Anticoagulation Flashcards

1
Q

What tends to drive clot formation in:

a) venous and intracardiac systems
b) arterial system

A

a) coagulation cascade

b) platelet activation

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2
Q

what is used as primary prevention for venous thromboembolism (DVTs and PEs)?

A

Heparin (usually LMWH)

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3
Q

Name two examples of heparins

A

enoxaparin

dalteparin

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4
Q

how are heparins administered and what is used to work out the dose?

A

subcutaenously

use weight to work out dose (200 units/kg)

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5
Q

what is the mechanism of action of heparins?

A

increase activity of antithrombin which inactivates clotting factors.

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6
Q

what can be used for primary prevention of DVT and PE other than heparins?

A

fondaparinux or DOACs

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7
Q

in what patients might you use unfractionated heparin to treat DVT or PE?

A

renal impairment

patients with an increased risk of bleeding

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8
Q

after starting warfarin, why do you have to continue giving a LMWH for 5 days?

A

warfarin only has effects on coagulation factors that are being newly synthesised so it takes a few days for it to reach a therapeutic level of anticoagulation

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9
Q

what drugs can be used as alternatives to warfarin?

A

DOACs

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10
Q

what is the main side effect of warfarin?

A

increased risk of bleeding

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11
Q

why should warfarin be avioded in patients with liver disease?

A

less able to metabolise it so they risk having too much warfarin in their system

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12
Q

warfarin has a low therapeutic index, what does this mean?

A

there is a fine line between the dose needed to prevent clotting and the dose that will cause bleeding

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13
Q

name some drugs that interact with warfarin and by doing so will reduce its effect making the person more susceptible to clotting

A

Rifampicin,carbamazepine (anti-epileptic),phenytoin (anti-epileptic),primidone (barbiturate anti-epileptic)

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14
Q

name some CYP inhibitors that reduce the metabolism of warfarin thus increase bleeding risk

A

fluconazole, metronidazole, amiodarone, gemfibrozil and sulfamethoxazole

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15
Q

how do some antibiotics cause an increase in the effects of warfarin due to their effects on gut flora?

A

some kill gut flora that synthesise vitamin K meaning there are even less clotting factors available.
especially cotrimoxazole, metronidazole, macrolides and fluoroquinolones

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16
Q

name the one DOAC that doesn’t have ‘xa’ in its name

A

dabigatran

17
Q

when would you use a DOAC?

A

for secondary prevention of a VTE or as primary prevention in patients undergoing elective hip or knee replacement surgery.

18
Q

what should you check before starting warfarin?

A

electrolytes and renal function

19
Q

how are DOACs metabolised and excreted? what effect does this have on who you should avoid prescribing it to?

A

cytochorme P450 and eliminated in faeces and urine.

avoid in hepatic or renal disease.

20
Q

what is the antidote for warfarin?

A

phytomenadione (vitamin K1), prothrombin complex concentrate, fresh frozen plasma

21
Q

what is the antidote to dabigatran overdose?

A

idarucizumab