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Pharmacology > Warfarin and Heparin > Flashcards

Warfarin and Heparin Flashcards

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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?

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A

3 days before

22
Q

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

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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?

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A

Bleeding

-subdural haemorrhage

24
Q

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

25
In which conditions is the target INR 2.5-4.5 on warfarin?
Mechanical prosthetic valve Recurrent thrombosis Thrombosis with inherited thrombophilia conditions
26
ADRs of warfarin?
Bleeding/bruising - intracranial - epistaxis - injection - GI loss Teratogenic
27
Steps that should be taken to reverse warfarin?
``` Stop warfarin Parenteral vitamin K (slow onset) Prothrombin complex Fresh frozen plasma (fast onset) Find source of bleeding, may require surgery ```
28
Before prescribing warfarin, what must be checked for in patient history?
Peptic ulcer disease History of subarachnoid haemorrhage Any bleeding disorder Age, mobility, falls risk score
29
What does warfarin have a lot of DDIs?
Metabolised by CYP450 | Heavily bound to albumin so can be displaced by other drugs
30
How can drugs potentiation warfarin and which do it?
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
Which drugs can inhibit warfarin and how?
Anti-epileptics except sodium valproate Rifampicin St John's wort Induce hepatic enzymes, increasing metabolism of warfarin and reducing INR
32
How to manage raised INR if between - 3.0-6.0 - 6.0-8.0 - 8+
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
What is an arterial thrombosis treated with in general?
Antiplatelets and thrombolysis
34
What are the two types of heparin?
Unfractionated | Low molecular weight
35
What is heparin made up of?
Linear mucopolysaccharide chains (glycosaminoglycans) of variable lengths and molecuar weights
36
How do heparins work?
Activate anti-thrombin III (ATIII) via a unique polysaccharide sequence This deactivates factor Xa, thrombin (IIa) and IXa
37
What is the composition of unfractionated heparin?
Mix of variable long length heparin chains | Have a unique pentasaccharide sequence which binds to ATIII
38
Mechanism of action of unfractionated heparin?
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
Why can unfractionated heparin inactivate IIa but not but not low molecular weight heparins (LMWH)?
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
Benefit of LMWH?
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
Mechanism of action of LMWH?
Has a sequence to bind to ATIII, activating it | Affects factor Xa specifically
42
How is LMWH cleared?
Kidneys | -care in renal failure
43
How are UFH and LMWH administered?
UFH - IV | LMWH - SC
44
Which type of heparin requires monitoring and why? How is it monitored?
UFH LMWH has little effect on APTT because it only affects factor Xa Monitored by APTT
45
Uses of heparin?
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
ADRs of heparin?
Bleeding - intracranial - injection sites - GI loss - epistaxis Heparin-induced thrombocytopenia Osteoporosis
47
What is seen in heparin-induced thrombocytopenia?
Autoimmune seen in 1-2 weeks of treatment | Can bleed/get serious thromboses
48
Pathophysiology in heparin-induced thrombocytopenia?
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
How is HIT treated?
Stop heparin | Give hirudin
50
How is heparin therapy reversed?
Protamine sulphate - dissociates heparin from ATIII a - irreversible binds to heparin Give in active bleeding

Pharmacology (23 decks)

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