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Polycythemia

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THE PRESENTATION INCLUDES INTRODUCTION, CLASSIFICATION( PRIMARY AND SECONDARY POLYCYTHEMIA), ETIOLOGY & PATHOPHYSIOLOGY, CLINICAL MENIFESTATIONS AND MANAGEMENT(MEDICAL AND NURSING) OF POLYCYTHEMIA.

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Polycythemia

  1. 1. SUBMITTED BY- CHANCHAL (B.Sc. NURSING )
  2. 2. INTRODUCTION • If you are even a casual fan of professional sports, you have probably heard about an athlete who was fined or kicked out of their sport due to blood doping. • When an athlete 'dopes' their blood, what they are really doing is injecting themselves with extra blood or a substance that increases the number of oxygen- carrying red blood cells in their body. • With more oxygen comes more endurance and an unfair edge over their competition.
  3. 3. INTRODUCTION • From a health standpoint, this is not such a great idea because the athlete is actually creating a blood condition known as polycythemia, which is a blood disorder in which there are too many red blood cells. • These extra cells thicken the blood, making a person more prone to blood clots, which in turn heightens their risk of heart attack or stroke.
  4. 4. INTRODUCTION • Polycythemia is a disorder that results in too many red blood cells • For instance, we see that the prefix 'poly' means many, the word 'cyt' refers to cells and the suffix 'emia' refers to in the blood • So polycythemia is literally 'many cells in the blood.‘
  5. 5. DEFINITION  POLYSTHEMIA is the production and presence of increased number of Red Blood Cells (RBC’s).  The increase in RBC’s can be so great that blood circulation is impaired as a result of increased blood viscosity (Hyperviscosity) and volume (Hypervolemia).
  6. 6.  POLYSTHEMIA is used when Hematocrites is elevated. > 55% in male. > 50% in female.
  7. 7. TYPES TYPES OF POLYCYTHEMIA PRIMARY POLYCYTHEMIA (POLYCYTHEMIA VERA) SECONDARY POLYCYTHEMIA
  8. 8. DEFINITION  POLYSTHEMIA VERA is overproduction (proliferation) of red blood cells due to bone marrow disease (myeloproliferative disorder).
  9. 9. ETIOLOGY AND PATHOPHYSIOLOGY JANUS KINASE-2 MUTATED GENE JAK-2 HEMATOPOIETIC STEM CELLACTIVATION INCREASED RBC’S PRODUCTION
  10. 10. DEFINITION  SECONDARY POLYSTHEMIA is an absolute increase in red blood cell mass that is caused by enhanced stimulation of red blood cell production.
  11. 11. TYPES TYPES OF SECONDARY POLYCYTHEMIA HYPOXIA DRIVEN SECONDARY POLYCYTHEMIA HYPOXIA INDEPENDENT SECONDARY POLYCYTHEMIA
  12. 12. ETIOLOGY AND PATHOPHYSIOLOGY OF SECONDARY POLYCYTHEMIA
  13. 13. HIGH ALTITUDE, CARDIOPULMONARY DISEASE, DEFECTIVE OXYGEN TRANSPORT HYPOXIA INCREASED ERYTHROPOITEN PRODUCTION IN KIDNEY INCREASE IN RBC’s PRODUCTION HYPOXIA DRIVEN SECONDARY POLYCYTHEMIA
  14. 14. RENAL CYST OR TUMOR, EXTERNAL TUMORS INCREASE ERYTHROPOIETIN PRODUCTION INCREASE IN RBC’s PRODUCTION HYPOXIA INDEPENDENT SECONDARY POLYCYTHEMIA
  15. 15. CLINICAL MANIFESTATION AND COMPLICATION  Hypertension caused by hypervolemia and hyperviscosity.  Subjective complaints of headache, vertigo, dizziness, tinnitus, and visual disturbance.  Generalised pruritus related to histamine release from an increased number of basophils.  Paresthesias and erythromelalgia.  Angina, heart failure, intermittent claudication, and thrombophlebitis, which may be complicated by embolization.  Hemorrhagic phenomena caused by either vessel rupture from over-distension on inadequate platelet function may result in prtrchiae, ecchymoses, epitaxis, or GI bleeding.
  16. 16. CLINICAL MANIFESTATION AND COMPLICATION  Hepatomegaly and splenomegaly from organ engorgrment may contribute to patient complaints of satiety and fullness.  Pain from peptic ulcer caused by either by increased gastric secretions or by liver and spleen engorgement.  Hyperuricemia is caused by the increase in RBC destruction that accompanies excessive RBC production.  Mylofibrosis and leukemia develope in some patients with polycythemia vera.
  17. 17. DIAGNOSTIC STUDIES 1. Elevated hemoglobin and RBC count with microcytosis. 2. EPO level 3. Elevated WBC count with basophilia 4. Elevated platelet count and platelet dysfunction 5. Elevated leucocytes alkaline phosphatase, uric acid and cobalamin levels 6. Elevated histamine levels. 7. Bone marrow examination.
  18. 18. COLLABORATIVE CARE  Phlebotomy  Avoid iron supplementation  Hydration therapy  Myelosuppressive agents like Hydroxyurea Busulfan Chlorambucil  Ruxolitinib ( drug inhibiting the expression of JAK-2 mutation)
  19. 19. COLLABORATIVE CARE  Low-dose aspirin  α-Interferon (α-INF is of particular use in women of childbearing age or those with intractable pruritus).  Anagrelide ( to reduce platelet count & inhibit platelet aaggregation)  Allopurinol (reduce the number of acute gouty attacks).
  20. 20. NURSING MANAGEMENT  Assist or perform phlebotomy. It may need to be done every 2 to 3 months, reducing the blood volume by about 500ml each time.  Evaluate fluid intake and output during hydration therapy to avoid fluid-overload or underhydration.  If myelosuppressive agents are used, administer the drug as ordered, observe patient, and teach the patient about medication side effects.  Assess the patient’s nutritional status.  Begin activities( like passive leg exercises and ambulation) or medications to decrease thrombus formation.

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