Acute reticulosis - a form of acute leukemia characterized by a hyperplastic process involving the reticular tissue of the stroma-forming organs and by aleukemic blood picture, in which the undifferentiated and immature hematopoietic elements do not enter the peripheral blood, or get it in small quantities.

Symptoms and flow. Is rare and occurs usually in the absence of clinical symptoms of hyperplasia of hematopoietic organs, but with rapidly progressive pancytopenia. It is characterized by sudden fever appears to 39-40, severe intoxication, sharp pains in the bones and joints.

According to the clinical picture and the composition of peripheral blood resembles aplastic (hypoplastic) anemia stop difference is that when reticulosis still often possible to identify, albeit slight, increase in the lymph nodes and spleen. Against the backdrop of the destroyed bone marrow observed elevated number of reticular elements found primarily in the form of syncytial fragments.

In some cases, acute reticulosis clinically occurs as a form of leukopenic hemocytoblastosis. At post-mortem examination revealed the widespread proliferation of the reticular elements.

Reticulose, flowing with the leading symptom of anemia, occurs mainly in the form of aleukemic option and only in the last stage of the disease in some cases, a transformation in hemocytoblastosis. In the differential diagnosis to exclude tuberculosis, hroniosepsis, hypoplastic anemia, osteodysplasia, chronic hemolytic anemia, malignant neoplasm.

Reticulose, flowing with predominant tumor growths, characteristic of the foreground rapid growth of blood-forming organs from the destruction of surrounding tissues. In this form of leukemia often manifest a symptoms of hemorrhagic pleurisy, pericarditis and ascites due to the infiltrative growth of tumor formation originating from the lymph nodes or other tissue organs hematopoiesis. Flow is subacute. The characteristic features of tumor-like growths are lymph nodes in the form of a conglomerate of various localization, increased liver and spleen, reaching the usually enormous size. This form of reticulosis identified with the reticuloendothelial (lymphocytes) sarcomatosis.

Blood in aleukemic reticulosis is characterized by reduction of red blood, a tendency to moderate leukocytosis, and thrombocytopenia expressed, however, not so sharp degree, as when hemocytoblastosis. Leucogram represented predominantly granulocytic elements or lymphocytes and monocytes, but more often occurs in the shift to single her immature and undifferentiated forms. If puncture of lymph nodes revealed hyperplasia of the reticular pattern of elements, usually represented as a syncytium or cells resembling hemohistioblast and hemocytoblasts.

Bone marrow punctate pattern shows increased immature and undifferentiated forms, but this increase does not adequately ensure what is observed in hemocytoblastosis. The number of mature granulocytes is reduced. Red sprout in most cases narrowed.

Recognition, especially aleukemic form reticulosis, often presents difficulties because of hemogram and myelogram number of undifferentiated elements is small. In order to clarify the diagnosis must take into account the full range of clinical symptoms, perform a thorough differential diagnosis of diseases such as sepsis, neoplastic process, tuberculosis, brucellosis, tularemia, etc.

In favor of the diagnosis of reticulosis indicates violation of one degree or another all haemopoesis according bone marrow, hyperplasia of reticular elements in the lymph nodes when they puncture or biopsy, and resorption of bone tissue and hyperplasia of reticular elements in preparations trepanobiopsy.

Treatment. Prednisolone at 1.5 mg / kg (an average of 80-60 mg / day) for 10-15 days followed by a gradual decrease in dose of 2.5 mg / 2 days to 30-40 mg per day, and that should be applied to the onset of clinical and hematological improvement. At the tumor forms of reticulosis, if they do not fall under the influence of steroid therapy should be to test the action of chemotherapy drugs, such as Cyclophosphamide of 200-400 mg / day. Heading dose varies widely (up to 3 of 6 g or more). Radiotherapy for local 50-200 daily or every other day.

With the development of anemia appoint transfusion of whole blood at 250 ml, or red blood cells of 125 ml. The frequency of transfusion depends on the degree of anemia. Since hemostatic purpose and to stimulate normal hematopoiesis appoint vitamins B2, B6, P, ascorbic acid, calcium preparations.

Hemophilia - a form of hemorrhagic diathesis, in which the tendency to bleeding due to an impaired blood coagulation due to deficiency of plasmic thromboplastin generation.

Etiology and pathogenesis. Hemophilia occurs in the form of congenital, rarely sporadic forms. Hemophiliacs suffer from male carriers of the disease are women.

A-form of Hemophilia associated with the lack anti-hemophilic globulin and occurs in 80-90% of patients with hemophilia.

B-form of Hemophilia is caused by lack of the plasmic thromboplastin component, occurs in 10-15% of patients with hemophilia.

C-form of Hemophilia characterized by lack of plasmic thromboplastin precursor, occurs in approximately 5% of patients with hemophilia.

D-form of Dhemophilia is the lack of Hageman’s factor.

Symptoms and flow. The main importance of hemorrhage in the form of large bruises on the soft tissue and is especially characteristic in the joints with the development of the strain them. Also observed bleeding from the mucous membranes of the mouth, nose, gastrointestinal tract, kidney, arising even for minor injuries, cuts, bruises. In most patients the disease manifests itself at an early age and goes heavily in childhood and adolescence. After 20 years of the disease is becoming calmer.

Recognition is based on laboratory studies, history of disease and typical hemarthrosis symptoms. The sharp slowdown in the blood clotting time, reduced consumption of prothrombin and modified thromboplastin test gives an opportunity to identify violations in the first phase of blood coagulation. Detection of haemophilia by direct determination of the deficit factor or by correlation of the ingredients of donated blood, or vice versa, mixing of donor blood and patient blood. Normalization or change the previously obtained parameters of blood coagulation provides an indication of violation in a link thrombocyte.

Treatment is symptomatic. The most effective are the repeated transfusion of fresh, no more than the daily prescription of blood or plasma by 400-500 ml of ink-jet method. In B-form hemophilia you can transfuse blood and plasma for longer periods of storage, because the plasma thromboplastin component in contrast anti-hemophilic globulin is stable in storage. In order to improve hemostasis prescribe corticosteroids (prednisolone 25-30 mg / day for 2-4 weeks). Anti-hemophilic globulin, isolated in pure form, is the most effective treatment for hemophilia.

By bleeding surface (mucosa of the nose, mouth) should have put hemostatic cotton, sponge, gauze cloth and thrombin or plasma.

When hemarthrosis immobilized limb, apply cold (ice) and a pressure bandage, and further local radiotherapy.

Various surgical interventions in hemophiliacs, including tooth extraction should be carried out in institutions with the use of various preventive measures in the preoperative period, at the time and after the operation. Most of these activities is the use of various hemostatic means - blood transfusion and plasma.

Acute Acquired Hemolytic Anemia

Etiology and pathogenesis. Arise as a result of infections (sepsis, malaria, etc.), intoxications hemolytic poisons (phosphorus, phenylhydrazine, or mushroom, snake venom, etc.), physical factors (cooling, burns). Increased hemolysis arises from the direct effects on red blood cells of the pathogenic factor and as a result of the influence of exogenous factors that lead to the formation of anti-erythrocyte antibodies in the application of certain medicinal substances. Thus, the use of Amidopyrine, Quinine, sulfanilamide and other drugs can lead to the formation of autoantibodies. As a result, connecting them with proteins and blood cells, these substances are autoantigens, causing the formation of antibodies to its own blood cells, including the red cells (heat and cold haemagglutinins, hemolysins, and other antibodies). Autoimmune hemolytic anemia are also observed in collagen disease, malignant tumors, leukemia, chlamydia, etc.

These anemia also arise when incompatible blood transfusion in the group and Rh factor. In such cases, hemolysis develops as a result of isoimmune antibodies that react with transfused red cells.

The presence in serum of patients with red cell antibody positivity recorded Coombs.

Symptoms and flow. The disease is characterized by acute onset. Chills, fever (up to 39-40В°), severe weakness, sometimes dyspeptic symptoms, the yellowness of the skin and visible mucous membranes. Since the cardiovascular system, expansion of the borders of the heart, tachycardia, systolic murmur, hypotension. In severe cases, collapse. In the blood revealed normocytic anemia or macrocytic type, normoeritro-blastosis, increased reticulocytosis, the shift of the blood to the left, increased the number of indirect bilirubin. Spleen and liver increased. The urine protein appears and free hemoglobin, resulting in urine becomes black. In some cases, a picture of thrombosis kidney pigments of red blood cells and debris from the development of severe necrotic changes, leading to anuria and azotemia.

In bone marrow erythroblast sharp reaction.

Recognition is based on progress of acute hemolytic anemia type, the presence of erythroblastic reaction in the bone marrow. The immune form of acute hemolytic anemia, Coombs’ positive test is confirmed. Acute hemolytic anemia in some cases have to differentiate with erythroleukemia. In favor of hemolytic anemia by the absence of gemotsitoblastnoy hyperplasia and higher reticulocytosis.

Treatment. The best effect was given with steroid hormones used in middle and high doses (30-60 mg daily) in combination with blood transfusions. When you take into account the hormonal preparation of the patient. At inclinations to violate water-salt metabolism is useful to apply triamsinolon and dexamethasone, in disorders of nitrogen metabolism and osteoporosis - prednisone or prednisolone. In acute and massive hemolysis, which is comparable with the action of corticosteroid therapy, shown splenectomy.

When the primary decrease in arterial hypotension and venous pressure is determined dysfunction neurohumoral system, regulating vascular tone. Secondary hypotension observed as a symptom with various infectious diseases and intoxications, ulcers and Addison’s disease.

Symptoms and flow. Complaints may be absent. Frequently observed functional disorders of the nervous and cardiovascular systems, as manifested by headaches, dizziness, general weakness, irritability, there are unpleasant sensations and pain in the heart, palpitations, sweating. Arterial and venous pressure is lowered (blood pressure 100/50 - 80/40 mm Hg. Art., Venous pressure below 80-60 mm of water. st.).

Periodically observed hypotonic crises, manifested in the sharp decline of strength, dizziness, bradycardia, failure of coronary circulation.

Treatment. Restorative and tonics (Strychnine, Caffeine, Ephedrine, Ginseng), therapeutic exercise. Nutrition with plenty of vitamins.

With persistent hypotension and no effect on the tonic treatment - intramuscular injections of 0.5% solution of Deoxycorticosterone Acetate and 1 ml daily in an amount of 10-15 injections per course of treatment.

Thalassemia

Etiology and pathogenesis. The disease is inherited family trait the predominance of red blood cells of fetal embryonic hemoglobin.

Symptoms and flow. There are large, small and minimal thalassemia. The first form of thalassemia in children-homozygotes, the latter two forms a child of heterozygotes. A typical symptom for thalassemia major is a progressive anemia with erythroblastosis, enlarged spleen and liver, osteoporosis, with peculiar changes in bones of the skull (disproportionate proliferation of parietal and occiput) as a consequence of abnormal proliferation of erythroblastic germ in the bone marrow. In the blood, anemia with eritroblastos, the presence of peculiar some special erythrocytes with increasing maximum and minimum simultaneously with a decrease in osmotic resistance.

In bone marrow at the background of general hyperplasia of cellular elements show an increase in red growth and a slight increase in the number of reticular cells. In the liver and spleen are determined extramedullary foci of erythropoiesis and leucopoiesis.

Treatment. In order to avoid the development of hemosiderosis hematherapy shown only when hemolytic crisis. Steroid hormones give temporary success. Splenectomy is effective not in all cases, and after the operation in the blood remain some special erythrocytes.

Sickle Cell Anemia

Etiology. The disease is congenital inferiority of red blood cells associated with the presence in the past to 60-90% of pathological hemoglobin S. Develops in children with homozygotes. Children heterozygote, inherited trait camber from one of the parents are carriers of sickle-cell abnormalities. Symptom of camber in red blood cells due to low solubility of hemoglobin S and its crystallization. Sickle-shaped red blood cells differ increased resistance to hypotonic solutions of sodium chloride.

Symptoms are similar to the pattern of congenital microspherocytic hemolytic anemia. Observed congenital defects of bones: skull tower, high sky. There is a tendency to osteoporosis in the bones, in the bones of the skull revealed subulate appendages. In the blood, anemia, bilirubinemia, increased urobilin in urine and stercobilin in feces. The disease is characterized by an undulating course, hemolytic crises are replaced by remissions. In the gallbladder pigment stones. In many cases, developed splenomegaly. A number of patients in the period of increased hemolysis appears a tendency to thrombosis of small vessels of various organs.

Recognition is based on the type of hemolytic anemia with the presence of peculiar crescent-shaped red blood cells and the application of special tests on the camber of red blood cells (with metabilsulfitom).

Treatment. During the period of anemia required blood transfusions. In marked splenomegaly, and especially the development of the spleen infarctions shown splenectomy.

Tendosynovitis - diseases of tendons and tendon sheaths. Generally affecting the extensor tendons of the muscles of hand and foot going through the narrow bone-fibrous feeds. As a consequence, the tendons exposed to minor trauma that leads to the development of the synovial membrane of a small tendon inflammation, which later can turn into chronic and lead to compaction and stenosis of the tendon.

Tendosynovitis of the hands develops mainly in women engaged in manual labor (dressmakers, typists, pianists, etc.). Is usually found in the long adductor tendon and the short extensor muscle of thumb, which manifests itself with pain in the area subulate appendages radiating to the thumb and the outer surface of the forearm. Pain intensifies under pressure, as well as abduction and extension of the thumb. Movement in the radiocarpal joint is free and painless. When moving the thumb and the wrist sometimes hear a small, dull crackling. In the transition to a chronic form develops chronic constrictive tendovaginitis (de Quervain’s disease) with fibrosis of the tendon and the formation of subulate appendages oblong, dense, sedentary and painless swelling. Movement of the thumb sharply painful. The X-ray sometimes with small Haygarth’s nodes in the subulate appendages radius.

Current chronic disease with a duration of several weeks to several months, and then (especially after wrist immobilization in a plaster bus) usually comes healing.

Tendosynovitis of the foot is rare. Arises as a result of microtrauma, cooling, muscle overexertion, vasomotor disturbances. Most often affects the tendons of the long common extensor of the fingers and anterior tibial muscles. In mild form, there are only a small hyperemia, but clinically small embarrassment and mild crepitus with motion in the foot. In the formation of effusion arises oblong painful, sometimes fluctuating swelling along the tendon. The course is favorable, but sometimes synovitis may pass into the chronic form. In these cases, the motion of the foot are difficult and painful on palpation feel the thickened tendon and sealed.

Recognition. Based on the presence of pain while reducing the individual muscle tendons, and these pains are localized outside the joint, passive movements which are usually free and painless. It is also probing compacted and painful tendons. For the differential diagnosis in relation to arthritis, it is important to the absence of inflammation in the joint (periarticular tissue swelling, effusion in the joint cavity, his pain on palpation and movement) and normal X-ray of the joint.

Treatment. Immobilization of the joint, the best in the cast. For pain use analgesics (Acetylsalicylic acid, Dipyrone and others), radiotherapy, local Hydrocortisone or Procaine (injections). In the absence of improvement (fibrosis tendon) is recommended surgery.

Endemic deforming arthritis - generalized osteoarthritis deformans with profound violation of the ossification process. Origin is unknown. It is believed that matter eating cereals contaminated by the fungus Fusarium sporotrichiella, or lack of calcium in water and soil. Well, they get children 6-14 years old. In the epiphysis of tubular bones develops a deep degenerative process (necrosis of cartilage, changes in articular surfaces with abundant marginal bone growths), leading to significant disfigurement of joints and bone dysplasia (short fingers, short stature).

Symptoms and flow. Characterized by slow progression of the disease with the gradual development of strains of small and large joints, the elbow flexion contracture, muscle atrophy, lordosis lumbar spine, stubby and short stature. Sometimes in a joint are severe pain and limitation of movement due to infringement of free intraarticular bodies - pieces of necrotic cartilage. Inflammatory changes in the joints are absent. Temperature and blood picture normal.

The X-ray - disfigurement and changing pattern spongy substance, epiphyses, flattening of joint surfaces, expressed Haygarth’s nodes.

Recognition on the basis of endemic disease, chronic progressive course, multiple strains of joints with stubby and stop the growth of the patient, the typical X-ray pictures.

Treatment. In order to reduce pain and improve function of joints used methods of physiotherapy and balneotherapy - general radon and hydrogen sulfide baths, paraffin and mud wraps. Effective treatment with brine and radioactive baths. In the early stages of the disease used fish oils, preparations of calcium and phosphorus (Calcium gluconate at 0.5 g 3-4 times a day, Phytin 0,5 g to 3 times a day).

Etiology and pathogenesis are not sufficiently clear. It is assumed that this common infectious-allergic disease associated with the presence in the body the focus of chronic infection (chronic tonsillitis, otitis, cholecystitis, etc.). Continuous flow in the blood of toxins from the infection focus leads to a change in immunological reactivity and the development of allergy. In the process of disorganization of connective tissue (mainly tissue of the joints), released a number of substances purchased properties autoantigens, against which antibodies are formed and the whole process takes autoimmune in nature, manifested by persistent, progressive course. In the blood of patients with infectious arthritis, there is a special macro globulin (rheumatoid factor), reinforcing agglutination, quite specific for this disease.

Symptoms and flow. The clinic is characterized by an unusually persistent and progressive chronic polyarthritis with a pronounced tendency to exacerbations. Are affected primarily the small joints of hands and feet (mostly middle interphalangeal), then the knees, wrist and all the other joints. Disease is often preceded by angina, influenza, cooling. The disease onset may be acute, the type of acute rheumatoid arthritis, but more often the disease begins and flows with subacute subfebrile temperature and low inflammation in the joints in the form of swelling, flushing and increased skin temperature, effusion into the cavity of the joint, pain on palpation of joints and movements . Later in the joints gradually develop proliferative effects, tissue of the joints are sealed, there are resistant strains due to the development of contractures, bursitis and subluxations of the joints. Function of the joints progressively worse until the complete ankylosis. At the same time near the affected joints develop pronounced muscle atrophy, trophic skin changes (thinning of the dryness), and nails. Under the skin of the forearm near the elbow sometimes form characteristic dense, painless education about the size of a pea (rheumatoid nodules).

On chest radiographs in the first (early) stages of osteoporosis epiphyses of bones found in the second - narrowing of the gap and the glenoid articular surfaces Uzury single in the third - Multiple Uzury, sometimes destroying the heads of bone subluxation, and the fourth (terminal) stage - the bone ankylosis. The edges of articular surfaces can be observed small Exostoses - the phenomenon of secondary osteoarthritis. In addition to joint damage, with Infectious arthritis may extraarticular lesions, most often in the form of Adenopathy, a small increase in the liver and spleen. There may also be observed pleurisy (pericarditis, peritonitis), generalized vasculitis (petechial rash, ecchymosis, bleeding), lung (focal or chronic interstitial pneumonia), heart (myocardial dystrophy, cardio with prolonged sluggish flow, sometimes with the formation of heart disease - lack mitral valve), the nervous system (from functional disorders to severe polyneuritis). Most importantly, renal damage type or focal nephritis, or, more often, the development of amyloidosis with renal failure and uremia, which is one of the causes of death in these patients.

The most difficult proceeds articular-visceral form with septic flow, which is based on generalized vasculitis. However, except for arthritis and multiple lesions of internal organs, there is a fever hectic type, a stunning chill and pouring sweat. The disease in this form of rapidly progressive and can result in the death of the patient within 1-2 years.

Combined form, when the disease takes place against a background of primary osteoarthritis, the most favorable. Characterized by small inflammation, slow progression and not sharp restriction of the joints. Infectious arthritis can also develop in patients with rheumatic diseases.

One of the clinical variants of the flow Infectious arthritis with the localization process in the small joints of the spine is Bechterew’s disease (ankylosing spondylitis, spondyloarthritis). Ill usually young men, and the process begins with the defeat of the sacroiliac joints and then spreads to the spine, hip and shoulder joints. Peripheral joints, which develop inflammation typical Infectious arthritis with outcome in ankylosis, are affected less frequently (in 20 - 25% of cases). Bechterew’s disease is manifested clinically severe pain and restriction of movements in the spine, the development of kyphosis, reduced lumbar lordosis, sciatica secondary phenomenon due to compression of nerve roots and, finally, complete immobility of the spine, and sometimes the large joints.

At first radiograph revealed changes in the sacroiliac joint, narrowing, and then the complete closure of the articular gap, more symmetrical ossification of longitudinal ligament of the spine and signs of ankylosis in the vertebral-rib joints. When ossification of ligaments and vertebral bodies, spinal fusion takes the form of a bamboo stick.

Etiology and pathogenesis. There is a neurosis regulating blood pressure points, leading to increased muscle tone of the arterial wall, narrowing of the lumen of small arteries and arterioles and increase blood pressure. Trigger a strain neuro-psychological sphere. For secondary mechanisms include renal ischemic and endocrine factors. Ischemia kidney juxtaglomerular apparatus allocates renin, which ultimately leads to increased blood pressure.

Increased secretion of aldosterone leading to sodium retention and accumulation of fluid in the walls of arterioles, which narrows their lumen and increases the pressure.

Symptoms and flow. Hypertensive heart disease is a chronic disease with different clinical manifestations depending on the stage of disease and predominant vascular lesions of the heart, brain and kidneys. There are three stages.

In the phase A of the I stage, blood pressure increased from time to time under the influence of negative emotions, nerve strain, cold, etc. In phase B are occasionally observed hypertensive crises, intermittent spasms of cerebral and coronary arteries. Subjective feelings can be absent or expressed in complaints of pain in the heart of a stabbing or aching character. Violations of the nervous system results in headaches, dizziness, insomnia, increased irritability, autonomic disorders - in sweat, expressed dermographism, etc.

Stage II of constant increase in blood pressure. It is unstable in the phase A, in the future (Phase B) blood pressure persistently elevated to significant digits. Subjective feelings are growing, declining productivity, were frequent hypertensive crises with strokes and cerebral blood flow due to spasm of blood vessels. Objectively determined left ventricular hypertrophy, accentuation of the second tone of the aorta, systolic noise on top. Reduces renal blood flow. Due to changes in the permeability of the renal vessels in the urine may appear white, red cells, hyaline cylinders. Changes in fundus expressed in narrowing and tortuosity of arteries, venous stasis.

Developing for stage II, mainly coronary atherosclerosis and cerebral vascular compounded stage III disease. It consistently high blood pressure often decreases after emerging myocardial infarction and stroke.

Grave prognostic significance is an isolated reduction in systolic blood pressure ( “decapitated” hypertension), which is due to the weakness of the heart muscle.

Rapidly progressive (malignant) variant of hypertensive disease occurs predominantly in young persons.

One of the first symptoms of the disease is impairment up to complete its loss. In the study of fundus hemorrhage set against the backdrop of papilledema and retina.

The most common form of cerebral expressed in persistent headaches, often accompanied by vomiting. Frequent violations of cerebral circulation and strokes due to bleeding into the brain.

Cardiac form manifests severe coronary insufficiency with attacks of angina, cardiac asthma, recurrent myocardial infarction.

Renal form is characterized by rapidly increasing renal insufficiency with an increase in blood residual nitrogen, oliguria and a clinical picture of uremia.

For the flow of a malignant variant is characterized by frequent crises.

Rapidly emerging weakness of the left ventricle entails bouts: cardiac asthma.

In stage III on the background of naturally developing atherosclerosis of the coronary vessels and vessels of the brain revealed severe functional and organic disorders of the heart and central nervous system. In the terminal stage of frequent crises, occurring with disorders of cerebral circulation (arteries spasm and thrombosis, hemorrhage as a result of atherosclerosis). As a result of scarring revealed renal insufficiency with a decrease in the proportion of urine, an increase in residual nitrogen of blood.

Chronic Posthemorrhagic Anemia is also known as Thalassemia or Cooley’s Anaemia.

Etiology. Arises as a result of repeated bleeding for a long period.

Symptoms and flow is characterized by gradually developing weakness, shortness of breath with movements, heart palpitations, dizziness. Pale skin and visible mucous membranes. The picture of blood to the forefront decline in hemoglobin and red blood cells. As a result of chronic bleeding there is increased loss of body iron stores, which affects a hypochromia of erythrocytes and thus to reduce the color index of blood to 0,6-0,7. Reveals the degenerative forms of erythrocytes: poykilotsity, anizotsity. The number of reticulocytes increased to 2-3%, Leukopenia. The platelet count remained within normal limits. In bone marrow increased erythrocyte germ, which increases the number of basophilic and polychromatic forms. Chronic hemorrhagic anemia is often hypo-regenerative.

Recognition is not difficult. More difficult are cases of blood loss from internal organs, particularly bleeding ulcers and tumors of the gastrointestinal tract. Chronic hemorrhagic anemia need to differentiate from sepsis, systemic neoplasm and chronic atrophic process (reticulosis, myeloma). Necessary to consider the data history for the presence of nasal bleeding, uterine, from the gastrointestinal tract.

Haemogram indicates a more or less than the combined reduction of hemoglobin and red blood cells, in contrast to iron deficiency anemia, in-which becomes more pronounced decrease in hemoglobin, and in contrast to the B12-deficient anemia, which is the most reduced number of red blood cells. When adenopathy and increased spleen size should be excluded hyperplastic leukemic process (aleukemic reticulosis).

Treatment is direct to remove the causes of bleeding, and then to the appointment of anti-anemia (transfusion of whole blood or red blood cells), the use of substances that stimulate hematopoiesis, substances, which are plastic materials needed to process blood. Vitamin B, C, iron, and liver medicines.