Etiology

• Polycythemia can be classified as:
  • Relative, ie normal red cell mass but PCV Hematology: packed cell volume increased due to reduced plasma volume.
  • Absolute, ie increased PCV Hematology: packed cell volume , red cell mass and [hemoglobin]:
    • Primary, iepolycythemia rubra vera Polycythemia: primary a rare myeloproliferative disorder (abnormal proliferation of erythroid precursors in bone marrow that occurs independent of erythropoietin).
    • Secondary (erythropoietin-mediated erythropoiesis): physiological, pathological.

Specific

• Physiological:
  • Chronic pulmonary disease.
  • Right to left shunts.
  • High altitudes.

• Pathological:
• • Renal disease:
  • • Renal cysts Kidney: polycystic disease.
    • Hydronephrosis Hydronephrosis / hydroureter.
  • Tumors producing erythropoietin like substances:
  • • Renal carcinoma Kidney: neoplasia.
    • Hepatoma Liver: neoplasia.
    • Pheochromocytoma Pheochromocytoma.
    • Ovarian carcinoma.
    • Uterine leiomyoma.
    • Adrenal adenoma/carcinoma (or hyperplasia).

Pathophysiology

• Increased packed cell volume (PCV Hematology: packed cell volume ) results in hyperviscosity → clinical signs.

• In a normal animal:
  • Erythropoietin (produced by the kidneys) stimulates proliferation of red cell precursors in bone marrow → increased production of red blood cells.
  • Erythropoietin produced in response to tissue hypoxia (physiological) → renal oxygen sensors → increased production and secretion of erythropoietin → increased red cell mass.
• Pathological polycythemia:
  • Primary polycythemia Polycythemia: primary: autonomous clonal expansion of red cell precursors in bone marrow (myeloproliferative disease).
  • Secondary polycythemia:
    • Production of erythropoietin-like substance by tumor which continually stimulates red cell production.
    • Functional renal neoplasia producing erythropoietin free from negative feedback mechanisms.

Timecourse

• Weeks to months.