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8 Cards in this Set

  • Front
  • Back
Aspirin
1. MECHANISM:
- irreversibly acetylates COX, which leads to decreased TXA2 production, thereby decreasing platelet aggregation
- at low doses, inhibits TXA2 production, but does not affect PGI2
- does not inhibit other platelet aggregation factors (ADP) so it is not a complete antithrombotic

2. CLINICAL:
- very effective in pts. with CVD
- not proven to be a good source of primary prevention

3. ADVERSE:
- dyspepsia and nausea
GI bleeding, hemorrhagic strokes, allergic rxn, asthma exacerbation
- may exacerbate gout
Thienopyridines: clopidogrel
1. MECHANISM:
- inhibit ADP-mediated activation of platelets
- irreversibly block P2Y12, which is needed for ADP activation

2. CLINICAL:
- used in pts allergic to aspirin. also to prevent thrombotic complications following percutaneous soronary stenting

3. ADVERSE:
- dyspepsia and diarrhea
glycoprotein IIb/ IIIa receptor antagonists: abciximab
1. MECHANISM:
- monoclonal Ab that inhibits the binding of activated platelet to fibrinogen and von Willebrand factor
- platelets cannot "stick together" inhibiting the formation of plug

2. CLINICAL:
- for pts undergoing percutaneous coronary interventions and high risk ACS
- must be given IV

3. ADVERSE:
- bleeding and thrombocytopenia
unfractioned Heparin (UFH)
1. MECHANISM:
- positively associates with antithrombin III (ATIII)
- reduces thrombin's ability to generate fibrin from fibrinogen
- also inhibits activated factor X
- antiplatelet activities by binding to von Willebrand factor

2. CLINICAL:
- parenteral administration
- unstable angina, non-STEMI, acute MI, PE or DVT

3. ADVERSE:
- bleeding
- heparin induced thrombocytopenia (HIT): most common type is direct heparin induced platelet aggregation. Rarer and more lethal is immune mediated. Abs are formed against heparin-platelet complex, causing thrombosis
low molecular weight heparins: enoxaparin
1. MECHANISM:
- preferentially inhibits factor Xa
- also inhibits thrombin via association with ATIII, but not as well as UFH
- have more prominent anticoagulation abilites v. UFH, fewer complications, less HIT

2. CLINICAL:
- prophylaxis against DVT following leg sx
- tx for DVT
- tx for ACS

3. ADVERSE:
- do not give to pts with a history of HIT
Fondaparinux
1. MECHANISM:
- binds to ATIII with very high affinity, thereby inhibiting factor Xa
- does not inactivate formed thrombin, does not affect platelet activity, or cause HIT
- long half life
- subQ

2. CLINICAL:
- prevention of DVT
- tx for DVT and PE
vitamin K antagonist: warfarin
1. MECHANISM:
- antagonizes vit K epoxide reductase, which inhibits vit K metabolism
- vit K needed for carboxylation of coagulation factors. these are inactive with warfarin
- vit K also activates coagulation inhibitors (protein C and S) so that warfarin aslo inactivates these factors

2. CLINCAL:
- long-term anticoagulation

3. ADVERSE:
- reduced dose in liver and hepatic dysfunction
- teratogenic. do not give during pregnancy, especially first trimester
fibrinolytics: alteplase (tPA)
1. MECHANISM:
- stimulates natural fibrinolytic system, transforming plasminogen into plasmin, thereby lysing fibrin clots
- bind preferentially to fibrin in a formed thrombus

2. CLINICAL:
- for use in acute STEMI. best to give within 30mins
- not effective in UA or NSTEMI

3. ADVERSE:
- contraindicated in pts with necessary fibrin clots (active peptic ulcer dx, hx of CVA, recovery from recent sx)