Thrombocytes : Anatomy and Physiology

• Thrombocytes


  - very small, disc-shaped cell fragments

  - 2-4 μm in diameter

  - unnucleated
• Thrombocytes: Development


  from the cytoplasm of megakaryocytes

  - RBW
• Thrombocytes: Cytoplasm


  - with granules

  - have substances that promote blood clotting

  - causes hemostasis
• Normal blood platelet count

  200 x 109/L - 350 x 109/L (200,000-350,000/mm3)
• Thrombopietin


  - from liver

  - stimulates platelet production
• Thrombocytes: Lifespan


  8-11 days
• Thrombocytes in the Spleen


  - 1/3 of total thrombocytes

  - emergency store

  - released to control excessive bleeding
• Hemostasis


  - bleeding stoppage

  - The more badly damaged the vessel wall is, the faster coagulation begins.
• The more badly damaged the vessel wall is, the faster coagulation begins, sometimes as quickly as _ after injury.


  The more badly damaged the vessel wall is, the faster coagulation begins, sometimes as quickly as15 seconds after injury.
• Hemostasis: Steps (3)


  1. Vasoconstriction

  2. Platelet plug formation

  3. Coagulation

  4. Thrombolysis
• Vasoconstriction


  platelets come into contact with a damaged blood vessel

  - surface becomes sticky

  - adhere to the damaged wall
• Vasoconstriction: Release of (2)


  1. Serotonin: 5-hydroxytryptamine, 5-HT

  2. Thromboxanes

  
  

  *constrict the vessel

  *reduce or stops blood flow
• Platelet plug formation


  - sticky platelets clump together

  - release Adenosine diphosphate (ADP)

  - positive feedback mechanism

  - plugs small holes in blood vessel walls
• Adenosine diphosphate (ADP)


  attract more platelets to the site
• Platelet plug


  - temporary seal

  - soft & easily disrupted

  - precursor to the far more durable blood clot
• Platelet plug formation: Duration

  complete within 6 minutes of injury
• Coagulation


  - complex process

  - positive feedback system
• Coagulation: Numbers


  based on order of discovery

  NOT order of participation
• Coagulation: Clotting Factors


  - activate each other in a specific order

  ☆ activation results in formation of prothrombin activator
• Prothrombin activator


  - first step in the final common pathway

  - activates prothrombin (inactive) into thrombin (active)
• Thrombin


  Fibrinogen (inactive) to Fibrin (active)
• Fibrin


  loose, insoluble threads
• Coagulation: Pathways (3)


  1. Extrinsic

  2. Intrinsic

  3. Final Common
• Extrinsic pathway


  Thromboplastin

  - releasedby damaged tissue cells

  - enters the blood
• Intrinsic pathway


  Platelets

  - adhere to damaged blood vessel lining
• Extrinsic & Intrinsic Pathways


  - need DIFFERENT sets of clotting factors

  - accomplish the same goal (Prothrombin activator)

  - missing a factor renders only ONE of the pathways useless, but blood clot formation is still doable using the other pathway with no missing factor
• No Clot Formation (2)


  1. missing factors from BOTH extrinsic and intrinsic pathways

  2. missing factor from common pathway
• Coagulation: Clot Formation


  - more stable than platelet. plug

  - stabilized by increased amounts of Fibrin from the common pathway
• Clotting Factors (13)


  I. Fibrinogen

  Il. Prothrombin

  III. Tissue factor (thromboplastin)

  IV. Calcium (Ca'*)

  V. Labile factor, proaccelerin, Ac-globulin

  
  

  VIl. Stable factor, proconvertin

  VIII. Antihaemophilic globulin (AHG), antihaemophilic factor A

  IX. Christmas factor, plasma thromboplastin component (PTC), antihaemophilic factor B

  X. Stuart-Prower factor

  XI. Plasma thromboplastin antecedent (PTA), antihaemophilic factor C

  XII. Hageman factor

  XIII. Fibrin stabilising factor
• Clotting Factors: There is no factor _


  There isno factor VI
• Vitamin K


  essential for the synthesis of factors II, VII, IX, and X
• Thrombolysis


  - destruction of a blood clot

  - healing blood vessel damage

  ☆ fibrinolysis
• Fibrinolysis


  - fibrin breakdown

  - first stage of fibrinolysis
• Thrombolysis: Steps (2)


  1. Activators: Plasminogen → Plasmin

  2. Plasmin: Fibrin → Breakdown producys
• Plasmin


  activated by activators from damaged endothelial cells
• Clot Formation


  - platelet shrinkage

  - draw edges of broken vessel together = CLOT RETRACTION (like wound retraction)
• Control of Coagulation


  - control & braking mechanisms

  - limit clotting to affected area

  - terminate the process at the appropriate time
• Control of Coagulation: Mechanisms (3)

  1. smoothness of normal blood vessel lining

  2. deactivation of activated clotting factors

  3. clearing of activated clotting factors
• smoothness of normal blood vessel lining


  prevents. platelet adhesion in healthy, undamaged blood vessels
• by anticoagulants, e.g., heparin, antithrombin III