Anticoagulant, Antiplatelet, Thrombolytic Drugs Flashcards
Coagulation cascade
Intrinsic or extrinsic pathways lead to formation of fibrin clot;
-Injured cells release prothrombin activator, prothrombin activator changes prothrombin to thrombin, thrombin changes fibrinogen to fibrin, fibrin forms insoluble web over injured area to stop blood flow
Clotting process
-Blood vessel injury causes vessel spasm (constriction)
-Platelets are attracted to and adhere to injured area
-Aggregation of platelets forms plug
-Formation of insoluble fibrin strand and coagulation (coagulation cascade)
Normal clotting occurs in six minutes
Fibrinolysis
Clot removal; initiated by release of tissue plasminogen activator (tPA) > tPA converts plasminogen to plasmin, plasmin digests fibrin strands-thus, circulation is restored.
Regulated so unwanted clots are removed and fibrin is left in wounds
Anticoagulants
Prevent formation of clots
- Most serious side effect to assess is bleeding; to assess internal bleeding: monitor CBC, lumbar pain, abdominal bulging, guaiac tests on stool
- Essential for patient safety to assess coagulation studies
Thrombolytics
Dissolve life-threatening clots; assess for exclusion to therapy, monitor baseline coagulation studies, monitor level of consciousness for symptoms of cerebral hemorrhage, observe for reperfusion arrhythmias, teach client about the risk of bleeding
Hemostatics
Prevent formation of clots; monitor for clotting, administer intrevenously, monitor site closely
- Assess for myopathy and myoglobinuria (reddish-brown urine), teach client to report symptoms of clotting or bleeding, DO NOT take aspirin!
- Prototype drug: aminocaproic acid (Amincar), mechanism of action: prevent fibrin from dissolving
Heparin
Mechanism of action: Anitcoagulant effect of heparin is mediated through its interaction with antithrombin III
Heparin monitoring
Activated partial thromboplastin time (aPTT):
-normal aPTT range = 26-33 seconds; heparin causes prolongation of aPTT
Heparin/pharmacokinetics
Not absorbed through GI tract, must be administered parentally (IV, SQ); onset of action: IV immediate/SQ 1-2 hours, half life: 1-2 hours (dose-dependent), clearance: reticuloendothelial system (RES), safe in pregnancy, not secreted in breast milk
Heparin/adverse effects
Hemorrhage/bleeding; hypersensitivity reaction
Management: mild: adjust infusion rate or stop infusion; severe: administer protamine sulfate 1 mg IV for every 100 units of heparin administered during the past 4 hours; administer protamine sulfate 50 mg IV over 10 min
Warfarin
Oral anticoagulant; antagonist vitamin K
-Blocks the biosynthesis of factors VII, IX, X and prothrombin; therapeutic uses: long-term prophylaxis of thrombosis
Aspirin (ASA)
Antiplatelet drug; inhibition of cyclooxygenase
-adverse effect: increased risk of GI bleeding
Ticlopidine (Ticlid)
Inhibits ADP-mediated aggregation; adverse effects: hematologic effects
Clopidogrel (Plavix)
ADP receptor antagonist
Management of STEMI
Adjuncts to reperfusion therapy; heparin, antiplatelet drugs
Drug management of STEMI
Thrombolytic drugs: alteplase (a tissue plasminogen activator), reteplase, streptokinase, tenecteplase, urokinase
-Percutaneous coronary intervention (PCI)
Primary percutaneous coronary intervention
Primary: refers to the use of angioplasty rather than fibrinolytic therapy; stents may be placed
-Goal: primary PCI within 90 minutes of patient contact; success rate w/ PCI somewhat higher than with thrombolytics
Fibrinolytic (Thrombolytic) therapy
Dissolves clots; converts plasminogen to plasmin (proteolytic enzyme)
- Alteplase, a tissue plasminogen activator
- Reteplase
- Streptokinase
- Tenecteplase
- Urokinase
Fibrinolytic (thrombolytic) therapy
Most effective when patient presents early; not given if pain has been present longer than 12 hours (best if given during first 4-6 hours)
Goal: to improve ventricular function, limit size of infarct, and reduce mortality; timely administration: opening of occluded artery in 80% of patients
-Guidelines suggest 30 minute target time, best for patients younger than 75 years
Adjuncts to reperfusion therapy: management of STEMI
-Unfractionated heparin used for treatment lasting less than 48 hours; low molecular weight (LMW) heparin used for treatment lasting longer than 48 hours
Complications of STEMI
Ventricular dysrhythmias, cardiogenic shock, heart failure, cardiac rupture
Adjuncts to reperfusion therapy: management of STEMI (drug therapy)
- Antiplatelet drugs: clopidogrel (plavix), glycoprotein (GP) IIb/IIIa inhibitors
- Low dose aspirin: may use concurrently with clopidogrel, should take indefinitely, higher dose for PCI patients
- Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs)
- Calcium channel blockers: antianginal, vasodilation, and antihypertensive actions
Secondary Prevention of STEMI
Discharge 6-10 days after event; 5% of patients have another infarct in first year. Outcome improved with risk factor reduction; All post-MI patients should take: beta blocker, ACE inhibitor, antiplatelet drug or anticoagulant
