Anemia Based on Mean Corpuscular Volume (MCV)

Have you tried understanding Anemia, and it looks like a mission-impossible task? I get it, a lot of people are still unable to understand what Anemia is, and so many people mistake Anemia for Pneumonia. In this post, we will get to know what anemia is, the types of anemia, and lab findings. Let's begin without wasting any time at all.

Overview of Anemia

Anemia is decreased (not enough), or hypo-functioning red blood cells (hemoglobin). Red blood cells are produced in the bone marrow and are responsible for carrying oxygen from the lungs to the body. Anemia can be classified based on the Mean Corpuscular Volume (MCV), where if the MCV is below 80, it is regarded low MCV, and diseases such as Iron-Deficiency Anemia, Sideroblastic Anemia, and Thalassemia are examples of low MCV anemia. When the Mean Corpuscular Volume is within the range of 80 to 99 MCV, it is regarded as normal, and diseases such as Anemia of chronic disease, Paroxysmal Nocturnal Hemoglobinuria, G6PD deficiency, Hereditary, and Spherocytosis fall under the normal MCV anemia. In high Mean Corpuscular Volume diseases, the disease must be above 100 MCV, and diseases are majorly folate deficiency anemia and B12 deficiency anemia.

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Iron-Deficiency Anemia

Iron deficiency anemia is the most common cause of anemia in the world. (just to state, males with iron deficiency anemia are usually believed to suffer from colon cancer until a test is done to prove it wrong, and in women, it could be said to menstruation unless a test). When a patient is diagnosed with iron deficiency anemia, they have low ferritin (iron), and high transferrin (iron binding capacity), the patient will be hypochromic (hypochromia is the paleness of the red blood cell) and have a low or microcytic mean corpuscular volume. An example of a disease associated with iron-deficiency anemia is Plummer-Vinson syndrome (which is a triad disease also made up of esophageal webs and dysphagia).

Sideroblastic Anemia

Is the anemia that arises as a result of abnormal utilization of iron during erythropoiesis, leading to abnormality in heme production in the porphyrin pathway. It could be as a result of aminolevulinic acid (ALA) synthase deficiency, lead poisoning (which inhibits the ferrochelatase enzyme), and drugs that could indirectly inhibit ALA synthase (Isoniazid) which inhibits B6. it is important to know that where there is an ALA synthase deficiency, it is difficult to produce heme. This would leave Iron to be freely availblein the mitochondria without being attached to heme.

Thalassemia

It is an abnormality in hemoglobin production which has to do the deletion of the genes that codes for heme production. 4 alpha gene and 2 beta genes that codes for heme production, so when there id an Alpha-Thalassemia, then the one or more alpha genes were deleted, and in Beta-Thalassemia, it means that one or more beta genes that codes for heme production is deleted.

When patients have 1 alpha gene deleted with Alpha-thalassemia, patients will be asymptomatic, having 2 alpha genes deleted will mean that the patient will suffer mild anemia where it can be CIS or TRANS deletion(where CIS occur on same chromosomes while TRANS occur on different chromosome), 3 alpha gene deletion will be severe anemia, while 4 alpha gene deletion in a patient will be regarded as hydrops fetalis. When there is a 1 gene deletion in the Beta gene, it is regarded as Beta Thalassemia Minor which is Asymptomatic while deletion of the 2 beta gene would lead to the production of Hemoglobin A2 (Beta Thalassemia Major).

Anemia of Chronic Disease

This is the body not being able to differentiate between a chronic inflammation and an infectious disease causing inflammation, thereby causing the body to activate Hepcidin which caused the gut to decrease iron absorption, increase iron storage as ferritin in the body (to prevent the infection from multiplying). Diseases such as Kidney disease, Rhematologic disease and autoimmune diseases could lead to Anemia of Chronic Disease.

Paroxysmal Nocturnal Hemoglobinuria

This is an anemia caused by a defect in phosphatidylinositol glycan class A (PIGA) gene which is made up of CD55 and CD59, thereby leading to the inability to produce CD55 and CD59. The red blood has both CD55 and CD59, encoded by the PIGA gene which inhibits C3 convertase, but with a defect in the PIGA gene both CD55 and CD59 will be absent in the blood causing C3 convertase to lyse the blood.

Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency

This occurs as result of oxidative stress on the red blood cells. Normally, NADP becomes NADPH when acted upon by G6PD, which inturn turns Glutathione to Reduced Glutathoine which then destroys free radicals which causes oxidative damage, but when there is a G6PD deficiency, The process of converting NADP to NADPH would not be possible, and NADPH will not be able to convert Glutathione to reduced Glutathione which means free radicals will be able to cause oxidative stress to the red blood cell. Patients who take Dapsone, Sulfa, Primaquine, L-Dopa, Fava- bean, free radicals are going to be activated, and when the patient doesn't have G6PD to clean the free radicals, the patient becomes Anemic. Their hemoglobin of the patient becomes denatured as a result of oxidative stress in form of Heinz bodies, which would be consumed by macrophages. Cells not completely engulfed are known as Bite cells.

Hereditary Spherocytosis

It is the most prevalent cause of hemolytic anemia, as a result of protein dysfunctions in Red blood cell skeleton. Proteins such as spectrin, Ankyrin, and Bands. When the proteins that are to make the red blood cell concave are absent, the Red Blood Cells become Spherical in shape which causes it to be difficult to pass through the spleen, leading to splenomegaly, after which the red blood cell start getting destroyed (hemolysis) causing Jaundice, and Howell-Jolly Bodies

B12 Deficiency

The gastro parental cells at the top of the stomach produces intrinsic factor which binds with B12 to form the B12-Intrinsic factor Complex which passes through the intestinal tract reaching the ileum where the B12 is being absorbed. When there is Pernicious Anemia, there is an autoimmune destruction of the Gastric parietal Cells, which leads to a decrease in the production of intrinsic factors which will lead to the inability to complex IF with B12 leading to the inability to absorb B12 in the ileum.

Conclusion

We have come to the end of this post today, and I didn't mention the diagnosis, and treatment of the types of Anemia because I wasn't looking into that today. the aim of the post is to help identify the types of anemia according to the Mean Corpuscular Volume (MCV) rate.

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