PRINCIPLES OF VETERINARY SURGERY

CHAPTER 4: PHYSIOLOGY OF HEMOSTASIS

1. Three Major Components of Hemostasis

A. Reflex vasoconstriction of blood vessel wall
B. Participation of blood platelets
C. Blood coagulation

A. Reflex vasoconstriction of blood vessel wall

 Following blood vessel injury, a brief local vasoconstriction reduces blood flow at the site.
Vasoactive components from adjacent platelets and surrounding tissues maintain vascular
contraction. The normal blood vessel wall endothelium has antithrombotic properties which is
maintained through active and passive mechanisms

 Active mechanism
a. Removal from the circulating blood compounds that promote platelet aggregation
(prostaglandin F1£, serotonin, adenine nucleotides, bradykinin and angiotensin I).
b. Synthesis and release of prostacyclin (prostaglandin I 2 or PGI2) which is a potent inhibitor
of platelet aggregation.
c. Antithrombotic proteoglycan components of blood vessel wall (heparin, heparin sulfate,
dermatan sulfate) that act against coagulation factors (thrombin, antithrombin III, factor X,
fibrinogen) and affect platelet functions (inhibit thrombin –collagen-induced aggregation
and binds to platelet factor 4 and growth factor derived from platelets).
 Passive Mechanism
a. Glycocalyx that protects the cell surface.
b. The negative charged vessel lumen that repels similarly charged cells such as platelets.
d. Presence of an £2 – macroglobulin which is a protease inhibitor.

 The endothelium is also capable of synthesizing von Willebrand factor protein, plasminogen
activator, fibronectin, types III and IV basement –membrane collagens, elastin, many enzymes
and prostacyclin.
 Pathology of the Endothelium includes atherosclerosis, thrombosis, DIC, defective hemostasis,
inflammation, vascular neoplasia, metastasis, prolonged hypotension, acidosis, hypoxia, and
dysproteinemias.

B. Participation of platelet to form platelet plug

 Disc-shaped structure that are derived from the extremities of megakaryocytes in the bone
marrow, lung and spleen. Platelet promote hemostasis by adhesion, aggregation and secretion
reactions and are an essential component of the initial hemostatic plug via the intrinsic coagulation
pathway.

 The following are the functions of platelets

 Hemostasis and thrombosis (endopthelial cells, coagulation, von Willebrand factor, collagen,
adenosine diphosphate, adrenalin, thrombin)
 Atherogenesis (platelet-derived growth factor, mitogens, cell-proliferating activity)
 Inflammation (specialized type of intravascular leukocyte, chemotaxis, phagocytosis)
 Prostaglandin metabolism
 Immunologic reactions (immune-complex disease)
 Endotoxin reactivity (Shwartzman reaction)
 Monoamines and serotoninergic synaptosomes (epinephrine and serotonin)
 Interactions with tumor cells (adhesions, aggregation, cell transformation, metastasis)
 Synthesis of proteins, lipids, carbohydrates and nucleotides.

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 CHAPTER 4: PHYSIOLOGY OF HEMOSTASIS

C. Blood Coagulation
 A series of sequential activating steps that results in the conversion of prothrombin to thrombin and
then fibrinogen to fibrin in the presence of calcium ions.

 Clotting Factors
Factor I Fibrinogen
Factor II Prothrombin
Factor III Tissue Thromboplastin
Factor IV Calcium
Factor V Proaccelerin, Labile Factor
Factor VII Proconvertin, Stable Factor
Factor VIII Antihemophilic Factor, Thromboplastinogen
Factor IX Plasma Thromboplastin Component, Christmas Factor
Factor X Stuart Factor
Factor XI Plasma Thromboplastin Antecedent (PTA)
Factor XII Hageman Factor, Glass Activation Factor
Factor XIII Fibrin Stabilizing Factor, Fibrinase, Laki-Lorand Factor

2. Fibrinolysis
 Involves a series of events that produce plasmin or fibrinolysin, the enzyme that digests fibrin and
initiates dissolution of hemostatic plugs to support vessel healing and repair. The process
parallels that of coagulation, as either direct or indirect activation of the fibrinolytic pathway that
converts plasminogen to active plasmin. Plasmin also digests fibrinogen and factors V and VIII.
 Physiologic control of fibrinolysis is maintained by fibrinolytic inhibitors (antiplasmins) so that
fibrinolysis is restricted to the area in and around a fibrin deposit.