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So good afternoon everyone. Uh My name is I'm one of the hematologists, uh originally graduated from University of two and I'm now practicing as a hematologist at um Helena Graham Cancer uh Center Research Institute in Delaware United States. And I'm, I'm glad to be sharing these uh slides with you today and I hope you'll benefit from hearing uh this presentation again. Feel free to email me with questions if you have any at the end, if we don't have time to cover them. So this is just a basic uh lecture to introduce to you um anemia and how to um uh approach a patient that comes to you with symptomatic anemia or if you find uh that the patient is anemic when you just do your uh regular screenings. OK. So, uh we're gonna talk about how um to define and how to grade anemia. We'll talk also about the common types of anemia, how to approach a patient that you think is anemic or you know, is anemic and how to take history. Uh I think this is really important for uh your level as medical students. I think if you don't know how to take history in a patient, you completely lose the point. I mean, taking history is very vital for whatever problem you're facing. For whatever kind of patient that comes in talking to the patient reviewing their records uh is vital. Ideally, by the end of doing your history, you should have your diagnosis at least you know about 50 to 60% minimum um confidence at the end of physical examination that should raise to maybe 70 to 80%. And then later laboratory data, I will complete your um assessment and you'll be able to diagnose and treat such patients at the end of the hour, we will be having a couple of examples. And I want you to kind of um if you can uh be interactive cause, I mean, these are uh the the the cases that resemble what you see generally in the emergency room or in your, in your office as a physician. Ok. So um anemia is very common and I'm sorry, I'm talking about American American patients, but this is where I practice. But um anemia is common everywhere in the world, especially in Africa. It's common in all kind of age groups from you know, infancy to uh geriatric patients. So it's very common, you will see it regardless of what specialty you choose. So um instead of referring patients to hematology should be able to kind of diagnose and treat the common types of anemia. So, anemia is defined when a hemoglobin is uh level of less than 12 g um in females and less than 13 g in males. And, and I'm talking about others here in pediatrics, the definition of that is by age. So, um in cancer patients, you rarely see a patient with normal hemoglobin. So the definition of anemia in cancer patient, if you come to, let's say CLL R I stage or you talk about multiple myeloma when you define anemia as an end organ damage, we use the level of uh 11. Ok. So mild anemia is um you know, anywhere between 10 to 12 or 10 to 13 based on the gender of the patients. And usually patients are generally asymptomatic when they have hemoglobin of less of more than 10, except if they have abrupt change in their hemoglobin level. And, and if, for example, they used the hemoglobin level of 10. Uh I'm sorry of 14 and they lose some blood or they develop hemolysis, their hemoglobin dropped to 10, then be they become symptomatic. But the most common types of anemia that we see like anemia of chronic disease and iron deficiency. They usually of insidious onset and patients are usually um you know, used to the level of hemoglobin. So they're not symptomatic and tell me that anemia is when your hemoglobin is less than 10 and above eight. severe anemia is when your hemoglobin is less than eight. And last creatinine, uh the hemoglobin is lower than that. And obviously, it's more, it's, it's worse if it's uh trending down further. So, the common types of anemia that we see regardless of patients, age is iron deficiency anemia in infants and Children in young females in elderly and adults is the most common type. And um usually due to blood loss and for you to be able to diagnose uh anemia of iron deficiency. Secondary to blood loss is usually kind of chronic, low grade blood loss. Acute blood loss does not cause features. Suggestive of iron deficiency anemia because their serum ferritin might be normal. Their M CV is gonna be fine. Their M CS is gonna be ok. Their RDW is gonna be ok, but they still have um any iron deficiency. And later on if you wait without replacing their iron stores, they will man manifest to you as the typical iron deficiency anemia. Ok. Uh sometimes it's due to poor absorption. So for somebody who has celiac disease, for example, people who are um infected with h pylori and people ha who take a lot of antacids. And also so these patients uh can have poor absorption a anemia. Uh of iron deficiency is very common in uh in bariatric surgery. Patients extremely common, not everybody who under who undergoes the uh bariatric surgery will be iron deficient but the majority of those patient end up needing some form of iron replacement. Um Well, vitamin deficiency anemias are also common. Um I know, all hematologist check B 12 and folate level. But believe it or not, patients with B 12 deficiency can come in with severe panto cy cytopenia, resembling uh apla anemia or something like acute leukemia. So, checking vitamin B 12 and folate level is very important. Uh It might, it might seem ridiculous, but again, it's, it will be um unfair that we miss those because they're readily replaceable and treatable. Ok. So, pernicious anemia is when you have um antibodies against parietal cell antibodies or uh parietal cells or intrinsic factor. And then there is a problem with B 12 absorption rather than the amount of B 12. The patient takes amy anemias are um you know, is a broad spectrum and they're not very common, but you have to recognize them because some of them can be very serious. So you have to pay attention to the parameters that can, you know, indicate hemolysis. Um hemolysis can occur if there is an an macroangiopathy process where the lining of the blood vessel is somehow disturbed whether by big changes such like a leaky valve or prosthetic valve or an aneurysm or by microangiopathic changes, such like such as disseminated intravascular coagulopathy where the endothelial lining of the blood vessel is damaged by the endotoxin. Um Similarly, TT P or thrombotic thrombocytopenic parra. Uh it belongs to this category uh of micro hemolytic process. Um You have the hem hemolytic uremic syndrome also uh causes hemolytic anemia there is a big category of autoimmune hemolytic anemia and this can be warm antibody or cold antibody. Again, patients come in with low hemoglobin, high M CV, high lactate dehydrogenase deficient lact dehydrogenase, uh low haptoglobin that will have high reticulocyte count if their bone marrow is able to compensate and have uh enough elements to do. So, we um have inherited hemolytic anemias and these are usually they usually present early. So, pediatric doctors tend to diagnose sickle cell anemia, thalassemia, um me and thalassemia intermediate. So G six PD is a periodic kind of um you know, um hemolytic anemia that comes after exposure to either um you know, drugs that are known to cause um um oxidation as well as um let's say some particular beans like beans or the light that, that cause oxidation as well. Yeah, part of it kinda is deficiency causes um kind of chronic hemolysis and it's um very hard to diagnose except if you pay attention and you know, you order the level. Ok, anemia of chronic disease. This is something that you see in patients who are um ha having multiple comorbidities including diabetes, hypertension, chronic kidney disease, patients who are undergoing chemotherapy or radiation therapy for cancer and patients with connective tissue disorder like, ok, lupus, rheumatoid, arthritis, psoriasis, all kind of chronic inflammation. Some patients who have foreign, foreign bodies, um they can have uh let's say prosthesis or whatever cosmetic um um insertions. One of the rare. Um anemias are because of the hematological disorder, like bone marrow disorder, like acute leukemia or um lymphoma uh that invading the bone marrow or alas anemia. These are very rare and they need a hematologist to diagnose and treat. Ok. So this diagram is just to simplify the common causes of anemia. Again, uh bleeding, uh chronic kidney disease, inflammation, hemolysis, whether for microangiopathic or microangiopathic process infection. Uh bone marrow involvement can be by cancer but can also be by granulomas or infection such as like mycobacterial infection, leishmaniasis, systemic Lemonis and the like again, um I mean, there are some uh this uh diagram on the previous list is not inclusive because I mean, there are other things that can cause anemia but they're very rare such like such as the splenic sequestration that can cause pancytopenia patients with huge spleen where all their blood is kind of instead of circulating in their uh blood vessels is is sequestered in the big spleen. So um a simple way of diagnosing um anemia and to kind of, you know, lo uh narrow. The list of differential is by looking at their um cell size and the amount of hemoglobin in each red blood cell. So to the, you know, differentiate them based on size and hemoglobin concentration. And usually when patients come to you, especially in the West, they already have some basic labs. Even even if uh they don't have it today, they'll have it from a month ago or a week, couple of weeks ago. So you will know if they have hypochromia microcytic anemia or normochromic normocytic or macrocytic anemia. And uh that will help you narrow um your um diagnostic list, differential diagnosis. All right. So a patient comes to you with normocytic normal chronic anemia. Um um these patients can um have bleeding, remember if acute bleeding happens, there is no chance to see the manifestation of iron deficiency. So, the cells will be normal in size. The cells will be um normal and hemoglobin concentration. Ok. So if you suspect that you have to kind of do a fecal occult blood, I mean patients can have a hematoma, they can have an internal bleeding, they can have an upper G I bleed, they can have significant epistaxis. Uh patient can have, you know, uh uterine bleeding. Ok. If a patient has a combined in and B 12 deficiency, they can still have a nor chronic normocytic anemia. So, an additional causes are something still to consider normocytic normal chronic anemia, anemia of chronic disease. Um is also very commonly can present as Noro normocytic, but it can present as hypochromia microcytic. Um um you know, pictures. So you need to check their kidney function. Hemolytic anemia usually presents as macrocytic anemia because of high reticulocyte count and the reticulocytes are big in size. So, if the body is able to produce significant number of reticulocyte hemolytic anemia presents as macrocytic anemia But if the number of reticulocyte is not big enough, then the person can present with normal chroma cytic anemia. Ok. So what you need to do that, you check their, uh check them for bleeding, you check them for a um renal problems. You check them for combined B 12 folate and iron deficiency anemia. And you check them for hemolysis by measuring their LDH hemoglobin reticulocyte count total bilirubin ac by looking at their preference, need to see, you know, micros spro sites or spherocyte and retic sites as well. Ok. So if no chromic chroma cytic anemia is, you know, after you do all of this and you don't know what's happening, then you start thinking about bone marrow processes such as multiple myeloma, you know, plastic anemia, lymphoma that's involving the bone marrow embo, right? But again, these are very rare. Ok. So these are normal looking red blood cells and your reference has to be a normal looking uh mature lymphocytes. So the size of the red blood cells should be similar to the size of the nucleus of the mature lymphocyte. And again, that's our reference. If the size is smaller, you call the cells macrocytic. If the size is we call a macrocytic. Again, the normal cells have a central pallor which reflects this indentation that you see in the in the center of the red blood cell. If the cent um center pallor is one third of the diameter, that's normal, that's normal um ha that's a normal chromic cell. But if the central pallor is more than this is hypo chromic cell, if there is no central pallor, we call it spherocyte. Ok. All right. These, some of the cells that you could possibly see in patients with anemia of chronic disease, secondary to renal insufficiency are bore cells. And these are cells that have um you know, some kind of around the projections are not sparky. If they're spiky, we call them acanthocyte. And do you see those with patients with advanced liver disease? Ok. Um Some of the um sickle cell patients are actually the majority of them come in with normochromic ma ma normochromic normocytic cells. Although they have some sickle cells, but somehow the machines um will not recognize those in when they, you know, measure the mean corpuscle volume. So they can count them as um normochromic no cytic anemia. All right. So these are the sickle cells. Oh man. And they're both shaved or banana shaped. Ok. So what if somebody comes to you with microcytic hypo chromic anemia? The first thing that comes to mind is iron deficiency anemia. So you need to check their serum ferritin and their serum fin is above 100. Then iron deficiency is ruled out and then serum ferritin is low. Then you know that you're dealing with um iron deficiency anemia. Uh some of the causes of I uh hypochromia microcytic anemias are uh thalassemia. But again, thalassemia is diagnosed. Um one is thalassemia, um intermediate or major. They're usually diagnosed at um childhood. So the patient will know that they're uh they have thalassemia. Some patients with thalassemia trait or thalassemia carriers don't know until they come to you. And this is a mys that's been going on for some time which is disproportional, the hemoglobin level. And um at that time, you suspect thalassemia and then you send for hemoglobin electrophoresis. Ok. Anemia of chronic disease can cause hypochromia and microcytosis. Ok. So again, these are the some of uh some of the causes of anemia of chronic disease. PB blastic anemia is not listed here. Another cause of hypochromia microcytic anemia. Lead poisoning can also lead to hypochromia microcytic anemia is and is not listed in this um diagram. So keep those in mind when um I mean, you would do all kind of work up and you find that these persons, they don't have anemia of chronic disease, they don't have thalassemia. Their iron studies are fine. So look for lead poisoning, um pseudo blastic anemia. Ok. So these, these are, I mean, remember we said the reference for your um red blood cell size is the nucleus of a mature lymphocyte. So if you look here compared to the size of this cell compared to the nucleus of the lymphocyte, C is clearly smaller. Ok. When you see hypochromia microcytic cells, you usually see some abnormal shapes on the left panel like OK, pencil shape, elongated shape. You see that the central pallor is more than one third of the diameter of the red blood cells. Um In this case, you call it a donut shape. And this picture is actually referred to as an iso poikilocytosis. So, red blood cells with different shapes and sizes and that's typical of c iron deficiency anemia, all righty. So um I'm pointing here some target cells because I mean, you could see them, these cells, you can see them in anemia. Um um uh uh related to severe liver disease, hemoglobinopathy such as hemoglobin C and D, you can see them in thalassemia as well. Um So just for you to know what target cells mean or look like. Ok. So what if you see a patient with macrocytic anemia? Somebody who has big M CV. And the first thing that comes to mind is B 12 and folate deficiency secondary, I mean Megaloblast causes. But uh many drugs can cause megaloblast changes including hydroxyurea. Uh AC T um you know, many of them anti psychotic and uh antiepileptic seizure medicines can cause macrocytosis. So you need to look at patient's medication list, then you go for their B 12 level folate. Uh remember sometimes B 12 level can be borderline normal, but they still can be um uh A B 12 deficiency. So you have to check their homocysteine level and the high me acid to exclude B 12 deficiency totally. Ok. Um keep in mind that patients with hemos can have high reticulocyte count and reticulocytosis can lead to high M CV. Some of the causes that ca uh that can lead to high M CD is liver disease and thyroid dysfunction as well. So, um uh the workup, uh it depends on if you have, they have B 12 or folate uh deficiency. If they don't, then you took for you. Uh look for other causes. Monos syndrome is a um a malignant hematological process that you should suspect when you see high M CD and two cell lines that are suppressed. So, if somebody comes in with anemia and neutropenia or anemia and thrombo, so mean and their M CD is elevated, then you think of M DS again, it happens for elderly, middle age and elderly patients. So, no, you don't suspect that in a young person except if they have a preexisting, you know, hematological disorders such as taco anemia, um or dyskeratosis, congenital um that inherited um hematological um disorders. Ok. So again, your reference is your uh red uh the nucleus of the lymphocytes. So, if you see red blood cells bigger than that, and then these are macrocyte, I'm showing you on the left panel here and uh hyper nucleated neutrophil and this is so, you know, it's kind of um an indication for vitamin B 12 deficiency and neutrophil that has five or more lobes is called hyper nucleated neutrophil. Ok. Um When if you have a hemolytic process, you see reticular size. And again, these are big and uh on the left panel, they increase the M CV. And here you see a nucleated red blood cell and red blood cell is the stage of erythropoiesis that precedes um reticularis. So the first, the nucleated red cell, uh you know, is it, it, it comes after the normal blast and when it loses its nucleus, it becomes a reticulocyte and the reticulocytes later becomes a mature red blood cell. So when you see a nu red blood cell in peripheral blood, that means the bone marrow is trying to compensate quickly and it's releasing immature forms like critical Cy and Rs. And that usually happens in hemolysis or acute blood loss. So the bomber is working tells you that the bomber is working and that's why um you know, this releasing these cells. You see here uh sickle cell. So this person in the left panel has acute sickle cell, uh hemolytic crisis and releasing S and in art disease. Um Here again, on the left panel, you see those um RN A reran that, that make the reticulocytes have this bluish who they're not pink, they're bluish kind of uh because of the RN A uh remnants. Ok. Some of the cells that you could see with acute hemolysis are spherocyte. So, spherocyte are small red blood cells that lack the central pallor. And again, this is a sign of hemolysis whether is um uh because of uh you know, autoimmune or autoimmune hemolysis cause of an infection, um or whatever thrombotic, thrombocytopenic prepper or T TB or hemolytic uremic syndrome. So you s you um see these and actually you count them um as you count the schistocytes in micro hemolytic process, they count as schistocytes. Ok. So these are schistocytes and these are broken cells that are eaten when they're circulated and circulate in the spleen because of um you know, um immune complexes because of an infection or TT P or Multi syndrome. So, um they call on fragmented cells or shes. Ok. So when you, when a patient with anemia comes to you, they usually come in with tiredness, the typical, you know, uh kind of decreased endurance, they feel short of breath with uh excessive activity. Some of them feel their heart beat like the, you know, their heart pacing. Ok. Um So uh these days, most of the patients are diagnosed with anemia before they become symptomatic. But believe it or not, some patients come in with very low hemoglobin and they have all these symptoms. So whenever you have a patient with a chief complaint, you need to know the duration, you need to ask them about the severity um about previous uh anemia, dysnea and exertion. Um you think of iron deficiency. So you talk to ask about bleeding for, you know, blood transfusion, prior um iron supplements, prior iron infusion. If you thinking of B 12 deficiency, then you're asking about tingling and numbness. Ok. Imbalance. Ok. If you think of hemolysis, then you ask about dark urine, yellowish discoloration of the sclera or skin. Um, dietary history is very important whether you uh you evaluate a patient with iron deficiency or B 12 deficiency. Ok. Um If you have a uh you know a female in child bearing age, you need to ask about pregnancies, you need to ask about their menstrual loss. And again, this is, this can be tricky. So you have to ask them about how many pads they use, if they have to wake up at night to change their pads. If they ever get soaked, uh, with uh the men blood, you have to ask about, um, if they see blood clots, anything more than five millimeter is significant. Ok? You ask about pregnancy and lactation, you know, blood loss other than uh administered blood loss is very important as well. Ok. So past medical history is extremely important for whatever you complain the person is coming in with. I will talk about chronic diseases. I mentioned the blood transfusion in the past history of cholecystectomy. For a person who have, you know, chronic hemolysis, like sickler, uh sickle cell patients or thalassemic patient, they can have um, gallstones. Ok. Um If some patient, you don't ask them, they wouldn't tell you they had a gastric bypass or gastric sleeve surgery. So it's always important to ask, ok. Medication is very important to have somebody who is coming in with high mc macrocytic anemia. Then you need to ask them about hydroxy antiepileptics, antipsychotic. If somebody whom you're suspecting iron deficient, and then you ask about uh um uh NSAID. Ok. If you're suspecting drug induced hemolysis, then you ask about antibiotics. So, drug history is very important. Family history is also important in patients with the bleeding disorder, but some patients that come in with severe iron deficiency anemia, secondary to Von Willebrand disease. So if you don't ask them about family history, Von Willebrand disease is not gonna come to your mind. So it's really important to ask about family members who need blood transfusion, family members who need iron infusion. If a patient has family history of hemophilia, which just generally diagnosed with like, ok, other um other ways rather than anemia, they usually come with significant bleeding, deep tissue hematomas, um bleeding inside their joints. Ok. Review of system is important cause this patient can have um you know, all kind of symptoms that can have um issues with their uh hair, their nails, uh patients with apla anemia, I mean they can have uh or dyskeratosis con they can, they can have barely gray hair, uh they can have brittle nails and other things. Ok. Um Social history is important and uh when you suspect lead poisoning, alcohol ingestion can cause um chronic liver disease that can cause esophageal varices, gastric varices, person can have subtle or acute blood, upper G I blood loss or lower G I blood loss. So, social history is very important. All right. So, um ok, now we already uh review interviewed the patient, examine the patient and then we're coming to interpret in the blood counts or the blood test. So, um serum iron is something that I don't generally look at because reflects the amount of iron patient took in the past 24 hours. So it wouldn't tell you about their iron stock. So if they didn't eat any iron containing food in that day, their iron level will be low. So I need the iron level only if I'm calculating their transfer in saturation. OK. So the total iron binding capacity is something that tells you how eager the body is for iron. So if it's elevated, it tells you that the body is iron deficient. Uh the transfer in saturation, it tells you um how saturated that transfer and which is responsible for transporting iron. And I use this mostly for patients with iron overload rather than iron deficiency. I also use this for a patient with iron deficiency secondary uh with iron deficiency anemia uh associated with anemia of chronic disease because this patient can have kind of borderline ferritin level. The ferritin level is not low, but at the same time, the transference saturation is low and that tells you they cannot metabolize iron wall and you need to get an iron infusion spro ferritin is the most important test for iron deficiency anemia. Again, a level of 100 above 100 rule out iron deficiency anemia. Ok. So, hemoglobin electrophoresis is something that you should order when you suspect thalassemia or hemoglobinopathy such as sickle cell anemia, hemoglobin c, hemoglobin D and all kind of hemoglobinopathy that are inherited. And um usually you um you see uh you're on the hemoglobin in this particular machine and based on the current uh the hemoglobin kind of um um subs where um the hemoglobin C, for example, uh uh in, in panel one, this particular patient has uh some of hemoglobin, a little bit of hemoglobin F and he a little bit of hemoglobin C and S. So this is sickle cell disease, hemoglobin sc. So they have combined sc hemoglobinopathy but they have some persistent hemoglobin F and a little bit of hemoglobin. A panel two. You, you see they don't have any hemoglobin C. They don't have hemoglobin F and other, the hemoglobin, you know, kind of settled by the sur C cell. Um This is sickle cell anemia patient. This particular patient in panel three is a sickle cell trait. They have half of their hemoglobin is hemoglobin S and half is hemoglobin A and, and you know, this is how we interpret hemoglobin electrophoresis patients with thalassemia alpha thalassemia. They will have only uh slightly elevated hemoglobin A two. OK. And no mo Yeah. I mean, they don't have hemoglobin srf, they have almost normal hemoglobin A and slightly elevated hemoglobin. A two patients with um alpha thalassemia, their hemoglobin elect fours is normal. So you, you have to do genetic testing for that. All those patients. Ok. So comms test is a test that we use in hematology um to um diagnose autoimmune and autoimmune hemolytic anemia. So for autoimmune hemolytic anemia, we use the direct coms test for autoimmune hemolytic anemia. We use the indirect comms test for the um direct comms test. Actually, you take um you know, you know that the body has already formed antibodies against its own red blood cells. So these red blood cells are already coated with antibodies. So all you need to do is you take these cells, you wash them and you add a sary agent. When you add comms agent, these cells were agglutinate and the CMBS red is like a complement. So when the complement uh uh you know, is attached to the antibodies and cells will aggregate and will lise and you know, if you have a positive cros test that tells you that patients have autoimmune positive direct crom test tells you that patients have autoimmune hemolytic anemia in autoimmune hemolytic anemia. Um the recipient or person has antibodies against foreign red blood cells. So what you need to do is you take the patient's serum that's already autoimmune has antibodies, you mix it with donor red blood cells and you add a comb to agent. So if the serum has antibodies against these particular red blood cells, agglutination will happen. And we, the administration with autoimmune, um you know, hemolytic anemia. Ok. So these are some of the cases. I think we have um you know, 25 minutes, I'll take my time. I'm going through these cases and we can um you know, um take some um questions later. So if a lady who's 16 year old, who just, you know, you know, that these ladies have started their period maybe a year or two or three ago and she comes to you with a normal um you know, easy fatigue ability, Dyne and exertion. Her hair is swallowing, her head is, you know, are breaking, she's craving ice, she's craving starch and you um you do a CBC and you find that her white cell count is totally normal. Her platelets are elevated. Her hemoglobin is serious low 6.3 and her mean corpuscle volume is low at 58 MC at 17.4 and RDW is 17.2% and RDW kinda reflects your an iso so the different shapes and sizes of um uh red cell width distribution is always elevated when uh you have, you know, variable uh kind of shapes and sizes of cell. The mean corpuscle volume uh reflects the means the average size of red blood cell. And the corus or hemoglobin is the main hemoglobin that um these cells contain. So by looking at this, I mean, this person obviously does not have a, you know, acute leukemia because her white cell count is fine. Uh She doesn't have something that has infiltrated the bone marrow because once something is infiltrating the bone marrow, whether it's lymphoma or myeloma or uh you know, leishmaniasis or mm you know, atypical macro bacterial infection, mycobacterial infection, it's not gonna only affect the red blood cell. It's gonna affect your platelets as well as white blood cells. So she has an isolated anemia. She has a reactive thrombocytosis. She has small cells and she has um pale cells that have different shapes and sizes. So um I don't know if anybody wants to, I know bitch him or participate. Ok. So let's move to the second slide. So after you see her CBC, you request her iron studies. So her serum iron is 4.7. But again, even if it's normal, it doesn't reflect except for the amount of iron she took in the past 24 hours, you look at her total iron binding capacity. And again, this is how hungry the body is to get to receive. Iron is elevated. Her trans saturation is low and her serum ferritin is extremely low. And I think this is a clear um you know, iron deficiency anemia most likely secondary to menstrual blood loss because she just achieved menarche. And uh you know, by the time you did your history. You found out already she has having significant menstrual bleeding uh when you see such patient, although she, you know she's young, but it's very important that you ask about family history of bleeding, iron deficiency anemia, postpartum hemorrhage because this particular girl could have von Willebrand disease manifesting as severe iron deficiency anemia. But if there is no family history, ok, we know that she has menorrhagia or micro menorrhagia because she just achieved um men then um straightforward iron deficiency anemia diagnosis 7 30 to uh um menorrhagia. So if a patient comes like this, I would definitely give them iron infusion and um later start them on iron s oral iron supplements. You know, I would consider sending them to the gyn doctor so they can give them some um hormonal therapy. Sometimes I use antifibrinolytic drugs such as tranexamic acid or a MOOC carbolic acid to slow down their menstrual blood loss in the 1st 3 to 5 days of e each menstrual be period. Again, something to um consider is that when a patient comes to you with significant anemia, you need to kind of check their blood levels periodically and check their iron levels periodically. Not to just give them iron supplement or iron infusion, let them go because likely they're gonna become iron deficient in a couple of months. So regular follow up and monitoring is very important. Ok. So we have a lady who comes in with asymptomatic anemia. So she's seen her primary care physician for the first time they did the CBC and they found that her hemoglobin is 11.6. Her MCV is disproportional low at 60.3 and her MCH is um low as well. Her RDW is normal. So I want you to pay attention to all these numbers. Her rbcs count is elevated. Usually the red blood cell count and iron deficiency anemia is low. But if the hemoglobin is 11.6 and the R BC count is elevated and the MCV is disproportionally low compared to the hemoglobin. That tells me this particular lady does not have iron deficiency anemia because if she has iron deficiency anemia, first of all, her R BC count should be low, it should be normal at the minimum, but usually it's low. Her MCT with this hemoglobin level should be maybe 78 close to normal because this is not severe iron deficiency anemia and her MC should be normal as well. Usually patients with iron deficiency, they have high platelet count, but that doesn't ex you know, normal platelet count do not um does not exclude uh iron deficiency. So this particular lady has very small cells and they're all similar in size because her RDW is normal. Um They're all, you know, uh not only similar in size but similar in shape. So cells that are small, similar in size, similar in shape, they have disproportionate smaller compared to the hemoglobin level. Uh tells me that this lady uh something else. So when I did her iron studies her uh serum iron again, I don't pay attention to that. Her T BC is within normal. Her transfer saturation is OK. Her serum ferritin is fine. So iron deficiency anem is excluded, excluded here. All righty. Um So because I suspect that Thalassa ordered, uh let's say, or you ordered her hemoglobin 46 and she um ends up having elevated hemoglobin A two and borderline hemoglobin A and that confirms um beta thalassemia. Again, this is beta thalassemia trait because if you have beta thalassemia major, this person would have been transfusion dependent. Since childhood patients with thalassemia intermedia, they tend to have a lower hemoglobin level around 99.5. And usually when they get pregnant or if they're sick, their hemoglobin drops further and you need to transfuse them. So, thalassemia too, they're usually asymptomatic because this hemoglobin level um is chronic. They're used to it. They were born with borderline hemoglobin. So they're usually asymptomatic and there's nothing except for genetic counseling that you need to do about those patients. Ok. So if a nine month old, um child comes to you with jaundice and anemia and you look at their parameters. They have, they're significantly anemic but they have normal M CV, normal M CS, normal RDW, the rest of the blood counts are fine. So the white blood cell is normal for this uh age group. The platelets are fine, but they're significantly anemic. So nine month old without uh you know, and they're, they're jaundice. So that, that tells you they have hemolysis. Um Again, the M CV is normal or so, I'm sorry, the M CV um slightly elevated for this child. So that tells you they have um some reticulocytes, reticulocytosis going on and with the jaundice, um you remember when we talked about normochromic normocytic anemia, you have to think of hemolysis, right? OK. So you do, they smear and you see these cells and they have some target cells, they have banana chip or blood chip cells. Ok. So, and then you do that hemoglobin and AIS the baby's hemoglobin A and you see hemoglobin S nine is 6.1% hemoglobin S is not normal. So you either have hemoglobin um uh uh uh sickle cell trait or sickle cell disease if, if you have some hemoglobin S. So this particular baby has 96.1% of hemoglobin S and this is like panel number two. And so he has sickle cell disease or sickle cell anemia. All right. So case number four, a five year old uh child who comes to you, I mean that young child came at nine month, but this one was normal all along, but all of a sudden he comes in with severe anemia and dark colored urine. Again, um Jaundice sometimes um is a a presenting symptom but sometimes is a sign. So sometimes patients or their family members don't notice, especially if they have all righty dark skin or dust clearer because of uh whatever reason or are abnormal, they might not notice the jaundice. But if the patient is fair skin and they have significant jaundice that can be noticed by the patient as well as their family members. So when you do their CBC, they have um white cell count that's slightly elevated. And I have to tell you one thing sometimes if a patient um who hemolyzing have white blood cells, it because the machine is counting nucleated red blood cells or white blood cells. Remember the machine will count whatever that has nucleus as red blood cells because platelets don't have nuclei and red blood cells mature red blood cells don't have nuclei. So, uh patients with acute chemosis will have um high white cell count because of the machine counting the nucleated RC as white blood cells. So this particular child has high white blood cells, has um no uh very low hemoglobin and very low um hematocrit. And they, he has had um high MC B which again uh secondary to high reticulocyte count. So high reticulocyte, high L DH, low haptoglobin and high white blood cells because of high nucleated RB CS. Now, some of the labs will give you the number for nucleated R BC that so that can help you. Um Again, the RDW is fine and the MC is OK. So this particular person doesn't, you shouldn't be thinking of iron deficiency at this stage. This is um clearly a hemolytic anemia and one um in general, this patient, they will have some dark urine because of the uru Biogen. So they, if they look at their urine, it's usually dark, they have acute hemolysis. So I want to explore further. I mean, you obviously did your history and you did your physical examination and you realize this is a new onset, a rapid very severe hemolytic process. Um you ask about family history and uh you know, kind of what kind of food the patient ingests. And then if there is exposure to whatever plus in Sudan malaria, but again, the patient will not come in with only anemia, they will have other things, high fevers. So you wouldn't be on isolated diagnosis of severe hemolytic anemia. You would you have other things that um la you know, direct you towards the infectious route. Ok. So when you look at their um sle and you see these cells, you call them blister cells. Uh So some um some of the cell wall is kind of separated from the rest of the red blood cells. And when you check them for G six PD level, you find it low. And again, um CG six PD level patients with G six PD deficiency has to be checked in the steady state because the reticulocytes in acute hemolysis, they have high G six PD level. So you should check the G six PD level when they are in their steady state. And the treatment for G six PD deficiency is to avoid, you know, um all kind of beans. There, there is a list of medications among them, respiratory and others. So you have to kind of provide those patients with list of things to avoid during an acute hemolysis. You give them folic acid and you support them with blood products, blood transfusion. Ok. So I think this is the last case. Um it could be a middle age, mostly an elderly person or a middle age female who had bariatric surgery or you know, an elderly patients who is eating only bread and you know, tea and bread or somebody who's a vegetarian and they come in with um white blood cell, the 4.8 but sometimes they come in with actually pancytopenia with low platelets and low uh white blood cells as well. Uh This particular patient has a low hemoglobin and and very elevated M CV. So when you look at their smear, you see this um these cells that are big. I mean, if you compare the nucleus of the red blood cell compared to the diameter of red blood cell is clearly different, you see uh the hyper nucleated um or hyper semente neutrophil. Again, the definition is five, more than five lobes or if you see more than five neutrophils that have five lobes, then this is an indication for megaloblast anemia, secondary to B 12 deficiency. So, generally, uh, for B 12 deficiency, um, patients who are diagnosed with this, uh, disorder, they end up being on B 12 replacement, lifelong cause whatever reason it's likely not gonna change. I mean, if they have bariatric surgery, they're not gonna have their stomach back. If they have, if they're vegetarian, they're not gonna, um, change their dietary habits. And if they um have pernicious anemia again, that's not gonna change. So, whenever I start the person on B 12 replacement, they're gonna end up staying on it again. B 12 is not important only for red blood cells but uh for hemoglobin. But it's also important for memory and nerves. And I think I'm done if anybody has any questions. Thank you very much doctor. Um I'm not sure if people want to, you can either write questions in the chat and I'll read them out on your behalf or you can raise your hand and un mute, unmute yourself. Um So please don't hesitate to ask questions. Now, someone has asked uh why do iron deficiency, why, why do iron deficient patients um have thrombocytosis? Oh. This is uh a good question. Actually, it's not known it's unknown. Um I haven't found an explanation for that. Um And again, not everybody with iron deficiency will have thrombocytosis. But um at least one third of patients do um you know, remember platelets are kind of uh a acute phase react. And so patients who undergo um significant surgery, they come in with thrombocytosis. Patients who have um acute blood loss while the, you know, B is trying to make red blood. So it releases a lot of platelets sometimes. So, platelets are reactive. A lot of patients who come into the hospital, um you know, say with burns, they have thrombocytosis. So it's, it's something like an acute phase reactant. Uh It's the way that the bone marrow tells you that I'm, you know, I'm comfortable and I'm affected by whatever is going on. Thank you, doctor. There's another question um asking if you can repeat how to diagnose anemia from the lab results. Ok. So um um from lab results, you look at the cell size, whether macrocytic or macrocytic and the amount of hemoglobin that each red blood cell has, whether hypo chromic or microcytic. So, if you have hypo chromic microcytic anemia, then you are thinking of iron deficiency anemia of chronic disease, sideroblastic anemia. Um um some, some cases of um you know, rare cases of lead um poisoning. Um you know, thalassemia, it's also hypochromia microcytic anemia. But again, with thalassemia, the difference is you have high R BC count and you have chronic hypochromia microcytic anemia. Again, you have disproportionally low M CV. So the PA the patient will have very low M CV with a hemoglobin of 11.8 or 11.6 So that tells you they have thalassemia, all that an iron deficiency. Well, if you're M CV and MC, it's still normal. But the patient is anemic, this is normal chromic, normal cytic anemia. And this can be secondary to many causes including combined B 12 and iron deficiency anemia of chronic disease. Some hemolytic anemias like anemia without compensatory reticulocytosis. They have normal chronic problems with anemia and, and anemia is secondary to bone or infiltration like, ok, whatever lymphoma or cancer or infectious process that are going on in the bone or the M CD and MC will be normal if you have macrocytic or big cells that um we call them macrocytic um anemia. Then you think of b 12 folate deficiency, you think of hemolysis, you have high reticulocyte count. You think of alcohol use. You think of thyroid disease, chronic liver disease, some drugs like uh we talked about hydroxy A ZT antiepileptics. Um Some of the anti um psychotic drugs can cause M CD. So it's based on the cell size and the hemoglobin concentration and you, you narrow your differential. Remember by the time you reach the lab, you have already, you know, or maybe, maybe not, but you have already talked to your patient. Figure out, figured out um um what type of anemia they might have? Thank you doctor. Um I think we're gonna have to end it here today. But if anyone has any further questions, could you share your email on the chat so they can send you questions. Sure I have it also on the last line. Um. Mhm or I can type it out if you tell me which email it is that ok? I'm there? Ok. Ok um I'm gonna put my personal email as well. That's great. Thank you so much. All righty you guys enjoy the rest of your day. Thank you very much. Have a great day. You too, welcome.