Anticoagulants Test Questions – Flashcards
Unlock all answers in this set
Unlock answersquestion
| what are the 3 main abnormal blood coagulation conditions? |
answer
| too little or too much coagulation, and presence of clots |
question
| what are some causes of coagulation deficiencies? |
answer
| genetic disorders (hemophila), aquired disorders (decubitus ulcers - bed sores), and tramua/sx |
question
| what are some specific coaguating agents? |
answer
| fresh blood, plasma, factor XIII, factor IX, vit K, thrombin, absorbable gelatin (gelfoam) |
question
| what is are fresh blood and plasma used for? |
answer
| replacement or supplement to lost blood -> can help supply missing clotting factors to pt |
question
| what is factor VIII used in? |
answer
| this is administered as plasma precipitate (fresh/frozen), can be produced from recombinant DNA and has a 8-12 hr half life. it is used in hemophila A |
question
| what is factor IX used in? |
answer
| this is used in hemophila B, and is derived from purified human factor (from plasma), it can be heat treated to reduce risk of disease transmission or produced from recombinant DNA |
question
| what are the vitamin K dependent factors? |
answer
| II, VII, IX, X |
question
| what is thrombin used for? how is it administered? |
answer
| thrombin is only used to arrest minor bleeding/oozing and can be in the form of bovine plasma, topical, or a powder. it activates platelets and converts V & VII to their active forms |
question
| what is absorbable gelatin (gelfoam) used for? how is it administered? |
answer
| this can be used for sx and trauma and is denatured collagen, available as sponge or powder, and is non antigenic. it doesn't have to be removed (will be broken down and absorbed - no wound-disturbing removal) |
question
| what is the risk of coagulating agents: blood, plasma, and factors VIII/IX? |
answer
| they could be carrying viral infections (hepatitis, AIDs, etc) |
question
| what are some reasons for using drugs that prevent coagulation? |
answer
| thrombo-emobolic diseases, extracorporeal devices (renal dialysis), and prophylatic tx |
question
| what are the injectable anti-coagulative agents? |
answer
| heparin, lepirudin, bivaliruden, and argatroban |
question
| how is heparin administered? what does it do? |
answer
| heparin is given SC or IV, (if given IM = hematoma). heparin potentiates antithrombin III, a serine protease inhibitor, causing more inactivation of thrombin |
question
| what are ADRs for heparin? |
answer
| unwanted bleeding in mucuous membranes, open wounds, and intracrainal & GI areas |
question
| what are in vivo indications for heparin? |
answer
| prevention and treatment of deep venous thrombosis, pulmonary embolisms, and arterial thrombosis |
question
| what is heparin used for in vitro? |
answer
| hemodialysis lines, indwelling vascular catheters, and some lab blood samples |
question
| is there an antagonist/reversing agent for heparing (in case of OD)? |
answer
| yes - protamine sulfate |
question
| what is used when pts have HIT (heparin induced thrombocytopenia) |
answer
| lepirudin and argatroban |
question
| what is the M/A for lepirudin? what is it a derivative of? |
answer
| it is a highly specific *irreversible thrombin inhibitor. it is a hirudin derivative |
question
| what are ADRs for lepirudin? |
answer
| hemorrage can occur at any site, which any unexpected call in hgb/BP should lead to consideration of -> therefore anticoagulation status should be monitored closely (aPTT) |
question
| what is bivaliruden? |
answer
| another hiruden derivative that has specific and *reversible direct thrombin inhibition. it has rapid on/off set and inhibits platelet activation (when you stop the IV, its effects will stop) |
question
| when is bivaliruden used? |
answer
| for percutanedous coronary angioplasty |
question
| what ADRs are associated with bivaliruden? |
answer
| hemmorage at any site, though most bleeding occurs at the site of arterial puncture |
question
| what does argatroban do? when is it used? |
answer
| argatroban has direct thrombin inhibition (both free & clot related) by inhibition of thrombin catalyzed OR induced reactions (including *fibrin formation and activation of coagulation factors V, VIII, and *XIII). its main indication is pts with HIT |
question
| what is the M/A for argatroban? |
answer
| it inhibits protein C activation, platelet aggregation, reversibly binds the thrombin active site (*does not require antithrombin III as a cofactor), and has rapid elimination (t 1/2: 39-51 min) |
question
| what are ADRs for argatroban? |
answer
| hemorrage at any site in the body, and intracranial hemorrage has been observed |
question
| what are the oral anticoagulants? |
answer
| warfarin, dabigatran etexilate, antiplatelet agents (NSAIDS, clopidogrel, ticlopidine, prasugrel, ticagrelor), dipyridamole, and prostacylin |
question
| what is warfarin? |
answer
| this is a PO administered vit K antagonist that leads to decreased synthesis of factors II, VII, IX, and X. is is named for the place in wisconson that sponsored its reasearch, and was developed originally as a rat poison (rats bled to death/cows were too big be affected: dose related) |
question
| ADRs for warfarin? |
answer
| unwanted bleeding (same as heparin). warfarin has a very tight therapeutic range -> pts on this must be monitored monthly. centrum silver has vit K! |
question
| what is given in the case of a warfarin OD? |
answer
| fresh blood -> has all the necessary factors? |
question
| can vit K be administered as an anticoagulation agent? |
answer
| yes in 2 formulations (aquamephyton and konakion) |
question
| what factors can decrease the effect of warfarin? |
answer
| enzyme induction (in liver), increased production of clotting factors, increased vit K absorption (supplements, diet), and inhibition of biotransformation |
question
| what factors would increase the effect of warfarin? |
answer
| decreased vit K absorption, displacement from plasma proteins (some NSAIDs, other drugs can do this), inhibition of platelet aggregation (things like ASA), and decreased production of clotting factors |
question
| what is dagbigatran etexilate? M/A? use? |
answer
| an anticoagulation agent that directly binds to and inhibits thrombin. it is used (only) to prevent venous thombosis events following total hip/knee sx. -> still in US trials, shows benefit over warfarin for a fib |
question
| what is the M/A for ASA? |
answer
| irreversible COX inhibitor (and there fore, the effect lasts the life of the platelet: 7-10 days); which als odecreases eicosanids (TXA 2) that stimulate platelet aggregation |
question
| what is clopidogrel (PLAVIX)? |
answer
| this NSAID inhibits the ADP-induced binding for fibrinogen to platelets by covalent *irreversible blockage of the ADP receptor on platelets |
question
| when is clopidogrel used? |
answer
| cardiovascular conditions that are prone to clot formation |
question
| what are side effects associated with clopidogrel? |
answer
| thrombotic thrombocytopenic purpura (TTP) |
question
| what is ticlopidine? |
answer
| an NSAID that inhibits platelet function by inducting a thrombasthenia-like state by *irreverible inhibition of ADP-induces platelet-fibrinogen binding and subsequent platelet-platelet interactions (same as clopidogrel) |
question
| what is the M/A for ticlopidine? |
answer
| irreversible binding to ADP-induced platelt-fibrinogen binding and subsequent platelet-platelet interactions (same as clopidogrel, used as an alternate if on a budget) |
question
| what is ticlopidine used for? |
answer
| it is mainly restricted to tx of acute cerebral ischemia (early stages stroke) |
question
| ADRs for ticlopidine? |
answer
| bleeding, nausea, some diarrhea and very rare neutropenia |
question
| what is the M/A for prasugrel? |
answer
| this NSAID inhibits platelet *activation which is mediated by the P2Y12 ADP receptor |
question
| what is the only indication for prasugrel? |
answer
| prevention of clots in pts undergoing angioplasty |
question
| what are side effects for prasugrel? |
answer
| it can cause significant bleeding (sometimes fatal) and TTP has been reported <- pt must be monitored |
question
| that is ticagrelor? does it require bioactivation |
answer
| this NSAID is a *reversible P2Y12 ADP receptor antagonist that does not require bioactivation = faster onset |
question
| what is ticagrelor used for? |
answer
| cardiovascular conditions prone to clot formation (like clopidogrel) |
question
| what are side effects for ticagrelor? |
answer
| breathing difficulty, heart rhythm abnormalities, major bleeding, and a slightly higher risk of minor bleeding |
question
| what is dypyridamole? |
answer
| an NSAID that increases cellular conc. of cyclic AMP in platelets (inhibits phosphodiesterase which breaks it down) that alone has little to no effect, but is usually used in combination with warfarin for prophylaxis of thromboemboli for prosthetic heart valves |
question
| what is prostacyclin (PGI2) used for? M/A? |
answer
| prostacyclin (PGI2) increases intraplatelet cyclic AMP (by stimulation of adenylate cyclase which synthsizes it) and blocks platelet adhesion and aggregation |
question
| what is a increase in cAMP associated with? which drugs address this? |
answer
| increase in cAMP = blocks aggregation and adhesion prostacyclin and dipyramole both address this |
question
| what are the fibrinolytic agents? |
answer
| streptokinase, urokinase, and tissue plasminogen activator |
question
| what is the M/A for streptokinase? |
answer
| streptokinase complexes with plasminogen, causing a conformational change and activates free plasminogen to plasmin -> producing a *non-clot specific systemic plasminogen activation. it has a half-life of 15-30 min |
question
| what is urokinase (derived from human urine/kidney cells)? |
answer
| urokinase cleaves the arg-arg 560-561 peptide bond in plasminogen, activating it to plasmin and produces a *non-clot specific systemic plasminogen activation |
question
| what can both streptokinase and urokinase be used for? |
answer
| cerebral vascular accidents (strokes) if used within a 3 hr window |
question
| what is tissue plasminogen activator (TPA)? |
answer
| TPA binds to fibrin and activates plasminogen by cleaving the arg-arg 560-561 bond of fibrin-bound plasminogen. it is *clot specific (inefficient at activating free systemic plasminogen) |
question
| what is anisoylated plasminogen streptokinase activator complex (APSAC)? |
answer
| APSAC prevents the proteolytic activity of plasminogen by acetylation at the active site of plasminogen, thereby inhibiting its action |
question
| what is the amniocaproic acid (AMICAR) used for? |
answer
| the antifibrinolytic agent aminocaproic acid binds to the lysine binding sites on plasmin/plasminogen and blocks binding to fibrin targets -> potent fibrinolysis inhibitor, but **cannot lyse new thrombi |
question
| how is aminocaproic acid administered? what is a major caveat for its use? ADRs? |
answer
| aminicaproic acid can be administered oral/IV. it can reverse excessive fibrinolysis, but not lyse new thrombi. ADRs include myopathy and muscle necrosis |
