Which of the following is NOT one of the four major physiologic events of hemostasis?
Hemostasis is a complex process and its function is to limit blood loss from an injured vessel. Four major physiologic events participate in the hemostatic process: vascular constriction, platelet plug formation, fibrin formation, and fibrinolysis. Though each tend to be activated in order, the four processes are interrelated so that there is a continuum and multiple reinforcements.
Which is required for platelet adherence to injured endothelium?
Platelets do not normally adhere to each other or to the vessel wall but can form a plug that aids in cessation of bleeding when vascular disruption occurs. Injury to the intimal layer in the vascular wall exposes subendothelial collagen to which platelets adhere. This process requires von Willebrand factor (vWF), a protein in the subendothelium that is lacking in patients with von Wille brand disease. vWF binds to glycoprotein (GP) I/IX/V on the platelet membrane. Following adhesion, platelets initiate a release reaction that recruits other platelets from the circulating blood to seal the disrupted vessel. Up to this point, this process is known as primary hemostasis. Platelet aggregation is reversible and is not associated with secretion. Additionally, heparin does not interfere with this reaction and thus hemostasis can occur in the heparinized patient. Adenosine diphosphate (ADP) and serotonin are the principal mediators in platelet aggregation.
Which of the following clotting factors is the first factor common to both intrinsic and extrinsic pathways?
The intrinsic pathway begins with the activation of factor XII that subsequently activates factors XI, IX, and VII. In this pathway, each of the primary factors is "intrinsic" to the circulating plasma, whereby no surface is required to initiate the process. In the extrinsic pathway, tissue factor (TF) is released or exposed on the surface of the endothelium, binding to circulating factor VII, facilitating its activation to VIla. Each of these pathways continues on to a common sequence that begins with the activation of factor X to Xa (in the presence of VIlla). Subsequently, Xa (with the help of factor Va) converts factor II (prothrombin) to thrombin and then factor I (fibrinogen) to fibrin. Clot formation occurs after fibrin monomers are cross-linked to polymers with the assistance of factor XIII.
Which congenital factor deficiency is associated with delayed bleeding after initial hemostasis?
Congenital factor XIII (FXIII) deficiency, originally recognized by Duckert in 1960, is a rare autosomal recessive disease usually associated with a severe bleeding diathesis. The male-to-female ratio is 1:1. Although acquired F XIII deficiency has been described in association with hepatic failure, inflammatory bowel disease, and myeloid leukemia, the only significant association with bleeding in children is the inherited deficiency. Bleeding is typically delayed because clots form normally but are susceptible to fibrinolysis. Umbilical stump bleeding is characteristic, and there is a high risk of intracranial bleeding. Spontaneous abortion is usual in women with F XIII deficiency unless they receive replacement therapy. Replacement can be accomplished with fresh frozen plasma(FFP), cryoprecipitate, or a F XIII concentrate. Levels of 1 to 2% are usually adequate for hemostasis.
In a previously unexposed patient, when does the platelet count fall in heparin-induced thrombocytopenia (HIT)?
Heparin-induced thrombocytopenia (HIT) is a form of drug-induced immune thrombocytopenia (ITP). It is an immunological event in which antibodies against platelet factor-4 (PF4) formed during exposure to heparin, affecting platelet activation and endothelial function with resultant thrombocytopenia and intravascular thrombosis. The platelet count typically begins to fall 5 to 7 days after heparin has been started, but if it is a re-exposure, the decrease in count may occur within 1 to 2 days.
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