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HSF II Cardiovascular - Hemostasis

Hemostasis collection of events that stops bleeding by turning a portion of the fluid blood into a semi-solid clot or thrombus
Two Aspects of Hemostasis 1) anticoagulant activity 2) procoagulant activity
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
Procoagulant Activity promotes hemostasis, predominate in damaged blood vessels and hemostasis initiates, a clot forms
Virchow's Triad factors for thrombosis: 1. injuries to vascular endothelium, 2. alterations in normal blood flow, 3. alterations in the constitution of blood
Causes of Abnormal Blood Flow immobility, venous obstruction, varicose veins, atherosclerosis, atrial fibrillation
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
Causes of Changes in Blood Constitution sepsis, chronic inflammation, hormonal changes/therapy, thrombophilia
Most important factor for maintaining normal pro- and anti-coagulant balance endothelial integrity
von Willebrand Factor (vWF) a procoagulant glycoprotein made by undamaged endothelium, binds and prevents the degradation of clotting factor VIII
Cause of Hemostasis Initiation when the balance of anticoagulants and procoagulants is shifted
Three Phases of Hemostasis 1) vascular spasm 2) platelet plug formation 3) coagulation (clotting)
Vascular Spasm (Hemostasis) smooth muscle contracts, causing vasoconstriction: a) pain, b) myogenic reflex, c) endothelins
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
Pain (vascular spasm) activates the sympathetic nervous system, increased sympathetic stimulation causes vasoconstriction
Myogenic Reflex (vascular spasm) direct response of smooth muscle to mechanical stimulation, stretch the muscle or deform it, causing mechanically gated ion channel
Endothelins (vascular spasm) cytokine proteins that constrict blood vessels. trauma to tunics increase endothelin production and shifts balance to vasoconstriction.
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
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
Created by: connorquinby
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