[TRANS] UNIT 3: INTRODUCTION TO HEMOSTASIS
OUTLINE
Introduction
Homeostatic Components
A. Extravascular
B. Vascular
C. Intravascular
III. Balance of Hemostasis
A. Normal
B. Hypocoagulation
C. Hypercoagulation
IV. Hemostatic Mechanism
A. Primary
B. Secondary
C. Fibrinolysis
V. Vascular Intima in Hemostasis
A. Anticoagulant Properties of Intact Vascular Intima
VI. Platelet Function & Contents
A.
Functions
B.
Content
I.
II.
INTRAVASCULAR COMPONENT
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Key components of intravascular hemostasis are:
o Platelets
o Biochemicals (procoagulants) in the plasma
The mentioned components are involved in the following:
o Coagulation (thrombus formation)
o Fibrinolysis (clot or thrombus dissolution)
Coagulation and fibrinolysis are the two essential
processes of hemostasis.
BALANCE OF HEMOSTASIS
PLT
HEMOSTASIS
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From the Greek meaning “the stoppage of blood flow.”
A complex physiologic process that keeps circulating blood
in a fluid state and then, when an injury occurs, produces a
clot to stop the bleeding, confines the clot to the site of
injury, and finally dissolves the clot as the wound heals.
Injured
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Coagulation
Healed
Fluid state
Clot
Dissolve clot
Imbalanced hemostasis system, hemorrhage (bleeding) or
thrombosis (pathological clotting) can be threatening.
Lifelong anatomic hemorrhage, chronic inflammation,
and transfusion dependence are due to the absence of a
single plasma procoagulant.
Absence of control protein = unchecked coagulation,
thrombosis, stroke, pulmonary embolism, deep vein
thrombosis, and cardiovascular events.
Thrombosis
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HEMOSTATIC COMPONENTS
There are three basic components of hemostasis:
A. Extravascular Component. The tissues surrounding
blood vessels.
B. Vascular Component. The blood vessels through
which blood flows.
C. Intravascular Component. The platelets and plasma
proteins that circulate within the blood vessels.
EXTRAVASCULAR COMPONENT
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Involves the tissues surrounding a vessel which become
involved when there is vessel injury.
Provides back pressure on the injured vessel through
swelling and the trapping of escaped blood. The pressure
that resulted collapses venules and capillaries.
The ability of these tissues to aid in hemostasis depends on
the following factors:
o Bulk or amount of surrounding tissues
o Type of tissue surrounding the injured vessel
o Tone of the surrounding tissue
VASCULAR COMPONENT
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Fibrinolysis
Involves the vessels through which the blood flows.
The role of these vessels in hemostasis depends on the
following:
o Size
o Amount of smooth muscle within their walls
o Integrity of the endothelial cell lining
Body
Bleeding
Vessels, coagulation and fibrinolysis proteins, and platelets
work together toward thrombus formation.
Platelets. Center of clot formation (thrombogenesis).
Swing to the right (excessive fibrinolysis or inadequate
coagulation) = bleeding
Swing to the left (excessive coagulation or inadequate
fibrinolysis) = pathologic clotting (thrombosis)
NORMAL HEMOSTATIC BALANCE
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Formation and dissolution of thrombi is maintained in a
delicate balance.
Without the balance, a person may experience the
following:
o Excessive bleeding
o Vasoocclusion
Hypocoagulable state. Conditions associated with
excessive bleeding.
Hypercoagulable state. Conditions in which there is
uncontrolled thrombosis.
HYPOCOAGULATION
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A.K.A. abnormal bleeding
Both inherited and acquired
Coagulation Factor Assay. Capable of diagnosing
conditions related to hypercoagulation.
Example: Hemophilia
HYPERCOAGULATION
A.K.A. thrombosis
Associated with the inappropriate formation of thrombi in
the vasculature that occlude normal blood flow.
Composition
of
thrombi:
leukocytes,
platelets,
erythrocytes held together by fibrin.
Associated with acquired diseases or altered physio states.
ANGELO JUDE C. COBACHA | BMLS 3D
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TRANS: INTRODUCTION TO HEMOSTASIS
HEMOSTATIC MECHANISM
VASCULAR INTIMA IN HEMOSTASIS
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OVERVIEW ON HEMOSTASIS
Hemostasis involves the interaction of vasoconstriction, platelet
adhesion and aggregation, and coagulation enzyme activation
to stop bleeding.
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KEY CELLULAR ELEMENTS
1.
2.
3.
Cells of the vascular intima
Extravascular tissue factor-bearing cells
Platelets
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PRIMARY HEMOSTASIS
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Involves the vascular (blood vessels) and platelet response
to vessel injury.
Blood vessels. Contract to seal the wound or reduce the
blood flow (vasoconstriction).
Platelets. Adhere to the site of injury, secrete the contents
of their granules, and aggregate with other platelets to form
a platelet plug.
Vasoconstriction and platelet plug formation comprise the
initial, rapid, short-lived response to vessel damage.
SECONDARY HEMOSTASIS
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Includes the response of the coagulation process to injury.
The activation of a series of coagulation proteins in the
plasma, mostly serine proteases, to form a fibrin clot.
These proteins circulate as inactive zymogens
(proenzymes) that become activated during the process of
coagulation and, in turn, form complexes that activate other
zymogens to ultimately generate thrombin, an enzyme that
converts fibrinogen to a localized fibrin clot.
Provides the interface between circulating blood and the
body tissues.
Innermost lining of blood vessels is a monolayer of
metabolically active endothelial cells (EC).
Role of ECs:
o Immune response
o Vascular permeability
o Proliferation
o Hemostasis
ECs form a smooth, unbroken surface that eases the fluid
passage of blood.
Fibroblast occupies the connective tissue layer and
produce collagen.
COMPOSITION
A.
Innermost Vascular Lining
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Endothelial cells (endothelium)
B. Supporting the endothelial cells
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Internal elastic lamina composed of elastin and
collagen
C. Subendothelial Connective Tissue
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Collagen and fibroblast in veins
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Collagen, fibroblasts, and smooth muscle cells in
arteries
TRUE or FALSE?
Smooth muscle cells in the walls of veins, venules, and
capillaries contract during primary hemostasis.
Answer: FALSE
Rationalization:
Smooth muscle cells in arteries and arterioles, BUT NOT in the
walls of veins, venules, or capillaries, contract during primary
hemostasis. -Rodak’s Hematology 5th ed. Page 643
ANTICOAGULANT PROPERTIES OF IVI
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IVI = Intact Vascular Intima
Normally, the intact vascular endothelium prevents
thrombosis by inhibiting platelet aggregation, preventing
coagulation activation and propagation, and enhancing
fibrinolysis.
Several specific anticoagulant mechanisms prevent
intravascular thrombosis:
FIBRINOLYSIS
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The final event of hemostasis
Occurs when healing start
Gradual digestion and removal of the fibrin clot
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Collagen. Promotes platelet adhesion.
Tissue factor. Activates coagulation.
ECs form a barrier to separate procoagulant proteins and
platelets from collagen and tissue factor.
The intact endothelial lining of blood vessels is
antithrombotic: it does not activate PLT or promote
coagulation. It promotes thrombosis.
ANGELO JUDE C. COBACHA | BMLS 3D
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TRANS: INTRODUCTION TO HEMOSTASIS
PLATELET FUNCTIONS & CONTENTS
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At the time of an injury, platelets adhere, aggregate, and
secrete the contents of their granules.
FUNCTIONAL CHARACTERISTICS
ADHESION
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Platelets bind nonplatelet surfaces.
VWF (Von Willebrand factor) links platelets to collagen in
areas of high shear stress such as arteries and arterioles.
Platelets may bind directly to collagen in damaged veins
and capillaries.
VWF binds platelets through their glycoprotein GP Ib/IX/V
VWF is essential for adhession
AGGREGATION
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Platelets bind to one another.
When platelets are activated, a change in the GP IIb/IIIa
receptor allows binding of fibrinogen, as well as VWF and
fibronectin.
Fibrinogen binds to GP IIb/IIIa receptors on adjacent
platelets and joins them together in the presence of ionized
calcium (Ca2+).
Fibrinogen binding is essential for platelet aggregation
SECRETION
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Platelets secrete the contents of their granules during
adhesion and aggregation, with most secretion occurring
late in the platelet activation process.
Platelets secrete procoagulants, such as factor V, VWF,
factor VIII, and fibrinogen, as well as control proteins, Ca21,
ADP, and other hemostatic molecules.
Summary of Platelet Function
PLATELET GRANULE CONTENT
ANGELO JUDE C. COBACHA | BMLS 3D
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