Coagulation Unit 1 Study Guide
Primary hemostasis, secondary hemostasis, fibrinolysis & what does it do and
how does it do it?
a. Disruption of the intact endothelium initiates hemostatic responses
i. Primary hemostasis → platelet plug formation
1. Vascular system response
2. PLTs adhere to endothelial wall
3. PLTs aggregate
4. PLTs release coagulant compounds
ii. Secondary hemostasis → fibrin clot formation
1. Coagulation cascade
iii. Fibrinolysis → digestion of the fibrin clot
1. Production of plasmin
b. Hemorrhage → vascular injury exceeding ability to form a PLT plug
c. Thrombus → stagnation of blood flow disturbs endothelial cell
anticoagulant effect
Pro and anticoagulant properties of vessels
d. Normal, intact endothelium is nonthrombogenic → resistant to PLTs,
leukocytes, and coagulation proteins
i. Anticoagulant properties of intact vessels
1. Maintain normal blood flow
○ Prostacyclin (PG12) → maintains normal blood flow
by inhibiting PLT aggregation and limits thrombus
formation beyond the damaged vessel
○ Tissue factor pathway inhibitors (TFPIs) → inhibit
factors Vlla (7a)/TF and factor X
2. Inhibitors of clot formation
○ Heparan sulfate → helps activate AT
○ Thrombomodulin → cofactor in protein C
activation when bound to thrombin
3. Fibrinolysis regulation
, ○ Tissue plasminogen activator (t-PA) → regulates
fibrinolysis, when bound to fibrin can activate
plasminogen to form plasmin
ii. Procoagulant properties of damaged vessels
1. Injured endothelial lining → promotes vasoconstriction
to minimize blood flow through the injured site
2. Collagen → binds vWF and PLTs
3. vWF → binds PLT receptor GP 1b/V/IX and collagen to
promote PLT adhesion, also a carrier for VIII (8)
4. TF → released after vascular trauma that initiates
coagulation by activating factor VII (7) with ionized Ca++
via the extrinsic pathway
5. Plasminogen activator inhibitors (PAIs) → neutralize the
activity of plasmin, plasminogen, and t-PA, are associated
with the risk of thrombosis
PLT structure and function
e. PLTs → anucleated cytoplasmic fragments of bone marrow
megakaryocytes
i. Lifespan = 7-10 days in circulation
ii. Normal PLT count = 150-400 x 10^3/uL
iii. Functions:
1. Provide a (-) charged phospholipid surfaces on which
secondary hemostasis can occur
2. Release substances that mediate vasoconstriction,
platelet aggregation, coagulation, and repair
3. Providing surface membrane GPs (like GP IIb and GP IIIa
to attach to other platelets via fibrinogen, and GP
Ib/V/IX to bind to collagen and subendothelium via vWF
f. Organelles
i. a-granules → the most numerous granules in PLTs, contain:
1. PF4
Primary hemostasis, secondary hemostasis, fibrinolysis & what does it do and
how does it do it?
a. Disruption of the intact endothelium initiates hemostatic responses
i. Primary hemostasis → platelet plug formation
1. Vascular system response
2. PLTs adhere to endothelial wall
3. PLTs aggregate
4. PLTs release coagulant compounds
ii. Secondary hemostasis → fibrin clot formation
1. Coagulation cascade
iii. Fibrinolysis → digestion of the fibrin clot
1. Production of plasmin
b. Hemorrhage → vascular injury exceeding ability to form a PLT plug
c. Thrombus → stagnation of blood flow disturbs endothelial cell
anticoagulant effect
Pro and anticoagulant properties of vessels
d. Normal, intact endothelium is nonthrombogenic → resistant to PLTs,
leukocytes, and coagulation proteins
i. Anticoagulant properties of intact vessels
1. Maintain normal blood flow
○ Prostacyclin (PG12) → maintains normal blood flow
by inhibiting PLT aggregation and limits thrombus
formation beyond the damaged vessel
○ Tissue factor pathway inhibitors (TFPIs) → inhibit
factors Vlla (7a)/TF and factor X
2. Inhibitors of clot formation
○ Heparan sulfate → helps activate AT
○ Thrombomodulin → cofactor in protein C
activation when bound to thrombin
3. Fibrinolysis regulation
, ○ Tissue plasminogen activator (t-PA) → regulates
fibrinolysis, when bound to fibrin can activate
plasminogen to form plasmin
ii. Procoagulant properties of damaged vessels
1. Injured endothelial lining → promotes vasoconstriction
to minimize blood flow through the injured site
2. Collagen → binds vWF and PLTs
3. vWF → binds PLT receptor GP 1b/V/IX and collagen to
promote PLT adhesion, also a carrier for VIII (8)
4. TF → released after vascular trauma that initiates
coagulation by activating factor VII (7) with ionized Ca++
via the extrinsic pathway
5. Plasminogen activator inhibitors (PAIs) → neutralize the
activity of plasmin, plasminogen, and t-PA, are associated
with the risk of thrombosis
PLT structure and function
e. PLTs → anucleated cytoplasmic fragments of bone marrow
megakaryocytes
i. Lifespan = 7-10 days in circulation
ii. Normal PLT count = 150-400 x 10^3/uL
iii. Functions:
1. Provide a (-) charged phospholipid surfaces on which
secondary hemostasis can occur
2. Release substances that mediate vasoconstriction,
platelet aggregation, coagulation, and repair
3. Providing surface membrane GPs (like GP IIb and GP IIIa
to attach to other platelets via fibrinogen, and GP
Ib/V/IX to bind to collagen and subendothelium via vWF
f. Organelles
i. a-granules → the most numerous granules in PLTs, contain:
1. PF4
