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Lecture 5

Lecture 5.docx

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Michelle French

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Lecture 5  Blood Clotting  hemostasis  Pathology  Asprin  Acetylsalicylic acid used in low dosages (baby asprin) to prevent heart stroke or blood clotting  Von Willebrand Disease  Most often an inherited genetic mutation leading to deficiency of the von Willebrand Factor (vWF)  a multimeric protein that is necessary for platelet adhesion to collagen and binds to Factor VIII in blood to increase its half- life  Most common coagulation disorder (1:100)  Areas with high numbers of capillary are most susceptible  Vasopressin can be administered that is an anti-diuretic hormone and can act on endothelium cells to increase vWF  Factor VIII (Anti-hemophilic Factor)  An essential blood clotting protein (Tissue Factor), also known as anti-hemophiliac factor (AHF)  administered to hemophiliac patients  Factor VIII is produced by the liver and is important in activating Factor X  Hemophilia A is a X-linked coagulation disorder  Tissue Plasminogen Activator (tPA)  A protein involved in the breakdown of blood clot by converting plasmogen into plasmin, the major enzyme involved in clot breakdown, administered to patients having a embolic or thrombolic stroke  tPA must be administered within 3-4 hours following a stroke, helps to break up clot and reduce tissue damage, must ensure stroke not caused by hemorrhage  Warfarin (coumadin)  blocks the action of vitamin K needed in regulated VIII in the blood, an essential Factor leading to activation of Factor X  Platelets are need for blood clotting  Platelets are derivatives from Megakaryocytes that belong to hematopoietic stem cell lineage; platelets are colorless cells with no nucleus, they are filled with granules and cytokines required for clotting  Megakaryocytes are giant cells with multiple copies of DNA in the nucleus  The edge of the megakaryocytes break off to form fragments called platelets which circulate the body  Half-life of platelets = 10 days  Thrombopoietin  stimulates the growth of megakaryocytes leading to increased platelet numbers  Homeostasis  The process of keeping blood within a damaged blood vessel. It involves 3 major steps:  1) Vascular Phase  2) Platelet Phase (platelet plug)  3) Coagulation phase  Too little homeostasis will result in excessive bleeding and too much will result in thrombus excess that can stop blood flow.  How is blood clotting regulated?  1) Vascular Phase  Damage to wall of blood vessel will expose collagen (connective tissue underlying the most inner cell well of vessel), that will lead to vasoconstriction  Vasoconstriction will lead to decreased blood flow and pressure for a temporary period  When a vessel is cut, it will constrict by neurogenic (local neurons) and myogenic (smooth muscle) control. The constriction will be reinforced by factors being secreted around the area because of tissue injury  Serotonin  Endothelin 1  Secreted by endothelial cells lining the blood vessels  Thromboxane A2  Secreted by platelets  2) Platelet Phase  Platelets are necessary for blood clotting as the human body on average only has 5L of blood  Platelets circulating near the damaged vessel will be activated, and start to release cytoplasmic granules that contain serotonin, ADP and thromboxane. ADP will attract more platelets and Thromboxane will support platelet aggregation and vasoconstriction. This cascade will result in aggregation of platelets into loose platelet plug (temporary hemostasis)  Von Willebrand factor  found in the blood, released from endothelial cells and platelets. It cross links collagen and platelets (adhere)  ADP  platelet aggregation  PAF (platelet activation factor)  platelet aggregation  Serotonin  platelet aggregation, vasoconstriction  Thromboxane A2  platelet aggregation, vasoconstriction  Platelet plug is reinforced by fibrin  Fibrin is a fibrous non globular protein involved in blood clotting, made from an inactive form of fibrinogen when converted by thrombin  Platelet Activation  Inactive platelets are small disk like cell fragments
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