Platelets = thrombocytes

Platelets = thrombocytes
Thrombopoiesis = Platelet formation
* requires thrombopoietin (from liver)
*occurs in the myeloid tissue
*myeloid stem cell
megakaryocytethousands of platelets(cell
*”lifespan” = 10 days(no nucleus, not even
complete cells
Hemostasis – stoppage of bleeding
• Hemostasis occurs in three stages:
I) Vascular spasm- nature of vessels , due to
pain and smooth muscle response
- enhanced by serotonin and thromboxane A2
released from platelets
II. Platelet plug formation – platelets aggregate
and form a plug. Why?
-enhanced by ADP and thromboxane A2
III. Blood coagulation – very complex, involves
many plasma proteins, most synthesized in
the liver. Vitamin K is found to be vital to
this process.
A) Intrinsic pathway- can happen in test tubes
or unbroken vessels. Slower. Triggered by
damaged endothelial cells (lining of blood
A’) Extrinsic pathway – Faster. Triggered by
damaged cells outside of bloodstream.
Prothrombin (pp) ----------prothrombin activator/ Ca++-----------------------Thrombin (enz)
Fibrinogen (pp) --------thrombin--------------------------Fibrin (mesh)
Clot dissolution
I. Fibrinolysis – dissolving (lysing)the fibrin
A) An inactive plasma protein (pp),
plasminogen, gets built into each clot. It is
eventually activated by healing tissues to
become an active enzyme called plasmin.
This enzyme helps to dissolve the fibrin.
Thrombosis is clotting in an unbroken vessel.
The clot is called a thrombus. If it dislodges
and travels to another part of the body, it is
then called an embolus. An example in
pulmonary embolism.
Other substances…..
• A) prostacyclin (from wbc’s) - inhibits
thromboxane A2 and platelet adhesion
• B) heparin (from wbc’s) – blocks thrombin
• C) aspirin – blocks thromboxane A2 and
prevents platelet aggregation
X – linked , recessive. Results in a lack of one or
more clotting factors involved in hemostasis.
Who is most susceptible?
MALES  one X chromosome