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Lecture 2

WEEK 2- Cardiovascular System Continued.pdf

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Humber College
BIOL 271

Blood (Continued from Cardiovascular System) Hemostasis: stoppage of bleeding when blood vessels are damaged must be quick, localized and carefully controlled three mechanisms: vascular spasm platelet plug formation coagulation (clotting) Vascular Spasm damage to arteries or arterioles —> immediate contraction of smooth muscle in vessel wall reduces blood loss for several minutes to several hours allows time for other hemostatic mechanisms to proceed Platelet Plug Formation 3 step process: platelet adhesion platelet release reaction platelet aggregation Platelet Adhesion platelets stick to collagen exposed when endothelium is damaged Platelet Release Reaction adhered platelets extend projections, contact other platelets and degranulate (release of clotting factors) thromboxane A2, ADP and serotonin released —> constriction of injured vessel, activation of other platelets Platelet Aggregation ADP activates more platelets that become sticky and form a platelet plug plug reinforced by fibrin threads formed during clotting process Blood Clotting blood normally remains liquid within vessels but thickens to a gel when removed gel separates into: serum (straw-coloured liquid) plasma minus clotting factors (they are used in the clot) clot (gel) cells trapped in a network of insoluble protein fibres (fibrin) Clotting Factors: chemicals required for clot formation (coagulation) include: inactive enzymes synthesized by liver cells molecules released by platelets or damaged tissues Clotting Cascade cascade of reactions that results in the formation of fibrin threads **prothrombinase (prothrombin activator) >requires Ca2> prothrombin >> thrombin >> fibrinogen >> fibrin fibrin is the substance that forms the clot **know slide (see diagram) prothrombinase formation is initiated by either or both of: intrinsic pathway activated by: damage to blood itself exposure of blood to collagen in traumatized vessel wall damaged platelets release phospholipids reaction requires several mins extrinsic pathway activated by chemicals from damaged tissue activated when thromboplastin (tissue factor from injured cells) leaks into bloodstream occurs rapidly (w/in secs) common pathway (after reaching prothrombinase, only 1 pathway) in the presence of Ca2+: prothrombinase converts prothrombin to thrombin thrombin converts soluble fibrinogen to insoluble fibrin, and activates factor XIII factor XIII (fibrin stabilizing factor) strengthens and stabilizes fibrin threads into a sturdy clot positive feedback effects of thrombin: accelerates formation of prothrombinase activates platelets >> increases platelet aggregation and phospholipid production Clot Retraction and Blood Vessel Repair requires adequate platelet count platelets pull on fibrin threads (retraction), drawing edges of damaged vessel closer together serum can still escape, but blood cells cannot clot eventually replaced by new endothelium (quick mitosis) and scar tissue produced by fibroblasts Role of Vitamin K fat-soluble vitamin (absorption dependent on lipid absorption) produced by bacteria in large intestine (waste product of bacteria) required for normal clotting not involved in clot formation, but required for synthesis of several clotting factors (haemophilia) Hemostatic Control Mechanisms fibrinolysis= dissolution of a clot fibrinolytic system dissolves small, intravascular clots and clots at a site of a completed repair plasminogen in the clot is converted to plasmin (fibrinolysin) which digests fibrin threads and inactivates several clotting factors clot formation remains localized because fibrin absorbs thrombin, and blood disperses clotting factors prostacyclin (produced by endothelial cells and WBCs) opposes platelet adhesion and release anticoagulants (ex: heparin, antithrombin) block or inactivate various clotting factors Intravascular Clotting thrombosis clot (thrombus) formation in an unbroken blood vessel due to: roughened endothelium (trauma, infection, atherosclerosis) stasis (decreased blood flow) causes local buildup of clotting factors thrombus may dissolve spontaneously or dislodge >> a thromboembolus (moving thrombus) venous emboli may cause pulmonary embolism arterial embo
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