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Platelet aggregation tests are carried out in specialized hematology laboratories if platelet dysfunction is suspected. These tests are usually indicated in patients presenting with mucocutaneous type of bleeding and in whom screening tests reveal normal platelet count, prolonged bleeding time, normal prothrombin time, and normal activated partial thromboplastin time. Platelet aggregation studies are carried out on platelet-rich plasma using aggregometer. When a platelet aggregating agent is added to platelet-rich plasma, platelets form aggregates and optical density falls (or light transmission increases); this is recorded by a chart recorder on a strip chart. Commonly used platelet aggregating agents are ADP (adenosine 5-diphosphate), epinephrine (adrenaline), collagen, arachidonic acid, and ristocetin. ADP (low dose) and epinephrine induce primary and secondary waves of aggregation (biphasic curve). Primary wave is due to the direct action of aggregating agent on platelets. Secondary wave is due to thromboxane A2 synthesis and secretion from platelets. Collagen, arachidonic acid and ristocetin induce a single wave of aggregation (monophasic curve) Normal aggregation curve is shown in Figure 804.1. Aggregation patterns in various platelet function defects are shown in Figures 804.2 to 804.4, and in Table 804.1.
 
Figure 804.1 Normal platelet aggregation curves
Figure 804.1 Normal platelet aggregation curves
 
Figure 804.2 Platelet aggregation curves in von Willebrand disease and Bernard Soulier syndrome absent aggregation with ristocetin normal aggregation with ADP epinephrine and arachidonic acid
Figure 804.2 Platelet aggregation curves in von Willebrand disease and Bernard-Soulier syndrome (absent aggregation with ristocetin, normal aggregation with ADP, epinephrine, and arachidonic acid)
 
Figure 804.3 Platelet aggregation curves in storage pool defect absent second wave of aggregation with ADP and epinephrine absent or greatly diminished aggregation with collagen and normal ristocetin aggregation
Figure 804.3 Platelet aggregation curves in storage pool defect (absent second wave of aggregation with ADP and epinephrine, absent or greatly diminished aggregation with collagen, and normal ristocetin aggregation)
 
Figure 804.4 Platelet aggregation curves in Glanzmanns thrombasthenia absent aggregation with all agonists except ristocetin
Figure 804.4 Platelet aggregation curves in Glanzmann’s thrombasthenia (absent aggregation with all agonists except ristocetin)
Box 802.1 Role of blood smear in thrombocytopeniaPlatelets are small, 1-3 μm in diameter, purple structures with tiny irregular projections on surface. In blood films prepared from non-anticoagulated blood (i.e. direct fingerstick), they occur in clumps. If platelet count is done on automated blood cell counters using EDTA-anticoagulated blood sample, about 1% of persons show falsely low count due to the presence in them of EDTA dependent antiplatelet antibody. Examination of a parallel blood film is useful in avoiding the false diagnosis of thrombocytopenia in such cases. Occasionally, platelets show rosetting around neutrophils (platelet satellitism) (see Figure 802.1). This is seen in patients with platelet antibodies and in apparently normal persons. Blood smear examination can be helpful in determining underlying cause of thrombocytopenia such as leukemia, lymphoma, or microangiopathic hemolytic anemia (Box 802.1).
 
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Platelets

  • 26 May 2017

Description: PLATELETS is the definitive current source of state-of-the-art knowledge about platelets and covers the entire field of platelet biology, pathophysiology, and clinical medicine. Recently there has been a rapid expansion of knowledge in both basic biology and the clinical approach to platelet-related diseases including thrombosis and hemorrhage. Novel platelet function tests, drugs, blood bank storage methods, and gene therapies have been incorporated into patient care or are in development. This book draws all this information into a single, comprehensive and authoritative resource. Comprehensive and definitive source of knowledge about platelets for clinicians, pathologists and scientists Integrates the entire field of platelet biology, pathophysiology, and clinical medicine Full color reference comprising 64 chapters, 1400 pages, and 16,000 references Contributions from 126 world leaders in their fields New chapters on topics such as the regulation of platelet life span, platelet microRNAs, GPVI and CLEC-2, monitoring of antiplatelet therapy, novel antiplatelet therapy, and making platelets ex vivo

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