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Anemia: Overview

by Carlo Raj, MD

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    00:02 This is an overview that you want to pay attention to when you’re dealing with anemia.

    00:05 All we’re doing here is the overview and what we will do later on is then divide and dive into each one of these categories of different types of anemias, is that clear? So for example, under microcytic anemia, which we will take on at first, first and foremost, you pay attention to MCV being less than 80.

    00:26 And under microcytic anemia, we will then walk through the differentials that you see here.

    00:30 And these include your iron-deficiency anemia of chronic disease, sideroblastic, and also your thalassemias.

    00:36 And will tell you how to approach this when the time is right, because really what you’re doing here is hemoglobin.

    00:42 And so therefore, you divide for pathologic purposes to make your life easier with diseases, you’ll divide it into heme and globin, do that for me and you’ll be in good shape.

    00:52 And when we deal with heme, there are a lot of things that we need to talk about there with biochemistry.

    00:57 Biochemistry, you should be thinking about the porphyria pathway.

    00:59 And if you’re not familiar with it, perhaps it will be a good time for you to take a look at the porphyria pathway with heme synthesis whereas your globin would then be the gene, you don’t have control over genes, that’s something that you’re given and we’ll talk about the alpha, beta, gamma, delta and such.

    01:13 Under macrocytic, really -- Under macrocytic, we’ll divide this into megaloblastic and nonmegaloblastic and that becomes really important for us.

    01:22 So for example, the megaloblastics here that are often tested are your folate deficiency and vitamin B12 deficiency.

    01:31 There are a couple of others that we have to address as well under megaloblastic.

    01:36 And those include your Diamond-Blackfan anemia and then you also have orotic aciduria, all right? So those are things that have shown up, are showing up, and will show up and stick with me here, and I will constantly feed you current information constantly.

    01:51 But what I’m saying is, “Dr. Raj, I thought megaloblastic was always macrocytic?” That is true, okay? But the macrocytic always doesn’t have to be megaloblastic, really.

    01:59 "I thought they were interchangeable." No, they’re not.

    02:02 Please pay attention.

    02:04 So you can have macrocytic megaloblastic or you can have macrocytic nonmegaloblastic.

    02:10 Is that clear? So what’s the difference? The difference is the following.

    02:13 What you’re measuring with macrocytic is going to be, for the most part, the size of that RBC in serum.

    02:21 Is that clear? That to you means circulation.

    02:24 So therefore, if you’re thinking about folate and B12 deficiency, then don’t you need that for proper DNA synthesis, either pyrimidine or purine? Sure.

    02:33 So if you don’t have proper folate and B12 available, how in the world can you properly form normal RBCs? You cannot.

    02:43 Not only can you not form proper RBCs, you have many, many other issues including your WBCs and such as well.

    02:50 Would you please tell me what an immature cell is called in your bone marrow? Oh! I see what you’re getting at.

    02:58 That’s a blast, isn’t it? There you go.

    03:01 So whenever you have a blast, this to you should mean that you have a problem in the bone marrow.

    03:06 Whereas if you take a look at the category of nonmegaloblastic, it’s still macrocytic, so what does that mean? MCV.

    03:15 They’re greater than 100.

    03:16 Now, you can be more technical in terms of dividing megaloblastic and nonmegaloblastic with 110 femtoliters, but that’s a bit much right now.

    03:24 But under nonmegaloblastic though, this would mean that from the bone marrow, there’s no problem.

    03:29 Not B12, not folate deficiency.

    03:31 Under nonmegaloblastic, you have things like liver disease, alcoholism, and reticulocytosis, all right? So those are things that I will mention, but in terms of going into detail, if I were you, I’d be paying attention to alcohol.

    03:44 Alcohol does a lot of things.

    03:46 “Dr. Raj, I thought alcohol would then consume your folate.” Yes, it does.

    03:49 So be smart though.

    03:52 So if your alcoholic has megaloblastic anemia, it most likely was due to? There you go.

    03:56 Folate deficiency.

    03:57 See where I’m getting at? What else could alcohol do? We’ll talk, we’ll talk, we’ll talk.

    04:02 Alcohol could also result in a very common form of acquired type of sideroblastic anemia.

    04:09 And with sideroblastic anemia, take a look, microcytic.

    04:12 You see this.

    04:12 Okay, so these are things that – All we’re doing here is setting up an overview.

    04:15 I am spending a little bit of time here so that you keep these arms and branches of your anemias all, well, organized shall we say.

    04:24 Okay.

    04:26 Then what do we do? Well, divide our normocytics.

    04:28 So normocytics are going to be the largest of all of the anemias.

    04:34 So be careful.

    04:34 Just because you find an MCV, take a look, between 80 and 100, all it does is put you in the category of? Anemia.

    04:43 Normocytic specifically.

    04:46 And your patient is going to what? Come with fatigue and tiredness, right? That’s all he or she knows and then you will then take the proper history and then you’ll figure out.

    04:54 And the way that you want to do this, ladies and gentlemen, all I’m doing here is setting up the organization pattern.

    05:01 It’s divided into nonhemolytic and hemolytic.

    05:03 So I would like for you to take a look at the category in the far left here and those are all nonhemolytics.

    05:10 What does that mean? For the most part, as a rule of thumb, for example, let’s say that you have a patient that has parvovirus B19.

    05:18 Reflex, you’re thinking plastic anemia, correct? Maybe your patient is taking chloramphenicol.

    05:24 Maybe your patient is receiving chemotherapy.

    05:25 Maybe, maybe, the kidney’s got damaged.

    05:29 What does all of this have in common? Kidney’s got damaged.

    05:33 No erythropoietin, no erythropoiesis.

    05:34 Oh, okay.

    05:36 Next, chemotherapy, bone marrow shut down, suppression, oh, no bone marrow function, okay? Parvovirus B19, it hits the bone, what happens? Aplastic.

    05:45 Okay, you see my point.

    05:48 If you’re never able to properly form your RBCs from the bone marrow, how in the world can you possibly destroy them? You cannot.

    05:57 So therefore, these are nonhemolytic. Are we clear? Now, you tell me where the gravesite is for an RBC.

    06:03 The gravesite for an RBC.

    06:04 Good, the spleen.

    06:07 And so therefore, the two categories that you see here, the one in the middle and the one on the right for you, those are all hemolytics.

    06:15 And we’ll walk through all of these in detail.

    06:17 So all of these will at some point then up at the spleen or maybe even perhaps intravascular.

    06:22 But guaranteed, there’s going to be destruction of that RBC because there was no problem with your bone marrow.

    06:27 Hence, we call it hemolytic anemia.

    06:31 Before I move on, there is one other concept that I have to introduce now and then we’ll go on to greater detail when the time is right.

    06:38 And there’s going to be what’s known as – Well, current day practice, it’s called reticulocyte production index or RPI.

    06:43 It’s a concept that you want to know and really it comes down to what’s known as corrective reticulocytes and luckily now, there’s calculations and such, you can just plug it into your computer, app, or whatever, and it will tell you the proper RPI.

    06:56 But before you go here though, you must understand what’s happening.

    07:00 Let me ask you something, if the bone marrow, which is the first column or first category, normocytic here has been shut down.

    07:07 I’m not able to produce any RBCs, right? So if you’re not able to produce any RBCs, we’re you able to produce any type of reticulocytes.

    07:18 What is a reticulocyte? Well, we’ll go into detail about reticulocyte.

    07:23 It’s the fact that it’s an immature RBC.

    07:25 But point is this, if your bone marrow has been shut down, there’s no way that you’re going to produce any reticulocyte.

    07:31 So what do expect your RPI or corrected reticulocyte count to be? Know the concept first.

    07:37 Decreased.

    07:38 Good.

    07:39 So here, you’re thinking less than 3%.

    07:41 Whereas, the RBCs are being destroyed in mass by the spleen or intravascular.

    07:48 So now what happens? Bone marrow has to churn, churn, churn, right? It's put it into overdrive.

    07:55 Overdrive.

    07:56 And what are you churning out? The bone marrow spitting out reticulocytes, clear? So therefore, you would expect there to be an increase in reticulocytes.

    08:07 And we call this greater.

    08:10 We mean actual value greater than 3% and that will be for any hemolytic.

    08:15 So now, well, you’ll ask more questions later on, but understand the concept.

    08:19 So here’s a nice little overview.

    08:21 Not to worry.

    08:22 Obviously we’re going to repeat, repeat, repeat everything that I said.

    08:25 But hopefully, you have now developed a proper oganization pattern.


    About the Lecture

    The lecture Anemia: Overview by Carlo Raj, MD is from the course Introduction to Red Blood Cell Disorders.


    Included Quiz Questions

    1. Anemia due to iron deficiency
    2. Anemia due to vitamin B12 deficiency
    3. Anemia due to acute blood loss
    4. Anemia due to alcoholism
    5. Anemia due to liver disease
    1. Deficiency of folic acid
    2. Deficiency of vitamin B12
    3. Bone marrow suppression
    4. Liver disease
    5. Deficiency of vitamin B6
    1. Infection with parvovirus B19
    2. Hereditary spherocytosis
    3. Pyruvate kinase deficiency
    4. Malaria
    5. Sickle cell disease
    1. Intrinsic RBC membrane defect
    2. Hemoglobinopathies
    3. Bone marrow suppression
    4. Extrinsic RBC defect
    5. RBC enzyme deficiency

    Author of lecture Anemia: Overview

     Carlo Raj, MD

    Carlo Raj, MD


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    Great professor!
    By Iqra S. on 16. December 2018 for Anemia: Overview

    I feel like I'm in good hands with Dr. Raj! I especially like how he comes back to a point multiple times to emphasize it/make it stick.