Normal red cell Size 7µм MCV 82-98fl MCH 27-32pg MCHC 31 0 -34 0 g/l
Anemia is a symptom of disease that requires investigation to determine the underlying aetiology . Anemia is strictly defined as a decrease in red blood cell (RBC) mass . I n practice, anemia is usually discovered and quantified by measurement of the RBC count, hemoglobin (Hb) concentration, and hematocrit (Hct)
Iron deficiency is defined as a decreased total iron body conten t
Iron deficiency anemia occurs when iron deficiency is sufficiently severe to diminish erythropoiesis and cause the development of anemia
Iron deficiency is the most prevalent single deficiency state on a worldwide basis
In healthy subjects, the body concentration of iron is regulated carefully by absorptive cells in the proximal small intestine
Persistent errors in iron balance lead to either iron deficiency anemia or hemosiderosis
Dietary iron enters the enterocyte after being reduced to the ferrous state by duodenal cytochrome b (Dcytb) and being transported by the divalent metal transporter (DMT1). Hephaestin facilitates iron export by ferroportin. Hepatocytes take up either free or transferrin-bound iron and release it back into the circulation via the action of ferroportin. Ferroportin also releases iron from macrophages. Ferroportin-mediated release of iron is inhibited by hepcidin.
E stablishing the diagnosis and reason for the iron deficiency
T he iron deficiency should be treated with oral iron therapy, and the underlying etiology should be corrected so the deficiency does not re o cur.
The most economical and effective medication in the treatment of iron deficiency anemia is the oral administration of ferrous iron salts ( ferrous sulfate )
Reserve parenteral iron for patients who are either unable to absorb oral iron or who have increasing anemia despite adequate doses of oral iron. It is expensive and has greater morbidity than oral preparations of iron.
Ferrous sulfate - Mainstay treatment for treating patients with iron deficiency anemia. They should be continued for about 2 mo after correction of the anemia and its etiological cause in order to replenish body stores of iron. Ferrous sulfate is the most common and cheapest form of iron utilized. Tablets contain 50-60 mg of iron salt. Other ferrous salts are used and may cause less intestinal discomfort because they contain a smaller dose of iron (25-50 mg).
Documented hypersensitivity; microcytic anemias without laboratory documentation of iron deficiency
Calcium supplementation decreases bioavailability of iron when metals are ingested simultaneously; absorption is enhanced by ascorbic acid; interferes with tetracycline absorption; food and antacids impair absorption
Iron deficiency anemia is an easily treated disorder with an excellent outcome; however, it may be caused by an underlying condition with a poor prognosis, such as neoplasia. Similarly, the prognosis may be altered by a comorbid condition such as coronary artery disease.
Failure to investigate the etiology of the iron deficiency anemia causing a delayed or missed diagnosis of neoplasm
Anaphylaxis pursuant to the use of parenteral iron therapy in patients who should be treated with oral iron
Megaloblastic anemias are a heterogeneous group of disorders that share common morphologic characteristics
The most common causes of megaloblastosis are cobalamin (vitamin B-12) and folate deficiencies (vitamin B9)
Folate deficiency is usually due to folate-poor diets but may also occur in patients with sprue, during pregnancy, and in patients on antifolate or other medications
The molecular basis for megaloblastosis is a failure in the synthesis and assembly of DNA
The assimilation of cobalamin. On entering the stomach, dietary cobalamin (Cbl) forms a complex with R binding protein. As this protein is digested in the small intestine, cobalamin is transferred to intrinsic factor (IF). This complex passes through the intestine until it reaches specific receptors on the mucosa of the distal ileum. The internalized Cbl is then transferred to transcobalamin II (TC II), which circulates in the plasma until it binds to receptors on cells throughout the body and is internalized.
Folate is essential for the de novo synthesis of purines, serving as an intermediate carrier of 1-carbon fragments used in the biosynthesis of these compounds. Its active form is tetrahydrofolate (THF)..
COBALAMIN DEFICIENCY I. Inadequate intake: vegetarians (rare) II. Malabsorption A. Defective release of cobalamin from food : ( Gastric achlorhydria ; Partial gastrectomy ; Drugs that block acid secretion ) B. Inadequate production of intrinsic factor (IF) : ( Pernicious anemia ; Total gastrectomy ; Congenital absence or functional abnormality of IF (rare) ) C. Disorders of terminal ileum : ( Tropical sprue ; Nontropical sprue ; Regional enteritis ; Intestinal resection ; Neoplasms and granulomatous disorders (rare) ; Selective cobalamin malabsorption ) D. Competition for cobalamin : ( Fish tapeworm (Diphyllobothrium latum) ; Bacteria: "blind loop" syndrome ; Drugs: p - aminosalicylic acid, colchicine, neomycin ) III. Other A. Nitrous oxide B. Transcobalamin II deficiency (rare)
Hematologycal symptoms: anemia; rare granulocyto or thrombocytopenia
Gastrointestinal symptoms: mucosal trophic changes; loss of appetite, weight loss, nausea, and constipation.
Neurological symptoms : paresthesias in the feet and fingers, poor gait, and memory loss. At later stages, patients can have severe disturbances in gait, loss of position sense, blindness due to optic atrophy, and psychiatric disturbances. In some patients, neurological impairment can occur without anemia. Therefore, neurological symptoms may range from mild to severe, and cobalamin deficiency should be considered even with minimal neurological symptoms and the absence of anemia.
This marrow section demonstrates so-called nuclear-cytoplasmic dissociation; The slow nuclear maturation is related to a decrease in DNA synthesis related to an insufficient supply of reduced folate to synthesize thymidylate. DNA synthesis inhibitors can produce this picture, as can folate and B12 deficiency.
Most patients with megaloblastosis are treated with cobalamin and folate therapy to treat deficiencies in these substances
Transfusion therapy should be restricted to patients with severe, uncompensated, and life-threatening anemia
Because megaloblastic anemias usually develop gradually, most patients have adjusted to low Hb levels and do not require transfusions.
Cobalamin (1000 mcg) should be given parenterally daily for 2 weeks, then weekly until the hematocrit value is normal, and then monthly for life. This dose is large, but it may be required in some patients
Folate should be administered orally (150-400 (400-800) g/d)
Patients who have undergone either total or partial gastrectomies should receive lifelong monthly doses of cobalamin (1000 mcg IM).
Prognosis is good if the etiology of megaloblastosis is identified and appropriate treatment is instituted. However, patients are at risk for complications of anemia, such as cardiac impairment and hypokalemia, during therapy for cobalamin deficiency.