POLYCYTHEMIA
| |POLYCYTHEMIA |ANEMIA |
|Difference between |Increase in red blood cell production |“Reduction in total number of erythrocytes in |
|polycythemia and | |blood or a decrease in the quality or quantity |
|anemia |2 types: relative polycythemia – |of hemoglobin” (Mansen & McCance, 2006, p. |
| |most common type |927). |
| | | |
| |Absolute or primary/ also |Decreased capacity to carry oxygen in the blood|
| |known as polycythemia |cells, leading to hypoxia of the tissues. |
| |vera (PV) or polycythemia | |
| |rubra vera, or erythemia |Caused by: excessive blood loss, hemolysis, and|
| | |deficient RBC production. (may be caused by |
| |Relative includes: Relative polycythemia is temporary|poor nutrition or bone marrow failure) |
| |and is corrected by increasing vascular fluid | |
| |volumes. |Anemia is not considered a disease BUT an |
| | |indication of altered body function. |
| |Absolute or primary includes: abnormality of the bone| |
| |marrow stem cells, may be acquired or inherited, |“Erythropoietin causes a compensatory increase |
| |familial or congenital |in erythrocyte production if the oxygen content|
| | |of blood decreases because of anemia” (McCance,|
| |Formation of red blood cells continues despite |2006, p. 909). |
| |hypoxia or renal failure (production of | |
| |erythropoietin by the peritubular cells of the kidney|Most common blood disorder (). |
| |normally provide compensatory erythrocyte production | |
| |when O2 content falls). | |
|Physiology review |Stems cells in bone marrow reproduce, proliferate, |Hemoglobin “constitutes approximately 90% of |
| |and differentiate into various blood cells, i.e. RBC |the cell’s dry weight” (McCance, 2006, p. 905).|
| |WBC, etc. Pluripotent stem cells divide into myeloid |Hemoglobin is a family of molecules that form a|
| |or lymphoid stem cells. In polycythemia we are |polypeptide chain called a tetrahedron (2 prs. |
| |concerned with myeloid stem cells. Myeloid stem cells|Of identical chains). Hemoglobin is made up of |
| |develop in bone marrow. Further, myeloid cells |four heme groups and therefore carries 4 |
| |differentiate into progenitor cells. (include RBC, |molecules of oxygen. |
| |platelets, monocytes, eosinophils, basophils). |(Adapted from McCance, 2006). |
| |Progenitor cell develop into either colony forming | |
| |units (CFU), precursor cells, T lymphoblasts, and B | |
| |lymphoblasts. CFU-E produces erythrocytes the primary| |
| |culprit in polycythemia (adapted from Tortora & | |
| |Grabowski, 2003). | |
|Pathology |Primary PV - classified as a chronic |Classified either by etiology (evaluation of |
| |myeloproliferative disorders (CMPD). |production, destruction, and loss) or |
| | |morphology (Mansen & McCance, 2006; |
| |PV - is a non malignant |) |
| |proliferative disease of the | |
| |pluripotent cells of the bone |Most often classified morphologically (groups |
| |marrow stem cells |anemia by RBC size, use MCV) (). |
| |(Gaspard, 2005; Mansen & |Divided into two cellular characteristics: |
| |McCance, 2006). |Size: “cytic” |
| |there is a net increase in the total number of blood | |
| |cells, primarily RBC’s and to a lesser extent |Hemoglobin |
| |platelets and WBC’s. |content: “ chromic” |
| | |Several types of anemia’s |
| |Findings associated with PV are conflicting and |Macrocytic-normochromic – pernicious anemia |
| |include: RBC lifespan is no longer than normal; RBC |Microcytic-hypochromic –iron deficiency anemia |
| |production is increased but not at the expense of WBC|Normocytic- normochromic – aplastic anemia |
| |production, which may be unchanged or increased; RBC |(Mansen & McCance, 2006). |
| |production is not affected by phlebotomy; formation | |
| |of red blood cells continues (as usual) in the |Anemia occurs due to: |
| |presence of hypoxia or renal failure; and |Impaired erythrocyte production (ineffective |
| |erythropoietin levels are lower than normal, which |hematopoiesis), |
| |one would anticipate results in decrease RBC |Blood loss – acute or chronic, i.e. hemorrhage |
| |production. |Increased destruction of erythrocytes |
| | |(hemolysis), |
| |Erythrocytosis is essential to diagnosis of PV. |all three. |
| |This disorder is oversensitive to endogenous hormones| |
| |or growth factors. |“Erythropoietin causes a compensatory increase |
| |Negative feedback loop is dysregulated |in erythrocyte production if the oxygen content|
| |Notable increase in red cell count, hemoglobin, and |of blood decreases because of anemia” (McCance,|
| |hematocrit (Gaspard, 2005). |2006, p. 909). |
| |Increased blood volume and viscosity – interferes | |
| |with cardiac output |Examples of how anemia may be manifested in the|
| |Hypertension is common |body: |
| |Thromboembolism – 15 – 60% in those with PV (Gaspard,| |
| |2005). |Poor nutrition to the cells slows erythrocyte |
| |Rarely malignant |production thus reducing the number of |
| |Hallmark of polycythemia is an elevated hematocrit |functional erythrocytes available to carry |
| |>55% |hemoglobin. |
| | | |
| |CMPD’s include PV, idiopathic myelofibrosis, and |Cardiovascular system alterations and |
| |essential throbocytosis, CML. |compensations as a result of hemorrhage – |
| | |reduced RBC volume, fluid moves from ECF into |
| |Secondary polycythemia |blood vessels to expand plasma volume in an |
| |- increase levels of |attempt to maintain appropriate blood volume. |
| |erythropoietin, (this is most |Blood becomes diluted and flows faster. Hypoxia|
| |likely a compensatory |causes arterial dilation decreasing resistance |
| |mechanism as result of |in blood vessels as well as activating |
| |hypoxia) |sympathetic nervous system response thus |
| |- Loss of plasma volume |increasing heart rate. Results in possible CHF.|
| |results without the | |
| |corresponding decrease in |Tissue hypoxia due to decreased hemoglobin: |
| |RBC’s evidenced by |May manifest itself in respiratory, |
| |dehydration, diarrhea, |hematological system, as well as skin, nails, |
| |vomiting, or excessive use if |lips, conjunctivae - pale |
| |diuretics. |Vit B12 defiency- nervous system |
| |-overproduction of RBC’s | |
| |may be a reaction to |GI tract – decreased 02 results in pain to |
| |chronically low O2 levels – |abdomen, N&V, anorexia |
| |ie. COPD, living at high | |
| |altitudes, or increased CO in |Severe or rapid anemia – symptoms of shock |
| |blood due to smoking, renal | |
| |or liver tumors, heart or lung | |
| |diseases. | |
| |-athletes will train at high | |
| |altitudes to increase the | |
| |oxygen carrying capacity of | |
| |the blood, “blood doping” | |
| |(Mansen & McCance, 2006; | |
| |Tortora & Grabowski, 2003). | |
| |Primary source Mansen, T.J., & McCance, K.L. (2006). |Primary source Mansen, T.J., & McCance, K.L. |
| |Alterations in erythrocyte function. In K.L. McCance |(2006). Alterations in erythrocyte function. In|
| |& S.E. Huether (Ed.), Pathophysiology: The biologic |K.L. McCance & S.E. Huether (Ed.), |
| |basis for disease in adults and children (5th ed.). |Pathophysiology: The biologic basis for disease|
| |St. Louis, MO: Elsevier Mosby. |in adults and children (5th ed.). St. Louis, |
| | |MO: Elsevier Mosby. |
Nadine and Lisa
References
Gaspard, K.J. (2005). Red blood cell disorders. In C.M. Porth (Ed.). Pathopysiology: Concepts of altered health states (7th ed.). pp. 314-315. Philadelphia, P.A. : Lippincott, Williams, & Wilkens.
Mansen, T.J., & McCance, K.L. (2006). Alterations in erythrocyte function. In K.L. McCance & S.E. Huether (Ed.). pp. 948 – 949. Pathophysiology: The biologic basis for disease in adults and children (5th ed.). St. Louis, MO: Elsevier Mosby.
McCance, K.L. (2006). The hematologic system. In K.L. McCance & S.E. Huether (Ed.). pp.
893-906. Pathophysiology: The biologic basis for disease in adults and children (5th ed.). St. Louis, MO: Elsevier Mosby.
Tortora, G.J., & Grabowski, S.R. (2003). Principles of anatomy and pathophysiology (10th ed.). New York, NY: John Wiley & Sons.
Wikipedia. (2008). Retrieved on June 17, 2008 from wiki/Anemia.
Wikipedia. (2008). Retrieved on June 17, 2008 from wiki/Polycythemia.
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