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Lymphadenopathy: Signs and Symptoms of Multiple Myeloma – White Blood Cell Pathology

by Carlo Raj, MD
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    00:01 Continuing our discussion of multiple myeloma.

    00:04 Apart from serum protein electrophoresis, what are the feature that you’d expect to find? Well, if you take a look at the skull, you’ll find that you have punched out lesions.

    00:15 It’s a monoclonal gammopathy, you’d expect there to be IgG or IgA, but not IgM, and these light chains.

    00:22 Light chains are once again either kappa or lambda.

    00:25 And majority of them will be kappa.

    00:27 And as the picture would show you, oftentimes, actually almost on your boards, they have to give you – If they want you to choose multiple myeloma, they’ll give you lytic bone lesions and these are punched out lesions, not wide areas of complete destruction of the bone.

    00:44 The reason I bring that to your attention is, when we talk about Langerhans cell histiocytosis, there will be a subtype called eosinophilic granuloma, and that type is where you would also find destruction of the bone, but it’s quite chaotic.

    00:58 It’s not so chaotic in plasma cell multiple myeloma.

    01:02 What I mean by that is it’s punched out lesion, almost looks as though that the skull was shot by a bullet, going right through it.

    01:12 Now, I have to be careful as to how I use the word chaotic though because it is going to cause chaos in your body.

    01:20 So once you start having these lytic bone lesions, the bone is very, very weak.

    01:24 Your patient is now prone to pathologic fractures.

    01:27 In addition, the bone which is the major reservoir for calcium, the calcium is now being leaked into circulation at great quantity.

    01:37 You can expect your patient no doubt to have hypercalcemia.

    01:41 That calcium is going to pass through the glomerulus.

    01:44 You can absolutely expect your patient to have hypercalciuria, and with all this calcium that’s now in your urine, would you not expect there to be calcium stones? Everything’s a story.

    01:58 Make sure you understand as to how the disease initiates from the bone marrow.

    02:02 with plasma cells, IgG and IgA, and how it wreaks havoc on the bone specifically.

    02:09 A couple of other things in terms of symptoms, I’m giving you the fundamentals of multiple myeloma, there’ll be other things such as rouleaux formation, but that is nonspecific, and I’ll give you a little bit of detail about that.

    02:21 And there could be issues with the kidney or Bence Jones protein.

    02:24 But Bence Jones just means light chains.

    02:27 You can find light chains in other diseases.

    02:29 Lytic bone lesion, bone marrow.

    02:31 Plasma cell, multiple myeloma, IgG, IgA, gamma spike, nonspecific.

    02:37 Is that enough information? Absolutely.

    02:39 Get your question right.

    02:43 The picture that you’re seeing here upon histology would be from the bone marrow.

    02:48 A bone marrow aspirate in which you would then find tons of plasma cells.

    02:52 How can you identify these plasma cells? Rows upon rows of rough endoplasmic reticulum.

    02:58 And if it’s multiple myeloma specifically, from the bone marrow, and what kind of immunoglobulins are these then producing, please? IgG or IgA.

    03:09 With all these being produced, then what wave is then going to be affected? Good.

    03:14 The gamma wave.

    03:15 And now you have created a gamma spike.

    03:21 Signs and symptoms of multiple myeloma, we’ll talk about that bone.

    03:25 So here, you might have osteoclastic activating factor.

    03:28 Many times, interleukin 1 or 6 might be involved.

    03:32 Remember that from immunology.

    03:34 Interleukin 1 or 6.

    03:37 All that osteoclastic activity then causing bone infiltration.

    03:40 There will be chronic pain.

    03:41 The bone is now weakened.

    03:43 Your patient is now susceptible to pathologic fracture.

    03:46 With all that bone being destroyed, well, no doubt that the patient is suffering hypercalcemia, hypercalceuria, and perhaps calcium stones.

    03:57 The immunoglobulin that’s being produced in great quantity.

    04:00 You’re producing the light chains, that then deposits on your glomerulus.

    04:03 You’re going to have amyloid production.

    04:07 And this amyloid then is stained with your Congo red, which give you what color? Good.

    04:13 Apple green birefringence.

    04:17 In addition, you have these Bence Jones proteins, but then you also have Tamm, Horsfall, CAS, and all of these is then going to cause major damage to the tubules, eventually leading into renal failure, amyloid deposition.

    04:35 What’s interesting about plasma cell neoplasms or multiple myeloma? You would think, you know, just by theory, “Dr. Raj, you’re producing all these immunoglobulins, how is it possible that the patient is susceptible to infection?” You completely lose the proper, proper protocol for isotypes switching of your immunoglobulin.

    04:57 Remember, you have to have IgM 1.

    04:59 You have to have isotype switching into the type of immunoglobulin that’s necessary to fend off the antigen or infection.

    05:09 In plasma cell multiple myeloma, my goodness, you lose that isotype protocol.

    05:14 So therefore, even though you might be producing all these immunoglobulins, it doesn’t mean that you’re hyper immune, in fact, just the opposite.

    05:23 Your immunity is impaired or compromised.

    05:26 Your patient is susceptible to infection.

    05:28 You’re producing the wrong – You’ve lost the proper organization of your immunoglobulin.

    05:37 Clinically, who’s your patient? Almost always older.

    05:42 Now, unfortunately, we don’t have proper methods of controlling multiple myeloma, not yet.

    05:48 The older the patient gets with multiple myeloma, I can almost say guaranteed death, unfortunately.

    05:54 Very scary.

    05:56 Incidence increases with age.

    05:58 Prognosis is very poor.

    05:59 Look at this, three years survival.

    06:06 There are variants here, a little bit more detailed than what’s necessary, but understand there are variants.

    06:11 I’ll have you focus on the one that we have been discussing.

    06:15 You have smoldering type, your indolent type, you have an osteosclerotic type even, but then here’s your nonsecretory that’s also quite rare.

    06:23 But the one that we looked at by far, would be one in which it’s a classic, classic multiple myeloma in which you’re going to produce lots of immunoglobulin.

    06:31 And it will be IgG or it would be IgA.

    06:34 However, just keep in mind, I cannot guarantee that that is only what they’ll ask.

    06:40 So just to make sure that we’re complete, here are variants.

    06:43 You can actually have a nonsecretory type of variant.

    06:46 Has all other characteristics of multiple myeloma, but then your M protein, which represents your IgG or IgA and such, it’s negative.


    About the Lecture

    The lecture Lymphadenopathy: Signs and Symptoms of Multiple Myeloma – White Blood Cell Pathology by Carlo Raj, MD is from the course Lymphadenopathy – White Blood Cell Pathology (WBC).


    Included Quiz Questions

    1. Lytic lesions in bone
    2. Scorbutic rosary
    3. Bone within a bone appearance
    4. Thinned cortices
    5. Empty box appearance
    1. Osteosclerotic myeloma
    2. Smoldering
    3. Indolent
    4. Non-secretory myeloma
    5. Osteosclerotic
    1. 50-70 years
    2. 20-30 years
    3. 40-50 years
    4. 35-40 years
    5. 25-35 years

    Author of lecture Lymphadenopathy: Signs and Symptoms of Multiple Myeloma – White Blood Cell Pathology

     Carlo Raj, MD

    Carlo Raj, MD


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