Anemia Presentation PDF

Hematopoietic Agents: Growth Factors, Minerals, and Vitamins  The finite life span of most mature blood cells requires their continues replacement, a process termed hematopoiesis. New cell production must respond to basal needs and states of increased demand. RBC : Anemia and hypoxe...

Hematopoietic Agents: Growth Factors, Minerals, and Vitamins  The finite life span of most mature blood cells requires their continues replacement, a process termed hematopoiesis. New cell production must respond to basal needs and states of increased demand. RBC : Anemia and hypoxemia WBC: Systemic infection Platelet: Thrombocytopenia  Hematopoiesis requires an adequate supply of hormones, cytokines. Minerals (e.g., iron, cobalt, and copper). Vitamins (e.g., folic acid, vitamin B12, pyridoxines, ascorbic acid, and riboflavin); Deficiencies generally result in characteristic anemias, or, less frequently, a general failure of Hematopoiesis.  VITAMIN B12 Vitamin B12 and folic acid are dietary essentials A deficiency of either vitamin results in defective synthesis of DNA in any cell in which chrosomal replication and division are taking place An early sign of deficiency is a megaloblastic anemia VITAMIN B12  VITAMIN B12 Cyanocobalamin Hydroxocobalamin Methylcobalamin 5-Deoxyadenosylcobalamin  ADME and Daily Requirements Gastric acid and pancreatic proteases. Gastric intrinsic factor-B12 complex. Receptor mediated active transport into circulation. Vitamin B12 deficiency in adults is rarely the result of a deficient diet per se. Antibodies to parietal cells or intrinsic factor. Pancreatic disorders, bacterial overgrowth, intestinal parasites, sprue, and localized damage to ileal mucosal cells.  Vitamin B12 Deficiency The plasma concentrations of vitamin B12 (~200-900 pg/ml). Hepatic disease or a myeloproliferative disorder (Tc I and Tc III). Congenital absence of Tc II. Impact on hematopoietic and nervous systems (pancytopenia). Diagnosis (serum vitamin B12 or serum methylmalonate levels). Schilling test.  VITAMIN B12 Metabolic functions The active coenzymes CH3 B12 and Deoxyadensoyl B12 are essential for cell growth and replacation. CH3 B12 is required for the formation of methionine and its derivative S-adenosylmethionine from homocysteine and consequently interferes with protein biosynthesis, a number of methylation reactions, and the synthesis of polyamines. Methyltetrahydrofolate trapped. 5-Deoxyadenosylcobalamin is requred for the isomerization of L-methylmalonyl CoA to succinyl CoA.  Relationships between vitamin B12 and folic acid Deoxyadenosyl B12 is a cofactor for the mitochondrial mutate enzyme (carbohydrate and lipid metabolism). methylcobalamin supports the methionine synthetase reaction, which is essential for normal metabolism of folate (conversion of homocysteine to methionine). This folate-cobalamin interaction is pivotal for normal synthesis of purines and pyrimidines, and therefore of DNA. The reaction is largely responsible for the control of the recycling of folate cofactors, and maintenance of a number of methylation reactions.  Relationships between vitamin B12 and folic acid Adequate supply of tetrahydrofolate (H4PteGlu1). Conversion of serine to glycine (CH2H4PteGlu). Conversion of dUMP to dTMP (DNA synthesis). Conversion of CH2H4PteGlu to H2PteGlu. Reduction of H2PteGlu by DHFR ( Methotrexate).  Relationships between vitamin B12 and folic acid In the presence of deficiency of either vitamin B12 or folate, the decreased synthesis of methionine and s- adenosylmethionine interferes with protein biosynthesis, a number of methylation reactions, and the synthesis of polyamines. The methyltetrahydrofolate then is trapped by lack of sufficient vitamin B12. (common basis for the development of megaloblastic anemia). Relationships between vitamin B12 and folic acid Neuropathy (damage to the myelin sheath). Methionine synthetase deficiency Nitrous oxide (N2O) megaloblastic changes and neuropathy. Prevention by methionine feeding.  Vitamin B12 Therapy Vitamin B12 is available for injection or oral administration. Oral administration can not be relied on the effective therapy in the patient with a marked deficiency of the vitamin. The treatment of choice for vitamin B12 deficiency is cyanocobalamine administered by IM or SC injection, never IV.  Vitamin B12 Therapy Vitamin B12 should be given prophylactically (dietary deficiency, the predictable malabsorption, and certain disease of small intestine) When GI function is normal, an oral prophylactic supplement of vitamins and minerals, including Vitamin B12 may be indicated. Otherwise, patient should receive monthly injection of cyanocobaslamin.  Vitamin B12 Therapy Therapy always should be as specific as possible. Severe anemic patients need blood transfusions and immediate therapy with folic acid and Vitamin B12 to guarantee rapid recovery.  FOLIC ACID Metabolic Functions Conversion of homocysteine to methionine (CH3H4PteGlu) Conversion of serine to glycine (H4PteGlu) Synthesis of thymidilate (5,10- CH2H4PteGlu) Histidine metabolism (H4PteGlu) Synthesis of purines Utilization or generation of formate  Therapeutic Use of Folate Oral tablets Aqueous solution for injection Combination with other vitamins and minerals Folinic acid (Leucovorin calcium,  Untoward Effects Folic acid in large amounts may counteract the anti-epileptic effect of phenobarbital, phenytoin, and primidone and increase the frequency of seizures in susceptible children.