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58 Cards in this Set
- Front
- Back
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Name the anticoagulant drugs
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Heparin
Low Molecular Weight Heparins (Dalteparin sodium, Enoxaparin) Warfarin (Coumadin) |
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Name a procoagulant
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Desmopressin acetate
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Name the antiplatelet drugs
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Acetylsalicylic acid (Aspirin)
Clopidogrel bisulfate (Plavix) Abciximab (ReoPro) |
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Fibrinolytic drugs
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t-PA, Activase
Streptokinase |
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Arterial vs Venous thrombosis
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Arterial- medium vessels, atherosclerosis, platelet rich plaque
Venous- static blood, rich in fibrin |
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clot adhering to a vessel wall
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thrombus
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detached clot circulating in the vascular system
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embolus
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3 reasons for no coagulation normally
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dilution of factors
plasma inhibitors factors rapidly removed by liver |
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Major risks for thromboembolism
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abnormal blood flow- atrial fib
abnormal surfaces- heart valves abnormalities of clotting factors |
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Platelet aggregation and formation of a platelet plug
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wall injury exoses collagen
collagen binds GpIa vWF binds GpIa Platelets secrete ADP, TXA2 and serotonin Aggregation through GpIIb/IIIa Fibrinogen, fibrin monomers bind, fibrin mesh Activated platelets round up Coagulation Contraction of clot Leukocyte infiltration |
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These trigger poweful vasospasms and are released by platelets
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TXA2 and serotonin (5-HT)
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Coagulation occurs due to trauma originating from the extra-vascular space
(formation of a macromolecular complex involving Thromboplastin /Tissue Factor, and Factor VII) the most important in vivo |
Extrinsic
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Coagulation is triggered by trauma to the blood itself
(from large glycoprotein complexes released by platelets) |
Intrinsic
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XII to XIIa, XI to XIa, IX to IXa, X to Xa
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Intrinsic
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VII to VIIa, X to Xa
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Extrinsic
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counteracting system to limit coagulation
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fibrinolytic system
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fibrinolytic system
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Plasminogen to Plasmin which degrades Fibrinogen and Fibrin
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Direct acting anticoagulants
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Calcium chelators (Sodium citrate, EDTA)
Heparins |
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Indirect acting anticoagulants
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Warfarin (Coumadin)
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Heparin
active in vivo or in vitro? what kind of a molecule? how is it made? what does it do? |
both
mucopolysaccharide made from bovine lung and porcine intestinal mucosa Forms a complex with ATIII which binds clotting factors which causes them to be degraded |
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Accelerates the process of ATIII binding to clotting factors
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Heparin
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Binds and irreversibly inactivates thrombin and Xa
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Heparin/ATIII
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Immediate anticoagulation after administration
Acts on preformed blood components |
Heparin
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Blocks conversion of prothrombin to thrombin and thus inhibits synthesis of fibrin from fibrinogen
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Heparin
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At low doses, neutralizes Xa
At high doses, prevents thrombin induced activation of platelets, and activation of V and VIII |
Heparin
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Side effect of Heparin
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thrombocytopenia
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How is heparin administered?
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IV or subQ
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Does Heparin cross the placenta?
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No, can be used for pregnant women
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Heparin overdose
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withdrawl
Protamine sulfate- basic peptide that binds Heparin and neutralizes its effects |
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How is Heparin monitored?
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aPTT
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What is Heparin used for?
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DVT, PE, acute MI
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Binds ATIII
Doesn't inhibit thrombin, just Xa more specific inactivator |
LMW Heparins
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Advantages of LMWH over UFH?
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Equal efficacy
More predictable outcome Half life is twice Increased bioavailability Less frequent dosing Less frequent bleeding |
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How are LMWH monitored?
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not by aPTT
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specific thrombin inhibitors
bind to free and meshed thrombin |
Lepirudin (Refludan)
Bivalirudin (Angiomax) |
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the most common oral anticoagulant
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Warfarin (Coumadin)
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When is Warfarin (Coumadin) active?
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only in vivo after a latent period of 12 to 24 hours
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structural analogue of vitamin K
effects are like vit K depletion interfere with normal posttranslational modification of clotting factors in the liver- a vit K dependent process |
Warfarin (Coumadin)
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Down regulates protein C which causes procoagulant activity in early therapy
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Warfarin (Coumadin)
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vitamin K dependent factors
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VII, IX, X, prothrombin
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How do you measure Warfarin?
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PT
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largely bound to plasma albumin and metabolizes by liver cytochrome P450
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Warfarin (Coumadin)
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can warfarin pass the placenta?
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Yes
abortion and birth defects |
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Warfarin overdose?
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withdrawl
vitamin K supplementatin (24 hr delay) transfusion of whole blood or plasma |
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Drugs that diminish response to warfarin
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Inhibit drug absorption in gut
Induce hepatic microsomal enzymes Stimulate clotting factor synthesis |
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Drugs that increase the response to Warfarin
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Drugs that
Displace anticoag from plasma prots Inhibit hepatic microsomal enzymes Reduce vit K Inhibit synthesis of clotting factors Decrease platelet aggegation (Aspirin) |
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a synthetic analogue of ADH
stimulates VIII procoagulant |
Desmopressin Acetate
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For treatment of Hemophilia A with low VIII
VIII abs severe classic von Willebrands disease abnormal VIII |
Desmopressin Acetate
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Inhibits synthesis of TXA2 by blocking COX irreversibly
Inhibits release of ADP by platelets and their aggregation |
Aspirin
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antiplatelet drug
treatment of recurrent stroke Inhibits response of ADP on its platelet receptor and prevents aggregation by impairing GPIIb/IIIa |
Ticlopidine (Ticlid)
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antiplatelet drug
treatment of recurrent stroke Inhibits response of ADP on its platelet receptor and prevents aggregation by impairing GPIIb/IIIa LESS side effects |
Clopidogrel bisulfate (Plavix)
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a chimeric monoclonal ab inhibitor of platelet GPIIb/IIIa
prevents binding of fibrinogen and vWF prevents platelet aggregation |
Abciximab (ReoPro)
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When to use thrombolytic therapy?
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extensive PE
severe iliofemoral throbophlebitis acute coronary occlusion |
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released from endothelial cells in response to stasis produced by vascular occlusion
binds to fibrin and converts plasminogen to plasmin |
t-PA
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enzyme that converts plasminogen to plasmin
little activity unless bound to fibrin selective for plasminogen bound to fibrin |
t-PA
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protein produced by beta hemolytic bacteria
forms a complex with plasminogen produces a conformational change that causes it to be cleaved to pplasmin |
Streptokinase
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Contraindications to thrombolytic therapy
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surgery within last 10 days
GI bleed HTN active bleeding CVA or intracranial bleed |
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prevents binding of plasminogen and plasmin to fibrin
potent inhibitor for fibrinolysis and can reverse states that are associated with excess fibrinolysis |
Aminocaproic acid
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