It is the process that produces red blood cells (erythrocytes), which is the development of the erythropoietic stem cell for the mature red cell.
It is stimulated by the decrease in O 2 in the circulation, which is detected by the kidneys, which secrete the hormone erythropoietin.
2. What is the role of iron in erythropoiesis? How is iron stored in the body?
The peptide hormone hepcidin may play a role in regulating hemoglobin production and, therefore, affect erythropoiesis. The liver produces hepcidin. Hepcidin controls the absorption of iron in the gastrointestinal tract and the release of iron from reticuloendothelial tissue. Iron must be released from macrophages in the bone marrow to be incorporated into the heme group of hemoglobin in erythrocytes. There are colony-forming units that cells follow during their formation. These cells are referred to as compromised cells, including colony-forming units of granulocyte monocytes.
Hepcidin secretion is inhibited by another hormone, erythroferrone, produced by erythroblasts in response to erythropoietin and identified in 2014. It appears that this links the erythropoiesis caused by erythropoietin with the mobilization of iron required for hemoglobin synthesis.
3. What is the role of transferrin?
The main role of transferrin is to supply iron from the absorption centers in the macrophages of the duodenum and white blood cells to all tissues. Transferrin plays a key role in areas where erythropoiesis and active cell division occur. The receptor helps to maintain iron homeostasis in cells by controlling iron concentrations.
4. What is the role of folate in erythropoiesis?
Production of thymine, to direct the bone marrow, for DNA synthesis.
5. What is the role of vitamin B12 in erythropoiesis?
Folates like vitamin B12 are indispensable for the synthesis of thymidine, one of the nucleotides that make up DNA, and the lack of one of them results in less DNA synthesis. Vitamin B12 participates indirectly in this reaction, acting as a coenzyme for the conversion of homocysteine to methionine, simultaneously transforming 5-methyltetrahydrofolate into tetrahydrofolate, the active form of folate that participates in the synthesis of thymidine. In the absence of vitamin B12, folate is transformed into 5-methyltetrahydrofolate, a form of transport of folate, useless for the synthesis of thymidine and DNA.
6. Characterize iron deficiency anemia.
The scheme would be iron absorption, Iron II → Iron III → Diphrene transferrin → Erythroblast in the marrow → Erythrocyte.
The patient shows pallor, tiredness, drowsiness and dizziness. In the most severe cases, there is shortness of breath, heart failure and palpitations. "The person does not eat properly and can develop bizarre habits, such as eating dirt or sucking on ice"
Effect in reducing anemia.
Reduced renal O2 stress → Increased erythropoietin production → Increased stimulus to differentiate early erythroid precursors → Increased number of polychromatic reticulocytes ("stress") released in peripheral blood → Increased erythrocyte mass
