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Pharmacology > Warfarin and Heparin > Flashcards

Warfarin and Heparin Flashcards

1
Q

What is a venous thrombosis treated with?

A

Anticoagulants

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2
Q

Give examples of types of an arterial thrombosis

A

CVA

MI

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3
Q

Give examples of types of venous thrombosis

A

DVT

PE

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4
Q

Give the parts of Virchow’s triad and what they can be caused by

A

Hypercoagulability

  • genetic
  • acquired - smoking, OCP, malignancy, prosthetic heart valve

Endothelial damage

  • atheroma - MI, CVA
  • hypertension
  • toxins - smoking, homocysteine

Stasis

  • immobility - health, post-op, travel
  • cardiac abnormality eg AF, HF, valve disease, post-MI
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5
Q

What are anti-coagulants used for?

A

Prevention and treatment of thromboembolism (venous and arterial) and intravascular clotting

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6
Q

What is fibrinolysis used for?

A

Breakdown of existing clot

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7
Q

Uses of anti-platelets?

A

Treat vascular disease (mainly arterial) eg IHD, cerebrovascular disease

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8
Q

How is an arterial thrombus formed?

A

Rupture of an atherosclerotic plaque leading to platelet actions

  • adhesion, activation and aggregation of platelets
  • secretion of mediators e.g. ADP
  • synthesis of mediators e.g. platelet activating factor and thromboxane A2
  • they increase activation and aggregation of platelets
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9
Q

What happens in the intrinsic pathway of the clotting cascade?

A 
Blood exposed to collagen, activates factor XIIa
XI to XIa
XIa + Ca -> IX to IXa
X -> Xa
Converts prothrombin to thrombin 
Converts fibrinogen to fibrin 
Fibrin cross links platelets
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10
Q

What activates the intrinsic pathway in the clotting cascade?

A

When blood is exposed to collagen

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11
Q

What activates the extrinsic pathway

A

Damage to endothelial cells - trauma

Exposes the blood to collagen in blood vessel wall

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12
Q

What can activate the intrinsic pathway?

A

Begins in the bloodstream eg in sepsis, hyperlipidaemia, inflammation
-intrinsic is less common, not normally seen in healthy people

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13
Q

What happens in the extrinsic pathway?

A

Damage to endothelial cells
Release of factor III (tissue factor)
TF + Ca -> VII to VIIa
VIIa activates Xa (prothrombinase)

Xa + Va + calcium convert prothrombin to thrombin (IIa)
This converts fibrinogen to fibrin
Cross-linking of fibrin strands with help from fibrin-stabilising factor

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14
Q

Mechanism of action of warfarin?

A

Competitively inhibits vitamin K reductase
Prevents Vit K being converted back to its active, reduced form in the liver
So anatomises Vit K
Leads to synthesis of non-functional coagulation factors, reducing clotting

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15
Q

Which factors is vitamin K required for?

A

VII, IX, X (prothrombinase)

Proteins C and S

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16
Q

How long is warfarin’s onset?

A

Couple of days - due to turnover of clotting factors

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17
Q

Indications for warfarin?

A 
DVT - taken for 3-6 months after
PE - taken for 6 months after 
AF 
Mechanical prosthetic valves
Patients with recurrent thrombosis 
Thrombosis associated with inherited thrombophilia conditions 
Cardiac thrombus
CVA
Cardiomyopathy
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18
Q

Administration and absorption of warfarin?

A

Orally

Easily absorbed in gut

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19
Q

Metabolism of warfarin?

A

CYP450 enzymes

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20
Q

What is given as a short term cover for warfarin?

A

Heparin

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21
Q

If having surgery, when must warfarin be stopped?

A

3 days before

22
Q

In which conditions must care be taken with warfarin or not given?

A

Care in patients with liver disease

Crosses placenta

  • not in first trimester - teratogenic
  • nor in third trimester - risk of brain haemorrhage of baby during vaginal delivery due to head distortion
23
Q

What does a higher INR increase the risk of?

A

Bleeding

-subdural haemorrhage

24
Q

In which conditions is the target INR 2-3 with warfarin?

A

DVT
PE
AF

25
Q

In which conditions is the target INR 2.5-4.5 on warfarin?

A

Mechanical prosthetic valve
Recurrent thrombosis
Thrombosis with inherited thrombophilia conditions

26
Q

ADRs of warfarin?

A

Bleeding/bruising

  • intracranial
  • epistaxis
  • injection
  • GI loss

Teratogenic

27
Q

Steps that should be taken to reverse warfarin?

A 
Stop warfarin 
Parenteral vitamin K (slow onset)
Prothrombin complex
Fresh frozen plasma (fast onset) 
Find source of bleeding, may require surgery
28
Q

Before prescribing warfarin, what must be checked for in patient history?

A

Peptic ulcer disease
History of subarachnoid haemorrhage
Any bleeding disorder
Age, mobility, falls risk score

29
Q

What does warfarin have a lot of DDIs?

A

Metabolised by CYP450

Heavily bound to albumin so can be displaced by other drugs

30
Q

How can drugs potentiation warfarin and which do it?

A

Inhibit hepatic metabolism - amiodarone, quinolone, metronidazole, cimetidine, alcohol, cranberry/grapefruit juice

Inhibit platelet function - aspirin

Albumin displacement - NSAIDs

Reduced vit K production from gut bacteria - cephalosporin abx

31
Q

Which drugs can inhibit warfarin and how?

A

Anti-epileptics except sodium valproate
Rifampicin
St John’s wort

Induce hepatic enzymes, increasing metabolism of warfarin and reducing INR

32
Q

How to manage raised INR if between

  • 3.0-6.0
  • 6.0-8.0
  • 8+
A

3-6 - stop warfarin, begin again when below 5

6-8 - stop warfarin and begin when below 5

> 8.0 - same again, if there are risk factors for bleeding, give low dose vit K

33
Q

What is an arterial thrombosis treated with in general?

A

Antiplatelets and thrombolysis

34
Q

What are the two types of heparin?

A

Unfractionated

Low molecular weight

35
Q

What is heparin made up of?

A

Linear mucopolysaccharide chains (glycosaminoglycans) of variable lengths and molecuar weights

36
Q

How do heparins work?

A

Activate anti-thrombin III (ATIII) via a unique polysaccharide sequence
This deactivates factor Xa, thrombin (IIa) and IXa

37
Q

What is the composition of unfractionated heparin?

A

Mix of variable long length heparin chains

Have a unique pentasaccharide sequence which binds to ATIII

38
Q

Mechanism of action of unfractionated heparin?

A

Pentasaccharide sequences binds to ATIII
Causes a conformational change and increased ATIII activity
ATIII inactivates thrombin (IIa) and Xa

To catalyse inhibition of IIa

39
Q

Why can unfractionated heparin inactivate IIa but not but not low molecular weight heparins (LMWH)?

A

Heparin needs to bind to IIa and ATIII at the same time to catalyse inhibition of IIa
Unfractionated heparin is large enough, LMWH is not

40
Q

Benefit of LMWH?

A

Smaller chains allow it be absorbed more uniformly and has a high bioavailability of >90%

Predictable dose response as does not bind to macrophages, endothelial cells or plasma proteins

Less likely to cause thrombocytopenia

41
Q

Mechanism of action of LMWH?

A

Has a sequence to bind to ATIII, activating it

Affects factor Xa specifically

42
Q

How is LMWH cleared?

A

Kidneys

-care in renal failure

43
Q

How are UFH and LMWH administered?

A

UFH - IV

LMWH - SC

44
Q

Which type of heparin requires monitoring and why? How is it monitored?

A

UFH
LMWH has little effect on APTT because it only affects factor Xa
Monitored by APTT

45
Q

Uses of heparin?

A

Prevent thrombo-embolism

  • peri-operative: LMWH low dose
  • immobility (HF, frail, unwell)

DVT/PE/AF

  • quick onset to cover patient whilst warfarin loading is achieved
  • LMWH normally used

Acute coronary syndromes

  • reduces coronary artery thrombosis
  • MI/unstable angina

Pregnancy
-in place of warfarin

46
Q

ADRs of heparin?

A

Bleeding

  • intracranial
  • injection sites
  • GI loss
  • epistaxis

Heparin-induced thrombocytopenia

Osteoporosis

47
Q

What is seen in heparin-induced thrombocytopenia?

A

Autoimmune seen in 1-2 weeks of treatment

Can bleed/get serious thromboses

48
Q

Pathophysiology in heparin-induced thrombocytopenia?

A

Heparin and PF4 on platelet surface are immunogenic
Immune complexes activate more platelets
Release of more PF4
Forms more IgG and complexes
Leads to depletion of platelets and thrombosis

49
Q

How is HIT treated?

A

Stop heparin

Give hirudin

50
Q

How is heparin therapy reversed?

A

Protamine sulphate

  • dissociates heparin from ATIII a
  • irreversible binds to heparin

Give in active bleeding

Pharmacology (23 decks)

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