platelets physiology
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Hemostasis
Definition:
Prevention of blood loss.
Events Involved In Hemostasis
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.
Vascular Constriction
• In ruptured blood vessel
1. Pain impulses from the site of trauma
as well as from the surrounding
nervous tissue originate and reach the
spinal cord.
• From the spinal cord order signal arise.
• The order signals pass 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.
• As the vessel wall is damaged the
action potential developed along the
vessel wall lead to vasoconstriction.
• The vasospasm lasts for almost half an
hour and it is directly proportional to
the intensity of trauma.
Vasoconstriction resulting from local
myogenic contraction of the blood
vessels is initiated by direct damage to
the vascular wall.
In the smaller vessels, the platelets are
responsible for much of the
vasoconstriction by releasing a
vasoconstrictor substance,
thromboxane A2.
Formation of the Platelet Plug
Platelets
• 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
• Development: From the pluripotentstem
cells in the bone marrow.
• CFU-M Colony forming megakaryocytes
• Megakaryoblast
• Promegakaryoctye
• Megakaryocytes
• Platelets
Normal concentration:
• 150,000 to 300,000 per microliter.
• Structure:
• Cell membrane
• Microtubule
• Cytoplasm
Cell Membrane of Platelet
• 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.
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.
Cytoplasm The cytoplasm of the platelets include:
• Golgi apparatus
• Endoplasmic reticulum
• Mitochondria
• Microtubule
• Microvessels
• Microfilaments
• Granules
Cytoplasm also contains:
• Proteins
• Enzymes
• Hormones.
• Chemical substances
Proteins
The major proteins present are
contractile proteins which are
responsible for the contraction of
platelets:
• Actin
• Myosin
• Thrombosthenin
Chemical substances:
• Calcium ions
• Mg- ions.
• Adenosine triphosphate (ATP)
• Adenosine diphosphate (ADP)
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.
• 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
Life span O f Platelets
• Platelets are eliminated from the
circulation mainly by the tissue
macrophage system in the spleen.
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.
• 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
• 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
• 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.
• 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
• 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.
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.
Formation Of Blood Clot
• If there is a large defect in the vessel
then blood clot + platelet plug are
required to stop bleeding.
• As clot on the top of platelet plug
supports it and reinforces the seal over
the break in the vessel.
Onset Of Formation Of Blood Clot:
• 15 – 20 sec…… in severe trauma.
• 1 – 2 min…… in minor trauma.
• 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
• 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.
• 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.
• The cross linkage process which is
catalyzed by a clotting factor known as
factor XIII (Fibrin stabilizing factor).
Fibrous Organization or Dissolution of the Blood
Clot
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.
• 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.
• 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.
• Special substances within the clot itself
usually become activated. These
function as enzymes to dissolve the
clot.
Mechanism of BloodCoagulation
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.
• 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.
• 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.
Three Essential Steps Involved In Clotting:
(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.
(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.
• 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.
• All elements necessary to bring about clotting by means of the intrinsic pathway are present in the blood.
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