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15 Cards in this Set

  • Front
  • Back
White Thrombus
Forms in high pressure arteries and is the result of platelet binding to damaged endothelium and aggregation with little involvement of fibrin.
Red Thrombus
Forms in low-pressure veins and in the heart: result of platelet binding and aggregation followed by formation of bulky fibrin tails in which red blood cells become enmeshed
Regulate the function and synthesis of clotting factors
-Primarily used to prevent clots from forming in the venous system and heart (red thrombi)
Inhibit platelet function
-Primarily used to prevent clots from forming in the arteries (white thrombi)
Destroy blood clots after they are formed
-Re-establish blood flow through vessels once clots have formed
Clinical uses for Anti-coagulants
Protect against embolic stroke, pulmonary emboli
Administer to patients with deep vein thrombosis, atrial arrhythmias
SIDE EFFECTS: Excessive Bleeding
Parenteral Anti-Coagulant
Oral Anti-Coagulant
Trade name = Coumadin
Mechanism of action: Heparin
Binds to & stimulates Antithrombin III, an endogenous inhibitor of clotting factors in the intrinsic system
-Molecular weight determines activity
Unfractioned Heparin (UFH)-->more activity
Low Molecular Weight Heparin (LMW) --> less activity
Common uses=prevention of emboli during surgery, heparin locks prevent clots from forming in catheters
Mechanism of action: Warfarin
Prevents Vitamin K re-activation
Delayed onset of action
**Many drug interactions
Common uses-->outpatient tx of deep vein thrombosis
Mechanism of action: Fibrinolytic Drugs
Destroy blood clots after they have formed
Clinical Uses
-Embolic/Thrombotic Stroke
-Acute MI
-Pulmonary Emboli
-Clear occluded IV catheters
Tissue Plasminogen Activator (t-PA) for Tx of Stroke
Most effective on embolic stroke within 3 hours of onset
**Can worsen damage produced by hemhorrhagic stroke
Mechanism of action: Anti-Thrombotics (Anti-platelet drugs)
-Thromboxane A2 (TXA2)-prostaglandin derived from arachondic acid via COX pathway that is released from platelets and promotes aggregation and local vasoconstriction
**Aspirin inhibits COX1 and thereby reduces synthesis of Thromboxane A2

-ADP (Adenosine Diphosphate)- Nucleotide released from activated platelets. Binds to receptors on other platelets resulting in aggregation.
**ADP Receptor Blockers prevent ADP from binding to platelet receptors CLOPIDROGEL
ADP Receptor Blocker
Platelet Receptor Antagonists
Antagonize receptors on platelet cell membranes to prevent physical interaction of platelets with fibrinogen and therefore platelet aggregation.
**Used to treat unstable angina and may be useful for treatment of acute MI