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Terms in this set (30)

A1: Reacts with two membrane integrins to induce full aggregation/secretion, monophasic secondary aggregation, secretes ATP
Reduced ATP= storage pool defect
A2: Induces aggregation via cyclooxygenase, biphasic
Suboptimum/Primary aggregation= platelet release disorders, not enough ADP, reaction dies
Excess- simultaneous shape change, secretion, aggregation= monophasic secondary
Decreased aggregation= storage pool defect, NSAIDS, cyclooxygenase pathway enzyme deficiency
A3: Induces aggregation via cyclooxygenase, biphasic
Decreased aggregation= storage pool defect, release defect, NSAIDS
A4: Intact membrane receptors/proteins, cyclooxygenase, Induces platelets to secrete ADP and form TXA2, lag time and only secondary (monophasic)
Decreased aggregation= storage pool defect, release defect, NSAIDS
A5: Part of cyclooxygenase pathway, no lag time, only secondary (monophasic)
Decreased aggregation= NSAIDs, sometimes storage pool defect
A6: Antibiotic produces thrombocytopenia, vWF must be present to aggregate, monophasic, induces aggregation/agglutination
Decreased aggregation= NSAIDS, vWD (except subtype IIb)- can be corrected w/ exogenous vWF, bernard soulier can not be corrected
Cofactor- platelet poor plasma agglutinates with risocetin, time= amount of vWF
B: PF3 is needed for conversion of prothrombin to thrombin and is released when platelets are activated by kaolin or cellite, causes decrease in clotting time
28-36 sec=normal like platelin, above 36=abnormal like platelet poor
C: Simulation of adhesion/aggregation from vascular injury
Membrane is coated with collagen (activation) and then either ADP or epinephrine (agonists for degranulation-aggregation)
Normal values EPI= 93-193 (low=intrinsic platelet defects- secretion/storage/aspirin), ADP= 71-118 (low=qualitative or vWF abnormality)