BIOL 271 Lecture Notes - Lecture 2: Prothrombinase, Tissue Plasminogen Activator, Vasospasm

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9 Mar 2014
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Blood (Continued from Cardiovascular System)
Hemostasis: stoppage of bleeding when blood vessels are damaged
must be quick, localized and carefully controlled
three mechanisms:
vascular spasm
platelet plug formation
coagulation (clotting)
Vascular Spasm
damage to arteries or arterioles —> immediate contraction of
smooth muscle in vessel wall
reduces blood loss for several minutes to several hours
allows time for other hemostatic mechanisms to proceed
Platelet Plug Formation
3 step process:
platelet adhesion
platelet release reaction
platelet aggregation
Platelet Adhesion
platelets stick to collagen exposed when endothelium is
damaged
Platelet Release Reaction
adhered platelets extend projections, contact other platelets
and degranulate (release of clotting factors)
thromboxane A2, ADP and serotonin released —> constriction
of injured vessel, activation of other platelets
Platelet Aggregation
ADP activates more platelets that become sticky and form a
platelet plug
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plug reinforced by fibrin threads formed during clotting
process
Blood Clotting
blood normally remains liquid within vessels but thickens to a gel
when removed
gel separates into:
serum (straw-coloured liquid)
plasma minus clotting factors (they are used in the clot)
clot (gel)
cells trapped in a network of insoluble protein fibres
(fibrin)
Clotting Factors:
chemicals required for clot formation (coagulation)
include:
inactive enzymes synthesized by liver cells
molecules released by platelets or damaged tissues
Clotting Cascade
cascade of reactions that results in the formation of fibrin threads
**prothrombinase (prothrombin activator) >requires Ca2>
prothrombin >> thrombin >> fibrinogen >> fibrin
fibrin is the substance that forms the clot
**know slide (see diagram)
prothrombinase formation is initiated by either or both of:
intrinsic pathway
activated by:
damage to blood itself
exposure of blood to collagen in traumatized vessel
wall
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damaged platelets release phospholipids
reaction requires several mins
extrinsic pathway
activated by chemicals from damaged tissue
activated when thromboplastin (tissue factor from injured
cells) leaks into bloodstream
occurs rapidly (w/in secs)
common pathway (after reaching prothrombinase, only 1
pathway)
in the presence of Ca2+:
prothrombinase converts prothrombin to thrombin
thrombin converts soluble fibrinogen to insoluble
fibrin, and activates factor XIII
factor XIII (fibrin stabilizing factor) strengthens
and stabilizes fibrin threads into a sturdy clot
positive feedback effects of thrombin:
accelerates formation of prothrombinase
activates platelets >> increases platelet aggregation
and phospholipid production
Clot Retraction and Blood Vessel Repair
requires adequate platelet count
platelets pull on fibrin threads (retraction), drawing edges of
damaged vessel closer together
serum can still escape, but blood cells cannot
clot eventually replaced by new endothelium (quick mitosis) and
scar tissue produced by fibroblasts
Role of Vitamin K
fat-soluble vitamin (absorption dependent on lipid absorption)
produced by bacteria in large intestine (waste product of bacteria)
required for normal clotting
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