Platelets: anucleated cell fragments; technically not true cells.
Red blood cells (erythrocytes) also anucleated ➔ both classified, with leukocytes, as "formed elements" rather than blood cells.
Trigger: vessel wall laceration exposes sub-endothelial collagen to blood.
Three tightly linked phases:
Vasoconstriction
Platelet plug formation
Coagulation (fibrin clot) and subsequent clot removal/repair
Smooth muscle around injured site contracts ➔ reduces lumen diameter & blood flow.
Maintains some flow to deliver clotting factors/platelets while minimizing loss.
Collagen exposure = adhesion site; endothelium normally prevents adhesion via nitric oxide.
Platelets bind collagen & each other ➔ initial plug.
Secrete Platelet-Activating Factor (PAF): positive feedback, recruits more platelets.
Release serotonin & thromboxane A2 ➔ sustain/enhance vasoconstriction.
Fibrin needed to cement platelets.
Circulating fibrinogen (inactive) converted to fibrin (active) by enzyme thrombin.
\text{fibrinogen} \xrightarrow{\text{thrombin}} \text{fibrin}
Fibrin mesh + platelet mass = stable clot sealing vessel.
Clot narrows lumen; must be removed after tissue repair.
Plasminogen (inactive) converted to plasmin by tissue plasminogen activator (tPA):
\text{plasminogen} \xrightarrow{\text{tPA}} \text{plasmin}
Plasmin digests fibrin ➔ clot dissolution, lumen returns to normal.
Growth factors (not detailed here) rebuild endothelium & collagen layer post-injury.
Positive feedback loop: PAF ↑ platelets ↑ PAF, accelerating plug formation.