anemia

Anemia (syn .: anemia) - a group of diverse pathological conditions, which are based on a decrease in hemoglobin and (or) of red blood cells. There are anemia due to blood loss (posthemorrhagic), increased destruction of red blood cells (hemolytic) and violation of their education.

Anemia due to blood loss (posthemorrhagic):

Acute hemorrhagic anemia is due to injuries associated with impaired blood vessel integrity, bleeding from internal organs (often with lesions of the gastrointestinal tract, uterus, lung), hemorrhage after acute complications of pregnancy and childbirth, disorders of hemostasis.

In acute blood loss (1000 ml or more) for a short time to perform first signs of collapse and shock. Clinically, this anemia is characterized by pallor of the skin and visible mucous membranes, weakness, dizziness, dry mouth, thirst, tinnitus, cold sticky sweat, rapid breathing (first deep, then the surface), a sharp decrease in blood pressure and body temperature, frequent pulse weak filling (filamentous), systolic murmur at all points of auscultation of the heart, agitation, successive fainting, sometimes vomiting, cyanosis, convulsions. The ECG can be detected segment depression ST, which sometimes leads to erroneous diagnosis of myocardial infarction. Is lost a significant amount of iron (500 mg or more). The hemogram is often marked by a small leukocytosis , leukocyte formula shift to the left to myelocytes, reticulocytosis.

Treatment consists of compensation of blood loss. Prehospital replenish blood volume (CBV) using an infusion of isotonic sodium chloride solution, glucose solution, polyglucin, hospital patient transfused blood products (blood loss of more than 1 liter), continue therapy such blood substitutes as polyglukin, albumin and saline solutions in volume depending on the magnitude of blood loss. With the development of iron deficiency in the following prescribed iron supplements.

Prognosis depends on the duration of the bleeding, the volume of blood lost; compensatory capacity of the organism and regenerative capacity of the bone marrow.

Chronic hemorrhagic anemia is a consequence of repeated minor hemorrhage of the gastrointestinal tract, uterus, hemorrhoids izyazvivshihsya et al. They lead to the depletion of iron stores and reducing regenerative ability of the bone marrow.

The clinical picture is consistent with iron deficiency anemia (see. Below).

The efforts of health workers should be aimed primarily at identifying and eliminating the causes of blood loss, as well as the replenishment of iron deficiency (iron supplements are recommended for 2 - 3 months or more under the control of erythrocyte hemoglobin and iron content in blood serum).

Anemia due to increased destruction of red blood cells (hemolytic) arise in cases where the destruction of red blood cells predominates over their recovery. Hemolysis in hemolytic anemia can be caused by a deficiency of red blood cells themselves, often congenital, and vneeritrotsitnymi factors (primarily the acquisition of the character). Common to all forms of hemolytic anemia symptoms can be caused by increased hemolysis (increased blood concentrations of the free fraction of bilirubin in severe hemolysis with development of jaundice, splenomegaly), increased release stercobilin with feces and urobilinovyh bodies in the urine, sometimes hemoglobinemia and hemoglobinuria with a corresponding change in urine color ) and enhanced red cell regeneration (increasing the number of reticulocytes, erythrocytes polihromaziya, bone marrow and erythroblastosis al.).

Hereditary haemolytic anemia associated with red blood cell changes include microspherocytic hemolytic anemia (a disease or Minkowski - Chauffard) nesferotsitarnye hemolytic anemia, such ovalotsitarnuyu hemolytic anemia, hemoglobinopathies, and others.

Microspherocytic hemolytic anemia - a chronic disease, an inherited dominant type, usually detected in late childhood or adolescence. The main clinical signs of it are the yellowness of the skin, sclera and mucous membranes, the intensity of which can vary; weakness, shortness of breath , sometimes (more often in women) acute hemolytic crises arising with pain in the right upper quadrant and biliary colic. In most patients, increased spleen; enlargement of the liver occurs in half of patients. Over the years, patients have characteristic facial skull deformity. The examination reveal mild anemia, hemolysis, symptoms and recovering red blood cells (reticulocytes content increased to 20% and more) as well as spherocytosis (reduced volume of erythrocytes having a spherical shape) and a decrease in their osmotic resistance. To find out the cause of jaundice allows comprehensive examination of the patient and identify signs of disease in relatives. The main treatment - splenectomy. In severe anemia during a severe hemolytic crisis shows the transfusion of red cells. The prognosis for timely favorable splenectomy.

Ovalotsitarnaya hemolytic anemia is also a hereditary disease characterized by the presence of an increased amount in the blood erythrocytes oval (ovalocytes). Clinical presentation and treatment are basically the same as when microspherocytic hemolytic anemia.

Haemoglobin in red blood cells due to the presence of abnormal (pathological and unusual) hemoglobin (qualitative hemoglobinopathies) or violation of the formation of normal hemoglobin chains (Quantitative hemoglobinopathies). Qualitative hemoglobin disorders include, for example, sickle cell anemia, quantitative - thalassemia. Some forms of hemoglobinopathies clinically manifest, others occur with severe hemolytic crisis (jaundice, fever , vomiting), requiring immediate hospitalization.

Acquired hemolytic anemia. These include paroxysmal nocturnal hemoglobinuria (or disease Marchiafava - Miksli), which is characterized by the appearance of red blood cells, with increased sensitivity to normal plasma complement; hemolytic anemia (autoimmune, and isoimmune geteroimmunnye) caused damage to the red blood cell antibodies; hemolytic anemia associated with mechanical red cell damage that occurs, for example, after the aortic or mitral valve; toxic anemia, which can develop in some infectious diseases, such as leishmaniasis, malaria. These are usually accompanied by anemia, jaundice staining of the skin and visible mucous membranes, so they should be differentiated from diseases of the liver (determined concentrations of hemoglobin and bilirubin fraction). Of the most important therapeutic measures is to eliminate the causes of anemia. In paroxysmal nocturnal hemoglobinuria prescribe transfusions of red cells; Treatment of hemolytic anemia, damage due to erythrocyte antibodies by using glucocorticoids, immunosuppressants, splenectomy performed.

In severe hemolytic anemia can be anemic (hemolytic) coma . The risk is particularly high for its development in autoimmune hemolytic anemia. Characteristic signs of anemic (hemolytic) are confusion, coma, tachycardia , intense jaundice , oliguria, collapse ; content of the erythrocytes significantly increased the number of indirect bilirubin in the serum in the blood is reduced. Such patients need to be hospitalized. The prognosis for a favorable treatment promptly initiated.

Anemia due to violations of the formation of red blood cells. There are scarce, hypoplastic (aplastic) and metaplastic anemia.

Deficiency anemia can be caused by the failure of such factors hematopoiesis, iron (iron deficiency anemia), vitamin B12 and folic acid (megaloblastic anemia).

Iron deficiency anemia, in addition to posthemorrhagic described above may be alimentary, t. E. Associated with eating disorders, and endogenous. In rare cases, nutritional anemia are polidefitsitnymi, t. E. Caused by deficiency of iron, protein, vitamin B12, and others. More often, iron deficiency anemia caused by iron deficiency endogenous. This is due to insufficient absorption of iron in the normal admission into the body that can be observed in the resection of the stomach, intestine, enteritis, taking drugs which depress the absorption of iron; due to the increased demand for iron body, such a transition in adolescents aged (particularly female), in pregnancy and lactation, resulting in increased iron loss (for example, then when operating in hot shops and in hot climates).

The patient marked weakness, fatigue, paleness of the skin and visible mucous membranes, ringing or noise in the ears, dizziness , shortness of breath , palpitations, with little physical activity, the so-called anemic murmurs are heard over the heart and jugular vein. Also characteristic nail changes (brittleness, striation, spoon-shaped form), hair loss; marked glossitis, perleche functional alterations of the cardiovascular system and gastrointestinal tract, taste perversion (eating paints, starch, clay, ice, chalk) and odor in some cases dysuria, particularly urinary incontinence . The blood was hypochromic anemia - decrease in hemoglobin and low color index (0.6 - 0.5 and below), and Anisocytosis poikilocytosis, reduction of iron and ferritin in blood serum.

Treatment is aimed at eliminating the causes of anemia and to eliminate iron deficiency (iron supplementation).

Prevention of iron deficiency anemia is conducted in individuals at risk (donor, giving blood for a long time, women with hypermenorrhea et al.). They prescribe iron supplements in small doses; recommended food rich in proteins, vitamins, iron and other micronutrients (meat, fruit).

When vitamin B12 deficiency, and (or) of folic acid appear B12-deficiency anemia and (or) folic acid deficiency anemia. The cause of B12 deficiency anemia is a lack of intrinsic factor Castle - gastromukoproteina produced by the gastric mucosa. Biermerin necessary for mastering the external factor Castle - vitamin B12 deficiency at which maturation of erythroblasts in the bone marrow is disrupted. At the same immature cells (megaloblasts) die, the blood comes defective red blood cells - megalocytes undergoing premature hemolysis. The causes of vitamin B12 deficiency may be atrophy of the gastric mucosa (the most common cause), gastric resection, inflammatory bowel disease, destruction of its specific areas, parasitic infestation, lack of vitamin B12 in food (found in meat, beans).

Classical B12-deficiency anemia (malignant or pernicious) occurs in people over the age of 40 years, evolving gradually. Clinically is characterized by lesions of hematopoietic tissue (patients concerned about shortness of breath , weakness, palpitations), digestive (lack of appetite, burning pains in the tongue, abdominal pain, constipation , diarrhea), and nervous system (paresthesia, irritability, depression, disorders of color). On examination revealed abnormal gait and skin sensitivity, functional (anemic), heart murmur, smoothed and redness of the tongue papillae ( "polish language"), loss of reflexes, staggering in Romberg, possible fever . The liver and spleen are enlarged. The disease occurs with exacerbations. Severe complication is anemic coma , which is manifested by loss of consciousness, fever, sometimes fever, frequent shallow breathing, tachycardia, decreased blood pressure, a sharp drop in hemoglobin. The skin is pale in patients with mild jaundice shade and moist. In addition, there may be clonic-tonic convulsions , meningeal symptoms, oliguria.

In blood observed hyperchromic anemia - a decrease in the number of red blood cells, hemoglobin saturated; red blood cells are larger (megalocytes) color index is typically 1.1 - 1.3; found fragments of erythrocyte nuclei (calf Jolly), giant gipersegmentirovannye neutrophils, marked leukopenia and thrombocytopenia. In the bone marrow revealed megaloblasts in large quantities.

Treatment - introduction of cyanocobalamin (vitamin B12) intramuscularly. With anemic coma patients urgently hospitalized. The prognosis for a favorable treatment promptly initiated. Patients B12-deficiency anemia are at the dispensary. To prevent recurrence prescribe injections of vitamin B12.

Folisvodefitsitnye anemia may result from inadequate intake of folic acid in the absence in the diet of gray products, while increased demand for it (in pregnant women), in patients with malabsorption of folic acid in patients with alcoholism, sprue, celiac disease, and OE), the appointment of some anti-epileptic drugs. Folievodefitsitnys anemia occur easier than B12-deficient; nervous system lesions does not happen. In the blood, signs of anemia hyperchromic (the presence of large red blood cells), revealed a giant stab leukocytes polisegmentatsiya their nuclei and thrombocytopenia; in the bone marrow - megaloblasts. If folic acid deficiency anemia appointed interior folic acid.

Hypoplastic (aplastic) anemia due to suppression of hematopoietic function of bone marrow and pancytopenia appear - insufficient formation of red blood cells, white blood cells and platelets. In most cases the cause of the disease is unknown. In some patients with aplastic anemia can result from the inhibitory effect on hemopoiesis several exogenous factors (e.g., anti ,. anticonvulsant drugs, antibiotics, insecticides, ionizing radiation) or effects of endogenous (e.g., immunological conflict dysfunction of the endocrine glands, prolonged infection ). Possible bone marrow hypoplasia in old age.

Typical clinical signs include pale skin, bleeding in the mucous membranes and skin, nasal, uterine, and other bleeding. Frequently observed infectious complications such as pneumonia , otitis media , pyelitis, inflammatory changes of oral mucosa, the rectum. The spleen and lymph nodes were not enlarged. In some patients revealed a slight increase in liver. In the blood, reduced the contents of all formed elements in marrow adipose tissue dominates myeloid.

Treatment - transfusion of red cells and platelets, corticosteroid anabolic hormones, immunosuppressants, splenectomy, the introduction of equine globulin antimonotsitarnogo, sometimes a bone marrow transplant. When bleeding shown hemostatic agents (platelet mass, aminocaproic acid, and others.). Prevention is to monitor the composition of the blood in the appointment of drugs (antibiotics, tranquilizers, anticonvulsants, etc.), Causing blood oppression.

Metaplastic anemia develop metastasis in malignant tumors of the bone marrow, as well as leukemias. Most often it is observed in breast, thyroid, prostate, lung, stomach, intestines. Distinctive features of these anemias are expressed eritronormoblastoz and leukemoid blood picture, in some cases, may develop pancytopenia.