PLATELETS AND
HEMOSTASIS
Platelets
• Platelets are the smallest formed elements.
• Develops from the process known as
thrombopoiesis or thrombocytopoiesis in the bone
marrow.
Stages of Development
• Stem cells (Pluripotent stem cells, committed stem cells
and CFU-Mega)
• Megakaryoblast
• Megakaryocytes
• Platelets
Pluripotent stem cells
Committed stem cells
CFU-Mega
Megakaryoblast
Basophil megakaryocyte
Granular megakaryocyte
Mature megakaryocyte
Platelets
Structure of Platelets
• Small, granulated, spherical or oval bodies
• Diameter: 1 to 4 micrometers
• Normal count: 150,000 -300,000 per microliter. Count
<50,000/mm3 of blood is critical count.
• Cytoplasm contains:
1. actin and myosin molecules
2. Thrombosthenin, a contractile protein
3. endoplasmic reticulum and the Golgi apparatus that synthesize
various enzymes.
4. Mitochondria
5. fibrin-stabilizing factor
6. Platelet granules
• Cell membrane contains:
1. coat of glycoproteins that repulses adherence to
normal endothelium but causes adherence to injured
areas of the vessel wall.
2. phospholipids
• Half life: 4 days.
• Elimination: macrophages in spleen
Platelet granules
• Two types: alpha granules and dense granules
• Alpha granules: 50-80 granules.
• Contain chemicals like:
1. von Willebrand factor
2. Platelet derived growth factor (PDGF)
3. Platelet activating factor (PAF)
4. Plasminogen
5. Platelet fibrinogen
6. Proaccelerin
7. Tissue plasminogen activator (tPA)
• Dense granules: 3-8 dense granules per
platelet
• Contain chemicals like:
1. Serotonin
2. ADP
3. Calcium
4. ATP
Properties of platelets
• Adhesion
• Aggregation
• Activation and release
Functions of Platelets
• Temporary hemostasis
• Blood coagulation
• Clot retraction
• Phagocytosis
• Storage and transport
• Vascular growth by platelet derived growth factor.
HEMOSTASIS
Hemostasis
Process of forming clots in the wall of damaged
blood vessels and preventing blood loss while
maintaining blood in the fluid state.
Ref: Ganong’s review of Physiology
Hemostasis
Response to injury:
1. vascular constriction
2. formation of a platelet plug (temporary hemostatic plug)
3. blood coagulation (definitive hemostatic plug)
Vascular constriction
• local myogenic spasm
• Nervous reflexes
• vasoconstrictor substance, thromboxane A2 and
serotonin.
Formation of platelet plug
• Platelet adhesion: platelets have high affinity
to adhere to the exposed vascular wall.
• Exposed collagen and von Willebrand factor in
the injured vessel wall attract platelets.
Platelet activation and release
• adhesion of platelets to damaged vascular
endothelium activates the platelets.
• ADP, serotonin, thromboxane A2 are released
from the platelets.
ADP and thromboxane A2 stimulate other platelets
to become activated and release additional
chemicals.
Platelet aggregation
• ADP, thromboxane A2 and platelet activating
factor produced from the activated platelets
further facilitate it.
• Thus, accumulation of more platelets occurs at
the site of vascular injury.
• Platelet aggregation leads to temporary
hemostatic plug formation.
Why does the platelet plug not continue to develop and
expand over the surface of the adjacent normal vessel
lining?
prostacyclin and nitric oxide release from the adjacent
normal endothelium which inhibit platelet aggregation.
Formation of Definitive hemostatic plug or blood
coagulation
• The loose aggregation of platelets in the temporary
plug is bound together and converted into the
definitive clot by fibrin.
• Occurs due to activation of clotting factors.
• fundamental reaction in the clotting of blood is
conversion of the soluble plasma protein fibrinogen to
insoluble fibrin.
• The conversion of fibrinogen to fibrin is catalyzed by
thrombin.
• activated factor X converts prothrombin into
thrombin.
• Factor X can be activated by reactions in either of two
pathways, an intrinsic pathway and an extrinsic
pathway.
Extrinsic Pathway
Intrinsic Pathway
Bleeding time
Clotting time
Role of calcium in coagulation
• for promotion or acceleration of all the blood-
clotting reactions.
• This fact is utilised to keep blood uncoagulated
outside the body.
Clot Retraction
• Shrinking of the clot expressing serum out of it is called
clot retraction.
• A retracted clot is a consolidated and stable thrombus,
which firmly seals the opening in the injured vessel
• Functions of Clot Retraction
1. Strongly seals injured vessel
2. Facilitates wound healing
3. Prevents thrombolysis
Anticoagulation process
• Anticoagulation process activated with the
coagulation.
• It limits coagulation, otherwise all the blood in the
body would be coagulated once coagulation has
started anywhere in the CVS.
Coagulation antagonised in the body by:
• Prostacyclin
• about 85 to 90 per cent of the thrombin becomes adsorbed to
the fibrin fibers as they develop preventing excessive spread
of the clot.
• Antithrombin III in plasma along with heparin prevents the
activity of factor IXa, Xa, XIa XIIa.
• Circulating blood carries away the activated factors from the
site of thrombus and the factors are then destroyed by liver
• Thrombomodulin, a protein expressed on endothelial cells,
binds to thrombin and modulates its action
• tPA (Tissue Plasminogen Activator) breaks down fibrin.
The fibrinolytic system
Anticoagulants
• Anticoagulants for Blood Collection
1. EDTA (ethylenediamine tetra-acetic acid)
2. Sodium citrate
3. Double Oxalate
4. Heparin
Anticoagulants for Treatment
1. Vitamin K antagonists (warfarin)
2. Heparin
Abnormalities of Coagulation
Hemophilia A
• Also known as classical hemophilia
• Occurs due to deficiency of factor VIII.
• X-linked recessive hereditary disease
Vitamin K deficiency
• Vitamin K is required for the synthesis of prothrombin (factor
II) and factors VII, IX and X in the liver.
Purpura
• The clinical condition in which the capillary abnormality
results in bleeding is known as Purpura.
• Reduction in platelet count- thrombocytopenia.
The End
