2. Hemostsis &Thrombosis: Definition
• Hemostasis is result from well regulated process that maintain blood in a
fluid clot free state in a normal vessel while inducing a rapid formation of
localized hemostatic plug at the site of vascular injury.
• haemostasis—the rapid arrest of blood loss upon vascular damage, in
order to maintain a relatively constant blood volume.
• The process by which blood is maintained in a fluid state and confined to
the circulatory system
• The formation of blood clot (Thrombus) in uninjured vessel.
• Thrombotic occlusion of a vessel after a relatively minor injury.
3. 1. Platelets adhesion and aggregation,
formation of the platelet plug
3. Blood clotting
4. Final repair by connective tissue
NB!The phases are not separated but rather
5. Classics of blood clotting
Alexander Schmidt and Paul Morawitz
discovered the enzymatic cascade nature of
1st phase –
2nd phase --
converted to soluble
3rd phase –
8. Factors influencing platelets adhesion
Collageen and plasma vonWillebrand factor
(vWf) iniate adhesion.
Adhesion is blocked by negative surface charge
of platelets, certain biochemical regulators (e.g.
NO, prostacyclin etc), and endothelial barrier
between collagen and blood.
•and matrix deposition.
Fig. 1. Wound healing is a
encompassing a number of
overlapping phases, including
•the formation of a blood clot re-
establishes hemostasis and provides a
provisional matrix for cell migration.
•CK play significant role in the evolution of
granulation tissue through
• recruitment of inflammatory leukocytes
•and stimulation of fibroblasts and
21. 31-08-2015 21
The disulfide rings are region containing 3 di-sulfide bonds cyclic linking homologous segment of , and
chains. N-linked polysaccharides are represented by filled hexagons.TheArg-Gly bonds that are cleaved by
thrombin in fibrin activation are indicated
23. The extrinsic pathway is critical in
initiating of blood clotting.
The intrinsic pathway plays an important
role in maintenance of coagulation.
There is no bleeding disorders in case of
25. Antithrombin III, tissue factor pathway
inhibitor (TFPI), alpha2-macroglobulin,
C1 inhibitor jt.
Antithrombin III inhibits mainly factor
X, and factorsVII, IX, XI, XII.
Heparin and glycosaminoglycans
increase the antithrombin III activity
26. Thrombomodulin and protein C are
members of an endogenous anticoagulant
Thrombin complexed with
thrombomodulin loses its procoagulatory
activity, while readily activating protein C
Proteiin C destroys factorsV andVIII
aspect of anti-
It may activated by infectious
agents, hemodynamic factors
plasma mediators & CK
29. There is no coagulation in case of intact endothelium
Endothelial cells can produce IL-1 orTNF tissue factor,
under influence of thrombin, which has procoagulatory
The surface of endothelial cells contains heparin-like
compounds, which bind antithrombin III and block
Endothelial cells can produce the plasminogen activators.
30. Platelets contain procoagulant anticoagulant
Polymorphonuclear leukocytes and monocytes
produce tissue factor, factorV and present
phospholipids, which all support blood
32. • HemophiliaA (lack
• Hemofiilia B (lack of
Vitamiin K is
important to add
(gla) to factors II,
VII, IX ja X.
33. Platelets contain both substances which
activate or inhibit blood clotting
Neutrophilic granulocytes and monocytes
produce the tissue factor, the factorV, and
phospholipids which all support blood clotting
34. In case of intact endothelium there is no clotting
Endothelial cells can produce under influence of
thrombin, IL-1,TNF the tissue factor, which can iniate
external pathway of blood clotting
On the surface of endothelium are heparin-like
substances which bind antithrombin III ühendid, mis
seovad antitrombiin III and inhibit thrombin activity.
Endothelial cells produce plasminogen activators.
A good overview and illustrations: http://ntri.tamuk.edu/homepage-ntri/lectures/clotting.html