered um low mean corpuscular volume but also normal mean corpuscular volume so this is a great segue into the normal diseases anything with a mean corpuscular volume from 80 to 99 is considered normal so it's not low it's not high it's normal so anemia of chronic disease can be normal or low my experience is that usually you'll see it on the normal side but it can be low the other diseases in this normal section that we're going to talk about are paroxysmal nocturnal hemoglobinuria g6pd deficiency and hereditary spherocytosis then we're going to talk about high mcv diseases so any time the mean corpuscular volume is 100 or higher we're talking about a high mcv and these are classically your b12 and folate deficiency so here's the overview of today's lecture and i'm going to go through each of these individually touch on all the high yields through our little mnemonics and we'll be on our way we'll be learning anemia together um one thing i do want to point out before we get started is that this is not an all-inclusive list there are other lower yield diseases not on this slide if you are interested in learning about those i would refer you to pathoma sitar does an absolutely wonderful job of summarizing all of those i'm just not going to waste your time so let's start from the left side and work our way across the slide towards the right so we'll do all the lows then all the normals and all the highs so with that said we're going to start with iron deficiency anemia so iron deficiency anemia is the most common cause of anemia right there right off the bat you've got a high yield point most common cause of anemia is iron deficiency anemia so this will classically present in someone with some type of bleeding if you have a patient who is iron deficient anemic you know iron deficiency anemia and you don't know why if it's an older male it's colon cancer until proven otherwise in a female it could be related to her menstrual period but you know that remains to be seen because there's lots of different causes of iron deficiency anemia and that'll be your job to investigate once you're a clinician but for the purposes of usmle and comlex let's talk about some labs so the labs that we'll see in iron deficiency anemia are low ferritin high transference tibc i'm going to use those words interchangeably you'll have hypochromia and again we talked about a microacidic mean corpuscular volume so ferritin is the storage form of iron that's how i want you to think of it so in when you're iron deficient you're going to have decreased ferritin because you don't want to store iron you want more iron free in the body so the storage form will be low slash tibc which stands for total iron binding capacity is basically something that represents the body's willingness to want iron or to have iron so in an iron deficient state we want more iron and therefore the tibc transferrin which carries the iron around is going to be high because we're trying to get more iron free in the body hypochromia is kind of like a pale a pellish color of the red blood cell that you'll see on a slide and the reason that it's pale is because when you're iron deficient your hemoglobin is is really not working so you have less hemoglobin which appears hypochromic when you actually look at a red blood cell and then we said it's microcytic it's mean corpuscular volume is going to be less than 80. so those are your labs and the labs are really high yield for iron deficiency anemia because a lot of times on your exam they'll just give you labs they'll describe a patient who probably has some questionable bleeding or you know some some type of bleeding disorder and they'll want you to pick iron deficiency anemia so be familiar with these labs be familiar with ferritin being storage transferrin such tibc being like the the transport or the body's willingness to want more iron hypochromia the paleness of the red blood cell because the hemoglobins just simply decreased or not working and it's microcytic so high-yield stuff right there a high-yield disease association is plummer-vinson syndrome so plumber-vinson syndrome is a triad of three things esophageal webs iron deficiency anemia and dysphagia memorize it guys three things esophageal webs iron deficiency anemia and dysphagia and the mnemonic here is w-i-d and the reason that w-i-d is the mnemonic is because plumber sounds like plumber and when do you need a plumber to fix your toilet when i diarrhea so when i diarrhea i need to call a plumber to unclog the toilet wid for when i diarrhea wid for webs iron dysphagia it's a triad it's plumber vinson syndrome don't forget it that is iron deficiency anemia here's a beautiful slide showing hypochromia so hypochromia are slightly paler red blood cells again because hemoglobin is just not in its normal state this is what that looks like compare this to a normal red blood cell and you'll definitely notice the difference but this is hypochromia that's iron deficiency anemia so we're already done one let's talk about citroblastic anemia so citroblastic anemia is an abnormality of heme production in the porphyrin pathway and what you see on the left part of the slide is the porphyrin pathway you do need to know the portform pathway i'm not going to go through it right now but i again i would refer you to pathoma and sitar who does an excellent job covering this but what i want you to be familiar with is what i've circled and marked in red here so citroblastic anemia the most common cause is an ala synthetase deficiency and that's the enzyme shown there in red the other causes of citroblastic anemia can be lead poisoning and administration of some drugs which are going to indirectly inhibit ala synthase so let's kind of go through this one at a time when this is the mitochondria that you're seeing shown there in that light blue and in the mitochondria you have the ultimate production of heme now if you have an ala synthetase deficiency you can't produce heme so there there's going to be decreased heme now what happens is heme combines with iron in the mitochondria and that's kind of how the heme and the iron get linked up for use in hemoglobin but since heme is not being produced you're going to have iron sitting around inside the mitochondria and we're going to come back to that in just a second but iron is going to be built up because it can't combine with heme now besides an ala synthetase deficiency which is a genetic deficiency of the enzyme that ultimately leads to the production of heme the other ways that you can get citroblastic anemia are from lead and from the drug isoniazid so isoniazid causes a b6 deficiency so isoni is isoniazid basically inhibits b6 and that's important because b6 is a cofactor in the step that uses ala synthase so isoniazid decreases b6 which decreases ala synthase which decreases heme when heme is decreased there's no heme so hemoglobin doesn't work and you become anemic and then iron builds up in the mitochondria which is bad you get iron overload in the mitochondria the other ways is to be lead poison so lead inhibits the enzyme ferro ketolace um furokilatase is one of the enzymes also involved in the production of heme so in some instances if the patient has lead poisoning feral kilo taste won't work you won't get heme hemoglobin works you become anemic and then iron builds up in the cell these are all various causes of citroblastic anemia so spend some time on this slide rewind the video and look at what i said but when this happens heme doesn't get produced now i told you that when heme doesn't get produced it can't combine with iron and if iron can't combine with heme to be exported and used in hemoglobin then you have an iron building up in the mitochondria that looks like this and the reason that this is important is because one of the ways they go after citroblastic anemia on usmle and comlex is they'll show you a picture of something that is stained with a prussian blue stain that looks like this so this is called a ringed citroblast and what you're seeing all those blue specks are iron accumulating in the mitochondria around the nucleus iron can not get out of the mitochondria it's accumulating and it is it's causing what's called a ringed citroblast so you see that picture it's citroblastic anemia because iron is building up in the mitochondria it has no heme to combine with probably because ala synthetase isn't working but possibly because the patient is a tb patient on isoniazid or they have lead poisoning because they live in a house that was built before 1972 secondary to lead paint whatever it is it's citroblastic anemia so ringed citroblast looks like this know it cold that's citroblastic anemia um and your labs you're gonna have increased iron because iron is accumulating right we got iron overload increase ferritin because iron is accumulating and we're trying to store it and decrease tibc transferrin because the body's like no no no i don't want any more iron that is citroblastic anemia so we're done with the first two let's talk about thalassemia so thalassemia has historically given everyone nightmares thalassemia is not fun to learn i'm gonna do my best to simplify it but i'm gonna be honest and forthcoming thalassemia is hard it sucks so spend some time on thalassemia so thalassemia is an abnormality and hemoglobin production basically you've got different types of genes that code for for heme production you have four alpha genes and two beta genes and the way that thalassemia works is that the deletion is given in the name so alpha thalassemia means that an alpha gene was deleted beta thalassemia means you know one or more of the beta genes was deleted so that's how the name the naming convention works so let's start with alpha thalassemia so if you have one deletion in an alpha gene you're asymptomatic doesn't matter you're probably fine two deletion of two alpha genes you're going to have a mild anemia that's the one that they go after the most on boards and and i'll come back to that in just a second three deletions you're gonna have severe anemia and four deletions it's it's high drops fatalis it is incompatible with life so baby is just not gonna make it now let's go back to the two deletions of two alpha genes that's the mild anemia this one is what they go after on boards and the reason is because it creates a mild anemia that anemia can be confused with other types of anemia so they want to make sure that you understand thalassemia and that you're going to identify it on usmle and complex so so this is what they like to go after what i want you to know is that there's two types of alpha thalassemias with the double deletion there's a cis deletion and a trans deletion now the cis deletion is going to as the name implies occur on the same chromosome the trans deletion is going to occur on different chromosomes um asian patients typically have the systolation and african patients usually have the trans deletion one deletion of a beta gene will cause beta thalassemia minor which is going to be asymptomatic pretty much two deletions of a beta gene causes beta thalassemia major and in that case you have production of hemoglobin a2 so because both of the betas are deleted you have two a's that's where the name comes from i think so lots of hemoglobin a2 i would know that and then i would know that there is this association which is called a chipmunk facey um or chipmunk faces chipmunk faces so basically what's happening is because you have beta thalassemia major hematopoiesis is royally screwed what the body tries to do is produce blood cells in other locations one of them is on the skull because there's a lot of surface area of bone there so the skull tries to do hematopoiesis and then the skull gets really deformed and the way that it's classically described is as a chipmunk facey so i guess you look like a chipmunk i don't really see that um similarity but that is what it's it's said to look like um the way that i remember this is that beta thalassemia major reminds me of the drum major who wears that hilarious funky hat which sits right on the skull so beta thalassemia major looks like the drum major the drum major wears the hat on the skull that reminds me that um there's extra medullary hematopoiesis at the skull which causes chipmunk faces in beta thalassemia major the way that i remember alpha thalassemia is that it's all the a's so the asian and african patients with the deletions will have alpha thalassemia and then beta thalassemia major looks like drum major extra medullary hematopoiesis which means that it's hematopoiesis occurring outside of the medullary portion of bone it occurs on the skull of the face which is going to cause chipmunk faces so that is thalassemia i think this is a really easy way of breaking it all down but i think you should definitely go through this slide a couple times and get comfortable with the different types of thalassemias because they are particularly high yield we're going to move on to talk about anemia of chronic disease now so anemia of chronic disease is an anemia that is secondary to some type of chronic inflammation so basically the body is unable to differentiate if it's getting destroyed from a really bad infection or if it's just some type of chronic inflammation or chronic inflammatory disease that causes inflammation in the body so this could be like someone has the bubonic plague and it's actually infected by something terrible and deadly and on the other hand it could be something like rheumatoid arthritis which is just a disease that causes chronic inflammation in the body so from the body's perspective it doesn't know which of the two it is but in either scenario it activates um an acute inflammatory product called hep cytin and hep cydin goes to the gut and tells the gut yo we're getting screwed by chronic chronic inflammation right now and i don't know if it's infectious or not but either way we gotta hide iron now the reason that it's hiding iron is because infectious processes use iron to multiply so when the body is experiencing chronic inflammation one of the pro-inflammatory mediators that come out is hepsidine and hepsidine's job is to go to the gut and say yo chill on the iron absorption so we have decreased iron absorption in the gut and then it's to go to ferritin and say hey ferritin bro you got to increase your iron storage because we got to hide the iron in the event that this is something truly infectious now again and i'm stressing this because this is very important it doesn't matter if it's an actual infection or if it's some type of disease that just causes chronic inflammation the body can't tell the difference because as evolved and amazing as our bodies are they're really quite stupid when it comes to anemia so hepsidine causes decreased iron absorption from the gut and increased iron storage in the body because of this the labs are going to be decreased iron because we're hiding iron increased ferritin because we're storing hiding iron in the form of ferritin and decreased transferrin tibc because the body doesn't want iron it's trying to hide it so that's anemia of chronic disease and the three things that i want you to remember in addition to an actual infection are kidney disease autoimmunity and anything rheumatologic so any of those things will cause anemia of chronic disease so like lupus rheumatoid arthritis chronic kidney disease whatever and the way that i remember this is that anemia of chronic disease chronic disease cd you listen to cds in the car car k a r i know i spelled it wrong whatever kidney disease autoimmunity rheumatologic diseases so we listen to the cd we listen to the chronic disease in the car k.a.r kidney autoimmunity anything rheumatologic so again infections chronic diseases doesn't matter the body is stupid and wants to hide iron that's anemia of chronic disease that's that's a normal mcv and a low mcv now let's talk about paroxysmal nocturnal hemoglobin area or pnh so this is caused by a defect in something called the piga gene right the piga gene and the piga gene encodes two things cd55 and cd59 cd55 cd55 is also known as decay accelerating factor aka daf so when you have an abnormality or a defect in this pika gene you don't get cd55 and you don't get cd59 now how does that contribute to peroxisal nocturnal hemoglobin area well let's say that this is a red blood cell normally the red blood cell will have these two products on it right it'll have cd55 known as decay accelerating factor and it will have cd59 these are both encoded by the piga gene when the piga gene is messed up you don't get these so that's what i want you to know so far now in complement complement usually works like this there's the gene c3 convertase which converts c3 into its c3b active form c3b activates the membrane attack complex which causes lysis of cells now normally the red blood cell has cd55 and cd59 on it and what these things do is inhibit c3 convertase so c3 convertase activates all its [ __ ] and that thing comes to the red blood cell and says red blood cell my name is complement i am here to destroy you and the red blood cell says not so fast bro here's cd55 here's cd59 and these two things slap c3 convertase across the face and inhibit it that's what normally happens but if you have a defect in the piga gene and you don't have cd55 and you don't have cd59 complement will occur and lyse the red blood cell so this is what's happening in paroxysmal nocturnal hemoglobin area now the way that i remember this is there are three things you need to know about pnh and the mnemonic is literally pnh you get pancytopenia so decrease in all the types of cells um there's a negative coombs test because a coombs test measures an auto antibody and there is no auto antibody in this in this instance and this occurs when you sleep at night and i use the h as this occurs when you're hibernating so as a really quick aside the reason that this typically occurs at night we believe this is because at night patients hypoventilate which causes some type of acidic change in the body that causes more complement to occur that's way beyond the scope of usmle and comlex so don't worry about that but i'm just trying to you know make more memory connections for you guys here so paroxysmal nocturnal hemoglobin area so the name sort of gives away what it does but just remember pnh pancytopenia negative coombs occurs during hibernation aka occurs during sleep and this is a defect in the pika gene which knocks out cd55 and cd59 so complement goes unchecked and lyses red blood cells which of course causes anemia so that's pnh not too bad right let's talk about g6pd deficiency so g6pd deficiency is pretty high yield so what happens this is this is due to oxidative stress being imposed on red blood cells so normally in the hexose shunt you have glutathione that turns into reduced glutathione and what mediates that for the glutathione being turned into reduced glutathione is the nadph nadph turns glutathione into reduced glutathione and then reduced glutathione goes around and it destroys free radicals which usually cause oxidative damage so that's the normal now there's an enzyme called g6pd which turns nadp into nadph so as you can see if there's no g6pd so if you have a g6pd deficiency you can't make nadph which means you cannot reduce glutathione which means you cannot cleanse free radicals and if free radicals are running around like crazy mad men like radical mad men as you see here then they're going to cause a lot of damage in the body and that's what happens when you have a g6pd deficiency now what's really high yield to know for your exams are two things one is that certain types of oxidative stress will cause the formation of free radicals so someone who has g6pd deficiency might be asymptomatic for a while but then all of a sudden they're going to incur some type of oxidative stress and because they have a deficiency in the g6pd enzyme they can't clean up all the free radicals that are forming as a result of this sudden burst of oxidative stress so what is it that causes the oxidative stress well the mnemonic instead of g6p is d6p and d6p stands for dapsone sulfa and primaqueen i also include fava beans but everybody knows that like favorite beans is the biggest buzzword for g6p deficiency g6pd deficiency so it's not part of my mnemonic but everyone pretty much knows that so dapzone sulfa drugs primoquine fava beans if a patient has that stuff ingest that stuff takes the drug and they're g6pd deficient they're going to become anemic it's going to be a normocytic anemia so look for the clinical vignette where the patient is taking some antibiotic and all of a sudden they become anemic it's probably a sulfa drug they're being treated for malaria and all of a sudden they become anemic it's primoqueen they go to some foreign country and they eat the local food and then they become anemic it's favorite beans they have an infection and then they become anemic might be g6pd deficiency how they'll get you on the test is with these super high yield pictures so please know these pictures cold what you're seeing here on the left are heinz bodies and on the right are bite cells so basically in a g6pd deficiency the patient will have denatured hemoglobin as a result of the oxidative stress causing the anemia and when that accumulates it accumulates in little clumps which are called heinz bodies you see them on the left now the body doesn't like heinz bodies so what it does is it sends macrophages and says yo there's heinz bodies over there go get them get rid of them so the macrophages literally walk up to the red blood cell and take a bite out of that red blood cell and what you see is called a bite cell and that's shown in the right so it looks like a red blood cell with literally like a bite taken out of it hence the name bite cells so if you see heinz bodies or you see bite cells it's a g6pd deficiency no again that g6pd deficiency is caused by oxidative stress due to the inability to reduce glutathione which means free radicals are roaming free as a result of the oxidative stressors which causes heinz bodies and bite cells so that's g6pd deficiency let's wrap up the normocytic anemias by talking about hereditary spherocytosis so hereditary spherocytosis is due to a dysfunctional red blood cell skeleton protein and there are a couple proteins that can cause this it can be to due to dysfunctional spectrum anchoring or some type of band so it'll say something like band 3.1 or band and then it'll list a number whatever that is it's hereditary spherocytosis so the red blood cell relies on these proteins to build its kind of perimeter and i love this diagram because it shows you that from the molecular point of view when you lack those proteins what should be that normal biconcave shape of the red blood cell turns into a sphere hence the name spherocytosis so when you have that sphere a couple things happen one is that the red blood cell loses its ability to pass through the spleen appropriately and as a result of that red blood cells are going to accumulate and become stuck in the spleen so you get splenomegaly you're going to have a coombs negative test because again there's no autoantibodies here so coombs is that's what it's testing for there's no auto antibodies it's going to be coombs negative you're going to get an increased indirect bilirubin and jaundice because of extravascular hemolysis so these red blood cells are going to be destroyed extravascularly and you get jaundice as a result of that the highest yield thing that i want you to know is that you get howl jolly bodies shown here in that image so usually what happens in the spleen is that red blood cells lose their nuclear remnants in this in the situation of hereditary spherocytosis the spleen cannot remove the nuclear remnants so you literally have basophilic nuclear remnants clumping up in little balls and staying in the red blood cell inappropriately when in fact they should have been removed in the spleen but they couldn't be because the spleen is really screwed up because these sphere-shaped red blood cells are accumulating in the spleen and causing problems with the spleen so that's hereditary spherocytosis and that wraps up all of the high-yield normal acidic anemias that you should know about the last category we're going to get into are the mcvs that are high so they're going to be 100 or higher and these are just b12 and folate deficiency these are particularly high yields so i really want you to pay attention here b12 deficiency i think to understand this we should start with a diagram of the stomach so there's your stomach and somewhere near the top of the stomach you have your gastric parietal cells which i marked there as gpc and if you followed the intestines you'd eventually reach the ilium so for simplicity's sake i marked the end of this diagram as the ilium what happens in b12 deficiency or you know what let's start with what happens normally so the gastric parietal cells will secrete something known as intrinsic factor or if and when you take in b12 and i show b12 they're coming down the esophagus intrinsic factor and b12 bind together and form this complex and they pass through the intestines together in this complex until they reach the ilium and at the ilium the ilium breaks the connection and absorbs the b12 so b12 is absorbed at the ilium that's really really high yield and intrinsic factor complexes with b12 which is secreted by the gastric parietal cells so the most common cause of b12 deficiency is what's caused called pernicious anemia so in pernicious anemia you have autoimmune destruction of gastric parietal cells and when that happens the gastric parietal cells don't make intrinsic factors so you have a decrease in if and when that happens you can't complex if to b12 so you have a decrease in that complex and then when that happens you can't absorb b12 at the ilium so you have a b12 deficiency b12 and folate but we're talking about b12 right now b12 and folate are both involved in dna synthesis so it's very important that you get these substances in in order to make dna and that's where sort of the anemia ties in so pernicious anemia is the most common cause of b12 deficiency and as you'll see when we briefly touch on folate you need foley because you don't get a lot of folate stores but b12 the body has so many b12 stores that it can literally it's very hard to become b12 deficient by not eating b12 because you've stored up so much that lasts such a long time so the number one cause of b12 deficiency is in fact this autoimmune condition called pernicious anemia something that's really high yield that i would like to point out is that because b12 is absorbed at the ilium another type of another cause of b12 deficiency would be if we knocked out the ilium so any type of gi disease that knocks out the ilium or you know trauma surgery whatever you can't absorb b12 you'll become b12 deficient so that's really high yield so what do the labs look like in both b12 and folate deficiency you have an increase in something called homocysteine but only in b12 deficiency do you also have an increase in something called mma that's methylmalonic acid this is really high yield because sometimes on exams they'll make you differentiate between b12 and folate deficiency so what gives it away is the increased mma that always goes with b12 deficiency so how do we remember this mma to me is mixed martial arts and here's a picture of an mma fighter kicking someone right in the ilium and in my head i'm saying they're knocking out the ileum which is what absorbs b12 so if you have mma you have b12 deficiency that's really really high yield another thing taking this a step further is that one of the symptoms of a b12 deficiency are neuropsychiatric symptoms subacute combined degeneration is what you'll see on exams and the reason is because b12 is used uh in the synthesis of the myelin sheath and without the myelin sheath you're going to get neuropsychiatric symptoms like numbness tingling lack of reflexes etc so that's that's one of the symptoms that you'll see really far down the line after the anemia once you're b12 deficient and the way that i remember that is again our mma fighter is now kicking somebody in the head which is causing neuropsychiatric symptoms so that's b12 deficiency we got mma kicking them in the ilium ilium is what absorbs b12 so mma elevated is b12 deficiency normal mma for folate deficiency and then again the mma fighter kicking someone in the head reminds me of the neuropsychiatric symptoms as a result of that elevated mma causing damage to the myelin sheath which causes neuropsychiatric symptoms so that's b12 deficiency in both b12 deficiency and folate deficiency not only do you have an elevated homocysteine but you have this hyper segmented neutrophils this is a very very high yield image which is why i blew it up and put it in really nice quality because you have to be able to recognize this if you see this picture it could be either b12 or folate deficiency you don't really know yet you're gonna have to look at other things like is mma elevated do they maybe have pernicious anemia how's their diet are they alcoholic things like that um you'll kind of go from there but where you start if you see this picture it's macrocytic it's megaloblastic it's going to be b12 or folate deficiency now i don't have a slide for folate deficiency because folate deficiency is pretty straightforward folate deficiency is a macroacidic right 100 or higher mcv it's a macrocytic megaloblastic anemia that's usually caused because of a nutritional deficiency so unlike b12 which is we have lots of stores of b12 in our body a folate deficiency is going to be because the person has terrible nutrition so like an alcoholic who you find on the bench might have a folate deficiency things like that so if you folate think more nutritional b12 think more pernicious anemia if you see neurosymptoms or an elevated mma it's b12 deficiency if you see hypersegmented neutrophils it could be either so that's it guys we've gone through all the types of anemia i know i kind of flew through this but i threw in mnemonics i talked about labs i showed you pictures and i think this is a really really good start if you combine this video with maybe something like um pathoma's video then i believe it's actually two videos on patholoma because it really takes a while to go through anemia then you should be pretty golden when it comes to answering these questions