Anticoagulants and antiplatelets Flashcards

1
Q

Example of oral anticoagulant

A

Warfarin

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2
Q

What does warfarin do

A

Vitamin K antagonist

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3
Q

Mechanism of action of warfarin

A

1) New factor formed from liver (it is a precursor)
2) new factor is chemically modified (still the precursor)
3) Precursor undergoes in the coagulation cascade
4) The system is Vitamin K dependent
5) Therefore warfarin blocks Vitamin K reductase which is needed for Vitamin K fo act as a cofactor
6) Therefore the production of the proper coagulation factors is inhibited by warfarin

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4
Q

How long does warfarin take ti impact on the production of coagulation factors

A

3 days

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5
Q

what is warfarin used for

A
  • In patients with replaced heart valves
  • Atrial fibrillation
  • DVT
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6
Q

What is the dose of warfarin determined by

A

INR

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7
Q

What does the INR measure

A

Anticoagulation of the patient

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8
Q

What are examples of injectable anticoagulants

A

Unfractionated heparin

Low molecular weight heparins eg enoxaparin

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9
Q

Difference between warfarin and enoxaparin

A

Enoxaparin acts immediately

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10
Q

What does enoxaparin do

A

Activates antithrombin III which inactivates some clotting factors and thrombin by complexing with serine protease of the factors (interferes with coagulation factors)

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11
Q

What is the use of heparin

A

Used to prevent thrombosis and used to prevent blood clotting on collection

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12
Q

When is heparin particularly used

A

Used whilst warfarin takes effect because warfarin takes 3 days to take effect

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13
Q

What are DOACs

A

Drugs which directly inhibit the coagulation factors

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14
Q

Benefits of DOACs

A

Fewer complications and less drug reactions

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15
Q

Drawback of DOACs

A

Warfarin is reversible but DOACs are expensive and challenging to reverse ie if the patient is bleeding and you want to reverse it

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16
Q

What are prostacyclin and nitric oxide derived from

A

Endothelial cells

17
Q

Function of prostacyclin

A
  • Stops platelets from sticking (acts on platelets to increase cAMP)
  • Vasodilator
18
Q

Function fo nitric oxide

A

Regulate blood pressure and blood flow and also prevents platelets from sticking

19
Q

How are prostacyclin, prostaglandins and thromboxane synthesises from arachidonic acid

A

1) arachidonic acid found in membrane
2) PLA2 breaks that down to free AA’s
3) Cyclo-oxygenase (COX) which is an enzyme breaks that down to endoperoxides which in turn form prostacyclin, prostaglandins and thromboxane

20
Q

Role of thromboxane

A

Promotes aggregation and decreases cAMP

21
Q

Effects of aspirin

A

Antiplatelet drug

22
Q

What is aspirin used for

A

Preventing myocardial infarction in patients who have previously had a MI

23
Q

What else does aspirin do

A

Inhibits cyclo-oxygenase irreversibly

24
Q

Aspirin inhibits cyclo-oxygenase which means that the production of prostacyclin is inhibited as well as thromboxane which is counter intuitive. therefore how is aspirin an anticoagulant

A

The nucleus of the endothelial cell which has been inhibited to produce thromboxane and prostacyclin produced the mRNA for cyclooxyrgenase so prostacyclin is pumped out of the endothelial cells

25
Q

Why is use of aspirin irreversible in platelets

A

Because platelets do not have a nucleus and so there is no possibility of producing mRNA for cycle-oxygenase

26
Q

Therefore overall effect of aspirin

A

Platelets have no nuclei so can’t produce any more cyclo=oxygenase so no more thromboxane produced until new platelets have been synthesised

-endothelial cells have nuclei so can produce more cycle-oxygenase to produce prostacyclin

27
Q

Effective anti-platelet drug

A

Low dose aspirin

28
Q

What is clopidogrel

A

-Antiplatelet drug

29
Q

What does clopidogrel do

A

Binds to ADP receptors and stops ADP from activating the platelets

30
Q

When is fibrinolysis activated

A

When coagulation is taking place

31
Q

When are thrombolytics used

A
  • In thromboembolic stroke

- Pulmonary embolism