The causes of thalassemia are directly linked to genetics and how the genes that affecthemoglobin production are inherited. People with moderate to severe forms received variantgenes from both parents. People who are carriers of the disease received variant genes fromone parent and normal genes from the other parent. Regardless of the causes of thalassemia, treatment options are available for all forms of the disease.
Mild jaundiceThalassemia major
Retarded physical and mental growth
Pronouncial hepatomegaly and splenomegaly
Thickening of the cranium and malillary cavity, caused by bone marrow hyperplasialeading to an appearance presembling doven syndrome
FOLIC ACID DEFICIENCY ANEMIA
VITAMIN B12 DEFICIENCY
Vitamin B12 is necessary for DNA synthesis and is almost exclusively found in foods derivedfrom animals. Vit.B12 deficiency occurs when inadequate VitB12 is consumed, or morecommonly, when it is poorly absorbed from the gastrointestinal tract. Deficiency of thisvitamin impairs cell division and maturation, especially in rapidly proliferating red bloodcells. As a result, microlytic, misshapen (oval rather than concave) RBCs with thinmembranes are produced. Great numbers of these large, immature RBCs enter thecirculation. These cells are fragile, incapable of carrying adequate amounts of oxygen andhave a shortened life span.
ETIOLOGY OF VITB12 DEICIENCY:
Resection of the stomach/ileum
Loss of pancreatic secretions
Chronic gastritis (affect vitB12 absorption)
Dietary deficiency of vitB12 (occurs among strict vegetarians)
Manifestations develop gradually as bodily stores of the vitamin are depleted
Pallor/slight jaundice and weakness develop
Paresthesias (altered sensations, such as numbness or tingling) inextremities
Problems with proprioception ( sense of one’s position in place)
Are a group of disorders caused by impaired DNA synthesis resulting in defective RBCs. Theseanemias share the morphology of megablast (then large, abnormal, and premature RBCs) inthe blood and bone marrow.