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Platelets physiology
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Platelets physiology


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  • 1. Hemostasis Definition: Prevention of blood loss.
  • 2. Events Involved In Hemostasis
  • 3.
    • Whenever a vessel is ruptured, hemostasis is achieved by:
    • Vascular constriction
    • Formation of a platelet plug
    • Formation of a blood clot as a result of blood coagulation.
    • Eventual growth of fibrous tissue into the blood clot to close the hole in the vessel permanently.
  • 4. Vascular Constriction
  • 5.
    • In ruptured blood vessel
    • 1. Pain impulses from the site of trauma as well as from the surrounding nervous tissue originate and reach the spinal cord.
    • From the spinal cord order signal arise.
  • 6.
    • The order signals pass through the sympathatic nerves
    • Lead to spasm of the vessel .
    • 2. Local muscle also contribute to the vascular vasospasm.
    • 3. local autacoid factors from the traumatized tissues and blood platelets.
  • 7.
    • As the vessel wall is damaged the action potential developed along the vessel wall lead to vasoconstriction.
    • The vasospasm lasts for almost half an hour and it is directly proportional to the intensity of trauma .
  • 8.
    • Vasoconstriction resulting from local myogenic contraction of the blood vessels is initiated by direct damage to the vascular wall.
    • In the smaller vessels , the platelets are responsible for much of the vasoconstriction by releasing a vasoconstrictor substance , thromboxane A 2 .
  • 9. Formation of the Platelet Plug
  • 10. Platelets
  • 11.
    • Platelets or thrombocytes are small colorless , non nucleated cells.
    • Shape is spherical or rod shaped and become oval or disc shaped when inactivated.
    • Size: 1 to 4 micrometers in diameter.
    • Life span: 10 - days
  • 12.  
  • 13.  
  • 14.
    • Development: From the pluripotentstem
    • cells in the bone marrow.
    • CFU-M Colony forming megakaryocytes
    • Megakaryoblast
    • Promegakaryoctye
    • Megakaryocytes
    • Platelets
  • 15.
    • Normal concentration :
    • 150,000 to 300,000 per microliter.
    • Structure:
    • Cell membrane
    • Microtubule
    • Cytoplasm
  • 16. Cell Membrane of Platelet
  • 17.
    • It is 6 nm thick and contain lipids (phospholipids, cholesterol and glycolipids), Carbohydrates (glycocalyx), Proteins and glycoproteins.
    • Out of all glycoprotein and phospholipids are functionally important.
  • 18. Glycopropteins
    • Prevents the adherence of platelets to normal endothelium.
    • Accelerates the adherence of platelets to collagen and damaged endothelium in ruptured blood vessels.
    • Forms a receptor for ADP and thrombin.
  • 19.  
  • 20. Cytoplasm
    • The cytoplasm of the platelets include:
    • Golgi apparatus
    • Endoplasmic reticulum
    • Mitochondria
    • Microtubule
    • Microvessels
    • Microfilaments
    • Granules
  • 21.
    • Cytoplasm also contains:
    • Proteins
    • Enzymes
    • Hormones.
    • Chemical substances
  • 22. Proteins
    • The major proteins present are contractile proteins which are responsible for the contraction of platelets :
    • Actin
    • Myosin
    • Thrombosthenin
  • 23. Chemical substances :
    • Calcium ions
    • Mg- ions.
    • Adenosine triphosphate (ATP)
    • Adenosine diphosphate (ADP)
  • 24. Function Of Platelets
    • Its surface has glycoprotein coat that adhere it to injured endothelial cells… …. preventing bleeding .
    • Actin, myosin & thrombosthenin that are contractile proteins…. cause clot retraction.
  • 25.
    • Secretes growth factor that promotes growth & multiplication of vascular endothelial cells, vascular smooth cells & fibroblasts…. repair damaged vascular wall.
    • Its membrane has phospholipids that activate intrinsic system of blood clotting
  • 26. Life span O f Platelets
    • Platelets are eliminated from the circulation mainly by the tissue macrophage system in the spleen.
  • 27. Mechanism of the Platelet Plug
    • When platelets come in contact with a damaged vascular surface, platelets attach to the exposed collagen fibers in the vascular wall.
    • Platelets immediately change their own characteristics.
  • 28.  
  • 29.
    • Platelets begin to swell and assume irregular forms with numerous irradiating pseudopods protruding from their surfaces
    • Contractile proteins in the platelets contract forcefully and cause the release of granules that contain multiple active factors
  • 30.  
  • 31.  
  • 32.
    • Adenosine diphosphate (ADP) is released which causes surface of nearby circulating platelets to become sticky and it adheres to the first layer of aggregated platelets
  • 33.  
  • 34.  
  • 35.
    • The aggregated platelets adhere to the von Willebrand factor that leaks into the traumatized tissue from the plasma
    • It leads to the release of more ADP , which cause more platelets to pile up at the defected site.
  • 36.  
  • 37.
    • The aggregating process is reinforced by the formation of Thromboxane A 2.
    • It directly promotes platelet aggregation and further enhances it indirectly by triggering the release of even more ADP from the platelet granules.
    • Formation of platelet plug takes place
  • 38.
    • Thirdly, the platelet plug release other chemical substances that play a role in blood clotting.
    • Platelet plugging mechanism alone is sufficient to seal tears in the capillaries and small vessels but, large holes require formation of blood clot to stop bleeding.
  • 39. Limitation of Platelet Plug
    • Normal endothelium of the vessel release Prostacyclin which prevents platelet aggregation.
    • So, platelet plug is limited to the defected part of the vessel and does not spread to the normal vascular tissue.
  • 40. Formation Of Blood Clot
    • If there is a large defect in the vessel then blood clot + platelet plug are required to stop bleeding.
    • As clot on the top of platelet plug supports it and reinforces the seal over the break in the vessel.
  • 41.
    • Onset Of Formation Of Blood Clot:
    • 15 – 20 sec …… in severe trauma.
    • 1 – 2 min …… in minor trauma.
  • 42.
    • Ultimate step in clot formation is the conversion of fibrinogen which is a soluble protein that is produced by the liver and is normally always present in the plasma to fibrin which is insoluble thread like molecule.
    • thrombin
    • Fibrinogen Fibrin
  • 43.
    • Fibrin molecules adhere to the damaged vessel surface forming a loose netlike meshwork that traps the cellular elements of blood .
    • The clot appears red because of abundance of RBC that are trapped in it.
  • 44.  
  • 45.
    • The original fibrin web is weak because the fibrin threads are loosely interlaced.
    • Rapidly, various chemical linkages are formed between adjacent strands to strengthen and stabilize the clot mesh work.
  • 46.
    • The cross linkage process which is catalyzed by a clotting factor known as factor XIII (Fibrin stabilizing factor).
  • 47.  
  • 48. Fibrous Organization or Dissolution of the Blood Clot
  • 49.
    • Once a blood clot has formed , it can follow one of two courses:
    • It can become invaded by fibroblast s , which subsequently form connective tissue all through the clot.
    • It can dissolve.
  • 50.
    • The usual course for a clot that forms in a small hole of a vessel wall…… is invasion by fibroblasts , beginning within a few hours after the clot is formed.
    • This event is promoted at least partially by growth factor secreted by platelets.
  • 51.
    • Complete organization of the clot into fibrous tissue takes place within 1 to 2 weeks.
    • When excess blood has leaked into the tissues and tissue clots have occurred where they are not needed.
  • 52.
    • Special substances within the clot itself usually become activated. These function as enzymes to dissolve the clot.
  • 53. Mechanism of Blood Coagulation
  • 54.
    • Procoagulants:
    • Substances that cause or affect blood coagulation that have been found in the blood and in the tissues…. promote coagulation
    • Anticoagulants:
    • Substances that inhibit coagulation are called Anticoagulants.
  • 55.
    • Whether blood will coagulate depends on the balance between these two groups of substances.
    • In the blood stream, the anticoagulants normally predominate, so that the blood does not coagulate while it is circulating in the blood vessels.
  • 56.
    • But when a vessel is ruptured, procoagulants from the area of tissue damage become “activated” and override the anticoagulants, and then a clot does develop.
  • 57. Three Essential Steps Involved In Clotting:
  • 58.
    • (1) In response to rupture of the vessel or damage to the blood itself, a complex cascade of chemical reactions occurs in the blood involving more than a dozen blood coagulation factors.
    • Formation of a complex of activated substances collectively called prothrombin activator.
  • 59.
    • (2) The prothrombin activator catalyzes conversion of prothrombin into thrombin in the presence of sufficient amounts of ionic Ca++ .
    • (3) The thrombin acts as an enzyme to convert fibrinogen into fibrin fibers that mesh with platelets, blood cells, and plasma to form the clot .
  • 60.  
  • 61.
    • The clotting cascade may be triggered by the intrinsic pathway or the extrinsic pathway:
    • The intrinsic pathway precipitates clotting within damaged vessels as well as clotting of blood samples in test tubes.
  • 62.
    • All elements necessary to bring about clotting by means of the intrinsic pathway are present in the blood.
  • 63.