Term
|
Definition
| decrease in the number of platelets in the peripheral blood below the reference range for an individual laboratory |
|
|
Term
|
Definition
| an increase in the number of platelets in the peripheral blood above the reference range for an individual laboratory |
|
|
Term
| expected platelet count in thrombocytopenia |
|
Definition
|
|
Term
| expected platelet count in thrombocytosis |
|
Definition
|
|
Term
|
Definition
| (< 3mm) are small, pinhead-sized purple spots causes by blood escaping from capillaries into intact skin. These are associated with platelet and vascular disorders |
|
|
Term
|
Definition
| (3mm-1cm) are purple discolorations of the skin caused by petechiae and/or ecchymoses |
|
|
Term
|
Definition
| (> 1cm) are bruises (bluish-black discoloration of the skin) that is larger than 3mm in diameter caused by bleeding from arterioles into subcutaneous tissues without disruption of intact skin |
|
|
Term
|
Definition
| localized collections of blood under the skin or in other organs caused by a break in the wall of the blood vessel |
|
|
Term
|
Definition
| is a common manifestation in disorders of primary hemostasis. Bruises usually appear on trunk without recognized trauma. Easy bruisability can also be associated with excessive and prolonged bleeding from cuts. |
|
|
Term
| Laboratory tests that can be ordered to screen for abnormalities of the hemostatic system |
|
Definition
| screening tests like PT, APTT, quantitative platelet count, BT, and fibrinogen assay |
|
|
Term
| expected clinical consequences when a patient has an abnormality of platelets or blood vessels |
|
Definition
| petechiae, ecchymoses, epistaxis (nose bleed), excessive bleeding from superficial wounds, bleeding into retina, gastrointestinal bleeding, bleeding in the urinary tract, hypermenorrhea, gingival bleeding (gums), increased bleeding after tooth extraction, and intracranial bleeding. |
|
|
Term
| Increased platelet counts correlation with disease maniestations |
|
Definition
| can be due to primary thrombocytosis (megakaryocyte proliferation and maturation bypass regulatory mechanisms, plt > 1000 x 103/ µL, seen in chronic myeloproliferative disorders), secondary thrombocytosis (reactive, increase in platelets caused by another disease, plt > 1000 x 103/ µL), or transient thrombocytosis |
|
|
Term
| decreased platelet counts correlation with disease manifestations |
|
Definition
| can be due to increased destruction of platelets which can be immune or non immune or decreased production of platelets which can be due to megakaryocyte hypoplasia (bone marrow), replacement of normal marrow (transplant), ineffective thrombopoiesis, or inherited disorders. Thrombocytopenia can also be due to increased splenic sequestration (90% of platelets held in spleen), dilutional thrombocytopenia (due to massive transfusions) or conditions with multiple mechanisms of thrombocytopenia |
|
|
Term
| Hematologic disorders characterized by thrombcytopenia |
|
Definition
| idiopathic immune thrombocytopenia, neonatal alloimmune thrombocytopenia, drug-induced thrombocytopenias, heparin associated thrombocytopenia, heparin induced thrombocytopenia or secondary to collagen diseases, autoimmune diseases, lymphoporliferative disorders, infections or vaccines. Thrombocytosis can also be related to disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome and mechanical destruction. |
|
|
Term
| Hematologic disorders characterized by thrombocytosis |
|
Definition
| Thrombocytosis is seen in chronic myeloproliferative disorders and myelodysplasia, reactive thrombocytosis (malignancies, chronic inflammation, IDA, or hemolytic anemia) |
|
|
Term
| Immune mediated Thrombocytopenia etiology |
|
Definition
| platelets which are sensitized by antibody are removed by splenic macrophages in the spleen |
|
|
Term
| Immune mediated Thrombocytopenia pathophysiology |
|
Definition
| caused by antibodoies which sensitize the platelets |
|
|
Term
| Immune mediated Thrombocytopenia laboratory findings |
|
Definition
| Mean platelet volume and platelet count are used to evaluate platelets (high MPV with decreased plt count). Bone marrow shows increased megakaryocytes with increased ploidy. |
|
|
Term
|
Definition
| auto reactive antibodies bind to platelets via receptors which shortens their life span |
|
|
Term
|
Definition
| idiopathic thrombocytopenia, autoimmune disorder |
|
|
Term
| Laboratory findings of ITP |
|
Definition
| Peripheral blood shows increased reticulated platelets, an increased in thrombopoetin. Can be chronic (seen in adults), acute (seen in children) or transplacental (newborns of mothers with ITP). |
|
|
Term
| Etiology of Neonatal alloimmune thrombocytopenia |
|
Definition
| maternal antibodies produced against fetal platelets (HPA-1a) that baby inhereited from father and mother lacks |
|
|
Term
| Pathophysiology of Neonatal alloimmune thrombocytopenia |
|
Definition
| platelet destruction by alloantibodies stimulated by foreign antigens during pregnancy or after blood transfusions |
|
|
Term
| laboratory findings of Neonatal alloimmune thrombocytopenia |
|
Definition
| high mortality rate due to bleeding into the CNS, bone marrow aspirations evaluates megakaryocytes and rules out other causes of thrombocytopenias, increased, markedly relfecting stimulation by TPO to increase platelet production, MPV is increased, PBS has increased platelets, normal TPO levels |
|
|
Term
| Etiology of Drug-induced thrombocytopenias |
|
Definition
| Heparin associated thrombocytopenia: non immune mediated in which heparin causes direct activation of plateletsHeparin induced thrombocytopenia: immune mediated in which heparin dependant platelet activating IgG against PF4 is bound by antibody an attached to platelet surface via platelets FcGamma receptors, causes an increase in platelet clearance. |
|
|
Term
| Pathophysiology of Drug-induced thrombocytopenias |
|
Definition
| generalzied hemoatopoietic supression, decrease in platelet production, increased destruction of platlets with cirulating immunoglobulins |
|
|
Term
| Laboratory findings of Drug-induced thrombocytopenias |
|
Definition
| very low platelet count, bleeding, withdrawl of drug reduces symptoms |
|
|
Term
| Etiology of Megakaryocyte hypoplasia |
|
Definition
| failure of bone marrow to deliver adequate platelets to the peripheral blood |
|
|
Term
| Pathophysiology of Megakaryocyte hypoplasia |
|
Definition
| due to drug or radiation therapy for malignant disease (decreased megakaryocyte syndromes), or pancytopenia and bone marrow hypoplasia (aplastic anemia |
|
|
Term
| Laboratory findings of Megakaryocyte hypoplasia |
|
Definition
| decreased platelet count appears before hypoplasia of other cell lineages, last lineage to return to normal, normal MPV, increased PDW (variation in size), increased TPO = aplasic anemia |
|
|
Term
| Primary malinant thrombocytosis |
|
Definition
| issue with megakaryocyte proliferation and maturation which bypasses the normal regulatory mechanisms, seen in chronic myeloproliferatative disorders and myelodysplasia. |
|
|
Term
| Secondary reactive thrombocytosis |
|
Definition
| an increase in platelets due to another disease or condition |
|
|
Term
| Effect of aspirin on platelets |
|
Definition
| Aspirin impairs acetylation and irreversible inhibition of platelet COX-1 which effects the platelet for its lifetime. It acetylates COX-1 in endothelial cells which blocks synthesis of PGI2 which affects the ability of the platelets to aggregate. |
|
|
Term
| What is the duration of asprin effects on platelets |
|
Definition
| the platelets entire lifetime, 7-10 days |
|
|
Term
| Bernard Soulier Syndrome clinical features |
|
Definition
| bleeding symptoms in homozygotes |
|
|
Term
| Bernard Soulier cause of clinical features |
|
Definition
| cause of large platelets is unknown, quantitative decrease or abnormal function of the GPIb/IX complex from mutation in gene that codes for proteins in GP complexes, lack of functional GPIb/IX complex prevents interaction of the platelets with vWF and the subsequent platelet adhesion to collagen |
|
|
Term
| Bernard Soulier laboratory features |
|
Definition
| moderate to severe thrombocytopenia, large platelets with uneven distribution, prolonged BT, normal platelet aggregation with ADP, collagen and epinephrine, abnormal platelet aggregation with ristocetin and VWF |
|
|
Term
| Glanzmanns thrombasthenia clincial features |
|
Definition
| bleeding problems in homozygotes |
|
|
Term
| Glanzmanns thrombasthenia cause of clincal features |
|
Definition
| defective GPIIb/IIA complex, platelet aggregation does not occur because platelets lack the site for attachment of fibrinogen, adhesion and secretion are normal |
|
|
Term
| Glanzmanns thrombasthenia laboratory features |
|
Definition
| prolonged BT, abnormal platelet aggregation in response to ADP, collagen, thrombin, and epinephrine, normal aggregation in response to ristocetin and VWF |
|
|
Term
| Delta storage pool disease clinical features |
|
Definition
|
|
Term
| Delta storage pool disease cause of clinical features |
|
Definition
| platelet aggregation abnormalities are due to the lack of ADP release from the DG so that secondary aggregation does not occur with ADP or epinephrine |
|
|
Term
| Delta storage pool disease laboratory features |
|
Definition
| prolonged BT, second wave of aggregation with ADP and EPI but absent with collagen |
|
|
Term
| Alpha storage pool disease clinical features |
|
Definition
| gray platelets, bleeding diathesis |
|
|
Term
| Alpha storage pool disease cause of clinical features |
|
Definition
| defect in targeting endogenously synthesized proteins to the developing alpha granules |
|
|
Term
| Alpha storage pool disease laboratory features |
|
Definition
| mild thrombocytopenia with prolonged BT, platelet aggregation studies are normal (as opposed to delta storage disease) |
|
|
Term
| Thrombocytopenias due to increased destruction |
|
Definition
| immune destruction = ITP, NAIT, drug-induced thrombocytopenias (HIT and HAT), miscellaneous immunne thrombocytopenia, non-immune thrombocytopenia |
|
|
Term
| Thrombocytopenias due to decreased production |
|
Definition
| megakaryotcyte hypoplasia |
|
|
Term
|
Definition
| chronic myeloproliferative disorders and myelodysplasia |
|
|
Term
|
Definition
| reactive thrombocytosis in which the increase in platelets is caused by another disorder or condition |
|
|
Term
|
Definition
| spikes and the returns to normal, childbirth |
|
|
Term
|
Definition
| immune destruction by autoreactive antibodies |
|
|
Term
|
Definition
| autoreactive antibodies to GPIIb-IIIa, GPIb-IX-V, and GPIa-IIa, bind to platelets and cause a shortened life span |
|
|
Term
|
Definition
| increased reticulated platelets (can be decreased if autoantibodis impede megakaryocyte differentiaion and platelet release), TPO can be normal to slighty increased, platelet count less than 20x 10^9/L, increased lymphocytes or mild eosinophilia, marrow shows normal or increased megakaryocytes |
|
|
Term
|
Definition
| alloimmune thrombocytopenia, 1st pregnancy |
|
|
Term
|
Definition
| maternal antibodies produced agaisnt epitopes of paternal HPA-1a antigens on fetal platelets |
|
|
Term
|
Definition
|
|
Term
| Drug-induced thrombocytopenia Etiology |
|
Definition
| drugs, generalized hematopoietic supression, selective suppression of platelet production or increased platelet destruction via IgG coated platelets |
|
|
Term
| Drug-induced thrombocytopenia pathophysiology Hapten theory |
|
Definition
| penicillin binds to platelets causing drug-platelet antigen complex and the drug-dependenet antibody binds to complex. |
|
|
Term
| Drug-induced thrombocytopenia laboratory findings of HIT |
|
Definition
| increased platelet clearance |
|
|
Term
| Drug-induced thrombocytopenia pathophysiology innocent bystander mechanism-HIT |
|
Definition
| Heparin binds to plasma protein (PF4)and the antibody response binds to the heparin, the immune complex nonspecifically binds to circulating platelets via Fc portion of antibody which binds to IgG FcGammaIIa receptor |
|
|
Term
| Drug-induced thrombocytopenia pathophysiology Drug-dependent antibody against epitopes |
|
Definition
| epitopes created by assocition of quinidine with proteins on platelet surface, quinidine binds on platelet surface via GPIb/IX or GPIIb/IIIa and leads to production of neoepitpopes |
|
|
Term
|
Definition
| non-immune mediated mechanism |
|
|
Term
|
Definition
| heparin causes direct platelet activation which causes thrombocytopenia |
|
|
Term
| Miscellaneous Immune Thrombocytopenia Etiology |
|
Definition
| secondary to collagen dieases, autoimmune duseases, lymophoroliferative disorders, and infections (vaccinations) |
|
|
Term
| Miscellaneous Immune Thrombocytopenia Pathophysiology |
|
Definition
| cross reacting antibody causes thrombocytopenia |
|
|
Term
| Miscellaneous Immune Thrombocytopenia laboratory findings |
|
Definition
| platelet count not less than 50 x 10^9/L, resolves when infection is treated, reduced platelet count in fections, shortened platelet survvial, increased megakaryocytes in bone marrow and large platelets on peripheal blood smear |
|
|
Term
| Non-immune mechanisms of destruction etiology |
|
Definition
| DIC, TTP, HUS and artifical heart values |
|
|
Term
| Non-immune mechanisms of destruction pathophysiology |
|
Definition
| platelets are activated and consumes by aggregation within the circulation |
|
|
Term
| Non-immune mechanisms of destruction laboatory findings |
|
Definition
|
|
Term
| Non-immune mechanisms of descreased production etiology |
|
Definition
| megakaryocyte hypolasia in bone marrow, ineffective thrombopoiesis, and hereditary or aquired conditions |
|
|
Term
| Non-immune mechanisms of decreased production pathophysiology |
|
Definition
| failure of bone marrow to deliver adequate platelets to the peripheral blood |
|
|
Term
| Non-immune mechanisms of decreased production laboatory findings |
|
Definition
| bone marrow function is abnormal, decreased platelet count |
|
|
Term
| Primary Thrombocytosis etiology |
|
Definition
| Chronic myeloproliferative disorders and myelodysplasia |
|
|
Term
| Primary Thrombocytosis pathophysiology |
|
Definition
| megakaryocyte proliferation and maturation bypass normal regulatory mechanisms |
|
|
Term
| Primary Thrombocytosis laboratory findings |
|
Definition
| platelet counts more than 1000 x 10^9/L |
|
|
Term
| seondary Thrombocytosis etiology |
|
Definition
| acute hemorrhage, surgery, post splenectomy, recovery form thrombocytopenia, malignantcy, chronic inflammatory diseases, IDA, and hemolytic anemia |
|
|
Term
| seondary Thrombocytosis pathophysiology |
|
Definition
| increased platelets caused by another disease or condition |
|
|
Term
| secondary Thrombocytosis laboratory findings |
|
Definition
| less than 1000 x 10^9/L platelet count but higher than normal |
|
|
Term
|
Definition
| occurs in children, abrupt onset of bleeding, petechiae and superfical bleeding, infection common 1-3 weeks prior, no gender predilection, hemorrhagic bullar in mouth present in severe cases, duration in 2-6 weeks and sponteneous remissions occur in 93% of cases |
|
|
Term
| Acute ITP laboratory data |
|
Definition
| inital platelet count <20 x 10^9/L, eosinophilia and lymphocytosis are common |
|
|
Term
| Chronic ITP clinical data |
|
Definition
| occurs in adults, insidious onset of bleeding, petechiae and superfical bleeding, infection in unusual prior, gender predilection toward females (3:1), hemorrhagic bullar in mouth are usually absent, duration of mouths to years, and sponteneous remissions is rare, the course of the disease fluccuates |
|
|
Term
| Chronic ITP laboratory data |
|
Definition
| inital platelet count 30-80 x 10^9/L, eosinophilia and lymphocytosis are rare |
|
|
Term
| Pathophysiology of Thromocytopenia |
|
Definition
| could be due to increased destruction (immune mediated, drug mediated) or decreased production (acquired or inherited) |
|
|
Term
| Pathophysiology of thromocytosis |
|
Definition
| primary disease, secondary to another disease, or transient |
|
|
Term
| Bernard-Soulier Syndrome etiology |
|
Definition
| autosomal recessive trait, defect in platelet-vessel wall interactuon, disorder of adhesion |
|
|
Term
| Bernard-Soulier Syndrome pathophysiology |
|
Definition
| deficiency or defect in GP-Ib/IX/V |
|
|
Term
| Bernard-Soulier Syndrome clinical features |
|
Definition
| bleeding symptoms in homozygotes- pupura, epistaxis, gingival bleeding, menorrhaga without hemarthroses, deep visceral hematomas, can range from mild brusing to severe, recurrent mucocutaneous bleeding |
|
|
Term
| Bernard-Soulier Syndrome laboratory features |
|
Definition
| moderate to severe thrombocytopenia, large platelets with heterogenous size distribution on PBS, prolonged PT, absent platelet agglutination by ristocetin and vWF (not corrected by mixing studies), decreased GP-Ib/Ix/ and V by flow cytometrey |
|
|
Term
| Glantzmanns Thrombasthenia etiology |
|
Definition
| inherited qualitative platelet disorder in which there is defect in platelet-platelet interaction, autosomal recessive |
|
|
Term
| Glantzmanns Thrombasthenia pathophysiology |
|
Definition
| deficiency or defect in GPIIb/IIIa |
|
|
Term
| Glantzmanns Thrombasthenia clinical features |
|
Definition
| bleeding symptoms in homozygotes- purpura, epistaxis, gingival bleeding, mennorhagia, ranges from mild brusing to severe recurrent mucocutaneous bleeding beginnin at birth |
|
|
Term
| Glantzmanns Thrombasthenia labotaory features |
|
Definition
| normal platlet count and morphology, prolonged BT, absent platelet aggregationin response to ADP, collagen, thrombin and epinephrine, clot retraction, decreased GP-IIa/IIIa by flow cytometry, decreased platelet fibrinogen in alpha granules |
|
|
Term
| Delta storage pool disease etiology |
|
Definition
| inheretid qualitative platelet disorder in which there is defects of platelet secretion and signal transduction |
|
|
Term
| Delta storage pool disease pathophysiology |
|
Definition
| deficieny of platelet dense granules |
|
|
Term
| Delta storage pool disease clinical features |
|
Definition
| mild to moderate bleeding diathesis |
|
|
Term
| Delta storage pool disease laboratory features |
|
Definition
| prolonged BT, second wave of aggregation with ADP and EPI is absent and with collagen is decreased, ratio of ATP:ADP in increased |
|
|
Term
| Alpha storage pool disease etiology |
|
Definition
| inherited qualitative platlet defect, autosomal recessive |
|
|
Term
| Alpha storage pool disease pathophysiology |
|
Definition
| deficiencies in platelet alpha granules |
|
|
Term
| Alpha storage pool disease clinical features |
|
Definition
| lifelong bleeding diathesis |
|
|
Term
| Alpha storage pool disease laboratory features |
|
Definition
| gray platelets, mild thrombocytopenia with prolonged BT, platelet aggregation studies are normal |
|
|
Term
| defect in platlet agonist interaction etiology |
|
Definition
|
|
Term
| defect in platelet agonist interaction pathophysiology |
|
Definition
| single agonist in platelet aggregation assays, abnormality is usually at the level of the platelet surface receptor for a specific agonist |
|
|
Term
| defect in platelet agonist interaction clincal features |
|
Definition
|
|
Term
| defect in platelet agonist interaction laboratory features |
|
Definition
| normal platelet count, prlongs BT, normal platelet aggregation, abnormal second wave with ADP and collagen |
|
|
Term
| Biochemical mechanism for the effect of aspirin on platelet function |
|
Definition
| Aspirin impairs platelet aggregation by inhibition the acetylation of platelet cyclooxygenase. |
|
|
Term
| Recommended time frame for patients to refrain from taking aspirin before platelet function testing |
|
Definition
|
|
Term
| What platelet count indicates thrombocytopenia? |
|
Definition
|
|
Term
| What laboratory tests are most often ordered to screen for abnormalities of the hemostatic system? |
|
Definition
|
|
Term
| An average of 20 platelets pr field was counted on a blood smear from an EDTA specimen with a 1000x magnification. What is the platelet count estimate? |
|
Definition
|
|
Term
| What are purple lesions that are larger than 1 cm in diameter that are not raised called? |
|
Definition
|
|
Term
| In which hematologic disorder would you expect to observe a decreased platelet count? |
|
Definition
|
|
Term
| How long should a patient be off aspirin or aspirin-containing products before having platelet function testing? |
|
Definition
|
|
Term
| What can result in a falsely decreased platelet count on an automated hematology counter? |
|
Definition
|
|
Term
| what level of platelet count is associated with a risk of life-threatening bleed into the central nervous system? |
|
Definition
|
|
Term
|
Definition
| a platelet count above the reference range |
|
|
Term
| Platelet satillitism and platelet agglutination seen on a peripheral blood smear occur only |
|
Definition
| in blood collected in EDTA anticoagulant |
|
|
Term
| What disorder is probably indicated by a boy with petchiae on ankles, nosebleeds, recent infection? |
|
Definition
|
|
Term
| If a bone marrow examination had been performed on a child with suspected ITP, what morphology could it likley have shown? |
|
Definition
| normal to abnormal numbers of megakaryocytes |
|
|
Term
| What is the mechanism of platelet destruction in immuno thrombocytopenia |
|
Definition
| removal of antibody-coated platelets by splenic macrophages |
|
|
Term
| The small purple dots on a boys ankle are most probably? |
|
Definition
|
|
Term
| What is the boy suspected of ITP, prognosis? |
|
Definition
| complete spontaneous recovery within 6 months |
|
|
Term
| What is characteristic in a patient with bernard souliers? |
|
Definition
| abnormal platelet aggregation with ristocetin |
|
|
Term
| What is found in Glanzmanns Thrombasthenia |
|
Definition
| genetic abnormality of GP IIb/IIIa |
|
|
Term
| Hereditary telangiestasia is characterized by |
|
Definition
| skin lesions that are arterioles connected directly to venules |
|
|
Term
| Platelet aggregation studies were performed and showed a primary wave of aggregation with ADP the returned to the baseline with no secondary wave, What is consistent with these results? |
|
Definition
|
|
Term
| Reactve thrombocytosis is assciated with |
|
Definition
|
|
Term
| A patient who has small (less than 3 mm diameter) purple lesions on the extremities and a platelet count of 20 x 10^9/L probably has |
|
Definition
|
|
Term
| Which platelet count is consistent with thrombocytosis? |
|
Definition
|
|
Term
| A patient with a platelet count of 6 x 10^9/L might have which of the following symptoms? |
|
Definition
| petechiae, intracranial bleeding, and profuse bleeding from cuts in the skin |
|
|
Term
| Sites of bleeding in patients with thrombocytopenia are usually: |
|
Definition
| external skin and mucous membranes |
|
|
Term
| Chronic idiopathic thrombocytopenic purpura (ITP) is most common in |
|
Definition
| adult females between the ages of 20 and 40 |
|
|
Term
| A screening test for primary hemostasis is |
|
Definition
|
|
Term
| It is important to perform platelet counts on patients with thrombosis that are receiving heparin because |
|
Definition
| A significant number of patients will develop heparin-induced thrombocytopenia |
|
|
Term
| A patient with folic acid deficiency is likely to have |
|
Definition
|
|
Term
| In which condition is a patient most likely to have a platelet count of 1500 x 10^9/L ? |
|
Definition
| essential thrombocythemia |
|
|
Term
| A patient with a severe nosebleed was seen in the emergency room of your hospital. When performing the evaluation of the peripheral blood smear, you noticed that at least 75% of the platelets were large- or giant-size. The platelets had abnormal morphology and appeared to have a large complement of granules. What condition may this patient have? |
|
Definition
|
|
Term
| Acute ITP is usually seen in |
|
Definition
| children 2 to 6 years old |
|
|
Term
| In which condition would a patient demonstrate a decreased platelet count because of ineffective thrombopoiesis? |
|
Definition
|
|
Term
| Which of the following is a characteristic laboratory finding in patients with Bernard-Soulier syndrome? |
|
Definition
| abnormal platelet aggregation response to ristocetin |
|
|
Term
| A patient with Bernard-Soulier syndrome will most probably have a mutation in the gene for: |
|
Definition
|
|
Term
| A 25-year old female patient presented with a severe nosebleed and several spontaneous bruises but no other significant history. Laboratory tests showed a platelet count of 35 x 109/L. All other hematology parameters were within reference ranges. The most probable condition is: |
|
Definition
| chronic idiopathic thrombocytopenic purpura |
|
|
Term
| Which of the following is an acquired vascular disorder? |
|
Definition
| Henoch-Schoenlein purpura |
|
|
Term
| On questioning prior to drawing a blood sample for a platelet closure time and platelet aggregation studies, a patient told the clinical laboratory scientist that she had been taking three aspirin tablets a day for the past week for headaches. Which of the following is the correct action for the clinical laboratory scientist to take? |
|
Definition
| Inform the physician to request that the patient refrain from taking any more aspirin and return in 10 days for testing. |
|
|
Term
| Platelet adhesion is abnormal in patients with Bernard-Soulier syndrome because: |
|
Definition
| Glycoprotein Ib of the platelet membrane is defective. |
|
|
Term
| What is the mechanism of platelet destruction in patients with acute idiopathic thrombocytopenic purpura? |
|
Definition
| removal of antibody-coated platelets by splenic macrophages |
|
|
Term
| Daily platelet counts were performed on a patient who was started on heparin therapy. On the fifth day after therapy started, the platelet count suddenly dropped from the usual 300 x 109/L to 50 x 109/L. What is the most likely reason for the decrease in the platelet count? |
|
Definition
| heparin-induced thrombocytopenia |
|
|
Term
| Petechiae and several brusies on a patients arm causes which tests to be ordered? |
|
Definition
| platelet count, PT, and aPTT as screening tests. |
|
|
Term
| What results of these tests for a patient with petechiae and several brusies on arm would you expect (normal or abnormal) in this patient? |
|
Definition
| Petechiae indicated a platelet abnormality, the most common of which is thrombocytopenia. You would expect the platelet count to be decreased, the PT and aPTT would be normal in platelet abnormalities that are not complicated or accompanied by abnormalities of fibrin formation |
|
|
Term
| Patient has an average of 14 platelets per high power field on a peripheal blood smear prepared from a needle tip and your laboratory allowed correltation between the direct intrument count and the blood smear estimate of 20%, what range would you expect the instrument to be? |
|
Definition
| 14 x 15 x 10^9/L = 210 x 10^9/L |
|
|
Term
| Is a platelet count of an average of 14 platelets per high power field on a peripheal blood smear within an acceptable reference range? |
|
Definition
| An acceptable range of the instrument count would be 168-252 x 10^9/L, which is within acceptable reference range |
|
|
Term
| How many platelets per 1000 x field would you expect to observe on the peripheral blood smear of a patient with acute ITP? |
|
Definition
| You would expect to see an aveage of fewer than 6 platelets per field. It can be difficult to find platelets on the blood smear of patients with ITP |
|
|
Term
| a 6 year old boy comes into his doctor because his mother noticed small pink spots on his legs, several bruises on his arms and legs, platelet count was 20 x 10^9/L, PT and aPTT were within normal limits. The CBC was normal escept for the low platelets. No previous history of bleeding but he got the spots after the hepatitis vaccine. What is the most probable type of thrombocytopenia? Should other coagulation tests be performed at this time? |
|
Definition
| The most probable type of thrombocytopenia experienced by this patient is an immune type of increased destruction, which is reportedly associated with viral infections in some children. Other coagulation tests are not neccesary |
|
|
Term
| What is the pathophysiology of thrombocytopenia in megaloblastic anemia? |
|
Definition
| Thrombocytopenia occurs in megaloblastic anemia because of ineffective production of all myeloid cell lines in the bone marrow |
|
|
Term
| Why is primary thrombocytosis associated with abnormal platelet function while secondary thromcytosis is not? |
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Definition
| Primary thrombocytosis is associated with the myeloproliferative disorders, which are clonal disorders of the pluripotent stem cell. The abnormal clone grows autonomously and not in resposne to normal regualtory factors. It is likley that abnormalities in platelet function are aquired along with the ability to grow autonomously. In secondary thrombocytosis the platelets are increased because the normal regualtory routes in response to a need for more platelets |
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Term
| platelet aggregation studies in plateelet adhesion disorders |
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Definition
| Platelet adhesion to collagen requires that the vWF attached to platelet GPIb/IX receptros bridge the platelet to the collagen fiber. Aggregation studies are abnormal with ristocetin because it takes the place of collagen in the test. |
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Term
| Why are the bleeding time test and closure time abnormal for up to 7 days flollowing ingestion of aspirin? |
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Definition
| Aspirin inhibits the platelet enzyme cyclooxygenase, which is neccesary for production of thromboxane A2. TXA2 is necesary in the activated platelet for secretion of granule contents and therefore the function of the platelets is impaired. The defective platelets continue to circulate for their normal life spin (10 days), because they are ciculating the bone marrow is not overstimulated to produce new platelets to replace defective ones |
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Term
| platelet aggregation studies in aggregation disorders |
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Definition
| involved abnormalities in the GPIIb/IIIa receptor or in fibrinogen. Other routine agonists require GPIIb/IIIa receptor and fibrinogen as the bridge to attach one platelet to another platele. Platelet aggregation studies will be abnormal with all agonists except ristocetin |
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Term
| platelet aggregation studies in secretion disorders |
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Definition
| platelets are able to respond to agonists in the primary wave of aggregation but are unable to release their own ADP and manufacture their own Thromboxane A2, so that the secondary wave of aggregation seen with ADP and epinephrine and wave of aggregation with collagen are abnormal |
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