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17 Cards in this Set
- Front
- Back
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What factors are inhibited by ATIII?
What is the role of Heparin when it comes to ATIII? When someone is on Heparin, what do you expect their ATIII levels to be relatively? |
ATIII inhibits Factors 2, 7, 9, 10, 11, and 12 (but mainly 2 and 10)
Heparin causes conformational change in ATIII accelerating binding to enzymes (1000x better). ATIII should be LOW when person is on Heparin (because it gets cleared) |
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What is the test we use to monitor Heparin's effects in the body?
Describe the pathogenesis of HIT? How do you treat it? |
Test= PTT (because it includes factors 11 and 12)
HIT- antibodies form against Heparin-PF4 leading to 1) platelet destruction --> thrombocytopenia and 2) platelet activation --> platelet aggregation and thrombosis *patients can develop DVTs, PE, MIs, Ischemic Strokes. REMOVE HEPARIN! And start Lepirudin/argatroban. |
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What is the advantage of using a LMWH?
In what patients is it absolutely contraindicated? How do we monitor it? |
LMWH = greater bioavailability, longer half life, less side effects (less HIT, less bleeding). Better anti-factor Xa activity. Does NOT cross placenta (use in pregnancy)
Monitor Anti Factor Xa levels (can't use PTT because it targets F10a which is common pathway). Cannot use in patients with decreased kidney fxn (renal clearance), or obese. |
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What is the only bad point about LMWH?
What is an antidote of HEPARIN? |
Bad= irreversible (no antidote...protamine doesn't completely reverse)
Protamine = antidote for heparin |
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Describe (in relative detail) the mechanism of action of Warfarin. What factors does it inhibit?
What is the test used for measuring Warfarin? Ideal goal for the therapeutic level? |
Warfarin inhibits gamma carboxylation of Factor 2,7,9,10 and Protein C. Prevents ability to bind surface of platelet.
Use INR (PT) to measure Warfarin's effects. Ideal = 2-3 for most VTE and PE prophylaxis. |
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If someone has a DVT, what is the Warfarin regimen that you should use?
Why? |
Start them on Heparin and Warfarin, keep them on Heparin for 5 days and then discontinue.
Reason for this is it takes at least 5 days for all the clotting factor levels to fall below anticoagulation threshold. |
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What is warfarin metabolized by?
What drugs potentiate it's anticoag effect? What drugs antagonize it's anticoag effect? |
Metabolized in the liver by CYP450 (specifically CYP2C9 and CYP1A2). Give low dose for someone with liver disease.
Potentiate = CYP450 inhibitors (Cimitidine, clofibrate, "azoles", and grapfruit juice) Antagonize= barbiturate, rifampin, CBZ, chronic ETOH use, and cholestyramine (↓ absorption) |
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What is the importance of the CYP2C9 variant on warfarin dosing?
What about Vit K epoxide reductase enzyme? |
CYP2C9 variants have 3x INCREASED risk of bleeding (because of decreased clearance in these patients)
VKORC1 enzyme recycles reduced vit K, genetic variants can increase or decrease dosing of Warfarin |
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Risk for hemorrhage from Warfarin increases above an INR of ____.
In what population is warfarin use ABSOLUTELY contraindicated? |
INR >4 (risk for hemorrhage increases)
NEVER give to pregnant women (warfarin toxicity) |
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What is the treatment for reversing Warfarin? What do you use when there's an acute bleed?
What medication is proven to have fewest recurrence of clot, and thus ideal for DVT, or PE patients? |
Give vitamin K (PO is best), and FFP (fresh frozen plasma- with all cofactors)- used with acute bleed.
LMWH is actually superior to warfarin. Fewer recurrent clots. Use LMWH for 3-6 months and then indefinitely keep person on warfarin or LMWH. |
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If a person has a DVT, what do you give them if...
1. Reversible risk factor is present (ocp, indwelling catheter) 2. First unprovoked DVT 3. First unprovoked PE 4. Second unprovoked DVT |
1. Reversible risk factor present - anticoagulate for 3 months only
2. First unprovoked DVT- at least 3 months anti coag, consider long term 3. First unprovoked PE- 3 months anticoag + long term anticoag 4. Second unprovoked DVT- add long-term anticoag |
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What is the role of Plasmin?
Role of tPA and alpha-2 antiplasmin inhibitor? Role of PAI (Plasminogen activator inhibitor)? |
It limits clot formation by cleaving fibrin--> d-dimer
Fibrin stimulates tPA release from endothelial cells. tPA cleaves plasminogen -- plasmin. a-2 antiplasmin inhibitor inactivates plasmin. PAI inactivates tPA. |
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What are the major indications for fibrinolytic therapies (tPA, streptokinase, urokinase)?
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Acute MI, Thrombotic stroke within 3 hrs, Acute artery occlusion, massive PE
*very dangerous, potent drugs, use only in very bad situations |
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What is the mechanism of action of Streptokinase? Why does it have the possibility of causing allergic reactions?
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Streptokinase (not a kinase) comes from B-hemolytic Strep. It binds ot plasminogen and auto-cleaves it to plasmin (no need for tPA).
People who have had prior strep infection may develop rxn against streptokinase. |
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What are some recombinant t-PA drugs?
What is mechanism of action of Recombinant Factor VIIa (7)? |
Alteplase, Reteplase, Tenecteplase (only use in very serious situations!)
Recombinant Factor 7- sits on platelet and directly causes activation of factor 10 --> thrombin. Very potent! Only to be used in serious bleeding situations. |
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What is the mechanism of action of Tranexamic acid, Amicar and Aprotinin?
What are they used for? |
Adjunctive therapy for hemophilia (excessive bleeding), overdose of Fibrinolytic therapy, prophylaxis for rebleeding intracranial hemorrhages
Inhibits Plasminogen activation by binding to it and preventing it from binding to fibrin. |
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What are contraindications to Thrombolytic Therapy?
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Active GI bleed
Aortic dissection Head injury or IC hemorrhage Neurosurgery Intracranial aneurysm **PROLIFERATIVE DIABETIC RETINOPATHY (the person can become blind and bleed). Any situation that causes high risk bleeding should be avoided. |
