What is Hemostasis?

• Derived from Greek meaning “the stoppage of blood flow”.

• An integral balance that maintains blood in a fluid state, promotes clotting when
needed (wounds) and also responsible for lysing the clot when no longer needed.
• involves the interaction of vasoconstriction, platelet adhesion and aggregation, and
coagulation enzyme activation to stop bleeding.

NORMAL HEMOSTASIS:
 Normal process by which bleeding from injured blood vessels was stopped through
blood coagulation and fibrinolysis.
 Without balance, an individual may experience either excessive
bleeding(hypocoagulable state) or vaso-occlusion (hypercoagulable state)

platelet adhesion

release of granule contents

platelet aggregation

primary (temporary) hemostatic plug

activation of coagulation system

fibrin formation

secondary (permanent) hemostatic plug

 Events:
1. Vasoconstriction
2. Platelet adhesion to exposed sub-endothelial connective tissue.
3. Platelet aggregation to initial platelet plug.

Three Hemostatic Components :

1. Extravascular component (outside)

 Involves the tissues surrounding a vessel which aids in hemostasis
 Provides back pressure on the injured vessel through:
1) Swelling
2) Trapping of escaped blood
 Increase pressure tends to collapse venules and cappilaries
 Depends on:
1) Bulk or amount of surrounding tissues
2) Type of tissue surrounding the injured vessel
 3) Tone of surrounding tissues

2. Vascular Component: (inside)

 Consist of the blood vessel through which blood flows
 It is dependent on:
1) size
2) amount of smooth muscles within their walls
3) integrity of the BV

3. Intravascular Component: (within the BV)

 Consist of complex sequence of physiochemical reactions which transform fluid
blood into a firm fibrin clot and involve various factors like platelets and
coagulation factors (plasma proteins) and subsequent lysis (fibrinolysis) of
formed fibrin clot.

Primary Hemostasis:
refers to the role of blood vessels and platelets in response to vascular injury, or the
common place desquamation of dying or damaged endothelial cells.

 Involves vascular and platelet response to injury

blood vessels contract to seal the wound or reduce the blood flow
 Formation of Hemostatic Platelet plug
platelets become activated, adhere to the site of injury, secrete the contents of
their granules and aggregate with other platelets

Systems involved in Hemostasis:

 Vascular system
Composed of arteries, veins and capillary system
 Endothelial lining
 b. Basement membrane
 Collagen material – stimulate platelets

 Connective tissue
 Elastic fibers – provide support around vessel

 Platelet system
 In response to vascular injury, platelets are stimulated to initiate the formation
of a primary hemostatic plug,
 the platelet contributes phospholipid (sometimes referred to as platelet factor 3
or PF3) to the coagulation cascade

 Coagulation system
 Composed of 14 coagulation factors which are interdependent
 Final product is a fibrin mesh or clot which completely stops bleeding.
 Slow contraction and lysis of the clot occurs.
 Fibrinolytic system
 Plasminogen is converted to plasmin
 Plasmin enzymatically attacks the fibrin molecule producing fibrin degradation
products (FDPs, sometimes called FSPs) that are cleared from the circulation by
macrophages

 Coagulation inhibition system

• Provides balance and control of clotting mechanisms

Natural inhibitors and anticoagulants circulate in the plasma .

Primary Hemostatic Plug:

platelets adhere to subendothelial structures at the site of injury. The platelets change their
shape and release granule contents. The released contents cause platelet aggregation and form a
primary hemostatic plug.

EVENTS IN PLATELET ACTIVATION

1. Platelet Adhesion and Shape Change

- initial step is adhesion of platelets to subendothelial structures at the site of injury.
The link is mainly through receptor sites (GpIb-IX) on the platelet with subendothelial
von Willebrand factor (vWF). vWF is synthesized by both endothelial cells and
megakaryocytes.
- platelets change their shape from round to spherical to stellate, thereby markedly
increasing the surface area.

2. Platelet Secretion (Release Action)

- soon after adhesion, platelets release granule contents which contains pro-
aggregatory substances like ADP, serotonin (5-hydroxytryptamine), fibrinogen and vWF.
Calcium is also released and is required for the coagulation.

3. Platelet Aggregation
- the secreted products recruit additional platelets and cause aggregation to each other
through the receptor sites (Gp IIb-IIIa) using fibrinogen as an intracellular bridge.
- these clumps of platelets so formed quickly stop bleeding from the site of injury and
are known as primary hemostatic plug. The process of primary hemostatic plug
formation is termed as primary hemostasis.
Secondary Hemostatic Plug:
exposure of tissue factor at the site of vascular injury activates the extrinsic coagulation
system. The fibrin formed develops into a secondary hemostatic plug.

CLASSIFICATION OF HEMOSTATIC DISORDERS

1. Bleeding Disorders: (hemorrhagic disorder/ hemorrhagic diathesis)

- bleeding disorders have an abnormal tendency to bleed due to failure of hemostasis.
2. Thrombotic Disorders:
they can cause thrombus formation.

BLEEDING DISORDERS CAUSED BY VESSEL WALL ABNORMALITIES

Vascular Purpura (Nonthrombocytopenic Purpura):

is a group of disorder of blood vessels that results in bleeding. They should be
distinguished from bleeding disorders due to abnormalities of platelets.
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 Compiled by: Medicah S. Peligrino

References:
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Applications (Fifth Edition) Elsevier (Singapore) Pte. Ltd.; Elsevier Inc.
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Edition) New Delhi, India; Jaypee Brothers Medical Publishers
-Steininger, C.A., Martin, E.A., Keopke, J.A.,; (1992) Clinical Hematology: Principles, Procedures,
Correlations Philadelphia, U.S.A.; J.B. Lippincott
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Brothers Medical Publishers
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U.S.A.; Lippincott William and Wilkins