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Organisation of the Body

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Question
Answer
Physiological challenges   Do not harm when all is normal - do not obstruct Automatically seal vascular punctures Prevent loss of blood Recruit healing helpers Resolve when healed  
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Stages of hemostasis   Vascular spasm in response to injury Primary - platelet plug formation Secondary - blood clotting (coagulation) Removing clots (fibrinolysis)  
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Arteriolar vasoconstriction   Damaged endothelium initiates sympathetic reflex (noradrenaline and neuropeptides) releases endothelin-1, a vasoconstrictor Arteriolar smooth muscle contraction restricts flow  
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The platelet   Small cytoplasmic fragments of megakaryocytes Life span of 8-10 days Abundant in blood Packed with granules  
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Platelet aggregation reaction   Adhesion to vessel wall - platelet GPIa/IIa binds collagen and GPIIb/IIIa binds fibronectin Activating platelet changes shape releasing granule contents Aggregation of platelets Release of ADP and TxA2 GPIb binds vWF to induce further aggregation  
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Platelet granule functions   Further activation Leukocyte recruitment Endothelial repair Secondary hemostasis Further aggregation Defence protein  
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Thrombopoiesis   TPO produced by liver and kidneys acts at every stage HSC - MPP - CMP - EMk - MkP All have CD110 receptors Negative feedback - platelets internalise TPO to reduce production  
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Platelet disorders   Hereditary thrombocytopenia Small platelets e.g. Wiskott-Aldrich syndrome Large platelets e.g. Bernard-Soulier syndrome Extreme folate/Vit B12 deficiency Infections Drugs Autoimmunity  
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The coagulation cascade   Signal amplification by a series of protease reactions Initiated by exposed charged surface and release of tissue factor and phospholipid from endothelium Generates insoluble fibrin mesh Regulated  
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Fibrinogen   Present in plasma at high concentrations High molecular weight Made in the liver 6 polypeptides - 2 alpha, 2 beta and 2 gamma Fibrinopeptides cleaved by thrombin to allow aggregation  
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Fibrin polymerization   Thrombin cleaves fibrinopeptides in fibrinogen Exposed regions spontaneously aggregate Meshwork traps platelets, rbc etc to stabilise plug Further crosslinking GLN-LYS by factor XIIIa to form gamma dimers  
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Vitamin K dependent zymogens   Signal peptide Gla domain - gamma carboxylated glutamate Kringle domains for regulation - cleaved off by prothrombinase Catalytic domain - serine protease  
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Vitamin K deficiency   Needed for gamma carboxyglutamate Gla residues bind 7 calciums to orientate hydrophobic residues into the membrane Epoxide reductase needed for VitK reduction inhibited by warfarin  
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The common pathway   Prothrombin Activated by FXa Also by FVa Requires phospholipid Restricts reaction to surface of activated platelets Serine protease that activates factors I V VIII XI XIII  
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Inhibitors of clotting   Endothelial glycosaminoglycans e.g. heparan sulphate Activated Protein C Thrombomodulin EPI Anti thrombin III  
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Antithrombin III   A serine protease inhibitor encoded in the human genome Also alpha 1 anti trypsin, Complement C1q inhibitor, PLA-1 ATIII-thrombin interaction enhanced 1000 fold by hepSO4 GAG and heparin  
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Haemophilia   X linked Often a recent mutation due to elderly spermatogenesis Cannot produce tenase complex Treated with clotting factors May be able to recombinantly produce these from DNA clones in mammalian cells  
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Fibrinolysis   Breakdown clots - used in treatment of clotting e.g. in strokes Plasminogen broken down to plasmin which is a serine protease - converts fibrin to fibrin degradation products  
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