Archive for the 'Thrombolytic Therapy' Category

12 Nov

Anticoagulation and Thrombolytic Therapy: Warfarin sodium

Warfarin sodium is rapidly and almost completely absorbed from the alimentary tract and is almost entirely bound to albumin in plasma (~99%). Because the unbound drug is pharmacologically active, interactions with simultaneously administered medications which displace albumin-bound warfarin, ie, phenylbutazone, will potentiate the anticoagulant effect, prolong the PT, and increase the risk of hemorrhage. Potentiation […]

11 Nov

Anticoagulation and Thrombolytic Therapy: Oral Anticoagulation

Osteoporosis and hypoaldosteronism are additional toxic effects of heparin administration but are rarely observed. Heparin is also associated with an increased incidence of fetal demise (20%) and prematurity (~14%) when used during pregnancy; however, in contrast to warfarin sodium (Coumadin), no teratogenicity or transplacental transport has been observed and heparin remains the anticoagulant of choice […]

10 Nov

Anticoagulation and Thrombolytic Therapy: Diagnosis of HAT

The diagnosis of HAT is confirmed by in vitro platelet aggregation studies, in which spontaneous platelet aggregation occurs in patient platelet-rich plasma (PRP) following the addition of heparin alone or in normal PRP to which patient platelet-poor plasma or heat-treated serum is added with exogenous heparin. Treatment consists of discontinuing the unfractionated heparin and substituting […]

09 Nov

Anticoagulation and Thrombolytic Therapy: HAT

In vivo investigations indicate that thrombotic events are propagated by continuous incorporation of new fibrin, even during physiologic or pharmacologic fibrinolysis. Heparin impedes the formation and deposition of new fibrin, and therefore, pretreatment or simultaneous administration of heparin with thrombolytic agents may greatly enhance therapeutic efficacy by preventing thrombus extension or reocclusion. In addition, heparin […]

08 Nov

Anticoagulation and Thrombolytic Therapy: Heparin

Coagulation activity is modulated most effectively by naturally circulating inhibitors of serine proteases (antithrombin III) and inhibitors of factors V and VIII (protein C and its cofactor protein S). The congenital or acquired deficiency of antithrombin III, protein C, or protein S is associated with a predisposition to recurrent venous thrombosis and, rarely, to arterial […]

07 Nov

Anticoagulation and Thrombolytic Therapy: Thrombin generation

The intrinsic and extrinsic pathways merge at the point of factor Xa activation, which can be achieved either by the proteolytic effects of a factor IX, factor VIII, Ca+2, and phospholipid complex, or by the action of a multimolecular complex of factor VII, Ca+2, and tissue thromboplastin derived from damaged extravascular (“extrinsic”) cells. Thrombin, a […]

06 Nov

Anticoagulation and Thrombolytic Therapy: The Intrinsic and Extrinsic Pathways

In vivo testing of platelet function is accomplished with the template bleeding time, a standardized procedure that depends on platelet number, aggregation function, platelet interaction with subendothelial components (adhesion), and the presence of normal subendothelial matrix collagen. Prolonged bleeding times are usually observed following the use of aspirin, NSAIDs (except sulfinpyrozone), and prostacyclin, but not […]

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