This is a sample of our (approximately) 4 page long Haemostasis notes, which we sell as part of the Biochemistry Notes collection, a First package written at Oxford in 2014 that contains (approximately) 216 pages of notes across 33 different documents.
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-Platelets play a central role in haemostasis- process that stops blood loss after blood vessel injury Three components to Haemostasis
-Platelet activation to form a loose plug
-Local vasoconstriction to reduce blood flow to the affected area
-Activation of the coagulation cascade to convert soluable fibrinogen to fibrin strands that form a mesh around the platelet plug and trap other blood cells, to generate a more permanent repair Vasoconstriction
-Damage to the endothelial cells leads to smooth muscle contraction, arterial contraction-lowers downstream blood pressure, key mediateors are serotonin, thrombaxane A2 i) Platelet activation (Platelets are small cytoplasmic fragments of megakaroycytes, life span of 8-10 days in circulation-abundant in blood)
-injured endothelial cells release von Willebrand factor - these attach to the underlying collagen
-Glycoprotein 1B receptor on the platelet membranes bind to von Willebrand factor, other glycoprotein receptors bind to collagen
-This leads to platelet adhesion
-Stimulation of the glycoprotein receptors triggers the platelet activation pathway
-activation of glycoprotein receptor Ib activation of Phospholipase A2, forms arachidonic acid. Cyclo-oxygenase enzyme (inhibited by aspirin) converts arachidonic acid into Thromboxane A2- this is a platelet aggregator and vasoconstrictor
-Thromboxane A2 bind to receptors on the platelet membrane and lead to increase in internal calcium concentrations which leads to platelet activation, through rise in internal calcium concentrations Rise in intracellular calcium:
-Release of granules:
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