Ateneo de Davao University – College of

Nursing; BSN-3H

Thrombocytopenia
Platelet disease with high Bleeding Tendencies
A group-collaboration for the Oral Revalida

Group Members
Group 1
Agravante, Keane Jim
Ajoc, Kit Lorenzo
Altarejos, Mary Frances
Armada, Cenon Francis
Bagares, Louraine Mae
Bauzon, Onaiza Paula
Bonifacio, Verity
Braga, Rojae Marie
Cachuela, Gwen Clarisse
Celeste, Celeste Dominique
Group 4
Perpetua, Micah Noel
Puray, Joni
Rubia, Arnikka
Santillan, Ma. Princess Gccae
Segura, Riel
Sinoy, Beverly
Suasin,
Group 1: Agravante, Ajoc,Anne Michelle
Alarejos, Armada, Bagares, Bauzon, Bonifacio, Braga,
Tandog, Jesse Nigel Cachuela, Celeste
Zamorra,
Group 4: Perpetua, Harrison
Puray, Rubia,Ford
Sanitillian, Segura, Sinoy, Suasin, Tandog,
Zarra, Von Lovel Zamorra, Zarra
Ateneo de Davao University – College of Nursing; BSN-3H
DEFINITION
Thrombocytopenia
• Thrombocytopenia refers to decreased circulating platelets and an increased tendency to bleed.
 Idiopathic Thrombocytopenia Purpura
→ Idiopathic thrombocytopenia purpura is an immune mediated thrombocytopenia that occurs in the absence of toxin or drug exposure or a disease
known to be associated with decreased platelets.
 Thrombotic Thrombocytopenic Purpura

→ Thrombotic thrombocytopenic purpura (TTP) is a rare blood condition characterised by the formation of small clots (thrombi) within the circulation,
which results in the consumption of platelets and thus a low platelet count (thrombocytopenia).
 Drug-induced Thrombocytopenia
→ Drug-induced thrombocytopenia (DIT) is a relatively common clinical disorder. It is imperative to provide rapid identification and removal of the
offending agent before clinically significant bleeding or, in the case of heparin, thrombosis occurs. DIT can be distinguished from idiopathic
thrombocytopenic purpura (ITP), a bleeding disorder caused by thrombocytopenia not associated with a systemic disease, based on the history of drug
ingestion or injection and laboratory findings. DIT disorders can be a consequence of decreased platelet production (bone marrow suppression) or
accelerated platelet destruction (especially immune-mediated destruction).
Source: Copstead, L.(2005).Pathophysiology. Missouri:Elsevier Saunders.
Thrombocytopenia
Thrombocytopenia is a decrease in the number of circulating platelets to a level less than 100,00/µL 9. However, spontaneous bleeding usually does not occur until the
platelet count falls below 20, 000/µL9.
Idiopathic Thombocytopenic Purpura
Idiopathic Thombocytopenic Purpura is an autoimmune disorder, result in platelet antibody formation and excess destruction of platelets. The immunoglobulin G antibody
commonly binds to two identified membrane glycoproteins while in the circulation. The platelets which are made more susceptible to phagocytosis because of the antibody, are
destroyed in the spleen and the liver.
Drug-induced Thrombocytopenia
come drugs, such quinine, quinidine, and certain sulfa-containing antibiotics, may induce thrombocytopenia. These drugs act as haptens and induce antigen-antibody
responses and formation of immune complexes that cause platelet destruction by complement-mediated lysis.
Thrombotic Thrombocytopenic Purpura
Thrombotic Thrombocytopenic Purpura is a microvascular disease characterized by widespread platelet thrombi in arterioles and capillaries of the heart, brain and
kidneys.
Source:
Porth, C. (2007). Essentials of Pathophysiology. Lippincott Williams & Wilkins: Philippines
THROMBOCYTOPENIA
Thrombocytopenia is a decrease in circulating platelet count (less than 100, 000/mm 3) and is the most common cause of bleeding disorders. It may be congenital or
acquired, and results from decreased platelet production, as in aplastic anemia, myelofibrosis, radiation therapy, or leukemia; increased platelet destruction, as in certain
infections, drug toxicity, or disseminated intravascular coagulation; abnormal distribution or sequestration in spleen; or dilutional thrombocytopenia after hemorrhage or red blood
cell transfusions. Severe thrombocytopenia may cause death as a result of blood loss or bleeding into vital organs.
 An autoimmune form of thrombocytopenia, idiopathic thrombocytopenic purpura (ITP), results from destruction of platelets by antiplatelet antibodies. Acute ITP typically
follows a viral illness and is more common in children. Eighty to ninety percent of patients recover uneventfully. Chronic ITP (more than 6-month course) is most common at ages
20 to 40, and is more common in women than men.
Drug-induced immune thrombocytopenia is a condition in which the use of certain drugs leads to the formation of antibodies against clot-forming cells in the blood
(platelets). These antibodies can cause a low platelet count, which makes bleeding more likely.
Thrombocytopenic purpura is a bleeding disorder characterized by a marked decrease in the number of platelets, resulting in multiple bruises, petechiae, and
hemorrhage into the tissues. Causes include infection and drug sensitivity and toxicity. The acute form usually occurs in children between 2 and 6 years of age and is benign, with
complete recovery usually apparent within 6 weeks. The chronic form usually occurs in adults between 2- and 5- years of age. Recovery is rarely spontaneous and often requires
adrenocortical steroids or splenectomy.
Thrombotic thrombocytopenic purpura (TTP) is a disorder characterized by thrombocytopenia, hemolytic anemia, and neurologic abnormalities. It is accompanied by a
generalized purpura with the deposition of microthrombi within the capillaries and smaller arterioles.
Source:
Nettina, S. (2006). Lippincott Manual of Nursing Practice Handbook, 3rd edition, pp. 919-922; Philadelphia: Lippincott Williams & Wilkins

ETIOLOGY
Rationale
Predisposing factors
• Age (children) Thrombocytopenia is a disease of younger people, with a peak incidence
between the ages 18-40. (Porth, C. 2007. Pathophysiology, p. 294)
• Gender (Women) The disease is seen as twice as often in women as in men. (Porth, C. 2007.
Pathophysiology, p. 294) In addition only women have the risk of being
preeclamptic.
Precipitating factors
• Blood loss Since platelets are one of the major blood components, severe blood loss could
cause the circulating platelets to decrease in number.
• Pregnancy (Preeclampsi) Thrombocytopenia is the most common hematologic complication of
preeclampsia among pregnant women. The cause of thrombocytopenia has been
ascribed to platelet deposition at the site of endothelial injury.
• Decreased or defective platelet production in the bone
marrow
a) Hematologic malignancy such as leukemia a) Immature WBC crowd out normal bone marrow cells thus platelet production
b) Anemia (Aplastic and Pernicious) decreases
c) Radiation therapy b) Bone marrow does not produce enough platelets
d) Drug therapy (thiazides, chemotherapy agents, c) Bone marrow activity is suppressed
estrogens) d) Bone marrow aplasia or hypoplasia occurs
e) HIV infection e) An infection with HIV suppresses the production of megakaryocytes, the
platelet precursors.
• Increased platelet destruction outside the bone marrow
a) Drug therapy (antibiotics, sulfonamides, gold salts) a)
b) Idiopathic causes
b) Antibodies form and attack platelets
c) Blood transfusions
c)
d) Disseminated intravascular coagulation d) Clotting factors are consumed including platelets
• Abnormal distribution of platelets
a) Splenomegaly a) Platelets collect in spleen; circulating platelets decreases

SYMPTOMATOLOGY
Symptoms Rationale
 Because platelets form temporary mucous plugs that quickly stop bleeding and promote key reactions in the coagulation cascade,
spontaneous bleeding associated with platelet disorders most often involves the small blood vessels. The common sites are the skin
BLEEDING
and the mucous membranes of the gastrointestinal and genitourinary tracts. Petechiae and purpura are common manifestation
resulting bleeding into the skin.
p. 204 of Porth, C. (2007). Essentials of Pathophysiology. Lippincott Williams & Wilkins: Philippines
MALAISE, GENERAL
Due to blood loss and poor oxygenation.
WEAKNESS AND
FATIGUE

EXAMPLES

1. Petechiae - red spots under the skin surface caused by intradermal hemorrhage

2. Ecchymoses (purple) - blood in subcutaneous tissue

3. Larged blood-filled bullae in the
- a blister on the skin more than 5 mm (about 3/16 inch) in diameter
mouth
- blood in the stool
4. Melena
Bleeding of the G.I.
- blood in the urine
5. Hematuria
Bleeding of the G.U.
Menorrhagia
6. Other
Epistaxis

ANATOMY AND PHYSIOLOGY

Bone Marrow is the flexible tissue found in the hollow interior of bones. In adults, marrow in large bones produces new blood cells. It constitutes 4% of total body weight, i.e.
approximately 2.6kg/5.7lbs in adults
Marrow types: There are two types of bone marrow:red marrow (consisting mainly ofmyeloid tissue) and yellow marrow(consisting mainly of fat cells). Red blood
cells, platelets and most white blood cells arise in red marrow. Both types of bone marrow contain numerous blood vessels and capillaries. At birth, all bone marrow is red. With
age, more and more of it is converted to the yellow type. About half of the bone marrow is red. [1] Red marrow is found mainly in the flat bones, such as the hip bone, breast
bone, skull, ribs, vertebraeand shoulder blades, and in thecancellous ("spongy") material at the epiphyseal ends of the long bonessuch as the femur and humerus. Yellow marrow
is found in the hollow interior of the middle portion of long bones. In cases of severe blood loss, the body can convert yellow marrow back to red marrow to increase blood cell
production.
Stroma: The stroma of the bone marrow is all tissue that isn't directly involved in the primary function of hematopoiesis. The yellow bone marrow belongs here, and makes the
majority of the bone marrow stroma, in addition to stromal cells located in the red bone marrow. Still, the stroma is indirectly involved in hematopoiesis, since it provides
thehematopoietic microenvironment that facilitates hematopoiesis by theparenchymal cells. For instance, they generate colony stimulating factors, affecting hematopoiesis. Cells
that constitute the bone marrow stroma are: fibroblasts (reticular connective tissue), macrophages, adipocytes, osteoblasts, osteoclasts, endothelial cells forming the sinusoids,
Macrophages contribute especially to red blood cell production. They deliver iron for hemoglobin-production.
Bone marrow barrier: The blood vessels constitute a barrier, inhibiting immature blood cells from leaving the bone marrow. Only mature blood cells contain the membrane
proteins required to attach to and pass the blood vessel endothelium. Hematopoietic stem cells may also cross the bone marrow barrier, and may thus be harvested from blood.
Stem cells: The bone marrow stroma contain mesenchymal stem cells (also calledmarrow stromal cells). These cells are multipotent stem cells that candifferentiate into a variety
of cell types. Cell types that MSCs have been shown to differentiate into in vitro or in vivo include osteoblasts,chondrocytes, myocytes, adipocytes, and, as described lately, beta-
pancreatic islets cells. They can also transdifferentiate into neuronal cells.
Compartmentalization: There is biologic compartmentalization in the bone marrow, in that certaincell types tend to aggregate in specific areas. For
instance, erythrocytes,macrophages and their precursors tend to gather around blood vessels, while granulocytes gather at the borders of the bone marrow.
Types of stem cells
- Hematopoietic stem cells give rise to the three classes of blood cells that are found in the circulation: white blood cells (leukocytes), red blood cells (erythrocytes),
and platelets (thrombocytes).
 - Mesenchymal stem cells are found arrayed around the central sinus in the bone marrow. They have the capability to differentiate
intoosteoblasts, chondrocytes, myocytes, and many other types of cells. They also function as "gatekeeper" cells of the bone marrow.
- Endothelial stem cells

Blood is a specialized bodily fluid that delivers necessary substances to the body's cells — such as nutrients and oxygen — and transports wasteproducts away from those same
cells.
In vertebrates it is composed of blood cells suspended in a liquid called blood plasma. Plasma, which comprises 55% of blood fluid, is mostly water (90% by volume), and contains
dissolved proteins, glucose, mineral ions,hormones, carbon dioxide (plasma being the main medium for excretory product transportation), platelets and blood cells themselves.
The blood cells present in blood are mainly red blood cells (also called RBCs or erythrocytes) and white blood cells, including leukocytes andplatelets (also called thrombocytes).
The most abundant cells in vertebrate blood are red blood cells. These contain hemoglobin, an iron-containing protein, which facilitates transportation of oxygen by reversibly
binding to this respiratory gas and greatly increasing its solubility in blood. In contrast, carbon dioxide is almost entirely transported extracellularly dissolved in plasma
asbicarbonate ion.
Vertebrate blood is bright red when its hemoglobin is oxygenated. Some animals, such as crustaceans and mollusks, use hemocyanin to carry oxygen, instead of
hemoglobin. Insects and some molluscs use a fluid called hemolymph instead of blood, the difference being that hemolymph is not contained in a closed circulatory system. In
most insects, this "blood" does not contain oxygen-carrying molecules such as hemoglobin because their bodies are small enough that their tracheal system suffices for supplying
oxygen.
Jawed vertebrates have an adaptive immune system, based largely onwhite blood cells. White blood cells help to resist infections and parasites.Platelets are important in
the clotting of blood.[1] Arthropods, using hemolymph, have hemocytes as part of their immune system.
Blood is circulated around the body through blood vessels by the pumping action of the heart. In animals having lungs, arterial blood carries oxygen from inhaled air to the tissues
of the body, and venous blood carries carbon dioxide, a waste product of metabolism produced by cells, from the tissues to the lungs to be exhaled.
Medical terms related to blood often begin with hemo- or hemato- (BrE:haemo- and haemato-) from the Greek word "αἷμα" for "blood." Anatomicallyand histologically, blood is
considered a specialized form of connective tissue, given its origin in the bones and the presence of potential molecular fibers in the form of fibrinogen.

Erythropoiesis is the process by which red blood cells (erythrocytes) are produced.[1] In human adults, this usually occurs within the bone marrow. In the early fetus,
erythropoiesis takes place in the mesodermal cells of theyolk sac. By the third or fourth month, erythropoiesis moves to the spleen and liver.[2] In humans with certain diseases
and in some animals, erythropoiesis also occurs outside the bone marrow, within the spleen orliver. This is termed extramedullary erythropoiesis.
The tibia and femur cease to be important sites of hematopoiesis by about age 25; the vertebrae, sternum, pelvis and ribs, and cranium bones continue to produce red blood cells
throughout life.

Platelets, or thrombocytes, are small cytoplasmic bodies derived from cells. They circulate in the blood ofmammals and are involved inhemostasis leading to the formation
of blood clots. Like red blood cells, platelets have no nucleus.
If the number of platelets is too low, excessive bleeding can occur; however, if the number of platelets is too high, blood clots can form (thrombosis), which block blood vessels,
and may cause a stroke and/or a heart attack. An abnormality or disease of the platelets is called a thrombocytopathy[1], which could be either a low number (thrombocytopenia),
a decrease in function (thrombasthenia) or an increase in number (thrombocytosis).
Kinetics
- Platelets are produced in blood cell formation (thrombopoiesis) in bone marrow, by budding off from megakaryocytes.
- The physiological range for platelets is 150-400 x 109 per litre.
- Around 1 x 1011 platelets are produced each day by an average adult.
- The lifespan of circulating platelets is 7-10 days.
- This process is regulated by thrombopoietin, a hormone usually produced by the liver and kidney.
- Each megakaryocyte produces between 5,000 and 10,000 platelets.
- Old platelets are destroyed by the spleen and by Kupffer cells in theliver.
Thrombus formation
The function of platelets is the maintenance of haemostasis. Primarily, this is achieved by the formation of thrombi, when damage to the endothelium ofblood vessels occurs. On
the converse, thrombus formation must be inhibited at times when there is no damage to the endothelium.
Activation
The inner surface of blood vessels is lined with a thin layer of endothelialcells that, in normal hemostasis, acts to inhibit platelet activation with the production of endothelial-
ADPase, noradrenaline, and PGI2. Endothelial-ADPase clears away ADP, a platelet activator, from platelet surface receptors. Endothelial cells produce a protein called von
Willebrand factor, a cell adhesion ligand, which helps endothelial cells adhere to collagen in thebasement membrane. Under physiological conditions, collagen does not pass into
the bloodstream; however vWF is secreted constitutively into the plasma by the endothelial cells that produce it, or otherwise is stored within the endothelial cell or in platelets.
When endothelial damage occurs, platelets come into contact with exposed collagen and vWF, causing a reduction in secretion of endothelium platelet inhibitors.The inner
surface of blood vessels is lined with a thin layer of endothelialcells. Under this is a layer of collagen. When the endothelial layer is injured, the collagen is exposed. When the
platelets contact collagen, they are activated. They are also activated by thrombin (primarily through PAR-1) and ADP receptors (P2Y1and P2Y12) expressed on platelets. They can
also be activated by a negatively-charged surface, such as glass. Platelet activation further results in the scramblase-mediated transport of negatively-charged phospholipids to
the platelet surface. These phospholipids provide a catalytic surface (with the charge provided byphosphatidylserine and phosphatidylethanolamine) for
the tenase andprothrombinase complexes.
Shape Change
Activated platelets change in shape to become more spherical, and pseudopods form on their surface. Thus they assume a stellate [star-like] shape.
Granule Secretion
Platelets contain alpha and dense granules. Activated platelets excrete the contents of these granules into their canalicular systems and into surrounding blood. There are two
types of granules: dense granules (containing ADP or ATP, calcium, and serotonin), α-granules (containing platelet factor 4, PDGF, fibronectin, B-thromboglobulin, vWF, fibrinogen,
and coagulation factors V and XIII).
Thromboxane A2 Synthesisis
Platelet activation initiates the arachidonic acid pathway to produce TXA2. TXA2 is involved in activating other platelets.
Adhesion and aggregation
Platelets aggregate, or clump together, using fibrinogen of vWF as a connecting agent. The most abundant platelet aggregation receptor is glycoprotein (GP) IIb/IIIa; this is a
calcium-dependent receptor for fibrinogen, fibronectin, vitronectin, thrombospondin, and von Willebrand factor (vWF). Other receptors include GPIb-V-IX complex (vWF) and GPVI
(collagen). Activated platelets will adhere, via glycoprotein (GP) Ia, to the collagen that is exposed by endothelial damage. Aggregation and adhesion act together to form the
platelet plug. Myosin andactin filaments in platelets are stimulated to contract during aggregation, further reinforcing the plug. Platelet aggregation is stimulated
by ADP, thromboxane and α2 receptor-activation, but inhibited by other inflammatory products like PGI2 andPGD2. Platelet aggregation is enhanced by exogenous administration
of anabolic steroids.
 Predisposing Factor: Precipitating Factor:
-age -blood loss
-gender -pregnancy (preeclampsia)
-decreased or defective
platelet production in the
bone marrow
-increase platelet destruction
outside the bone marrow
-abnormal distribution of

Drugs act as
Aggregation Platelet ENLARGED SPLEEN Damage to the
haptens
of platelets Immunoglobulin G bone marrow
and antibody Formation
Antigen antibody activation of Spleen harbour
response coagulation Binds to many platelets
in the small glycoproteins Diminished Diminished or
blood vessels GpIIb/IIa and platelet absent
Formation of Decrease number production megakaryocyt
immune complexes Platelets become of platelets in the despite the es in marrow
Platelets are
more susceptible to circulation presence of
consumed in
phagocytosis megakaryocyt
the
Destruction of es in marrow No production
coagulation
platelets by of
process
complement thrombocytes
Platelet destroyed
mediated lysis
in the spleen and
liver

Increase destruction
of platelets
Massive blood
replacement or
exchange transfusion

loss of platelet
viability in stored
blood

Platelets become
diluted

THROMBOCYTOPENIA

IF TREATED IF NOT TREATED

-rise in the level of platelets -sharp decrease of platelets
-prognosis(ni riel) -fatal bleeding
-patient cheats death! -tachycardia
-loss of consciousness
-shock
-death
Treatment

Medications
ITP
1. Immune globulin intravenous is a sterilized solution made from human plasma. It contains the antibodies to help your body
protect itself against infection from various diseases.
Immune globulin is used to treat primary immune deficiency, and to reduce the risk of infection in individuals with poorly
functioning immune systems. IGIV is also used to increase platelets (blood clotting cells) in people with idiopathic
thrombocytopenic purpura (ITP).
IGIV such as (brand names):
Carimune, Flebogamma, Gamimune N 10%, Gammagard
2. Steroids-Steroids help prevent bleeding by decreasing the rate of platelet destruction. Steroids, if effective, will result in an
increase in platelet counts seen within two to three weeks. Side effects may include irritability, stomach irritation, weight
gain, hypertension and acne.
Includes:
3. Corticosteroids-It blocks the effects produced by the antibodies that destroys the platelets.
Includes: Acetocot, Cinalone, Deltasone, Methylprednisolone, Triamcinolone
4. Rituximab and Vincristine are cancer medications that interfere with the growth of cancer cells and slows their growth and
spread in the body. For Thrombocytopenic purpura, it interfere with the actions of the antibodies that destroys and decreases
the platelet count.
TTP

1. Cyclosporine A- An immunosuppressive drug which suppresses cell-mediated immune reactions and some humoral
immunity, but exact mechanism is not known.
2. See other medications of TTP in ITP and HUS
HUS
1. Antiplatelet agent such as the aspirin and the dipyridamole- Inhibits prostaglandin synthesis, which prevents platelet-
aggregating thromboxane A2 formation, prevents thrombus formation, and shortens thrombocytopenia. Used in combination
with plasma exchange because not beneficial alone.

Exam Definition Normal Value Indication of Abnormal Results

CBC A complete blood count 150,000 to 400,000/mm3 If the number of platelets is below normal
(CBC) test measures the (thrombocytopenia), the cause may be:
following:

• Cancer chemotherapy
• The number of • Disseminated intravascular
red blood cells coagulation (DIC)
(RBCs)
• Hemolytic anemia
• The number of
white blood cells • Hypersplenism
(WBCs) • Idiopathic thrombocytopenic
• The total purpura (ITP)
amount of • Leukemia
hemoglobin in
the blood
• Massive blood transfusion

• The fraction of • Prosthetic heart valve

the blood
composed of red
blood cells
(hematocrit)
• The size of the
red blood cells
(mean
corpuscular
volume, or MCV)

The CBC test also

provides specific
information the size and
hemoglobin content of
individual red blood cells.
This is determined from
the additional following
measurements:

• Mean
corpuscular
hemoglobin
 (MCH)
• Mean
corpuscular
hemoglobin
concentration
(MCHC)
The platelet count is also
usually included in the
CBC.
Bone Marrow Bone marrow is the soft
Aspiration tissue inside bones that
helps form blood cells. It
is found in the hollow
part of most bones. Bone
marrow aspiration is the
removal of a small
amount of this tissue in
liquid form for
examination.
Partial thromboplastin
Partial time (PTT) is a blood test
thromboplastin that looks at how long it
time (PTT) takes for blood to clot. It
can help tell if you have
bleeding or clotting
problems.
Prothrombin time (PT) is
Prothrombin time a blood test that
(PT) measures the time it
takes for the liquid
portion (plasma) of your
blood to clot
The marrow should contain
blood-forming
(hematopoietic) cells, fat
cells, and connective
tissues
The normal value will vary
between laboratories. In
general, clotting should
occur between 25 to 35
seconds. If the person is
taking blood thinners,
clotting takes up to two and
a half times longer.
The normal range is 11 to
13.5 seconds. However,
"normal" varies from lab to
lab.
The PT time will be longer
in persons who take blood
thinners.
Abnormal (Low production of platelets in the
bone marrow) results may be due to:
• Acute lymphocytic leukemia
• Acute nonlymphocytic leukemia
(AML)
• Anemia of B12 deficiency
• Anemia of folate deficiency
• Chronic lymphocytic leukemia
(CLL)
• Chronic myelogenous leukemia
(CML)
• Idiopathic thrombocytopenic
purpura (ITP)
• Lymphoma
• Macroglobulinemia of Waldenstrom
• Megaloblastic anemia
• Multiple myeloma
• Myelofibrosis
• Pernicious anemia
• Primary thrombocytopenia
An abnormal (too long) PTT result may be
due to:
• Cirrhosis
• Disseminated intravascular
coagulation (DIC)
• Factor XII deficiency
• Hemophilia A
• Hemophilia B
• Hypofibrinogenemia
• Malabsorption
• Von Willebrand's disease
• Lupus anticoagulants
Increased PT times may be due to:
• Bile duct obstruction
• Cirrhosis
• Disseminated intravascular
coagulation
• Hepatitis
• Malabsorption
• Vitamin K deficiency
• Coumadin (warfarin) therapy
• Factor VII deficiency
• Factor X deficiency
 • Factor II (prothrombin) deficiency
• Factor V deficiency

• Factor I (fibrinogen) deficiency

A test for platelet- A negative test is normal. Abnormal results show the person has
Platelet associated associated antibodies antiplatelet antibodies. These are that
antibodies shows whether you have attach to platelets and destroy them. This
abnormal antiplatelet causes a low platelet count, which can lead
antibodies in your blood to excessive bleeding. Antiplatelet
antibodies may appear in the blood for
unknown reasons (idiopathic
thrombocytopenic purpura), or as a side
effect of certain drugs such as heparin.
These drugs can sometimes cause the
immune system to identify its own platelets
as abnormal or foreign, and attack them.

Exams and Tests for Thrombocytopenia

• CBC shows low platelets

• Bone marrow aspiration or biopsy may be normal or may show low megakaryocytes (platelet precursors) or an infiltrating
disease.
• PTT clotting study is normal
• PT clotting study is normal
• Platelet associated antibodies may be present

Source: http://www.nlm.nih.gov/medlineplus/ency/article/000586.htm
Priority Nursing Diagnoses:

1. Risk for injury related to bleeding tendency

2. Risk for infection related to inadequate secondary defences
3. High risk for fluid volume deficit related to hemorrhage
4. Altered tissue perfusion (peripheral) related to hypovolemia
5. High risk for trauma related to abnormal blood profile
6. Acute pain related to hemorrhage

Nursing Management:

1. Monitor for changes in vital signs such as increase in PR, RR, and decrease in BP.
2. Assess/ Monitor for signs of bleeding: epistaxis, bleeding of gums, vagina or rectum.
3. Monitor for systemic signs of bleeding and hypovolemia.
4. Instruct patient to avoid contact sports (e.g. basketball).
5. Avoid invasive procedures including rectal temperature taking.
6. Use soft- bristled toothbrush.
7. Avoid NSAIDs (e.g. aspirin) for these are sulfa-containing meds that alter platelet function and increase bleeding tendencies.
8. Evaluate use of contraceptives (e.g. IUD) as these may increase the risk for bleeding tendencies.
9. Advise patient to avoid flossing.
10. Fluid replacement for rapid loss of blood.
11. Administer blood transfusion (e.g. cryoprecipitate or Fresh Frozen Plasma) as ordered to replace clotting factors.
12. Monitor for changes in neurological status (e.g. headache, confusion, visual disturbances).
13. Apply direct pressure for 5-10 minutes then a pressure dressing (to promote clotting and to reduce blood loss) to all
venipuncture sites and monitor it carefully for 24 hours.
14. Treat nausea aggressively to prevent vomiting as severe nausea causes GI bleeding.