Anti- platelet and anti- coagulants Flashcards

1
Q

What is the difference in appearance, consequence and method of prevention of arterial vs venous clots?

A

Appearance: arterial= red// venous= white
Consequence: A–> MI, stroke// V–> DVT, PE
Prevention: A need anti-platelets, V need anti- coagulants

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2
Q

What activates the intrinsic and extrinsic pathways??

A
Intrinsic= exposure of tissue factor in basement membrane- activates factor X
Extrinsic= abnormal surface (class, collagen) leading to factor XII activation
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3
Q

What 3 factors lead to increased coagulability? (virchows triad)

A
  • abnormality in vessel wall
  • abnormality in flow
  • abnormality in blood components
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4
Q

How does warfarin work?

A

inhibits production of vitamin K dependant clotting factors (VII, IX and X)

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5
Q

Why do most people need to take heparin as well for the first 3 days of starting warfarin?

A

Because it takes a few days for the existing clotting factor to be used up and not replaced

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6
Q

What effect will alcohol and NSAIDS have on warfarins effect?

A

Both will increase effect, alcohol because it inhibits the CYP enzyme which metabolised warfarin and NSAIDS because it displaces warfarin from plasma proteins it binds to.

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7
Q

Why is warfarin avoided in young women?

A

It is teratogenic

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8
Q

Name 3 things which will inhibit warfarins effect

A

Leafy greens, cererals, antiepileptics, rifampicin, st johns wort–> these induce CYP450s

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9
Q

Give 3 indications of warfarin

A

AF, DVT, PE, prosthetic heart valve

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10
Q

Give 3 side effects of warfarin

A

bleeding, bruises, severe headache, vomiting, confusion

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11
Q

How can warfarin be reversed?

A
  • Stop warfarin (needs 3 days to get back to normal)
  • Give vitamin K IV if acutely unwelll
  • Consider giving fresh frozen plasma and prothombin complex concentrate if severe bleeding
  • Consider surgery to find source of bleeding
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12
Q

What are the two types of heparin and whats the difference between them?

A

Low molecular weight heparin- eg dalteparin, daily sub cut injections
Unfractionated heparin - IV bolus infusion

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13
Q

How does heparin work?

A

Heparins are glycosaminoglycans which bind and activate anti- thrombin III which then deactivates factor Xa. Unfractioned heparin also inhibits IIa by activating anti- thrombin III.

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14
Q

Describe the monitoring required of LMWH and unfractioned heparin

A

LMWH does need monitoring as response is very predictable. Unfractioned isn’t so requires monitoring

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15
Q

How fast do heparins work?

A

Fairly rapidly, also reverse fast on stopping use

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16
Q

Briefly describe the initiation of warfarin

A

Loading dose of 10mg, usually. Dose on second day will depend on INR response, gradually dose lowered until INR is within required range (usually 2-3). Cover first 3 days with heparin.

17
Q

When is heparin used?

A
  • LMWH peri operatively in low doses as youve removed warfarin
  • LMWH during first few days of initiating warfarin treatment
  • Reduce reoccurance/ extension of coronary artery thrombosis in unstable angina and MI
  • Instead of warfarin in pregnancy
18
Q

Give 3 ADRs of heparin

A
  • intracranial bleeds
  • bleeding at injection sites
  • thrombocytopenia (may trigger autoimmune destruction of platelets)
  • osteoporosis with long term use
19
Q

How is heparin reversed?

A

Using protamine sulphate - dissociates heparin by binding to anti- thrombin III

20
Q

How does dabigatran work?

A

It is a thrombin (factor IIa) inhibitor

21
Q

List 3 anti-platelet drugs

A

Aspirin, dipyridamole, clopidogrel

22
Q

How does dipyridamole work? when is it used?

A

phosphodiesterase inhibitor, this in turn inhibits platelet activation- uses lots in secondary preventions of strokes but can cause flushings and headaches

23
Q

How does clopidogrel work and when is it used?

A

ADP antagonist, used in acute coronary syndromes and post PCI

24
Q

Name two fibrinolytics other than streptokinase

A

Alteplase, reteplase

25
Q

How do alteplase and reteplase work?

A

They are tissue plasminogen activators (tPA), tPA cleaves plasminogen into plasmin, which breaks down fibrin in the clot. It also breaks down fibrinogen systemically (bad), but less so than streptokinase.