Fibrinolysis

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  • 1. Prepared By : Muhammad Halmii (016-3626470) TEAM GENESIS
  • 2.  DEFINE  CAUSE (-)  DISEASE PROCESS (PATHOGENESIS) (X)  TYPES (X)  EFFECT (- )  CLINICAL MENIFESTATIONS (SIGNS & SYMPTOMS) TEAM GENESIS
  • 3. Blood Clot: A thickened mass in the blood formed by tiny substances called platelets. Clots form to stop bleeding preventing excessive blood loss Fibronolysis: (Lysis Of Fibrin) Fibrinolysis is a process that prevents blood clots from growing and becoming pathologic BOTH PROCESS ARE STEPS OF WOUND HEALING & PHYSIOLOGICAL TEAM GENESIS
  • 4. Anticoagulant Coagulant Eg: Heparin, Antithrombin Eg: Fibrin Thrombin Excessive:Hemophilia Excessive:Thrombosis TEAM GENESIS
  • 5. Haemostasis Inflammation GranulationRemodelling / Maturation Proliferative Angiogenesis Overlaps Blood Clot Fibrinolysis TEAM GENESIS
  • 6. TEAM GENESIS
  • 7. Local Response : Release Thromboxane Systemic Response : Adrenal Medulla Regulates Hormones (i.e epinephrine & norepinephrine) Stimulates Cross Bridge Of Smooth Muscle Cell {i.e. contraction} Exposes Large area of collagen surface to BV & Limits Blood Loss Initiates Platelet Activation TEAM GENESIS
  • 8. Primary Secondary TEAM GENESIS
  • 9.  Made In Bone Marrow From The Megakaryocytes’ Cytoplasm  Not A Cell  Below Normal Count = Thrombocytopenia  High Normal Count = Thrombisis  F(x) = Hemostatic Plug etc.  Binding Site = Between Platelets , VWFTEAM GENESIS
  • 10.  Immediate Initiation (20 sec) & Immediate Completion (Few Minutes)  Platelets Undergo Conformational Shape Change To Enhance Clot  Main Components : Platelets 100%  Moderately Stable TEAM GENESIS
  • 11.  Platelet adhesion: First event in hemostasis is the adhesion of platelets to exposed subendothelium. mediated by von Willebrand factor (vWf), which binds to glycoprotein Ib.  Platelet activation:The adhesion of platelets to the vessel wall activates them, causing the platelets to change shape & activates the receptor glycoprotein IIb/IIIa. Upon activation, platelets synthesize and release thromboxane A2 (TXA2) and platelet activating factor (PAF), which are potent platelet aggregating agonists and vasoconstrictors. {POSITIVE FEEDBACK}  PRIMARY HEMOSTASIS TEAM GENESIS
  • 12.  Synthesized At Gene No. 12  F(x) = Grips Platelets At Glycoprotein Ib To Stabilize Clot TEAM GENESIS
  • 13.  Converts Fibrinogen To Fibrin  Activates Factor 13 (Hardening Of )  Generates Procoagulant Activity  Activates (Protein C) Fibrinolysis After A While TEAM GENESIS
  • 14.  Involves Both Intrinsic (Inside BV) & Extrinsic (Outside BV) Activity To Generate Thrombin Which Ultimately Generates Fibrin  Happens After Primary Hemostasis  Extrinsic Initiate But Produces Little Fibrin While Intrinsic Amplifies Action  INtrinsic  Twelve  Eleven  Nina  Eight  Ten 12 11 9 8 10 5 7 TEAM GENESIS
  • 15.  Initiation of coagulation: The coagulation cascade is initiated by the extrinsic pathway with the generation/exposure of tissue factor. Tissue factor then binds to factor VII and this complex activates factor X. Factor X, in the presence of factor V, calcium and platelet phospholipid ("prothrombinase complex") then activate prothrombin to thrombin. This pathway is rapidly inhibited by a lipoprotein-associated molecule, called tissue factor pathway inhibitor. However, the small amount of thrombin generated by this pathway (before inhibition) activates factor XI of the intrinsic pathway, which amplifies the coagulation cascade.  Amplification of coagulation: The coagulation cascade is amplified by the small amounts of thrombin generated by the extrinsic pathway. This thrombin activates the intrinsic pathway by activation of factors TENET. generating large amounts of thrombin. Thrombin, in turn, then cleaves fibrinogen to form soluble fibrin monomers, which then spontaneously polymerize to form the soluble fibrin polymer. Thrombin also activates factor XIII, which, together with calcium, serves to crosslink and stabilize the soluble fibrin polymer, forming cross linked (insoluble) fibrin. TEAM GENESIS
  • 16. TEAM GENESIS
  • 17.  Clot Would Be Dangerous If It Were To Expand Beyond Boundary Thus They Are Inhibited By: Clotting Factors Are Rapidly Inhibited At Other Places (Enzymes In Blood Inactivate Clotting Factors) End Product Inhibition Of Fibrin (The Higher Fibrin, The Higher The Intensity Of Thrombin Inhibition) TEAM GENESIS
  • 18.  Activated Protein C & Protein S  Tissue Factor Inhibitor  Anti-Thrombin  Heparin Cofactor II GO AND READ YRSELF  In Short, They Prevent Unnecessary Clotting At Unwounded Areas PREVENTS CLOT FORMATION BUT DOES NOT DESTROYS THE CLOT !!!!! TAKE NOTE TEAM GENESIS
  • 19.  The Clot Stimulates Tissue Plasmin Activator  TPA Converts Plasminogen To Plasmin  Plasminogen Is Found In Blood  Clot Removal Happens At A Slow Pace To Enable Endothelial To Divide For Healing TEAM GENESIS
  • 20.  Destroys Fibrinogen & Fibrin  Produces D-Dimer TEAM GENESIS
  • 21.  Reaction Time Is Delayed  Prolonged Clotting Time  Increase Blood Loss TEAM GENESIS
  • 22.  Vascular Disorder  Scurvy (Scurvy is a disease resulting from a deficiency of vitamin C, which is required for the synthesis of collagen in humans.)  Bruising Vulneribility (Lack Of Endothelial Integrity)  Platelets Disorder  Thrombocytopenia (Platelet count below 50,000 per microlitre.)  Platelets Dysfunction (Platelets Lacking Of Receptors)  Coagulation Disorder  Hemophilia (Lacking Of Intrinsic Factors) TEAM GENESIS
  • 23.  Blood Count  Bleeding Time (Diagnose Thrombocytopenia)  Prothrombin Time (Measure Extrinsic Factor) PT Excellent  Activated Partial Thromboplastin Time (Intrinsic & Common)  Thrombin Time (Tome For Fibrinogen To Fibrin Formation)  Mixing Test (Detect Factor Dificiency) TEAM GENESIS