Classification of erythrocytosis
Erythrocytosis is divided into three main groups depending on the mechanisms of development:
- Primary: associated with neoplastic transformation of hematopoietic tissue (e.g., polycythemia vera).
- Secondary: act as a symptom of other diseases, accompanied by the activation of erythropoiesis.
- Relative: occur when plasma volume decreases or red blood cells leave storage depots without an increase in their total count in the body.
Secondary absolute erythrocytosis
They develop as a result of non-neoplastic stimulation of erythropoiesis. The main regulator is the hormone erythropoietin. Its secretion increases during:
- Chronic hypoxia (respiratory or heart failure, anemia).
- Neoplastic processes in the kidneys or liver.
Unlike polycythemia vera, thrombocytosis and leukocytosis are usually absent here, and eliminating the cause of hypoxia leads to the normalization of blood parameters.
Relative erythrocytosis
In these conditions, red blood cell production in the bone marrow is unchanged. Two mechanisms are distinguished:
- Hemoconcentration: fluid loss (vomiting, diarrhea, burns) leading to polycythemic hypovolemia.
- Redistribution: release of stored red blood cells into the bloodstream during stress or acute hypoxia, causing polycythemic hypervolemia.
Hemodynamic consequences
High blood viscosity in erythrocytosis inevitably leads to circulatory disorders:
- Arterial hypertension.
- Microcirculatory disorders (sludge phenomenon, stasis).
- Thrombotic syndrome.
- Paradoxical bleeding due to functional inferiority of platelets.
Briefly: answers to topical questions
In what pathological conditions does the secretion of erythropoietin increase, causing secondary erythrocytosis?
Erythropoietin secretion/production increases in secondary absolute erythrocytosis in the following situations:
- Hypoxia of any type: in chronic anemia, respiratory failure (RF), heart failure (HF), as well as in generalized tissue hypoxia with arterial hypoxemia.
- Local renal ischemia: causes renal erythrocytosis; the kidneys are the source of erythropoietins.
- Tumors of the kidneys, liver, and other organs: accompanied by excessive synthesis of erythropoietin; in paraneoplastic erythrocytosis, the tumor is the source of erythropoietins.
What changes in peripheral blood, apart from an increase in red blood cells, are characteristic of polycythemia vera (Vaquez's disease)?
Polycythemia vera (Vaquez's disease) is characterized by an increase in the number of red blood cells, as well as other blood formed elements. The following are observed in the peripheral blood:
- Leukocytosis.
- Thrombocythemia (thrombocytosis).
- Increased hemoglobin concentration and elevated hematocrit.
- Increased blood viscosity.
Polycythemia vera is accompanied by thrombocytosis and leukocytosis, unlike secondary erythrocytosis.
"Absolute — bone marrow is active, Relative — plasma is gone or depot is open."
Class and exam questions
What is the main difference between secondary erythrocytosis and polycythemia vera?
Secondary erythrocytosis is a symptom of another disease, lacking the thrombocytosis and leukocytosis characteristic of polycythemia vera.
Why can bleeding occur in erythrocytosis?
This is a paradoxical effect caused by the functional inferiority of platelets and overstretching of the vascular wall due to an excessive blood volume.
What is polycythemic hypovolemia?
This is a condition where the concentration of red blood cells increases due to a decrease in plasma volume (e.g., during dehydration).
What else to study on this topic
- Molecular mechanisms of cellular sensitivity to erythropoietin.
- Differential diagnosis of erythrocytosis in various types of hypoxia.
- Pathophysiology of the sludge phenomenon in the microvasculature.
- The role of catecholamines in the mobilization of red blood cells from storage depots.
- Clinical markers of the transition of secondary erythrocytosis to the chronic stage.
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