Blood disorders such as Anemia are cases nurses encounter many times with patients. Anemia is an abnormality in the presence of red blood cells or hemoglobin in blood. Gender, age and ethnicity influence how anemic disorders affect the patients. There are different forms of anemia including sideroblastic anemia, folate deficiency, pernicious post- hemorrhagic and chronic inflammation anemia ( Schmitz-Abe et al., 2015) .
Iron deficiency anemia is a form of anemia and is as a result of decreased absorption, increased demand or increased loss of iron. The deficiency and sideroblastic anemia have similarities in their causes such as dizziness and feeling weak ( Auerbach et al., 2016) . The causes can be divided based on factors such as age, gender and ethnicity. Iron is important for production of hemoglobin and iron deficiency may be as a result of bleeding in the occult gastro intestines. This deficiency leads to microcytic hypochromic anemia on the peripheral blood smear (Schmitz-Abe et al., 2015) . Usually, iron is distributed in storage pools which are very active. Iron absorption is determined by the type of iron molecule and other substances that are taken in. The absorption is best when the food taken has meat. When iron is depleted, there is increase in absorption as a result of suppression of hepcidin. Iron from intestinal cells is transferred to transferrin then to other receptors. Transferrin synthesis increases with iron deficiency and decreases with chronic diseases (Schmitz-Abe et al., 2015) . Iron is stored in form of perritin and hemosiderin. Ferritin is the most important form as it is readily available in the body. Iron deficiency occurs in stages. First, the need for iron in the body exceeds the rate of iron intake leading to decrease in iron stores in the bone marrow. As this happens more iron is taken in as compensation. In the last stage, iron synthesis is disabled eventually leading to anemia. Causes of iron deficiency anemia based on age include exclusive breastfeeding for infants after 6 months (infants aged six to twelve months are at high risk of getting iron deficiency disorder), malnutrition and excessive intake of cow’s milk for children (Schmitz-Abe et al., 2015) . Cow milk disrupts iron absorption.
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Menstruation in adolescents is also a cause. In adults, iron deficiency anemia can be caused by pregnancy in the females and ulcers in the males ( Gupta et al., 2016) . Hookworms are also a major cause for adults mostly aged 50 years and above. Iron loss can be caused by bleeding and even frequent blood donation. Decreased intake can be caused by vegan diets, cereal based diets and undernutrition.Decreased iron absorption is caused by inflammatory bowel disease and bariatric surgery. Increased demand for iron is caused by pregnancy, lactation, EPO therapy. Iron deficiency anemia can affect mental development in adolescents and children and may even affect visual functioning. It could also lead to behavioral problems and poor school performance. The prevalence of iron deficiency anemia is higher in women who are in their reproductive age regardless of their race. It is higher in black women and very low in men
Sideroblastic anemia, unlike iron deficiency, is caused by too much iron. The condition is characterized by breathing difficulties, fatigue as well as feeling weak. People with this disorder often feel angina-like chest pains. While most forms of anemia are caused by iron deficiencies, people suffering from sideroblastic anemia usually have abnormally high iron levels in their blood. Some patients inherit the disorder while others acquire it meaning it can either be congenital or acquired ( Tesarova et al., 2019) . Congenital sideroblastic anemia is categorized into X- linked, autosomal recessive, and the mitochondrial DNA defect and wolfram. This hereditary type of anemia usually shows dimorphic red cells which are divided into normocytic normochromic and microcytic hypochromic unlike the acquired sideroblastic anemia which exhibits normocytic or macrocytic red cells. Congenital sideroblastic anemia is identified when there is change in genes that are related to intra mitochondrial heme-iron metabolism which includes the iron sulphur cluster biosynthesis, mitochondrial protein synthesis and heme biosynthesis. Heme biosynthesis defect involves the aminolevulinate synthase. The activity of aminolevulinate synthase is decreased in the bone marrow of patients with congenital sideroblastic anemia meaning that if the heme biosynthesis is impaired it leads to sideroblastic anemia. X- Linked sideroblastic anemia with ataxia is inherited the same way X- linked sideroblastic anemia is (Schmitz-Abe et al., 2015) . Patients with the defect have mild anemia. The defect is due to changes in adenosine triphosphate binding cassette gene. Acquired sideroblastic anemia is viewed as either primary or secondary.
The primary type is what is called myelodysplasia while the secondary is as a result of alcohol, drugs and lead poisoning ( Fernández-Murray et al., 2016) . Severe sideroblastic anemia can be recognized in an infant while mild anemia may be recognized later on. X- Linked sideroblastic anemia in elderly women is as a result of skewing with age. School age children have the lowest prevalence of anemia while people aged between eighty to eighty five years have the highest prevalence. Blacks are most affected by the disorder regardless of gender. It is more common in males than females. Acquired sideroblastic anemia is mostly seen in older patients of both genders usually 65 years and above but cases have been reported for people in their mid-50s ( Gupta et al., 2016) .
In conclusion, while iron deficiency anemia and other common forms of anemia are caused by not having enough iron, sideroblastic is caused by having too much too much and can be hereditary unlike iron deficiency. Patients with both disorders show signs of fatigue and weakness but iron deficiency anemia has more effects especially on children and adolescents.
References
Auerbach, M., & Adamson, J. W. (2016). How we diagnose and treat iron deficiency anemia. American journal of hematology , 91 (1), 31-38.
Camaschella, C. (2015). Iron-deficiency anemia. New England journal of medicine , 372 (19), 1832-1843.
Fernández-Murray, J. P., Prykhozhij, S. V., Dufay, J. N., Steele, S. L., Gaston, D., Nasrallah, G. K., ... & McMaster, C. R. (2016). Glycine and folate ameliorate models of congenital sideroblastic anemia. PLoS genetics , 12 (1), e1005783.
Gupta, P., Perrine, C., Mei, Z., & Scanlon, K. (2016). Iron, anemia, and iron deficiency anemia among young children in the United States. Nutrients , 8 (6), 330.
Schmitz-Abe, K., Ciesielski, S. J., Schmidt, P. J., Campagna, D. R., Rahimov, F., Schilke, B. A., ... & Sendamarai, A. K. (2015). Congenital sideroblastic anemia due to mutations in the mitochondrial HSP70 homologue HSPA9. Blood , 126 (25), 2734-2738.
Tesarova, M., Vondrackova, A., Stufkova, H., Veprekova, L., Stranecky, V., Berankova, K., ... & Vodickova, E. (2019). Sideroblastic anemia associated with multisystem mitochondrial disorders. Pediatric blood & cancer , 66 (4), e27591.
