Figure 4-6 Normal hemostasis. (A).

 Major systems involved in maintaining hemostasis:

After vascular injury, local 1. Blood vessels
neurohumoral factors induce a 2. Platelets
(transient vasoconstriction. B). Platelets 3. Coagulation proteins

adhere (via GpIb receptors) to exposed 4. Fibrinolysis

extracellular matrix (ECM) by binding 5. Serine protease inhibitors

to von Willebrand factor (vWF) and are  Major systems involved in maintaining hemostasis:

activated, undergoing a shape change 1. Kinin system

and granule release. Released 2. Complement system

 Imbalance bleeding and thrombosis
adenosine diphosphate (ADP) and
thromboxane A2 (TXA2) lead to further
Platelet
platelet aggregation (via binding of
fibrinogen to platelet GpIIb-IIIa Platelet’s functions in hemostasis:
receptors), to form the primary
hemostatic plug. (C). Local activation 1. Providing a negatively charged phospholipid surface for factor X and

of the coagulation cascade (involving prothrombin activation.

tissue factor and platelet phospholipids) 2. Releasing substances that mediate vasoconstriction, platelet aggregation,
results in fibrin polymerization, coagulation (thrombin generation), and vascular repair.
"cementing" the platelets into a 3. Providing surface membrane glycoproteins such as GPIIb and GPIIIa to attach
definitive secondary hemostatic plug. to other platelet via fibrinogen, and GPIb to bind to collagen and subendothelium
(D). Counter-regulatory mechanisms, via vWF.
such as release of t-PA (tissue
plasminogen activator, a fibrinolytic
product) and thrombomodulin
(interfering with the coagulation
cascade), limit the hemostatic process to
the site of injury.

 Hemostasis  complex process

by which the body spontaneously stops
bleeding and maintains blood in the
fluid state within vascular compartment
 Major role of hemostatic
system: maintain a complete balance
of the body’s tendency toward clotting and bleeding