پاورپوینت کامل Hemostasis 64 اسلاید در PowerPoint

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پاورپوینت کامل Hemostasis 64 اسلاید در PowerPoint

اسلاید ۴: Local vasoconstrictionis due to local spasm of the smooth muscle (symp. reflex)can be maintained by platelet vasoconstrictors

اسلاید ۵: Formation of platelet aggregateInjured blood vessel releases ADP, which attracts platelets (PLT)PLT comming in contact with exposed collagen release: serotonin, ADP, TXA2, which accelerate vasoconstriction and causes PLT to swell and become more sticky

اسلاید ۶: The micrograph shows activated platelets adhering to some damaged cells

اسلاید ۷: Formation of blood clotIn the formation of the clot, an enzyme called thrombin converts fibrinogen into insoluble protein, fibrin Fibrin aggregates to form a meshlike network at the site of vascular damage

اسلاید ۸: The intrinsic system is more complex and present only in „higher” life forms (e.g. birds and reptiles possess only extrinsic system) The complex sequence of events that produce fibrin are divided into three stagesCoagulation mechanism is composed of an extrinsic and intrinsic pathway, which eventually merge into one

اسلاید ۹: Extrinsic pathway:1. When blood comes in contact with injured tissue – tissue thromboplastin (F III) interacts with proconvertin (F VII), and Ca2+ activating Stuart factor (F X).Stage I: Formation of prothrombin activatorCa2+Stuart factorAnti- hemophilic factorChristmas factor

اسلاید ۱۰: Intrinsic pathway:2. Exposed collagen activates Hageman factor (F XII). Activated F XII activates plasma enzyme – plasma thromboplastin antecedent (PTA; F XI, which in the presence of Ca 2+ activates Christmas factor (F IX). F IX interacts with antihemophilic factor (F VIII), Ca 2+ to form a complex that activates Stuart factor (F X).Stage I: Formation of prothrombin activatorCa2+Christmas factorAnti- hemophilic factorStuart factor

اسلاید ۱۱: Stage I: Formation of prothrombin activator3. Common pathway:Activated F X in the presence of Ca 2+ forms complexes with accelerin (F V) to form prothrombin activatorCa2+Christmas factorAnti- hemophilic factorStuart factor

اسلاید ۱۲:

اسلاید ۱۳: Stage II: conversion of prothrombin to thrombinProthrombin – inactive precursor of enzyme thrombinIn the presence of prothrombin activator and Ca2+ prothrombin is converted to thrombinThrombin itself increases its own rate of formation (positive feedback mechanism)Ca2+

اسلاید ۱۴: Stage III: conversion of fibrinogen to fibrinFibrinogen – plasma protein produced by the liverThrombin converts fibrinogen to fibrinThrombin also activates fibrin-stabilizing factor (F XIII), which in the presence of Ca2+, stabilizes the fibrin polymer through covalent bonding of fibrin monomersfibrin-stabilizing factor

اسلاید ۱۵: Calcium ionsAre required for promotion and acceleration of almost all blood clotting reactionsExcept: activation of XII and XI (intrinsic mechanism)Ca2+http://w/biosci/esp/2002_general/Esp/folder_structure/tr/m1/s7/trm1s7_3.htm

اسلاید ۱۶: Ca2+Ca2+Christmas factorAnti- hemophilic factorStuart factorFibrin-stabilizing factor

اسلاید ۱۷:

اسلاید ۱۸: Fibrinolysis

اسلاید ۱۹: Clot DissolutionPlasmin is formed from plasminogen – enzyme called activator (e.g. enzymes from urine, tears, saliva or bacterial enzyme streptokinase)Plasmin as an enzyme is involved in breaking down fibrin into soluble fragments (fibrinolysis) Plasminogen Plasmin Activator (e.g. t-PA)Fibrin soluble fragmentsPlasminogen may be produced by eosinophils

اسلاید ۲۰:

اسلاید ۲۱: AnticoagulantsHirudo medicinalis produce Hirudin that inhibits Thrombin

اسلاید ۲۲: AnticoagulantsAlthough tissue breakdown and platelets destruction are normal events in the absence of trauma, intravascular clotting does not usually occur because:the amounts of procoagulants released are very smallnatural anticoagulants are present (Antithrombin III, Heparin, Antithromboplastin, Protein C and S, fibrin fibers)

اسلاید ۲۳: Natural anticoagulantsAntithrombin III – inhibits factor X and thrombin Heparin from basophils and mast cells potentiates effects of antithrombin III (together they inhibit IX, X, XI, XII and thrombin)Antithromboplastin (inhibits „tissue factors” – tissue thromboplastins)Protein C and S – activated by thrombin; degrade factor Va and VIIIa

اسلاید ۲۴: Abnormalities of hemostasis

اسلاید ۲۵: ThrombocytopeniaSevere reduction in the number of PLTs – thrombocytopeniathis causes spontaneous bleeding as a reaction to minor traumain the skin – reddish-purple blotchy rashit may result from:decreased production (toxins, radiation, infection, leukemias)increased destruction (autoimmune processes)increased PLTs consumption (DIC)Hemorrhagic spots (petechiae)

اسلاید ۲۶: ThrombocytopeniaLethal when PLTs<10G/LBleeding occurs when PLTs<50G/LNorm: 150-400G/L

اسلاید ۲۷: Hepatic failureMost of the clotting factors are formed in the liverSubconjunctival hemorrhage

اسلاید ۲۸: Disseminated intravascular coagulation (DIC)Widespread coagulation thrombosis in small blood vessels increased fibrinolysis, and depletion of coagulating factors generalized bleedingIt may result from:bacterial infections (endothelial damage)disseminated cancers (release of procoagulants)complications of pregnancysevere catabolic statesDisseminated cervical cancer metastases (PET imaging)

اسلاید ۲۹: Hemophilia A (lack of F VIII) and B (lack of F IX) are transmitted genetically and affect only males. Females carry the gen but do not show symptoms.Von Willebrand’s disease – loss of large component of fVIII

اسلاید ۳۰: Hemophilia A (lack of F VIII; 85%)Spontaneous or traumatic subcutaneous bleedingBlood in the urineBleeding in the mouth, lips, tongueBleeding to the joints, CNS, gastrointestinal tractMild hemophilia after injection in buttock

اسلاید ۳۱: Son of the last Tsar of Russia – Aleksy Romanow suffered from Hemophilia A

اسلاید ۳۲: Tests of coagulation

اسلاید ۳۳: “Intrinsic” and “extrinsic” coagulation pathwaysN: 9.9 – ۱۳ secActivated Partial Thromboplastin TimeN: 25-35 sec Prothrombin Time

اسلاید ۳۴: Prothrombin time (PT) test – norm 11 -15 sec evaluates extrinsic system (VII, X, V, II, fibrinogen)prolonged PT indicates a deficiency in any of factors VII, X, V, prothrombin (factor II), or fibrinogen (factor I). Prolonged PT:- a vitamin K deficiency (vitamin K is a co-factor in the