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WEEK 19:
Pharmacology of Anticoagulants, Antiplatelet drugs & Fibrinolytics:
| Question | Answer |
|---|---|
| uses of warfarin (4) | in patients with replaced heart valves, AF, PE, and DVT |
| purpose of warfarin | prevent thrombosis |
| how long does warfarin take to act | days |
| mechanism of warfarin | |
| increased actions lead to | bleeding |
| examples of bleeding from increased actions (6) | gastric, cerebral, haemoptysis, blood in faces, blood in urine and easy bruising |
| INR | |
| examples of unfractionated heparin/ LMWH | enoxaparin and tinzaparin |
| how does unfractionated heparin/ LMWH work** | activates antithrombin III which then itself inactivates clotting factors and thrombin by complexing with serine protease of the factors |
| heparin action | immediate |
| heparin use | prevent blood clotting on collection and thrombosis (venous, unstable angina) WHILST warfarin takes effect |
| unfractionated heparins monitored by what | APTT |
| warfarins are monitored by what | INR |
| novel oral anticoagulants (NOACs) | |
| dabigatran | oral thrombin inhibitor which prevents thromboembolism |
| advantage with dabigatran over warfarin | less bleeding, fewer drug interactions, and does not need monitoring |
| issues with warfarin | need to measure INF regularly |
| rivaroxaban and apixaban | oral inhibitor of activated factor X |
| RE-LY trial** | |
| prostacyclin (PGI2) / NO | vasodilators in endothelial (cell lining of blood vessels) |
| PGI2 | prevents platelet aggregation to increase cAMP |
| thromboxane (TXA2) | promotes aggregation, to decrease cAMP |
| NO | prevents both platelet adhesion and aggregation by increasing platelet cGMP |
| how is NO made | L-arginine + O2 -> NO + citrulline via NO synthase |
| example of antiplatelet drug | aspirin and dipyridamole |
| antiplatelet drugs | used to prevent MI in patients who have previously had MI (secondary prevention) and reduces incidence of stroke |
| antiplatelet drugs inhibit | cyclo-oxygenase permanently (its irreversible) |
| **29 | |
| ADP from aggregating platelets leads to | expression of GP llb/ lla |
| GP llb/ lla | binds to fibrinogen leading to cross-linking of platelets |
| clopidogrel | inhibits ADP induced expression of GP |
| who can take clopidogrel | patients who cannot take aspirin/ can be used with aspirin |
| Abciximab | monoclonal antibody against GP llb/ lla |
| who can take Abciximab | patients undergoing angioplasty (only use once) |
| fibrinolysis/ streptokinase | endogenous system dissolve clots |
| when is fibrinolysis activated | in parallel with clotting system |
| how does fibrinolysis occur | plasmin from plasminogen digests fibrin of the clot and some clotting factors |
| fibrinolytic agents (clot busters) activate what | plasminogen to plasmin |
| when are thrombolytics given | after MI to dissolve thrombus causing MI, PE, and thromboembolic stroke |
| primary treatment for MI | emergency angioplasty |
| when are thrombolytics most effective | when with aspirin, but can cause bleeding |
| treatment for ischaemic stroke | alteplase |
| alteplase | used for ischaemic strokes to dissolve clot to restore blood flow in brain |
Created by:
kablooey
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