Oral Anticoagulants — NOACs, Antiplatelets & Fibrinolytics
Heparins, Warfarin, DOACs, Antiplatelet Drugs, Fibrinolytics & Reversal Agents
Past RGUHS + DNB + MPMSU + MUHS + VNSGU · 49
MPMSUOct '25
MPMSUJan '25
RGUHSJun '24
RGUHSJun '24
MUHSWinter '24
MPMSUJun '23
DNBOct '23
VNSGUJun '23
RGUHSNov '22
RGUHSMay '22
RGUHSJul '21
MPMSUAug '21
DNBDec '21
MUHSSummer '21
RGUHSNov '20
MPMSUJul '20
DNBJun '20
RGUHSNov '19
RGUHSMay '19
MPMSUMay '19
MPMSU2019
MUHSSummer '19
MUHSWinter '19
RGUHSMay '18
RGUHSMay '18
RGUHSMay '18
MPMSUMay '18
MPMSUMay '18
MPMSU2017
MPMSUJun '17
MUHSSummer '17
MUHSSummer '16
VNSGUApr '16
MPMSU2014
DNBDec '14
DNBDec '14
MUHSWinter '14
DNBDec '13
DNBDec '12
RGUHSMay '11
MPMSU2011
MPMSU2011
DNBDec '11
RGUHSOct '10
RGUHSMay '09
RGUHSOct '08
RGUHSApr '08
RGUHSApr '06
MPMSU2004
Introduction
- Haemostasis is the regulated arrest of blood loss while blood stays fluid in intact vessels — a balance between coagulation and fibrinolysis. Therapeutic antithrombotic drugs tip this balance to prevent or treat pathological thrombosis.
- Three drug families act on different limbs: anticoagulants (inhibit fibrin formation), antiplatelet drugs (inhibit platelet activation/aggregation) and fibrinolytics/thrombolytics (dissolve formed thrombi).
- Therapeutic corollary of thrombus type — arterial = platelet-rich "white" thrombi (high shear) → antiplatelets primary; venous = fibrin-rich "red" thrombi (sluggish flow) → anticoagulants primary.
- Anticoagulants prevent thrombus extension and embolism by slowing fibrin formation — they do not dissolve an existing clot (that is the fibrinolytics' role).
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Oral Anticoagulants Noacs
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