Term
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Definition
| anti plateletirreversibly inhibits platelet release action and cyclooxygenase which eventually creates TXA2 (increases platelet activation and aggregation (promotes GPIIb/IIIa) |
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Term
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Definition
| on platelets binds fibrinogen |
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Term
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Definition
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Term
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Definition
| VIIa + tissue factor (Ca); or VIIIa, IXa, lipid and Ca |
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Term
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Definition
| Xa +Va (Ca and phospholipid) |
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Term
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Definition
| Activates V, VIII, XIII and of course fibrin (I); when activates by thrombomodulin it can activate protein C, also directly activates platelets |
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Term
| Dipyradamole (w/ aspirin for? w/ warfarin for?) |
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Definition
| antiplatelet0 coronary vasodilary, interferes w/ platelet function by increasing cAMP --> inhibiting cyclic nucleotide phosphodiesterase and or blocks adenosine uptake (both increase cAMP), most effective w/ warfarin for postoperative primary prophylaxis in patients w/ prosthetic heart valves, or in combo w/ aspirin as secondary prophylaxis in patients w/ prior strokes |
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Term
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Definition
| antiplatelet- increased cAMP by inhibiting ADP binding to it's receptor (P2Y12)- prolongs bleeding time, used for prevention of thrombosis in cerebrovascular and coronary artery disease, indicates for patients that do not do well w/ aspirin; combo w/ aspirin good b/c work separately good combo for patient undergoing angioplasty- Only approved use is to reduce risk of thrombotic stroke in patients who have experienced stroke precursors-oral |
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Term
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Definition
| anti platelet- Like ticlopidine (inhibit ADP binding it's receptor, raises cAMP) w/ a better toxicity profile (less thrombocytopenia, leukopenia), has replaced ticlopidine-oral |
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Term
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Definition
| humanized monocolonal antibody against gpIIb/IIa receptor (fibrinogen binder) and also vitronectin; parenteral; for use w/ coronary angioplasty to prevent coronary thromboses, works 18-24 hours-Parenteral |
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Term
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Definition
| Cyclic peptide inhibit of fibrinogen binding site on IIb/IIIa (looks like fibrin/binds receptors and blocks)- works for 6-12 hours, used for unstable angina and angioplastic ronary interventions-PARENTERAL |
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Term
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Definition
| nonpeptide inhibitor that owkrs like eptifibatide (nhibit of fibrinogen binding site on IIb/IIIa)-PARENTERAL |
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Term
| What is contact activation |
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Definition
| When prekallikrein, HMWKinogen and XII bind collagen and activate each other, synonym for instrinsic pathway |
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Term
| Vitamin K dependent molecules, what does K do? |
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Definition
| K puts 10-13 gamma carboxyglutamic residues on proteases - II, VII, IX, X, protein C and protein S and protein Z (probably breaks down X) |
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Term
Warfarin
1. absorption- good/bad?
2. 1/2 life long short? most effective?
-can cross placenta |
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Definition
1. good, way better than dicumarol
2. long-36 hours, plasma protein bound, peak effect at 36-72 hours |
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Term
1. warfarin - how metabolized?
2. side effects |
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Definition
1. microsomal enzymes in liver --> bile
2. bleeding, dermatitis, skin necrosis, small intestine necrosis |
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Term
| Phenprocumon, indandione derivates |
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Definition
| long 1/2 life warfarin like, not used in US |
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Term
warfarin mechanism
random: early can increase clotting because inhibits protein C and S; also takes a while to start working (must wait for old preformed Vit K dependent cofactors to degrade) so usually heparin first (w/ warfarin to prevent pro-coagulant features) and then switch over |
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Definition
| blocks vitamin K epoxide reductase |
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Term
1. heparin produced by
2. heparan sulfate?
-very very negative mucopolysaccharide |
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Definition
1.mast cells
2. endothelial cells, naturally preventing coagulation |
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Term
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Definition
1. binds to antithrombin II and makes more active -antithrombin cleaves IXa, Xa and thrombin - antithrombin II binds and blocks them and then when complexed w/ thrombin it cleaves-notes say that it irreversibly inhibits
2. activates loportein lipase from endothelial cells and may also decrease platelet adhesiveness to endothelial cells |
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Term
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Definition
| I is when thrombin is absorbed onto fibrinogen after cleaving, II is the one that works w/ heparin, III is heparin independent |
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Term
1. heparin activity monitred by?
-takes 1-2 hours subcu to take effect, IV immediately |
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Definition
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Term
| 1. how is LMW heparin different |
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Definition
1. acts primarily on factor Xa,
2. more predictable pharmaokinetic profile
3. no routine requirement for lab monitoring
4. lower incidence of thrombocytopenia |
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Term
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Definition
| 1.mainly hemorrhage, thrombocytopenia, fever, osteoporosis, HSN rxn, antibody binding to complex of heparin and platelet factor 4 leading to platelet activation and aggregation --> clots |
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Term
| 1. tx w/ serious heparin induced hemorrhage |
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Definition
| 1. protamine sulfate, low MW positively harged protein binds and forms inert complex |
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Term
1. heparin breakdown
heparin preferred for pregnancy (stays in intravascular compartment, doesn't cross placenta) |
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Definition
| liver metabolism and renal excretion (of heparin and it's metabolite), ie problems if renal failure |
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Term
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Definition
| structure of antitorhombin binding region of heparin, inhibits factor Xa but no effect on thrombin; no need for coag monitoring, less likely side effets, give prophylactically hip/knee surgery-parenteral |
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Term
| hirudin- action, monitor how? |
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Definition
thrombin inhibitor (binds binding site), v. potent, monitor by aPTT
Parenteral |
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Term
| lepirudin - action/how excreted |
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Definition
recombinant derivative of hirudin, for use w/ heparin induced thrombocytopenia, excreted by kidney AKA look out renal failure- DAILY monitoring recommended
parenteral! |
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Term
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Definition
| like lepirudin and hirudin |
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Term
| argatroban - what is, how different then other like it |
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Definition
| thrombin inhibitor, looks like arginine, binds catalytic site of thrombin (others bind catalytic and substrate recongition site) parenteral |
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Term
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Definition
| recombinant for of activated protein C, used for patients at risk of death from severe sepsis |
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Term
| fibrinolysis mediated by? how activated? |
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Definition
1. plasmin degrades fibrin (plasminogen binds plasminogen activator-fibrin complex)
2. tPA, urokinase type PA |
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Term
1. what happens to free plasmin
2. why is does plasmin only act where activated |
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Definition
1. rapidly inactivated by a2 antiplasmin
2. b/c it is absored and restricted to use btw fibrin strands |
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Term
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Definition
| fibrin, factor I, V and VII and it can activate itself! |
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Term
| excess circulating plasmin produces? |
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Definition
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Term
| 1. explain first and 2nd gen thrombolytics |
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Definition
| both are plasminogen activators - first gen not clot selective and syttem fibrinogenolysis occurs, 2nd gen bind selctively to fibrin and cause clot slective fibrionlysis |
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Term
| 1. most important agent in therapy of MI? |
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Definition
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Term
| serious cases of bleeding from thrombolytic agents stopped how? mechanism? |
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Definition
| aminocaproic acid or tranexamic acid, bind plasmin at binding site for fibrin and stop interaction |
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Term
1. what does streptokinase have to do with this?
causes hemorrhage, pyrexia and allergic-anaphylic |
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Definition
| 1. non enzymatic protein that forms 1:1 complex w/ plasminogen causes fonromational changes to it and exposes active site (plasmin cleaves plasminogen --> increase) |
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Term
| alteplase, reteplase, tenecteplase - what are, how different |
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Definition
| alteplase is recombinant t-pa (2nd gen thrombolytic), reteplase and tenecteplase are also but slightly different w/ increased 1/2 life b/c increased resistant to inhibition by PAI-I |
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