platelets physiology
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TRANSCRIPT
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Hemostasis
Defination:
Prevention of blood loss.
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Events Involved In Hemostasis
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Whenever a vessel is ruptured, hemostasis is achieved by:
1. Vascular constriction
2. Formation of a platelet plug
3. Formation of a blood clot as a result
of blood coagulation.
4. Eventual growth of fibrous tissue into
the blood clot to close the hole in the
vessel permanently.
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Vascular Constriction
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• In ruptured blood vessel
1. Pain impulses from the site of trauma
reach the spinal cord.
• From the spinal cord order signal arise.
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• through the sympathatic nerves
• Lead to spasm of the vessel.
2. Local muscle also contribute to the
vascular vasospasm.
3. local autacoid factors from the
traumatized tissues and blood
platelets.
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• The vasospasm lasts for almost half an
hour and it is directly proportional to
the intensity of trauma.
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In the smaller vessels, the platelets are
responsible for much of the
vasoconstriction by releasing a
vasoconstrictor substance,
thromboxane A2.
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Formation of the Platelet Plug
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Platelets
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• Platelets or thrombocytes are small
colorless, non nucleated cells.
• Shape is spherical or rod shaped and
become oval or disc shaped when
inactivated.
• Size: 1 to 4 micrometers in diameter.
• Life span: 10 - days
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• Development: From the pluripotentstem
cells in the bone marrow.
• CFU-M Colony forming megakaryocytes
• Megakaryoblast
• Promegakaryoctye
• Megakaryocytes
• Platelets
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Normal concentration:
• 150,000 to 300,000 per microliter.
• Structure:
• Cell membrane
• Cytoplasm
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Cell Membrane of Platelet
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• It is 6 nm thick and contain lipids
(phospholipids, cholesterol and
glycolipids),Carbohydrates(glycocalyx),
Proteins and glycoproteins.
• Out of all glycoprotein and
phospholipids are functionally
important.
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Glycopropteins
• Prevents the adherence of platelets to
normal endothelium.
• Accelerates the adherence of platelets
to collagen and damaged endothelium
in ruptured blood vessels.
• Forms a receptor for ADP and
thrombin.
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Cytoplasm The cytoplasm of the platelets include:
• Golgi apparatus
• Endoplasmic reticulum
• Mitochondria
• Microtubule
• Microvessels
• Microfilaments
• Granules
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Cytoplasm also contains:
• Proteins
• Enzymes
• Hormones.
• Chemical substances
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Proteins
The major proteins present are
contractile proteins which are
responsible for the contraction of
platelets:
• Actin
• Myosin
• Thrombosthenin
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Chemical substances:
• Calcium ions
• Mg- ions.
• Adenosine triphosphate (ATP)
• Adenosine diphosphate (ADP)
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Function Of Platelets
• Its surface has glycoprotein coat that
adhere it to injured endothelial cells…
….preventing bleeding.
• Actin, myosin & thrombosthenin that
are contractile proteins…. cause clot
retraction.
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• Secretes growth factor that promotes
growth & multiplication of vascular
endothelial cells, vascular smooth cells
& fibroblasts…. repair damaged
vascular wall.
• Its membrane has phospholipids that
activate intrinsic system of blood
clotting
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Life span Of Platelets
• Platelets are eliminated from the
circulation mainly by the tissue
macrophage system in the spleen.
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Mechanism of the Platelet Plug
• When platelets come in contact with a
damaged vascular surface, platelets
attach to the exposed collagen fibers in
the vascular wall.
• Platelets immediately change their own
characteristics.
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• Platelets begin to swell and assume
irregular forms with numerous
irradiating pseudopods protruding from
their surfaces
• Contractile proteins in the platelets
contract forcefully and cause the
release of granules that contain
multiple active factors
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• Adenosine diphosphate (ADP) is
released which causes surface of
nearby circulating platelets to become
sticky and it adheres to the first layer of
aggregated platelets
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• The aggregated platelets adhere to the
von Willebrand factor that leaks into
the traumatized tissue from the plasma
• It leads to the release of more ADP ,
which cause more platelets to pile up at
the defected site.
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• The aggregating process is reinforced
by the formation of Thromboxane A2.
• It directly promotes platelet
aggregation and further enhances it
indirectly by triggering the release of
even more ADP from the platelet
granules.
• Formation of platelet plug takes place
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• Thirdly, the platelet plug release other
chemical substances that play a role in
blood clotting.
• Platelet plugging mechanism alone is
sufficient to seal tears in the capillaries
and small vessels but, large holes
require formation of blood clot to stop
bleeding.
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Limitation of Platelet Plug
• Normal endothelium of the vessel
release Prostacyclin which prevents
platelet aggregation.
• So, platelet plug is limited to the
defected part of the vessel and does
not spread to the normal vascular
tissue.
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Formation Of Blood Clot
• If there is a large defect in the vessel
then blood clot + platelet plug are
required to stop bleeding.
• A clot on the top of platelet plug
supports it and reinforces the seal over
the break in the vessel.
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Onset Of Formation Of Blood Clot:
• 15 – 20 sec…… in severe trauma.
• 1 – 2 min…… in minor trauma.
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• Ultimate step in clot formation is the
conversion of fibrinogen which is a
soluble protein that is produced by the
liver and is normally always present in the
plasma to fibrin which is insoluble thread
like molecule.
thrombin
Fibrinogen Fibrin
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• Fibrin molecules adhere to the
damaged vessel surface forming a
loose netlike meshwork that traps the
cellular elements of blood.
• The clot appears red because of
abundance of RBC that are trapped in
it.
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• The original fibrin web is weak
because the fibrin threads are loosely
interlaced.
• Rapidly, various chemical linkages are
formed between adjacent strands to
strengthen and stabilize the clot mesh
work.
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• The cross linkage process which is
catalyzed by a clotting factor known as
factor XIII (Fibrin stabilizing factor).
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Fibrous Organization or Dissolution of the Blood
Clot
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Once a blood clot has formed, it can
follow one of two courses:
• It can become invaded by fibroblasts,
which subsequently form connective
tissue all through the clot.
• It can dissolve.
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• The usual course for a clot that forms
in a small hole of a vessel wall…… is
invasion by fibroblasts, beginning
within a few hours after the clot is
formed.
• This event is promoted at least partially
by growth factor secreted by platelets.
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• Complete organization of the clot into
fibrous tissue takes place within 1 to 2
weeks.
• When excess blood has leaked into the
tissues and tissue clots have occurred
where they are not needed.
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• Special substances within the clot itself
usually become activated. These
function as enzymes to dissolve the
clot.
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Mechanism of BloodCoagulation
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Procoagulants:
• Substances that cause or affect blood
coagulation that have been found in
the blood and in the tissues…. promote
coagulation
Anticoagulants:
• Substances that inhibit coagulation are
called Anticoagulants.
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• Whether blood will coagulate depends
on the balance between these two
groups of substances.
• In the blood stream, the anticoagulants
normally predominate, so that the
blood does not coagulate while it is
circulating in the blood vessels.
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• But when a vessel is ruptured,
procoagulants from the area of tissue
damage become “activated” and
override the anticoagulants, and then a
clot does develop.
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Three Essential Steps Involved In Clotting:
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(1) In response to rupture of the vessel or
damage to the blood itself, a complex
cascade of chemical reactions occurs
in the blood involving more than a
dozen blood coagulation factors.
• Formation of a complex of activated
substances collectively called
prothrombin activator.
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(2) The prothrombin activator catalyzes
conversion of prothrombin into
thrombin in the presence of
sufficient amounts of ionic Ca++.
(3) The thrombin acts as an enzyme to
convert fibrinogen into fibrin fibers that
mesh with platelets, blood cells, and
plasma to form the clot.
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• The clotting cascade may be triggered
by the intrinsic pathway or the extrinsic
pathway:
• The intrinsic pathway precipitates
clotting within damaged vessels as well
as clotting of blood samples in test
tubes.
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• All elements necessary to bring about clotting by means of the intrinsic pathway are present in the blood.
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Extrinsic pathway for initiating clotting
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