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30 Cards in this Set
- Front
- Back
Anticoagulants: Warfarin - Overview |
Warfarin (Coumadin): - Is a vitamin K antagonist and is the most commonly prescribed oral anticoagulant. - It is a potent rodenticide (used to kill rats) - Similar to Heparin it is used to prevent thrombosis - Has a delayed onset of action thus making it inappropriate for emergency use - Does NOT require injection, ideal for long-term prophylactic treatment - Significant risk for hemorrhage - a number of drug interactions which can contribute to hemorrhage risk |
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Warfarin: Mechanism of Action |
Warfarin supresses vitamin K dependent clotting factors (ie. VII, IX, X, prothrombin) - Inhibits Vit. K epoxide reductase complex 1 (enzyme) needed to convert vit. K to its active form - reduces vit K dependant factors by 30-50% |
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Warfarin: Pharmacokinetics |
Oral: - Half life: 0.5-3 days; Onset: 12-24 hrs; Peak 3-4 days; Duration 3-5 days - Delayed onset as Warfarin has no effect on clotting factors already present in circulation - Coagulation remains inhibited for 2-5 days after discontinuation because of long half life |
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Warfarin: Indications |
Most frequently prescribed for the long-term prophylactic treatment of thrombosis. - Prevention/tx of venous thrombosis and associated PE (ie. DVT) - Prevention of thromboembolism in pt.'s with prosthetic heart valves - Prevention of thrombosis in pt.'s with atrial fibrillation - Atrial fibrillation = high risk of CVA secondary to clot formation in artiums -- if dislodged can cause artery blockage = ischemic stroke
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Warfarin: Contraindications |
a) Active bleeding process or high risk of such occurence b) Thrombocytopenia - low platelets - Normal range: 150-400 x10^9/L - Leukemia - Small cohort of women develop thrombocytopenia during pregnancy c) Surgery: warfarin should be dc days prior to elective surgery; vit. K given prior to emergent cases for those on warfarin (antidote) |
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Warfarin: Adverse Effects |
a) Hemorrhage: considered a major complication of therapy and can occur at any time. - Monitor for bleeding: BP, HR, bruising, petechiae, hematomas, black/red stool, discolored urine, pelvic pain, lumbar pain (ie. adrenal hemorrhage), headache (cerebral hemorrhage) - Bleeding: dc warfarin, antidote = vit. K, avoid razors; soft toothbrush
b) Fetal hemorrhage and teratogenesis (pregnancy): FDA classification = risk outweighs benefit of drug administration. - Warfarin crosses placenta and can result in fetal hemorrhage, malformation, CNS defects, optis atrophy and death. - Women of child-bearing age and considering pregnancy should be aware of teratogenic effects: postpone pregnancy? termination of pregnancy if on warfarin? warfarin enters breast milk ie. can't breast feed - Heparin is an alternative as it doesn't cross placental barrier |
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International Normalized Ratio (INR) |
Internationally recognized blood test that measures the effectiveness of warfarin therapy. - Objective of warfarin therapy is to increase INR = less chance for thrombus formation
INR levels vary for the condition being treated: - Acute MI, atrial fib., valvular heart disease, PE, & venous thrombosis = 2-3 - Mechanical heart valves = 3- 4.5 - Systemic embolism - prevention = 2-3 - Systemic embolism - recurrent = 3- 4.5 |
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Warfarin: Interactions |
Subject to a large number of clinically significant drug interactions: - Drugs that incr. the effect of warfarin: Asprin, acetaminophen, cimetidine, trimethoprim- sulfamethoxazole, cephalosporins - Drugs that promote bleeding: Aspirin, clopidogrel (plavix), heparins, glucocorticoids, indomethacin - Drugs that decrease the effect of warfarin: Dilantin, rifampin, phenobarbital, oral contraceptives, vitamin K |
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Anticoagulants: Heparin (Hepalean) -Overview |
Rapid acting anticoagulant (SC/IV only) NOT IM! |
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Heparin: Mechanism of Action |
Heparin administration --> activation of anti-thrombin --> promotes inactivation of thrombin factor Xa = supression of fibrin
- Fibrin forms the framework of thrombi in veins. Heparin is therefore useful in prophylactic tx. of venous thrombosis |
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Heparin: Pharmacokinetics |
Half-life:1-2hrs Onset: SC - 20-60mins; IV - immediate Peak: 2-4 hrs Duration: dose dependent |
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Heparin: Indications |
a) Anticoagulant of choice for pregnancy as it does not cross the placenta b) Critical/emergent situations: PE, evolving CVA (stroke), DVT, adjunct to acute MI management c) Open heart surgery & renal dialysis: heparin prevents coagulation in devices (ie. heart/lung machines) d) Post-operative prevention of venous thrombosis |
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Heparin: Contraindications |
In those at high risk for bleeding: - Hemophilia, severe hypertension, dissecting aneurysm, peptic ulcer disease - Thrombocytopenia - during/immediately after eye, brain, spinal cord injury |
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Heparin: Adverse Effects |
a) Hemorrhage: - bleeding occurs in aprox. 10% of pt.'s - bleeding can occur at any site - monitor pt. carefully for blood loss: BP, HR, bruising, petechiae, hematomas, black/red stool, discolored urine, pelvic pain, lumbar pain (ie. adrenal hemorrhage), headache (cerebral hemorrhage)
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Activated Partial Thromboplastin Time (aPTT): |
- normal: 27-38 seconds - Therapeutic goal is 1.5-2 times the normal (ie. 60-80 seconds) - Heparin drip- frequent lab tests to determine therapeutic effect - protamine sulfate is antidote for heparin |
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Heparin: Interactions |
Platelet aggregation is the only remaining defense in those treated with heparin - Avoid aspirin or other antiplatelet medications |
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Antiplatelet: Aspirin - Overview |
- Anti-inflammatory, analgesic, anti-pyretic, clot prevention - Prevention of thrombosis in arteries - where as warfarin and heparin prevent formation of thrombus in veins |
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Aspirin: Mechanism of Action |
-Suppresses platelet aggregation by causing irreversable inhibition of cyclooxygenase (enzyme) that is required by paltelets to synthesize thromboxane A2. - Thromboxane A2 promotes platelet aggregation and vasoconstriction - Asprin supresses vasoconstriction, and platelet aggregation, thus reducing risk for arterial thrombosis |
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Aspirin: Pharmocokinetics |
Oral: - Half-life: 3.5-4.5 hours - Onset: 15-30 mins - Peak: 1-2 hours - Duration: 4-6 hours |
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Aspirin: Indications |
a) Ischemic stroke and TIA: reduce the risk of death and non-fatal stroke b) Chronic stable angina, unstable angina, previous MI: Reduce risk of MI and death c) Coronanry Stent Placement: to prevent re-occlusion d) Acute MI: reduce risk of vascular death e) Primary prevention of MI: prevent first MI in men and in women over 65 years old - Research (2002) - in those at risk for cardiovascular event in next 5 years, aspirin lowers the risk of MI by 28%, it doesn't however, reduce the risk of death |
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Aspirin: Contraindications |
- Thrombocytopenia - Active bleeding - Leukemia - Traumatic Injury - Gastric ulcer - Vitamin K deficiency - Recent stroke (CVA) |
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Aspirin: Adverse Effects |
a) Increase risk of GI bleed and hemorrhagic stroke: even at low doses - study - apsirin usage for at least 5 yrs: 2-4 bleeding episodes per 1000 pt.'s; 0-2 hemorrhagic strokes per 1000 pt.'s
b) Enteric coated aspirin may not reduce risk of GI bleeding: may need proton pump inhibitor - pantoprazole (protonix) - AKA GI protection |
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Aspirin: Interactions |
a) NSAIDS/heparin: additive anti-platelet activity and increased bleeding potential b) Hypoglycemic medications: large doses of aspirin may enhance the effect of oral hypogylcemic drugs c) Steroids: Can increase risk of gastric ulcers/bleeding |
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Thrombolytic: Alteplase (tPA) - Overview |
- Clot buster - AKA Tissue Plasminogen Activator is made through recombinant DNA and modified hamster ovary cells - Clot specific: doesn't produce systemic lyses - Naturally occurring in body, therefore does not induce antibody-antigen response |
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Alteplase (tPA): Mechanism of action |
Alteplase binds with plasminogen to form an active complex (alteplase-plasminogen complex) - Complex converts other plasminogen molecules into plasmin (enzyme) that breaks down fibrin -- essentially it is a fibrinolytic |
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Alteplase (tPA): Parmacokinetics |
IV: Half-life: 5 mins Onset: unknown Peak: varies with dose Duration: unknown - 80% cleared within 10 mins after stopping infusion |
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Alteplase (tPA): Indications |
- Acute MI - Acute ischemic stroke - Acute massive PE
Global utilization of Streptokinase and tPA for Occluded Coronary Artery - large trial looked at benefits of thrombolytic drugs in pt.'s with MI: - treated within 2 hrs of symptom onset - death rate 5.4% - treated 2-4 hrs after symptom onset - death rate 6.6% - treated 4-6 hrs after symptom onset - Death rate 9.4% |
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Alteplase (tPA): Contraindications |
- Other medications altering clotting |
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Alteplase (tPA): Adverse Effects |
Bleeding: - Destroys pre-existing clots from recent injuries that have healed and can interfere with new clot formation -- Intracranial hemorrhage (ICH) is the most concerning -- recent wounds, needle punture sites, invasive? - Management: Pressure dressings, Blood products (PRBCs), IV aminocaporic acid (prevents activation of plasminogen and inhibits plasmin) |
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Alteplase (tPA): Interactions |
- Minimize physical manipulation - Avoid SC and IM injections - Minimize invasive procedures - Minimize anticoagulant and antiplatelet use |