1 megakarocyte produces 1-2000 platelets. Matures in 5 days
2/3 platelets circulate in blood
1/3 platelets sequestered in spleen
Old platelets phagocytized by the RE system (mainly spleen)
Platelet function in hemostasis
Endothelium is damaged, platelets will being to interact with exposed sub-endothelium tissues.
Platelets are activated by exposure to the sub-endothelium, they lose their disk shapes to form pseudopods that extend and attach to exposed collagen
Platelets "tie up" to collagen and other platelets with proteins that bind with different glycoprotein receptors.
Plasma and Platelets
Attaches to other platelets with Fibrinogen
Attaches to collagen with vWF
Platelets "stick" to the surfaces of damaged blood vessels
Platelets sticking to each other at the damaged vessel
Promoted by: Collagen, Thrombin, Serotonin, TXA2
Inhibited by: Aspirin, Some prostaglandins
Impairs the synthesis of thromboxane (TXA2), stimulates platelet granule release.
Platelet aggregation is impaired for the entire life span of the platelet.
Commonly prescribed to inhibit vascular occlusions (clots) in patients at risk for coronary occlusions
Effect on platelet's take place within 5-15 minutes after ingestion.
Inhibits platelet GP IIb/IIIa
When people die from hemostasis disorders, they usually die from excessive clotting
Quantitaive and Qualitative Platelet Tests
A normal platelet count does not necessarily imply normal function.
Excessive bruising or bleeding with a normal platelet count suggests a qualitative platelet disorder.
Thrombocytopenic patients can be transfused with platelets
Blood (plasma) coagulation proteins
Synthesized in liver
"Cascading-domino" sequence of chemical interactions between the proteins, tissue substances and calcium leads to the formation of an insoluble protein-the fibrin clot at the site of the injured blood vessel.
The fibrin clot seals off the damaged blood vessel and limits blood loss.
Other proteins in the fibrinolytic system limit fibrin formation and eventually its dissolution.
Activated Factor IIa
Inactivated Factor II
Coagulation proteins can be measured
Individually (factor assays test, fibrinogen)
Collectively (PT and PTT tests)
Group I Fibrinogen
Consumed during clotting (absent in serum)
Factors 5 and 8 extremely liable
Increased in inflammation, pregancy, and oral contraceptives
Not consumed during clotting (except 2)
Requires Vitamin K for synthesis
(11, 12, PK, HMWK)
Not consumed during clotting
Soluble plasma protein precursor to fibrin
Stable precursor of thrombin
Active form of prothrombin
Thrombin converts fibrinogen--fibrin
Promotes platelet aggregation
Any tissue (non-plasma) phospholipid substance (cell membrane guts)
Only ionized Ca is active in hemostasis
Very liable (1/2 life=16 hours)
Consumed during clotting
2 Complex components
High Molecular Weight: vWF, VIII RCo (Platelet aggregation), VIII Ag (Antigenic site)
Low Molecular Weight: VIII C (Procoagulant), VIII Ag (Antigenic Site)
Plasma Thromboplastin Component
Plasma Thromboplastin Antecedent
Fibrin Stabilizing Factor
Mechanisms of the coagulation proteins
Activated by contact with tissue phospholipids following endothelial damage.
Activated by contact with negatively charged solid surfaces (collagen, glass)
Represents the merging of the extrinsic and intrinsic pathway