Transcription
This is a video as a continuation of our series on anemia. If you haven't watched the previous videos, please go ahead and watch them first. I will link them in the description.
So today we'll talk about the causes and mechanism of anemia. Remember symptoms of anemia: pale and tired, tired and pale.
So regarding causes of anemia, except for acute blood loss or sequestration, the most common cause of anemia is either a hypoproliferative cause or a survival defect. Again, so the main causes are hypoproliferative or survival problems. Okay, that is if we have ruled out the acute blood loss and sequestration.
So let's get more specific. Remember what we have just said: except for blood loss and sequestration, the main causes of anemia are hypoproliferative or survival. Okay. Hypoproliferative includes production defects and maturation defects. Production defects like what? Like a problem in the bone marrow, such as what? Let's say bone marrow damage will have production defect or decrease in EPO, like what? Kidney damage. So bone marrow damage, kidney damage. Also, we can have a hypometabolic state, such as hypothyroidism, can cause anemia. Okay, in this category, what do you predict the reticulocyte count will be? High or low? It will be low. The factory is broken, so both baby RBCs and RBCs are decreased.
Number two, maturation defects. They can be either cytoplasmic or nuclear. Cytoplasmic, like what? Like maybe a problem in hemoglobin synthesis, such as iron deficiency anemia. Okay, perfect. Or a problem in globin synthesis—you know hemoglobin has heme and globin—so globin alone, such as thalassemia. That's cytoplasmic. Nuclear: DNA synthesis problems, such as B12 deficiency, folate deficiency, myelodysplasia, and so forth.
Number three, survival defects. The RBC is produced normally, but it cannot survive, such as what? Maybe intrinsic defects or extrinsic, outside defects. Intrinsic means intrinsically in the RBC; could be in the membrane. Membrane defect, could be an enzyme, could be the hemoglobin itself. Okay, membranes, such as what? Such as spherocytosis, elliptocytosis. Okay, enzymes, such as what? G6PD deficiency. Hemoglobin problems, such as what? Such as sickle cell disease. Okay, that's it for intrinsic. Or extrinsic problems, such as what? Extrinsic problems will be something like antibodies against the red blood cell valve. When the RBC is coming through the valve and gets sheared and damaged by this valve, we call this microangiopathic hemolytic anemia. Also, may be damaged by a complement cascade attacking the RBC. That's it for survival defects.
Sequestration: the only place where sequestration takes place is the spleen. Okay, we got to have hypersplenism, increase of the spleen function. The spleen is brutal and cruel and damaging our red blood cells, such as in portal hypertension. Since the portal vein, okay, splenic vein goes into the portal vein, so portal hypertension will cause blood to back up and accumulate here, causing hypersplenism and splenic sequestration, as we have said before when we discussed portal hypertension and topics like portal vein thrombosis.
Number five is blood loss. Not just blood loss, it has to be acute. Okay, chronic blood loss will take a long time, but acute blood loss will cause anemia right away. So acute blood loss, like what? Like a car accident where you get injured and you have hemorrhagic shock. Also, stuff like peptic ulcer disease that's very common, okay, to cause acute blood loss. Okay, or sometimes can be chronic as well. The most common cause of anemia in the U.S. is iron deficiency anemia, probably due to acute blood loss. That's the most common cause of anemia in the U.S.
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