anti-platelets + anticoagulants + thrombolytics Flashcards
example of thrombolytics
streptokinase
alteplase
unistreplase
urokinase
MOA of thrombolytics
activate tissue plasminogen to plasmin which can break down insoluble fibrin mesh
PK: intracoronary injection, IV
use of thrombolytics
- emergency treatment of coronary artery thrombosis
- peripheral arterial thrombosis and embolism
ischaemic stroke (very narrow time window and must first ensure it is not haemorrhagic stroke)
types of anticoagulants
heparin
warfarin
MOA of heparin
amplify effect of anti thrombin III by causing conformational change that exposes acitve site of ATIII
use: prevent further thrombosis
PK: IV
AE of heparin
haemorrhage
if have, stop heparin and give protamine sulfate which binds tightly to heparin and sequesters it
MOA of warfarin
inhibit vit K reductase, causing vit K to remain oxidised so vit K cannot carry out post translational modification of factors 2,7,9,10
PK: oral so quick absorption
types of anti-platelet drugs
NSAIDs eg aspirin
GP IIB/IIA receptor
ADP receptor blocker
ODE inhibitor
MOA of aspirin
inhibit COX, preventing converion of arachidonic acid to thromboxane A2
use: prophylaxis for transient cerebral ischaemia and protective effect post MI
why is the effect of aspirin irreversible
once platelet has been deactivated, platelet remains dysfunctional and can only be replaced through synthesis of new platelets
AE of aspirin/NSAID
bleeding, gastric ulcer and GI bleed
MOA of GP IIB/IIA receptor
blocking recepotr prevents binding of fibrin to platelet and cross linking cannot occur -> clot cannot be formed
use of GP IIB/IIA receptor
prevent restenosis after angioplasty where rute force is wused which can cause damage and activate clotting
vessel can easily restenose and plaque can reform
ADP receptor blocker
eg ticlopidine, clopidogrel
prevent binding of ADP to ADP receptor to activate platelet to aggregate
advantage of clopidogrel over ticlopidine
less neutropenia side effect
