Anticoagulant drugs Flashcards
1
Q
Clinical uses of anticoagulants
A
- Prevention of deep vein thrombosis
- In treatment of deep vein thrombosis/ prevention of pulmonary emboli
- Prevention of thrombosis on prosthetic heart valves
2
Q
Mechanism of action of warfarin
A
- It prevents the carboxylation of factors II, XII, IX and X by inhibiting vitamin K reductase
- The tissue factors cant then localize to the right place (on platelets) and cant stimulate the conversion of fibrinogen to fibrin
3
Q
clinical use of warfarin
A
Prolonged therapy
4
Q
administration of warfarin
A
- Orally
* Is rapidly absorbed by GI tract
5
Q
Rate of onset of warfarin
A
- Rate of onset is slow as already carboxylated tissue factors have to be broken down and factor VII has a half life of 6h which is the fastest
- Rate of onset therefore 6-12h
6
Q
duration of action/ half life of warfarin
A
Duration 4-5 days
It strongly binds to plasma proteins
Its own half life = 40 hours and is metabolized in the liver
7
Q
Warfarins actions are potentiated by
A
- Drugs which displace warfarin from plasma proteins (Aspirin) → As it would cause an increased amount of free warfarin in the blood stream
- Drugs which interfere with liver function (sulphonamides)→ reducing the livers function would decrease warfarin clearance
- Drugs which interfere with platelet function (NSAID)
- Liver disease (decreases factor production and warfarrin clearance)
- Decreased Vit K availability
8
Q
Warfarins actions are decreased by
A
- Drugs which induce metabolizing enzymes (Barbiturates) → so warfarin clearance is increased
- Promoted clotting factor synthesis (Vitamin K)
- Reduced warfarrin adsorption (colestipol) → many patients with DVT also have high LDL levels so are on drugs to prevent absorption in the gut
9
Q
Unwanted side effects of warfarin
A
•Haemorrhage – bowel or brain
10
Q
who can warfarin not be administered to
A
•Pregnant women as it is teratogenic
11
Q
What is the mechanism of action of heparin
A
- It has a negative charge and binds and activates antithrombin III (AT3) which has a positve charge
- Antithrombin III inhibits Factor IIa (thrombin) and Factor Xa
- Heparin/ AT3 more potent action at factor IIa than factor Xa
12
Q
Clinical use (time) of heparin
A
•Acutely (short term therapy)
13
Q
Limitations in heparin use
A
- Activity modified by platelet factor 4 which is released from platelts and inhibits heparin action
- If factor Xa is already bound to fibrin, it cannot interact with AT3/heparin complex
14
Q
Administration of heparin
A
IV
15
Q
pharmacokinetics of heparin
A
- Complex due to high plasma protein binding
- There is an initial rapid removal of heparin due to binding to endothelial and macrophage cells therefore an initial big bolus is given to saturate this followed by slow infusion
- Slower subsequent removal by renal excretion
