Dicumarol inhibition of vit k dependent factors

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Unformatted text preview: onents in blood & trauma to blood or exposure to collagen (or foreign surface) To trigger clot fiber net that traps RBCs PGG2 - PGH2 = plug PG12 - no plug (bleed) Anticoagulants vs Lysis of clots •  Anticoagulants –  prevents clots from forming •  chelators-tye up calcium (citrate, oxylate) •  heparin- complexes with Antithrobin III •  dicumarol-inhibition of Vit. K dependent factors –  factors II, VII, IX, X (synthesized by hepatocytes Activators of Plasminogen •  Endogenous Activators –  tissues –  plasma –  urine •  Exogenous Activators –  streptokinase –  tPA (tissue plasminogen activator) TPA - used to clear clots immediately after strokes •  Lysis of Clots –  Plasmin (from plasminogen) Plasmin breaks down fibrin into fibrin split Aspirin & Ibuprofen •  Block both thromboxane A2 & prostacyclin production by blocking fatty acid cyclooxygenase which converts arachidonic acid to PGG2 & PGH2 (intermediates) •  Why take aspirin to prevent heart attacks? Because it prevents clotting Reperfusion injury •  Most of the frank tissue damage associated with infarction occurs upon reperfusion •  associated with the formation of highly reactive oxygen species with unpaired electrons. free radicals •  When pressure on tissues relieved & again perfused with blood, free radicals are generated (this when frank damage occurs) Free radicals - rip electrons from tissue to become stratified Reperfusion of tissue causes damage - not ischemia of it bc of production of ROS 3 Collateralization •  The ability to open up alternate routes of blood flow to compensate for a blocked vessel –  Angiogenesis Ability to form new vessels –  Vasodilatation Enlarging blood vessels –  Role of the SNS ?? •  May impede Cx of bv •  May augment Neuropeptide Y Protective mechanism Blood Coagulation- Thrombosis •  Extrinsic mechanism-initiated by chemical factors released by damaged tissues •  Intrinsic mechanism-requires only components in blood & trauma to blood or exposure to collagen (or foreign surface) Clotting factors •  •  •  •  •  •  •  I- fibrinogen II- Prothrombin III- Thromboplastin IV- Calcium V- Proaccelerin VII- Serum prothombin conversion acclerator VIII- antihemophilic factor (A) Clotting factors (cont.) •  IX- antihemophilic factor B christmas factor •  X- Stuart factor •  XI- antihemophilic factor C •  XII- Hageman factor •  XIII- Fibrin-stabilizing factor •  Prekallikrein- Fletcher factor •  High molecular weight kininogen •  Platelets Sex linked on x chromosome Hepatocytes role in clotting •  Liver synthesizes 5 clotting factors –  I (fibrinogen) –  II (prothrombin) –  VII (SPCA) –  IX (AHF B) –  X (Stuart factor) Hemophilia •  Sex linked on X chromosome –  occurs almost exclusively in males –  85% of cases- defect in factor VIII –  15% of cases- defect in factor IX •  varying degree of severity from mild ⇒ severe <5% - defect i n factor XI •  Coumarin (warfarin or cumadin) depresses liver formation of II, VII, IX, X by blocking action of vitamin K 4 Ca required for steps 3- the end Blood Coagulation •  The key step is the conversion of fibrinogen to fibrin which requires thrombin »  thrombin Intrinsic pathway •  Factor XII activated when blood contacts a negatively charged surface (collagen, glass) •  Activated XII + Kalikrein+ Kinnogen will activate Factor XI •  Activated XI + Ca++ will activate both Factors IX & VIII •  Activated IX + VIII + Phospholipid + Ca++ will activate Factors X & V •  Activated X + V + Pho...
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This note was uploaded on 05/03/2011 for the course PHYS 339 taught by Professor Free during the Spring '11 term at Palmer Chiropractic.

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