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Thrombosis treatment

Groce, J.B., III. Patient outcomes and cost analysis associated with an outpatient deep venous thrombosis treatment program. Pharmacotherapy 1998, 18 (6 Pt. 3), 175S-180S. [Pg.69]

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. [Pg.309]

Platelets play a central role in primary hemostasis. They are also important in pathological processes leading to thrombosis. Antiplatelet drugs are primarily directed against platelets and inhibit platelet activation by a number of different mechanisms. They are used for the prevention and treatment of thrombotic processes, especially in the arterial vascular system. [Pg.167]

Aspirin has been remarkably successful in the treatment of the pain and swelling of inflammatory disease and in fact, an estimated 45,000 tons of aspirin are still consumed each year. This success resulted in the syntheses of many other aspirin-like drugs , now referred to as NSAIDs. Aspirin, however, continues to have a unique use in the prevention of thrombosis. Since it produces irreversible inhibition of COX-1 by acetylation of serine at position 530 in the active site, a daily low dose of aspirin will cause a cumulative inhibition of COX-1 in platelets, in the portal circulation. A gradual inhibition of platelet aggregation occurs, reducing the possibility of occlusion of coronary or cerebral vessels by platelet thrombi. However, there are no systemic... [Pg.404]

Erythropoietin (Eprex ) is physiologically produced in the kidney and regulates proliferation of committed progenitors of red blood cells. It is used to substitute erythropoietin in severe anemias due to end stage renal disease or treatment of cancer with cytostatic agents. Side effects include hypertension and increased risk of thrombosis. [Pg.411]

Since plasmin in free form (not bound to fibrin) is extremely and rapidly inactivated by the inhibitor system (Fig. 4), plasminogen activators are used for treatment of thrombosis. Under such a condition, if plasmin is formed by the activators (especially by tPA) at the site of fibrin, the bound form can degrade fibrin because it is protected against the inhibitor system. In the medical practice, mainly two endogenous plasminogen activators, tPA and uPA, and one exogenous, the streptokinase (SK) are used [1,4]. [Pg.505]

Prevention and treatment of venous thrombosis, PE, peripheral arterial embolism ... [Pg.424]

The IV solutions of plasma expanders include hetastarch (Hespan), low-molecular-weight dextran (Dextran 40), and high-molecular-weight dextran (Dextran 70, Dextran 75). Plasma expanders are used to expand plasma volume when shock is caused by bums, hemorrhage surgery, and otiier trauma and for prophylaxis of venous thrombosis and diromboembolism. When used in die treatment of shock, plasma expanders are not a substitute for whole blood or plasma, but tiiey are of value as emergency measures until die latter substances can be used. [Pg.635]

Figure 24.4 The decision-analytic model shows the three strategies that were examined by Arnold and researchers [22] to evaluate the financial implications of the direct thrombin inhibitor argatroban for early treatment (<48 hours after thrombocytopenia onset), compared with delayed treatment, of heparin-induced thrombocytopenia (HIT) with or without thrombosis. Figure 24.4 The decision-analytic model shows the three strategies that were examined by Arnold and researchers [22] to evaluate the financial implications of the direct thrombin inhibitor argatroban for early treatment (<48 hours after thrombocytopenia onset), compared with delayed treatment, of heparin-induced thrombocytopenia (HIT) with or without thrombosis.
Arnold R, Kim R, Zhou Y, Tang B. Budgetary impact of heparin-induced thrombocytopenia with thrombosis and treatment with the direct thrombin inhibitor Argatroban (P401E). ASHP 39th Midyear Clinical Meeting. Orlando, FL, 2004. [Pg.588]

Heparin and warfarin are widely used in the treatment of thrombotic and thromboembolic conditions, such as deep vein thrombosis and pulmonary embolus. Heparin is administered first, because of its prompt onset of action, whereas warfarin takes several days to reach full effect. Their effects are closely monitored by use of appropriate tests of coagulation (see below) because of the risk of producing hemorrhage. [Pg.604]

Fibrinolysins are produced by both staphylococci (staphylokinase) and streptococci (streptokinase). These toxins dissolve fibrin clots, formed by the host around wounds and lesions to seal them, by indirect activation of plasminogen, thereby increasing the likelihood of organism spread. Streptokinase m be employed elinieally in conjunction with streptodomase (Chapter 25) in the treatment of thrombosis. [Pg.83]

Streptokinase is administered by intravenous or intra-arterial infusion in the treatment of thrombo-embolic disorders, e g. pulmonary embolism, deep-vein thrombosis and arterial occlusiorrs. It is also used in acute myocardial irtfarclioa... [Pg.475]

Junghans U, Seitz RJ, Wittsack HJ, Aulich A, Siebler M. Treatment of acute basilar artery thrombosis with a combination of systemic alteplase and tirofiban, a nonpeptide platelet glycoprotein Ilb/HIa inhibitor report of four cases. Radiology 2001 221 795-801. [Pg.116]

Einhaupl KM, Villringer A, Meister W, Mehraein S, Garner C, PeUkofer M, Haberl RL, Pfister HW, Schiedek P. Heparin treatment in sinus venous thrombosis. Lancet 1991 338 597-600. [Pg.161]

Tsai FY, Wang AM, Matovich VB, Lavin M, Berberian B, Simonson TM, Yuh W. MR staging of acute dural sinus thrombosis correlation with venous pressure measurements and implications for treatment and prognosis. Am J Neuroradiol 1995 16 1021-1029. [Pg.161]

Horowitz M, Purdy P, Unwin H, Carstens G, Greenlee R, Hise J, Kopitnik T, Batjer H, Rollins N, Samson D. Treatment of dural sinus thrombosis using selective catheterization and urokinase. Ann Neurol 1995 38 58-67. [Pg.161]

Di Rocco C, lannelli A, Leone G, Moschini M, Valori VM. Heparin-urokinase treatment in aseptic dural sinus thrombosis. Arch Neurol 1981 38 431 35. [Pg.161]

Holder CA, Bell DA, Lundell AL, Ulmer JL, Glazier SS. Isolated straight sinus and deep cerebral venous thrombosis successful treatment with local infusion of urokinase. J Neurosurgery 1997 86 704-707. [Pg.161]


See other pages where Thrombosis treatment is mentioned: [Pg.297]    [Pg.410]    [Pg.131]    [Pg.297]    [Pg.410]    [Pg.131]    [Pg.536]    [Pg.177]    [Pg.310]    [Pg.313]    [Pg.330]    [Pg.112]    [Pg.145]    [Pg.170]    [Pg.1022]    [Pg.419]    [Pg.297]    [Pg.576]    [Pg.578]    [Pg.578]    [Pg.104]    [Pg.153]    [Pg.161]   
See also in sourсe #XX -- [ Pg.115 ]

See also in sourсe #XX -- [ Pg.30 , Pg.839 , Pg.840 ]

See also in sourсe #XX -- [ Pg.839 , Pg.840 ]




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Arterial thrombosis, treatment

Cerebral venous thrombosis treatment

Coronary artery thrombosis, treatment

Coronary thrombosis treatment

Deep vein thrombosis treatment

Fibrinolytic enzyme in thrombosis treatment

Peripheral arterial thrombosis, treatment

Pulmonary thrombosis treatment

Thrombosis

Thrombosis treatment abciximab

Venous thrombosis, treatment

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