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HEMOSTASIS
24
Transcript
HEMOSTASIS
HEMOSTASIS
- Process that stops bleeding and prevents blood loss through vessel walls
- Allows repair after tissue damage
- 3 overlapping phases:
- - Vascular phase
- - Platelet phase
- - Coagulation phase
VASCULAR PHASE
VASCULAR PHASE
- A cut in wall of a blood vessels
- - Triggers vascular spasm (contraction of vessel smooth muscle)
- Lasts 30minutes
- Endothelial cells become sticky
- - May block opening completely
PLATELET PHASE
- Begins within 15seconds after injury
- Platelets are activated, aggregate at site, adhere to damaged surfaces
- - To form platelet plug
COAGULATION PHASE
- Begins 30seconds or more after the injury
- Involves complex sequence of events
- - Converts fibrinogen into fibrin (clot)
COAGULATION
- Requires clotting factors that
- - Converts soluble fibrinogen into insoluble fibrin
- As fibrin network grows
- - Blood cells and platelets are trapped within tangle to form a blood clot
- - Seals off damaged part of vessel
CLOTTING FACTORS
- Consist of:
- - 11 plasma proteins
- > Most are produced by liver
- > Exist as proenzymes:
- > activated when there is a cut
- > remains inactivated; "inert"
- - Calcium ions (factor IV)
- Interact with substances produced by platelets and damaged endothelial cells to form a clot
- - Via a casade mechanism
CASCADE MECHANISM
CASCADE MECHANISM
- Consists of chain reactions
- - 1 clotting factors (proenzyme) is coverted into an enzyme that activates a second clotting factor
- - activated by calcium
- EG:
- Factor III converted to activated Factor III, leads to an inert Factor IX converted to active Factor IX
CASCADE MECHANISM
- Forms 3 pathways which ultimately results in a blood clot
- - Extrinsic pathway
- - Intrinsic pathway
- - Common pathway
- Extrinsic and Intrinsic pathways are initiated when a blood vessel is damaged
EXTRINSIC PATHWAY
- Shorter, faster pathway
- Begins in vessel wall
- - Damaged endothelial cells release tissue factor (TF)
- - TF combines with Ca (calcium) and factor VII to activate other factors
- Eventually activates Factor X
EXTRINSIC PATHWAY
INTRINSIC PATHWAY
INTRINSIC PATHWAY
- Occurs within bloodstream
- Begins with activation of clotting factors exposed to collagen
- Requires assistance of platelet factors
- Eventually activates Factor X
COMMON PATHWAY
COMMON PATHWAY
- Final pathway
- Enzymes from both pathways activates Factor X
- Forms enzyme prothrombinase
- - Converts prothrombin to thrombin
- Thrombin converts fibrinogen to fibrin
CALCIUM AND VITAMIN K
- All 3 pathways require Calcium ions
- Vitamin K is also required for production of clotting factors
- - injected into newborns
CALCIUM AND VITAMIN K
CLOT RETRACTION
CLOT RETRACTION
- After clot has formed
- - Platelets contract and pull torn area together
- Reduces size of damaged area
FIBRINOLYSIS
- Gradual dissolution of clot
- Begins with conversion of plasminogen into plasmin
- - By thrombin, tissue plasminogen activator (t-PA)
- Plasmin digests fibrin and breaks down clot which restores circulation
ANTI-COAGULANTS
ANTI-COAGULANTS
- Clotting can be prevented through drugs that:
- - Depress clotting response:
- > EG: Heparin, Coumadin, Aspirin
- - Dissolve existing clots:
- > EG: t-PA, Streptokinase, Urokinase
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