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24 Cards in this Set
- Front
- Back
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What are the major classes of anticoagulant medications? |
Factor IXa and/or Xa inhibitors - heparin enoxaparin, fondaparinux
Vitamin K antagonist - warfarin
Direct Xa inhibitor - rivaroxaban
Direct thrombin inhibitor - dabigatran |
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What is the prototypical fibrinolytic agent? |
Plasminogen activator - Alteplase (r-tPA) |
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What is the mechanism of HMW heparin?
How is it administered?
Why must it be tested? |
Heparin activates anti-thrombin III, which subsequently inhibits clotting factors IXa and Xa
Too large to absorbed by GI, thus given IM |
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What are the therapeutic uses of HMW heparin? |
Venous thrombosis and pulmonary embolism Angina Acute MI AFib Vascular surgery A or V catheter placement DOES NOT CROSS PLACENTA - best for preggers |
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What are the adverse effects of heparin?
What are the contraindications of heparin?
What can be used to inactivate heparin? |
Side effects: hemorrhage, osteoporosis, fractures and 1-4% get heparin induced thrombocytopenia which is a hypercoagulable state
Cx in pts. with (intracranial hemorrhage), HTN, thrombocytopenia, hepatic/renal disease, endocarditis
Can use protamine sulfate to inactivate heparin |
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What is HIT?
How is it treated? |
Occurs 1-2 wks after therapy starts; ≥50% decrease in platelets and body forms abs against heparin-platelet combo which activates platelets; leads to systemic coagulation = DVT, PE, MI, CVA, organ death, death death
Stop heparin, give hirudin and alternate anticoagulant. DON'T give platelets. |
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How is HMW heparin monitored? |
Activated partial thromboplastin time (aPTT) should be 2-2.5x normal.
Only monitored when given IV.
If long-term therapy is needed, use HMW heparin until warfarin takes effect |
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What is the mechanism of LMW heparin?
What are its therapeutic uses?
What is monitored?
Can it be inactivated by protamine sulfate? |
Activates antithrombin to bind factor Xa
Venous thromboembolism, thrombosis, PE, UA
Monitor Xa activity in CKD, obesity or preggers
Incomplete inactivation by protamine sulfate
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What are the advantages of LMW heparin over HMW heparin? |
Longer t1/2 and faster absorption time Lower risk of thrombocytopenia and osteopo Once daily SC injections as outpatient Less frequent monitoring
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What is the mechanism of warfarin? |
Inhibition of vitamin K epoxide reductase which is the enzyme that activates clotting factors VII, IX, X and prothrombin.
Thus biologically inactive clotting factors are made and coagulation is inhibited.
Requires 3-5 days to achieve full effect |
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What are the therapeutic uses of warfarin?
What are the adverse effects of warfarin?
Why is patient history important before starting warfarin? |
Acute DVT, PE, venous thromboembolism, post acute MI, prosthetic heart valve placement, afib
Hemorrhage (can be reversed w/ supp. vit K), can cross placenta (bone defects), cutaneous necrosis can occur during initiation of therapy
MANY DRUG INTERACTIONS |
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How is warfarin monitored? |
Every couple of weeks must monitor the prothrombin time and calculate the INR (normal is 1, therapeutic index is 2-3) |
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What is the mechanism of dabigatran?
What is its therapeutic use?
What are its adverse effects? |
Direct inhibition of thrombin, thus no formation of fibrin from fibrinogen
Stroke prevention in patients with nonvalvular afib
Hemorrhage, increased risk of MI, GI upset |
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What are the pros and cons of dabigatran compared to warfarin? |
Pros: no monitoring required, rapid onset and no drug interactions
Cons: expen$ive, no antagonist |
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What is the mechanism of rivaroxaban? What are the benefits of its use? What's its therapeutic use? What are the adverse effects and cx? |
Direct inhibition of clotting factor Xa Given as a fixed dose, rapid onset, no monitoring Prevention of thromboembolism following knee or hip surgery Side effect of hemorrhage and may be cx in patients with renal dysfunction |
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What are the recommendations for oral anticoagulants in patients with afib? |
Warfarin is superior to ASA/Clopidigrel combo
Warfarin and dabigatran have equal efficacy in reducing stroke |
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What is the mechanism of alteplase (tPA)?
Where is it metabolized? t1/2?
When is it effective?
What inhibits tPA? |
Directly converts plasminogen to plasmin and chomps up the fibrin
Metabolized in the liver. t1/2 is 3-8 minutes
Only effective if used directly after the onset of thrombosis.
Inhibited by aminocaproic acid |
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What are the therapeutic uses of tPA? |
In-hospital IV administration for acute ischemic stroke, acute MI, PE, severe DVT and ascending thrombophlebitis |
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What is the major adverse effect of tPA?
What are the cx of tPA? |
Hemorrhage is the major concern, esp. intracranial
Cx if brain tumor, aneurysm, stroke, major surgery in last two weeks, active GI or GU bleed, uncontrolled HTN, thrombocytopenia or coagulation disorder |
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What is the mechanism of streptokinase?
Where in the circulation does it act?
When is it used?
When is it Cx? |
Catalyzes the conversion of plasminogen
Acts throughout circulation, not just at clot
Used to treat acute MI the first time (then tPA)
Cx in patients with allergy or acute ischemic CVA |
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Where does tPA act? |
Acts only at the site of the clot because it binds to plasminogen that is bound to fibrin |
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Why is vitamin K important to the body?
What can lead to a vit. K deficiency?
What are the symptoms? |
Vitamin K activates several of the factors of the clotting cascade
Poor (hospital) diet, surgery, Abx can cause vit K deficiency
Symptoms are incr. bleeding and osteoporosis |
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How is a vitamin K deficiency treated?
What are side effects of rapid IV administration? |
Supplemental vitamin K is given, but takes 24 hours to be fully effective
Rapid IV can cause dyspnea, angina, death |
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What is the cause of disease in hemophilia a and b? |
hemophilia a = factor VIII deficiency
hemophilia b = factor IX deficiency |
