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Hamostasis and blood coagulation


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Hamostasis and blood coagulation

  1. 1. Prof. M.C. Bansal MBBS ., MS., MICOG . , FICOG.Fonder principal & Control, Jhalwar Medical College & Hospital Jhalawar Ex principal & Controller MGMC & Hospital Sitapura ., Jaipur.
  2. 2. intra vascular coagulation is linked with three different interrelated systems.1. Coagulation System .2. Coagulation Inhibitory System .3. Fibrinolytic System .
  3. 3.  Hemostasis means prevention of blood loss after blood vessel is severed or ruptured. It is achieved by a complex mechanism . 1, Vascular constriction. 2, Formation of Platelet plug . 3, Clot formation by coagulation process switched on by trauma, 4, Eventual fibrosis in clot closed to the hole in blood vessel.
  4. 4.  It is brought about by -- a. Local auto acid factor released from traumatized tissue ., b. spontaneous and its own Spasm of myofibrils of blood vessel. c . Nervous reflex ---traumatized sensory nerve endings convey to higher center and efferent nerves carry action orders to myofibrils . d. Thromboxane A produced by Platelets .
  5. 5.  Small holes are immediately closed by platelet plugs. Platelet Cytoplasm has many active factors like Actin, myocine molecules , thromboplastin , Adenoplasmin Reticulum , Golgi apparatus ( synthesize Various enzymes and store Ca ++ ), Mitochondria and enzyme system capable to produce ATP, ADP , Prostgandins , fibrin stabilizing factor and growth factor. Growth factor growth of and repair of vascular endothelium myofibrils and fibroblasts needed for blood vessel repair. Platelet membrane is coated with glycoprotein which prevent their adherence to healthy endothelium .but once endothelium is damaged the platelets quickly and abundantly adhere to damaged endothelium and exposed collegen fibers in the vessel wall there by plugging the hole / defect. Platelet membrane also contain phospholipids.
  6. 6. It starts to develop with in 15-20 seconds of injury to blood vessel . clotting process activating substances are released from traumatized tissue , vascular endothelium, platelets and plasma proteins.If vascular hole is small , it is plugged with in 2-3 minutes but in case of large defect it may take 20 minutes to 1 hour .The clot formed in damaged followed by repaired site retracts and further closes the vessel.Platelets also play an important role in clot retraction .
  7. 7.  Once the clot is formed , blood vessel defect is repaired the clot is invaded by fibroblasts ( promoted by Growth factor produced by platelets ) . This continues till complete organization of clot in to fibrous tissue is completed with in 1-2 weeks . Extra vagated blood is also clotted similarly and is dissolved by fibrinolysis activity.
  8. 8.  The smoothness of vascular endothelium prevents platelet adhesion and contact activation of intrinsic clotting cascade. A layer of Glycocalyx on endothelium repels platelets and intrinsic factor to contact . Protein bound to endothelium called Trombomodulin binds with Thrombin and slows the process of clotting and their complex molecule “ Thrombomodulin-thrombin “ activates protein C ., inhibits factor V and VIII.
  9. 9.  In damaged / rough endothelium –Glycocalyx and Thrombomodulin is lost hence both factor XII, platelet adhesion and intrinsic factor initiate the clotting cascade . Anti Coagulants are also present in blood itself ----They remove thrombin from the blood. 1 Fibrin fibers . 2 Alpha globulin also called antithrombin III or antithrombin Co factor. This prevents excessive clot formation . 3 free Thrombin combines with fibrin fibers and anti thrombin III , so free thrombin is no more available to fibrinogen to form fibrin clot.Heparin –secreted by mast cells , its physiological role is limited and insignificant , but pharmacological use is very common in clotting disorders in clinical practice.
  10. 10.  Plasma proteins contain euglobin called Plasminogen when activated changes into Plasmin ( Fibrinlysin ) . It is proteolytic like trypsin enzyme . It digests fibrin fibers , fibrinogen , factor V , VIII , IX and prothrombin , causing dissolution of clot . After few days of trauma when bleeding is stopped , repair work / healing process starts Endothelium librates a powerful activator called tissue plasminogen activator (t-PA ) , which converts plasminogen in to plasmin to remove the undesired clot to facilited neo vascularisation and patency of blood vessel necessary for tissue perfusion .
  11. 11. Test Value Bleeding Time – Duke’s Method 1-3 Mins Ivy’s Method 1-9 MinsCoagulation Time- Wright’s Tube Method 3-7 Mins Lee & White’s Methods 4-9 Mins Clot Observation Test (Weiner’s) 6-12 Mins Clot Retraction Time 30 Mins Fibrindex Or Thrombin Test Formation Of A Clot In 1 Min Prothrombin Time 11-17 Mins Thrombin Time 10-15 Secs Platelet Count 1.5-4 Lacs/Cumm Fibrin Degeneration Products 0-5 Micro G/Ml Euglobin Clot Lysis Time 2-4 Hours Fibrinogren 300-600 Mg% D-dimer 0-200 Mg/Ml
  12. 12. Test Method Of Collection Of Amount Of Blood Blood In Test Tube / Vial Hb% Or PCV EDTA Vial 2 Ml ABO & Rh Group Plain (Clotted) And 3.8% 2 Ml & Few Drops Sodium Citrate Solution Vdrl Plain (Clotted) 2mlDirect / Indirect Coomb’s Plain (Clotted) 2ml Test Prothrombin Time 0.5 Ml Of 3.8 % Sodium 4.5 Ml Citrate Solution Fibrinogen EDTA Vial 2ml Platelet EDTA Vial 2ml Edp Special Tubes Supplied With Kits Eclt Citrate Solution 4.5 Ml D-dimer EDTA Vial 2 Ml
  13. 13.  Deficiency of one / more blood clotting factors . Vit. K . Deficiency . Hemophillia . Thrombocytopenia. Liver disease ==not able to produce clotting factors . DIC
  14. 14.  Abnormal that develops in blood vessel being loosely attached may get detached and flow in circulation –get lodged at distance is called Embolus ( in pulmonary or aortic circulation - --chocks the end arteries).the affected area / organ does not get O2 resulting in Acute Ischemia and infarction .
  15. 15.  Roughened breeched endothelium in blood vessels ---arteriosclerosis , atheroscerosis , infection , traumatic . Blood flow is very slow or stagnant . Intra venous therapy cannulatios left in situ for a longer time , trombophlebitis . Intravenous thrombosis ----Central sinus vein , deep veins of calf and pelvis . Intramural thrombus in heart chambers . Its incidences increases in pregnancy , puerperium LSCS ( hyper coagulability state of pregnancy , tissue trauma, inflammation , dehydration , prolong bed rest ) , pelvic surgery