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| smallest version of heparin that allows for antithrombin activity. Pentasachharide. MOA: allosteric binding exposing arginine of antithrombin, which is then attacked by activated protease (Xa). Irreversible indirect xa inhibitor (protamine sulfate wont work here). No need to be monitored. NO HIT occuring. Cleared exclusively by kidneys s o dont give to patients with elevated creatinine. |
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| Direct thrombin inhibitor. Monitored via PTT. Can be used for treatment of HIT , excreted exlucivey by urine. Ab may bind to it, and this complex cant be removedd by kidney so increased halflife and effective dose. |
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| Direct thrombin inhibitor, mostly metabolic clearance. |
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| Direct thrombin inhibitor. Sythetic deriative of argaine. Monitored by aPTT . Cleared mostly by liver. |
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| inhibito of vitamin K epoxide reductase., blocks carboxylation of 2,7,9,10 factors. Orally bioavailable. Highly boudnt o plasmaproteins so any change in binding causes effective dose to o way up. .Prolongs PT (EX PresidenT went to WAR). DONT GIVE ALONEFOR FIRST FEW Days- factor VII will deplete fast (short halflife) giving illusion of logner bleeding time, protein C goes down fast too- skin necrosis- worst with patietns with underlying Protein C defieincy. toxicity: teratogenic. In case of overdose: stop warfarin, if minor bleeding: low dose Vit K. If majro bleeding, throw in clotting factors concentrates. conditiosn that alter warfarin response: affecting metabolism , palsma protein binding, so anythign that also decreases plasma portein levels, Depletion of bacteria, ghigh vit k diet. Very low therapuetic index of warfarin (2x) . |
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| oral DTI, demonsrated as effective sa warffarin |
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| low level- inhibits platelet Cox-1 , wihc lowers thormboxane A2 production. High levels will lower cox-1 endothelium which is needed for prostacylin which is a plattelet inhibitor (so high levels may increase coag). |
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| adp receptor antagonist on platelets- pltelts can activate. And aggregate, irreversible |
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| irreverisble inhibotrs of ADP receptors. |
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| monoclonal antibody against GpIIb/IIIa receptor. |
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| analog which competitively inhibits GPIIb/IIIA receptor |
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| analog which competitively inhibits GPIIb/IIIA receptor |
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| inhibits binding of plasminogen bjidnign to fibrin. . Can be used in hemophelissa, or as antidote to tpA. |
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| stored in mast cells. bad bioavailbility- continous IV administratio with constant . monitoring via PTT. Enchancing activity ofAT III , immediate onset. Not consumed, ocne it activates ATIII it is free to go to other molecules. . Also binds thrombin . May also displace TFPI from endothelium, furtheri nhibiting clot formation.. Complications: bleeding (reversible via Protamine Sulfate ). Mild platelet dysfunction, ostoeperosis is a commonn problem, heparin resistance . HIT0 Heparan induced Thrombocytopenia. Binding with pf4 receptor on Platelets, this complex is recognziedb y antibodies, which causes both platelet destruction adn activation. |
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| More anti-Xa activity than thrombin activity. More predictable response so don’t have to monitor except in pregnancy renal inssufeicney and pediatric population, more bioavailability . Monitoring method:b anti-XA. SubQ aministration. Less HIT occuring (still contraindicated in patients with HIT), and longer halflife than HMW. Also doe not snospecifically bind to plasma proteins like Heparin does.. Complications: Lessbleeding, less thrombocytopenia, however only partially reversible with protamine sulfate. |
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| arterial thrombotic disorder s tratment |
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| antiplatelete aents as opposedt o anticoagulants. |
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| adminsitered as bolus. Fibrinolysis by activating conversion from plasminogen to plasmin. |
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