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, Anne Michelle Group 1: Agravante, Ajoc, Alarejos, Armada, Bagares, Bauzon, Bonifacio, Braga, Tandog, Jesse Nigel Cachuela, Celeste Zamorra, Harrison Ford Group 4: Perpetua, Puray, Rubia, 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) • Gender (Women) Thrombocytopenia is a disease of younger people, with a peak incidence between the ages 18-40. (Porth, C. 2007. Pathophysiology, p. 294) 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. Since platelets are one of the major blood components, severe blood loss could cause the circulating platelets to decrease in number. 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. a) b) c) d) e) Immature WBC crowd out normal bone marrow cells thus platelet production decreases Bone marrow does not produce enough platelets Bone marrow activity is suppressed Bone marrow aplasia or hypoplasia occurs An infection with HIV suppresses the production of megakaryocytes, the platelet precursors.

Precipitating factors • Blood loss • • Pregnancy (Preeclampsi) Decreased or defective platelet production in the bone marrow a) Hematologic malignancy such as leukemia b) Anemia (Aplastic and Pernicious) c) Radiation therapy d) Drug therapy (thiazides, chemotherapy agents, estrogens) e) HIV infection Increased platelet destruction outside the bone marrow a) Drug therapy (antibiotics, sulfonamides, gold salts) b) Idiopathic causes c) Blood transfusions d) Disseminated intravascular coagulation Abnormal distribution of platelets a) Splenomegaly

a) b) c) d) a) Antibodies form and attack platelets Clotting factors are consumed including platelets 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, BLEEDING spontaneous bleeding associated with platelet disorders most often involves the small blood vessels. The common sites are the skin 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 WEAKNESS AND FATIGUE Due to blood loss and poor oxygenation.

EXAMPLES 1. Petechiae 2. Ecchymoses (purple) 3. Larged blood-filled bullae in the mouth 4. Melena 5. Hematuria 6. Other - red spots under the skin surface caused by intradermal hemorrhage - blood in subcutaneous tissue - a blister on the skin more than 5 mm (about 3/16 inch) in diameter - blood in the stool Bleeding of the G.I. - blood in the urine Bleeding of the G.U. Menorrhagia 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, betapancreatic 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

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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).

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Mesenchymal stem cells are found arrayed around the central sinus in the bone marrow. They have the intoosteoblasts, chondrocytes, myocytes, and many other types of cells. They also function as "gatekeeper" cells of the bone marrow. Endothelial stem cells

capability

to

differentiate

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

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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.

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- 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 endothelialADPase, 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: -age -gender

Precipitating Factor:
-blood loss -pregnancy (preeclampsia) -decreased or defective platelet production in the bone marrow -increase platelet destruction outside the bone marrow -abnormal distribution of

Drugs act as haptens Antigen antibody response

Formation of immune complexes

Aggregation of platelets and activation of coagulation in the small blood vessels Platelets are consumed in the coagulation process

Platelet Immunoglobulin G antibody Formation Binds to glycoproteins GpIIb/IIa and Platelets become more susceptible to phagocytosis

ENLARGED SPLEEN

Damage to the bone marrow

Spleen harbour many platelets Diminished platelet production despite the presence of megakaryocyt es in marrow Diminished or absent megakaryocyt es in marrow

Decrease number of platelets in the circulation

Destruction of platelets by complement mediated lysis

Platelet destroyed in the spleen and liver

No production of thrombocytes

Increase destruction of platelets

Massive blood replacement or exchange transfusion

loss of platelet viability in stored blood

Platelets become diluted

THROMBOCYTOPENIA

IF TREATED -rise in the level of platelets -prognosis(ni riel) -patient cheats death!

IF NOT TREATED -sharp decrease of platelets -fatal bleeding -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.

3. 4. TTP 1. 2. HUS

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: Corticosteroids-It blocks the effects produced by the antibodies that destroys the platelets. Includes: Acetocot, Cinalone, Deltasone, Methylprednisolone, Triamcinolone 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.

Cyclosporine A- An immunosuppressive drug which suppresses cell-mediated immune reactions and some humoral immunity, but exact mechanism is not known. See other medications of TTP in ITP and HUS Antiplatelet agent such as the aspirin and the dipyridamole- Inhibits prostaglandin synthesis, which prevents plateletaggregating thromboxane A2 formation, prevents thrombus formation, and shortens thrombocytopenia. Used in combination with plasma exchange because not beneficial alone. Exam Definition A complete blood count (CBC) test measures the following: Normal Value 150,000 to 400,000/mm3 Indication of Abnormal Results If the number of platelets is below normal (thrombocytopenia), the cause may be:

1.

CBC

• • •

The number of red blood cells (RBCs) The number of white blood cells (WBCs) The total amount of hemoglobin in the blood The fraction of the blood composed of red blood cells (hematocrit) The size of the red blood cells (mean corpuscular volume, or MCV)

• • • • • • • •

Cancer chemotherapy Disseminated intravascular coagulation (DIC) Hemolytic anemia Hypersplenism Idiopathic thrombocytopenic purpura (ITP) Leukemia Massive blood transfusion Prosthetic heart valve

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)

Bone Marrow Aspiration

The platelet count is also usually included in the CBC. Bone marrow is the soft 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.

The marrow should contain blood-forming (hematopoietic) cells, fat cells, and connective tissues

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

Partial thromboplastin time (PTT)

Partial thromboplastin time (PTT) is a blood test that looks at how long it takes for blood to clot. It can help tell if you have bleeding or clotting problems.

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.

• 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

Prothrombin time (PT)

Prothrombin time (PT) is a blood test that measures the time it takes for the liquid portion (plasma) of your blood to clot

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.

• 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

Platelet associated antibodies

A test for plateletassociated antibodies shows whether you have abnormal antiplatelet antibodies in your blood

A negative test is normal.

• Factor I (fibrinogen) deficiency Abnormal results show the person has antiplatelet antibodies. These are that attach to platelets and destroy them. This causes a low platelet count, which can lead 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. 2. 3. 4. 5. 6. Risk for injury related to bleeding tendency Risk for infection related to inadequate secondary defences High risk for fluid volume deficit related to hemorrhage Altered tissue perfusion (peripheral) related to hypovolemia High risk for trauma related to abnormal blood profile Acute pain related to hemorrhage

Nursing Management: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. Monitor for changes in vital signs such as increase in PR, RR, and decrease in BP. Assess/ Monitor for signs of bleeding: epistaxis, bleeding of gums, vagina or rectum. Monitor for systemic signs of bleeding and hypovolemia. Instruct patient to avoid contact sports (e.g. basketball). Avoid invasive procedures including rectal temperature taking. Use soft- bristled toothbrush. Avoid NSAIDs (e.g. aspirin) for these are sulfa-containing meds that alter platelet function and increase bleeding tendencies. Evaluate use of contraceptives (e.g. IUD) as these may increase the risk for bleeding tendencies. Advise patient to avoid flossing. Fluid replacement for rapid loss of blood. Administer blood transfusion (e.g. cryoprecipitate or Fresh Frozen Plasma) as ordered to replace clotting factors. Monitor for changes in neurological status (e.g. headache, confusion, visual disturbances). 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.

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