Heamostasis
- 1. MODERATOR – DR. ASHISH RAI PRESENTER – DR. SADAF RAHMAN PG 1st YR
- 2. INTRODUCTION HEAMOSTASIS MECHANISM OF HEAMOSTASIS METHOD OF HEAMOSTASIS
- 3. Blood is considered as fluid of life as it carries oxygen and carbondioxide. Fluid of growth as it carries nutritive substance. Fluid of health as it protects body against disease.
- 4. 1. Color- red , arterial blood is scarlet in color and venous blood is purple red 2. Volume- adult (5L), new born (450ml), female(4.5l) 3. Reaction and ph – 7.4 4. Viscosity – 5 times more viscous than water.
- 5. Three types of cells are present in blood- 1. Red blood cells or erythrocytes 2. White blood cells or leukocytes 3. Platelets or thrombocytes
- 6. Ranges- 4-5.5 millon per cu mm of blood Male – 5 millions/cu mm Female – 4.5 millions/ cu mm Lifespan – 120 days It plays vital role in transport of respiratory gases. Red color is due to presence of hemoglobin.
- 7. Transport of oxygen from lungs to the tissue Transport carbondioxide from the tissue to the lungs Buffering action in blood In blood group determination
- 8. Total wbc count- 4,000 – 11,000/cu mm of blood Colorless Plays vital role in defense mechanism of body and protects the body from invading organism by acting like soldiers
- 9. Based on presence or absence of granules Granulocytes 1. Neutrophilis 2. Eosinophilis 3. Basophilis Agranulocytes 1. Monocytes 2. lymphocytes
- 10. Lifespan Neutrophilis – 2-5 days Eosinophilis – 7-12 days Basophilis – 12-15 days Monocytes – 2-5 days Lymphocyte – half to 1 day
- 11. Neutrophilis plays an important role in defense mechanism . First line of defense is against the invading microorganism. Eosinophilis mainly against parasite. Basophilis plays important role in healing Lymphocyte in immunity
- 12. It is also known as thrombocytes. Total count- 150000 – 450000 cc mm of blood Life span- 8-9 days. It helps in formation of blood clot and prevent from bleeding.
- 13. It is a normal physiological process for the prevention and stopping of bleeding/heomorrahge whenever a vessel is ruptured.
- 14. To maintain the blood in fluid state while it remains circulating within vascular system. To maintain the integrity of the vessels wall. To arrest bleeding at the site of injury or blood loss by the formation of haemostatic plug. Eventual removal of plug when healing is complete.
- 18. Endothelial cells produce vasoconstrictors such as angiotensin II and serotonin which help in vasoconstriction. Activated platelets produce thromboxane A2 (TXA2) which is a potent vasoconstrictor
- 19. With in 1-2 sec after injury to blood vessel, hemostatic process begins & proceed as 1. platelet adhesion 2. platelets activation 3. platelets release reaction 4. platelets aggregation
- 20. Platelets attach to non-platelet surfaces, such as collagen fibers in the subendothelium. Platelets move from the blood vessels and into the tissues. Exposure to surfaces in the tissues causes them to bind to collagen with the presence of von Willebrand factor ( vWF) and Glycoprotein IbIX, making a bridge formation. Binding via GpI b initiates activation of platelet.
- 21. The adhesion of platelets to the vessel wall activates them. Platelets undergo a shape change from disc to tiny sphere with projecting pseudopodes. Activation required for hemostatic plug formation. Activators released or synthesized at the site of injury
- 22. Immediately after adhesion & activation process of release reaction or secretion begins. In this process content of platelets organelles are released to the exterior.
- 23. Secretion of α granules a) Fibrinogen b) Factor V c) Fibronectin d) PDGF
- 24. Secretion of dense granules: ADP, GTP, GDP Calcium, serotonin Histamin, epinephrin
- 25. Process by which platelets interact with one another to form a hemostatic plug. Chemical changes cause platelets to aggregate and stick to one another GPIIb-IIIa complex binds vWF, undergoes Ca++dependent structural change, then acts as receptor for fibrinogen Fibrinogen activated platelets serve as a bridge between two platelets .
- 26. Clot develops in 15 -20s if trauma is severe. 1-2 mints if trauma has been minor. If vessel opening is not too large it fills within 3-6 mints.
- 27. Once blood clot is formed it follows two courses 1. It can become invaded by fibroblast, which forms connective tissue all through the clot. 2. It can dissolve 3. The usual course for clot that forms in a small hole of a vessel wall is invasion by fibroblast, within few hours after the clot is formed. This continues to complete organization of the clot into fibrous tissue within about 1-2 weeks.
- 28. Procoagulant that promote coagulation, anticoagulant that inhibit coagulation Blood coagulation depends upon these two group Clotting takes place in three steps 1. In response to rupture of the vessel or damage to the blood itself 2. Prothrombin activator catalyse the conversion of prothrombin into thrombin. 3. Thrombin acts as a enzyme to convert fibrinogen into fibrin fibers that enmesh the platelets, blood cell and plasma to form clot.
- 30. First physiological response to vascular injury, which is mediated by platelets, in order to arrest bleeding Mechanism: Activation of platelets via stimulators such as thrombin Adhesion of platelets to subendothelium via interaction between GPIb and von Willebrand Factor (VWF) Release of platelet granule products in order to recruit more platelets to the injured site Aggregation of platelets via interaction between GPIIb/IIIa (aIIb3) and fibrinogen to form the initial plug. Triggers secondary hemostasis (coagulation proteins)
- 31. Process of blood coagulation Mechanism: Coagulation proteins work in concern to generate thrombin Thrombin converts fibrinogen to fibrin Fibrin consolidates the platelet plug made in primary hemostasis such that a thrombus (secondary hemostatic plug) is formed Prevents further blood loss from the injury site
- 34. Calcium ions are required for promotion or acceleration of all the blood clotting reactions. Therefore in the absence of calcium ions, blood clotting by either pathway does not occur When blood is removed from a person, it can be prevented from clotting by reducing the calcium ion concentration below the threshold level for clotting.
- 35. Fibrinolysis is due to action of proteolytic enzyme fibrinolysis or plasmin. It is present in inactive plasminogen which gets converted to plasmin by action of thrombin and tissue plasminogen activator. Plasmin lyses fibrin and fibrinogen with the production of fibrinogen degradation product that inhibit thrombin
- 36. Procedural Factors Type of procedure Patient position Surgical incisions Exposed bone (eg, spinal reconstructive procedures) Large surfaces of exposed capillaries Unseen sources of bleeding • Tissues that cannot be sutured or low-pressure suture lines Adhesions stripped during surgery
- 37. Patient Factors Specific anatomical considerations Medications (eg, anticoagulants) Coagulopathies Platelet dysfunction or deficiency Fibrinolytic activity Coagulation factor deficiencies Medical conditions Nutritional status
- 38. 1. Mechanical methods Direct pressure Fabric pads/gauze sponges/sponges Sutures/staples/ligating clips
- 39. Electrosurgery Monopolar Bipolar Bipolar vessel sealing device Argon enhanced coagulation Ultrasonic device Laser
- 40. Pharmacological agents Topical hemostatic agents Epinephrine Vitamin K Protamine Desmopressin Lysine analogues (eg, aminocaproic acid, tranexamic acid)
- 41. 1. Passive (ie, mechanical) agents Collagen-based products Cellulose Gelatin Polysaccharide spheres
- 42. 2. Active agents Thrombin products 3. Flowables 4. Sealants Fibrin sealants Polyethylene glycol (PEG) polymers Albumin and glutaraldehyde Cyanoacrylate
- 43. 1. Bleeding time Time from onset of bleeding to stoppage of bleeding (1-5 min) 2. Clotting time Time from the onset of bleeding till the clot formation (2-8 min) 3. Prothrombin time Time required for coagulation to take place (12-16 s)
- 44. 4. Appt (activated partial thromboplastin time) 5. Factor assay 6. D-Dimer
- 45. 1. Haemophilia It is also known as haemophilia A Sex linked inherited disorder Males It involves total lack of factor 8 activity. The level of coagulation factor 8 in blood may be less than 1% of normal individual. cryoprecipitate Fresh blood or fresh frozen plasma
- 46. 2. Christmas disease It is also known as haemophilia B Deficiency of factor 9 Cryoprecipitate Fresh frozen plasma
- 47. 3. Von willebrands disease Low plasma level of factor 8 Platelet abnormlities Bizarre episodic bleeding Bleeding more from mucous membrane than from the mucoskeletal system