CH 38: Anticoagulants Flashcards
Coagulation Modifiers: Thrombolytics - what do they do?
aka fibrinolytics - alteplase (tPa), tenecteplase (TNK-tPa)
- dissolves bonds that hold existing thrombi together
Coagulation modifiers: Antifibrinolytics - what do they do?
aminocaproic acid & tranexamic acid
- inhibit activation of plasminogen to plasmin, prevent break-up of fibrin & maintain clot stability
- used to prevent excessive bleeding
- used to stabilize post surgical bleeds
Anticoagulants - what are the parental and oral drugs?
parental:
- heparin
- low-molecular-weight heparins (only subcu)
- fondaprinuxn (chemically r/t LMWH)
- direct thrombin inhibitors
oral (preferred route):
- warfarin
- dabigatran
What are some considerations for anticoagulants?
- baseline blood tests
- monitor aPTT every 6 hours when adjusting dose (follow PPOs in IHA)
- monitor for signs of bleeding
- apply firm pressure x5 min venous & x10 mins for arterial needle sticks
- reduce risk of trauma
-** keep heparin antidote readily available (protamine sulfate)**
What are the 5 contraindications for all blood thinners?
- hemorrhagic stroke
- GI bleed
- trauma
- surgery - heparin stopped 24h before surgery, start again 24h after
- blood disorders, e.g., hemophilia
What are the INR levels for warfarin?
- below 1 if not going for surgery/is normal
- between 2-3 if at risk for clotting
Anticoagulants - patient education?
- no razors, wax instead or use electric razor
- soft bristled toothbrush
- no high impact activities (will bruise more easily)
- if bleeding, e.g., nosebleed or fingercut, > 30 min, go to hospital
- if GI bleed (coffee ground emesis or melena), go to hospital
oral anticoagulants- what is the prototype drug?
warfarin (Coumadin)
therapeutic: anticoagulant
pharmacologic: vitamin K antagonist
warfarin - therapeutic effects/uses & mechanism of action
therapeutic effects/uses:
- prophylaxis arterial thromboembolism (prevention of CVA/MI)
- DVT/PE
- long-term indwelling catheters
- prevent thromboembolic events in high-risk patients
mechanism of action:
- inhibits 2 enzymes involved in formation of activated vit K
- inhibits synthesis of new clotting factors
What are some considerations for warfarin?
- assess for risk of thromboemboli
- monitor PT/INR
- monitor urine, stool, liver function, blood
- monitor risk groups for nonadherence
- teach pts to avoid, or eat sparingly, foods rich in vit K, such as broccoli, leafy greens, etc
Warfarin - pt education?
- monitor for signs of bleeding
- apply firm pressure x 5 min venous & x10 mins for arterial needle sticks
- reduce risk of trauma
Heparin - classifications, therapeutic uses/effects & mechanism of action?
therapeutic class: anticoagulant
pharmacologic: indirect thrombin inhibitor
effects/uses:
- acute thromboembolic disorders
- DVT/PE
- unstable angina/evolving MI
- prophylaxis
mechanism of action:
- activates anti-thrombin III, which inhibits thrombin and to a lesser extent, factor Xa (prevents formation of clots)
Heparin - any considerations?
- baseline blood tests
- monitor aPTT q6h when adjusting dose (follow PPOs in IHA)
- monitor for signs of bleeding
- apply firm pressure x 5min venous & x10 mins for arterial needle sticks
- reduce risk of trauma
- keep heparin antidote readily available (protamine sulfate)
What are ADP receptor blockers?
what do they do?
- aka P2Y12 inhibitors
- antiplatelet agents prescribed for prevention & treatment of arterial thrombosis
- inhibits aggregation (decr ability to clot, doesn’t come to spot of bleeding)
- makes blood less “sticky”
ADP Receptor Blockers/P2Y12 Inhibitors - what are the agents?
reversible:
- Ticlopidine (Ticlid) BID - stroke prophylaxis
- cangrelor
irreversible - MI & stroke
- clopidogrel (Plavix)
- prasugrel
Adverse effects of ADP receptor blockers?
- bleeding
- neutropenia/agranulocytosis
- thrombotic thrombocytopenic purpura
ADP receptor blockers: prototype drug?
clopidogrel (Plavix)
therapeutic: antiplatelet agent
pharmacologic: ADP receptor blocker
3 new P2Y12 receptor inhibitors: prasugrel, cangrelor, ticagrelor
clopidogrel: therapeutic uses/effects?
- reduce risk of CVA/MI (doesn’t break down clot directly) - more preventative
- reducing thrombolytic events post-CVA/MI
- prevent DVT
- prevent thrombi formation unstable angina / coronary stents
clopidogrel - mechanism of action?
- inhibits ADP receptors on platelets and prolongs bleeding time by irreversibly inhibiting platelet aggregation
- CYP450 interaction
What are the drawbacks of clopidogrel?
- delayed onset of action
- large inter-individual variability in platelet response
- genetic polymorphism of metabolizing enzyme
- drug-drug interactions (DDIs)
- 2-step activation process catalyzed by series of ctyochrome P450 (CYP) isoenzymes
–> prodrug, requires hepatic conversion to an active metabolite resulting in delayed onset of action and inter-individual variability
Thrombolytics - what are they called?
“-plase” or “-nase”
What are some thrombolytics?
streptokinase (SK)/ Urokinase (UK)
- older, slower, more side effects, cheap, allergenic
- for PE, MI, DVT
newer drugs have fewer side effects
- tenecteplase (TNK-tPA)
- alteplase (tPA)
What risks do thrombolytics have?
risk of bleeding may outweight benefits - watch for s/s hemorrhagic stroke (LOC)
Antifibrinolytics: therapeutic uses / effects?
- aplastic anemia
- hepatic cirrhosis
- postop cardiac surgery (@ risk for excessive bleeding
- certain carcinomas
- hemophilia A
- excessive post surgical bleeds
Antifibrinolytics - what are they for?
- aka hemostatics/tranexamic acid, to promote formation of clots
- more commonly prescribed in surgical pts
- occupies binding sites on plasminogen and plasmin
- prevents digestion of fibrin clot by plasmin
- stabilizes clot
