ANEMIA (anemia; the Greek negative an-and haima prefix — blood; synonym anemia) — the state which is characterized by reduction of quantity of erythrocytes and decrease in a hemoglobin content in unit volume of blood. At And. in peripheral blood also qualitative changes of erythrocytes — their sizes, a form and coloring quite often are found. At some And. in blood nuclear prestages of erythrocytes (erythroblasts, normoblasts, megaloblasts), unripe forms of erythrocytes (polychromophils), erythrocytes containing various inclusions appear: cytoplasmatic — siderocytes, basphilic and aurofiljno-punktirovanny erythrocytes and nuclear — chromatinic motes, Cabot's rings, Joly's little bodies (tsvetn. fig. 1).
From true And. it is necessary to distinguish hemodilution, i.e. the fluidifying of blood due to plentiful inflow of an intercellular lymph observed, e.g., at patients in the period of a convergence of hypostases after operation using artificial circulation. Similar pseudo-anemia passes as the «hypostasis of blood» which caused it disappears. True And. can mask a pachemia, e.g., at plentiful vomiting or profuse ponosa; at the same time owing to reduction of volume of plasma the quantity of erythrocytes in unit volume of blood can be normal and even raised.
Idiosyncrasy true And. is or an absolute degrowth of erythrocytes — erythron, or functional insufficiency of erythron owing to reduction of a hemoglobin content in each separate erythrocyte.
At an anemia in an organism oxidizing processes are broken and develops hypoxia (see). Development of a hypoxia is influenced by not only degree of an anemia, but also speed of its development, and also degree and speed of adaptation of an organism to the changed living conditions.
Compensatory mechanisms at anemia
the Clinical physician quite often observes discrepancy between weight of an anemia and an active condition of the patient that is explained by the compensatory mechanisms providing the physiological need of fabrics for oxygen.
The main role in compensation of an anemic state belongs to nervous and cardiovascular systems: the hypoxia leads to the fact that nedookislenny metabolic products come to blood. The last, influencing the central regulation of blood circulation, and also the neuromuscular device of heart, cause increase of a cordial rhythm and acceleration of a blood-groove therefore the minute volume of the blood which is thrown out by a left ventricle increases twice (to 8 l instead of 4 l normal). Besides, at And. the spasm of peripheral vessels develops and blood reserves from fabric depots, hl come to a circulatory bed. obr. from hypodermic cellulose. In more mild cases And. providing fabrics with enough oxygen is reached by increase in physiological activity of erythrocytes and permeability of a capillary wall for blood gases. The known significance in compensation of a hypoxia is attached to the ferriferous enzymes (cytochrome oxydase, a catalase) which are potential carriers of oxygen and also processes of oxygen-free breath with the participation of glutathione.
The major role in elimination And. and recovery of normal composition of blood belongs to marrow, its erythropoietic function.
About a condition of erythropoietic function of marrow judge by a morphological picture of sternal punctate (by a method M. And. Arinkina), in particular on a quantitative ratio eritro-and leykoblastichesky elements; in normal conditions this ratio makes 1:3 or 1:4. At the increased regeneration of red blood when marrow functions preferential in the direction of an erythrogenesis, the ratio eritro:leyko changes in favor of erythroblasts, reaching 1:1 or 2:1 and even 3:1.
Depending on dominance in sternal punctate of this or that type of erythroblasts distinguish the following types of an erythrogenesis: a) erythroblastic, b) pro-normoblastic, c) normoblastic, d) megaloblasticheskiya.
The final stage of erythropoietic function of marrow is process of receipt of mature, nuclear-free erythrocytes of marrow in the circulating blood. This major eliminiruyushchy function of marrow comes to light a dynamic research of the main indicators of red blood — hemoglobin contents, quantities of erythrocytes and percent of reticulocytes.
Etiology and pathogeny
And. arises or when the decrease of erythrocytes in blood (owing to blood loss or, a krovorazrusheniya) on this interval of time exceeds the maximum opportunities of regeneration of marrow, or owing to insufficient erythropoietic function of marrow. The last in turn depends or on deficit of substances, necessary for a normal hemopoiesis (iron, vitamin B 12 , folic to - you — so-called scarce anemias), or from not digestion (non-use) of these substances marrow (so-called akhrestichesky anemias).
Pathogeny of some And. it is connected with genetic features: in one cases enzymatic structures of erythrocytes can be broken that results in their hypersensitivity in relation to various external agents (to medicines, vegetable products) with the subsequent massive intravascular hemolysis; in other cases under the influence of the hereditary or acquired factors synthesis a subject is broken (see. Gemoglobin ), what leads to a condition of an akhreziya, i.e. non-use of a number of metabolites, first of all iron and vitamins of a hemopoiesis (vitamins B 12 , B 6 , folic to - you).
the set of classifications Is developed And. According to a morphological and functional condition of marrow, its ability to regeneration and compensation of an anemic state distinguish the following forms A.: hyper regenerator, regenerator (at acute blood loss, hemolysis), hyporegenerative (at chronic blood loss), hypoplastic, aplastic (at a panmyelophthisis), dysplastic or dizeritropoetichesky [at B 12 - (foliyevo) scarce states, inborn multinuclear eritroblastoz].
On the classification offered by G. A. Alekseev distinguish three basic groups of anemias: And. owing to blood losses — posthemorrhagic; And. owing to the broken krovoobrazovaniye; And. owing to the raised krovorazrusheniye — hemolitic (see the tab.). Distinguish also acute and hron. And.
At And. the complex of the changes reflecting acute or hron comes to light. insufficiency of blood supply. The nature of changes depends on a form A., phases of development and the carried-out therapy. Pallor and quite often yellowness of skin is macroscopically noted. At hron. And. development of a hypodermic fatty tissue, fatty tissue in a mesentery, an epiploon and around internals is noted. The muscle of heart flabby, dim, in papillary muscles can be observed yellow specks. A liver on a section of pale gray color, the drawing of segments is erased. The spleen is often reduced in sizes, the capsule of a morshchinist, on a section a pulp gives scraping. In the thickness of fatty tissue of mesenteries nodes of dark red color can come to light multiple small (0,3 — 0,4 cm in the diameter) limf. Marrow of flat bones of a usual look, in an average and lower third of a hip fatty, with sites of a hemopoiesis of rose-red color. Sometimes marrow becomes active throughout a hip. Microscopic examination reveals fatty dystrophy in a muscle of heart and in a liver, and also adjournment of lipids in cytoplasm of cells of an endothelium of vessels of a brain, parenchymatous bodies. The changes found in marrow are various depending on sharpness and a form of process and efficiency of the carried-out treatment. The histologic research of biopsies of marrow allows to specify extent of its defeat and promotes differentiation with other diseases. Studying of biopsies of marrow in course of disease allows to establish efficiency of therapy and activity of processes of regeneration of marrow.
A clinical picture
Symptoms of a disease are more or less expressed depending on degree of an anemization and adaptation of the patient. Weakness, bystry fatigue, an asthma and heartbeat at an exercise stress is usually noted, pallor of skin and mucous membranes. At deep And., especially at its bystry development, there are frequent dizzinesses, a sonitus, a vision disorder in the form of flashing of «front sights» before eyes, decrease in visual acuity, sometimes up to a full amaurosis in connection with disturbance of food of optic nerves as a result of a hypoxia. During the listening of heart the «blowing» systolic noise at a top and on an anastomosis, resulting from a hydremia and compensatory acceleration of a blood-groove is defined.
Anemia agastrichesky arises usually after full removal (gastrektomip) or a subtotal resection of a stomach. The partial resection which is widely applied at stomach ulcer, as a rule, is not followed by A. Lish at a part of patients (preferential at women) iron deficiency A.
Agastricheskaya A. is observed there is iron deficiency also B 12 - (foliyevo) scarce; it is shown usually in terms from 3 to 5 years after operation of a gastrectomy, sometimes earlier — in 1 — 1/2 years.
From classical pernicious anemia of Addison — Birmera agastrichesky B 12 - scarce And. differs in smaller expressiveness of symptoms of intra marrowy hemolysis (because of a dizeritropoez).
Prevention agastrichesky And. consists in timely (even before development of the phenomena of B 12 - insufficiency) purpose of vitamin B 12 in injections to 100 — 200 mkg of 1 — 2 time a month, since first months after operation. Iron preparations are used according to indications (at a hypochromia of erythrocytes, a sideropenia).
Anemia ankilostomny is caused by helminths from a class of nematodes — ankylostomas (see. Ankilostomidoza ). Grizinger (W. Griesinger, 1854) showed that ankylostomas are activators of a so-called Egyptian chlorosis; «mountain anemia», or the anemia of miners observed as a mass disease of the navvies working during the making of the Saint Gothard tunnel was also ankilostomny origin. Pathogeny ankilostomny And. it is connected with a loss of blood. It proceeds as iron deficiency Ampere-second a low color indicator (0,4 — 0,6), a microcythemia and a moderate reticulocytosis. In hard cases the amount of hemoglobin falls to 2 — 3 g of %. The picture of white blood is characterized by a leukopenia and a high eosinophilia (to 74%). The diagnosis is made on the basis of detection of eggs of ankylostomas in excrements or duodenal contents; in the last it is possible to find also live puberal individuals. The major medical and preventive action is deworming (see), at expressed And. — after a preliminary course of antianemic treatment by high doses of iron.
Anemia anenteralny. Under this name combine various forms A., the absorptions connected with disturbance in a small bowel of proteins, minerals and vitamins. The pernicious and anemic states arising at long enterita, especially at a spra are most known (so-called pernicious spru-anemia — tsvetn. fig. 2 and 3). Pernitsiozopodobnye A. arise quite often in connection with organic lesions of intestines (polyposes, malignant tumors, a reticulum cell sarcomatosis, a lymphogranulomatosis), at diverticulums, strictures and extensive resections thin, especially ileal, guts, at regional (terminal) ileitises. Pathogeny of B 12 - scarce And. in the last cases connect with loss of function of intestinal protein acceptor. In an origin of these forms A. disturbance of absorption in the affected intestines of both iron, and antianemic factors — vitamin B matters 12 , folic to - you. Has value and dysbacteriosis, as a result to-rogo processes of biosynthesis folic to - you are broken by lactobacilli, and the colibacillus breeding in a small bowel competes with a macroorganism in use of food vitamin B 12 and folic to - you.
The defeats of a small bowel which are followed by the general (proteinaceous, mineral and polyvitaminic) insufficiency, lead to emergence mixed, B 12 - (foliyevo) - iron deficiency, A. Izvestna also anenteralny iron deficiency And., proceeding as a chlorosis, with a low color indicator, low content of iron of plasma, but with a macrocytosis of erythrocytes.
Treatment anenteralny And. carry out by the general rules of treatment iron-, vitamin, B 12 - (foliyevo) scarce anemias. Considering disturbance of intestinal absorption, it is necessary to appoint all antianemic drugs parenterally.
Anemia akhrestichesky (Izraelsa — Wilkinson a disease) arises because marrow is not able to use the antianemic substances which are available in an organism. In a crust. time is considered by nek-ry scientists as erythremic myelosis (see).
Anemia of B 12 - (foliyevo) scarce. Under this name combine group of the anemic conditions of various etiology resulting from insufficiency of vitamin B 12 and (or) folic to - you of which increase in a color indicator (1,2 — 1,8) and emergence of pathological forms of erythrocytes is characteristic, in particular, (tsvetn. fig. 2). See. Pernicious anemia .
Anemia benzene — see. Hypoplastic anemia .
Anemia hemolitic — see. Hemolitic anemia .
Anemia hypochromia — see. Iron deficiency anemia .
Anemia hyperchromic — see. Pernicious anemia .
Anemia hyporegenerative most often arises as a final stage hron. posthemorrhagic And., and also in connection with the general intoxication, a cachexia and exhaustion of erythrocytes of substances, necessary for creation — iron, proteins, vitamins, microelements. A picture of blood at hyporegenerative And. it is characterized normo-or a hypochromatism, rarely by a hyperchromasia, with the expressed degenerative changes of erythrocytes (anizo-or noykilotsitoz) at the normal or slightly lowered quantity of leukocytes (granulocytes) and normal quantity of platelets.
Difference hyporegenerative And. from actually hypoplastic And. consists in the following: 1) as a rule, primary moment in development hyporegenerative And. bleeding, therefore, pathogenetic this anemia — posthemorrhagic is; 2) hyporegenerative And. never passes into a full aplasia; 3) a marrowy hemopoiesis corresponds to a condition of hyporegeneration more (but not hypoplasias); among erythroblasts basphilic forms prevail; therefore, there is not an aplasia of parent elements of an erythrogenesis, but exhaustion of funds of iron, the proteins and vitamins necessary for creation of mature forms of red blood; 4) this state is reversible: prolonged and systematic complex treatment brings marrow out of a torpid state, there occurs practical recovery.
Anemia dizeritropoetichesky — see. Dizeritropoetichesky anemia .
Anemia difillobotriozny. Etiological role of a wide tape-worm in development And. it is proved by treatment of patients after exile of a parasite what S. P. Botkin for the first time paid attention (1884) to. The research of a gastric juice at the persons infested by a wide tape-worm showed the normal maintenance of an internal antianemic factor. Emergence And. connect with disturbance of assimilation or destruction of antianemic substances (vitamin B 12 , folic to - you). The picture of blood at the height of a disease is similar that at pernicious And. also differs only in the expressed eosinophilia (to 30 — 40%). A marrowy hemopoiesis represents a picture of a megaloblastichesky erythrogenesis. Treatment helminthic And. comes down to exile of a parasite. At true difillobotriozny And. after deworming patients quickly recover without special antianemic therapy. At a heavy current the previous antianemic therapy is necessary (vitamin B 12 ), the effect a cut is shown even before exile of a parasite. Prevention consists in the prevention of helminthic invasions.
Iron deficiency anemia — see. Iron deficiency anemia .
Anemia zhelezorefrakterny (tsvetn. fig. 6) — the general name for extensive group of the anemic states combined on the basis of the high content of iron in plasma and a refrakternost to treatment by iron is more detailed — see. Zhelezorefrakternaya anemia .
Lederer's anemia — see. Hemolitic anemia .
Anemia medicamentous — not so frequent phenomenon if to take modern scales of use of chemotherapeutic means and antibiotics into account. In the wide plan distinguish two groups of medicinal
A. K to the first group carry myelotoxic And., arising in connection with cytostatic (himio-or beam) the therapy which is carried out concerning a tumoral disease or system pathology of blood. Potentially any cytostatic means possessing miyelodepressivny action is capable to cause And. hypoplastic type. Carry to the second group medicamentous And., which emergence is connected with individually hypersensitivity of an organism to certain medicinal substances.
Majority medicamentous And. consider or in respect of anti-vitamin activity of drug, or in aspect of autoimmune aggression where medicine plays a role of hapten (see. Antigens ), or in aspect of the individual inferiority of enzymatic structures of erythrocytes causing «hemolitic readiness» in connection with reception of some medicines. At prolonged use of massive doses of streptocides and some antibiotics (biomycin, chloramphenicol, synthomycin, levomycetinum) bacteriostatic action of these drugs on microbic flora of a small bowel is shown; as a result of dysbacteriosis biosynthesis of a number of vitamins, in particular folic to - you is broken.
Are of interest of B 12 - (foliyevo) scarce And., provoked by reception of some antimalarial, (Daraprimum) and antiepileptic means — dipheninum (diphenylhydantoin, Phenytoinum), a hexamidine (Primidonum), Mesantoinum, luminal (phenobarbital) and other barbiturates, and also a furadonin (nitrofurantoin) and butadiene (phenylbutazone). Pathogenetic communication of Ampere-second anti-folic activity of these drugs is proved by decrease in concentration folic to - you in blood of the persons accepting them and positive effect of treatment folic to - that (in doses of 50 — 100 mg a day). Treatment by vitamin B is less effective 12 .
B 12 - (foliyevo) scarce And. medicamentous genesis is followed by symptoms of a vitamin deficiency of group B, in particular folic and nicotinic acids (a glossitis, a hyperkeratosis, a diarrhea, changes of mentality), develops at the weak, exhausted patients more often.
From classical pernicious anemia of Addison — Birmera medicamentous B 12 - (foliyevo) scarce And. differs in safety of gastric secretion, normal concentration of vitamin B 12 in blood (at normal absorption of vitamin B, marked on cobalt 12 in intestines) and lack of neurologic symptoms.
There are descriptions And., arising in connection with reception of antitubercular drugs. Pathogeny of this And. difficult; there are bases to consider it as the zhelezorefrakterny anemia caused by disturbance of synthesis a subject in connection with disorder of exchange of B6 vitamin (pyridoxine-piridoksal-phosphate).
Treatment medicamentous And. consists in the termination of the administration of drug which caused And., and introduction folic to - you.
Anemia medicamentous hemolitic (enzimodefitsitny) — see. Enzimopenichesky anemia .
Anemia myelotoxic — And. owing to toxic oppression of marrow at various exogenous (benzene) and endogenous (at damage of kidneys, a liver) intoxications (see. Hypoplastic anemia ).
Anemia mishenevidnokletochny — see. Thalassemia .
Anemia pernicious — see. Pernicious anemia .
Anemia at a renal failure in most cases has the hypochromia character inherent to iron deficiency A. U of some patients hyperchromic pernitsiozopodobny A. Otmechayetsya a neutrophylic leukocytosis (with preservation of eosinophils) develops, at uraemia to 12000 — 20000 in 1 mkl. The known role in development And. at a renal failure plays defeat went. - kish. path. In the light of data about erythropoetins (see) the opinion is expressed that the reason And. at a renal failure dysfunction of the juxtaglomerular device of kidneys is. According to other authors who established the braking influence of blood serum of renal patients on proliferative activity of erythroblasts of marrow, And. at a renal failure arises under the influence of accumulation in blood of inhibitors of erythropoetin. The inactivation of inhibitors of erythropoetin is connected with the unknown still function of kidneys.
Treatment — vitamin therapy, transfusion of eritrotsitny weight. In the long term — development of receiving erythropoetins.
Anemia at damages of a liver. At hron. diffusion damages of a liver (hepatitises), irrespective of an etiology of process, arises macrocytic And. normokhromny or moderately hyperchromic type that is connected with disturbance of deposition and utilization of vitamin B 12 , and also folic to - you. At subacute dystrophy of a liver macrocytic And. hyperchromic type is one of the most important indicators of a heavy abnormal liver function and has serious predictive value.
Development heavy pernitsiozopodobny And. at metastatic cancer of a liver can serve as the instruction on primary localization of cancer in a stomach.
At hron. active (so-called lupoid) the hepatitises, cirrhoses of a liver developing on the autoagressivny mechanism quite often arises hemolitic And., proceeding as the acquired autoimmune hemolysis, with positive direct test of Koombs (see. Koombs reaction ).
Anemia at metastasises of cancer in marrow most often develops at cancer of prostatic, milk, thyroid glands, lung cancer, a hypernephroma. At innidiation of a malignant tumor in marrow (miyelokartsinoz) a syndrome And. takes the leading place in a clinical picture of a disease. The initial center of process (the tumor which gave a metastasis of cancer in a bone) is quite often so small that by any methods of a research does not come to light. Distinctiveness of this And. are extraordinary expressed eritronormoblastoz and a leukemoid picture of blood. However in a third of cases, even at very considerable distribution of metastasises on bones, the leukemoid test can not be observed. The picture of blood depends not only on a mechanical factor — implantation in marrow of cancer cells, but also on reactivity of marrow. Between type of a tumor and the nature of reaction of marrow there is no visible communication.
Sternal puncture (see) gives the chance to diagnose metastasises in marrow even in the absence of clinical data (tsvetn. fig. 4). Cytologic diagnosis does not present special difficulties; the most important sign of cancer cells is their atypia in comparison with surrounding myeloid fabric. Along with cells atipichesky, not inherent to marrow, in marrowy punctate neoplastic cells which in the conditions of the environment of marrow are exposed to a peculiar metaplasia meet, gaining some properties of myeloid elements, in particular azurophilic granularity. At a diffusion metaplasia of marrow foreign fabric the picture of blood can approach that what is observed at hron. myeloleukemia or acute miyeloblastny leukosis (see).
Anemia lead develops under the influence of intoxication of an organism lead (see) or its connections. In a crust. time is considered as a prototype And., connected with disturbance of synthesis a subject.
Rimington (Rimington, 1938) for the first time expressed opinion that lead interferes with entry of iron into a porphyrinic ring and by that breaks formation a subject from protoporphyrin and iron. Modern researchers found in urine of patients lead And. considerable contents δ-aminolevulinic to - you to - you to - you (((δ-ALCOHOL). Lead, blocking the fermental systems participating in synthesis of porphyrines slows down synthesis a subject and at earlier stage — education from δ-ALCOHOL of porphobilinogen. As believe, the main essence of toxic effect of lead consists in blocking of sulphhydryl groups of enzymes. The subject plays a direct role in disturbance of synthesis suppression of activity of the following fermental systems: dehydrogenases of δ-ALCOHOL, decarboxylase of uroporphyrinogen, gemsintetaza. Investigation (not the reason!) a defective hemopoiesis shortening of a life cycle of erythrocytes and accelerated eritroliz, followed by symptoms of quasihemolitic jaundice is (a hyperbilirubinemia, an urobilinuria, the increased content of stercobilin in Calais).
The clinical picture of lead intoxication is diverse: symptoms of defeat went. - kish. path, nervous and cardiovascular systems, hemopoietic bodies. Already in an initial stage and at easy degree of lead intoxication a picture of blood (tsvetn. fig. 5) finds characteristic changes in a type of a considerable reticulocytosis and basphilic stippling of erythrocytes. At more expressed intoxication develops And. usually hypochromia type, with decrease in hemoglobin in hard cases to 8 — 6 g of %. Along with the expressed hypochromia of erythrocytes the high content of iron in serum is noted. Marrowy punctate is characterized by the expressed erythronormoblastic reaction and sideroblastozy with dominance of ring-shaped forms.
The diagnosis of lead intoxication is made on the basis of the anamnesis, a characteristic picture of blood (basphilic stippling of erythrocytes and a hyper reticulocytosis, inadequate degrees of anemia and hemolysis); finally is confirmed by detection in urine of lead; especially large amounts of lead (to 2 mg) are allocated for 1 l of urine after introduction of a complexon. The known diagnostic value, especially at an early stage of lead intoxication, can have detection in urine δ-aminolevulinic to - you to - you to - you, being the most precursory biochemical symptom of the broken synthesis a subject.
As a specific antidote apply to treatment kompleksen — dinatriykaltsiyevy salt ethylene diamine tetraacetic to - you are (Tetacinum-calcium), forming the strong complex which is easily deleted from an organism with lead. The drug is administered in a vein in the form of 10% of solution on 20 ml daily within 5 days. Carry usually out 3 — 4 courses with 4 — 5-day intervals. Apply also other complexons: kompletsin — inside in tablets (on 2 g every other day within 20 days) or in a vein (in the form of 10% of solution on 20 ml a day within 5 days), D-Penicillaminum (in a vein in a single dose of 1 g).
The system of dispensary observation developed in the USSR for workers of the productions connected with production, smelting or use of lead promotes early detection of easy forms and the prevention of severe forms of lead intoxication.
Anemia drepanocytic — see. Drepanocytic anemia .
Anemia splenogenny is considered in a crust. time as first stage of a general disease of a spleen, liver and marrow, so-called miyelo-gepato-lienal syndrome, or Banti of a syndrome (see). The picture of peripheral blood is characterized by a pancytopenia, i.e. quantitative reduction of all cellular forms. At the same time actually anemia, i.e. an erythrocytopenia, is not so expressed; quite often into the forefront the leukopenia (a so-called splenic gipoleykiya) or thrombocytopenia acts, the cut sometimes accompanies hemorrhagic diathesis (see. Werlhof's disease ). From actually splenogenny And. it is necessary to distinguish And., developing owing to went. - kish. bleedings because of thrombosis of a splenic vein at patients from tromboflebitichesky splenomegaly (see). At splenogenny And. operation of removal of a spleen is shown, however indications to operation shall be considered individually.
Anemia spherocytic — see. Hemolitic anemia .
Anemia thyroprival develops on the soil hypothyroidism (see). Distinguish three look thyroprival And.: normokhromny, hypochromia, hyperchromic (pernitsiozopodobny). Believe that deficit of thyroxine leads to disorder of utilization of specific factors of a hemopoiesis (iron, folic to - you, vitamin B 12 ).
Anemia at a Hashimoto's disease (see. Hashimoto disease ) consider in a crust, time in aspect of the autoimmune conflict. In this regard a combination of a hypothyroidism with pernicious (B 12 - scarce) And. it can be interpreted as result of organospetsifichesky immunization that is proved by detection of antibodies of the directed action both against cells of a thyroid gland (thyreoglobulin), and against covering cells of fundal glands (an internal factor of Kasl).
At And., proceeding against the background of a hypothyroidism, the best medical effect is reached by use of iron and cyanocobalamine (vitamin B 12 in a usual dosage) in combination with Thyreoidinum (0,1 — 0,2 g 3 times a day).
Anemia at children
At early age And. it is observed very often that is explained by functional lability of the hemopoietic device of the child. Even insignificant and incontinuous errors in food, unfavorable conditions of life, insufficient use of fresh air and daylight, accidental diseases etc. easily cause And., and specific features of the child are of great importance; the role of heredity is big. The broken hemogenesis at children, especially in the first years of life, gains lines of embryonal type with tendency to development of leukemoid tests. At the same time at elimination of the reason which caused And., the expressed ability of the hemopoietic device to regeneration and recovery of normal composition of blood is noted.
Alimentary anemia it is usually observed at children of 6 — 18 months receiving uniform milk or flour food (tsvetn. fig. 7).
On a clinical picture distinguish forms lungs when the general condition of the child is almost not broken, moderately severe and heavy. At And. moderately severe the general pastosity, pallor of skin and mucous membranes, increase in a stomach, a moderate hyperplasia limf, nodes and almonds, locks is noted. The amount of hemoglobin goes down to 8 — 10 g of %, number of erythrocytes — to 4000000, is rare to 3000000, a color indicator 0,5 — 0,7; polychromatophilia, moderate reticulocytosis, single normoblasts; number of leukocytes, a leukocytic formula, thrombocytes — within norm. The combination of an alimentary factor to an infection considerably worsens a current And.
Severe form And. (alimentary and infectious, Yaksh's anemia — Gayema; tsvetn. fig. 8) in a crust, time almost does not meet. The general condition of the child heavy, mucous membranes are very pale, skin of wax-like or yellowish color with hemorrhages, is almost always observed heavy rickets, the liver and a spleen are strongly increased; the amount of hemoglobin and number of erythrocytes are sharply reduced, the number of leukocytes reaches 15 — 20 thousand, sometimes it is more, in a leukocytic formula lymphocytes or neutrophils prevail, it is a lot of nuclear forms of erythrocytes and unripe forms of neutrophilic leukocytes.
Sometimes alimentary And. on the overall clinical and hematologic picture (tsvetn. fig. 9) approaches pernicious; describe it under the name psevdoper-nitsiozny or alimentary (nutritive) megaloblastichesky And., edges develops because of uniform feeding by goat milk or dry milk blends. In a pathogeny — insufficient quantity in food folic to - you and vitamin B 12 ; has value and deficit of the vitamin C which is taking part in education from folic to - you tetrahydrofolic; insufficient products of gastromucoprotein, disturbance of acid-base equilibrium, an endointoxication as a result of the strengthened processes of rotting in intestines. Children are uneasy, badly eat, the increase in weight is insufficient, mucous membranes are pale, skin with a grayish shade; the liver and a spleen are increased. And. normo-, sometimes hyperchromic, is more rare than gipokhromyy character.
The number of erythrocytes can decrease to 1000000 and below, the anisocytosis, a poikilocytosis, nuclear forms of erythrocytes, retikulotsnt is not enough, basophilic stippling in erythrocytes, is more rare — single megaloblasts, Joly's little bodies, Cabot's rings. The number of leukocytes is a little lowered or within norm, bent to hypersegmentation of neutrophilic leukocytes; the number of thrombocytes is lowered, also the level of iron of serum is quite often reduced; in a picture of a miyelogramma — the strengthened megaloblastichesky erythrogenesis.
In treatment the main thing — a balanced diet with the sufficient content of proteins, vitamins, iron. Drugs with ascorbic to - that are shown, to the promoting stabilization of easily assimilable bivalent iron, and 1 — 2% solution divorced salt to - you, necessary for assimilation of food iron. 3 — 4 times a day give Ferrum reductum on 0,1 — 0,3 g; salts of bivalent iron (a gluconate and ascorbas of iron) — on 0,2 — 0,5 g 2 — 3 times a day, they do not concede by efficiency to Ferrum reductum and do not cause in children of the dispeptic phenomena. At difficulties in reception of powders and tablets it is possible to appoint 10% aqueous solution of lemon and ammoniac iron on 1 chaya. l. 2 — 3 times a day. Has good effect Haemostimulinum (see) which is applied on 0,25 — 0,5 g by 3 times a day. It is reasonable to appoint iron preparations in intervals between meals. Before and right after reception of iron it is not recommended to give tea, fat and flour products in order to avoid formation of insoluble compounds. At persistent And. the combined treatment by iron preparations and vitamin B is more effective 12 on 50 — 100 mkg every other day, 10 — 15 injections. At intolerance of administration of drugs orally and disturbance of absorption it can be applied ferkoven 1 — 2 ml intravenously only in stationary conditions. In resistant cases apply a transfusion of zritrotsitny weight on 30 — 75 ml daily 5 — 7 days.
Fankoni's anemia — the inborn family pancytopenia which clearly is coming to light most often at the age of 5 — 7 years — see. Hypoplastic anemia .
Family hypoplastic anemia of Estrenum — Damesheka — see. Hypoplastic anemia .
Daymond's anemia — Blekfana — see. Hypoplastic anemia .
Pernicious anemia like Addison — Birmera at children it is observed extremely seldom — see. Pernicious anemia .
Recently several rare forms pernitsiozopo-dobny are described And., including disease Imerslund (The lake of Imerslund) — family B 12 - scarce Ampere-second the kept internal factor of Kasl and a proteinuria, and juvenile B 12 - scarce And. — a consequence of functional insufficiency of glands of a stomach producing glandulyarny mucoprotein at a normal morphological condition of a mucous membrane of a stomach and the kept secretion salt to - you.
Hereditary megaloblastichesky anemia (disturbance of metabolism of pyrimidines, in particular orotovy acid) it is described at two children of three-months age; it is inherited, apparently, on autosomal recessively type. This form A. has pernitsiozopodobny character with expressed anizopoykilotsitozy and an anizokhromiya; erythroblasts, Joly's little bodies, Cabot's ring; neutropenia, moderate thrombocytopenia; in marrow — a megaloblastichesky erythrogenesis, narrowing of a granulotsitarny sprout in the presence of huge miyelo-and metamyelocytes. Orotatsiduriya. Delay of physical development. With the medical purpose appoint uridine.
From true And. it is necessary to distinguish seeming, or imaginary, anemia. Children — are almost healthy and usually there are no complaints; in peripheral blood a normal hemoglobin content and erythrocytes. Pallor of skin at such children is explained by features of an arrangement and krovenapolneniye of skin capillaries, the arterial pressure which sometimes is a little lowered. These children demand only careful observance of the mode corresponding to their age.
Anemia at pregnant women
Pregnancy — the special physiological condition which is followed by deep reorganization of all types of exchange of edge, however, does not cause development of special forms A., inherent only in pregnant women. Pregnancy of the woman healthy before, apparently, not often provokes A. Chashche's development pregnancy reveals latentno the proceeding pathological process or aggravates the course of the disease existing earlier. Usual clinical forms A occur at pregnant women., which are widespread among the population in general.
It is necessary to distinguish from true And. at pregnant women sometimes the condition of hemodilution accompanying pregnancy — the fluidifying of blood disproportionately increasing volume of plasma which is incorrectly called by «pseudo-anemia» or «physiological anemia» of pregnant women. F. L. Adair and soavt. counted that the volume of blood at healthy women during pregnancy increases on average by 23% (plasmas — for 25%, the mass of erythrocytes — for 20%). On the 16th week of pregnancy the accruing tendency to decrease in quantity of erythrocytes and hemoglobin is found. To the 32nd week the hemoglobin content in peripheral blood decreases by 15% of initial size. Indicators of the admissible lower bound of hemodilution: a hematocrit — 33/67 — 30/70, hemoglobin — 11 g of % and number of erythrocytes — 3600000. Gemodilyushchsh clinically is not shown, the reasons of its development are not clear. A certain value has probably strengthening of secretion of corticosteroids which, undoubtedly, participate in mobilization of liquid from inside - and extracellular spaces in blood [M. G. Kolpakov; Blomstedt]. Hemodilution is not inherent to healthy women with the uncomplicated course of pregnancy [Hyutten, Peyntin, Bayet, Lund, Sisson (Hytten and Paintin; Bast; Lund and Sisson].
Iron deficiency anemia wins first place among And. at pregnant women. It is found in 15 — 30% of pregnant women that makes 75 — 95% among patients And. pregnant women.
According to WHO statistics, iron deficiency And. comes to light at 21 — 80% of pregnant women at a research only of hemoglobin and at 40 — 99% at use of more exact diagnostic test — saturation of transferrin. A major factor in a pathogeny is the lack of iron, is more often than utilization character. At pregnancy the organism of the woman in addition needs 900 — 1100 mg of iron, and for needs of a fruit and creation of a placenta are spent by from 375 to 500 mg (WHO; Bayet). Than less iron comes to an organism of the pregnant woman from the outside or rezorbirutsya from went. - kish. a path, subjects deficit develops quicker. In similar cases the deposited iron is spent. Exhaustion of reserves of iron is promoted by frequent childbirth, a long lactation, long disturbances of food, parasitic diseases. Undoubtedly and value of deficit of vitamin D, And, With, a complex B. Oppression of an erythrogenesis is promoted also by surplus of steroids, especially эстрадиола-17β and estrone.
Pregnant women with hemoglobin there is lower than 11 are g in %, color indicator lower than 0,8, number of erythrocytes by less than 3600000, a hematocrit less than 33/67 and the content of serumal iron below 60 mkg of % consider as patients iron deficiency And. (WHO). The clinic of an iron deficiency anemia at pregnant women is shown by usual symptoms for this form A. (see. Iron deficiency anemia ). The considerable .opasnost is represented by complications of pregnancy against the background of And., especially late toxicoses and premature amotio of normally located placenta. Full placental detachment is observed in 2,9% of cases, premature births — in 11,3%, perinatal child mortality — from 4,5 to 20,7%.
Pernitsiozopodobny, B 12 - (foliyevo) scarce anemia pregnant women becomes frequent in December — April. Average age of sick 28 — 30 years, multipara prevail. The disease begins preferential in the second half of pregnancy, is more rare — in a puerperal period. After the delivery usually there occurs recovery, but aggravations at the subsequent pregnancies are possible. The disease begins slowly. Sometimes frustration join went. - kish. path. Hypostases, hypertensia and a proteinuria often mask true nature of a disease. Unlike pernicious And., severe defeats of a nervous system are not observed, paresthesias are sometimes noted. The forecast adverse as for mother (a lethality of 4%), and for a fruit; premature births make 36%, mortinatality — 12% [Guzen (Page J. G. Goosen)].
Differential diagnosis between a severe form iron deficiency and megaloblastny And. is based on set of clinical signs, a picture of peripheral blood and punctate of marrow.
Treatment And. at pregnant women depends on character And. At deficit of iron it is recommended to appoint at the same time the drugs containing iron, copper and cobalt (Ferrocalum, Ferrobionum, ferratol, Haemostimulinum, Ferrohaemotagenum, ferkoven). At B 12 - (foliyevo) scarce anemias — vitamin B 12 and folic to - that.
It is necessary to consider also interests of the fruit developing in conditions hron. hypoxias, the accruing avitaminosis and a metabolic acidosis. Therefore vitamins should be entered in the maximum doses, to carry out an oxygenotherapy and correction of acid-base equilibrium of blood. According to indications — hemotransfusions. A question of preservation of pregnancy at And. it is necessary to solve to the therapist and the obstetrician jointly.
Radio isotope diagnosis
it is possible to define by radioisotopes true or false And., synthesis of hemoglobin, size of an erythrogenesis, speed and places of preferential destruction of erythrocytes.
Main techniques and drugs: scoping of the circulating erythrocytes is carried out by means of Cr 51 , a research of life expectancy of erythrocytes — with Cr 51 or P 32 (diizopropilflyuoro-phosphonate), places of preferential destruction of erythrocytes — with Cr 51 , existence and the size of the concealed hemorrhages — with Cr 51 , intensity of an erythrogenesis — with Cr 51 or Fe 59 , absorptions of iron — with Fe 59 and absorptions of vitamin B 12 — with Co 58 (see. Absorption , radio isotope research). The majority of tests carry out in vivo; synthesis of hemoglobin is studied by in vitro.
Indicator amounts of drugs depending on test fluctuate from 1 — 5 mkkyura of Cr 51 , Co 58 , Fe 59 to 200 mkkyura of Cr 5 1. Measuring equipment: counters are scintillation liquid, and also with integral and well crystals, scanners and gamma cameras. Indicators of norm for the majority of methods have relative value since depend on details of the applied techniques.
Informational content of tracer techniques is more, than not isotope.
Unlike earlier extended method of differential agglutination, at Krom life expectancy only of the donor (poured) erythrocytes is defined, the tracer technique allows to define life expectancy and erythrocytes of the recipient. In clinical practice the only method allowing to determine the mass of the deposited erythrocytes is the isotope method. The tracer technique is more sensitive, than not isotope methods of identification went. - kish. bleedings. It gives the chance to quantitatively determine the size of blood loss throughout rather long time that is important in assessment of blood loss as a factor, defiant posthemorrhagic And. (see. Gastrointestinal bleeding , radio isotope diagnosis).
Use of radio isotope tests at difficulties in diagnosis of such anemias as iron-and B is especially reasonable 12 - scarce, zhelezorefrakterny, Markiafava — Mikeli (fig. 1), aplastic. The diagnosis of a α-thalassemia can be made only by means of a tracer technique. In fig. 2 it is shown that inclusion of C14 - asparaginic to - you in α-and β-chains of a globin almost equally is normal. At a β-thalassemia inclusion of C14 - asparaginic to - you in a β-chain is reduced, at a α-thalassemia — — in a α-chain.
Radio isotope definition of rate of decay of erythrocytes in a spleen at hemolitic And. helps to establish indications to a splenectomy.
for the purpose of studying of origins And., processes of regeneration of blood, detection of insufficiency of the hemopoietic system and development of methods of therapy the anemia at animals artificially is reproduced.
Experimental And. it is possible to cause bloodletting, destruction of erythrocytes hemolitic poisons, disturbance of integrity of various textural features of a nervous system, removal of bodies, etc.
Posthemorrhagic anemia is caused bloodletting, a cut 10 — 15 times on 10 — 12% do once in number of 30 — 40% of volume of the circulating blood (28 — 35 ml/kg) or repeatedly; at cats it is possible to remove 40 — 50% of volume of blood, at rats and rabbits — no more than 30%. Loss of 60 — 70% of blood is deadly.
Massive bloodletting causes in dogs braking of function of bark of big hemispheres within 7 — 8 days, change of vascular and respiratory reflexes, lowering of arterial pressure, an anoxemia and air hunger. The volume of blood decreases only at the very beginning of blood loss, then is recovered at the expense of the liquid arriving from fabrics. Hemoglobin, number of erythrocytes, content of proteins of plasma decreases. Serum of animals within 5 — 7 days gains hemolitic properties: there is a destruction of a part of erythrocytes and further decrease in quantity of erythrocytes and hemoglobin. These changes especially are expressed, than massivny bloodletting. Decomposition products of erythrocytes promote strengthening of production of the erythropoetin stimulating an erythrogenesis. The quantity of leukocytes within 4 — 8 days increases generally at the expense of neutrophylic with shift to young to the left. The number of reticulocytes begins to increase in several hours and reaches the maximum size on 5 — the 6th day, then gradually decreases. The number of thrombocytes decreases a little in the beginning, but is quickly recovered and exceeds initial level within several days. Erythropoietic activity of marrow amplifies without high-quality disturbances of a hemopoiesis.
Character and current And. depend on the size of blood loss and regenerator ability of the hemopoietic fabric.
At repeated bloodlettings strengthening of a hemopoiesis can be replaced by oppression in connection with exhaustion of the hemopoietic fabric. After loss of 40% of volume of blood recovery of indicators of peripheral blood occurs in 20 — 25 days.
At repeated blood losses recovery of a hemoglobin content lags behind recovery of quantity of erythrocytes in connection with exhaustion of a reserve of iron; respectively the color indicator decreases; it is observed anizo-, the poikilocytosis, a polychromatophilia of erythrocytes, appear normoblasts in peripheral blood. At exhaustion of the hemopoietic fabric the number of reticulocytes and leukocytes decreases. Terms of regeneration depend on a reference functional state of an organism and regenerator ability of the hemopoietic fabric, a floor, food, seasonal fluctuations, conditions of keeping of animals in a vivarium, etc.
Hemolitic anemia is caused most often by introduction phenyl of a hydrazine which destroys old erythrocytes. At the same time decomposition products of erythrocytes stimulate an erythrogenesis; therefore recovery of indicators of peripheral blood happens quicker, than at posthemorrhagic And.
2 — 5% enter aqueous solution of phenylhydrazine to dogs and rabbits under skin or intramusculary 4 — 12 times with intervals in 2 — 3 days or daily at the rate of 0,02 — 0,04 mg/kg on an injection; to rats and mice enter once intraperitoneally at the rate of 2 — 8 mg on 100 g of weight.
Degree and speed of development And. depend on a dose phenyl of a hydrazine. Under the influence of high doses the quantity of erythrocytes decreases in 2 — 3 days by 40 — 50%, the color indicator raises, there are in peripheral blood polychromatophilous, vacuolated and supporting pathological structures erythrocytes; considerably the maximum osmotic resistance of erythrocytes increases, the number of reticulocytes raises; the moderate leukocytosis without disturbance of a leukocytic formula develops; viscosity and coagulability of blood increases.
At long administration of phenylhydrazine there are megaloytes and megaloblasts, adjournment of hemosiderin in marrow, a spleen and a liver is observed. With 8 — the 10th day the centers of an extramedullary gemotsoez develop, the spleen and a liver increase in a size. In a leukocytic formula — shift to the left to myelocytes. High doses can cause phenyl of a hydrazine aplastic And.
Hyperchromic megaloblastichesky anemia at animals is caused by intravenous administration of aqueous solution of a saponin in number of 1 — 5 mg/kg within 5 days in increasing (on 1 mg a day) a dose. The number of erythrocytes decreases by 50%, hemoglobin — for 25 — 30%. Indicators of peripheral blood are recovered in 20 — 25 days. At a combination of a saponin with colloid silver (0,3 — 0,5 mg/kg) And. it is supported up to 40 days. Mesoxalyl urea (180 mg/kg in the form of 10% of solution) causes And. at animals in 2 — 3 days. As hemolitic poison is applied by lead, tolylenediamine, pyrogallol, hydrogen arsenide, but they cause also other displays of intoxication.
Neurogenic anemia can be caused by disturbance of integrity of various textural features of a nervous system, napr, denervation of a sinocarotid reflexogenic zone, a spleen, kidneys, a small bowel, etc. And. it is possible to cause also repeated introduction animal under skin of acetylcholine, Carbacholinum and other cholinergic substances. Moderate hypochromia A. Kolichestvo of hemoglobin develops and erythrocytes as much as possible decreases on 9 — the 15th day after operation. In blood at the same time find the substances oppressing an erythrogenesis. Recovery of indicators of peripheral blood happens within 20 — 40 days.
Organoprivny anemias develop at animals after removal of a part or all stomach, a part of a small bowel or a liver, at hron. to loss of bile (through a fistula of a gall bladder), after a hypophysectomy. At a combination of a gastrectomy to disturbance of food at dogs develops hypoplastic And.
Alimentary anemia. Long decrease in caloric content of food, especially depletion by her squirrels, and also causes a lack of iron, copper, cobalt in animals And. various character and; deficit folic to - you and vitamin B 12 causes hyperchromic megaloblastichesky And.
Reproduction of diseases at animals for experimental and therapeutic researches, under the editorship of N. V. Lazarev, page 296, L., 1954; Goldberg of A. I. Agastricheskiye B 12 - scarce anemias, Tomsk, 1962, bibliogr.; An iron deficiency anemia and some questions of regulation of an erythrogenesis, under the editorship of S. I. Ryabov, L., 1970; Idelson L. I. Disturbances of porphyrinic exchange in clinic, L., 1968, bibliogr.; Kassirsky I. A. and Alekseev G. A. Clinical hematology, page 149, M., 1970, bibliogr; Mosyagina E. N. Anemias of children's age, M., 1969, bibliogr.; Mukhamedzyanova G. S. Hypoplastic anemias at children, M., 1970, bibliogr.; Sarkisov D. S. and Remezov P. I. Reproduction of diseases of the person in an experiment, page 84, M., 1960; Feinstein F. E. Aplastic and hypoplastic anemias, M., 1965; Begemann H., Rastetter J. u. Kaboth W. Klinische Hämatologie, Stuttgart, 1970, Bibliogr.; Recent advances in hematology, ed. by A. Goldberg a. M. G. Brain, Edinburgh, 1971, bibliogr.
Pathological anatomy And.
A. I apricots. Private pathological anatomy, century 1, page 274, M. — L., 1947; Davydovsky I. V. Pathological anatomy and patogenee diseases of the person, t. 2, M., 1958; Nemenova N. M., Protasov T. G. and Voronin V. M. A biopsy of marrow in diagnosis of diseases of system of blood, Arkh. patol., t. 33, No. 3, page 3, 1971; Strukov A. I. Pathological anatomy, page 286, M., 1971; Burkhardt R. Farbatlas der klinischen Histiopathologie, B. u. a., 1970.
Radio isotope diagnosis And. — Layta L. G. Use of isotopes in hematology, the lane with English, M., 1963, bibliogr.; Tsfasman A. Z. Use of radioactive chrome in clinic, M., 1964; Radioisotopes in medical diagnosis, ed. by E. H. Belchek a. H. Vetter, L., 1971.
And. pregnant women
Abdurakhmanov M. K. Some indicators of exchange of oryzamins, B2, B6, C, A, D at the normal and complicated iron deficiency hypochromia anemia at pregnant women, Akush. and ginek., No. 6, page 10, 1971, bibliogr.; Hakimova S. H. To an etiology and a pathogeny of an iron deficiency anemia at pregnant women, in the same place, page 3, bibliogr.; André R. et Najman A. Interprétation des anémies de la grossesse, Sem. Hop. Paris, t. 45, p. 2306, 1965; Bast G. Anämien in der Schwangerschaft, Z. ges. inn. Med., S. 46, 49, 1966, Bibliogr.; Goosen G. J. Anaemias of pregnancy in afr leans, J. Obstet. Gynaec. Brit. Emp., v, 68, p. 994, 1961, bibliogr.; Malinac P. Les frontières de l'anémie &##225;u cours de la grossesse, Concours méd., t. 90, p. 1527, 1968; Nair G. T. R., Agarwal K. N. a. Kotwani B. G. Nutrition deficiency anaemias in later months of pregnancy, J. Obstet. Gynaec. India, v. 20, p. 594, 1970; Rothman D. Folic acid in pregnancy, Amer. J. Obstet. Gynec., v. 108, p. 149, 1970, bibliogr.
G. A. Alekseev; N. M. Nemenova (stalemate. An.), A. F. Tour (ped.), N. A. Fedorov, M. G. Katekhelidze (And. experimental), C.X. Hakimova (And. pregnant women), A. Z. Tsfasman (I am glad.).