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Thalassemias are inherited blood disorders that result in abnormal hemoglobin. [7] Symptoms depend on the type of thalassemia and can vary from none to severe. [1] Often there is mild to severe anemia (low red blood cells or hemoglobin) as thalassemia can affect the production of red blood cells and also affect how long the red blood cells live. [1]
Sickle-cell versions of hemoglobin stick to themselves, stacking to form fibers that distort the shape of red blood cells carrying the protein. These sickle-shaped cells no longer flow smoothly through blood vessels, having a tendency to clog or degrade, causing the medical problems associated with this disease. [citation needed]
Sickle-cell disease was the genetic disorder to be linked to a mutation of a specific protein. Pauling introduced his fundamentally important concept of sickle cell anemia as a genetically transmitted molecular disease. [20] This vein (4) shows the interaction between the malaria sporozoites (6) with sickle cells (3) and regular cells (1).
Autosplenectomy caused by sickle cell anemia or hyposplenism in coeliac disease [3] In patients with obstructive liver disease, lecithin cholesterol acetyltransferase activity is depressed, which increases the cholesterol-to-phospholipid ratio and produces an absolute increase in the surface area of the red cell membrane.
Whereas normal adults have less than 1% of hemoglobin F, patients with only one disease gene have 5-30%. Patients with two disease copies can have hemoglobin F in up to 100% of red blood cells. [31] As other diseases such as sickle cell disease could also cause a higher level of hemoglobin F to be present, it can sometimes be misdiagnosed. [32]
Fifth disease, also known as erythema infectiosum and slapped cheek syndrome, [3] is a common and contagious disease caused by infection with parvovirus B19. [4] This virus was discovered in 1975 and can cause other diseases besides fifth disease. [5] Fifth disease typically presents as a rash and is most common in children.
[3] [4] In the most common variant of sickle-cell disease, the 20th nucleotide of the gene for the beta chain of hemoglobin is altered from the codon GAG to GTG. Thus, the 6th amino acid glutamic acid is substituted by valine—notated as an "E6V" mutation—and the protein is sufficiently altered to cause the sickle-cell disease. [5]
There is no red cell effect with Ho-2 compared to Hemoglobin S, which changes the shape of the cell to become sickled. The Hopkins-2 variant of hemoglobin is not involved in forming sickle cells. There is a lack of phenotypic expression of Ho-2 in terms of sickle cell, so a person with sickle cell and hemoglobin Hopkins-2 would be asymptomatic.