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Bone Marrow Failure (BMF)

by Carlo Raj, MD
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    00:01 Now moving forward, apart from acute blood loss and still in the realm of normocytic non-hemolytic anemia, let us now move in to the bone marrow.

    00:11 And for whatever reason, we’re going to shut it down.

    00:14 If you shut down your bone marrow, then what happens? Well you can’t produce reticulocytes, can you? So therefore, what’s the concept? It’s the fact that you have a decreased reticulocyte production index or as it says here inadequate reticulocytosis.

    00:29 And that magic corrected reticulocyte number is less than 3%.

    00:35 That you’ll have to memorize but the concept is clear.

    00:38 It’s a fact that the bone marrow has been shut down.

    00:42 Why? Well, we’ll get into this in a second.

    00:44 Bone marrow cellularity rule-of-thumb.

    00:47 So if the bone marrow has been shut down, think about what the bone marrow should look like.

    00:51 It should be nice and empty.

    00:52 There should be lipid.

    00:54 There should be fat vacuoles and obviously, there should be hematopoietic stem cells.

    00:58 And there should be those primitive type of blasts, right? Now, not too much and not too little, just right.

    01:07 And so that you can then produce a proper homeostatic churning or synthesis of the stem cells that we require.

    01:15 However, if the bone marrow for whatever reason, let’s say that this patient has aplastic anemia, then understand that at this point, the bone marrow is completely dead and is pretty empty.

    01:24 I’ll show you pictures.

    01:26 Now, as a rule-of-thumb which you can use as 100 minus age gives you approximate normal cellularity of your bone marrow.

    01:33 Just the generality, but as far as your concern, it would work.

    01:38 Now the causes, what’s causing aplastic anemia? What is then causing the bone marrow to become aplastic or hypocellular? Well, pancytopenia is just a term that we use for what, please? Usually it’s in reference to the trilineage.

    01:54 And by trilineage we are referring to, obviously, the RBCs, the platelets.

    01:59 And of all the granulocytes, which one do we normally have in our body circulating predominantly? Good, neutrophils.

    02:07 So that’s usually what you were referring to when you say pancytopenia and each one of those loss of the lineages is going to give you different symptoms in your patient.

    02:15 For example, if there is no RBC, your patient is going to present how? Fatigued and tired.

    02:21 If your patient has not enough platelets, what is that presenting with? Obviously excess bleeding that can form a clot.

    02:30 And if they don’t have neutrophils, what does that mean to you? Oh, they are now susceptible to infection.

    02:38 Those are three that you want to take a look at when you have pancytopenia.

    02:41 Earlier, we have talked about this in terms of megaloblastic anemia, right? In megaloblastic anemia, remember please, you were still producing your cells but they were blasts.

    02:54 But just because you’ve formed a cell, if it hasn’t matured then it can’t carry out its function, can it? Of course not.

    03:03 So those megaloblastic anemia or the megaloblastic cells and hypersegmented neutrophils with B12 and folate, yes, there is pancytopenia but that is not aplastic anemia.

    03:13 Is that clear? By definition, if it’s aplastic anemia, it means that you had no cells being produced because the bone marrow had been shut down and so therefore in the category of normocytic non-hemolytic anemia.

    03:25 Keep that in mind as you move forward.

    03:29 Now bone marrow failure, idiopathic/autoimmune being the most common.

    03:32 You find that occurring with many organ damage.

    03:36 Drugs including chloramphenicol and chemotherapy.

    03:39 Chemosuppression, right, in general or bone marrow suppression.

    03:43 Usually looking at those cells that like to divide.

    03:45 Tell me about your stem cells.

    03:47 What kind of cells are they? They are labile, aren't they? They love to proliferate, proliferate, proliferate.

    03:53 And so therefore with chemotherapy, looking at those cells that love to proliferate and unfortunately instead of attacking the cancer, may also have collateral damage.

    04:01 You’ve heard of bone marrow suppression.

    04:03 You’ve heard of hair loss.

    04:04 And there is massive diarrhea, isn't there? In those patients that are taking chemotherapy unfortunately.

    04:09 Quite a bit of pain.

    04:10 Sometimes the chemo is worse than the disease itself.

    04:14 Infection, we have parvovirus B19.

    04:16 Now, what we’ll do here, is well, is anytime parvovirus -- is it possible that you might have a patient that has another type of anemia such as hemolytic anemia and then may then have a parvovirus B19 virus infection? Sure.

    04:31 And so therefore, at that point, where do you move in to? What’s my topic here or category? Normocytic non-hemolytic because the bone marrow has been shut down.

    04:40 Now, with Diamond-Blackfan syndrome, we’ll talk about this a little bit more.

    04:44 But what I do wish for you to keep in mind is the following.

    04:47 Diamond-Blackfan syndrome can come under either your bone marrow failure where this is normocytic non-hemolytic and please be careful because Diamond-Blackfan could also be part of your megaloblastic anemia.

    04:59 We’ll talk more about that later.

    05:00 But that is one that you want to pay attention to.

    05:03 Fanconi’s anemia, there, what you want to pay attention to is do not confuse that with Fanconi’s syndrome which is a problem with the proximal convoluted tubule in the kidney.

    05:12 One has nothing to do with the other.

    05:14 These are all the different causes that you want to be quite familiar with with bone marrow failure.

    05:20 So what is Diamond Blackfan syndrome?


    About the Lecture

    The lecture Bone Marrow Failure (BMF) by Carlo Raj, MD is from the course Normocytic Anemia – Red Blood Cell Pathology (RBC).


    Included Quiz Questions

    1. Hypercoagulable state
    2. Fatigue
    3. Bleeding diathesis
    4. Increased risk of infections
    5. Decreased reticulocytosis
    1. Decreased DNA synthesis
    2. Chemotherapy
    3. Bone marrow suppression
    4. Fanconi anemia
    5. Parvovirus B19 infection
    1. Diamond-Blackfan anemia
    2. Iron deficiency anemia
    3. Sideroblastic anemia
    4. Anemia of chronic disease
    5. Thalassemia

    Author of lecture Bone Marrow Failure (BMF)

     Carlo Raj, MD

    Carlo Raj, MD


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