Folic acid with vitamin

Anemias, reductions in the number of red blood cells or of hemoglobin in the blood, can reflect impaired synthesis of hemoglobin (eg, in iron deficiency Chapter 51) or impaired production of erythrocytes (eg, in folic acid or vitamin Bjj deficiency Chapter 45). Diagnosis of anemias begins with spectroscopic measurement of blood hemoglobin levels. 

Explain the optimal use of folic acid and vitamin B12 in patients with macrocytic anemia. 

A modification of the above serum folic assay method was recently described (W4). The investigators confirmed the validity of this technique as a practical means of differentiating patients with folic acid from vitamin B12 megaloblastic anemias. Another modification of this method was also described (C4). These investigators reduced the over-all sensitivity by high serum dilutions and thus made the assay, as they used it, valueless as a diagnostic tool. 

Folic acid the vitamin precursor to a family of coenzymes involved with the metabolism of one-carbon fragments. 

Formation of THF from dihydrofolate (DHF) is catalyzed by the enzyme dihydrofolate reductase. DHF is made from folic acid, a vitamin that cannot be synthesized in the body, but must be taken up from exogenous sources. Most bacteria do not have a requirement for folate, because they are capable of synthesizing folate, more precisely DHF, from precursors. Selective interference with bacterial biosynthesis of THF can be achieved with sulfonamides and trimethoprim. 

C. The only effective treatment of pernicious anemia is supplementation of vitamin B12.It is important to determine whether megaloblastic anemia is from a deficiency of folic acid or vitamin B12. Treatment of vitamin Bi2-deficient anemia with folic acid may result in neurological damage if vitamin Bi2 is not adequately supplemented. 

Deficiency of either folic acid or vitamin B12 results in a clinically similar megaloblastic anemia because of the neurological damage that accompanies the megaloblastic anemia of vitamin B12 deficiency, the condition is generally known as pernicious anemia. Suhoptimal folate status is also associated with increased incidence of neural tube defects (Section 10.9.4), hyperhomocys-teinemia leading to increased risk of cardiovascular disease (Section 10.3.4.2), and undermethylation of DNAleadingto increased cancerrisk (Section 10.9.5). 

Because flavin coenzymes are widely distributed in intermediary metabolism, the consequences of deficiency maybe widespread. Because riboflavin coenzymes are involved in the metabohsm of folic acid, pyridoxine, vitamin K, and niacin, deficiency will affect enzyme systems other than those requiring flavin coenzymes. With increasing riboflavin deficiency, tissue concentrations of FMN and FAD fall, as does flavokinase activity, thus further decreasing FMN concentrations. FMN concentrations are decreased proportionally more than FAD concentrations. Decreases in the activities of enzymes requiring FMN generally follow the fall in tissue concentrations, whereas the FAD-dependent enzymes are more variably affected. ... 

Because all vitamins are essential, it is difficult to state that one vitamin is more important than another. Nevertheless, folic acid, with its coenzyme role in purine biosynthesis, can be considered crucial for some of the cells most fundamental biochemistry, cell division. This vitamin is intimately tied to vitamin (cobalamin), which has made estimating its DRIs difficult. Also, conditions that can cause a folic acid deficiency also can result in a vitamin Bi2 deficiency. 

One of the most prevalent clinical problems observed in the elderly is anemia, although it is not an inevitable outcome of aging. The anemia is associated with an increased risk of mortality, poor health, and decreased physical functioning. Those with iron deficiency may have concurrent folic acid or vitamin B12 deficiency. 

MCV represents the average volume of RBCs. Cells are said to be macrocytic if they are larger than normal, microcytic if they are smaller than normal, and normocytic if their size falls within normal limits. Folic acid and vitamin B12 deficiency anemias yield macrocytic morphology, whereas iron deficiency and thalassemia are examples of microcytic anemias. A falsely elevated MCV occurs with reticulo-cytosis because reticulocytes are larger than erythrocytes. The MCV is also falsely elevated in the presence of cold agglutinins and hyperglycemia. When IDA (decreased MCV) is accompanied by folate deficiency (increased MCV), failure to understand that the MCV rep-... 

Patients with anemia of critical iUness need the necessary substrates of iron, folic acid, and vitamin B12 for RBC production in order for the physiologic response for anemia correction to occur. Iron stores are usually insufficient to meet physiologic demands, hence the administration of supplemental iron in the oral or parenteral form is necessary to support erythropoiesis. Parenteral iron is often utilized in this population, as often patients are on enteral therapy or there are concerns regarding inadequate iron absorption. The disadvantage of parenteral therapy is the theoretical risk of infection. The low iron concentrations in critically iU patients may be a defense mechanism, as microbes require iron for sustenance. Therefore diminished iron levels may inhibit bacterial growth. 

Myelosuppression increased in patients with elevated cystathioneine or homocysteine concentrations. Folic acid and vitamin B12 supplementation decrease myelosuppression by decreasing elevated cystathionine and homocysteine levels. 

Anemia has frequently, but not consistently, been reported in association with scurvy in clinical cases, both in adults and infants, and in experimental scurvy in guinea pigs and monkeys. The extensive literature has been cited (M18, L19, V2). The anemias were not constant in type or severity, although all were reheved when ascorbic acid was reintroduced to tbe diet. In contrast, no anemia or abnormality of the blood picture was ever seen in experimental human scurvy. The therapeutic effect of ascorbic acid on the anemia cannot be accepted as proof of its etiology, since associated deficiencies would also be made good with the return of normal appetite. It is well recognized that the clinical cases of scurvy usually have associated deficiencies. Often, there is iron deficiency in the milk-fed infants, and folic acid or vitamin B12 deficiency in the malnourished adult. ... 

Liver Extract. An extract made from the livers of mammals. Upon ingestion or injection in a suitable dosage form it increases the numbar of red blood corpuscles in the blood of persons afflicted with pernicious anemia. Contains folic acid and vitamin BL1 activity. 

Although a therapeutic trial with small amounts of vitamin Bj, can help confirm the diagnosis, acutely Ul, elderly patients may not be able to tolerate the delay in the correction of a severe anemia. Such patients require supplemental blood transfusions and immediate therapy with folic acid and vitamin B to guarantee rapid recovery. 

Mr. Veere s malnourished state was reflected in his admission laboratory profile. The results of hematologic studies were consistent with an iron deficiency anemia complicated by low levels of folic acid and vitamin Bi2, two vitamins that can affect the development of normal red blood cells. His low serum albumin level was caused by insufficient protein intake and a shortage of essential amino acids, which result in a reduced ability to synthesize body proteins. The psychiatrist requested a consultation with a hospital dietician to evaluate the extent of Mr. Veere s marasmus (malnutrition caused by a deficiency of both protein and total calories) as well as his vitamin and mineral deficiencies. 

Deficiencies of folic acid or vitamin Bp are the most common causes of megaloblastic anemia. If a patient with this type of anemia has a normal serum vitamin Bp concentration, folate deficiency is the most likely cause of the anemia. The answer is (C). 

The client is prescribed folic acid, a vitamin. Which information should the nurse discuss with the client ... 

The use of oral contraceptive agents (OCAs) is widespread and is being increasingly encouraged in developing countries. Their use has been associated with a number of side effects, in particular, a possible increased risk of thrombotic and embolic vascular disease. There is also evidence that OCAs may affect the metabolism of a number of vitamins. Evidence for deficiency of thiamine, riboflb vin, ascorbic acid, pyridoxine, folic acid, and vitamin B12, and for excess accumulation of vitamin A has been reported. This is of particular concern to populations in which vitamin nutrition may already be suboptimal and has been the subject of recent brief reviews (02, R4, Tl, W13). 

The compositions and properties of the Valery ampoules are described in armotations. We succeeded in combining a glycine amino acid, widely used vitamin and antioxidant (ascorbic acid) with a biostimulator, antidote and strong Cresazin antioxidant in Trecresan-C gel. Our Cresazin is superior as an antidote and antioxidant to the classical standards — succinic, ascorbic and folic acids, and vitamin E (a-tocopherol) (Tables 1,2). 

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