ANTI COAGULANT DRUGS
Drugtargets in thrombosis
Antiplatelets platelet function
Fi brinolytics Enhance fibrin breakdown e.g Streptokinase
Anticoagulants Fibrin formation coagulation cascade
NB Anticoags
are of better
use in veins as
the blood flows
slower and so
is composed of
more fibrin
Anti coagulantdrugs
I 1 Non
Heparin Coumarins vitamin K
Un fractionated warfarin direct oral anticoagulant
Low molecular NOACSIDOACS
weight
, A Heparin Released from intact blood vessel
endothelium to prevent uncontrolled clotting
chain
Family of glycosaminoglycans of variable
length un fractionated Heparin CU FH crude
mix of all chain
lengths
Fractionated into low molecular
weight heparin
CC MW H longer duration and more predictable
anti effect
coag
Mechanism of action
Binds to and activates antithrombin 111 CAT111
break in the cascade
coagulation
U EH AT 111 complex then inactivates thrombins
IIA and X A No conversion of
fibrinogen to
fibre is
L M WH is not inactivate thrombin
long enough to
so its main effect is to inactivate Xa
Pharmacokinetics
Large highly charged molecules so can not be
absorbed by GLT
U FH C due to chains
given i v
large and subcu
and is
immediately active The 40 90 mins C
at A dosage due to metabolic pathways in lover
Drugtargets in thrombosis
Antiplatelets platelet function
Fi brinolytics Enhance fibrin breakdown e.g Streptokinase
Anticoagulants Fibrin formation coagulation cascade
NB Anticoags
are of better
use in veins as
the blood flows
slower and so
is composed of
more fibrin
Anti coagulantdrugs
I 1 Non
Heparin Coumarins vitamin K
Un fractionated warfarin direct oral anticoagulant
Low molecular NOACSIDOACS
weight
, A Heparin Released from intact blood vessel
endothelium to prevent uncontrolled clotting
chain
Family of glycosaminoglycans of variable
length un fractionated Heparin CU FH crude
mix of all chain
lengths
Fractionated into low molecular
weight heparin
CC MW H longer duration and more predictable
anti effect
coag
Mechanism of action
Binds to and activates antithrombin 111 CAT111
break in the cascade
coagulation
U EH AT 111 complex then inactivates thrombins
IIA and X A No conversion of
fibrinogen to
fibre is
L M WH is not inactivate thrombin
long enough to
so its main effect is to inactivate Xa
Pharmacokinetics
Large highly charged molecules so can not be
absorbed by GLT
U FH C due to chains
given i v
large and subcu
and is
immediately active The 40 90 mins C
at A dosage due to metabolic pathways in lover
