1. Unit Six: Blood Cells, Immunity, and Blood Coagulation
Chapter 36: Hemostasis and Blood Coagulation
Guyton and Hall, Textbook of Medical Physiology, 12th edition

2. Events in Hemostasis
Vascular Constriction
Local myogenic spasm-most effective
Local autacoid factors
Nervous reflexes-from pain receptors
Formation of a Platelet Plug
Small cut in a vessel; have a plug
instead of the complete clotting
mechanism

3. Events in Hemostasis
Platelets
Fragmented megakaryocytes
150, ,000
Do not have nuclei and cannot reproduce
Contain actin and myosin (thrombosthenin)
Produce ATP
Release prostaglandins
Release endothelial cell growth factor
Surface glycoproteins for adherence to damaged
vessels
i. Half-live of 8-12 days

4. Events in Hemostasis
Mechanism of the Platelet Plug
Platelets swell; irregular shape with pseudopods
Become sticky and adhere to collagen
Thromboxane A2 and ADP enhance adherence
Damaged wall activates increasing numbers of
platelets
Important in closing small tears or ruptures in very
small vessels

5. Blood Coagulation
Basic Theory
Depends on the activation of 50 or more possible
blood procoagulants
Formation of prothrombin activator
Conversion of prothrombin to thrombin
Conversion of fibrinogen to fibrin

6. Fig. 36.2

7. Blood Coagulation
Conversion of Prothrombin to Thrombin
Prothrombin activator is formed as a result of
damage to a blood vessel
In the presence of Ca++ causes the conversion
of prothrombin to thrombin
Thrombin causes the polymerization of
fibrinogen molecules into fibrin fibers
Prothrombin attaches to receptors on platelets
Prothrombin is a plasma protein formed
continually by the liver
Vitamin K is required for the production of
prothrombin

8. Blood Coagulation
Conversion of Fibrinogen into Fibrin
Fibrinogen is produced by the liver
In the early stages of polymerization, the molecules
are held together by hydrogen bonds
Fibrin-stabilizing factor is released by platelets;
acts as an enzyme to form covalent bonding and
multiple cross-linkages

9. Blood Coagulation
Blood Clot
Meshwork of fibrin fibers running in all directions
and entrapping blood cells, platelets, and plasma
Within a few minutes the clot contracts and
expresses fluid (serum)
Platelets contribute directly by activation
thrombosthenin and myosin (contractile proteins)
Positive Feedback of Clot Formation

10. Blood Coagulation
Initiation of Coagulation
Trauma to the vascular wall and adjacent tissues
Trauma to the blood
Contact of the blood with damaged endothelial
cells or collagen and other tissue elements
d. All lead to the formation of prothrombin activator

11. Blood Coagulation
Extrinsic Pathway
Release of tissue factor
Activation of Factor X-role of Factor VII and tissue
factor
Effect of Xa to form prothrombin activator-role of
Factor V in the presence of calcium to split
prothrombin to thrombin

12. Fig. 36.3 Extrinsic pathway for initiating blood clotting

13. Blood Coagulation
Intrinsic Pathway
Blood trauma causes activation Factor XII and
release of platelet phospholipids
Activation of Factor XI
Activation of Factor IX by activated XI
Activation of Factor X-role of Factor VIII
Action of activated Factor X to form prothrombin
activator-role of Factor V

14. Fig. 36.4 Intrinsic pathway for initiating blood clotting

15. Blood Coagulation
Role of Calcium in Extrinsic and Intrinsic Pathways
Except for the first two steps in the intrinsic
pathway, calcium ions are required for promotion
or acceleration of all blood clotting reactions
Normally, calcium levels do not fall low enough to
affect blood clotting mechanisms

16. Blood Coagulation
Interaction Between Extrinsic and Intrinsic Pathways
Clotting occurs by both pathways simultaneously
Extrinsic pathway is more explosive and faster (as little
as 15 seconds)
Intrinsic is slower requiring 1-6 minutes

17. Blood Coagulation
Intravascular Anticoagulants- prevention of blood
clotting in the normal vascular system
Endothelial surface factors-smoothness, glycocalyx,
thrombomodulin (binds thrombin), protein C (inhibits
Factors V and VIII
Antithrombin action of fibrin and antithrombin III
Heparin-released by basophils and mast cells
Plasmin-digests fibrin fibers and other clotting factors
(from plasminogen-serum protein trapped in clot)

18. Excessive Bleeding
Decreased Prothrombin, Factors VII, IX, and X Caused
By Vitamin K Deficiency
Hemophilia
Thrombocytopenia