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17. Clinical Pharmacology and Therapeutics > 14. Anti-Platelets and Anticoagulants > Flashcards

14. Anti-Platelets and Anticoagulants Flashcards

1
Q

What is the difference between white clots and red clots?

A

White clots are rich in platelets, red clots are rich in clotting factors.

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2
Q

What are the three components of Virchow’s triad?

A

Hypercoagulability, endothelial damage, and stasis.

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3
Q

What can cause hypercoagulability?

A

Genetics - protein C/S deficient, factor V leiden. Acquired - SLE, OCP, smoking, malignancy.

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4
Q

What can cause endothelial damage?

A

Atheroma in MI/CVA, hypertension, toxins - cigarettes/homocysteine.

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5
Q

What can cause stasis?

A

Immobility - ill health, post-op, economy class; cardiac abnormality - AF, CCF, mitral valve disease, post MI.

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6
Q

Name an anticoagulant.

A

Warfarin.

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7
Q

What is the mechanism of action of Warfarin?

A

Inhibits production of vitamin K dependent clotting factors so less II, VII, IX, and X (extrinsic pathway). This is by competitive inhibition.

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8
Q

What is the onset time for Warfarin to have an effect?

A

Days - slow half life of clotting factors.

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9
Q

Why can warfarin be given orally?

A

Good GI absorption.

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10
Q

Why is heparin needed alongside warfarin initially?

A

Because warfarin has a slow onset of action.

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11
Q

Why must warfarin be stopped 3 days before surgery?

A

It has a slow offset due to long half life, stopping early allow time to synthesise new clotting factors.

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12
Q

How is warfarin metabolised?

A

Hepatic metabolism using cytochrome p450 system.

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13
Q

Why must warfarin be avoided during pregnancy?

A

T1 - teratogenic, T3 - brain haemorrhage.

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14
Q

How can warfarin be monitored?

A

Extrinsic pathway factors, prothrombin time, INR (international normalised ratio).

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15
Q

What is the prothrombin time?

A

Citrated plasma clotting time after adding calcium and thromboplastins.

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16
Q

What is the purpose of having an international normalised ratio (INR)?

A

Allows a standard value corrected for different lab thromboplastin reagents.

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17
Q

What are the drug interactions to be wary of with warfarin?

A

Effects on anticoagulation - most increase anticoagulant effect, some do decrease it.

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18
Q

Name a drug that inhibits hepatic metabolism and the effect it has on warfarin.

A

Amiodarone, quinolone, metronidazole, cimetidine, alcohol. All potentiate warfarin.

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19
Q

Name a drug that inhibits platelet function and the effect it has on warfarin.

A

Aspirin, potentiates effect.

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20
Q

Name a drug that reduces vitamin K from gut bacteria and the effect it has on warfarin.

A

Cephalosporin antibiotics, potentiates effect.

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21
Q

How do NSAIDs impact action of warfarin?

A

They displace binding to albumin so potentiates warfarin effect slightly.

22
Q

Name a drug that inhibits warfarin.

A

Antiepileptics, rifampicin, St Johns Wort.

23
Q

How do inhibitors of warfarin work?

A

Induce hepatice enzymes so increase metabolism.

24
Q

What are the indications of use of warfarin?

A

DVT, PE, atrial fibrillation, mechanical prosthetic valves, recurrent thromboses on warfarin, thrombosis associated with inherited thrombophilia conditions.

25
Q

How long should warfarin be use in the cases of DVT, PE, and AF?

A

DVT 3-6 months, PE 6 months, AF until risk > benefit.

26
Q

What is the goal INR for warfarin therapy in DVT, PE and AF?

A

2.0-3.0.

27
Q

What is the goal INR for warfarin use in mechanical prosthetic valves, recurrent thromboses, or thrombophilia?

A

2.5-4.5.

28
Q

What are the ADRs of warfarin?

A

Bleeding/bruising intracranially, epistaxis, injection, or in GI tract. Also teratogenic.

29
Q

What is a safety issue with a high INR?

A

Risk of brain haemorrhage if over 3.5.

30
Q

How can warfarin therapy be reversed?

A

Parenteral vitamin K (slow effect), or fresh frozen plasma (fast effect).

31
Q

What should be considered when prescribing warfarin?

A

Indications, PMH, medication (DDIs), age, mobility, falls risk score, blood tests, loading dose and heparin cover, and when to start.

32
Q

What should be discussed with the patient before starting warfarin therapy?

A

Side effects, if female talk about teratogenicity, interactions with other medications and OTC and alcohol/cranberry juice/grapefruit juice, need to INR monitoring, and give them an anticoagulant card.

33
Q

What is the mechanism of action for heparins?

A

Activate anti-thrombin III.

34
Q

What are the two types of heparin molecule?

A

Unfractionated heperan with variety of molecular weights, low molecular weight heparins.

35
Q

What is the route of administration for unfractionated heparin and LMWH?

A

UH - IV, LMWH - SC.

36
Q

What is the mechanism of action of unfractionated heparin?

A

Binds to anti-thrombin III to increase activity, this inactivates thrombin and factor Xa.

37
Q

Which types of heparin can inhibit thrombin and inhibit factor Xa?

A

Thrombin - only unfractionated heparin is large enough. Xa - both can bind.

38
Q

How does LMWH differ from UH in terms of size, bioavailability, half life, and dose response?

A

LMWH is smaller (<18 saccharide units), higher bioavailability with more uniform absorption, longer half life, more predictable dose response.

39
Q

What is the mechanism of action of LMWH?

A

Affect factor Xa specificially.

40
Q

What is the route of clearance of LMWH?

A

Kidneys.

41
Q

Why must heparin be given parenterally?

A

Poor GI absorption.

42
Q

How fast is onset/offset of heparin?

A

Rapid.

43
Q

How is UFH monitored?

A

APTT test.

44
Q

What are the indications for use of heparin?

A

Peri-operative, immobility, DVT/PE and AF, acute coronary syndromes, pregnancy.

45
Q

What are the ADRs of heparin?

A

Bruising/bleeding sites (intracranial, injection sites, GI, epistaxis), thrombocytopenia (HIT), osteoporosis (long term use).

46
Q

What is thrombocytopenia?

A

An autoimmune condition causing bleed or serious thromboses, with depleted platelets.

47
Q

How can heparin therapy be reversed?

A

Protamine sulphate - dissociates heparin from anti-thrombin III.

48
Q

Name an anti-platelet drug and a brief mechanism of action.

A

Aspirin (COX-1 inhibition), dipyridamole (phosphodiesterase inhibitors), clopidogrel (ADP antagonists), glycoprotein IIb/IIIa inhibitors.

49
Q

What is the process of thrombotic occlusion by platelets?

A

Plaque fissure/rupture, platelet aggregation, platelet activation, platelet aggregation, thrombotic occlusion.

50
Q

When is clopidogrel used?

A

With aspiring and cardiac indications.

51
Q

What is dipyridamole used for?

A

Secondary prevention of stroke.

52
Q

What are the uses of glycoprotein IIb/IIIa receptor antagonists?

A

High risk ACS, post PCI.

17. Clinical Pharmacology and Therapeutics (25 decks)

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