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Mild, moderate and severe anemia. Anemia - symptoms, causes, types, treatment and prevention of anemia Moderate anemia treatment drugs

Anemia is a decrease in the number of red blood cells (erythrocytes) in the blood below 4.0x109/l, or a decrease in hemoglobin level below 130 g/l in men and below 120 g/l in women. Anemia during pregnancy is characterized by a decrease in hemoglobin below 110 g/l.

This is not an independent disease; anemia occurs as a syndrome in a number of diseases and leads to disruption of the oxygen supply to all organs and tissues of the body, which, in turn, provokes the development of many other diseases and pathological conditions.

Severity

Depending on the concentration of hemoglobin, it is customary to distinguish three degrees of severity of anemia:

Grade 1 anemia is registered when the hemoglobin level decreases by more than 20% of the normal value;
anemia of the 2nd degree is characterized by a decrease in hemoglobin content by approximately 20−40% of the normal level;
Anemia of the 3rd degree is the most severe form of the disease, when hemoglobin decreases by more than 40% of the normal value.

Only a blood test can clearly show that a patient has stage 1 or a more severe stage.

Reasons

What is it: anemia, that is, anemia, is nothing more than. Namely, hemoglobin carries oxygen throughout all tissues of the body. That is, anemia is caused precisely by a lack of oxygen in the cells of all organs and systems.

Nature of nutrition. With insufficient consumption of iron-containing foods, it can develop, this is more typical for population groups where there is already a high level of nutritional anemia;
Disturbances in the gastrointestinal tract (in case of disturbances in the absorption process). Since iron absorption occurs in the stomach and upper part of the small intestine, if the absorption process is disrupted by the mucous membrane of the digestive tract, this disease develops.
Chronic blood loss (gastrointestinal bleeding, nosebleeds, hemoptysis, hematuria, uterine bleeding). Belongs to one of the most important causes of iron deficiency conditions.

Iron deficiency anemia

The most common form of anemia. It is based on a violation of the synthesis of hemoglobin (oxygen carrier) due to iron deficiency. It is manifested by dizziness, flickering of spots before the eyes, and palpitations. Dry skin, pallor,... Typical manifestations There are brittle and layered nails, and they have pepper striations.

Aplastic anemia

This is often an acquired acute, subacute or chronic disease of the blood system, which is based on a violation of the hematopoietic function of the bone marrow, namely sharp decline its ability to produce blood cells.

Sometimes aplastic anemia begins acutely and develops quickly. But more often, the disease occurs gradually and does not manifest itself with clear symptoms for quite a long time. The symptoms of aplastic anemia include all the symptoms characteristic of, and.

B12 deficiency anemia

Occurs when there is a lack of vitamin B12 in the body, which is necessary for the growth and maturation of red blood cells in bone marrow, as well as for the proper functioning of the nervous system. For this reason, one of the distinctive symptoms Vitamin B12 deficiency anemia causes tingling and numbness in the fingers and an unsteady gait.

Hemolysis occurs under the influence of antibodies. These may be maternal antibodies directed against the child’s red blood cells if the child and mother are incompatible with the Rh antigen and, much less frequently, with the ABO system antigens. Antibodies against one's own red blood cells can be active at normal temperatures or only when cooled.

They can appear without apparent reason or due to the fixation on erythrocytes of incomplete antigens-haptens foreign to the body.

Signs

We list the main signs of anemia that can worry a person.

pale skin;
increased heart rate and breathing;
fatigue;
dizziness;
tinnitus;
spots in the eyes;
muscle weakness;
difficulty concentrating;
irritability;
lethargy;
slight increase in temperature.

Symptoms of anemia

Among the symptoms of anemia, the leading ones are those directly related to hypoxia. Degree clinical manifestations depends on the severity of the decrease in hemoglobin number.

With a mild degree (hemoglobin level 115-90 g/l), general weakness, increased fatigue, and decreased concentration may be observed.
With moderate levels (90-70 g/l), patients complain of shortness of breath, rapid heartbeat, frequent headaches, sleep disturbances, tinnitus, decreased appetite, and lack of sexual desire. Patients are distinguished by pale skin.
In case severe(hemoglobin less than 70 g/l) develop.

With anemia, in many cases there are no symptoms. The disease can only be detected through laboratory blood tests.

Diagnosis of the disease

In order to understand how to treat anemia, it is important to determine its type and the cause of its development. The main diagnostic method of this disease is a study of the patient's blood.

Are considered:

for men 130-160 grams per liter of blood.
for women 120-147 g/l.
for pregnant women, the lower limit of the norm is 110 g/l.

Treatment of anemia

Naturally, methods of treating anemia differ radically depending on the type of anemia, its cause and severity. But the basic principle of treating anemia of any kind is the same - it is necessary to fight the cause that caused the decrease in hemoglobin.

If you have anemia caused by blood loss, you need to stop the bleeding as quickly as possible. In case of large blood loss that threatens life, donor blood transfusion is used.
For iron deficiency anemia, you should eat foods rich in iron, vitamin B12 and folic acid (they improve iron absorption and hematopoietic processes); your doctor may also prescribe medications containing these substances. Folk remedies are often effective.
For anemia caused by infectious diseases and intoxication, it is necessary to treat the underlying disease, conduct urgent measures to detoxify the body.

In case of anemia, an important condition for treatment is a healthy lifestyle - correct balanced diet, alternating loads and rest. It is also necessary to avoid contact with chemical or toxic substances and petroleum products.

Nutrition

An important component of treatment is a diet with foods rich in substances and microelements that are necessary for the process of hematopoiesis. What foods should be eaten for anemia in a child and an adult? Here is the list:

meat, sausages;
offal - especially liver;
fish;
egg yolks;
whole grain flour products;
seeds - pumpkin, sunflower, sesame;
nuts - especially pistachios;
spinach, cabbage, Brussels sprouts, fennel, parsley leaves;
beet;
black currant;
sprouts, wheat germ;
apricots, prunes, figs, dates;

You should avoid drinking drinks containing caffeine (for example, tea, coffee, cola), especially during meals, because caffeine interferes with iron absorption.

Iron supplements for anemia

Iron supplements for anemia are much more effective. The absorption of this microelement in the digestive tract from iron preparations is 15-20 times higher than from food.

This allows you to effectively use iron supplements for anemia: quickly increase hemoglobin, restore iron reserves, eliminate general weakness, fatigue and other symptoms.

Ferretab composite (0154g ferrous fumarate and 0.0005g folic acid). Additionally, it is advisable to take ascorbic acid in a daily dose of 0.2-0.3 g).
(0.32 g of ferrous sulfate and 0.06 g of vitamin C) is available in pills, daily dosage depending on the degree of anemia, 2-3 times a day.
Totema - available in 10 milliliter bottles, the content of elements is the same as in the sorbifer. It is used internally, can be diluted with water, it can be prescribed for intolerance to tablet forms of iron. Daily dose 1-2 doses.
(0.15g, ferrous sulfate, 0.05g vitamin C, vitamins B2, B6, 0.005g calcium pantothenate.
Vitamin B12 in 1 ml ampoules of 0.02% and 0.05%.
Folic acid in tablets 1 mg.
Ampoule iron preparations for intramuscular and intravenous administration are sold only by prescription and require injections only in hospital settings due to the high frequency of allergic reactions to these drugs.

You should not take iron supplements together with medications that reduce their absorption: Levomycytin, Calcium supplements, Tetracyclines, Antacids. As a rule, iron supplements are prescribed before meals if medicine no vitamin C required additional dose ascorbic acid in a daily dose of 0.2-0.3 g.

For each patient, the daily requirement for iron is specially calculated, as well as the duration of the course of treatment, and the absorption of the specific drug prescribed and the iron content in it are taken into account. Usually long courses of treatment are prescribed, therapeutic doses are taken for 1.5-2 months, and prophylactic doses are taken in the next 2-3 months.

Consequences

Iron deficiency anemia untreated early stage, may have severe consequences. Severe degree progresses to heart failure associated with,. Sometimes people end up in the hospital with a sudden loss of consciousness, the cause of which is undertreated or not detected in time anemia.

Therefore, if you suspect this disease or are prone to low hemoglobin, then it is worth taking a control blood test every three months.

Materials are presented from the RUDN textbook

Anemia. Clinic, diagnosis and treatment / Stuklov N.I., Alpidovsky V.K., Ogurtsov P.P. – M.: Medical Information Agency LLC, 2013. – 264 p.

Copying and reproducing materials without indicating the authors is prohibited and is punishable by law.

Anemia or anemia is a pathological condition that is characterized by a decrease in hemoglobin content, the number of red blood cells and/or hematocrit level per unit volume of circulating blood. With true anemia, a decrease in hemoglobin content and the number of red blood cells corresponds to a decrease in the mass of circulating red blood cells, and due to a compensatory increase in the amount of plasma, the total volume of circulating blood does not change significantly. The exception is anemia after acute blood loss, in which there is a simultaneous, rapid decrease in both the mass of circulating red blood cells and the volume of circulating plasma. In men, the lower limit of H concentration b corresponds to 130 g/l, for women – 120 g/l.

One should distinguish from true anemia relative anemia or so-called false anemia, in which a decrease in hemoglobin levels is caused not by a decrease in red blood cell mass, but by an increase in the volume of circulating plasma or a kind of dilution of the blood. “False anemia,” which cannot be considered as a result of a violation of erythropoiesis or erythron disease, can be observed both during pregnancy (hydremia of pregnancy) and with fluid retention in patients with the oliguric form of renal failure, in patients with severe circulatory failure, in some chronic diseases, occurring with hypoalbuminemia, liver cirrhosis and splenomegaly of various origins. So currently, the normal hemoglobin concentration during pregnancy is considered to be 110 g/l in the first and third trimesters and 105 g/l in the second.

The clinical manifestations of anemia are determined by a number of factors: the degree of anemia, the speed of its development, the characteristics of the underlying disease that caused the onset of anemia, the adaptive abilities of the cardiovascular and pulmonary systems of the body, and the age of the patient. With the gradual development of anemia, a decrease in hemoglobin level to 80 g/l is often not accompanied by any pathological symptoms and the patient’s state of health remains quite satisfactory. On the contrary, acute blood loss at the same level of hemoglobin can cause the development of shock due to rapidly occurring hypovolemia.

Classification of anemia by severity

Lightweight– hemoglobin level above 90 g/l;

Moderate– hemoglobin within 90 – 70 g/l;

Heavy– hemoglobin level less than 70 g/l.

Depending on the origin, symptoms common to all types of anemia can be divided into two groups:

1. symptoms due to functioning compensatory mechanisms aimed at preventing or reducing tissue hypoxia;

2. symptoms directly related to tissue hypoxia.

The symptoms of the first group, which predominate in the clinical picture of anemia, include pallor of the skin, tachycardia, the appearance of hemodynamic noise, a feeling of lack of air, shortness of breath and other signs of cardiovascular failure.

Pale skin, which appears when the hemoglobin level decreases to 70 g/l, is often the first symptom that forces a patient with anemia to consult a doctor. Paleness of the skin develops as a result of capillary spasm, which is part of the redistribution adaptation mechanism aimed at improving blood supply to vital important organs. It should be remembered that jaundice, cyanosis and skin pigmentation can mask the pallor of the skin during anemia, so pallor of the oral mucosa, upper palate, conjunctiva, lips and nail bed is more demonstrative.

With anemia, the heart responds to a decrease in the ability of blood to bind and carry oxygen by increasing cardiac output, which is clinically manifested by tachycardia, increased arterial and capillary pulsation and the appearance of hemodynamic murmurs: systolic, which is better heard at the apex of the heart and pulmonary artery, and less often – diastolic. Normal myocardium can tolerate long-term increased loads caused by anemia. However, profound anemia, in which the oxygen needs of the heart muscle are not fully satisfied, may be accompanied by pain in the heart area, cardiomegaly, shortness of breath, signs of pulmonary congestion and edema. It should be noted that increased breathing and shortness of breath appear long before the development of heart failure and are a consequence of a compensatory increase in lung function in response to hypoxia and hypercapnia of the respiratory center.

Despite the mobilization of compensatory mechanisms, with severe anemia tissue hypoxia still develops, to which the brain is especially sensitive. Insufficient oxygen supply to the brain is manifested by weakness, increased fatigue, headache, muscle cramps, dizziness and the appearance of “floaters” before the eyes.

To characterize anemia, morphological signs of red blood cells and the number of reticulocytes are used, the combination of which makes it possible with a high degree of probability to suggest the cause of the development of anemia, take action for further examination and the most effective therapy.

Morphological classification of anemia

Classification of anemia by red blood cell volume

I. Macrocytic anemia (MCV > 100 fL, erythrocyte diameter > 8 µm) – deficiency of vitamin B 12 and folic acid, liver disease, myelodysplastic syndrome (MDS).

II. Microcytic anemia (MCV)<80 фл, диаметр эритроцитов < 6 мкм) – дефицит железа, нарушения синтеза глобина, нарушение синтеза порфирина и гема.

III. Normocytic anemia (MCV 80–100 fL, erythrocyte diameter 6–8 μm) – acute blood loss, hemolysis of unchanged erythrocytes, aplastic anemia, decreased production of erythrocytes in bone marrow failure (erythropoietin-dependent anemia) – anemia of chronic disease (ACD) and chronic renal failure . ACB are most often found in infectious diseases, systemic collagenosis, and malignant tumors (anemia of malignant disease - ACD).

Classification of anemia according to the hemoglobin content in the erythrocyte (MSI indicator,color index - CPU)

I. Hypochromic anemia (MSI color index< 0,8) – железодефицитная анемия, сидероахрестическая анемия, талассемии.

II. Anemia is normochromic, color index 0.8 - 1.05 - anemia in chronic renal failure (CRF), aplastic anemia, anemia in liver diseases, acute post-hemorrhagic anemia.

III. Hyperchromic anemia, color index > 1.05 – B 12-deficiency anemia, folate deficiency anemia.

Classification of anemia depending on the ability of bone marrow to regenerate

I. Regenerative form of anemia (with sufficient compensatory activation of bone marrow function) - reticulocytes more than 12 ‰ (hemolytic anemia, acute posthemorrhagic anemia, regenerative stage of iron deficiency anemia, reticulocyte crisis in the treatment of pernicious anemia with vitamin B 12).

II. Hyporegenerative form of anemia(with inadequate reduced regenerative function of the bone marrow) – reticulocytes 2 – 12‰ (erythropoietin-dependent anemia - ACHB, ADN, hyporegenerative stage of iron deficiency anemia).

III. Hypoplastic or aplastic formanemia (with a sharp inhibition of erythropoiesis processes) – reticulocytes less than 2‰ (vitamin B 12, folate deficiency anemia, erythropoietin-dependent anemia - chronic renal failure anemia).

Correct use of MCH or CPU and MS indicators V helps to most simply and quickly determine the cause of a decrease in hemoglobin. B85 – 90% of cases hypochromic anemia indicates iron deficiency anemia. Anemia with a normal volume of red blood cells and a normal content of hemoglobin in red blood cells allows us to exclude almost all hereditary hemoglobinopathies and membranopathies. Hyperchromic and macrocytic anemias most often occur with a deficiency of vitamins B 12 and folic acid, sometimes requiring the exclusion of MDS. Severe reticulocytosis (more than 100‰ ), mainly associated with active hemolysis, reticulocytosis 20 – 100‰, as a rule, due to the reparative activity of the bone marrow after blood loss (peptic ulcer of the stomach, duodenum, menometrorrhagia). Reticulocytosis more than 100‰ in combination with hypochromia and microcytosis almost unambiguously indicates hereditary hemolytic anemia (when combined with jaundice, increased indirect bilirubin and splenomegaly). On the contrary, with inadequate activity of erythropoiesis - hypo- and regenerative anemia, the presence of ACHD, ADN, and chronic renal failure is most likely.

The most accurate assessment of the nature of anemia is possible when known reason and the mechanism of its development. Understanding such processes makes it possible to prevent the development of anemia, stop the progression of the disease and carry out adequate therapeutic measures. To optimize diagnostic and therapeutic approaches, a pathogenetic or etiopathogenetic classification of anemia has been developed.

Pathogenetic (etiopathogenetic) classification of anemia

I. Anemia due to predominantly impaired red blood cell production

A. Anemia caused by impaired erythropoiesis at the level of early erythropoiesis precursors and stem cells

1. Aplastic anemia

2. Myelodysplastic syndrome

3. Partial red cell aplasia

B. Anemia caused by impaired erythropoiesis at the level of morphologically distinguishable erythropoietic progenitor cells.

1. Anemia caused by impaired DNA synthesis (megaloblastic)

- In 12 - deficiency anemia, folate deficiency anemia:

due to reduced dietary intake;

due to impaired absorption;

due to impaired transport and metabolism;

due to increased consumption.

- Megaloblastic anemia not associated with vitamin B12 or folate deficiency.

2. Anemia caused by impaired heme synthesis

- iron deficiency anemia;

- anemia due to impaired porphyrin metabolism – sideroachrestic (hereditary and acquired).

3. Erythropoietin dependent anemia

- anemia in chronic renal failure.

4. Anemia due to multiple and/or unknown causes

- anemia of chronic disease;

- anemia of malignant disease;

- anemia of pregnancy;

- anemia due to diseases of the thyroid gland, pituitary gland, adrenal glands;

- anemia due to protein deficiency (kwashiorkor);

- anemia due to bone marrow infiltration (leukemia, tumor metastases, lymphomas).

II. Anemia due to increased destruction of red blood cells

A. Anemia caused by defective red blood cells themselves (usually hereditary)

1. Hemolytic anemia associated with disruption of the red blood cell membrane (membranopathy)

- hereditary spherocytosis (Minkowski-Schaffard disease);

- hereditary elliptocytosis;

- hereditary stomatocytosis;

- hereditary acanthocytosis;

- paroxysmal nocturnal hemoglobinuria (Marchiaf-Micheli disease).

2. Hemolytic anemia associated with impaired activity of erythrocyte enzymes (enzymopathies)

- hemolytic anemia due to a deficiency in the activity of enzymes of glycolysis (pyruvate kinase), the glutathione cycle and those involved in the use of ATP;

- hemolytic anemia with deficiency of the activity of enzymes of the pentose phosphate cycle (G-6-FDG, GFGD).

3. Hemolytic anemia associated with the presence of abnormal hemoglobin in red blood cells - qualitative hemoglobinopathies

- sickle cell anemia;

- anemia with other stable abnormal hemoglobins ( c, d, e, etc.);

- anemia caused by carriage of unstable hemoglobins;

- hemoglobinopathies-M, caused by amino acid substitution in the hemin pocket, which causes an increased affinity for oxygen and is clinically manifested by cyanosis and erythrocytosis.

4. Anemia caused by impaired synthesis normal hemoglobins due to a defect in the synthesis of α- and β-chains of globin (homozygous α- and β-thalassemia) - quantitative hemoglobinopathies.

B. Anemia developing as a result of extra-erythrocyte effects (more often acquired)

1. Antibody-associated hemolytic anemias

- isoimmune anemia: hemolytic disease of the newborn, post-transfusion hemolytic anemia

- autoimmune hemolytic anemia.

2. Hemolytic anemia associated with mechanical damage to red blood cells

- March hemoglobinuria;

- hemolytic anemia in pathology of vessels of medium and large diameter;

- microangiopathic hemolytic anemia (thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome, atypical hemolytic-uremic syndrome).

4. Anemia due to poisoning with hemolytic poisons

5. Hemolytic anemia caused by increased sequestration by cells of the phagocytic mononuclear cell system

- anemia in acute infections;

- anemia due to hypersplenism.

III. Anemia due to acute blood loss (posthemorrhagic anemia)

1. Acute posthemorrhagic anemia;

2. Chronic posthemorrhagic anemia.

Anemia of the 2nd degree is a blood condition in the human body with a low level of hemoglobin, a substance that is part of red blood cells. It performs the respiratory function of the human body on cellular level. Oxygen entering through the lungs is absorbed into the blood and tends to form compounds with hemoglobin and be transported with it to each cell. In return, hemoglobin takes carbon dioxide from the cell and returns it to the lungs, thereby performing gas exchange in the body.

Causes and dangers of low hemoglobin

A decrease in hemoglobin disrupts the gas exchange process, which affects all vital processes in the body. Anemia may result medium degree gravity. This is an intermediate stage, between mild and severe, and moderate anemia is very important.

This is explained as follows:

With a mild degree of anemia, a person’s condition often does not give noticeable signs of this condition, and only in the blood can one see a decrease in the level of hemoglobin, this is 110 - 90 g/l.
The second is the average degree, in which a person experiences symptoms of anemia, a blood test will show hemoglobin levels of 90 - 70 g/l.
If this period is missed and anemia is not treated, then severe third degree occurs, in which irreversible consequences develop. At this degree, the hemoglobin level in the blood will be less than 70 g/l.

There are many reasons that affect the composition of the blood and contribute to the occurrence of anemia. They can be individual for each type and form of the disease.

But there are common ones that unite all varieties:

acute or chronic blood loss;
shortening the life cycle of red blood cells;
failure of the bone marrow to perform its functions.

At normal composition blood anemia can occur due to blood loss. This occurs due to damage to the skin and mucous membranes by various factors. Injuries and surgical interventions can lead to significant, acute loss blood.

Donors experience blood loss from donating it to small quantities, unable to harm them. In this case, the normal state of a person is quickly restored. With chronic bleeding, there is a constant, seemingly imperceptible, loss of blood.

This can happen for various reasons:

For heavy periods in women or bleeding hemorrhoids.
Each cell in the human body has its own life cycle. Red blood cells have a normal lifespan of 120 days. This period can be shortened if there is a lack of proteins, vitamins B12, B6 and folic acid, as well as vitamin C, which are involved in hematopoiesis or trace elements, copper and iron.
Also hereditary disorders may affect the life cycle of red blood cells. Red blood cells born with the defect are irregular in shape and do not participate in the transport of gases. Such cells are quickly destroyed in large quantities, this is called hemolysis.
The bone marrow ceases to perform the function of reproducing blood cells due to a deficiency of substances that promote this process or its replacement with fibrous or fatty compounds. Kidney diseases and the development of endocrine disorders also affect hematopoiesis.

Symptoms of moderate anemia

Moderate anemia is characterized by vivid symptoms and is manifested by various external signs:

severe fatigue, even after sleep;
general malaise;
constant weakness;
tachycardia;
shortness of breath even with low exertion;

there is noise in the ears and flashing of flies before the eyes;
decreased mood;
change in taste preferences;
pale skin and blue circles under the eyes;
jaundice;
increase internal organs.

A healthy person gets tired after work or playing sports. With severe anemia, fatigue becomes chronic and occurs without visible stress. Even when waking up in the morning, a person already feels this feeling of fatigue.

The general condition of a person can be described as follows:

Constant general malaise and weakness, even with minor physical activity, deprive a person of his usual activities. Shortness of breath and tachycardia also occur due to a lack of oxygen in the body. The heart, working with double force, beats twice as fast normal rhythm to quickly deliver the missing oxygen to the cells.

The pressure in the blood vessels is low and insufficient blood flows to the brain, thereby causing cerebrovascular accidents, which cause depressed mood, tinnitus and poor sleep. The reason for poor sleep and memory, absent-minded attention also lies in the disruption of oxygen supply to the brain.
Digestive disorders develop against the background of anemia due to changes in fermentation and thinning of the mucous membrane. This entails a change in taste preferences. Food that was previously consumed is no longer attractive, and various inedible substances seem tasty and people eat them: earth, clay, chalk.
A person’s appearance also changes, the skin first becomes pale and then yellow. This affects the lips, they crack, these wounds do not heal even with treatment.
Lower and upper limbs go numb, and sometimes there is a tingling feeling. Due to problems with the heart and kidneys, the legs swell and an unsteady gait occurs.

Diagnostic methods

Sometimes it is enough to make a diagnosis general test blood.

But for a complete examination you need:

urine tests;
biochemical blood test;
X-ray examination;
bone marrow biopsy;
endoscopy.

In this case:

A blood test shows a low hemoglobin concentration and a decreasing red blood cell count.
The color of the urine is dark due to the large amount of bilirubin excreted.
A biochemical blood test determines the amount of free, not bound hemoglobin in it, bilirubin, which in this state enters the liver for further utilization there.
Ultrasound determines the condition of internal organs and changes in them. The liver and spleen are enlarged, renal, gastric and intestinal pathologies are observed.
In women, the uterus is examined to identify the causes of uterine bleeding.

To determine hidden bleeding, endoscopy of internal organs and intestines is performed. If hematopoiesis is impaired, bone x-rays are taken to diagnose pathologies in the bone marrow due to the proliferation of connective or fatty tissue, and in case of injuries, the presence of fractures and internal injuries is determined. A bone marrow biopsy determines the cause of the defective red blood cells, as well as its cellular composition.

Treatment

Moderate anemia is treated in inpatient department taking into account the diagnostic results and the reasons that caused it.

The treatment regimen is selected individually for each patient and looks something like this:

identifying and eliminating the causes of blood loss;
use of iron supplements according to indications;
prescribing vitamins to improve hematopoiesis;
blood transfusion;
therapeutic nutrition;
symptomatic treatment;
hormone therapy;
splenectomy;
bone marrow transplantation.

The resulting anemia due to bleeding cannot be fully treated without eliminating the causes that caused the blood loss.

To do this you need:

Stop blood loss from internal organs surgically.
Next, blood transfusion is performed to restore the normal volume of circulating blood in the body. Blood and red blood cell transfusions are also done for extensive hemolysis and leukemia, malignant anemia.

In almost all cases of anemic conditions, it is due to iron deficiency, except for hemolytic anemia. Therefore, treatment with iron supplements is prescribed immediately after diagnosis and continues until the normal blood picture is restored.

Iron deficiency leads to impaired absorption of B vitamins by the digestive system. Injections of vitamin B12, and for children also vitamin B6, folic and ascorbic acid are also used to treat anemia. There is also a correction in the patient’s diet.

Food products must contain:

iron;
protein;
vitamins;
microelements.

For concomitant diseases from internal organs and systems, symptomatic treatment is used. For inflammation and infections, antibacterial therapy and corticosteroid drugs may be used.

Sometimes the spleen must be removed to treat anemia. Operation splenectomy helps stop the increased process of destruction of red blood cells or prevent the danger of rupture of this organ.

Pernicious anemia is treated by transplanting red bone marrow and stem cells to restore hematopoiesis. This requires a compatible donor. If it is not there, then cells for transplantation are taken from the patient himself; this treatment can improve the composition of the blood. Recovery occurs when stable remission is achieved, when the concentration of red blood cells in a blood test is 120 g/l.

To prevent disease, it is necessary to promptly treat all diseases in the body. Periodically donate blood for analysis to monitor the concentration of hemoglobin in it. Human nutrition should be varied and contain foods with a high content of all necessary vital substances.

Food must contain:

animal meat;
liver;
legumes;
green;
fruits;
vegetables.

Moderate exercise and walks in the fresh air improve blood circulation and respiratory function of the body.

Oxygen entering through the lungs is absorbed into the blood and tends to form compounds with hemoglobin and be transported with it to each cell. In return, hemoglobin takes carbon dioxide from the cell and returns it to the lungs, thereby performing gas exchange in the body.

Causes and dangers of low hemoglobin

This is explained as follows:

With a mild degree of anemia, a person’s condition often does not give noticeable signs of this condition, and only in the blood can one see a decrease in the level of hemoglobin, this is 110 - 90 g/l.
The second is the average degree, in which a person experiences symptoms of anemia, a blood test will show hemoglobin levels of 90 - 70 g/l.
If this period is missed and anemia is not treated, then severe third degree occurs, in which irreversible consequences develop. At this degree, the hemoglobin level in the blood will be less than 70 g/l.

There are many reasons that affect the composition of the blood and contribute to the occurrence of anemia. They can be individual for each type and form of the disease.

But there are common ones that unite all varieties:

acute or chronic blood loss;
shortening the life cycle of red blood cells;
failure of the bone marrow to perform its functions.

With normal blood composition, anemia can occur due to blood loss. This occurs due to disruption of the skin and mucous membranes by various factors. Trauma and surgery can result in significant, acute blood loss.

Donors experience blood loss from donating small amounts that cannot harm them. In this case, the normal state of a person is quickly restored. With chronic bleeding, there is a constant, seemingly imperceptible, loss of blood.

This can happen for various reasons:

For heavy periods in women or bleeding hemorrhoids.
Each cell in the human body has its own life cycle. Red blood cells have a normal lifespan of 120 days. This period can be shortened if there is a lack of proteins, vitamins B12, B6 and folic acid, as well as vitamin C, which are involved in hematopoiesis or trace elements, copper and iron.
Also, hereditary disorders can affect the life cycle of red blood cells. Red blood cells born with the defect are irregular in shape and do not participate in the transport of gases. Such cells are quickly destroyed in large quantities, this is called hemolysis.
The bone marrow ceases to perform the function of reproducing blood cells due to a deficiency of substances that promote this process or its replacement with fibrous or fatty compounds. Kidney diseases and the development of endocrine disorders also affect hematopoiesis.

Symptoms of moderate anemia

Moderate anemia is characterized by vivid symptoms and is manifested by various external signs:

severe fatigue, even after sleep;
general malaise;
constant weakness;
tachycardia;
shortness of breath even with low exertion;

there is noise in the ears and flashing of flies before the eyes;
decreased mood;
change in taste preferences;
pale skin and blue circles under the eyes;
jaundice;
enlargement of internal organs.

A healthy person gets tired after work or playing sports. With severe anemia, fatigue becomes chronic and occurs without visible stress. Even when waking up in the morning, a person already feels this feeling of fatigue.

The general condition of a person can be described as follows:

Constant general malaise and weakness, even with minor physical activity, deprive a person of his usual activities. Shortness of breath and tachycardia also occur due to a lack of oxygen in the body. The heart, working with double force, beats twice as fast as the normal rhythm in order to quickly deliver the missing oxygen to the cells.

The pressure in the blood vessels is low and insufficient blood flows to the brain, thereby causing cerebrovascular accidents, which cause depressed mood, tinnitus and poor sleep. The reason for poor sleep and memory, absent-minded attention also lies in the disruption of oxygen supply to the brain.
Digestive disorders develop against the background of anemia due to changes in fermentation and thinning of the mucous membrane. This entails a change in taste preferences. Food that was previously consumed is no longer attractive, and various inedible substances seem tasty and people eat them: earth, clay, chalk.
A person’s appearance also changes, the skin first becomes pale and then yellow. This affects the lips, they crack, these wounds do not heal even with treatment.
The lower and upper limbs become numb, and sometimes a tingling sensation occurs. Due to problems with the heart and kidneys, the legs swell and an unsteady gait occurs.

Diagnostic methods

A general blood test is sometimes sufficient to make a diagnosis.

But for a complete examination you need:

urine tests;
biochemical blood test;
X-ray examination;
bone marrow biopsy;
endoscopy.

A blood test shows a low hemoglobin concentration and a decreasing red blood cell count.
The color of the urine is dark due to the large amount of bilirubin excreted.
A biochemical blood test determines the amount of free, unbound hemoglobin in it, bilirubin, which in this state enters the liver for further utilization there.
Ultrasound determines the condition of internal organs and changes in them. The liver and spleen are enlarged, renal, gastric and intestinal pathologies are observed.
In women, the uterus is examined to identify the causes of uterine bleeding.

Treatment

The treatment regimen is selected individually for each patient and looks something like this:

identifying and eliminating the causes of blood loss;
use of iron supplements according to indications;
prescribing vitamins to improve hematopoiesis;
blood transfusion;
therapeutic nutrition;
symptomatic treatment;
hormone therapy;
splenectomy;
bone marrow transplantation.

The resulting anemia due to bleeding cannot be fully treated without eliminating the causes that caused the blood loss.

To do this you need:

Stop blood loss from internal organs surgically.
Next, blood transfusion is performed to restore the normal volume of circulating blood in the body. Blood and red blood cell transfusions are also done for extensive hemolysis and leukemia, malignant anemia.

In almost all cases of anemic conditions, it is due to iron deficiency, except for hemolytic anemia. Therefore, treatment with iron supplements is prescribed immediately after diagnosis and continues until the normal blood picture is restored.

Iron deficiency leads to impaired absorption of B vitamins by the digestive system. Injections of vitamin B12, and for children also vitamin B6, folic and ascorbic acids are also used to treat anemia. There is also a correction in the patient’s diet.

Food products must contain:

For concomitant diseases of internal organs and systems, symptomatic treatment is used. For inflammation and infections, antibacterial therapy and corticosteroid drugs may be used.

Food must contain:

Moderate exercise and walks in the fresh air improve blood circulation and respiratory function of the body.

I only had moderate anemia during pregnancy. In the first place, hemoglobin fell after childbirth, in the second during pregnancy, and immediately after childbirth it returned to normal. I felt the decrease in iron very strongly - I was crawling along the walls, shortness of breath, weakness, and I was breaking into a sweat. My norm was always 140+, and during pregnancy, hemoglobin dropped to 90. But for the third time after giving birth, it dropped to 74, but the most interesting thing is that I didn’t feel it at all. I jumped and jumped around the department, and the doctor said that with such hemoglobin it was time to go to the hospital. For a very long time I raised it in every possible way. Iron levels returned to normal only after six months.

After reading the article, I don’t even want to think that such changes in a person’s blood are akin to a death sentence. I have encountered thrombocytopenia, but this is a lack of platelets in the blood and, as a result, insufficient blood clotting. I know for sure that you can’t give up and fight to the end. Take care of yourself and be healthy!

Half a year ago. I have encountered this disease.

At first I thought everything was fine.

But then I began to notice that even after sleep I was tired and felt some weakness.

Rapid shortness of breath after going up to the 5th floor.

But before that, I wasn’t tired at all, because I was doing CrossFit.

So when I went to the doctors, they diagnosed second degree anemia!

Anemia 1st degree

Anemia of the 1st degree is the most mild manifestation a whole complex of diseases that are characterized by a decrease in hemoglobin concentration or the number of red blood cells. As a result of anemia, many changes begin in the body, which are caused by insufficient oxygen supply to organs and tissues. Manifestations and pathological changes in the body directly depend on the severity of the disease.

Anemia 1st degree

Classification

The classification of anemia is quite simple. They are distinguished depending on the causes of occurrence into the following types:

Posthemorrhagic anemia, which develops as a result of a decrease in the number of blood cells, red blood cells, as a result of acute or chronic blood loss. Their causes may be trauma, difficult and frequent childbirth, heavy menstruation, or gastric ulcer. In infants, posthemorrhagic anemia most often develops as a result of birth trauma, internal hemorrhages, placental bleeding, and hemorrhagic diathesis.
Hemolytic anemia occurs as a result of the pathological breakdown of red blood cells. This form of the disease is quite rare and occurs under the influence of various autoimmune and hereditary factors.
Deficiency anemia caused by impaired erythropoiesis. This group of anemias is the most common. This includes iron deficiency anemia, which occurs in the vast majority of cases, megaloblastic anemia, caused by a lack of vitamin or folic acid. Sometimes so-called multifactorial anemia develops, caused by a simultaneous deficiency of iron and B12.
Hypoplastic and aplastic anemia resulting from dysfunction of the bone marrow. This variety is extremely rare. It is either hereditary in nature or develops after severe chronic diseases, the effects of medications, or chemicals.

In addition, to prescribe the correct treatment regimen, it is necessary to determine the degree of anemia by hemoglobin. This is calculated based on the deviation of the hemoglobin value from the norm. Hemoglobin is the main iron-containing coloring element of red blood cells, which is “responsible” for the transport of oxygen with blood throughout the body.

For an adult man, the hemoglobin concentration is 135 – 160 g/l. For women, this value is slightly lower and ranges from 120 to 140 g/l. For children, the normal hemoglobin level depends on age. These values are shown in the table:

Age

For teenagers aged 16 and over, adult standards apply.

Reasons

Most of the iron contained in the body is found in red blood cells; there are also reserves of this substance in the muscles, liver and bone marrow. Daily requirement for an adult, the iron content is about 10–15 mg. Of this amount, no more than 1.5 mg is absorbed into the blood; approximately the same amount is normal daily physiological losses through sweat, urine and feces. As for children, the daily need infant in iron is 0.5 - 1.2 mg, this figure increases with age, and a two-year-old child needs about 10 mg of iron per day.

Here you will find detailed information about treatment methods

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How to treat anemia? What helped me with iron deficiency?

The causes of iron deficiency anemia are most often not too abundant, but chronic blood loss due to hemorrhoidal bleeding, acute course peptic ulcer, heavy menstruation and others similar conditions. Insufficient intake of iron from food or impaired absorption of iron after gastric surgery also plays a role in the development of iron deficiency anemia.

Iron deficiency anemia often develops in premature babies, since many substances necessary for normal hematopoiesis are formed in the last two months of pregnancy. The cause of this disease in infants can also be iron deficiency anemia of varying severity in a woman during pregnancy.

B12 - deficiency anemia develops due to insufficient intake of this vitamin from food, since it is not synthesized in the body. B12 is absorbed in the gastrointestinal tract with the help of a special enzyme called gastromucoprotein (also called Castle factor). After gastrectomy, with gastritis, chronic alcohol consumption, the secretion of Castle factor sharply decreases and, as a result, B12 deficiency develops.

There are certain reserves of folic acid in our body. It also comes with food and is absorbed in the duodenum and ileum. This process can be disrupted under the influence of alcohol, long-term use hormonal contraceptives, anticonvulsants, some antibacterial drugs, in particular trimethoprim or sulfomethoxazole.

Clinical manifestations

Symptoms largely depend on the severity of the disease. Moreover, with each subsequent stage, existing symptoms worsen and new ones may appear.

First degree anemia is practically asymptomatic. Sometimes a person complains of slight weakness, malaise, and fatigue. There is noticeable pallor of the skin, sweating, and loss of appetite. Mild anemia in infants is characterized by increased excitability child, tearfulness, excessive regurgitation after feeding (or vomiting in older children).
Moderate anemia is manifested by headaches and dizziness associated with insufficient oxygen supply. Children with this form of anemia get tired very quickly and have difficulty withstanding even the lightest physical activity. A child under one year old may even experience regression in the development of motor skills. There is roughness or dryness of the skin, very painful cracks in the corners of the mouth, and digestive disorders may occur, which manifest themselves in the form of diarrhea or constipation, and flatulence. From the cardiovascular system, tachycardia and heart murmurs may be observed.
Anemia of the 3rd degree is characterized by changes in the structure of nails and hair (they acquire a matte tint and become very brittle), hair loss, a feeling of coldness and numbness in the extremities, and a distorted perception of smells and tastes. Stomatitis and caries (even tooth decay) may appear. Children may be behind in physical and psychological development. On ultrasound of organs abdominal cavity noticeable enlargement of the liver and spleen. If left untreated, severe anemia is dangerous and can cause extremely serious consequences.

The severity of symptoms may vary depending on the general condition of the child or adult suffering from anemia. Also, the likelihood of one or another clinical sign depends on the cause of the disease.

Diagnostics

You can assume the development of this disease in yourself or in a child by simply clinical analysis blood, which can be donated without a doctor’s referral in any laboratory. If the hemoglobin concentration decreases below normal, you should mandatory consult a therapist or pediatrician.

Then a biochemical blood test is prescribed. There is a decrease in the amount of serum iron, the level of ferritin (a protein that helps maintain iron stores), and transferrin saturation with iron.

Naturally, the doctor pays attention to the general symptoms of anemia and conducts a comprehensive examination to determine what changes this disease has caused in the body.

Treatment of first degree anemia

Anemia of the 1st degree in children and adults is usually very mild and in most cases does not require medical correction. It is enough to make certain changes in your diet and daily routine. Long walks in the fresh air and moderate physical activity are recommended.

If grade 1 anemia is detected, then the diet for children and adults should be formulated taking into account the following principles:

Increase your protein intake. To do this you need to eat eggs, fermented milk products, liver, kidneys, fish and meat.
Limit milk and strong tea, as these drinks slow down the absorption of iron from gastrointestinal tract. Preservatives, oxalates, phosphates and some medications, for example, antacids and tetracycline antibiotics, have the same effect.
Instead of animal fats, it is necessary to give preference to vegetable ones. You need to use butter, season salads with a variety of vegetable oils (sunflower, olive, grape and the like).
If there is no acute problem with overweight, then the amount of carbohydrates in the diet can not be limited.
Vitamins C and group B contribute to better absorption of iron. Therefore, it is advisable to introduce products that contain them into the menu. These are citrus fruits, greens, legumes, many berries, etc.
Consumption of iron-containing foods (beef liver, rabbit and turkey meat, buckwheat and oatmeal, millet, caviar).

It is worth noting that it is imperative to monitor blood dynamics and control hemoglobin levels. In most cases, with proper adherence to the diet, its value increases to normal numbers, and further prescription of medications is not required.

Treatment of anemia of 2 and 3 degrees

Treatment of anemia of moderate degree or more severe form consists of prescribing special medications depending on the cause of the disease. Thus, iron deficiency anemia requires long-term treatment with iron supplements in a dosage of 100–120 mg per day. It is worth noting that medication must be continued after the patient’s condition has normalized and hemoglobin levels have been restored. This is due to the fact that in addition to eliminating the deficiency state, it is necessary to replenish iron reserves in the body. In most cases, for the convenience of the patient, medications are prescribed in tablets. Parenteral administration indicated when the absorption of this element in the digestive tract is impaired.

Treatment of B12 deficiency anemia is carried out using injections of cyanocobalamin or hydroxocobalamin at a dosage of 400 - 500 mcg per day for the first week. Then they switch to maintenance therapy, during which the same injection is given once every 7 days. The total duration of therapy is about two months. If the cause of such anemia cannot be eliminated, then it is necessary to give preventive injections of cyanocobalamin several times a year to maintain normal B12 levels.

Treatment of grades 2 and 3 folate deficiency anemia is the same. Prescribed 5 mg of folic acid three times a day.

Treatment of rarer forms of anemia is much more difficult. For hemolytic anemia, a long course of prednisolone is indicated. Aplastic anemia was previously considered incurable and often ended fatal. On at the moment This disease is treated with a bone marrow transplant.

Features of the treatment of anemia in children

Anemia treatment should be carried out under the strict supervision of a physician. If infants are bottle-fed, it is recommended special mixtures with high iron content. Child with iron deficiency anemia It is recommended to introduce complementary foods a few weeks earlier and start with applesauce and oatmeal and buckwheat porridge.

Anemia of the 2nd degree in children cannot be treated with simple nutritional correction. The use of drugs that contain ferric iron is required. These are maltofer, ferrum lek, ferlatum, etc. For this form of the disease, they are given in the form of drops or syrup. Parenteral administration of drugs is indicated for third degree anemia. In parallel with these medications, multivitamin complexes are also prescribed, because this disease is accompanied by vitamin deficiency.

When severe anemia develops in infants, recombinant human erythropoietin is also prescribed. These are drugs such as Recormon, Eprex, Epocrine. The same drugs are also prescribed to premature babies born at 4–5 weeks. ahead of schedule. Typically, the dosage of such medications is 250 IU per kg of body weight three times a week, but the younger the child, the larger the dose required for effective treatment.

In addition to drug therapy, long walks, a strict daily routine, and elimination of psychological stress are recommended. The effect of treating anemia in children is noticeable already on the seventh day. If there is no effect after two weeks of therapy, then a re-examination is carried out or the dose of medication is adjusted.

In general, the most common types of deficiency anemia are easily treated, even at the most severe stage of the course. However, medication can be avoided if proper diet nutrition and active lifestyle.

All information on the site is presented for informational purposes. Before using any recommendations, be sure to consult your doctor.

Anemia

In the vast majority of cases, a reduced concentration of hemoglobin in a person’s blood is associated with iron deficiency in the body. This condition is called anemia, and according to official medical statistics it is diagnosed in almost 20 percent of the population.

The normal hemoglobin content in the body of an adult healthy person is determined within the following limits: g/l for women and/l for men.

Along with a decrease in hemoglobin during anemia, there is also a decrease in the number of erythrocytes in the blood (red blood cells).

Causes of anemia

The main causes of iron deficiency and subsequent anemia include significant blood loss that occurs during extensive operating, gastric, uterine, and nasal bleeding; as well as with constant donation.

Besides prolonged bleeding accompanied by heavy blood loss, the causes of anemia can be acute and chronic diseases gastrointestinal tract, in which the function of iron absorption in the human body is impaired.

Periods of increased body need for iron supplements are also accompanied by a decrease in hemoglobin in the blood. Often this condition develops in women during pregnancy, childbirth and breastfeeding.

The causes of anemia can definitely be attributed to long-term vegetarianism, poor nutrition, and strict adherence to starvation diets. All of the listed nutritional deficiencies and errors significantly increase the risk of developing anemia even in a completely healthy person.

The causes of anemia in children lie in the child’s still physiologically immature hematopoietic system. Anemia progresses in children against the background of the same unfavorable factors listed above as in the adult population.

Degrees of anemia

Experts distinguish three main degrees of anemia, which are divided into mild, moderate and severe. It is very difficult to determine by eye, without the use of laboratory tests, what degree of anemia a particular case of the disease belongs to, even for medical worker. The fact is that the main criterion for the degree of anemia is the level of hemoglobin content and its level can be determined solely on the basis of a patient’s blood test.

Mild, first-degree anemia is characterized by a slight decrease in hemoglobin levels with the following indicators g/l in men and/l in women.

Typically, patients do not experience any changes in their condition. As a treatment for this type of anemia, following a diet and consuming foods with a high iron content are recommended.

With the second, moderate degree of anemia, hemoglobin has a more significant decrease - dog/l. This condition is characterized by the appearance the following symptoms anemia and complaints: headaches, slight dizziness, etc. In this case, nutritional adjustments alone are not enough, and iron supplements are prescribed.

Severe, third degree anemia is considered life-threatening. Hemoglobin drops to a level of 70 g/l and below. There are disturbances in the functioning of the cardiovascular system, blood thinning occurs, and the general condition of the body deteriorates significantly.

Symptoms of anemia

Common symptoms characteristic of anemia are as follows. Patients usually complain of increased fatigue, weakness, trembling of the limbs (tremor) and constant dizziness. With further progression of the disease by anemia, the development of fainting conditions is also possible.

The appearance of people suffering from anemia is easily determined by external examination. Skin such patients are dry and have very pale, sometimes bluish tint, mucous membranes are also unnaturally pale in color.

Even minor physical activity causes severe shortness of breath and palpitations in an anemic person. Without timely treatment anemia patients may develop symptoms coronary disease hearts.

Treatment of anemia

Regular consumption of iron-containing foods can be recommended as the main remedy for self-treatment anemia and prevention of its occurrence. Such means include a whole list of accessible and inexpensive plant products, growing in our domestic beds.

Carrots, beets, sorrel, celery, pumpkin, rutabaga, turnips - all these vegetables, eaten daily as salads or freshly squeezed juices, will become a reliable obstacle to the occurrence of such a serious disease as anemia.

In addition to garden vegetables, it is advisable to take infusions and decoctions of some wild plants to treat anemia. Clover flowers, dandelion roots, nettle and many other natural preparations will effectively help you increase hemoglobin levels in the blood.

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The information is generalized and is provided for informational purposes. At the first signs of illness, consult a doctor. Self-medication is dangerous to health!

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Anemia (anemia) is a very common and serious disease that is observed when a wide variety of organs and systems are affected and has very different clinical significance. The pathogenetic classification of anemia given below, which is followed by a description of the various forms of anemic conditions, indicates simpler mechanisms of their occurrence, more easily accessible to clarification in the clinic. Participation violation nervous regulation is of great importance in the origin of each of the given pathogenetic groups of anemia and should be taken into account in the clinic with special care.

Acute anemia from blood loss-- “anemia” in the narrow sense of the word: in the first hours after blood loss, a smaller amount of qualitatively unchanged blood circulates in the vessels, which leads primarily to acute vascular failure and sometimes even death. By the end of the first half day, normal blood mass is restored due to the absorption of tissue fluid and signs of hemoglobin and iron deficiency appear.
Lack of iron in the body, due to impaired absorption of iron contained in food, or its low content in food, as well as as a result of repeated blood loss, leads to anemia, in which red blood cells, even with a sufficient number of them, are poor in pigment (hemoglobin) - hypochromic chloranemia, united by the main factor by the term iron deficiency anemia.
In another group of anemias, the ripening of red blood cells is affected due to lack of anti-anemic substance, formed from food under the influence of the hematopoietic enzyme Castle in the stomach and deposited in the liver; in this case, large immature red blood cells well stained with hemoglobin are formed - hyperchromic, megalo- and macrocytic anemia.
Regardless of a sufficient amount of hematopoietic substances and good bone marrow function, anemia occurs from increased breakdown of red blood cells in certain metabolic disorders, poisoning and infections - hemolytic anemia.
Regardless of the presence of hematopoietic substances in the body, anemia occurs when the bone marrow is destroyed, displaced, for example, by a tumor or bone growths, with paralysis, inhibition of its function - and plastic and hypoplastic anemia.

Some rare pathogenetically and etiologically insufficiently clear forms of anemia do not fit into these groups.

Numerous other previously proposed classifications of anemia are less clinically justified. Thus, a distinction is often made between primary anemia - for diseases of the blood system itself - and secondary, or symptomatic anemia - for diseases of the stomach, kidneys, infections, etc. However, the development of classic primary anemia - malignant anemia and chlorosis - is currently associated mainly with damage to other systems - violation gastrointestinal digestion and absorption and nervous regulation. True, in every anemic or, more broadly, hematological syndrome, it is important to highlight symptomatic forms, establish the main cause of the disease in this case, especially if this cause can be eliminated. Likewise, hemolytic and aplastic anemias, which are often not clinically associated with damage to any organ, arise as a result of intoxication, metabolic disorders and hyperergic reactions, which in turn arise as a result of disturbances in nervous regulation. Botkin attached primary importance to the neurogenic factor in the origin of anemia, distinguishing anemia from damage to the centers of the brain and peripheral neuroreflex forms. However, the neurogenic factor has not been studied to such an extent that it can now be used as the basis for the practical classification of anemia.

The division of anemia into hemolytic and hyporegenerative is of great importance, but, for example, hemolysis may be based on defects in the structure of red blood cells (their underripening in malignant anemia) or at the same time an increased function of the cellular blood-destructive system (as in chronic hemolytic anemia), or, finally, the presence of hemolysins in the blood, which is why, from a practical point of view, it is not advisable to combine, for example, all anomies with increased blood breakdown into one pathogenetic group.

The morphological or narrow hematological divisions of anemia according to the characteristics of erythrocytes into hyperchromic and hypochromic, megalo-, macro- and microcytic, megaloblastic and normoblastic are essentially close to the identification of two main forms that arise as a result of insufficiency of the main hematopoietic substances - anti-anemic substance and iron. But morphological features, for example, in relation to the color indicator, are not so conclusive, since a color indicator above one can also occur with a lack of antianemic substance. And for hemolytic anemia; microcytosis can also develop as a result of not only iron deficiency, but also as a result of increased hemolysis, therefore these headings do not give the clinician direct instructions on the necessary pathogenetic therapy. Morphological signs of peripheral blood do not always correspond to the state of the bone marrow and therefore may be of less fundamental importance, while the study of bone marrow puncture does not always give unambiguous results and is somewhat difficult for everyday use. Establishing etiological factors in various hematological syndromes is widely used for practical purposes of prevention and treatment.

Anemia (anemia) - decrease general level hemoglobin (Hb), often manifested in a decrease in it per unit volume of blood. True anemia differs from pseudoanemia in the size of the hematocrit (in adults it is 36-48%).

In the world, about 30% of the population suffers from anemia, and half of them, 600 million people, have iron deficiency. Separation of anemias by red blood cell size (MCV) indicates probable cause. Red blood cells in the bone marrow must accumulate a minimum level of hemoglobin. Red blood cell precursors undergo division, which is regulated by erythropoietin. If the required amount of hemoglobin is not delivered to the red blood cells, more cell divisions than normal will occur before they are released into the blood, and the volume of the red blood cell will be reduced. MCV may become smaller due to a lack of components needed for the hemoglobin molecule. In iron deficiency, there is not enough iron; in thalassemia - globin chains; in congenital sideroblastic anemia - heme rings; and sometimes lack of iron utilization leads to anemia of chronic diseases. In megaloblastic anemia, biochemical disorders caused by a deficiency of vitamin B 12 or folate inhibit the synthesis of new bases for building DNA. A similar defect in cell division in the bone marrow is observed under the influence of cytostatics and in some hematological diseases, for example, myelodysplasia. In this case, the cells receive enough hemoglobin, but undergo fewer divisions, as a result, circulating red blood cells increase MCV. The erythrocyte membrane is built like a double lipid layer, which easily exchanges with plasma lipids. Liver disease, hypothyroidism, hyperlipidemia and pregnancy accompanied by an increase in plasma lipids can cause an increase in MCV.

The term “anemia” refers to a decrease in the number of red blood cells, hemoglobin (the main indicator for anemia) and/or hematocrit with a normal, as a rule, total blood volume. Immediately after acute massive blood loss, with dehydration or overhydration, the diagnosis of anemia can be made only after the restoration of blood volume. The pathogenetic classification of anemia reflects the violation of individual stages of erythropoiesis, as well as the life expectancy of red blood cells circulating in the blood (hemolytic anemia).

Erythropoiesis disorders occur when:

impairment or absence of differentiation of pluripotent hematopoietic stem cells (aplastic anemia in panmyelopathy or acute myeloblastic leukemia);
transitory (with viral infections) or a constant decrease in only erythropoiesis precursor cells (isolated aplastic anemia) due to the formation of autoantibodies against erythropoietin or membrane proteins of erythropoiesis precursor cells;
erythropoietin deficiency in kidney pathology (so-called renal anemia);
chronic inflammation or tumors that activate, among other things, interleukins that suppress erythropoiesis (secondary anemia);
impaired cell differentiation (ineffective erythropoiesis), the cause of which, in addition to genetic defects, may be a deficiency of folate or vitamin B 12 (megaloblastic anemia);
disorders of hemoglobin synthesis (microcytic hypochromic anemia).

Acute posthemorrhagic anemia

Causes of acute posthemorrhagic anemia

The occurrence of the disease is promoted by:

all kinds of injuries, especially with damage to large vessels;
ectopic pregnancy;
various diseases of internal organs accompanied by acute bleeding (peptic ulcer and DNA, varicose veins veins of the esophagus with cirrhosis of the liver, disintegrating tumor of the stomach; tuberculosis, lung abscess and bronchoectasis);
hemorrhagic diathesis, especially hemophilia.

A condition associated with rapid loss of a significant volume of blood (20-25% of blood over approximately 1 hour). The factor determining the degree of dysfunction and their compensation is uncorrectable hypovolemia.

Stages of compensation for acute blood loss

Reflex phase of compensation. Occurs on the 1st day after acute blood loss due to activation of the sympathoadrenal system: peripheral vascular resistance increases, blood is redistributed (centralization of blood circulation).

Hydraemic phase of compensation. It occurs on the 2-4th day and consists of the movement of fluid from the extracellular space into the vessels. One of the mechanisms of the hydremic phase is catecholamine-induced hyperglycemia due to glycogenolysis in the liver; the content of basic electrolytes in plasma remains virtually unchanged.

Bone marrow compensation phase. In this phase, activation of the formation of erythropoietins in the kidneys against the background of severe hypoxia is important.

In the first time after blood loss, due to a decrease in the volume of the vascular bed, a decrease in the content of hemoglobin and red blood cells is usually not detected, and the hematocrit indicator also does not change.

Due to hydremia, a gradual drop in hemoglobin and red blood cell levels begins.

Treatment of acute posthemorrhagic anemia

Aimed at fast recovery volume of circulating blood: blood transfusions, administration of colloid or saline solutions. For hemostasis, calcium chloride, vikasol, sewage plasma, fibrinogen, and aminocaproic acid are administered intravenously. If necessary, surgical stopping of bleeding is performed.

Chronic posthemorrhagic anemia

Anemia that develops as a result of repeated losses of small volumes of blood during bleeding from the gastrointestinal tract, with renal, uterine, nasal and hemorrhoidal bleeding.

Peripheral blood is characterized by a decrease color index, microcytosis, moderate leukocytosis with a neutrophilic shift to the left. With a long course of the disease, anemia becomes hyporegenerative in nature.

Anemia associated with impaired blood formation

1. Dysregulatory- caused by a violation of the regulation of hematopoiesis with a decrease in the production of erythropoietins or an increase in the number of their inhibitors (chronic kidney disease, hypofunction of the pituitary gland, adrenal glands, thyroid gland).

2. Scarce- occurs when there is a lack of substances necessary for erythropoiesis (iron, vitamins, protein).

Iron deficiency anemia accounts for up to 80% of all anemia and develops as a result of an imbalance between the intake of iron into the body, its use and loss.
Iron losses are observed with repeated and prolonged bleeding - uterine, gastrointestinal, renal, pulmonary, and with hemorrhagic diathesis.

In some cases, nutritional iron deficiency (less than 2 mg per day) is possible, for example, with a small amount of meat consumption, with artificial feeding or with late complementary feeding in childhood.

Reduced iron absorption is observed with hypoacid gastritis, chronic enteritis, or with resection of parts of the gastrointestinal tract.

Impaired iron transport is possible with hereditary or acquired hypotransferrinemia.

Increased iron consumption develops during periods of growth and maturation, during pregnancy and lactation, and in chronic inflammatory diseases.

Iron deficiency is accompanied by an increase in ineffective erythropoiesis and a decrease in the lifespan of erythrocytes.

The blood picture is characterized by a decrease in hemoglobin content (from 100 to 20 g/l), the erythrocyte content may be normal or significantly reduced, and hypochromia is detected. A tendency to microcytosis, poikilocytosis, and the regenerative or hyporegenerative nature of anemia are also typical.

In the peripheral blood there are: serum iron levels below 30 mcg/l; ferritin content in the blood is below 40 mcg/l.

Serum iron deficiency is manifested by increased fatigue, distortion of taste and smell, general weakness, and headaches. Iron deficiency also leads to a decrease in the level of myoglobin and the activity of tissue respiration enzymes. The consequence of hypoxia is degenerative processes in organs and tissues. Layered and brittle nails, stomatitis, caries, atrophic gastritis, etc. are common.

Anemia caused by vitamin B12 deficiency (pernicious)

Vitamin B 12 deficiency can develop due to a violation of its supply, absorption, transport, deposition and assimilation at the bone marrow level.

Malabsorption is likely in the absence of internal Castle factor (transcorrin), in atrophic processes on the part of the gastric mucosa, in a hereditary selective disorder of vitamin production, in autoimmune destruction, in the agastric form of deficiency.

The absorption of vitamin B|2 is sharply limited in case of widespread damage to the small intestine - with enteritis, celiac disease, as well as with its resection.

The pathogenetic role of the competitive consumption of vitamin is shown during invasion by the broad tapeworm, as well as in the “cecal intestine” syndrome (when anastomoses are performed, sections of the small intestine remain).

In some cases, vitamin B12 deficiency is caused by a lack of transcobalamin.

Vitamin B 12 deficiency causes a disruption in the formation of DNA and further a disorder in the division of hematopoietic cells, i.e. slowing down the mitotic process and reducing the number of mitoses. Under such conditions, a megaloblastic type of hematopoiesis, similar to the embryonic one, is formed.

The development of anemia is associated with the following mechanisms.

Decreased mitotic activity.
Ineffective erythropoiesis due to intramedullary destruction of megaloblasts.
Extravascular hemolysis in the spleen due to increased size of megalocytes.
Intravascular hemolysis due to a decrease in the osmotic resistance of the megalocyte membrane.

In the peripheral blood, severe anemia is detected, predominantly hyperchromic, hyporegenerative. The presence of nuclear residues, anisocytosis, and poikilocytosis are typical. Neutropenia and thrombocytopenia are also noted.

Folate deficiency anemia is close to vitamin B 12 deficiency in its development mechanism and blood picture.

Hypo- and aplastic anemia

These anemias are a set of syndromes in which, along with pancytopenia, inhibition of hematopoiesis in the bone marrow is detected.

According to etiology, aplastic anemia is divided as follows:

Genuine (idiopathic), constitutional-hereditary, caused by impaired reactivity of the body or endocrine insufficiency.
Aplastic anemia associated with the action of damaging factors: radiation, toxic factors (benzene, mercury), cytotoxic (chlorethylamine, ThioTEP, colchicine, 6-mercaptopurine, etc.), medicinal (amidopyrine, barbiturates, sulfonamides, aminazine), infectious (viral hepatitis A, B, generalized forms of tuberculosis, typhoid fever, salmonellosis, septic conditions).

The following mechanisms are important in pathogenesis:

A decrease in the number of stem cells or their defects.
Disruption of the microenvironment leading to changes in stem cells.
Immune influences causing disorders of stem cell function. The blood picture is characterized by pronounced, often normochromic, macrocytic, hyporegenerative anemia. There is significant granulocytopenia and thrombocytopenia. The number of myelokaryocytes in the bone marrow decreases. Clinical picture depends on the degree of disruption of individual hematopoietic germs and their combinations; it includes anemic, thrombocytopenic and granulocytopenic syndromes.

Hemolytic anemia

This group includes various anemias associated either with hereditary increased destruction of red blood cells or with the action hemolytic factors exogenous origin.

Hereditary hemolytic anemias

1. Anemia associated with disruption of the erythrocyte membrane (membranopathy). Hereditary microspherocytosis- autosomal dominant type of inheritance, characterized by an increase in the permeability of the erythrocyte membrane and an excessive intake of sodium ions into the cell. There is swelling of red blood cells, impaired ability to deform and a decrease in their life expectancy, destruction of the spleen by macrophages.

In microspherocytosis, the absence or disruption of binding of the membrane protein spectrin to protein 4.1 was revealed. It is assumed that the formation of the tetrameric form of spectrin from the dimeric form is disrupted, as well as the absence of erythrocyte membrane proteins, designated 4.2.

Usually the anemia is normochromic, regenerative. The blood picture is different to varying degrees severity, during a hemolytic crisis - more severe, but at the same time high reticulocytosis develops.

Membranopathies also include elliptocytosis (ovalocytosis), stomatocytosis (mouth-shaped red blood cells).

Acanthocytosis is caused by a violation of the lipid structure of the erythrocyte membrane.

2. Anemia associated with impaired activity of erythrocyte enzymes. Deficiency of enzymes involved in energy production in red blood cells leads to disruption of the ionic composition, decreased resistance to oxidizing agents and a decrease in the life expectancy of these cells.

Hereditary deficiency of lycolysis and ATP metabolism enzymes (hexokinase, hexophosphate isomerase, phosphofructokinase, pyruvate kinase, ATPase) has been described.

A deficiency of pentose phosphate cycle enzymes leads to a lack of NADP*H2, which is necessary for the reduction of glutathione, a factor that resists the action of oxidizing agents. This happens when there is a deficiency of glutathione synthesis enzymes - glutathione synthetase, glutathione reductase, glutathione peroxidase.

In such cases, anemia of varying severity is formed. Usually normochromic, with symptoms of anisocytosis, poikilocytosis, and polychromasia. The content of reticulocytes is increased, especially during exacerbations.

3. Anemia associated with impaired structure and synthesis of hemoglobin (hemoglobinopathies).

Immune hemolytic anemias

Heterogeneous group of diseases, combined by the participation of antibodies or immune lymphocytes in the damage and death of red blood cells or erythrokaryocytes.

Iso- or alloimmune anemias may develop due to hemolytic disease of the newborn or blood transfusion.

Heteroimmune anemia (haptenic) associated with the appearance of new antigens on the surface of erythrocytes (for example, as a result of fixation of drugs on erythrocytes - penicillin, sulfonamides). The hapten sometimes becomes a virus, also fixed on the surface of the erythrocyte.

Autoimmune hemolytic anemias- a group of diseases caused by the formation of antibodies against self-antigens of erythrocytes or erythrokaryocytes.
In addition to idiopathic, there are also symptomatic autoimmune anemia; in them, hemolysis develops against the background of other diseases (malignant tumors of various locations and hemoblastosis, systemic lupus erythematosus, rheumatoid polyarthritis, immunodeficiency states).

The most likely pathogenetic basis of autoimmune hemolytic anemia is a breakdown of immunological tolerance.

The blood picture shows mild anemia, often normochromic, with an increased content of reticulocytes. At hemolytic crises blood counts are disturbed to a greater extent, reticulocyte crises are possible with an increase in the content of reticulocytes to 80-90%.

B12 - deficiency (pernicious) anemia

Symptoms and signs. At 12 - deficiency anemia develops slowly, gradually. Increasing weakness, fatigue, and shortness of breath are noted.

The hemogram shows a decrease in the number of red blood cells with a high saturation of them with hemoglobin, MCH >31 pg. Red blood cells are of unequal size (anisocytosis), macrocytes predominate.

Diagnostics. The diagnosis is made in the presence of hyperchromic anemia with macrocytosis, leukopenia and thrombocytopenia, MSI >31 pg, autoimmune gastritis with achlorhydria, and signs of damage to the nervous system. It is confirmed by the hematological effect of treatment with vitamin B 12.

Treatment. It is carried out by subcutaneous injection of vitamin B 12.

Folate deficiency anemia

Folate deficiency anemia is much less common than B12 deficiency anemia, since folates are present in meat (meat, liver) and plant products.

Reasons. The development of the disease is caused by: extensive resections of the small intestine; celiac disease; long fasting(GULAG); taking anticonvulsants (diphenin, phenobarbital, etc.), antituberculosis and contraceptives; alcoholism (increases the need for folic acid); hemolytic anemia (the need for folic acid is increased due to constant proliferation processes in the bone marrow); pregnancy; culinary processing of food (boiling after 15 minutes folic acid is completely destroyed).

Symptoms and signs. The anemic syndrome is similar to that of B 12 deficiency anemia. The difference lies in the presence of complaints of gastrointestinal dysfunction; There is no funicular myelosis, but epilepsy, schizophrenia, and mental disorders are common.

In the blood there are signs of hyperchromic anemia, pronounced anisocytosis, a decrease in the number of erythrocytes, platelets and leukocytes. In the bone marrow there are megaloblasts.

Treatment. Carried out by folic acid; preventive intake of folic acid if the cause of its deficiency has not been eliminated.

Prevention. It is carried out in pregnant women and patients with hemolytic anemia - constant intake of folic acid (1 mg/day).

Anemia caused by impaired hemoglobin synthesis

Red blood cells are necessary for the transport of O 2 and CO 2, as well as for maintaining the buffering properties of the blood. Hemoglobin is important for all three of these functions. Its molecule consists of four subunits, each of which includes three components: protoporphyrin, iron (Fe 2+) and globin (α or β). When Fe 2+ is incorporated into the protoporphyrin structure, heme is formed. Hemoglobin synthesis is impaired when one of the heme components is deficient or defective. In these cases, the size of red blood cells usually decreases (MCV), and the hemoglobin content in them also decreases (MSI) (microcytic hypochromic anemia).

Disturbances in the synthesis of protoporphyrins arise as a result of hereditarily determined enzyme deficiency, for example, in hereditary sideroblastic anemia, in which the formation of δ-aminolevulinic acid (δ-ALA) from glycine and succinyl-CoA, and therefore the synthesis of heme, is impaired. Heme inhibits the activity of δ-ALA synthase according to the principle of negative feedback. In other words, if the heme concentration decreases, the inhibition of the enzyme stops and, despite the defect, a sufficient amount of heme is formed. Defects in enzymes that catalyze subsequent metabolic transformations lead to increased concentrations of intermediate products. Due to the increased rate of heme formation, these metabolites cause another disorder called porphyria.

Disorders of globin synthesis. Before birth, the baby has a type of hemoglobin that has an increased affinity for O 2, which is a mechanism of adaptation to low PO 2 in the blood vessels of the placenta. This fetal hemoglobin (HbF) contains γ chains instead of β chains.

The properties of hemoglobin (solubility, affinity for O 2, oxidability, etc.) depend on the sequence of amino acids in the protein part of the molecule. However, not all of the more than 300 known genetically mediated hemoglobin variants are characterized by a violation of the functional properties of hemoglobin. On the other hand, even a single “abnormal” amino acid (substitution of glutamine for valine in the 6th position of the β-chain with the formation of HbS) can lead to serious functional disorders observed in sickle cell anemia caused by a homozygous gene defect. In the oxidized state, HbS groups together so that the red blood cells take on a sickle shape. These cells are not able to deform; they form aggregates, clogging small blood vessels. RBC aggregation occurs within a few minutes, so it is more pronounced in capillaries with slow blood flow (spleen, vasa recta of the renal medulla). With a general slowdown in blood flow (shock) or hypoxia (at high altitudes, during air travel, during anesthesia), erythrocyte aggregation may increase in other organs (for example, in the heart). Occlusion of blood vessels impairs blood flow in the affected organs and tissues and PO 2 is further reduced, leading to a vicious circle. Sickle cell anemia occurs almost exclusively in dark-skinned people who either themselves or their ancestors migrated from regions of central Africa with a high prevalence of malaria. The “survival” of the defective gene in 40% of the population of Central Africa, despite the fact that until recently children homozygous for the given gene died, can be explained by the fact that heterozygous carriers of the gene are protected from severe forms malaria (selective advantage).

In β-thalassemia, the formation of β-chains is reduced, which leads to a deficiency of HbA. This can be partially compensated by increased formation of HbA 2 and HbF. Partially included in the composition of heme, therefore, some of the iron in erythrocytes remains unused (sideroachresia). Subsequently, Fe 2+ can accumulate in the body in excess quantities (secondary hemochromatosis). Although the osmotic resistance of red blood cells increases, their sensitivity to mechanical damage, so they are quickly destroyed in the spleen (early hemolysis). While the heterozygous form (thalassemia minor) is virtually asymptomatic, the homozygous form (thalassemia major) can lead to death in patients even before puberty. With rare α-thalassemia, fetal death is usually observed, because in the absence of the α-chain, HbF synthesis is also impaired. Hbγ 4, formed in this case in the fetus, and Hbβ 4, synthesized in the postnatal period, obviously are not able to adequately replace normal forms of hemoglobin.

Causes of anemia

Weakened or ineffective hematopoiesis

Lack of iron, vitamin B 12 or folate.
Kidney failure.
Hypoplasia.
Anemia of chronic diseases

Peripheral causes

Blood loss.
Hypersplenism
Hemolysis.

Symptoms and signs of anemia

The clinical picture of anemia is determined by the depth of oxygen deficiency and depends on the degree of anemia, the rate of its increase and the presence of cardiopulmonary pathology in the patient. The rapid development of anemia (for example, with bleeding) is accompanied by more severe symptoms than with its gradual increase. In patients suffering from cardiopulmonary diseases, symptoms of anemia may appear against the background of higher hemoglobin numbers than in persons with healthy hearts and lungs.

Diagnosis of anemia

When diagnosing anemia, it is necessary to take into account additional factors- pregnancy, living in high mountains, etc.

The diagnosis of anemia should reflect not only the severity of the course, but also indicate its cause. Diagnosis is based on anamnestic data, examination results, determination of all clinical indicators blood, viewing a blood smear and additional research methods.

Anamnesis

Iron deficiency anemia is the most common form in the world. Anamnestic data concerning the gastrointestinal tract are important; pay attention first of all to signs indicating blood loss. Heavy menstruation is one of the most typical reasons anemia in women. In women, it is necessary to be interested in the course of the menstrual cycle.
When assessing dietary patterns, it is necessary to determine the level of iron and folate intake in the body. Nutrition may be insufficient and not meet the needs of the body (for example, during pregnancy or during a period of intensive growth of a child or adolescent),
A history of past illnesses helps to identify a disease that is accompanied by anemia, for example rheumatoid arthritis, previous operations (resection of the stomach or small intestine, which lead to impaired absorption of iron and/or vitamin B 12).
Family history and the patient's ethnicity are important in diagnosing certain forms of hemolytic anemia, such as hemoglobinopathies and hereditary spherocytosis.
Determining the patient's medications will indicate drugs that can provoke blood loss (for example, aspirin and other anti-inflammatory drugs), hemolysis, or bone marrow aplasia.

Physical examination

Along with the general objective signs anemia, sometimes it is possible to identify signs indicating the origin of anemia. So, for example, in a patient you can feel a space-occupying formation in the right iliac region - cancer of the cecum; hemolytic anemias are manifested by jaundice; Vitamin B12 deficiency is accompanied by neurological symptoms in the form of peripheral neuropathy and dementia. Sickle cell anemia is sometimes accompanied by ulcers on the legs. Anemia can have several causative factors, and the absence of specific symptoms does not exclude the presence of a “hidden” pathology.

The patient's examination plan for anemia is often based on the size of red blood cells.

A normal MCV (normocytic anemia) suggests acute blood loss.
Small MCV (microcytic anemia) may indicate iron deficiency or thalassemia.
Large MCV (macrocytic anemia) is a sign of vitamin B 12 or folate deficiency.