Flashcards in Anticoagulants II Deck (40)
Prophylactic use: Prevention of thrombotic disorders
Therapeutic use: Treatment of established thrombus
Coumadin inhibits which factors
factors II, VII, IX, and X
warfarin's structure is similar to
All agents depress the formation of functional forms of factors II (prothrombin), VII, IX and X by inhibiting the carboxylation of glutamic acid in these proteins which is essential for Ca+2 binding. (blocks vit k synthesis)
factors are still present but not functional
onset of warfarin/coumadin
long- takes 8 to 10 hours before the amount of active factors decreases, 3-5 days before a pt is properly anti-coagulated.
due to binding of albumin in the plasma
therefore it is not use when a pt presents to the ER with a thrombus but can be given for them to take afterwards at home
bioavailability of warfarin/coumadin
metabolism of warfarin/coumadin
hydroxylated to inactive compounds by the hepatic endoplasmic reticulum.
varies greatly between patients therefore pts must be monitored
which pathway does warfarin/coumadin affect
what do you use to monitor warfarin/coumadins effects
Prothrombin time (PT)/INR
what deviation from baseline is needed for warfarin to be in the therapeudic range
a PT of 1.5 times baseline
Reagent based variations have been noted in the prothrombin time. To obtain uniform degrees of anticoagulation, the concept of international normalized ratio (INR) has been introduced.
The INR can be used universally to adjust the level of anticoagulant in a given patient. Thus it helps in the optimization of dosage .
ratio of the patients PT divided by the mean normal control
what are some factors that affect the dose of warfarin/coumadin that you want to give a patient
how does diet affect warfarin
green leafy vegetables high in vitamin K decrease the affects of warfarin/coumadin
how do Drugs cause warfarin potentiation
by causing vitamin K deficiency.
by displacing warfarin from protein binding sites.
by decreasing clotting-factor synthesis.
by suppressing or competing for microsomal enzymes.
by having antiplatelet aggregating properties.
how do drugs cause inhibition of the anticoagulant action of warfarin
by decreasing warfarin absorption.
by enhancing warfarin metabolism.
Toxicity of Warfarin
* hypoprothombinemia resulting in ecchymosis, purpura, hematuria, hemorrhage.
*All oral anticoagulants pass the placental barrier and may cause fetal malformation
necrosis (due to non-functionality of protein C)
how is protein C affected by warfarin and how does this affect the patient
protein C non-functioning in the presence of warfarin. functional protein C's levels drop before the other factors. Because protein C is an anticoagulant and inhibits factors V and VII, initially there is an increased tendency to clot
Treatment of oral anticoagulant overdose
1. Replacement of 4 factors. Infusion of whole fresh blood or frozen plasma.
2. Recombinant Factor VIIa
3. Vitamin K
Function of Vitamin K
Essential to the attachment of a calcium binding functional group to prothrombin protein (presence of γ carboxyglutamic acid).
Required for the synthesis of clottable coagulation factors (II, VII, IX and X).
Therapeutic use of Vitamin K
Drug induced hypoprothrombinemia antidote.
Intestinal disorders and surgery (gastrectomy).
Hypoprothrombinemias of newborn.
toxicity of Vitamin K
High doses sometime cause hemolysis in infants (mainly water soluble vitamin K).
Certain individuals who are sensitive to primaquine may develop hemolysis.
anti Xa agents
characteristics of new oral anticoagulants (anti-Xa and antithrombin)
oral anticoagulants (anti-Xa and antithrombin) uses
stroke prevention in people who previously had a DVT
or treatment of a DVT
advantages and disadvantages of oral anticoagulants (anti-Xa and antithrombin)
they do not need to be monitored but also a disadvantage is you cannot monitor them therefore is emergency surgery is needed you do not know how much is present.
fixed once per day