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HSF II Cardiovascular - Hemostasis

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Hemostasis   collection of events that stops bleeding by turning a portion of the fluid blood into a semi-solid clot or thrombus  
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Two Aspects of Hemostasis   1) anticoagulant activity 2) procoagulant activity  
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Anticoagulant Activity   maintains blood in a fluid state while circulating within the vascular system, does not promote hemostasis, predominate and inhibit hemostasis in normal conditions  
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Procoagulant Activity   promotes hemostasis, predominate in damaged blood vessels and hemostasis initiates, a clot forms  
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Virchow's Triad   factors for thrombosis: 1. injuries to vascular endothelium, 2. alterations in normal blood flow, 3. alterations in the constitution of blood  
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Causes of Abnormal Blood Flow   immobility, venous obstruction, varicose veins, atherosclerosis, atrial fibrillation  
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Deep Vein Thrombosis (DVT)   when blood clot (thrombus) forms in one or more of the deep veins in your body, usually in the legs. because venous flow from muscle pump  
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Causes of Changes in Blood Constitution   sepsis, chronic inflammation, hormonal changes/therapy, thrombophilia  
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Most important factor for maintaining normal pro- and anti-coagulant balance   endothelial integrity  
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von Willebrand Factor (vWF)   a procoagulant glycoprotein made by undamaged endothelium, binds and prevents the degradation of clotting factor VIII  
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Cause of Hemostasis Initiation   when the balance of anticoagulants and procoagulants is shifted  
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Three Phases of Hemostasis   1) vascular spasm 2) platelet plug formation 3) coagulation (clotting)  
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Vascular Spasm (Hemostasis)   smooth muscle contracts, causing vasoconstriction: a) pain, b) myogenic reflex, c) endothelins  
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Platelet Plug Formation (Hemostasis)   injury to lining of vessel exposes collagen fibers, platelets adhere. Platelets release chemicals that make nearby platelets sticky, and platelets form the clot  
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Pain (vascular spasm)   activates the sympathetic nervous system, increased sympathetic stimulation causes vasoconstriction  
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Myogenic Reflex (vascular spasm)   direct response of smooth muscle to mechanical stimulation, stretch the muscle or deform it, causing mechanically gated ion channel  
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Endothelins (vascular spasm)   cytokine proteins that constrict blood vessels. trauma to tunics increase endothelin production and shifts balance to vasoconstriction.  
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Platelet Phase   second phase in hemostasis, subendothelial vWF exposed, platelets bind to vWF and the exposed collagen via one membrane receptor, fibrinogen binds to the other  
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Platelet Release Reaction   aggregated platelets release 1) serotonin (5-HT) (vasoconstrictor) 2) ADP and 3) Thromboxane A2 (vasoconstrictor, eicosanoid). these all enhance platelet plug formation  
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