541
CHAPTER FOURTEEN
Blood
Fibroblasts
(see chapter 5, p. 153) invade blood clots that
form in ruptured vessels, producing connective tissue with
many F
bers throughout the clots, which helps strengthen
and seal vascular breaks. Many clots, including those that
form in tissues as a result of blood leakage (hematomas),
disappear in time. In clot dissolution, F brin threads absorb
a plasma protein called
plasminogen
(proF brinolysin). Then
a substance called plasminogen activator released from the
lysosomes of damaged tissue cells converts plasminogen to
plasmin.
Plasmin is a protein-splitting enzyme that can digest
F
brin threads and other proteins associated with blood clots.
Plasmin formation may dissolve a whole clot; however, clots
that F
ll large blood vessels are seldom removed naturally.
A blood clot abnormally forming in a vessel is a
throm-
bus
(throm
bus). A clot that dislodges, or a fragment of a clot
that breaks loose and is carried away by the blood fl
ow, is
called an
embolus
(em
bo-lus). Generally, emboli continue
to move until they reach narrow places in vessels where they
may lodge and block blood fl
ow, causing an
embolism.
A blood clot forming in a vessel that supplies a vital
organ, such as the heart (coronary thrombosis) or the brain
(cerebral thrombosis), blocks blood fl
ow and kills tissues the
vessel serves (
infarction
) and may be fatal. A blood clot that
extrinsic and intrinsic clotting mechanisms.
Table 14.9
lists
the clotting factors, their sources, and clotting mechanisms.
Laboratory tests commonly used to evaluate blood coagulation
mechanisms include
prothrombin time
(PT) and
partial thromboplastin
time
(PTT). These tests measure the time it takes for F
brin threads to
form in a sample of blood plasma. The prothrombin time test checks
the extrinsic clotting mechanism, whereas the partial thromboplastin
test evaluates intrinsic clotting.
Fate of Blood Clots
After a blood clot forms, it soon begins to retract as the tiny
processes extending from the platelet membranes adhere
to strands of F
brin within the clot and contract. The blood
clot shrinks, pulling the edges of the broken vessel closer
together and squeezing a fl
uid called
serum
from the clot.
Serum is essentially plasma minus all of its F brinogen and
most other clotting factors. Platelets associated with a blood
clot also release
platelet-derived growth factor
(PDG±), which
stimulates smooth muscle cells and F broblasts to repair dam-
aged blood vessel walls.
TABLE
14.8
|
Blood Coagulation
Steps
Extrinsic Clotting
Mechanism
Intrinsic Clotting Mechanism
Trigger
Damage to vessel or tissue
Blood contacts foreign surface
Initiation
Tissue thromboplastin
Hageman factor
Series of reactions involving several clotting factors and calcium ions (Ca
+2
) lead to the production of:
Prothrombin activator
Prothrombin activator
Prothrombin activator and calcium ions cause the conversion of:
Prothrombin to thrombin
Prothrombin to thrombin
Thrombin causes fragmentation, then joining of:
±ibrinogen to F
brin
±ibrinogen to F
brin
TABLE
14.9
|
Clotting Factors
Clotting Factor
Source
Mechanism(s)
I
(F
brinogen)
Synthesized in liver
Extrinsic and intrinsic
II
(prothrombin)
Synthesized in liver, requires vitamin K
Extrinsic and intrinsic
III
(tissue thromboplastin)
Damaged tissue
Extrinsic
IV
(calcium ions)
Diet, bone
Extrinsic and intrinsic
V
(proaccelerin)
Synthesized in liver, released by platelets
Extrinsic and intrinsic
VII
(serum prothrombin conversion accelerator)
Synthesized in liver, requires vitamin K
Extrinsic
VIII
(antihemophilic factor)
Released by platelets and endothelial cells
Intrinsic
IX
(plasma thromboplastin component)
Synthesized in liver, requires vitamin K
Intrinsic
X
(Stuart-Prower factor)
Synthesized in liver, requires vitamin K
Extrinsic and intrinsic
XI
(plasma thromboplastin antecedent)
Synthesized in liver
Intrinsic
XII
(Hageman factor)
Synthesized in liver
Intrinsic
XIII
(F
brin-stabilizing factor)
Synthesized in liver, released by platelets
Extrinsic and intrinsic
There is no clotting factor VI. The chemical once thought to be factor VI is apparently a combination of activated factors V and X.
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