Mechanisms of leukopenia development
The pathogenesis of decreased leukocyte count is based on four main mechanisms:
- Excessive cell destruction. Occurs in the vascular bed or hematopoietic organs. The main causes are penetrating radiation and antileukocyte antibodies. Medications (amidopyrine, sulfonamides, barbiturates) acting as haptens play an important role. They stimulate the formation of antibodies that cause agglutination and death of leukocytes.
- Redistribution of leukocytes. Under the influence of biologically active substances (chemotaxins, adhesion activators), cells temporarily accumulate in certain regions of the vascular bed. This leads to a decrease in their number in other areas and creates a picture of "false" (pseudo) leukopenia in peripheral blood.
- Increased loss by the body. Occurs in acute or chronic blood loss, as well as in massive plasmorrhagia and lymphorrhagia. Typical examples include extensive burns and chronic purulent processes (peritonitis, endometritis, osteomyelitis).
- Hemodilution leukopenia. Associated with blood dilution. It is observed in hypervolemia (transfusion of large volumes of plasma or plasma substitutes) or when fluid flows from tissues into vessels along an osmotic/oncotic pressure gradient (in hyperaldosteronism, hyperglycemia, hyperalbuminemia).
Clinical and morphological manifestations of leukopenia
The decrease in cell count can affect all differentiation pathways (general leukopenia) or predominantly one of them, causing isolated conditions: lymphocytopenia, monocytopenia, neutropenia, basopenia, or eosinopenia.
An important indicator is the dynamics of immature neutrophil forms (band cells, metamyelocytes):
- A decrease in their number in the early stages indicates suppression of the regenerative capacity of hematopoietic tissue.
- An increase in their number (shift to the left) against the background of persistent leukopenia after elimination of the causative factor indicates the activation of leukopoiesis.
In leukopenia, signs of cell degeneration and destruction (mainly in neutrophils and monocytes) are often detected. Morphological changes include:
- Changes in cell contour (poikilocytosis) and the presence of cells of varying sizes (anisocytosis).
- Shrinkage or swelling.
- Appearance of vacuoles, toxic granulation, and cytoplasmic inclusions.
- Hypersegmentation of nuclei.
- Nuclear shrinkage (pyknosis) and breakdown (karyorrhexis).
Degenerative nuclear shifts
Changes in the leukocyte formula (differential white blood cell count) in leukopenia are often accompanied by specific shifts:
- Degenerative left nuclear shift: a large number of degenerative leukocyte forms appear in the blood, the proportion of segmented neutrophils decreases, while there is a moderate increase in the content of band neutrophils and metamyelocytes.
- Degenerative right nuclear shift: characterized by an increase in the number of segmented leukocytes with pronounced signs of degeneration. There is no accompanying increase in the number of band cells.
Features of leukocytosis
The increase in the number of all leukocyte forms or their individual types (lymphocytosis, monocytosis, granulocytosis) directly depends on the nature of the causative factor. According to their biological significance, leukocytosis is divided into two main groups: physiological and pathological.
Hemoconcentration leukocytosis requires special attention:
- Cause: body hypohydration of various origins (repeated vomiting, diarrhea, polyuria) leading to hypovolemia.
- Pathogenesis: the total (absolute) number of leukocytes in the body remains normal, but their content per unit volume of blood increases due to hemoconcentration and a decrease in plasma volume.
- Diagnostic sign: simultaneously with leukocytosis, the blood levels of other formed elements—erythrocytes and platelets—are elevated.
Briefly: answers to topical questions
What are the pathogenetic mechanisms of pathological leukocytosis?
The mechanisms of pathological leukocytosis include leukocyte redistribution, hemoconcentration, and increased leukocyte production/proliferation.
The main pathogenetic mechanisms include:
- Redistributive — change in the localization of leukocytes in the vascular bed under the action of biologically active substances: chemotaxins, stimulators of adhesion, aggregation, and agglutination. The total number of leukocytes in the body remains normal, and the blood picture is "false" or relative.
- Hemoconcentration — during hypohydration, hypovolemia and hemoconcentration develop; the total number of leukocytes in the body is normal, but their content per unit volume of blood is increased due to a decrease in plasma volume.
- Stimulation of leukopoiesis under the action of a pathogenic factor: in allergic reactions, eosinophilia develops due to stimulation of eosinophilopoiesis; in bacterial infections, neutrophilia due to stimulation of myelopoiesis; in viral and specific infections, lymphocytosis due to stimulation of lymphopoiesis; in certain infectious diseases, monocytosis due to the activation of monocytopoiesis.
- In neoplastic blood diseases — activation of hemoblastosis cell proliferation, as well as stimulation of normal leukocyte division due to the appearance of tumor antigens, leukopoietins, and other growth factors.
For quick memorization of leukopenia mechanisms, use the rule "Four Ps" (or the Russian "Two D, Two R" equivalent): Destruction (antibodies, haptens), Dilution (hemodilution), Redistribution (pseudoleukopenia), Loss (burns, bleeding).
Class and exam questions
What is hemoconcentration leukocytosis and how to distinguish it?
This is a condition where the absolute leukocyte count is normal, but their concentration is increased due to blood thickening (in vomiting, diarrhea). The main distinguishing feature is the simultaneous increase in erythrocyte and platelet levels.
What does the appearance of band neutrophils against the background of leukopenia indicate?
If the action of the damaging factor has already ceased, such a left shift of the leukocyte differential is a favorable sign. It indicates the activation of leukopoiesis and the onset of recovery.
How can drugs cause leukopenia?
Certain drugs (e.g., sulfonamides, amidopyrine, barbiturates) act as haptens. They provoke the formation of antibodies that cause agglutination and subsequent destruction of leukocytes.
What else to study on this topic
- Classification of leukocytosis by biological significance (physiological and pathological)
- Types of partial leukopenia (neutropenia, lymphocytopenia, monocytopenia)
- The role of chemotaxins and adhesion activators in leukocyte redistribution
- Pathogenesis of degenerative changes: from poikilocytosis to karyorrhexis
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