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

1. SUBMITTED BY-
CHANCHAL
(B.Sc. NURSING )

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. 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. 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. 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.  POLYSTHEMIA is used when
Hematocrites is elevated.
> 55% in male.
> 50% in female.

7. TYPES
TYPES OF
POLYCYTHEMIA
PRIMARY
POLYCYTHEMIA
(POLYCYTHEMIA
VERA)
SECONDARY
POLYCYTHEMIA

9. DEFINITION
 POLYSTHEMIA VERA is
overproduction (proliferation) of red
blood cells due to bone marrow disease
(myeloproliferative disorder).

10. ETIOLOGY AND
PATHOPHYSIOLOGY
JANUS KINASE-2 MUTATED GENE
JAK-2
HEMATOPOIETIC STEM CELLACTIVATION
INCREASED RBC’S PRODUCTION

12. DEFINITION
 SECONDARY POLYSTHEMIA is an
absolute increase in red blood cell mass
that is caused by enhanced stimulation of
red blood cell production.

13. TYPES
TYPES OF SECONDARY
POLYCYTHEMIA
HYPOXIA
DRIVEN
SECONDARY
POLYCYTHEMIA
HYPOXIA
INDEPENDENT
SECONDARY
POLYCYTHEMIA

14. ETIOLOGY AND
PATHOPHYSIOLOGY
OF
SECONDARY
POLYCYTHEMIA

15. HIGH ALTITUDE, CARDIOPULMONARY DISEASE,
DEFECTIVE OXYGEN TRANSPORT
HYPOXIA
INCREASED ERYTHROPOITEN PRODUCTION IN KIDNEY
INCREASE IN RBC’s PRODUCTION
HYPOXIA DRIVEN SECONDARY POLYCYTHEMIA

16. RENAL CYST OR TUMOR,
EXTERNAL TUMORS
INCREASE ERYTHROPOIETIN PRODUCTION
INCREASE IN RBC’s PRODUCTION
HYPOXIA INDEPENDENT SECONDARY
POLYCYTHEMIA

18. 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.

19. 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.

20. 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.

21. COLLABORATIVE CARE
 Phlebotomy
 Avoid iron supplementation
 Hydration therapy
 Myelosuppressive agents like
Hydroxyurea
Busulfan
Chlorambucil
 Ruxolitinib ( drug inhibiting the expression of JAK-2
mutation)

22. 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).

23. 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.