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Suyasning HI
Tujuan pembelajaran
• Peranan hemostasis
• Komponen yang terlibat dalam proses
hemostasis
- Pembuluh darah
- Trombosit
- Faktor koagulasi
- Inhibitor koagulasi
- Fibrinolisis
- Kaskade kimia hemostasis
Hematopoiesis
HEMOSTASIS
DEPENDENT UPON:
Vessel Wall Integrity
Adequate Numbers of Platelets
Proper Functioning Platelets
Adequate Levels of Clotting Factors
Proper Function of Fibrinolytic Pathway
Platelets – cont.
Megakaryoblast
Megakaryocyte
Platelets
Regulation of Thrombopoiesis
9
Function of Platelets
• Plays a role in Hemostasis = prevention of blood loss.
• Adhesion
• Shape change
• Aggregation
• Release
• Clot Retraction
Platelet function
Adhesion
Aggregation
Secretion
Platelet Adhesion
• Platelets stick to exposed collagen underlying
damaged endothelial cells in vessel wall
Platelet Release Reaction
• Platelets activated by adhesion
• Extend projections to make contact with each other
• Release Thromboxin A2, Serotonin & ADP activating other platelets
• Serotonin & Thromboxin A2 are vasoconstrictors decreasing blood
flow through the injured vessel. ADP causes stickiness
Platelet Aggregation
• Activated platelets stick together and activate new platelets to
form a mass called a Platelet Plug
• Plug reinforced by fibrin threads formed during clotting
process
Platelet
1. Adhesion
Endothelium
2. Shape change
Resting platelet Activated platelet
Platelet shape change and
Aggregation
Platelet Plug Formation
1. Blood vessel injury.
2. Platelets come in contact with damaged blood vessel.
3. They become activated and adhere to the injured area.
4. This will activate even more platelets to come to the
injured area resulting in platelet plug formation.
Platelet haemostatic plug formation
Platelet Plug formation Cont.
FX F Xa
Blood
FV
PLTs, Ca++ clot
Prothrombin Thrombin
FINAL COMMON Fibrin
Fibrinogen
PATHWAY
Bleeding Disorders
• Hemophilia:
– ↑ bleeding tendency.
– X-linked disease.
– Affects males.
– 85% due to FVIII deficiency (hemophilia A), and 15% due to FIX
deficiency (hemophilia B).
Hemophilia FX F Xa
Blood
FV clot
PLTs, Ca++
Prothrombin Thrombin
Fibrinogen Fibrin
Anticoagulants
• Heparin
– Liver, lungs, mast cells, basophils
– Direct antithrombin
– Prevent the conversion of Prothrombin to Thrombin
– Injection only
– 6-8 hours
• Warfarin
– Almost all coagulation factors are synthesized in the liver.
– Suppresses the synthesis of Prothrombin, FVII, FIX, & FX vitamin
K dependent factors
– Orally
– 48 hours
HEMOSTASIS
1. VASCULAR PHASE
2. PLATELET PHASE
3. COAGULATION PHASE
4. FIBRINOLYTIC PHASE
PLATELET PHASE
PLATELETS ADHERE TO THE DAMAGED
SURFACE AND FORM A TEMPORARY PLUG.
Coagulation Phase
Notes:
Extrinsic Pathway-
Intrinsic Pathway-
Common Pathway-
COAGULATION PHASE
THROUGH TWO SEPARATE PATHWAYS
THE CONVERSION OF FIBRINOGEN
TO FIBRIN IS COMPLETE.
FIBRINOLYTIC PHASE
ANTICLOTTING MECHANISMS ARE ACTIVATED
TO ALLOW CLOT DISINTEGRATION AND REPAIR
OF THE DAMAGED VESSEL.
LABORATORY EVALUATION
• PLATELET COUNT
• BLEEDING TIME (BT)
• PROTHROMBIN TIME (PT)
• PARTIAL THROMBOPLASTIN TIME (PTT)
• THROMBIN TIME (TT)
PLATELET COUNT
NORMAL 100,000 - 400,000 CELLS/MM3
• Clot Retraction
• Fibrinolysis
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