L16 Anticoagulant, Thrombolytic &
Antiplatelet Agents I
1. INTRODUCTION TO THROMBOSIS
Thrombosis = formation of unwanted clot inside a blood vessel
- Most common hemostatic abnormality.
Treated with:
● Anticoagulants (prevent clot formation)
● Fibrinolytics/thrombolytics (dissolve clots)
Thrombotic Disorders
● Acute myocardial infarction
● Acute ischaemic stroke
● Deep vein thrombosis (DVT)
● Pulmonary embolism (PE)
Thrombus vs Embolus
● Thrombus – clot attached to vessel wall
● Embolus – floating clot; causes distal obstruction
○ From leg veins → lungs → Pulmonary embolism
○ From left heart → brain → stroke
, 2. PATHOPHYSIOLOGY OF THROMBOSIS
1) Venous stasis
Reduced blood flow → ↑ viscosity → microthrombi formation (thrombus may grow)
2) Coagulation activation
Endothelial interaction → cytokines → leukocyte adhesion to endothelium→ balance between
coagulation & fibrinolysis determines progression.
3) Endothelial damage
From trauma/surgery → hypercoagulable state due to ↑ tissue factor & ↓
antithrombin/fibrinolysins.
4) Decreased vein contractility & valve dysfunction
Leads to chronic venous insufficiency → varicose veins, oedema, venous ulcers.
3. PLATELET RESPONSE TO VASCULAR
INJURY
Resting state
● Endothelial prostacyclin (PGI₂) & NO inhibit platelet aggregation.
● Injury → ↓ PGI₂ → ↓ cAMP → ↑ aggregation.
Adhesion & Activation
Upon collagen exposure:
● Platelet granules release ADP, thromboxane A₂, serotonin, PAF, thrombin
● ↓ cAMP & ↑ Ca²⁺ → platelet activation
Antiplatelet Agents I
1. INTRODUCTION TO THROMBOSIS
Thrombosis = formation of unwanted clot inside a blood vessel
- Most common hemostatic abnormality.
Treated with:
● Anticoagulants (prevent clot formation)
● Fibrinolytics/thrombolytics (dissolve clots)
Thrombotic Disorders
● Acute myocardial infarction
● Acute ischaemic stroke
● Deep vein thrombosis (DVT)
● Pulmonary embolism (PE)
Thrombus vs Embolus
● Thrombus – clot attached to vessel wall
● Embolus – floating clot; causes distal obstruction
○ From leg veins → lungs → Pulmonary embolism
○ From left heart → brain → stroke
, 2. PATHOPHYSIOLOGY OF THROMBOSIS
1) Venous stasis
Reduced blood flow → ↑ viscosity → microthrombi formation (thrombus may grow)
2) Coagulation activation
Endothelial interaction → cytokines → leukocyte adhesion to endothelium→ balance between
coagulation & fibrinolysis determines progression.
3) Endothelial damage
From trauma/surgery → hypercoagulable state due to ↑ tissue factor & ↓
antithrombin/fibrinolysins.
4) Decreased vein contractility & valve dysfunction
Leads to chronic venous insufficiency → varicose veins, oedema, venous ulcers.
3. PLATELET RESPONSE TO VASCULAR
INJURY
Resting state
● Endothelial prostacyclin (PGI₂) & NO inhibit platelet aggregation.
● Injury → ↓ PGI₂ → ↓ cAMP → ↑ aggregation.
Adhesion & Activation
Upon collagen exposure:
● Platelet granules release ADP, thromboxane A₂, serotonin, PAF, thrombin
● ↓ cAMP & ↑ Ca²⁺ → platelet activation
