For further discussion of the plasma within the
context of blood and lymph structure and func-
tion please see the overview section “The Blood
and Lymph.”
See also BLOOD TRANSFUSION; ERYTHROCYTE; HEMA-
PHERESIS; HORMONE; LEUKOCYTE; LYMPHOCYTE; MONO-
CYTE.
plasmapheresis See HEMAPHERESIS.
platelet The cellular structure indispensable for
COAGULATION(clotting), also called a thrombocyte.
Platelets, which are actually cell fragments rather
than intact cells, separate from parent cells in the
BONE MARROWcalled megakaryocytes, the largest
cells in the BONEmarrow. When platelets emerge
into the circulation they become the smallest cell
particles in the circulating blood. Their small size
permits them to travel into any blood vessel, even
the tiniest arterioles and venules, to respond to
bleeding. Platelets lack nuclei and thus, like ery-
throcytes, cannot divide. They live in the circula-
tion for about 10 days.
The normal number of platelets in the blood is
130,000 to 400,000 per cubic milliliter. The SPLEEN
holds about 30 percent of the blood’s platelets
within its red pulp, releasing them into the circu-
lation when needed to respond to bleeding. This
containment helps reduce the risk for inadvertent
agglutination as platelets swirl into contact with
one another in the bloodstream.
Any breach in a blood vessel that allows blood
to escape results in the release of the enzyme tis-
sue factor (factor III), which attracts droves of
platelets to the site. As the platelets agglutinate
(come into contact with the damaged site and
with one another) they release chemicals such as
serotonin, thromboxane, and phospholipids that
extend and focus the coagulation cascade.
For further discussion of platelets within the
context of blood and lymph structure and func-
tion, please see the overview section “The Blood
and Lymph.”
See also ANTICOAGULATION THERAPY; ARTERY; CELL
STRUCTURE AND FUNCTION; CLOTTING FACTORS; HEMA-
PHERESIS; VEIN.
platelet aggregation The process through which
platelets respond to chemical signals in the BLOOD,
allowing them to adhere to each other and to col-
lagen fibers in the blood to form the hemostatic
plug that will become a blood clot at the conclu-
sion of the COAGULATIONcascade. The formation of
collagen and the conversion of fibrinogen (clotting
factor I) to the enzyme fibrin together initiate a
sequence of chemical conversions that alter
PLATELETsurface proteins as well as attract more
platelets to the location of the injury. As the coag-
ulation cascade continues, platelets accumulate.
The platelets change shape, developing threadlike
extensions called pseudopods that allow them to
extend like vines into the weave of collagen fibers.
The surface of the platelets continues to undergo
chemical changes that attract fibrinogen and
release arachidonic acid, which oxidizes to form
PROSTAGLANDINS, short-acting hormones that are
key players in the IMMUNE SYSTEM’s INFLAMMATION
response. Prostaglandins further attract platelets to
the site.
Converted CLOTTING FACTORS begin to weave
fibers of protein among the fibers of fibrin, throm-
bin, and collagen, forming a netlike structure that
entraps other cells flowing through the blood.
When the clot reaches critical mass additional
chemical reactions begin to shut down the coagula-
tion cascade, bringing the clotting process to a halt.
The surface proteins of circulating platelets revert,
and the platelets no longer adhere to each other.
The reversion also activates mechanisms within the
platelets that cause them to contract, pulling them
tightly into the clot structure. Other proteins cause
the clot to harden, cementing it in place.
Inflammation of the ARTERY walls, such as
occurs with CORONARY ARTERY DISEASE(CAD), attracts
platelets in the same manner as do wounds, set-
ting in motion the events of platelet aggregation in
ways that are detrimental to health. Doctors often
prescribe antiplatelet medications to slow platelet
aggregation in people who have had HEART ATTACK
OR STROKE, or who have CAD. Most of these med-
ications work by blocking the oxidation of arachi-
donic acid, which then inhibits prostaglandin
formation. The most commonly used antiplatelet
medication is aspirin. Platelet aggregation can also
occur as a SIDE EFFECTof medications or a dysfunc-
tion of coagulation.
See also ANTICOAGULATION THERAPY; ATHEROSCLE-
ROTIC PLAQUE; C-REACTIVE PROTEIN.platelet aggregation 163