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ANEMIA DUE TO TOXIC EXPOSURE OF THE BONE MARROW (MYETHOXICAL ANEMIA)
Thyroid wave anemia
Thioprivial anemia - anemia that develops on the basis of hypothyroidism. Experimental work confirms the important role of thyroid hormone - thyroxin - in stimulating normal blood formation. Animals deprived of the thyroid gland, quickly anemiziruyutsya, the introduction of the same thyroid preparations thyroidectomized animals cures them from the effects of thyroid-void cachexia, in particular from anemia.
The clinical picture of anemia in myxedema (hypothyroidism) is heterogeneous. There are three types of anemia: 1) normochromic (macrocytic), 2) hypochromic, 3) hyperchromic (pernicious).
The pathogenesis of thyroid-free anemia is heterogeneous. Thyroxine deficiency is thought to lead to a disorder in the utilization of specific hematopoietic factors (iron, folic acid, vitamin B12.
Anemia in thyroiditis Hashimoto (struma lymphomatosa) is considered by modern authors in the aspect of autoimmune conflict. In this regard, the combination of hypothyroidism with pernicious (B12-deficient) anemia can be interpreted as a result of organ-specific immunization, as evidenced by specific immunological studies that detect the presence of antibodies directed against the thyroid cells (or thyroglobulin) and the parietal fundus glands (or internal factor a).
Treatment. Clinical experience shows that with anemia occurring on the background of hypothyroidism, the best effect is achieved through the use of combination therapy with iron and vitamin B12 in the usual dosage in combination with thyroidin (0.1—0.2 g 3 times a day).
ANEMIA IN RENAL FAILURE
From true anemia, which is a consequence of renal failure (with chronic nephritis, wrinkled kidney, etc.), one should distinguish between “false anemia”, which depends both on the degree of skin edema and poor blood filling of the skin vessels, and on hydremia, i.e. swelling of the blood itself.
In most cases, anemia is hypochromic normo-or microcytic in nature, characteristic of iron deficiency anemia. However, in some patients with chronic nephritis with symptoms of renal failure, hyperchromic macrocytic, pernicious-like anemia develops.
Anemia in renal insufficiency is accompanied by changes in white blood in the form of neutrophilic leukocytosis (with preservation of eosinophils), reaching with uremia (not even complicated by infection), especially high numbers (12000—20000 in 1 mm3).
The lifetime study of bone marrow hematopoiesis in the case of anemia of brayts (G. A. Alekseev) revealed a picture of a deep disorder of erythropoiesis in the form of a violation of hemoglobinization and delayed maturation of erythroblasts.
What is the pathogenesis of anemia of the bratiks? With the exception of relatively rare cases, when patients with nephritis have prolonged gross hematuria and anemia is mainly post-hemorrhagic, anemia of braic is the result of autointoxication of the body associated with renal failure.
It can be assumed that azotemic gastritis and enterocolitis, which is observed during azotemia, is a known role in the development of anemia of brightkeys. A change in the function of the stomach, which becomes primarily an excretory organ (“the stomach urinates,” according to the figurative expression of M. P. Konchalovsky), as well as the intestine, cannot but adversely affect
secretion of free hydrochloric acid and gastromucoprotein, which in turn should lead to a breakdown of iron absorption.
In the light of the latest data on erythropoietin plasma (see above), it is suggested that the cause of anemia of the braic can be impaired function of the juxtaglomerular apparatus of the kidneys in the production of erythropoietin.
LOW COLOR AT DIFFUSIVE LIVER DAMAGE
In chronic diffuse lesions of the liver (chronic hepatitis), regardless of the etiology of the process, macrocytic anemia of the normochromic or slightly hyperchromic type occurs.
Studies by our employees (N. T. Fokina) and other authors who have found elevated levels of vitamin B12 in plasma give the right to argue that macrocytic anemia in chronic liver damage is associated with impaired deposition and utilization of vitamin B12, as well as folic acid.
In subacute liver dystrophy, hyperchromic macrocytic anemia is one of the most important indicators of severe liver dysfunction and has a serious prognostic value.
The development of severe pernicious anemia in metastatic liver cancer may indicate the primary localization of cancer in the stomach.
INFECTIOUS DISEASES ANEMIA
Anemias in infectious diseases are very diverse both in etiology and pathogenesis, and in clinical features.
Anemia in infectious diseases can occur because of a violation of the normal absorption of iron or hematopoietic substances (vitamin B12, folic acid). It may be associated with hemolysis, bleeding, hypersplenism, developing avitaminosis, finally, with the anemizing effect of chemotherapy drugs.
The development of iron deficiency anemia in infectious diseases is mainly due to the fact that iron is not used for the needs of erythropoiesis, but for the fight against infection. Being fixed in the tissues, iron participates as a catalyst of oxidative processes, increasing in febrile conditions, and as a stimulator of reticulohistiocytic (lymphoid) elements that produce immune antibodies. Additional factors contributing to the development of infectious hyposiderosis are reduced iron adsorption in the gastrointestinal tract, as well as impaired iron absorption and heme disorder in erythroblasts, as evidenced by the increased content of protoporphyrin in them and increased excretion of coproporphyrin.
An undoubted role in the development of hyposiderosis in infectious patients is also played by protein deficiency, in particular, deficiency of? -Globulin (transferrin), which plays a role in the delivery of iron to the bone marrow.
The above anemizing factors can be combined, for example, with a prolonged septic endocarditis, the toxic effect of the infective (streptococcus) on the bone marrow and its hemolytic effect and the development of hypersplenism takes place. Anemia is a characteristic symptom for many infections. These are protozoal diseases: malaria, trypanosomiasis, internal leishmaniasis, in which either red blood cells are affected, or reticulohistiocytic, resp. the hematopoietic system, as well as some acute and chronic bacterial septic infections, the causative agents of which cause anemia due to myelotoxic action. According to their pathogenesis, these anemias are either hemolytic (malaria, acute anaerobic or streptococcal sepsis), or anemia from impaired blood formation due to the direct toxic effects of pathogens on the bone marrow (visceral leishmaniasis).
Treatment. Therapy of infectious anemia consists in the treatment of the underlying disease.
Despite the relative rarity of drug-induced anemia, which indicates the role of the individual sensitivity of the organism in their occurrence, the issue of drug-induced anemia becomes particularly relevant, given the current scale of chemotherapeutic agents.
As it is known, chemotherapy drugs and some antibiotics (chloramphenicol) in relation to the macroorganism are antivitamins that, in affinity for microbes, compete with vitamins essential for the microbial cell - the so-called essential metabolites, such as para-aminobenzoic acid.
The bacteriostatic effect of sulfonamides and PAS is based on the structural similarity of these drugs with para-aminobenzoic acid. Replacing the latter of the association with a specific microbial protein, respiratory enzyme, and thus destroying the biologically active enzyme system vital for the microorganism, the chemotherapy drugs themselves bind to the same specific proteins, forming a biologically inactive system.
The bacteriostatic effect of chemotherapy drugs (sulfonamides) and some antibiotics (chloramphenicol) also extends to the intestinal flora useful for the microorganism, which is involved in the synthesis of a number of vitamins, in particular folic acid.
This explains the role of sulfonamides and antibiotics in the occurrence of disorders of hematopoiesis, especially with prolonged use of massive doses.
According to some reports, sulfonamides violate the synthesis of folic acid and directly, preventing the connection of para-aminobenzoic and pteroylglutamic acids.
It was experimentally possible to obtain macrocytic anemia in pigs by turning off folic acid from the diet and prescribing its antagonists simultaneously with sulfathiazole.
The anti-vitamin effect of sulfonamides and antibiotics on the human body is manifested, especially in weak, exhausted patients, in the form of pellagroznyh phenomena (glossitis, hyperkeratosis, enteritis) and macrocytic anemia, indicating deficiency of B vitamins, in particular nicotinic and folic acids.
Currently, most medicinal anemias, especially hemolytic, are considered in the aspect of the innate inferiority of the erythrocyte enzyme structures, which determine their "hemolytic readiness" in connection with taking certain medications (see Enzyme Deficiency Hemolytic Anemias).
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ANEMIA DUE TO TOXIC EXPOSURE OF THE BONE MARROW (MYETHOXICAL ANEMIA)
- Anemia due to bone marrow drainage, hypothyroidism, and aplastic anemia. MYELOPLASTIC SYNDROME
Despite the large number of studies devoted to the study of hypo-and aplastic anemias, it is still not possible to create a rational classification of these conditions, since not only the issues of pathomorphogenesis, but even the definition of the very concept of "hypo (a) plastic anemia" is debatable. In accordance with modern concepts of the genesis of hypo-
- Anemia due to blood loss, post-hemorrhagic anemia
Anemia due to blood loss, post-haemorrhagic
- PATHOLOGY OF BLOOD CELL AND BONE MARROW. ANEMIA
Hematological diseases may be primary, that is, caused by the disease of the blood-forming organs themselves, or secondary, reflecting the damage of any other systems. Secondary diseases are more common. The availability of morphological studies of blood cells, for example, in a smear of venous blood or bone marrow punctate, provides a direct study of the changes that have occurred. AT
- Dizerythropoietic anemia (due to impaired erythropoiesis)
This group of diseases includes: a) anemia, combined by a common mechanism of occurrence associated with impairment or termination of erythropoiesis as a result of a deficiency of substances necessary for normal blood formation - deficient anemia (B12 -, B6 -, B2 - folic acid, iron-copper cobalt-deficient, protein-deficient), as well as anemia, arising from the inability of the bone marrow
- Anemia due to impaired hemoptosis
DEFINITION Diamond-Blackfan Anemia is a group of congenital red cell aplasias that are usually diagnosed during the first year of life. EPIDEMIOLOGY Currently, hemolytic anemia due to vitamin E deficiency has largely disappeared due to the improved composition of mixtures for premature newborns containing lower concentrations of polyunsaturated fatty acids
- Hypo-and aplastic anemia. Syndrome of bone marrow failure
Anemia of this group can be acquired (secondary) and hereditary, congenital (primary). Acquired forms may develop under the influence of physical (ionizing radiation); chemical (benzene, arsenic, etc.) factors, drugs (some antibiotics, sulfonamides, antimetabolites - methotrexate, etc.), as well as due to a lack of hormones (myxedema,
- ANEMIA UNDER CONDITIONS OF FUNCTIONAL AGASTRY (AGASTRAL ANEMIA)
In contrast to the actual agastric anemia associated with partial or complete anatomical removal of the stomach, we distinguish anemia that develops in conditions of functional agastria, when the anatomically preserved stomach partially or completely turns off from the physiological process of digestion and, in particular, loses the ability to assimilate the external antianemic factor - Vitamin B12.
- Anemia associated with impaired synthesis of DNA and RNA (megaloblastic anemia)
Megaloblastic anemia unites a group of acquired and hereditary anemias, a common feature of which is the presence of megaloblasts in the bone marrow. Regardless of the etiology of the patients, hyperchromic anemia with characteristic changes in the erythrocyte morphology is revealed - oval red blood cells, large (up to 12-14 microns or more). There are red blood cells with basophilic cytoplasm, in many of
- Anemia associated with impaired synthesis or utilization of porphyrins (sideroachrestic, sideroblastic anemia)
This is a heterogeneous group of diseases, hereditary and acquired, associated with a violation of the activity of enzymes involved in the synthesis of porphyrins and heme. The term "sideroahresticheskaya anemia" was introduced by Iewer (1957). In case of sideroachrestric anemia, serum iron levels are elevated. In the bone marrow detect ring-shaped sideroblasts - nucleated red blood cells with a nucleolus corolla,
- APLASTIC (HYPOPLASTIC) ANEMIA
Previously, this anemia was called panmielophthysis - the consumption of bone marrow. This is a disease of the blood system, characterized by the inhibition of the hematopoietic function of the bone marrow and manifested by the insufficient formation of red blood cells, leukocytes and platelets - pancytopenia. There are congenital (constitutional) and acquired hypoplasias. In 1888, Erlich first described the disease in a young
Anemia (anemia) is a condition characterized by a decrease in hemoglobin concentration in a unit blood volume below normal. Often, but not always, this decrease occurs while simultaneously reducing the total mass of red blood cells per unit volume of blood. Anemia develops when the rate of their reproduction in the bone marrow decreases due to the destruction or loss of red blood cells. Therefore, there are two large
- ACQUIRED HEMOLYTIC ANEMIA
Acquired hemolytic anemias include: • immune hemolytic anemia; • drug hemolytic anemia; • traumatic and microangiopathic hemolytic anemia; • anemia caused by hemolytic poisons, chemicals, bacterial toxins; • paroxysmal night
- Hyporegenerative anemia
Hyporegenerative anemia is not so much a nosological as a functional-morphological concept. Essentially, hyporegenerative anemia is the biological variant of any anemia. Most often it occurs as the final stage of development of chronic post-hemorrhagic or auto-aggressive hemolytic anemia with a long-term process, as well as in connection with general intoxication
Anemia - a condition characterized by a decrease in hemoglobin per unit volume of blood by reducing its total amount in the body. In most cases, anemia is also accompanied by a decrease in the number of red blood cells per unit volume of blood. From true anemia should be distinguished hydremia - blood thinning due to tissue fluid. At the heart of the development of anemia are various pathological processes in
- Acquired hemolytic anemia
This is a heterogeneous group of hemolytic anemias that occur under the influence of a number of factors that have the ability to damage red blood cells and cause their premature destruction. Classification of acquired hemolytic anemia [Idelson LI, 1975] I. Hemolytic anemia associated with exposure to antibodies. 1. Isoimmune hemolytic anemia 1) hemolytic disease of the newborn
- Anemia Prematurity
Etiology and pathogenesis The isolation of this group of anemias is explained by the heterogeneity of the etiopathogenetic mechanisms leading to the development of the anemic syndrome. The main factors contributing to the occurrence of anemia in the first year of life in premature or low birth weight children are the cessation of erythropoiesis, iron deficiency, folate deficiency and vitamin E deficiency (Table 43).
- Hypo and aplastic anemia
Hypo- and aplastic anemias are a heterogeneous group of diseases, characterized by a sharp inhibition of blood formation. Differences between hypo-and aplastic anemias are mainly due to the degree of inhibition of bone marrow hematopoiesis. Naturally, this distinction leaves its mark on the clinical manifestations of the disease, the effectiveness of the treatment applied and