Physiology · Blood, hemostasis and basic immunity
Primary hemostasis and platelets !
- Mechanism
- Exam priority: high
When a vessel is cut it narrows and platelets stick to the wound, forming a soft plug in seconds to minutes.
Updated 2026-11-01
Also called: Platelet plug, Platelet adhesion and aggregation
What it is
Primary hemostasis is the first response to vessel injury: vasoconstriction and a platelet plug. Platelets adhere to exposed collagen through von Willebrand factor, activate, release signals that recruit more platelets, and link to each other through fibrinogen. The plug is fragile until the coagulation cascade reinforces it with fibrin (secondary hemostasis).
How it works, step by step
- Injury → reflex and endothelin-mediated vasoconstriction briefly reduce flow.
- Subendothelial collagen and tissue factor are exposed; vWF from endothelium and plasma binds collagen.
- Platelet GPIb binds vWF → platelets slow and adhere; GPVI and integrin α2β1 bind collagen directly.
- Adhesion activates platelets → shape change (spheres with pseudopods) and phosphatidylserine on the surface.
- Granules release ADP, serotonin and Ca²⁺; arachidonic acid is turned into TXA₂ by COX-1.
- ADP and TXA₂ recruit and activate passing platelets (positive feedback); thrombin is the strongest activator.
- Inside-out signalling changes GPIIb/IIIa → it binds fibrinogen and vWF → platelets aggregate into a plug.
- The activated platelet surface hosts the coagulation complexes; fibrin then stabilizes the plug and the clot retracts.
Reference values
| Parameter | Value | Note |
|---|---|---|
| Platelet count | ≈150 000–450 000/µL | |
| Platelet life span | ≈7–10 days | |
| Platelets held in the spleen | ≈one third of the total | more with splenomegaly |
| Spontaneous bleeding risk | rises markedly below ≈10 000–20 000/µL |
Approximate values for a healthy adult at rest; each laboratory sets its own ranges.
Regulation
- +Collagen, vWF, thrombin: Adhesion and strong activation
- +ADP (P2Y12) and thromboxane A₂: Recruit more platelets; amplify the plug
- +Thrombopoietin (liver): Raises megakaryocyte production
- −Prostacyclin (PGI₂) and nitric oxide: Raise cAMP/cGMP in platelets; keep healthy endothelium non-sticky
- −Aspirin, NSAIDs: Block TXA₂ synthesis (aspirin irreversibly)
Defects of primary hemostasis
| Defect | What fails | Count | Clue |
|---|---|---|---|
| Von Willebrand disease | vWF (adhesion) and low factor VIII | Normal | Mucosal bleeding; aPTT may be long |
| Bernard–Soulier syndrome | GPIb | Low, giant platelets | Fails ristocetin aggregation |
| Glanzmann thrombasthenia | GPIIb/IIIa | Normal | No aggregation to ADP or collagen |
| Aspirin or uremia | TXA₂ synthesis / platelet function | Normal | Prolonged platelet function tests |
| Thrombocytopenia (ITP, dengue) | Number of platelets | Low | Petechiae, purpura |
Test yourself
Think of the answer, then tap the question to see it.
Why does a single exposure to aspirin affect platelets for about a week?
Aspirin acetylates COX-1 irreversibly. Platelets have no nucleus and cannot make new enzyme, so TXA₂ synthesis stays low until new platelets replace them over 7–10 days.
Why can von Willebrand disease prolong the aPTT while the platelet count is normal?
vWF protects factor VIII from clearance. Low vWF lowers factor VIII, an intrinsic-pathway factor measured by the aPTT.
Why does bleeding from platelet defects start immediately after a cut, while hemophilia bleeding is often delayed?
The platelet plug is the first seal; without it bleeding starts at once. In hemophilia the plug forms but is not reinforced by fibrin, so it gives way later and bleeding restarts.
How does healthy endothelium prevent platelets from sticking?
It releases prostacyclin and nitric oxide, which raise cAMP and cGMP in platelets, degrades ADP with ectonucleotidases and hides collagen behind an intact lining.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- The coagulation cascade
- Coagulation tests: PT/INR, aPTT and platelets
- Thrombosis and bleeding: Virchow's triad and hemostatic defects
- Fibrinolysis and natural anticoagulants
Related conditions
In Biochemistry
In Pharmacology
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 18.5 Hemostasis (OpenStax (Rice University), 2022); 18.4 Leukocytes and Platelets (OpenStax (Rice University), 2022); Platelet Tests (MedlinePlus (U.S. National Library of Medicine), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 37). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.