Thrombocytopathies. Pathogenetic classification

Reduction in the number of red blood cells and hemoglobin content below standard sizes called anemia. Anemia is not an independent disease, but a symptom that accompanies many physiological and pathological processes and is relatively rarely caused by primary diseases of the hematopoietic system.

Based on hematocrit values, anemia can be divided into the following degrees of severity:

Mild anemia 36-42%;

Average 24-35%;

Severe less than 24%.

Hematocrit less than 15% requires emergency blood transfusion.

Pathogenetic classification (7) Anemia due to blood loss

Chronic posthemorrhagic anemia.

Anemia caused by insufficiency of erythropoiesis (hypoproliferative)

1. Hypochromic anemia:

Iron deficiency;

Anemia associated with impaired porfin synthesis.

2. Normochromic anemia:

Anemia of chronic diseases;

Anemia in chronic renal failure;

Aplastic anemia;

Anemia in tumor and metastatic lesions of the bone marrow.

3. Megaloblastic anemia:

Anemia due to vitamin deficiency

Folate deficiency anemia.

Anemia due to increased destruction of red blood cells (hemolytic anemia)

1. Anemia caused by extra-erythrocyte factors:

Immune hemolytic anemias:

Isoimmune hemolytic anemia;

Autoimmune hemolytic anemias.

Table 9

Algorithm differential diagnosis anemia (M.M.\Vlntrobe)

Hemolytic anemia caused by mechanical damage to red blood cells.

2. Anemia caused by erythrocyte factors:

Hemolytic anemia associated with a violation of the structure of the erythrocyte membrane (microspherocytic, ovalocytic, stomatocytic, acanthocytosis);

Hemolytic anemia caused by a deficiency of erythrocyte enzymes (glycolytic enzymes, pentose phosphate shunt enzymes, glutathione system enzymes);

Hemolytic anemia associated with impaired globin synthesis.

3. Hemolytic anemia caused by somatic mutation of myeloprogenitor cells.

Acute posthemorrhagic anemia

Acute posthemorrhagic anemia is a condition that develops as a result of rapid loss of a significant volume of blood. The cause of acute blood loss can be: violation of the integrity of the walls of the vessel due to its injury, damage by the pathological process in various diseases (stomach and intestinal ulcers, tumors, pathological childbirth, etc.); changes in capillary permeability (hemorrhagic diathesis) or disturbances in the hemostasis system. The consequences of these changes, regardless of the reasons that caused them, are the same.

The body's normal response to blood loss is characterized by activation of hematopoiesis.

The anemia that develops from 1-2 days after blood loss is normochromic in nature: CP is close to 1.0. The greatest changes in hematological parameters of peripheral blood are usually observed 4-5 days after blood loss. These changes are caused by active proliferation of bone marrow elements. The criterion for the activity of hematopoiesis (erythropoiesis) is an increase in the amount of

reticulocytes up to 2-10% or more, polychromatophils (Fig. 28). Reticulocytosis and polychromatophilia, as a rule, develop in parallel and indicate increased regeneration of erythrokaryocytes and their entry into the blood. The size of red blood cells increases slightly after bleeding (macrocytosis). Erythroblasts may appear. If the reticulocyte count does not decrease by the beginning of the second week, this may indicate ongoing bleeding.

The severity of anemia is diagnosed by indicators of Hb, red blood cells, reticulocytes, and iron metabolism.

On the 5-8th day after bleeding, moderate leukocytosis (1.2-1.8 times) and a slight band shift usually occur. Persistent leukocytosis occurs in the presence of an associated infection. The platelet count increases 1.5-2 times.

With small blood losses, deposited iron enters the bone marrow, where it is used for the synthesis of hemoglobin. The degree of increase in serum iron depends on the level of reserve iron, erythropoiesis activity and plasma transferrin concentration. With a single acute blood loss, there is a transient decrease in the level of serum iron in plasma. With large blood losses, serum iron remains low. Reserve iron deficiency is accompanied by sideropenia and the development of iron deficiency anemia. The degree of anemia is influenced by the volume and rate of blood loss, the time from the moment of bleeding, the iron reserve in the depot organs, the initial number of red blood cells and hemoglobin.

Tissue hypoxia, which develops during blood loss, leads to the accumulation of under-oxidized

metabolic products and acidosis, which at first is compensated. The progression of the process is accompanied by the development of uncompensated acidosis with a decrease in blood pH. In the terminal stage, alkalosis joins acidosis. The respiratory quotient increases. Hyperglycemia develops, the activity of the enzymes LDH and AST increases, which confirms damage to the liver and kidneys. In the serum, the concentration of Na and Ca decreases, the content of K, Mg, inorganic P and C1 increases, the concentration of the latter depends on the degree of acidosis and can decrease with its decompensation.

Chronic posthemorrhagic anemia

Chronic posthemorrhagic anemia is a hypochromic-normocytic anemia that occurs with prolonged moderate blood loss.

Such conditions are similar to iron deficiency anemia (IDA) and accompany:

Chronic gastrointestinal bleeding;

Inflammatory processes in the uterus;

Blood loss from the urinary tract.

Iron deficiency is possible with unbalanced artificial nutrition and infections of young animals, as a result of impaired absorption in the intestine (after extensive resection of the small intestine, with chronic enteritis, giardiasis, helminthic infestations).

Impaired transport of iron from the depot to the erythron occurs in the absence of transferrin synthesis, as well as liver diseases accompanied by impaired protein synthetic function (hepatitis, cirrhosis, liver cancer).

Therapy with recombinant erythropoietin leads to stimulation of erythropoiesis and increased iron consumption by erythrokaryocytes, which contributes to the development of IDA-

Table 10

Anemia due to blood loss

In each case, iron deficiency is preceded, first of all, by depletion of its reserves, then transport iron decreases, then the activity of iron-containing enzymes decreases, and lastly, the synthesis of Hb is disrupted.

With a long course of IDA, the proliferative activity of the bone marrow is depleted, ineffective erythropoiesis increases, which leads to a decrease in the number of myelokaryocytes, a decrease in the number of erythrocytes, the appearance of a population of erythrocytes with an increased volume, and a possible delay in the maturation of granulocytes.

During the examination, you need to pay attention to searching for the causes of minor prolonged bleeding: bleeding gums, severe flea infestation, etc.

Anemia associated with impaired porphin synthesis (sideroblastic anemia)

Anemias of this group (quite rare in animals) are caused by insufficient or abnormal utilization of intracellular iron during the synthesis of Hb, despite normal or even increased iron content in the mitochondria of erythrokaryocytes. Such defects may be associated with hereditary disorders or with an acquired nature of the lesion, for example, as a result of lead poisoning or vitamin B6 deficiency. A distinctive feature of this type of anemia is the saturation of the body with iron.

This anemia is characterized by signs of ineffective erythropoiesis, which is defined as anemia with relative or absolute reticulocytopenia. Serum iron content is significantly increased.

In the peripheral blood, the content of Hb gradually decreases by 2 or more times, erythrocytes with pronounced hypochromia (low CP, MCH, MCHC), aniso-poikilocytosis is detected, and basophilic punctuation of erythrocytes appears (Fig. 15).

Anemia of chronic diseases (ACD)

Anemia accompanying infectious, rheumatic and tumor diseases is conventionally called “anemia of chronic diseases” (ACD). Their frequency in these conditions reaches 100%. ACD ranks second in prevalence after IDA. ACD is characterized by a redistribution or functional deficiency of iron, due to the accumulation and blockade of iron release in tissue macrophages, which leads to a decrease in the delivery of iron to bone marrow erythrokaryocytes, impaired erythropoiesis and the development of anemia.

More often, anemia in ACD is normochromic, normocytic, and less often moderately hypochromic.

Table 11

Differential diagnosis of anemia ACD and IDA

Differential diagnosis of true and redistributive iron deficiency is possible only if the level of serum ferritin is determined. Misdiagnosis of IDA may lead to the prescription of iron supplements with the development of secondary hemosiderosis.

Anemia in chronic renal failure

Anemia is one of the most characteristic syndromes accompanying the course of chronic renal failure (CRF). When creatinine clearance decreases below ZOml/min, signs of anemia appear before the development of severe azotemia. The development of end-stage chronic renal failure is manifested by severe uremia, combined with severe anemia.

The reasons leading to the development of anemia include:

Deficiency of endogenous erythropoietin;

Shortening the lifespan of red blood cells;

Toxic effect on erythrocytes of nitrogen metabolism products that promote membrane-lytic processes;

Blood loss caused by a platelet defect.

In the peripheral blood, normochromic normocytic, less often hypochromic microcytic anemia is detected. The reticulocyte count in nephrogenic anemia is usually normal or slightly reduced.

Treatment of patients with chronic renal failure with recombinant erythropoietin drugs leads to partial correction of anemia, but due to stimulation of erythropoiesis it may

develop IDA, according to which it is necessary to study the parameters of iron metabolism during treatment.

Anemia in chronic renal failure is characterized by:

Low hematocrit;

Reduced number of red blood cells and Hb content in them;

Reduced number of reticulocytes;

Hypoplasia of erythroid elements of the bone marrow.

The severity of normocytic normochromic hypoplastic anemia is proportional to azotemia (due to the toxic effect of nitrogen metabolism products).

A blood test reveals: high levels of urea nitrogen, creatinine, P, Ca, low levels of bicarbonate and K, hypoproteinemia, hypoalbuminemia. The iron content in the blood serum is normal or reduced.

The urine shows: impaired urination, moderate proteinuria, and the presence of active sediment.

Cats should be screened for carriage of leukemia and immunodeficiency viruses to rule out myelodyscrasia associated with these viruses.

Aplastic anemia

Aplastic anemia (AA) is a disease characterized by a sharp inhibition of bone marrow hematopoiesis, inhibition of the processes of proliferation and differentiation of cellular elements with different

development of deep pancytopenia in the peripheral blood.

The clinical picture is determined by anemic and hemorrhagic syndromes. The main manifestations of AA are caused by inhibition of normal hematopoiesis, hypoxia of tissues and organs (shortness of breath, tachycardia, weakness) and severe thrombocytopenia (bruising, nosebleeds, etc.). As a result of severe neutropenia, pneumonia, otitis, sinusitis, pyelitis and other inflammatory processes develop, and sepsis is possible.

Peripheral blood is characterized by signs of severe normochromic anemia with a sharp decrease in the concentration of Hb, the number of red blood cells, moderate anisocytosis with a tendency to macrocytosis, and poikilocytosis. The content of reticulocytes varies from 0.3 to 0.9%, with hemolysis reaching 4-5%. Characteristic of AA is pronounced leukopenia (up to 2.5-0.55 thousand per µl) with absolute neutropenia (8-40%) and relative lymphocytosis. Thrombocytopenia is pronounced; sometimes platelets may be absent in peripheral blood smears. In most cases, AA is accelerated by ESR. Severe forms of AA include cases with the number of granulocytes in the blood less than 0.5 thousand per μl, platelets less than 20.0 thousand per μl.

The number of red blood cells and Hb is reduced, MSU and MCH are increased, MCHC means increased.

Blood samples are examined for ehrlichiosis, feline leukemia virus, antibodies to erythrocytes, leukocytes, platelets, and other autoimmune diseases (antinuclear antibodies to systemic lupus erythematosus).

Anemia in tumor and metastatic lesions of the bone marrow

Damage to the bone marrow in hemoblastoses and multiple metastases of solid tumors leads to inhibition of normal hematopoietic germs, including erythroid, which is accompanied by the development of anemia, which can occupy a major place in the clinical picture. Metastases to the bone marrow occur in tumors of various locations, but are most typical for breast cancer, prostate cancer, kidney cancer, lung cancer, thyroid cancer, and neuroblastoma.

More often, anemia is normochromic and normocytic in nature, the number of reticulocytes is increased. Pancytopenia often develops. Blood smears reveal anisocytosis, poikilocytosis, polychromatophilia, and erythrokaryocytes. A shift to myelocytes may be observed in the leukocyte formula. Morphological examination of bone marrow punctures reveals complexes of tumor cells.

Megaloblastic anemias

Anemia associated with impaired DNA synthesis can be either hereditary or acquired. A common feature of these anemias is the presence of megaloblastic hematopoiesis in the bone marrow. In megaloblastic anemia, the synthesis of nucleic acids is disrupted as a result of a deficiency of vitamin B or folic acid. Their combined deficiency is rare, only when intestinal absorption is impaired.

More often there is an isolated deficiency of vitamin B12, less often - folic acid. Reasons for the development of B]2 deficiency:

Malabsorption (atrophic gastritis, gastrectomy, damage to the small intestine);

Insufficient food intake;

Competitive consumption (wide tapeworm using B12 for its own growth);

Increased utilization of B12 (malignant neoplasms, hyperthyroidism);

Hereditary deficiency of transcobalamin-11.

In a clinical blood test, the number of red blood cells decreases to a greater extent than the Hb level. CPU is greater than 1.2. Hyperchromic anemia. Anisocytosis of erythrocytes due to microcytes, megalocytes. In erythrocytes one can find Jolly bodies (Fig. 22), less commonly Cabot rings (Fig. 16), and basophilic granularity is found (Fig. 15). The number of reticulocytes and leukocytes is reduced. There is a shift in the leukocyte formula to the right - large polysegmented neutrophils appear. The number of eosinophils and monocytes decreases, until they disappear. Relative lymphocytosis.

The diagnosis of B]2-deficiency anemia can only be established by morphological examination of the bone marrow, which is advisable to carry out before the administration of vitamin B2. Injection of B12 for 1-2 days changes the type of hematopoiesis in the bone marrow.

Hemolytic anemia

Hemolytic anemia is a large group of hereditary and acquired diseases in which

the processes of blood destruction prevail over the processes of blood formation. With them, the life expectancy of red blood cells is reduced. The destruction of red blood cells (hemolysis) can develop under the influence of endogenous and exogenous causes.

Endogenous causes include disruption of the structure of hemoglobin and red blood cells.

Exogenous - the impact of various toxic substances, antibodies, mechanical damage on red blood cells with unchanged morphological properties and functional activity.

The lifespan of red blood cells is 90-120 days. About 90% of aged erythrocytes are destroyed in the organs of the reticuloendothelial system (RES), mainly in the macrophages of the spleen and partly in the liver, with the formation of bile pigments, 10% of erythrocytes are destroyed in the capillaries of the vascular bed with the release of free hemoglobin, which binds in the blood to plasma protein - haptoglobin. The hemoglobin - haptoglobin complex is absorbed by the RES and destroyed by its cells. The ability of haptoglobin to bind hemoglobin prevents its extrarenal excretion. An excess of the reserve hemoglobin-binding capacity of haptoglobin or a decrease in its level in the blood is accompanied by the release of hemoglobin through the kidneys in the urine.

Hemolytic anemias are distinguished between intracellular (red blood cells are destroyed in tissues as a result of changes in plasticity) and intravascular hemolysis (destruction inside blood vessels).

The type of hemolysis determines the symptoms and treatment of the disease. Each type of hemolysis corresponds to certain laboratory parameters.

Table 12

Comparative characteristics of intracellular and intravascular hemolysis

Anemia, caused predominantly by intravascular hemolysis, usually has an acute onset of the disease and is characterized by an increase in the content of free hemoglobin in the blood serum, excretion

its loss in the urine and deposition of hemosiderin in the kidney tubules.

Anemia characterized by intracellular hemolysis is more likely to have a chronic course with hemolytic crises, remissions and splenomegaly, which develops in response to prolonged increased hemolysis of red blood cells. Hemolysis with intracellular localization of the process is accompanied by changes in the exchange of bile pigments with the deposition of hemosiderin in the spleen.

However, in some situations, for example, in the presence of two types of anti-erythrocyte antibodies (agglutinins and hemolysins) in the blood, signs of both intracellular and intravascular hemolysis may be detected. The degree of hemolysis depends on the activity of the RPE cells and the antibody titer.

A reduction in the lifespan of red blood cells is a common characteristic of all hemolytic anemias. If the intensity of hemolysis does not exceed the physiological level, then the excessive destruction of red blood cells is compensated by the regenerative proliferation of the bone marrow. At the same time, signs of activation of hematopoiesis are detected in the blood (reticulocytosis and polychromatophilia). Reticulocytes up to 8-10%, erythrocytes and Hb are normal. Leukocytosis and minor thrombocytosis are possible. Other signs of hemolysis are an increase in the concentration of unconjugated bilirubin, hemosiderinuria and hemoglobinemia.

With a pathological increase in the destruction of erythrocytes by more than 5 times and insufficient activity of hematopoiesis, anemia develops, the degree of which depends on the intensity of hemolysis, the initial hematological

Rice. 5.6. Dog bone marrow. Cells: granulocyte precursors (1), erythrocyte precursors (2). Uv. xYOOO

ical indicators and the state of erythropoiesis. Prolonged or frequently repeated intravascular hemolysis leads to iron deficiency in the body and the development of IDA. Reticulocytosis, polychromatophilia, and erythronoblastosis are observed in the peripheral blood.

Scheme of laboratory examination for hemolytic anemia

1 - direct Coombs test;

3 - search for immune diseases by counting platelets, etc.;

4 - search for infectious diseases, tumors of the lymphatic and monocytic systems;

5 - collecting anamnesis about medications taken, vaccines, the possibility of contact with poisons;

6 - cold or agglutination test;

7 - test of osmotic resistance of erythrocytes. The direct Coombs test is used to identify im-

munohemolytic anemia, in which, due to mostly unclear reasons, antibodies are formed directed against one’s own red blood cells (autoantibodies). These complete or incomplete antibodies and/or complement are located on the surface of red blood cells and thereby change their membrane. Subsequently, agglutination and/or hemolysis of red blood cells occurs, and they are phagocytosed in the RES (primarily the spleen) due to their altered surface. Secondary immunohemolytic anemias also occur, for example with

lupus erythematosus, tumors, lymphoproliferative diseases, infections, autoimmune diseases (thyroiditis, ulcerative colitis, type 1 diabetes, sarcoidosis) and allergies to medications.

In contrast to autoantibodies, isoantibodies act not on their own, but on foreign red blood cells. Isoantibodies are directed against certain blood groups and can occur due to improper blood transfusion.

Per unit volume of blood. Anemia accompanies many diseases and is an independent pathology.

Anemia can be classified by pathogenesis, which is convenient for understanding the mechanism of anemia development according to erythrocyte indices, peripheral blood smear and reticulocyte count, and also convenient for studying the clinical problem.

1. Anemia due to hypofunction of the bone marrow with reduced production of red blood cells - occurs as a result of the inability of the bone marrow to form new red blood cells.

• Replacement of hematopoietic bone marrow tissue (myelophthisic anemia associated with tumors or granulomas, tuberculosis). In the absence of severe anemia, or the appearance of nucleated red blood cells on a blood smear, may indicate miliary tuberculosis or bone marrow metastases.
• Bone marrow damage (hypoplastic and).
• Nutrient deficiency (megaloblastic anemia due to deficiency or).
• Endocrine hypofunction (pituitarism, hypofunction of the adrenal glands, thyroid gland; anemia in chronic renal failure).
• Bone marrow hypofunction due to decreased hemoglobin production (hypochromic microcytic anemia).

2. Incomplete synthesis of heme (iron deficiency anemia with reduced levels, pyroxidine-dependent anemia).

3. Incomplete synthesis of globin (thalassemia, hemoglobinopathy).

4. Excessive loss of red blood cells.

5. Hemolytic anemia:

• Hemolytic anemia caused by a genetic defect of red blood cells.

Abnormal form (hereditary spherocytosis, hereditary elliptocytosis).

Abnormal hemoglobin (sickle cell anemia, thalassemia, HbC disease).

Abnormalities of erythrocyte enzymes (congenital non-spherocytic hemolytic anemia, G-6-PDG deficiency).

• Hemolysis with acquired erythrocyte defects and positive.

Autoantibodies (cold or warm autoimmune), transfusion reactions, microangiopathic hemolytic anemia as in systemic lupus erythematosus, malignant lymphoma).

Exogenous allergens, such as penicillin allergy.

6. Excessive loss of normal red blood cells.

• Bleeding.
• Hypersplenism.
• Chemical agents (eg lead).
• Infectious agents (eg Clostridium welchii, Bartonella, malaria).
• Mixed diseases (eg, uremia, liver disease, cancer).
• Physical agents (eg burns).
• Mechanical injuries (eg, artificial heart valves).
• In patients with prosthetic heart valves, a blood smear reveals fragmented, oddly shaped red blood cells.

Anemias are multifactorial conditions. The final diagnosis depends on the dominant factor causing the anemia. The diagnosis should be re-evaluated after treating the underlying causes of the disease.

Department of Internal Medicine No. 1 with a course of cardiovascular pathology

METHODOLOGICAL DEVELOPMENT OF THE LECTURE

Academic discipline "Internal Medicine"

MODULE No. 1 “Fundamentals of internal medicine (endocrinology, cardiology, general issues, hematology)”

Lecture No. 1 “ANEMIA”

Course IV. Faculty: medical, international

Specialty: 7.12010001 "General Medicine"

7.12010002 “Pediatrics”

7.12010003 “Medical and preventive care”

Lecture discussed

At the methodological meeting of the department

D. Protocol No. 3.

Head of department

Doctor of Medical Sciences Yu.I. Karpenko

Odessa -2012

Lecture “Anemia” - 2 hours

І. Relevance of the topic. Rationale for the topic

ІІ. Purpose of the lecture

Learning objectives:

1. Have an idea of ​​the prevalence of the epidemiology of anemia.

2. Know the etiology and pathogenesis of anemia.

3. Know the clinical picture of anemia.

4. Know laboratory methods for diagnosing anemia.

5. Know the basic methods of treating anemia.

Educational goals:

1. Form deontological ideas when working with patients with anemia.

2. Using the material of the topic being studied, develop a sense of responsibility for the timeliness and correctness of professional actions

3. To form an idea of ​​the basics of a psychotherapeutic approach to patients

4. Form an idea of ​​medical ethics.

III. Lecture plan and organizational structure

Bibliography:

1. V.G. Perederiy, S.M. Weaver. Clinical lectures on internal medicine. – T.2. – Kyiv, 1998.

2. Perederiy V.G., Tkach S.M. Fundamentals of internal medicine. – Vinnytsia: Novaya kniga, 2009. – 784 p.

3. Internal diseases / Ed. B.I. Shulutko. – T.2. – S-P, 1994.

Questions:

1) Define anemia.

2) Know the clinical classification of anemia and the criteria underlying it.

3) Etiology and pathogenesis of anemia.

4) Clinical manifestations of anemia.

5) Differential diagnosis of anemia.

6) Principles and methods of treating anemia. The main classes of drugs used to treat anemia.

7) Preventive measures

IV. Lecture text

ANEMIA

Anemia is a decrease in the amount of Hb per unit volume of blood, often with a simultaneous decrease in the number of red blood cells (or the total volume of red blood cells).

The term “anemia” without detail does not define a specific disease, but indicates changes in blood tests, i.e. anemia should be considered one of the symptoms of various pathological conditions.

General laboratory signs of anemia. Hb content in the blood is less than 140 g/l or hematocrit (Ht) is less than 42% in adult men; Hb content is less than 120 g/l or Ht is less than 37% in adult women.

Classification. According to the morphology of erythrocytes - micro-, normo- and macrocytic anemia. Objective criterion - MSD (average carpuscular volume - measured directly using an automated counter. The normal MSD value is 80-95 fL (normocytosis). A decrease in MSD less than 80 fL is microcytosis. An increase in MSD over 95 fL is macrocytosis).

Based on the degree of saturation of erythrocytes with Hb (or serum iron content), hypo-, normo- and hyperchromic anemias are distinguished. The objective criterion is SSEG (the average hemoglobin content in an erythrocyte is normal - 27-33 picograms).

Based on the combination of the first and second criteria, hypochromic microcytic anemias are distinguished (low MSD and SSGE), macrocytic (increased MSD), normochromic normocytic (MSE and SSGE are within normal limits). According to the degree of red blood cell regeneration: hyporegenerative (aregenerative) and hypergenerative anemias. Determined by the number of blood reticulocytes or the reticulocyte index.

By severity: mild anemia (Hb 91-119 g/l), moderate anemia (Hb 70-90 g/l), severe (Hb less than 70 g/l).

Pathogenetic classification

I. Anemia due to impaired Hb synthesis and iron metabolism (hypochromic microcytic).

Iron deficiency anemia

Thalassemia

Sideroblastic anemia

Anemia in chronic diseases (60% hypochromic normocytic). II. Anemia due to impaired DNA synthesis (hyperchromic macrocytic with

megaloblastic type of hematopoiesis).

Pernicious anemia and other B 12 deficiency anemias

Folate deficiency anemia.

III. Other pathogenetic mechanisms (usually normochromic normocytic anemia).

1. Anemia combined with a decrease in the bone marrow response to erythropoietin: aplastic; hypoplastic; disorders characterized by cellular infiltration of the bone marrow (myelophthisic anemia).

2. Hyperregenerative anemia: acute posthemorrhagic; hemolytic.

IRON DEFICIENCY ANEMIA

IDA is a disease caused by depletion of iron reserves in the body, which entails a disruption in the synthesis of iron-containing proteins. The disease is manifested by a decrease in the concentration of hemoglobin in the blood and trophic disorders in the tissues.

Epidemiology. According to WHO experts, 700-800 million people around the world suffer from IDA or hidden iron deficiency.

Etiology. The most important reason for the development of IDA is blood loss. The main causes of blood loss: hyperpolymenorrhea, abortion, childbirth; chronic bleeding from the gastrointestinal tract (peptic ulcer of the stomach, duodenum; stomach tumors; tumors of the small intestine; tumors of the colon; hiatal hernia; esophagitis; erosive gastritis; Crohn's disease; diverticulosis; hemorrhoids); associated with taking medications (aspirin, NSAIDs, anticoagulants); nosebleeds; hematuria; hemoptysis; bleeding into closed body cavities; donation; acute blood loss (surgeries, wounds, trauma).

Nutritional IDA develops with a decrease in foods containing iron in the diet.

In women, frequent pregnancy and breastfeeding can cause IDA.

Pathogenesis. Depletion of iron stores leads to a decrease in hemoglobin synthesis in bone marrow erythrokaryocytes, which leads to a decrease in its concentration, and then in the concentration of erythrocytes per unit volume of blood. Adaptive mechanisms are an increase in cardiac output and increased release of oxygen in tissues, resulting from an increased concentration of 2-3-diphosphoglycyric acid in erythrocytes. With iron deficiency, muscle performance is impaired. The cause of functional muscle failure is the reduced activity of iron-containing enzymes, the main significance being the depletion of α-glycerophosphate dehydrogenase.

With severe iron deficiency, neurological disorders, distortion of taste and smell perception, and trophic disorders (increased fragility and hair loss, brittle nails, dry skin, angular stomatitis and atrophic glossitis) may develop.

Clinical picture.

General anemic complaints: weakness, dizziness, fainting, palpitations, shortness of breath.

Sideropenic syndrome: dry and atrophic skin, brittle nails and hair, hair loss. A very characteristic change in taste, addiction to eating chalk, toothpaste, clay, raw cereals, raw coffee, unpeeled sunflower seeds. The perception of smells changes. There is an addiction to the smell of gasoline, kerosene, nail polish (acetone), the smell of damp clay, and lime.

Neurological disorders: headache, paresthesia, difficulty swallowing solid food, urinary incontinence.

An objective examination reveals pallor of the skin and mucous membranes, dry, thinned skin, nails flatten and sometimes become concave (spoon-shaped) - koilonychia, angular stomatitis in the corners of the lips and redness of the tongue, smoothness of its papillae.

IDA is characterized by a decrease in the amount of hemoglobin and red blood cells. Anemia is hypochromic (microcytic) in nature. The reticulocyte count is within normal limits. The number of leukocytes, platelets and the nature of the leukocyte formula were not changed. In severe iron deficiency, along with severe hypochromic (microcytic) anemia, mild neutropenia and, less commonly, thrombocytopenia may occur.

Diagnostics.

The main criteria for IDA are the following: low color index (0.6-0.7); hypochromia of erythrocytes; anisocytosis (reduced red blood cells) and poikilocytosis (changes in the shape of red blood cells); decreased serum iron levels (less than 12 µmol/l); increase in the total iron-binding capacity of serum (more than 85 µmol/l); decreased serum ferritin levels; clinical manifestations of hyposiderosis (non-permanent sign); effectiveness of iron supplements.

The presence of a hypochromic nature of anemia makes one first of all suspect that the patient has IDA (all IDA are hypochromic!). However, the fact of the presence of hypochromic anemia in itself does not exclude other pathogenetic variants of anemia (not all hypochromic anemias are iron deficiency!).

For example, hypochromic anemia can occur when there is a defect in Hb synthesis as a result of a violation of the inclusion of iron in its molecule with normal or even elevated levels of iron in the blood serum. To distinguish between these conditions and thereby verify IDA, it is possible to study the iron content in the serum, which should be performed before prescribing iron medications to patients or carrying out red blood cell transfusions. Doctors, nursing staff (nurses, laboratory assistants), as well as patients themselves should be aware of this.

Along with determining the iron content in blood serum, an important laboratory indicator determined for IDA is the total iron-binding capacity of the serum, which reflects the degree of “starvation” of the serum and saturation of the transferrin protein with iron. The total iron-binding capacity of serum in IDA is always increased, in contrast to other hypochromic anemias associated not with iron deficiency, but with a violation of its inclusion in the hemoglobin molecule or with the redistribution of iron from erythroid cells to cells of the macrophage system (for example, during active inflammatory processes). Desferal test (iron excretion in urine) for IDA - below 0.2 mg/day.

A decrease in the level of the iron-containing protein ferritin is an essential diagnostic criterion for IDA with high specificity. Ferritin characterizes the amount of iron reserves in the body. Since depletion of iron stores is a mandatory stage in the formation of IDA, the level of ferritin is one of the specific signs of the iron deficiency nature of hypochromic anemia. It should, however, be borne in mind that the presence of a concomitant active inflammatory process in patients with IDA may mask hypoferritinemia.

Additional methods for determining iron stores in the body include counting the number of bone marrow erythroid cells containing iron granules (sideroblasts) and the amount of iron in the urine after administration of iron-binding drugs, such as desferrioxyamine. The number of sideroblasts in IDA is significantly reduced until they are completely absent, and the iron content in the urine does not increase after the administration of desferrioxyamine.

Pathomorphology of bone marrow. The picture of hematopoiesis in the bone marrow in patients with IDA is not much different from that in healthy individuals. There may be slight hyperplasia of the erythroid lineage. A sharp decrease or complete absence of iron reserves in the stromal and macrophage elements of the bone marrow, as well as a sharp decrease in the number of sideroblasts, is revealed.

It is necessary to differentiate IDA from other variants of hypochromic anemia: thalassemia; anemia in chronic inflammation.

Treatment. It is important to identify and, if possible, eliminate the cause of iron deficiency (surgical treatment of stomach and intestinal tumors, treatment of enteritis, correction of nutritional deficiency, etc.). For successful treatment of IDA, only medicinal forms of iron should be used; it is even theoretically impossible to replenish the required amount of iron by obtaining it from food due to limited absorption. From medicinal sources in patients with IDA, the absorption of iron increases at least 10 times compared to the absorption of iron from food, i.e. it is 20-25 mg/day. At this level of absorption, the hemoglobin level increases by approximately 1% per day.

In some cases, radical elimination of the cause of IDA is not possible, for example, with ongoing menorrhagia, hereditary hemorrhagic diathesis manifested by nosebleeds, in pregnant women and in some other situations. In such cases, pathogenetic therapy with iron-containing drugs becomes of primary importance.

In clinical practice, iron medications are used orally or parenterally. The route of administration of the drug in patients with IDA is determined by the specific clinical situation.

In most cases, to correct iron deficiency in the absence of special indications, iron supplements should be prescribed orally.

Treatment of iron deficiency anemia is continued until the level of hemoglobin in the blood normalizes, then iron supplements are used in smaller doses for several months to restore its reserves in the depot.

Iron preparations are produced in the form of various salts: iron gluconate (ferronal), iron polyisomaltose (ferrum-lek), iron sulfate (ferrocal, ferroplex, sorbifer durules, conferon, ferro-gradument, fenyuls, etc.), iron fumarate (ferretab comp. , heferol), iron chloride (hemofer). Only divalent iron preparations are taken orally, because Ferric iron compounds are practically not absorbed from the intestines. In iron deficiency conditions, Hb synthesis requires 50-100 mg of iron daily. Since when taking iron supplements orally, only 25% of the dose taken can be absorbed, then to quickly correct iron deficiency in the body, it must be used at a dose of 200^00 mg per day. If gastrointestinal disorders occur, it is possible to reduce the dose of iron, but in this case, iron deficiency is eliminated more slowly.

Iron gluconate is prescribed orally, after meals, 4-6 tablets per day; iron sulfate - after meals, 0.3-0.5 g 3-4 times a day.

Iron fumarate - 1 capsule per day on an empty stomach; if the effect is insufficient, you can take 1 capsule 2 times a day. Reception is continued after the blood picture has normalized. The duration of the saturation course of therapy is at least 1-1.5 months.

Iron chloride is taken at a dose of 4-6 mg/kg body weight per day, divided into 3-4 doses.

The basic principles of treatment with oral iron preparations are as follows:

Prescribing iron supplements with sufficient ferrous iron content;

Prescribing iron supplements containing substances that enhance iron absorption;

It is undesirable to simultaneously take nutrients and medications that reduce iron absorption;

It is inappropriate to simultaneously prescribe vitamins B, B12, and folic acid without special indications;

Avoid prescribing iron supplements orally if there are signs of impaired absorption in the intestine;

Sufficient duration of the saturating course of therapy (at least 1-1.5 months);

The need for maintenance therapy with iron supplements after normalization of hemoglobin levels in appropriate situations.

Treatment with oral medications should be carried out until hemoglobin levels normalize, and then for another 2 months at half the dose to replenish iron reserves in the depot. Long-term uncontrolled use of large doses can lead to hemosiderosis of internal organs.

Parenteral drugs should be used only in selected patients.

Ferrum LEK preparations are more often used for intramuscular administration (polyisomaltose) and for intravenous administration (sodium-saccharate complex); ectofer (sorbitol citrate complex) for intramuscular injection and venofer (iron saccharate) for intravenous administration. One ampoule of each of these drugs contains 100 mg of iron.

Indications for parenteral treatment with iron preparations:

Malabsorption in the intestine with severe enteritis;

Extensive resection of the small intestine;

Inability to take oral iron supplements.

The use of parenteral iron preparations does not allow one to actually shorten the treatment period and accelerate the rise in hemoglobin concentration to the desired level. To do this, if there are really significant indications, it is better to use red blood cell transfusion. The use of parenteral iron preparations is limited by the high risk of developing anaphylactic reactions, hemosiderosis of internal organs and painful, often abscessing infiltrates at the sites of drug administration.

Side effects when treated with iron preparations: facial flushing, nausea, dizziness, headache, allergic skin reactions. Less commonly - vomiting, diarrhea, abdominal pain, back pain, tachycardia, transient decrease in blood pressure. With intramuscular injection, abscesses may develop at the injection site.

Iron supplements are contraindicated for hemochromatosis and hypersensitivity to iron. Iron preparations should not be prescribed parenterally for hypertension, severe coronary insufficiency, allergic skin diseases, severe liver and kidney dysfunction. Iron supplements darken stool and can sometimes mask bleeding; may cause darkening of teeth.

Forecast. With proper treatment, the prognosis for IDA is favorable.

Prevention. The main population in need of IDA prevention are women with hyperpolymenorrhea. Every girl, from the moment the menstrual cycle is established, needs prophylactic intake of iron supplements if menstrual bleeding continues for more than 5 days without the formation of blood clots or more than 3 days with the formation of blood clots. Oral iron supplements are used at a dose of 300 mg/day, for 5 days monthly. If there are additional indications for this, oral contraceptives with a special iron supplement can be used. The duration of preventive measures is determined by the duration of menstrual blood loss in the specified volume and often coincides with the duration of the reproductive period.

Preventive intake of iron supplements is necessary for pregnant and lactating women throughout pregnancy and lactation. It is necessary to take the drugs at half the dose (150-250 mg/day). If, despite prophylactic use, a pregnant or lactating woman develops IDA, then use full doses of the drug according to the rules for treating IDA.

Related information.

P.S. To calculate the color index, you can use the following mnemonic rule:

According to the regenerative capacity of bone marrow All anemias can be classified as:

1. Regenerative (and hyperregenerative) - IR>2%;

2. Hypo-regenerative - IR<2%.

The reticulocyte index is calculated using the formula:

Reticulocytes (%) Ht bth (%)

IR= -------------- =2%

2 Ht normal (%)

In the first case, the number of reticulocytes in the peripheral blood and bone marrow exceeds the norm to varying degrees.

In the second case, it is reduced or there are practically no reticulocytes.

Regenerative anemias include anemia after blood loss and all hemolytic anemias outside of a crisis.

Hypo-regenerative: hypo-aplastic forms, sideroblastic anemia, B 12 (folate)-deficient and IDA.

Anemia can also be classified according to type of hematopoiesis. There are two possible options here: normoblastic and megaloblastic types of hematopoiesis.

The normoblastic type of hematopoiesis characterizes the production of red blood cells through various stages, starting with RBC, the founder of erythropoiesis, and ending with the reticulocyte/erythrocyte.

The other is the megaloblastic type of hematopoiesis, which partially replaces the normoblastic type, which is characteristic of a deficiency of vitamin B 12 and folate in the body. The lack of these factors can lead to disruption of DNA synthesis in dividing erythroid cells and, as a consequence, to dissociation between the processes of maturation of the nucleus and cytoplasm (immature nucleus and “overripe” cytoplasm). It is this type of discrepancy that leads to the appearance of huge cells of the precursors of erythropoiesis - megaloblasts (“megas” - huge) in the bone marrow, hence the name “megaloblastic”. This type of hematopoiesis is accompanied by the appearance in the peripheral blood of large-diameter red blood cells (megalocytes - 12-14 microns and macrocytes - 9-11 microns), which have an increased concentration of hemoglobin. Hence, this anemia belongs to the macro-megalocytic and hyperchromic type.

I. Anemia due to impaired blood formation

A.1. Iron deficiency anemia (IDA)

Worldwide, IDA accounts for about 70% of all anemias, and it is generally accepted that they most often occur in people belonging to the “poor population”, because in this case, their cause is poor nutrition. Other reasons may be associated with impaired iron metabolism in the body (diseases of the gastrointestinal tract, often the stomach), as well as chronic blood loss.

Vornik B.M.,

Department of Sexology and Medical Psychology KhMAPO Kiev Center for Sexology, Andrology and Reproduction

The classification of the phenomena being studied is rightly considered a fundamental direction in the development of any science. Classification issues are especially relevant in medicine, where they not only summarize scientific achievements, but also determine approaches to diagnosis and treatment.

In the process of developing a particular classification of various diseases, the following methodological approaches are most often used:

1. Phenomenological - diseases are classified according to external manifestations.
2. Symptomatic - diseases are classified according to internal and external manifestations.
3. Syndromological - diseases are classified according to the results of a combination of forming features or systems involved.
4. Etiological - diseases are classified according to the causes of the disorder.
5. Pathogenetic - diseases are classified according to the mechanisms of formation of the disorder.
6. Etiopathogenetic - diseases are classified according to the cause and mechanism of formation of the disorder.
7. Nosological - when the name developed historically, was given by the author who described this form, the situation in which the disease arises or the name comes from the essence of the problem.

The most justified is the etiopathogenetic approach, which is based on the results of an analysis of the etiology, pathogenesis, clinical picture, diagnosis, differential diagnosis, treatment and prevention of the disease, being the classic option, or the “gold standard” in the methodology for developing medical classifications.

The classification of sexual disorders is no exception to the rule, remaining for many years one of the most discussed issues in medical sexology.

Over the past decades, many different classifications of sexual disorders have been proposed. Some of them were revolutionary in terms of the development of medical sexology, others already have only historical interest. The proposed classifications of recent years are partly based on the etiopathogenetic principle, but in a number of works this approach, unfortunately, is not always fully disclosed and justified.

In recent years, classifications have increasingly appeared that are in the nature of a “classification of symptoms,” replacing the description of the patient’s symptoms or complaints. For example, the classification of erectile or ejaculation disorders, or the classification of libido disorders, which simply describe the manifestations of erectile, ejaculation or libido disorders, being only a statement of what is happening to the patient. At the moment, unfortunately, the classification of sexual disorders in ICD-10 is based on the same principle. Such a diagnosis does not guide the doctor either to understand the causes and mechanisms of the emerging disorder, or to the choice of etiopathogenetic therapy.

The existing multitude of classifications has led to the fact that the issue of classifying sexual disorders has long crossed the border of the scientifically progressive register and, especially in the last decade, has become an indicator of the ability or inability to make logical conclusions.

Methodology for diagnosing sexological disorders

When making a sexological diagnosis, it is necessary to remember that a sexual disorder is always a symptom of some disease and/or mental/psychological disorder, and/or an unfavorable social situation, and most often - together.

We must proceed from this postulate both in making a diagnosis or developing a classification, and in choosing methods for diagnosing and treating patients.

To make a diagnosis in sexopathology, the doctor must be able to: use general clinical, sexological, neurological, urological, psychological/pathopsychological, laboratory, instrumental examination methods, in addition, use questionnaires/questionnaires/scales (sexological, psychological, urological) to assess the patient’s condition, and also be able to correctly interpret their results.

In clinical practice, two approaches to diagnosis are used: assessment of the present condition (here and now) and longitudinal (lasting over time) characterization of the development of the disease. The latter approach is especially relevant for the diagnosis of psychogenic and mixed sexual dysfunctions. At the same time, regardless of the primary (basic) specialization of the doctor, the main diagnostic method in clinical sexology is the method of structural analysis of sexual disorders, based on the general theory of functional systems by P. K. Anokhin and the physiological concept of G. S. Vasilchenko on the stages and components of the copulatory cycle . Structural analysis is a set of diagnostic algorithms that provide a transition from symptoms to syndromes and culminate in a detailed clinical diagnosis of a sexual disorder, taking into account the state of the urogenital apparatus, hormonal support, elementary nervous regulations and the patient’s psyche, not in their opposition, but in their integral interaction .

In addition to this, the dynamics of the development of the pathological condition are necessarily characterized and pathogenic factors are identified, the combined action of which led to the emergence of a sexual disorder (with differentiation of factors whose action was limited to the initial stages (triggering) from factors that continue to maintain the disorder).

Only after this can the doctor formulate a diagnosis. Quite often, during the first appointment, it is difficult for the doctor to make a final diagnosis, without additional examination. In such cases, a preliminary diagnosis is made, which is not included in the list of final diagnoses until it is finally established. Due to the methodological paucity of the classification of sexual dysfunctions given in ICD-10, along with a sexological diagnosis, diagnoses of diseases or conditions that caused the occurrence of sexual dysfunction are also made.

Diagnosis is a brief summary of the patient’s physical and mental condition, reflecting the causes, mechanism of development, objective condition of the patient and directions of treatment.

Practitioners are often confused by the confusion in the literature between the terms “disease,” “disease,” “disorder,” and “dysfunction.”

ICD-10 clearly states that when formulating a diagnosis in relation to mental and behavioral disorders, the term “disorder” is used, because the terms “illness” and “disease” cause certain methodological and deontological difficulties when used. In relation to sexual disorders, it is customary to use the term “dysfunction” as the least psychotraumatic term, which, moreover, methodologically more accurately reflects the state and changes in a person’s sexual function.

In addition, the term “disorder” is more suitable for assessing the state of a function sign, for example, erectile dysfunction as one of the signs of sexual function. But isolated disorders of only one symptom almost never occur in sexological practice, and if they do occur, it is for a very short period of time at the very beginning of the disease. As a rule, a disorder of any of the signs causes a disorder of the entire sexual function, and therefore diagnosis options based on only one sign are considered incorrect in medical sexology. Disorder of one of the signs of sexual function, for example, erection, can be a symptom of several forms of sexual dysfunction, and the doctor’s task is to assess the mechanism of occurrence of this symptom, the presence of other hidden symptoms and determine which form of sexual dysfunction occurs in a given patient in order to correctly prescribe treatment .

The most significant issue is the practical use of certain classifications by practicing doctors, who are required to prescribe a diagnosis not only in the patient’s outpatient record (form 25/u), but also in other accounting and statistical forms, which subsequently allows for an examination and analytical assessment of the state of the sexual and reproductive health of the population.

To find ways to practically solve these problems, we analyzed the condition and preliminary diagnoses of 19,863 married/partnered couples and 2,813 male patients without a partner, aged from 16 to 84 years, who applied independently or with the referral of other doctors for help to the Kiev Center for Family Planning and Sexology and human reproduction for the period from 1996 to 2013.

A clinical analysis of the most commonly used classifications was carried out, the possibilities of their use in practice were assessed, taking into account the requirements of ICD-10 and the statistical and accounting systems existing in practical healthcare, and the frequency of occurrence of each form of sexual dysfunction was assessed, which allowed us to clarify and refine and propose an etiopathogenetic classification of sexual dysfunctions in men for practical use at outpatient appointments.

Classification. The modified classification we propose was based on the most common classifications in the post-Soviet space: I. M. Porudominsky, G. S. Vasilchenko, I. F. Yunda and V. V. Krishtal, which, despite their classicism, alas, are not always correspond to the assessment of the patient’s condition and, moreover, are quite often difficult not only to understand, but even to pronounce by some modern doctors, as well as the classification of sexual disorders given in ICD-10.

Since there are only four physiological manifestations of sexuality (libido, erection, ejaculation and orgasm), the symptoms of sexual dysfunction are practically the same in different forms, i.e. in practice there is no specificity of the clinical picture of various forms of sexual dysfunction.

Therefore, we attributed each specific case of the disease to one form or another of sexual dysfunction not on the basis of complaints and clinical manifestations, but based on the cause and mechanism of occurrence of sexual disorders, that is, we used an etiopathogenetic approach.

The results of the work allowed us to propose the following etiopathogenetic classification for practical use:

A. Sexual disharmony and dysgamy - 27.3%:

• socio-psychological form;
• somato-psychological form;
• mixed form.

B. Sexual dysfunctions - 72.7%:

I. Psychogenic sexual dysfunction - 42.8%:

• debutant;
• psychotraumatic;
• symptomatic;
• perverse;
• imaginary sexual disorder.

II. Neurogenic sexual dysfunction - 2.3%:

• cortical;
• diencephalic;
• spinal;
• conductor;
• receptor.

III. Genital sexual dysfunction - 5.3%:

• toxic;
• mechanical;
• pathoreflex.

IV. Vascular sexual dysfunction - 1.8%:

• arterial;
• venous;
• arteriovenous.

V. Endocrine sexual dysfunction - 2.7%:

• hypogonadal;
• discorrelative.

VI. Mixed sexual dysfunction - 44.2%:

• iatrogenic;
• involutive;
• symptomatic;
• disturbance of psychosexual and somatosexual development.

VII. Idiopathic sexual dysfunction - 0.9%:

• alibidemia;
• hypolibidemia;
• hyperlibidemia;
• hypoerection disorder;
• frequent painful erections;
• priapism - prolonged painful erections;
• intermittent nocturnal priapism;
• pathological emissions;
• pathological masturbation;
• aspermatism (complete, partial);
• retrograde ejaculation;
• anorgasmia;
• coitophobia.

Clinical characteristics of the main forms of sexual disorders. In modern medical sexology, it is customary to distinguish between sexual disharmony and sexual dysfunction. Our analysis showed that sexual disharmony occurs in 27.3% of patients, i.e. almost one third. But at the same time, they are extremely rarely diagnosed by doctors, who see only erectile dysfunction in such men. The remaining patients have various types of sexual dysfunction, among which the most common are mixed and psychogenic forms.

A. Sexual disharmony and dysgamy (27.3%). Sexual disharmony is a consequence of a mismatch in the sexual interaction of spouses/partners due to a violation of interpersonal relationships; they can be based on both internal personal factors of one of the spouses/partners and various biological factors.

With sexual disharmony, each of the spouses/partners is individually sexually healthy, that is, has no sexual disorders, but due to various factors, their relationship does not lead to sexual satisfaction for one of them or both.

In this case, a primary discrepancy arises in the interaction of one or more main marital factors - physiological, material, cultural, sexual, psychological, leading to a complex of consequences in the form of various sexual disorders. Often the occurrence of sexual disharmony is due to errors in choosing a partner.

Dysgamy is sexual disharmony between a man and a married woman. As a rule, dysgamy is especially hard for women. They often lead to discord in family relationships, divorce, and can also become one of the causes of various neuroses.

What these two definitions have in common is their functional nature: that is, disorders leading to sexual maladjustment and subsequent sexual disharmony, as well as the fact that diagnosis and correction of sexual disorders is possible only in a specific couple.

A large number of causes and factors causing sexual disharmony allowed V.V. Krishtal to identify the following types of disharmony: sociocultural disadaptation, sex-role, sexual-erotic, communicative, constitutional, biorhythmic, sexual aversion and virgogamy (virgin marriage). To facilitate its practical use by practicing urologists, andrologists, and sex therapists, we have reduced all types of disharmonies into three main clinical forms:

• socio-psychological;
• somato-psychological;
• mixed.

The socio-psychological form of sexual disharmony is a discrepancy between ideas, attitudes, expectations, and behavior in the sexual sphere, which is a consequence of different upbringings, cultural and religious views, as well as the personal characterological characteristics of partners/spouses.

Somato-psychological form of sexual disharmony observed when, with the relative preservation of a positive psychological “climate,” a couple experiences problems in sexual relations due to the presence of somatic diseases or diseases of the genital area of ​​both or one of the partners/spouses, or due to various physiological differences associated with sexual function (discrepancies in the size of the genital organs, anatomical features, etc.).

Mixed form of sexual disharmony combines signs of socio-psychological and somato-psychological sexual disharmony. The most pronounced variant of the last stage of the mixed form of sexual disharmony is sexual aversion, in which there is an extremely negative attitude towards both the sexual partner and sex in general.

Sexual aversion develops due to constant psychological or social dissatisfaction in relationships, which is aggravated by layered sexual dissatisfaction. As a result, the psychological aspects of interpersonal communication (psychological aversion) or sexual aspects (sexual aversion) are initially affected, which, in turn, inevitably have a negative impact on each other, that is, a “pathological circle” is formed. Sexual aversion, as a rule, leads to the development of various forms of neurotic disorders. Such couples rarely see a doctor. More often they turn to a psychologist or get divorced. Therefore, in practice, aversion occurs in 0.08% of cases of disharmony. The overall frequency of sexual disharmony was 27.3% of all cases of seeking sexological help. Sexual dysfunctions occurred in 72.7% of patients who applied for an appointment.

B. Sexual dysfunctions (72.7%). Analyzing the causes and mechanisms of development of sexual dysfunctions, it becomes clear that 3 groups of factors lead to sexual dysfunctions: psychogenic, somatogenic and mixed. Each of these groups has a different mechanism for the development of sexual dysfunction, but the symptoms of sexual dysfunction are often similar and almost always manifest as weakening or absence of erections. Despite the similarity of external manifestations, the treatment of each form of sexual dysfunction has its own specifics. In addition, sexological symptoms can occur against the background of clinical manifestations of another disease. Therefore, we built the classification of sexual dysfunctions based on etiology and pathogenesis, rather than complaints and clinical manifestations. The frequency of occurrence of various forms was calculated from those 72.7% of patients who were diagnosed with sexual dysfunction, taken as 100%.

I. Psychogenic sexual dysfunction (42.8%)- a disorder of sexual function, which is caused by various subjectively significant traumatic or stressful situations for a person and the characteristics of the individual reaction to them.

Features of psychogenic disorders are closely related to personality type.

Psychogenic sexual dysfunction can manifest itself in the following clinical forms:

1. Debutante - occurs in young men as a result of an unsuccessful start to sexual life. An unsuccessful start to sexual activity causes dissatisfaction with oneself, anxiety and fear of subsequent sexual contacts, and in the future, depending on personal characteristics, a person may develop the so-called “expectation of failure” neurosis, characterized by an obsessive fear of sexual intimacy, self-doubt, expectation that “nothing will work out”, vegetative manifestations.

2. Psychotraumatic - occurs as a result of exposure to acute or chronic stress or psychotrauma. Moreover, the degree of its severity depends on the characteristics of the individual. The disorder occurs according to the classical mechanism of development of psychosomatic disorders.

3. Symptomatic - occurs in psychopathological disorders of the psychotic and non-psychotic register as a symptom or as a consequence of the disease, and can also arise due to treatment as a complication of prescribed psychotropic drugs. May have different symptoms, depending on the underlying disease. So, with schizophrenia, epilepsy, there may be difficulty in the onset of ejaculation, and with neuroses, asthenia, on the contrary, there may be accelerated ejaculation, etc.

4. Perverse - arises as a result of the inability to realize one’s sexual preferences of a deviant nature.

5. Imaginary sexual disorder, or it is also called pseudo-impotence, arises as a result of misinformation regarding the psychohygiene of sexual life, the presentation of inflated demands on oneself that do not correspond to physiological capabilities.

II. Neurogenic sexual dysfunction (2.3%)- a disorder of male sexual function that occurs as a result of diseases of the central and peripheral nervous system, leading mainly to disruption of the neurohumoral component of male sexual function.

May manifest in the following clinical forms:

1. Cortical - occurs with functional or organic disturbances of processes occurring in the cerebral cortex, arising from mental disorders or organic diseases of the brain. Needs differential diagnosis with psychogenic sexual dysfunction.
2. Diencephalic - a violation of sexual function that occurs as a result of traumatic, toxic or other pathogenic effects on the hypothalamic centers by exogenous or endogenous factors.

Exogenous factors include: head injuries, including sports, industrial and household intoxications, long-term use of alcohol, drugs and other psychoactive substances, long-term use of certain medications, smoking, exposure to high-frequency energies, physical overexertion, occupational hazards (ionizing radiation, hypothermia , overheating, vibration, noise, chemicals - petroleum products, lead, mercury, etc.).

Endogenous factors include excessive mental and emotional stress, frequent stress, prolonged exhaustion from chronic somatic diseases, renal and liver failure, septic conditions, complications of past infectious diseases.

1. Spinal - occurs with injuries or diseases of the spinal cord, leading to both disturbances in the conduction of sexual impulses and disruptions in the functioning of the spinal centers of erection and/or ejaculation.
2. Conduction - sexual dysfunction caused by various diseases of the peripheral nerves, disrupting the afferent and efferent conduction of sensory and motor sexual impulses and leading to disruption of the innervation of the genital organs, blood vessels, and changes in receptor sensitivity. Occurs, in particular, during surgical interventions on the genitals, pelvic organs, etc.
3. Receptor - occurs when the receptors at the endings of the nerve fibers innervating the external and internal genital organs are damaged. In this case, both external receptors (exteroceptor) and internal (interoreceptor) can be damaged. Various pathological processes and diseases of the genital organs and accessory gonads lead to damage to the receptors.

III. Genital sexual dysfunction (5.3%) occurs with various disorders and pathological processes in the internal and external genital organs, as well as with their damage or developmental pathologies.

Genital sexual dysfunction, depending on the causes and mechanism of damage, manifests itself in the form of toxic, mechanical or pathoreflex clinical forms.

1. Toxic - occurs with inflammatory diseases of the accessory sex glands.
2. Mechanical - occurs with diseases of the penis that impair or limit the possibility of sexual intercourse.
3. Pathoreflex - occurs when the rhythm of functioning of the spinal centers of erection and/or ejaculation is disrupted due to frequent exhausting masturbation, frequent sexual intercourse, including without ejaculation, long periods of abstinence, long-term practice of interrupting sexual intercourse for the purpose of preventing pregnancy or prolonging sexual intercourse, leading to pathological irritative-depleting state of the function of the spinal centers of erection and ejaculation. In these cases, disturbances arise through the mechanism of consolidation of the pathological reflex.

All these forms are often accompanied by autonomic disorders, occurring with a predominance of the tone of the sympathetic or parasympathetic nervous system, which largely forms the symptom of the disorders.

IV. Vascular sexual dysfunction (1.8%) caused by pathology of the blood vessels of both the genital organs and the great vessels outside the reproductive system, for example, with Leriche syndrome, systemic vascular diseases, such as atherosclerosis, endothelial disorders, angiopathy, for example, with diabetes mellitus, with the use of certain medications and others.

There are arterial, venous and arteriovenous clinical forms of vascular sexual dysfunction. Some authors also highlight endothelial sexual dysfunction, but we have not encountered a single case of an independent isolated disorder of the endothelium as a cause of sexual dysfunction. Endothelial dysfunction always occurs in somatic systemic diseases and is only a link in the pathogenesis of both these diseases and sexual dysfunction.

1. Arterial - occurs when blood flow to the corpora cavernosa of the penis is impaired.
2. Venous - occurs when there is a pathological increase in the outflow of venous blood from the penis.
3. Arteriovenous - occurs when a combination of difficulty in blood flow to the penis and increased outflow.

V. Endocrine sexual dysfunction (2.7%)- occurs as a result of various disturbances in the activity of the endocrine glands, primarily the genital glands.

Manifests itself in the following clinical forms:

1. Hypogonadal - occurs as a consequence of any forms of hypogonadism and hypogonadal conditions.
2. Discorrelative - occurs as a result of diseases of the endocrine glands, leading to a violation of the relationship between hormone levels and, as a consequence, to obesity, diencephalic disorders, dysfunction of the gonads and other pathological conditions.

VI. Mixed sexual dysfunction (44.2%)- occurs when two or more forms of sexual dysfunction of different origins are combined. Mixed sexual dysfunction also includes those cases when psychopathological changes arise as a complication of neurogenic, genital, vascular and endocrine sexual dysfunction. It can manifest itself in the following clinical and etiological forms:

1. Iatrogenic - occurs as a result of mental or physical influence on the part of doctors and medical staff, causing harm to the psychological or somatic state of the patient.
2. Involutive - a violation of sexual function during the involutionary period, caused solely by the aging process, and not by diseases that arise in older age, that is, a genetically determined decrease in the production and activity of hormones, a decrease in the number of various receptors, a decrease in various types of tissue sensitivity, changes in the psychological state and social situation.
3. Symptomatic - a clinical form in which certain sexual dysfunctions are in the nature of a symptom of a disease and do not have independent significance. For example: decreased libido or weakened erection due to pneumonia or chronic renal failure, etc.
4. Disorders of psychosexual and somatosexual development - depending on the etiology, pathogenesis and clinical picture, these conditions may relate to psychogenic, endocrine or mixed forms of sexual dysfunction, depending on whether there are disorders of psychosexual or somatosexual development, or a combination thereof.

A violation of somatosexual development is manifested in a violation of the timing (delay, acceleration) of somatosexual development (hair growth, size of the genital organs, timbre of voice, height, etc.), which may be accompanied by a violation of gender-role behavior and sexual orientation.

Violation of psychosexual development is manifested in disturbances in the pace (delay, acceleration) of psychosexual development, as well as in violations of sexual identity, gender-role behavior, sexual orientation (homosexual orientation is excluded). Disorders of psychosexual development are often a consequence of disturbances of somatosexual development.

VII. Idiopathic sexual dysfunction (0.9%)- this is sexual dysfunction of unknown origin for reasons that cannot be identified at this stage of the examination. More often it manifests itself as a monosymptomatic sexual disorder, when a person experiences only a disorder of one sign of sexuality (symptom), which occurs as an independent disease, the cause of which the doctor cannot establish, but combinations of these symptoms are also possible, developing into a syndrome, but without any etiopathogenetic patterns. Sexual disorders in the idiopathic form can be manifested by such symptoms as alibidemia, hypolibidemia, hyperlibidemia, hypoerection disorder, priapism, pathological emissions, aspermatism (complete, partial), retrograde ejaculation, anorgasmia, coitophobia and others.

It is clear that all these conditions can also occur with various forms of sexual dysfunction or any somatic or mental disorders. But we are talking about those cases where their cause cannot be established.

Final (refined) diagnosis. When entering a diagnosis into the patient’s outpatient card, the sexological diagnosis is written first, based on the reason for the visit and the mechanism of development of dysfunction, that is, why the patient came to the appointment. Then they write a diagnosis of the disease or condition that led to the development of a sexual disorder, indicating the ICD-10 code, and then the diagnosis of concomitant diseases, if any.

Since not all sexological diagnoses accepted in practice are reflected in ICD-10 due to the lack of international consensus on this matter, the one of the established diagnoses that is in ICD-10 and most appropriate to the patient’s condition is written on the page for recording the final diagnoses in the outpatient card . If you need to code sexual dysfunction, then this is done according to the leading sign and there will be 2 codes in the list of specified diagnoses.

The same diagnosis will be coded in the static coupon. However, it must be remembered that ICD-10 has a mainly statistical mission, and in clinical practice, preference is still given to etiopathogenetic diagnosis and assessment of the reason for seeking help.

Examples of sexological diagnoses:

1. Psychogenic debutant sexual dysfunction, Anxiety disorder (F52.2+F41.3).
2. Psychogenic symptomatic sexual dysfunction; Neurasthenia (F52.2 +F48.0).
3. Mixed sexual dysfunction; Gender identity disorder, Transsexualism (F52.2+F64.0).
4. Neurogenic diencephalic sexual dysfunction; Chronic alcoholism (N48.1 + F10.2)
5. Neurogenic conductive sexual dysfunction; Multiple sclerosis (N48.1 + G35.0).
6. Genital mechanical sexual dysfunction; Fibroplastic induration of the penis (N48.1+ N48.6).
7. Genital toxic sexual dysfunction; Chronic prostatitis (N48.1 + N41.1).

For specified forms of somatic or mental disorders, the second code may change

Conclusion: Thus, the proposed forms clearly reflect the etiopathogenetic approach and confirm the independence of such a clinical discipline as medical sexology. The given frequency of various forms of sexual dysfunction, obtained from a huge amount of clinical material, in contrast to the existing opinion, shows a fairly high proportion of psychogenic sexual dysfunction and its negative impact on such somatic indicators as hormone levels, blood flow in the penis and others, which can often mislead the doctor regarding the etiology, pathogenesis and form of sexual dysfunction, as well as the direction of treatment.

The presence of a clear approach and a unified classification, easily used in practical healthcare, will lead to the opportunity to organize and implement into practice statistical reporting forms characterizing the state of sexual and reproductive health of the population, and conduct an objective analysis of morbidity, which will also help assess the situation and choose directions for further scientific research.

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