Required section · Section 2 of 6
Basic mental model
An intact endothelial surface is antithrombotic and vasodilatory. Nitric oxide and prostacyclin inhibit platelet adhesion, activation, and aggregation. Injury removes that local barrier and exposes subendothelial collagen with matrix-bound VWF. Injured or activated endothelium also releases endothelin-1, producing transient local vasoconstriction that reduces flow at the site.
At high shear, matrix-bound VWF rapidly and reversibly tethers circulating platelets through platelet GPIb-IX-V. Firm adhesion adds collagen receptors GPVI and integrin α2β1, with GPVI as the principal activating signaling receptor. The tethered platelet changes from a discoid cell to a spread, pseudopod-bearing cell and centralizes granules. This is a coordinated local response, not a set of independent test results.
Activation releases ADP and supports thromboxane A2 generation, recruiting additional platelets. Inside-out signaling raises the affinity of αIIbβ3, allowing fibrinogen to bridge adjacent platelets into an aggregate. The plug is temporary and needs fibrin reinforcement from secondary hemostasis for durable hemostasis. Localize an observation to tethering, activation, or aggregation before choosing a follow-up method.
Illustrative drawing — this picture was drawn rather than captured.
Reusable sequence for reasoning from an injured vessel to a temporary platelet plug.
Injury and flow reduction
Exposed matrix removes the local antithrombotic barrier; endothelin-1 contributes transient vasoconstriction.
Tether and adhere
VWF binds exposed matrix and platelet GPIb-IX-V; GPVI and α2β1 support firm collagen adhesion.
Activate and recruit
Shape change, dense-granule secretion, ADP, and thromboxane A2 recruit additional platelets.
Aggregate temporarily
Activated αIIbβ3 binds fibrinogen bridges between platelets; fibrin reinforcement remains outside primary hemostasis.
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