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the
megakaryocytes, bone marrow cells, to produce blood thrombocytes or, as we all know
as platelets. Another factor is due to stress. At times when you are in a stressful
situation, your sympathetic nervous system is stimulated and brings about the flight-orfight response to help you cope with it. Because the sympathetic nervous system is
stimulated, the adrenal medulla releases two similar hormones: epinephrine and
norepinephrine. Collectively, these hormones are called catecholamines. According to a
study done by Afossi and Trovati (1996, May), Human platelets exhibit both adrenergic
and dopaminergic receptors that are influenced by different catecholamines. alpha(2)Adrenoceptors of alpha(2A) subtype prevail on platelet membrane; through their
stimulation, catecholamines potentiate the effects of other agonists and, at higher
concentrations, initiate
arachidonate pathway activation. The third factor, which is one of the main causes,
would be due to the removal of the spleen (splenectomy). As we all know, the spleen is
the graveyard for blood components. Circulating platelets are reduced by trapping them
in the spleen. Without the spleen, accumulation of platelets in the blood will occur thus,
causes reactive thrombocytosis. Lastly, iron-deficiency anemia causes secondary
thombocytosis. The association of iron-deficieny anemia with thrombocytosis points to
an interrelationship between erythropoietic and thrombotic growth factors (Khan, et al.,
2009). Although its exact mechanism is not clearly understood, many studies have
observed that due to a deficiency of iron, platelet levels are high thus developing
thrombosis.
3. Discuss briefly the pathologic process.
Secondary thrombocytosis is generally a self-limiting condition that resolves with
the inciting condition. Basically, the increase in platelets is a normal physiological
response to the factors states (inflammation, infections, cancer, stress, etc.) that is,
however, exaggerated. This exaggeration causes the increase in platelets characterized
as greater than 400,000/mm3 (400,000 per cubic milimeter). Rarely, it increases up to 1
million/mm3 (1 million per cubic millimeter). It is only when it reaches this many that
clotting and bleeding occurs with secondary thrombocytosis.
4. Identify the different clinical manifestations as the disease condition progresses.
Normally, there are no significant group of clinical manifestations to differentiate
secondary thrombocytosis because the signs and symptoms would relate only to the
underlying cause. It is only from the labs that results to an increase in platelet levels
would
we
determine
that the
person is
experiencing
secondary or reactive
you have just read about this. According to Budde and Genderen (2007), For patients
with high platelet counts, an inverse relationship has been established between platelet
counts and large von Willebrand factor (vWf) multimers in plasma. vWf is like the glue
that is used to put platelets together upon clotting formation. The decrease of its number
is cause by the increased consumption of it by the platelets that is overcrowding the
blood. The following the manifestations when bleeding or thrombosis occurs:
5. What are the diagnostic studies and its relevance to the disease condition.
1. Complete Blood Count (CBC): To know how many platelets are in the blood.
2. Erythrocyte Sedimentation Rate (ESR): Indirectly measures how much
inflammation is in the body. This can help in determining if the cause of thrombocytosis
is due to inflammation.
3. TIBC (Total Iron Binding Capacity) Test: This is used to measure how much
iron is carried in your bloodstream. This can help determine if the person is
experiencing iron-deficiency anemia, a factor for secondary thrombocytosis.
4. Blood Smear: Often used as a follow-up test to abnormal results on a CBC.
This is useful to help diagnose or monitor numerous conditions that affect blood cell
population. In this case, the platelets will be of focus.
6. What are the medical/surgical management and discuss briefly.
Treatment is solely aimed at treating the underlying disorder that is causing the
reactive thrombocytosis. With successful management, the platelet count usually
returns to normal. In rare circumstance, treatments to protect against inappropriate clot
formation might be advised such as: (1) compression stocking, (2) ensuring you take
plenty of fluids, (3) keeping as mobile as possible, and (4) cessation of smoking. No
treatment is specifically indicated to directly reduce the platelet count. However, when
the platelet exceeds 1 million cubic millimeter, aspirin may be prescribed to prevent clot
formation.
7. Determing the nursing diagnosis based on the clinical manifestations.
Acute Pain r/t chest tightness secondary to thrombosis
Fatigue r/t anemia
Anxiety r/t temporary vision loss
Risk for Bleeding r/t high platelet count
Risk for Injury r/t altered clotting factors
Sources:
Clinical Practice Guideline for THROMBOCYTOSIS. (2008, July 22). Retrieved August
21, 2016, from http://www.asams.org/guidelines/Completed/NEW
Thrombocytosis.htm
Thrombocytosis. (n.d.). Retrieved July 21, 2016, from
http://www.mayoclinic.org/diseasesconditions/thrombocytosis/basics/symptoms/con-20032674
Acir, O., Borazan, M., & Dadaci, Z. (2014, September 8). Acute Central Retinal Vein
Occlusion Secondary to Reactive Thrombocytosis after Splenectomy. Retrieved
August 21, 2016, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172986/
Iron Deficiency Linked With Thrombosis. (2011, December 14). Retrieved August 21,
2016, from http://www.pulsetoday.co.uk/iron-deficiency-linked-withthrombosis/13223013.fullarticle
Olivares, J., Tingle, L., Khan, P., Nair, R., & Li, Z. (2009, January 22).
Postsplenectomy reactive thrombocytosis. Retrieved August 21, 2016, from
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626351/
G, A., & M, T. (1996, May 16). Role of catecholamines in platelet function:
Pathophysiological and clinical significance. Retrieved August 21, 2016, from
ttp://www.ncbi.nlm.nih.gov/pubmed/8796362
Precipitating Factors:
-Infection
-Chronic Inflammation (eg. Asthma, Chronic Peptic Ulcer,
TB, Kawasaki Disease, etc.)
-Iron deficiency anemia
-Malignant Disease
-Splenectomy
-Stress
Predisposing Factors:
All age, gender, and
race
Inflammation,
Infection,
Cancer
IL-6 are
produced at
site
Stress
Splenectomy
Activates fight
or flight
Accumulation
of platelets in
blood
Increase in
TPO
Release of
cetacholamine
Stimulates
megakaryocytes
Release of
cetacholamine
Irondeficiency
anema
Increase in
EPO
Increase in
thrombotic
growth
factors
Produces
blood
thrombocytes
Nsg Mgt:
-instruction on risk of hemorrhage
and thrombosis
-compression of stockings
-increase oral fluid intake
-keeping as mobile as possible
-cessation of smoking
Increased Platelets
(> 400,000/mm3)
Management:
-treating underlying cause
-Medication (prevention): Aspirin
Increased Platelets
(> 1,000,000/mm3)
Thrombosis
Bleeding
Decreased circulatory
platelets
Heart
Brain
Eyes
Extremities
Lungs
Chest
tightness
Stroke
Retinal vein
occlusion
DVT
Decrease in
0xygen
levels
Numbness
Heart Attack
Temporary
vision
changes
Weakness,
SOB