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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
– 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.
- Spring '11