Sickle Cell Anemia

             Imagine, that you have just had your newborn baby and as you take her to get her first check up, you find out she has sickle cell anemia. The first thing that goes through your mind is what is it and how did she get it?
             Sickle cell anemia disease is a group of inherited red blood cell disorders. Normal red blood cells are round like doughnuts, and they move through small blood tubes in the body to deliver oxygen. Sickle red blood cells become hard, sticky and shaped like the sickles that are used to cut wheat. When these hard and pointed red cells go through the small blood tube, they clog the flow and break apart. This can cause pain, damage and a low blood count, or anemia. A normal hemoglobin cell There is a substance in the red cell called hemoglobin that carries oxygen inside the cell. One little change in this substance causes the hemoglobin to form long rods in the red cell when it gives away oxygen. These rigid rods change the red cell into a sickle shape instead of the round shape.
             You can inherit sickle cell only one way, and that is from a parent who is a carrier and passes that trait to you. You inherit this trait just as you would eye color, hair color, and other physical traits. You can't catch it. You have to be born with it. The types of hemoglobin a person makes can be dependent on what hemoglobin genes were passed down from parents. Like most genes, you can just be a carrier and have the trait. Sickle Cell trait (AS) is an inherited condition in which both hemoglobin A and S are produced in the red blood cells, always more A than S. Sickle cell trait is not a type of sickle cell disease. People with sickle cell trait are generally healthy. Now, I will give the chance that your baby will have sickle cell. If one parent has sickle cell and the other parent is normal, the children will just carry the trait. If one parent ha
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Sickle Cell Anemia. (1969, December 31). In MegaEssays.com. Retrieved 07:26, March 29, 2024, from https://www.megaessays.com/viewpaper/13199.html