Hemostasis

HEMOSTASIS
HEMOSTASIS
• Spontaneous arrest or stoppage of bleeding from injured vessel by
physiological process
• Blood clots form at sites of vascular injury
• Heme: Blood
• Stasis: To halt/stop
A precisely orchestrated process involving platelets, clotting
factors, and endothelium that occurs at the site of vascular
injury and culminates in the formation of a blood clot, which
serves to prevent or limit the extent of bleeding
FUNCTIONS OF HEMOSTASIS
o To maintain blood in fluid state in the vessels
o To stop bleeding by formation of stable hemostatic plug
o To limit the process in the vicinity of the damage
o Eventual removal of the hemostatic plug when healing is complete
Endothelium
• Strategically located at the interface between tissue and blood.
• Pivotal for protecting against vascular injury and maintaining blood
fluidity.
• Anti-platelet properties;
• Prostacyclin and Nitric oxide, potent inhibitors of platelet and
monocyte activation and vasodilators.
• Expresses ecto-adenosine diphosphatase, which degrades adenosine
diphosphate and inhibits platelet aggregation;
Endothelium
• Tissue plasminogen activator, which activates the fibrinolysis
system.
• von Willebrand factor, which mediates platelet adhesion.
• Injury to endothelium is accompanied by loss of protective

molecules and expression of adhesive molecules.
• Activates procoagulant activities leading to development of
thrombosis.
Stages of Hemostasis
Vascular constriction
Formation of platelet plug
Formation of blood clot
Fibrinolysis
Vasoconstriction
• Immediate
• Reduces blood flow to the injured area.
• Mediated by reflex neurogenic mechanisms

• Augmented by endothelin, a potent endothelium-derived
vasoconstrictor
• Effect is transient
• Bleeding would resume if not for activation of platelets and
coagulation factors.
Formation of the platelet plug
• Immediate phenomenon appearing within seconds of injury
• Responsible for cessation of bleeding.
• Primary hemostasis involves three steps:
1. Platelet adhesion
2. Platelet granule release
3. Platelet aggregation
Platelet adhesion
• Mediated largely via interactions with vWF and exposed collagen.
• vWF acts as a bridge between the platelet surface receptor
glycoprotein Ib (GpIb) and collagen
Platelet granule release
• Platelets rapidly change shape
• Converted from smooth discs to spiky flat discs with greatly
increased surface area
• Release three types of granules from their cytoplasm:
• Dense granules, α-granules and lysosomal vesicles.
• Important products released from these granules are:
• ADP, ATP, calcium, serotonin, platelet factor 4, factor V, factor VIII,
platelet-derived growth factor (PDGF), vWF, fibronectin, fibrinogen,
plasminogen activator inhibitor –1 (PAI-1) and thromboxane A2.
Platelet aggregation
• This process is mediated by fibrinogen.
• Forms bridge between adjacent platelets via glycoprotein receptors
on platelets, GpIIb-IIIa.
Formation of blood clot
• Tissue factor is also exposed at the site of injury.
• Membrane bound glycoprotein (TF) acts in junction with factor VII
• Results in thrombin generation.
• Cleaves circulating fibrinogen into insoluble fibrin
• Creating a fibrin meshwork, leading to additional platelet
aggregation at the site of injury
Fibrinolysis
• Clot stabilization and resorption
• Polymerized fibrin and platelet aggregates undergo contraction to
form a solid, permanent plug that prevents further hemorrhage.
• At this stage, counterregulatory mechanisms are set into motion.
• e.g., tissue plasminogen activator, t-PA made by endothelial cells
that limit clotting to the site of injury and eventually lead to clot
resorption and tissue repair.
SUMMARY
• Endothelial injury exposes the underlying ECM;
• Platelets adhere to the ECM primarily through the binding of platelet GpIb
receptors to VWF.
• Adhesion leads to platelet activation
• An event associated with secretion of platelet granule contents, including
calcium and ADP; and changes in shape and membrane composition; and
activation of GpIIb/IIIa receptors.
• The GpIIb/IIIa receptors on activated platelets form bridging crosslinks with
fibrinogen, leading to platelet aggregation.
• Activation of thrombin promotes fibrin deposition, cementing the platelet plug
in place
• tissue plasminogen activator, t-PA made by endothelial cells that limit clotting
to the site of injury and eventually lead to clot resorption and tissue repair

Hemostasis

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Hemostasis

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HEMOSTASIS

• Blood clots form at sites of vascular injury

• Injury to endothelium is accompanied by loss of protective

Formation of platelet plug

Formation of blood clot

• Mediated by reflex neurogenic mechanisms

• Responsible for cessation of bleeding.

• Primary hemostasis involves three steps:

2. Platelet granule release

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