Causes and Classification of Anemia - Research Paper Example

APA Format Template: of Paper Goes Here Not Bold 12 pt. Font This research is devoted to the anemia disease. During the research the definition, causes and classification of anemia have been determined and analyzed. Firstly, the three main types of anemia: posthemorrhagic, hemolytic anemia and anemia associated with increased destruction of red blood cells were described. Secondly, the main subtypes of anemia have been described. Besides, it was found the main ways of anemia`s treatment. Special attention was given to the up to date scientific literature which describes the variety of types of anemia. As the result, there was generated and analyzed the current classification of the disease and possible mechanisms of treatment has been established. Also, the main methods of treatment which lies in blood oxygen balance restoration or transfusion were characterized. Another way of treatment is to provide the necessary amount of iron, which is necessary for the correct functioning of hemoglobin. Anemia Anemia is a pathological condition characterized by a decrease in the number of red blood cells and (or) hemoglobin per unit volume of blood (Halwachs-Baumann, 2012). Possible to speak about anemia as a condition that is characterized by a decrease in the formation of red blood cells or an increase in their degradation, or a combination of both factors. Red blood cells and hemoglobin, which is contained in them, play an important function of transporting oxygen to the tissues. Thus, reducing the number of red blood cells and hemoglobin causes insufficient provision of oxygen to tissues. According to the pathogenesis anemia is divided into 3 groups. 1) posthemorrhagic - as a result of blood loss; 2) hemolytic - due to enhanced destruction of red blood cells; 3) anemia associated with increased destruction of red blood cells. Posthemorrhagic anemia can be divided to acute and chronic forms. Acute posthemorrhagic anemia. Acute posthemorrhagic anemia is caused by rupture or erosion of the vessel wall through mechanical trauma, ulcerous disease of stomach, pulmonary tuberculosis and bronchiectasis. Color index = 0,85-1,1. Lack of qualitative and quantitative changes in erythrocytes is observed. Abrupt decrease in the number of circulating red blood cells causes hemic hypoxia to which kidneys respond by increased synthesis of erythropoietin. This peptide is a hormone of erythropoiesis and its role lies in stimulating the formation and maturation of erythroblasts in the bone marrow. Proliferation of erythroid sprout becomes noticeable at 4 and 6 days after hemorrhage. In the blood the number of reticulocytes and polychromatic red blood cells increases and also appears rare normocytes. These changes indicate a high regenerative ability of the bone marrow. It changes color to bright red and juicy color. Yellow fatty bone marrow turns to red one and becomes rich in erythropoietic cells. Also, the extramedullary hematopoiesis foci emerging in the spleen, lymph nodes, retrosternal glands, liver, kidneys, mucous and serous membranes. Under conditions of the rapid maturation red blood cells do not have time to accumulate a sufficient amount of hemoglobin. Color index gradually drops to 0.8 and lower, normochromic anemia turns into hypochromic one. Matters the fact that reserves of iron, which are required for hemoglobin synthesis, after blood loss are significantly reduced. At this stage erythrocytes with low hemoglobin levels appear. Such red blood cells under a microscope look like bagels with middle enlightenment and called the hypochromic erythrocytes. Chronic posthemorrhagic anemia occurs as a result of long-term repeated blood loss in patients with gastric ulcer and duodenal ulcer, gastric cancer, hemorrhoids, hemophilia and in women with uterine bleeding. Meanwhile, expressed regeneration occurs in the bone marrow. Due to the deficiency of iron depletion anemia gradually becomes hypochromic. In hypoxia develops fatty dystrophy of infarction, liver, kidney and also observed the dystrophic changes in the cells of the brain, multiple hemorrhages in the skin, stomach and serous membranes of internal organs. Treatment is mainly directed for liquidation of the source of bleeding and restoration of iron levels. Patients require a complete nutrition, iron supplements and vitamins. The clinical picture of acute posthemorrhagic anemia consists of acute circulatory failure syndromes (shock, collapse and swoon). Patients suffer from a "deadly pale" cold nose, dizziness, loss of consciousness, nausea, vomiting and seizures. Rapid pulse and lowered blood pressure is also symptoms of acute posthemorrhagic anemia. Diagnostics. After 1-2 days the lost blood is replaced by tissue fluids, volume of the vascular bed and come hemodilution (blood dilution) is restored. After 4-5 days bone marrow compensation phase is coming. During this phase number of reticulocytes and leukocytes with a shift to the left is increased. Treatment. Main role in the treatment of acute posthemorrhagic anemia takes the recovery of circulating blood volume by entering the blood and blood substitutes. To determine blood group and Rh-factor the transfusions of blood substitutes ­is conducted – firstly rapid jet intravenous injection, then switching to a drip in a total dose of 5-10 mg/kg body weight. When restoring circulating blood volume by blood substitutes it is necessary to keep the level of hematocrit not lower than 25% due to the risk of hemic hypoxia. For hemotransfusion it is used direct blood transfusion from a donor, diluted fresh blood, erythrocytes mass and washed red blood cells. Hemolytic anemia. Hemolytic anemia occurs when the process of destruction of red blood cells prevalence over their formation (Dhaliwal, Cornett, & Tierney, 2004). There are hereditary and acquired forms of hemolytic anemia. The hereditary hemolytic anemia. The hereditary anemia due to the nature of the genetic defect is divided into three groups: a) Membranopathies - associated with disruption of the structure of protein and lipid components of erythrocyte membranes;   b) Fermentopathies - associated with deficiency of erythrocyte enzymes that provide the pentose-phosphate cycle, glycolysis, synthesis of ATP and porphyrins, nucleotides and glutathione metabolism; c) Hemoglobinopathies - associated with disruption of the structure or synthesis of hemoglobin chains (Alaarg, Schiffelers, van Solinge, & van Wijk, 2013). Hereditary microspherocytosis belongs to hereditary membranopathies (Minkowski-Chauffard disease) with autosomal dominant inheritance. Membrane defect lies in the high permeability of erythrocyte membrane for sodium ions. Water directs in red blood cells, so they gain a spherical shape. The reason for high bandwidth of membranes for sodium is considered to be a violation of their protein and lipid structure. The destruction of red blood cells occurs primarily in macrophages of the spleen. Anemia may serve as an example of fermentopathies that occurs at glucose-6-phosphate dehydrogenase deficiency. The disease is inherited dominantly, linked with the X-chromosome. Permanent anemia is rare. Typically, the disease is manifested by hemolytic crises that occur after taking of some drugs - sulfanilamides, antimalarial and antituberculosis drugs. All these drugs can oxidize hemoglobin to exclude it from the respiratory function. Healthy individuals do not suffer from this disease due to the existence of the antioxidant system, an important component of which is reduced glutathione. At deficiency of glucose-6-phosphate dehydrogenase total amount of reduced glutathione is rapidly decreases. Sickle cell anemia is the most common for hemoglobinopathies. In patients with sickle cell anemia instead of synthesis of hemoglobin A occurs the synthesis of hemoglobin S. The main difference is that glutamic acid is replaced by valine in it in the sixth position of the b-chain. This change dramatically reduces the solubility of hemoglobin in hypoxic conditions. Reduced hemoglobin S is 100 times less soluble than oxidized and 50 times less soluble than hemoglobin A. In the acidic environment it precipitates as crystals and deforms red blood cells, giving them the crescent shape. Therefore, the membrane loses its strength and intravascular hemolysis begins. Symptomatic treatment is typical for hereditary hemolytic anemia. Acquired hemolytic anemia. Acquired hemolytic anemia is commonly divided into toxic, immune and mechanical forms. Toxic hemolytic anemia is caused by poisons. Nitrobenzenes, phenylhydrazine, phosphorus, salts of lead participate in lipids oxidizing or denaturation of proteins in red blood cells membranes and partially stroma that leads to their degradation. Poisons with biological origin (bee, snake, mushroom, strepto- and staphylolysin) have an enzymatic activity and cleave the lecithin of erythrocyte membranes. Some parasites that live in red blood cells cause their destruction. Immune hemolytic anemia - a group of diseases with a common pathogenesis: antibodies or immune cells are involved in the damage and hemolysis of red blood (Bass, Tuscano, & Tuscano, 2014). Hemolytic anemia associated with mechanical damage of red blood cells occurs after prosthesis of atrial septal, aortic and mitral valves. Rarely hemolytic crises occur in patients after long walk or running on hard surfaces (march hemoglobinuria). Red blood cells are destroyed in the capillaries of the feet. In the peripheral blood in hereditary hemolytic anemia cells of normal regeneration forms (large number of reticulocytes, polychromatophilic cells and normocytic red blood cells) and degenerative forms (anisocytes, poikilocytes and annulocyte) are located (Jung, 2013). With sufficient regenerative capacity of bone marrow common manifestation of their will be reticulocytosis. Anemias caused by deficient erythropoiesis. Anemias caused by deficient erythropoiesis are divided into deficient, hypoplastic and metaplastic. Iron deficiency anemia includes 80% of total anemias and is one of the most common diseases in the world (Kemmer, Novotny, & Ah Ping, 2008). This disease occurs as a result of iron imbalance, when its rate of replenishment from outside is lower than inside usage. In the etiology of the disease leading role is played by repeated bleeding, which devastates the reserves of iron stores and reduces its concentration in blood and bone marrow. Large and prolonged menstrual bleeding is often a cause of anemia in women (especially in the age over 40 years). Multiple pregnancy and lactation increase the need in iron and also lead to anemia. The monthly loss of 100-125 mg of iron after a half of year will lead to iron deficiency anemia. Iron deficiency anemia from time to time is found in the donors who give blood constantly. Treatment consists in the use of iron supplementation with rate of 5 mg/kg per day. Also it is necessary to have a valid nutrition - animal protein as meat products as they contain iron in the form of heme. In cases of a low level of hemoglobin - less than 50-40 g/l - blood transfusions is necessary (Buelvas, 2013). B12 and folate deficient anemias have many similarities in the etiology and pathogenesis, and therefore are considered together. Vitamin B12 deficiency is caused by three reasons - lack of intrinsic factor Castle, lesions of the small intestine and competitive absorption of vitamin by worms and intestinal flora. In all cases there is limit of its absorption into the bloodstream. Blockade of B12-dependent reactions that occur as a result of lack of vitamin has a great influence on the activity of the bone marrow, digestive tract and nervous system. In bone marrow erythropoiesis is distorted because erythroblastic type of hematopoiesis is replaced by megaloblastic one. Decelerations in maturation of red blood cells are also observed by the death of young forms in bone marrow and ejection of degenerative form into the bloodstream. Decreasing in production of white blood cells and platelets occur in the bone marrow. These pathological phenomena are explained by thymidine deficiency that causes the delay of DNA synthesis and bone marrow cells division. Lesions of the digestive canal are manifested by atrophic and inflammatory changes in the oral mucosa, stomach and intestines - stomatitis, gastritis, enteritis and colitis. This prevents the absorption of vitamin B12 and enhances its deficit consequences. The reason of atrophy is inhibition of proliferation of the digestive canal epithelium due to thymidine deficiency. Hypo- and aplastic anemia is caused by a direct lesion of the bone marrow by ionizing radiation, chemical toxins (benzene compounds of heavy metals), medicines (cytostatics, antibiotics, sulfanilamide drugs) and chronic infections (tuberculosis, syphilis, brucellosis). Some hypoplastic anemias have hereditary origin and represent the fermentopathies (Dolberg & Levy, 2014). Hypoplastic anemia usually combines with leuco- and thrombocytopenia. Metaplastic anemia belongs to anemias that arise in a result of the replacement of the red bone marrow by tumor cells (cancer, leukemia) (Marsh et al., 2009). Treatment. Treatment of B12-deficiency anemias begins with the elimination of it reasons. Carry out deworming, treat diarrheal diseases and prescribe a balanced diet. Pathogenetic therapy consists in appointment of vitamin B12 (parenteral). If the causes of B12 deficiency anemia are eliminated, there is no need for long-term therapy. In other cases it is recommended conducting a maintenance therapy (prophylactic courses 1 time per year). Treatment of folic deficiency anemia lies in the elimination of causes of folic acid deficiency. Assign also folic acid inside, even in case of the violation of its intestinal absorption. The daily dose is 10-30 mg – the course of treatment lasts 20-30 days. Treatment of iron deficiency anemia lies in the elimination of the root cause of the disease. One of the effective treatment and preventive measure is a long exposure on fresh air. It is necessary to remove the existing defects of feeding and appoint a balanced diet. Important links of complex therapy is the right organization in regime of the day and diet. Pathogenetic therapy of iron deficiency anemia involves appointment of iron preparations. In most cases, treatment is carried out by drugs for internal application. Cited works Alaarg, A., Schiffelers, R. M., van Solinge, W. W., & van Wijk, R. (2013). Red blood cell vesiculation in hereditary hemolytic anemia. Frontiers in Physiology, 4(December), 365. doi:10.3389/fphys.2013.00365 Bass, G. F., Tuscano, E. T., & Tuscano, J. M. (2014). Diagnosis and classification of autoimmune hemolytic anemia. Autoimmunity Reviews, 13(4-5), 560–4. doi:10.1016/j.autrev.2013.11.010 Buelvas, A. C. (2013). Anemia and transfusion of red blood cells. Colombia Médica, 44, 236–242. Dhaliwal, G., Cornett, P. a, & Tierney, L. M. (2004). Hemolytic anemia. American Family Physician, 69(11), 2599–606. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/15202694 Dolberg, O. J., & Levy, Y. (2014). Idiopathic aplastic anemia: diagnosis and classification. Autoimmunity Reviews, 13(4-5), 569–73. doi:10.1016/j.autrev.2014.01.014 Halwachs-Baumann, G. (2012). Diagnosis of anaemia: old things rearranged. Wiener Medizinische Wochenschrift (1946), 162(21-22), 478–88. doi:10.1007/s10354-012-0149-1 Jung, H. L. (2013). A new paradigm in the diagnosis of hereditary hemolytic anemia. Blood Research, 48(4), 237–239. doi:10.5045/br.2013.48.4.237 Kemmer, T. M., Novotny, R., & Ah Ping, I. (2008). Iron deficiency and anemia: disparity exists between children in American Samoa and children living within the US. European Journal of Clinical Nutrition, 62(6), 754–60. doi:10.1038/sj.ejcn.1602786 Marsh, J. C. W., Ball, S. E., Cavenagh, J., Darbyshire, P., Dokal, I., Gordon-Smith, E. C., … Yin, J. a L. (2009). Guidelines for the diagnosis and management of aplastic anaemia. British Journal of Haematology, 147(1), 43–70. doi:10.1111/j.1365-2141.2009.07842.x Read More