Hemostasis Flashcards
Platelets are derived from
GM-CSF thrombo
—> Megakaryocytes*
*hematopoietic linaege
Another name for platlets
Thrombocytes
When are platelets formed
They are active when they a fragments off the megakaryocytes
Normal levels of platelets
150,000-450,000 ul^3
What do platelets contain
Actin, myosin, thrombostatin, mitochondria, peroxioomes, COX2, Fribrin
2 granules
2 granules that platelets have
- a-granules : store Von Willebrand factor, fibrinogen, factor 5 (clotting)
- dense-core granules : store ATP, ADP, HT’5, Ca+2
Megakaryocytes and platelets take up what
Fibrinogen that they secrete in the liver for Hemostasis
3 steps for platelets
Adhesion
Activation
Aggregation
What regulates platelet formation
Thrombopoietin (TPO) made in liver and kidney
The C-terminal if it prolongs life of platelet
* increase production and function of hematopoietic stem cells and platelets
How does TPO act
It binds to the c-MPL (CD110) receptor on the Megakaryocytes
Low platelet count effect on TPO
High free TPOs
C-MPL is not internalized and degraded
High platelet count effect on TPO
Low free TPOs and c-MPL receptor is internalized and degraded
4 steps to healing injury
- Vascular Spasm : severed vessel
- Formation of platelet plug : Platelet agglutinate + fibrin appears
- Formation of blood clot
- Repair of Damage : clot retracts
What is vasospasm
Disrupt BF and keep it above the injury = avoid more blood loss
4 things that contribute to vasospasm
- Myogenic : reflex from damage to SM
- Platelet factor : serotonin, thromboxane A2
- Release of molecules from endothelial BV cells
- Neural reflex from pain or injury
How do platelets bind to the vessels
ADHESION
The platelets have glycoproteins
- Von Willebrand factor is released from endothelial cells —> GP 1b/a on platelet
- Injured endothelial cells expose collagen —> GP 1a/2a on platelet
- Laminitis and fibronectin is also exposed —> GP 1c/2a on platelet
What regulates adhesion of platelets
Negative charges and collagen on the surface
What activates the platelet
When the GP are bound on its surface
3 names for Von Willebrand disease
Psudohemophilia
Vascular hemophilia
Angiohemophilia
What happens after the GP receptors of the platelet are activated
- Phospholipase C is activated
- CA+2 influx
- = causes ATP, ADP, CA+2, HT’5 release from DENSE granules (inside platelet)
= a-granules release vWF, Factor 5, Fibrinogen, GFs - Finger like filopodia extensions
- Arachidonic acid—> Thromboxane A2 (by cyclooxgenase)
cyclooxgenase
Converts aracidonic acid —> Thromboxane A2
How do platelets aggregate
- ADP is released : —> bind to P2Y12 on other platelets
- HT’5 + thromboxane A2 activate other platelets also
- Fibrinogen activates another platelet and causes bridges between platelets = PLATELET PLUG
Aspirin on platelet aggregation
Inhibits cyclooxygenase
—I clotting (low thromboxane A2)
Clopidogrel (plavix) on platelet aggregation
Inhibits P2Y12 receptors = no further platelet activation and no aggregation
