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1.

Describe briefly the disease condition


Secondary Thombocytosis is also called reactive thrombocytosis. It is similar to
primary thombocythemia because this disease condition elevated the platelet levels in
the blood. The difference however is that primary thrombocythemia is a stem cell
disorder within the bone marrow, whereas secondary thrombocytosis, according to
American Society of Aerospace Medicine Specialists (2008), is most often a normal
physiologic response to a coexistent inflammatory condition of surgery.
2. Determine predisposing and precipitating factors and discuss.
There arent any particular predisposing factors for this disease because it is
caused mainly of precipitating factors. However, it is important to take note that females
at a young age (children) are more prevalent to have iron-deficiency anemia which is
also a precipitating factor. The following are the precipitating factors of secondary
thrombocytosis: Inflammation, Infection, Cancer, Stress, Splenectomy, and Irondeficiency Anemia. The most common among all these are those that causes tissue
damage inflammation, infection, and cancer. Due to the damage done, it stimulates
the normal inflammatory response that starts with the release of interleukin-6 (IL-6) at
the site of inflammation. IL-6 is a cytokine that has been shown to be a key player in
chronic inflammation. In relation to the topic, IL-6 stimulates thrombopoiesis through
increasing the thrombopoietin (TPO), a glycoprotein hormone produced by the liver and
kidney which regulates

the

production of platelets. TPO then stimulates 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

platelet responses, including aggregation, secretion and

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

thrombocytosis. However, when the platelet increases to more than 1 million/mm3 (1


million cubic millimeter), thrombosis and bleeding occurs; this phenomenon (symptoms
associated with bleeding and thrombosis) is very rare (Brunner and Suddarth, 2007). It
is already understandable how thrombosis occurs; this is basically due to the increase
in platelet, a blood-clotting factor. Bleeding, however, is somehow surprising to know if

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:

Bleeding: confusion, light-headedness, weakness, clammy skin, fainting, and


skin bruising.

Thrombosis: Chest pain, vision changes due to retinal vein occlusions,


numbness on extremities due to DVT, tingling, weakness
Thrombosis would then affect many organs such as:

Heart -> Heart Attack

Brain -> Stroke

Lungs -> Damage to lungs and other organs due to hypoxia

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)

Decrease in highmolecular weight


multimens of von
Willebrand factor

Thrombosis

Will continue to use up


available platelets

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

Signs and Symptoms:


confusion, light-headedness,
weakness, clammy skin, fainting, and
skin bruising.

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