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Lecture 23 - Coagulation: platelets, platelet disorders, & tests of platelet function
Terms in this set (20)
Identify the frequency of von Willebrand's disease, its pattern of inheritance and the type of bleeding that is observed in patients with von Willebrand's disease.
Frequency: Most prevalent bleeding disorder worldwide. Affects 1-3% of the world's population
Inheritance: Autosomal recessive
Bleeding: Mucosal membrane bleeding (nosebleed, bleeding from gums, bleeding after dental procedure, heavy menstrual bleeding) & rarely bleeding into joints
Identify the basic platelet defect that is observed in von Willebrand's disease
Deficiency/abnormality of vWf, essential protein for plt adhesion.
Plts look normal but unable to adhere collagen, affects plt adehesion
Identify laboratory test results that are abnormal in patients with von Willebrand's disease
Bleeding time test (or PFA-100 test)
Describe the procedure for performing the modified Ivy bleeding time test.
Blood pressure cuff placed on the arm and pressure inflated to 40mm Hg. Pressure maintained throughout procedure
Incision made on forearm using a spring-loaded device (Simplate or Surgicutt bleeding time device) and timer is started
After 30 seconds, the first drop of blood is wicked onto filter paper and repeated at 30 second intervals until bleeding stops. The bleeding time is reported in minutes, rounded to the nearest 1/2 minute.
Identify the reference range for the Ivy bleeding time test
Normal patients stop bleeding within 2-9 minutes
Describe ways aspirin affects platelet function
Impairs platelet aggregation by interfering with the synthesis of thromboxane A2 (TxA2), a potent platelet aggregator
Prolongs bleeding time
Describe the procedure for performing the platelet aggregation test and identify 4 agents used as agonists.
Involves platelet rich plasma (PRP) & platelet poor plasma (PPP) centrifuged in a special way.
Agonsists (aggregating agents) are added to the tubes of plasma to induce in vitro aggregation
Light transmittance is measured and plotted as a function of time. As aggregation increases, more light is transmitted through the solution. Patterns are generated that correspond with particular types of plt disorders
Platelet aggregation tes agonists
Using scanned images, identify platelet aggregation patterns observed in a) Bernard- Soulier disease b) von Willebrand's disease c) Glanzmann's thrombasthenia and d) storage pool disease
Identify the basic platelet defect that causes Bernard-Soulier disease.
Rare autosomal recessive disorder w/ abnormal plt adhesion
aka "giant platelet syndrome"
Missing Gplb and/or GpIX receptor precents the plt from binding with vWf
Describe platelet morphology as observed on a peripheral blood smear stained with Wright's stain in Bernard-Soulier.
Moderate to severe thrombocytopenia
↑giant platelets on smear 60-80%
Describe laboratory test results that are consistent with a diagnosis of Bernard-Soulier disease.
Prolonged Ivy bleeding time
Abnormal plt aggregation with ristocetin
Identify the basic platelet defect that causes Glanzmann's thrombasthenia.
Rare autosomal plt disorder w/ moderate bleeding
Deficiency of GpIIb/IIIa complex (site of fibrinogen attachment), results in no plt aggregation due to lack of binding site for fibrinogen
Describe platelet morphology as observed on a peripheral blood smear stained with Wright's stain in Glanzmann's thrombasthenia
Normal plt morphology
Identify platelet glycoproteins detected by flow cytometry that are found in patients with Glanzmann's thrombasthenia
Flow cytometry reveals the expression of CD41 (GpIIb) and CD61 (GpIIIa) surface an&gens.
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