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31 Cards in this Set

  • Front
  • Back
What are the Anticoagulants that we learned?
Danaparoid
Enoxaprin
Heparin
Lepirudin
Warfarin
What are the Thrombolytic Agents that we've learned?
Alteplase (tPA)
Streptokinase
What are the platelest Inhibitors that we've learned?
Abciximab
Aspirin
Clopidogrel
Dipyridamole
Eptifibatide
Ticlopidine
Tirofiban
Arterial thrombosis usually occurs in what sized vessels and what is their primary cause?
Arterial thrombosis usually occurs in medium-sized vessels and are rendered thrombogenic by surface lesions of endothelial cells caused by atherosclerosis. They are PLATELET rich!!
Under what conditions do venous thrombosis usually occur and what are they consistent of?
Venous thrombosis is triggered by blood stasis or inappropiate activation of the coagulation cascade. They are frequently due to defects in normal hemostatic defense mechanisms and composed of fibrin.
What is released by healthy intact endothelial cells that prevents formation of a hemostatic plug and how does it work?
They release prostacyclin and nitric oxide. Prostacyclin binds to platelet membrane receptors, causing synthesis of cAMP which stabilizes inactive GP IIb/IIa receptors and inhibits release of granules containing platelet aggregation agents or Ca2+
What are three compounds that can bind to platelet receptors and what is the associated process that eventually leads to platelt aggregation?
Thrombin, thromboxanes, and Exposed Collagen. They bind to the platelet receptors which then causes a cascade release of intracellular granules by the platelets ultimately leading to platelet aggregation.
How does dipyridamole work?
It inhibits phosphodiesterase which typically inactives cAMP. The increased life of cAMP prevents intracellular Ca++ release thereby preventing platelet degranulation
what does the elevated Ca++ in a platelet actually do?
Causes release of platelet granules
Activation of Thromboxane A2 synthesis
Activation of the GP IIb/IIIa receptors
How is fibrin actually formed?
Release of thrombin, a SERINE PROTEASE, causes conversion from fibrinogin to fibrin which binds to platelets and causes aggregation forming a hemostatic plug
How does aspirin work in a platelet?
It blocks Cyclooxygenase-1 (COX-1) conversion of Arachadonic acid to Prostaglandin H2 which typically ultimately becomes Thromboxane A2. Without thromboxane A2 clumping of platelets is greatly decreased..? (not detailed explanation)
What do the antiplatelet drugs clopidogrel and ticlopidine do?
They block ADP mediated platelet aggregation by blocking ADP receptor site binding on the platelet thereby preventing activation of the GP IIb/IIIa receptors
Which one is affected by food absorption ticlopidine or clopidogrel?
Ticlopidine is adversely affected. Both drugs bind plasma proteins upon entry and become active following cytochrome P450 modification
What is Abciximab and how does it work?
It is a monoclonal mouse Fab fragment attached to human immunoglobulin. It functions by binding and blocking GP IIb/IIIa which prevents platelet aggregation. Given as adjunctive therapy with aspirin or heparin. Works for 24-48 hours post infusion
How does Eptifibatide and Tirofiban work?
They work similarly to Abciximab except that Eptifibatide is a peptide and Tirofiban is not. They both block the GP IIb/IIIa binding site. Effects of duration about 4 hours post infusion. Tirofiban is excreted unchanged by the kidney and Eptifibatide's metabolite is excreted by the kidney.
How does dipyridamole work?
It increases intracellular levels of cAMP by inhibiting a phosphodiesterase thereby decreaseing thromboxane A2. However, it may potentiate PGI2 which is an antoginist to platelet stickiness. It is ineffective alone and must be used in combination with say aspirin or warfarin.
What is the first low molecular weight heparin available in the US?
Enoxaparin - This was to help you remember that enoxaparin is a Low Molecular Weight Heparin
How do heparins and LMWH's work?
Heparin (unfractionated) accelerate antithrombin III into binding with either Factor Xa or Thrombin reducing the opportunity for fibrinogen activation cascade. LMWHs stabilize antithrombin as well but only allows binding to Factor Xa.
Which anticoagulant is the primary treatment for PE and DVTs?
Heparin!
What is the anticoagulant treatment of choice for pregnant women?
Heparin and LMWH because of inability to cross the placenta
Because of the unpredictability of regular unfractionated heparin at what activated Partial Thromboplastin Time is suitable?
1.5 to 2.5 fold greater than normal.
How can heparin paradoxically cause a thrombosis?
Chronic or intermitten administration of heparin leads to a reduction in antithrombin III activity, thus decreasing the inactivation of coagulation factors and, thereby, increasing risk of thrombosis. To minimize risk, low dose therapy!
What are the various types of thrombocytopenias caused by heparin administration?
Type I: occurs within the first five days of treatment, and is not serious
Type II: platelets are activated by an immunoglobulin G mediated reaction with a heparin platelet factor IV complex causing platelet aggregation and release of platelet contents. Results in thombocytpoenia nad thrombosis around the fifth to 14th day of treatment
What is Lepirudin and how does it work?
it is a direct thrombin antagonist. It binds to thrombin resulting in a blockade of thrombogenic activity. effective in the treatment of heparin induced thrombocytopenia and other thromboembolic disorders.
What process typically designed to eliminate things in the body may prolong the effect of lepirudin?
Antibodies can be formed in about half of the patients on Lepirudin. Inspite of being bound the lepirudin is still functional and its life may be prolonged due to being bound by antibody.
What is Danaparoid?
Another Anti-factor Xa and antithrombin inhibitor though its anti-factor Xa function is much more powerful than its antithrombin activity it is made of heparin, dermatan, and chondroitin.
What are the vitamin K antagonists?
Coumarins such as warfarin anddicumarol
how do coumarins work?
By depleting the recirculating ability of Vitamin K there is a reduction of coagulating factors thereby preventing coagulation. Warfarin works 8-12 hours post administration
How do the thrombolytic drugs work?
They enhance the activation of plasminogen to plasmin which in turn increases the rate of degredation of fibrin, thereby dissolving clots.
How does the thrombolytic agent alteplase work?
In low doses it activates plasminogen that is bound to fibrin so that it is "fibrin selective."
How does the thrombolytic agent stremptokinase work?
acts on free plasminogen to cause degradation of both fibrin and fibrinogen