262
U N I T 3
Hematopoietic Function
called
thrombopoietin
that causes proliferation and
maturation of megakaryocytes.
2
Thrombopoietin is
produced in the liver, kidney, smooth muscle, and bone
marrow. Its production and release are regulated by the
number of platelets in the circulation.
Although platelets lack a nucleus, they have many of
the structural and functional characteristics of a whole
cell.
1–5
They contain an outer cell membrane, microtu-
bular structures, and inner organelles (Fig. 12-2). The
platelet cell membrane, which plays an important role in
platelet adhesion and the coagulation process, is covered
with a surface coat of glycocalyx, consisting of glycopro-
teins, glycosaminoglycans, and several coagulation fac-
tors adsorbed from the plasma.
2
One of the important
glycoproteins is glycoprotein IIb/IIIa (gpIIb/IIIa), which
binds fibrinogen (factor I) and acts to connect platelets
together to form large aggregates. Phospholipids, which
are also present in the platelet membrane, provide criti-
cal binding sites for calcium and coagulation factors
in the intrinsic coagulation pathway.
2,3
The cell mem-
brane is supported by a network of microtubules, actin
filaments, myosin, and actin-binding proteins. They
are arranged circumferentially and are responsible for
maintaining the platelet’s disk shape.
The central part of the platelet contains mitochon-
dria, enzymes needed for synthesis of adenosine tri-
phosphate (ATP) and the prostaglandin thromboxane
A
2
(TXA
2
), glycogen, and two specific types of granules
(
α
- and
δ
-granules) that release mediators for hemosta-
sis.
2–5
The
α
-granules contain fibrinogen, coagulation
factors, plasminogen, plasminogen activator inhibitor,
and platelet-derived growth factors. The contents of
these granules play an important role in platelet aggre-
gation, blood coagulation, and the initial phase of ves-
sel repair. The release of growth factors causes vascular
endothelial cells, smooth muscle cells, and fibroblasts to
proliferate and grow. The
δ
-granules, or dense granules,
mainly contain adenosine diphosphate (ADP), ATP, ion-
ized calcium, serotonin, and histamine, which facilitate
platelet adhesion and vasoconstriction at the site of ves-
sel injury.
The Coagulation System
The coagulation system uses plasma proteins that are
present as inactive procoagulation factors. Each of the
procoagulation or coagulation factors, identified by
Roman numerals, performs a specific step in the coagu-
lation process. The activation of one procoagulant or
proenzyme is designed to activate the next factor in the
sequence (i.e., cascade effect). Because most of the inac-
tive procoagulants are present in the blood at all times,
the multistep process ensures that a massive episode of
intravascular clotting does not occur by chance. It also
means that abnormalities of the clotting process occur
when one or more of the factors are deficient or when
conditions lead to inappropriate activation of any of
the steps.
Most of the coagulation factors are proteins synthe-
sized in the liver. Vitamin K is necessary for the synthe-
sis of factors VII, IX, and X; prothrombin (factor II);
and proteins C and S. Calcium (factor IV) is required
in all but the first two steps of the clotting process. The
body usually has sufficient amounts of calcium for these
reactions. Inactivation of the calcium ion prevents blood
from clotting once removed from the body. The addition
of citrate to blood stored for transfusion purposes pre-
vents clotting by chelating ionized calcium.
A clot is not expected to be a permanent solution to
vessel injury; thus, blood clotting is accompanied by
processes designed to control the coagulation cascade
and dissolve the clot once bleeding has been controlled.
FIGURE 12-1.
A scanning electron micrograph depicting a
number of red cells enmeshed in a fibrinous matrix on the
luminal surface of an indwelling catheter (magnification ×
5698). (From the Centers for Disease Control and Prevention
Public Health Images Library No. 7313. Courtesy of Janice
Carr.)
GPIIb/IIIa glycoprotein
δ
-Granules
α
-Granules
Glycogen
Actin
Myosin II
Microtubules
Plasma
membrane
Glycocalyx coat
Mitochondria
FIGURE 12-2.
Platelet structure.
