ANP 1105 Lecture Notes - Lecture 11: Liver Disease, Haemophilia, Cirrhosis

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ANP1105 – Lecture 11
Hemostasis
- Process by which the body stops bleeding upon injury and maintains blood in the fluid
state with vessel integrity
- Process is rapid and localized
- Platelets
○ Cytoplasmic fragments of megakaryocytes
○ Contain purple staining granules that contain clotting factors and enzymes
○ Anucleate
○ Lifespan = 10 days
○ Platelet formation regulated by thrombopoetin
○ 250 000 - 500 000 platelets /ul blood
- (3) phases
1. Vascular spasms
○ Vasonconstritcion of vessel in response to damage
○ Triggers - damage, chemicals from endothelial cells and platelets
○ Pain reflexes
○ Purpose - valuable bc a strongly constricted artery can significantly reduce blood loss
§ 20-30 min allow time for next steps
2. Platelet plug formation
○ Usu platelets do not stick to each other or to endothelial lining
○ NO and PGI2 (prostacyclin) produced by endothelial cells; inhibits platelet aggregation
in undamaged tissue
○ Exposure of collagen stimulates platelets to swell , become spiky and sticky
○ Adhere to exposed collagen (von Willebrand factor) - degranulation
○ ADP (adenosine diphosphate)
§ Enhances aggregation and degranulation
○ Serotonin and thromboxane A2
§ Enhances vascular spasm and aggregation
• Primary hemostasis
○ Platelets
§ Interact with injured blood vessel wall
§ Interact with each other
§ Produce primary hemostatic plug
○ Primary platelet plug
§ Fragile
§ Can easily be dislodged from the vessel wall
• Platelet function:
○ Provide negatively charged surface for factor x and prothrombin activation
○ Release substances that mediate vasoconstriction, platelet aggregation, coagulation and
vascular repair
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○ Provide surface mb, proteins to attach to other platelets, bind collagen and
subendothelium
• Aggregation
○ Platelet to platelet interaction
§ Begins 10-20 sec after vascular injury and platelet adhesion
§ Requires dense granule release from the adhering platelets
§ Requires Ca++ and ATP
§ Requires fibrinogen and fibrinogen receptors GPIIb and IIIa
§ Mechanism
- ADP released from platelet cytoplasm upon adherance induces exposure of fibrinogen
receptors of GPIIb and IIIa
- Fibrinogen binds to the exposed GPIIb and IIIa
- Extracellular Ca++ dependant fibrinogen bridges from between adjacent platelets
thereby promoting platelet aggregation
- This is primary or reversible aggregation
- Secondary aggregation begins with the release of dense granules
- Secondary aggregation is considered irreversible
• Secretion
○ Secondary aggregation begins with platelet secretion of dense granules
○ Dense granules contain large amounts of ADP
○ ADP binds to the platelet mb triggering the synthesis and release of TXA2
○ Release of large amounts of ADP combined with TXA2 amplifies the initial
aggregation of platelets into a large platelet mass
3. Coagulation
○ Reinforces the platelet plug with fibrin threads that act as 'molecular glue' for
aggregated platelets
○ Blood transformed from liquid to gel - clotting factors and procoagulants
§ Clotting factors - plasma proteins - produced in liver - I - XIII
○ 3 phases
A. Prothrombin activator formed
B. Prothrombin to thrombin
C. Fibrinogen molecules
- Fibrin mesh
- Also many procoagulants and anticoagulants; latter predominate in intact vessels
• (2) pathways to prothrombin activator
Intrinsic pathway Extrinsic pathway
- Clotting of blood outside body (ex tube) or in - Clotting of blood associated with body
and blood vessels
Slightly damaged vessel Damage
- Slower pathway to factor x and PA - Release of tssue factor
- Bypass many steps of intrinsic pathway
- Faster pathway to factor X and PA
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