HEMOSTASIS

• HEMOSTASIS

  • Retains the blood within the vascular system during periods of injury
  • Happens during vasoconstriction (pressure is applied = constrict to retain the blood = lumen is smaller to control the blood flow)
  • Vasodilation = lumen is bigger
• HEMOSTASIS

  • Localizes the reaction involved to the site of injury
  • PRIMARY HEMOSTASIS: platelet adhesion and aggregation
  • Platelet will begin to travel, and adhere, and aggregate to the site of puncture or the broken blood vessel
  • Complete occlusion = forming the platelet plug
• HEMOSTASIS

  • Repairs (platelet plug) and re-establishes blood flow through the injured vessels
  • Re-establishes thru sealing the platelet plug by (SECONDARY HEMOSTASIS):
  • COAGULATION FACTORS (sealer) = secure the platelet plug (w/o coagulation factor, the platelet plug may be dislodged anytime and bleeding will occur again)
  • After the clot and the bleeding is stopped, FIBRINOLYSIS is needed for dissolution of clot to re-establish the blood flow
• HEMOSTASIS

  • IT’S ALL ABOUT FORMING THE CLOT, SEALING THE BLOOD VESSELS IN ORDER TO ARREST BLEEDING
• EXTRAVASCULAR COMPONENTS

  • Outside the blood vessel
  • Play a part in hemostasis by providing back pressure on the injured vessel through swelling and entrapment of escaped blood
  • During the injury, the blood vessels are restricted because of the surrounding tissue
  • The surrounding tissues applied pressure on the blood vessel (surrounding tissue = swells around the blood vessel = restrict)
• CAPABILITY TO ARREST BLEEDING DEPENDS ON THE:

  Bulk or amount of surrounding tissue

  • Kind of tissue: fleshy part
  • Fleshy part = exerts more pressure = vasoconstriction = arrest bleeding immediately
• CAPABILITY TO ARREST BLEEDING DEPENDS ON THE:

  Type of tissue

  • Skeletal muscle = higher vasoconstriction
  • Skeletal muscle: more effective in constricting blood vessels than loose connective tissue
• CAPABILITY TO ARREST BLEEDING DEPENDS ON THE:

  Tone (elasticity/flexibility) of the surrounding tissue

  • Elasticity/flexibility depends on the age
  • Older = less elastic/flexible = slower in arresting bleeding
  • Varicose vein (in old age) = not effective in vasoconstriction
• EXTRAVASCULAR CELLS THAT PARTICIPATE IN HEMOSTASIS:

  1.     Fibroblast

  2.     Smooth muscle cell

  • These two are highly pro-coagulant (like to form clots)
  • Once they are released from the outside of the vein, they have the ability to go to the punctured vessel and seal it off temporarily
• VASCULAR COMPONENTS

  Depends on: Size of the blood vessels

  • From hard to easy to clot: (1) arteries, (2) veins, (3) capillaries
  • Arteries = hard to clot = pressure is very strong = excessive bleeding
  • Veins and capillaries = easy to clot = with small amount of pressure they can constrict
  • The thinner, the easily to seal off; the thicker, the harder for it to seal off
• VASCULAR COMPONENTS

  Depends on: Amount of smooth muscle within their wall (compare the walls of the arteries from that of the veins and capillaries)

  • More smooth muscle: arteries > vein
  • Arteries have thick walls that are almost resistant to bleeding, but once it is punctured, it can be the cause of death (as it is very hard to seal)
• VASCULAR COMPONENTS

  Depends on: Integrity of the endothelial cell lining

  • Platelets: contribute to the strength of endothelial cell lining and ability to withstand the pressure
• INTRAVASCULAR COMPONENTS

  • Inside the blood vessels
  • Platelets; biochemicals in the plasma (coagulation factors)
• LESS IMPORTANT SYSTEM THAT PARTICIPATES IN HEMOSTASIS:

  COMPLEMENT SYSTEM

  • C1-C9: they form the membrane attack complex
  • Inflammation goes hand-in-hand in coagulation
  • Once there is coagulation, the inflammatory responses are activated to further avoid complications in bleeding
• LESS IMPORTANT SYSTEM THAT PARTICIPATES IN HEMOSTASIS:

  KININ SYSTEM

  • Control the heartbeat during hemostasis
  • Once bleeding, the heart needs to be regulated = more pump = more blood supply
• LESS IMPORTANT SYSTEM THAT PARTICIPATES IN HEMOSTASIS:

  SERINE PROTEASE INHIBITORS

  • Are coagulation inhibitors that stop coagulation if not needed and turn off fibrinolysis
  • Are proteins from the liver
• PRIMARY HEMOSTASIS

  • End product: involves only platelet plug (temporary) formation
  • First responder in injury = platelets
• PRIMARY HEMOSTASIS

  • Involves vascular intima and platelets
  • Rapid, short-lived response
  • They can be dislodged based on the pressure of the blood = platelet plug is not strong enough to hold it
  • Ends with platelet plug formation
• PRIMARY HEMOSTASIS

  • Activator: desquamation or small tissue injury
  • Broken blood vessels = exposed endothelium = once exposed it is termed as desquamation (shedding of the endothelium)
• PRIMARY HEMOSTASIS

  • Tissue factor (one of the most important activator) and collagen are released from the damaged endothelium (broken blood vessel)
  • These travel in the blood vessels to call out the cascade:

  1. blood vessel constriction then calls the platelet
  2. platelet adhesion;
  3. platelet activation = changing in shape (holy leaf);
  4. once activated = secrete granules inside them
  5. after secretion = aggregation occurs as the secretion attracts more platelet to come
  6. aggregation = formation of platelet plug
• SECONDARY HEMOSTASIS

  • End product: fibrin clot (permanent) formation
  • Activator: tissue factor or large tissue injury
  • Tissue factor will travel (exposed on cell membrane), not just to attract platelets but also coagulation proteins/factors
• SECONDARY HEMOSTASIS

  • Involves activation of a series of plasma proteins (coagulation factors) in the coagulation system until fibrin clot formation
  • Zymogens (proenzymes): not active proteins
  • Trypsinogen (zymogen) to tripsin
  • Fibrinogen (zymogen) to fibrin (sealant of platelet clot)
  • CFX to CFXa
  • Once fibrinogen is activated to fibrin, stabilization of platelet plug will occur → fibrinolysis (dissolution of blood)
• SECONDARY HEMOSTASIS

  • Involves platelets and coagulation system
  • Platelets provide the cell membrane (particularly platelet phospholipid) which is the assembly area of coagulation factors
  • Without the platelet aggregated plug, the coagulation factors has no assembly area
  • Delayed, long-term response
  • Regulation: needs to stop in time, otherwise one will be hypercoagulable
  • Naturally occurring inhibitors = serine protease inhibitors