Platelets and Hemostasis

Study Notes

Platelets, also known as thrombocytes, are small, colorless cell fragments in blood.
Their role is to form clots to stop or prevent bleeding.
Platelets are produced in bone marrow.
Platelets have a lifespan of 8 days.

Blood vessel constriction occurs immediately after injury.
This constriction helps decrease blood loss at the injured site.
Causes of vasoconstriction include:
- Local myogenic contraction due to direct trauma.
- Nervous reflexes triggered by pain from the injured vessel.
- Local humoral factors released by platelets, such as ADP, serotonin, and thromboxane A2.

Platelet aggregation forms a temporary hemostatic plug in the early stages of hemostasis.
Injury to a vessel stimulates platelets to form a mechanical plug to seal the damaged area.

Platelet adhesion: Platelets adhere to exposed subendothelial collagen after blood vessel injury.
Platelet activation: After adhesion, platelets change shape and release granule contents.
Platelet release reaction: Platelets release granules containing ADP, serotonin, and thromboxane A2, playing a role in clot formation.
Platelet aggregation: Platelets adhere to each other at sites of vascular injury, crucial for hemostatic plug formation and thrombosis.
Platelet fusion: An irreversible slow process where aggregated platelets fuse at the injury site, caused by high ADP concentration and thrombin.

The clotting mechanism converts temporary platelets plugs into definitive clots using fibrin.
Coagulation factors, plasma proteins synthesized by the liver, are activated in a cascade.
The final step in coagulation is the formation of a fibrin mesh.

Intrinsic Pathway: Initiated within the blood itself by factors activated within the vascular system.
Extrinsic Pathway: Initiated by factors and tissues outside the bloodstream (e.g., trauma to the blood vessel.)