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I have hematology finals tomorrow and am not even worried as always.After watching your videos,i feel no need to memorize stuffs,just undastnd.!! youre second to none.
Mcv can be high in myelodysplasia. Because MDS is also a cause of non megaloblastic macrocytic anaemia. So MDS may have low mcv or high mcv. Low mcv- if MDS is a cause of sideroblastic anaemia and High mcv- if MDS is a cause of non megaloblastic macrocytic anaemia
But the question is when is mcv high in sideroblastic type of anemia and not other type like non megaloblastic macrocytic anemia... The stain is prussian stain.
a few miles away from Beirut 7 of my professors passed away because of covid-19 including this subject's professor but we still have to move on with our first exam this semester if it was't for this playlist i would've honestly given up and dissociated until the end of finals thank you for the awesome explanation and for your super-human power of simplifying even the most complicated points
You made me like Medicine, the way you simplify the information and the interesting way you conduct the lesson especially when you say "and this is the whole story morning glory" I even started to use it sometimes when I talk 😂 Thanks so much Dr ❤️ All my love from Sudan 🇸🇩
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lead poisoning is often listed in textbooks as a cause of sideroblastic anemia. It is the author's experience, however, that lead poisoning is not associated with sideroblastic changes [76]. Like sideroblastic anemia, lead poisoning can cause anemia, a low reticulocyte count, and neurologic changes. Like sideroblastic anemia, lead poisoning is associated with disordered heme synthesis. Unlike sideroblastic anemia, lead poisoning typically produces heavy basophilic stippling rather than Pappenheimer bodies in RBCs or ring sideroblasts. Unlike sideroblastic anemia, lead poisoning is associated with elevated blood lead levels.
It's MDS, because in this condition there is JAK 2 gene mutation, this gene codes for a protein called Juan kinase, it's a protein that transmit stimulations from hormones like EPO and thyroxine to the nucleus helping in cell differentiation, thus the cell will get the ability to have new functions like Hb synthesis. Each time the cell gets a new function, it's work-list increases so it will be less interrested by division instead of maturation. In the mutation of Jak2, the cell keeps it's ability of division but lose it's ability for maturattion,this mutation happens so early in the pathway before even pro-erythroblastic state. This mutation can alse affect others blasts from # lineage not only erythroblasts, so the divisions increase and they consume vit B12 so the cells becomes macrocytic instead of being blastic ( having big size). And because there is no maturation of RBC's, there will be no synthesis of Hb components cause there will be no EPO and other hormone stimulus cause there in no jak2. And then the mitochondria surrounding the nucleus charges with Fe and wait for it's clue (enzymes) essential for Hb synthesis, that will never come. So we will have macrocytic sideroblasts. In the case of alcohol yes we can have vit B12 deffeciency (causing macrocytosis) but in opposition we may have sideroblastosis and decrease in Hb synthesis (microcytosis), if both of them meets they can lead to normocytosis.
What does "they become macrocytic and not blastic"mean? Is it Because if the vit b12 gets over due to excess usage even the blasts won't be produced and whatever cells are already in circulation would be macrocytic.bcz now even the blasts can't be made
@@luffy101n2 No myelodysplasia is different from aplasia, the first one there will be blasts but few ones cause there is a lack of vit B12 not total absence, so there will be divisions that give big cells and those cells because they are big they remain few this is why we have anemia but in the case of Aplasia there is no Blasts at all. 0 bone marrow.
ANSWER: MCV is expected to be high in cases of Myelodysplastic Syndrome. Stain used for sideroblastic anemia are New Methylene Blue and Wright Stain. Correct me if I'm wrong. I'm grateful to you sir, thank you so much. P.S. more info in MDS pls. :)
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Congenital forms often present with normocytic or microcytic anemia while acquired forms of sideroblastic anemia are often normocytic or macrocytic. Congenital forms including X-linked SA, autosomal recessive SA, genetic syndromes Acquired forms including acquired clonal SA (which fall under the broader category of myelodysplastic syndromes (MDS)), acquired reversible SA (alcoholism, pyridoxine deficiency, lead poisoning, copper deficiency, excess zinc) Prussian blue stains iron
Thank you very much! I love the etymology thing very much as well! IMO sidero- means star, -blast means immature cell It is a type of immature cell that look like a starry sky It is not called siderocyte because siderocyte is a mature RBC that looks like a starry sky Please comment if I am wrong :P
+Lee Romeo I think “Sidero”- here means iron, as we say “hemosiderosis”... blast means: growing, germ, or cell with a nucleus. But thinking of it as a star or constellation helps during studying but I am not sure it’s scientifically accurate. That’s all that I know :)
Chronic alcohol use may lead to macrocytic but sideroblastic anemia. Iron can be visualised with prussian blue stain. Am I right? Thank you for the video
Iron stain is prussian blue. In acquired type MCV is high Ex. MDS ......... AND I HAVE A QUESTION TOO, WHY YOU DONOT COMMENT ON RETICULOCYTE? IN SIDEROBLASTIC ANAEMIA THERE IS INEFFECTIVE ERYTHOPOIESIS SO THERE WILL BE RETICULOCYTOPENIA IN RELATIONS TO ANAEMIA.
You made me like Medicine, the way you simplify the information and the interesting way you conduct the lesson especially when you say "and this is the whole story morning glory" I even started to use it sometimes when I talk 😂 Thanks so much Dr ❤️
Erythrocyte protoporphyrin - The erythrocyte protoporphyrin (PP) measurement has not been systematically examined in the majority of sideroblastic anemia types and has limited value in diagnosis. RBC PP values have been established in a few forms: ●In X-linked sideroblastic anemia (XLSA) and with defects in SLC25A38, the erythrocyte PP level is uniformly low because heme synthesis and hence protoporphyrin production are reduced ●In XLSA with ataxia (XLSA/A), erythrocyte PP is increased (mainly as zinc protoporphyrin) [9,10] ●In MDS disorders with ring sideroblasts, erythrocyte PP is characteristically increased up to 300 mcg/dL (normal: 20 to 80 mcg/dL)
MCV can be high ie macrocytic in acquired forms eg MDS, medication s eg isoniazid, chemotherapy etc, and also in alcohol abuse. Stain with Prussian blue
I am glad to know the nutritional equivalents to the body's absorption placement to help my acquired symptoms with no general defects. I combine my personal experience with food and your technical instructions. Keep posting! Thanks for helping me save my life!
Is it that the MCV would be high in the sideroblastic anemias caused by a myelodysplastic syndrome, having an underlying megaloblastic process as well? You can see stainable bone marrow iron by staining with the Prussian Blue stain.
I finally know what the heck Sideroblastic anemia is, thank you! Also MCV would be high in MDS And a personal request, can you make a video for MDS vs Aplastic Anemia, I know you have one video for each but it would be very helpful to make a comparison video to highlight the differences and similarities between the two conditions.
Can MCV be high in chronic alcoholism also? Due to both, direct alcohol toxicity on bone marrow, and B12 and/or folate deficiency secondary to poor nutrition.
@@mty6391 Sorry its been nine 9 months but I dont really know what caused it sorry. i've had it since I was born and I cannot remember an actual reason for it. Im sorry
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Ferritin is storage form of iron in liver and bone marrow .. and tibc is total iron binding capacity( max is 6 ) .. but I cannot understand why they are inversely proportional .. I'm asking a stupid question but I don't know . Help ?
a little late, but i think that the answer is intuitive. When the iron storage (ferritin) is high, you dont need the means of transportation to the deposits to be that eficient any more. you need the means of transportation to be very efficient only when the storage is empty.
my professor asked a question to the students after teaching us about microcytic anaemias: he said "if a patient only eats Spanish what type of anaemia would he get?" assuming he has normal levels of iron and folate. what do you think the answer is? I think the answer is sideroblastic & thalassemia but thalassemia is only caused by genetic disorders so do you think it's sideroblastic? I also thought of anaemia caused by vitamin b12 deficiency but I'm not sure if spinach provides the essential needs of it or not.