Essentials of Anatomy and Physiology

prothrombin, and that is also true. The stages of clot-
ting may be called a cascade, where one leads to the
next, as inevitable as water flowing downhill. Pro-
thrombin activator, the product of stage 1, brings
about the stage 2 reaction: converting prothrombin to
thrombin. The product of stage 2, thrombin, brings
about the stage 3 reaction: converting fibrinogen to
fibrin (see Box 11–6: Hemophilia).
The clot itself is made of fibrin, the product of
stage 3. Fibrin is a thread-like protein. Many strands
of fibrin form a mesh that traps RBCs and platelets,
and creates a wall across the break in the vessel.

Once the clot has formed and bleeding has stopped,

clot retractionand fibrinolysisoccur. Clot retraction

requires platelets, ATP, and Factor 13 and involves

folding of the fibrin threads to pull the edges of the

rupture in the vessel wall closer together. This will

make the area to be repaired smaller. The platelets

contribute in yet another way, because as they disinte-

grate they release platelet-derived growth factor

(PDGF), which stimulates the repair of blood vessels

(growth of their tissues). As repair begins, the clot is

dissolved, a process called fibrinolysis. It is important

that the clot be dissolved, because it is a rough surface,

266 Blood

Table 11–3 CHEMICAL CLOTTING

Clotting Stage Factors Needed Reaction

Stage 1

Stage 2

Stage 3

• Platelet factors


• Chemicals from damaged tissue
  (tissue thromboplastin)


• Factors 5,7,8,9,10,11,12


• Calcium ions


• Prothrombin activator from stage 1


• Prothrombin


• Calcium ions


• Thrombin from stage 2


• Fibrinogen


• Calcium ions


• Factor 13 (fibrin stabilizing factor)

Platelet factors tissue thromboplastin 

other clotting factors calcium ions

form prothrombin activator

Prothrombin activator converts prothrombin

to thrombin

Thrombin converts fibrinogen to fibrin

BOX11–6 HEMOPHILIA

cure) has become possible with factor 8 obtained

from blood donors. The Factor 8 is extracted from

the plasma of donated blood and administered in

concentrated form to hemophiliacs, enabling them

to live normal lives.

In what is perhaps the most tragic irony of med-

ical progress, many hemophiliacs were inadver-

tently infected with HIV, the virus that causes AIDS.

Before 1985, there was no test to detect HIV in

donated blood, and the virus was passed to hemo-

philiacs in the very blood product that was meant

to control their disease and prolong their lives.

Today, all donated blood and blood products are

tested for HIV, and the risk of AIDS transmission to

hemophiliacs, or anyone receiving donated blood,

is now very small.

There are several forms of hemophilia; all are

genetic and are characterized by the inability of

the blood to clot properly. Hemophilia A is the

most common form and involves a deficiency of

clotting Factor 8. The gene for hemophilia A is

located on the X chromosome, so this is a sex-

linked trait, with the same pattern of inheritance

as red-green color blindness and Duchenne’s mus-

cular dystrophy.

Without factor 8, the first stage of chemical

clotting cannot be completed, and prothrombin

activator is not formed. Without treatment, a

hemophiliac experiences prolonged bleeding after

even minor injuries and extensive internal bleeding,

especially in joints subjected to the stresses of

weight-bearing. In recent years, treatment (but not