Patient on anti-coagulant therapy Flashcards

(60 cards)

1
Q

What is dabigatran?

A

Dabigatran is an oral anticoagulant that works by being a direct thrombin inhibitor. It is an alternative to warfarin and does not require regular monitoring.

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2
Q

What are the main indications for dabigatran?

A

Dabigatran is used for prophylaxis of venous thromboembolism following hip or knee replacement surgery and for prevention of stroke in patients with non-valvular atrial fibrillation.

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3
Q

What risk factors indicate the use of dabigatran for stroke prevention?

A

Risk factors include:
1. Previous stroke, transient ischaemic attack or systemic embolism
2. Left ventricular ejection fraction below 40%
3. Symptomatic heart failure of NYHA class 2 or above
4. Age 75 years or older
5. Age 65 years or older with diabetes mellitus, coronary artery disease or hypertension

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4
Q

What are the known side effects of dabigatran?

A

The major adverse effect of dabigatran is haemorrhage.

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5
Q

How should dabigatran dosing be adjusted in patients with kidney disease?

A

Doses should be reduced in chronic kidney disease and dabigatran should not be prescribed if the creatinine clearance is < 30 ml/min.

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6
Q

What is used for rapid reversal of dabigatran’s anticoagulant effects?

A

Idarucizumab can be used for rapid reversal of the anticoagulant effects of dabigatran.

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7
Q

What did the RE-ALIGN study reveal about dabigatran?

A

The RE-ALIGN study showed significantly higher bleeding and thrombotic events in patients with recent mechanical heart valve replacement using dabigatran compared with warfarin.

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8
Q

What is the current guidance regarding dabigatran use in patients with prosthetic heart valves?

A

Dabigatran is now contraindicated in patients with prosthetic heart valves.

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9
Q

What are direct oral anticoagulants (DOACs) used for?

A

DOACs are used for the prevention of stroke in non-valvular atrial fibrillation (AF), prevention of VTE following hip/knee surgery, and treatment of DVT and PE.

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10
Q

What risk factors are considered for stroke prevention in non-valvular AF with DOACs?

A

Risk factors include prior stroke or transient ischaemic attack, age 75 years or older, hypertension, diabetes mellitus, and heart failure.

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11
Q

What is the mechanism of action for Dabigatran?

A

Dabigatran is a direct thrombin inhibitor.

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12
Q

What is the mechanism of action for Rivaroxaban, Apixaban, and Edoxaban?

A

Rivaroxaban, Apixaban, and Edoxaban are direct factor Xa inhibitors.

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13
Q

How is Dabigatran primarily excreted?

A

Dabigatran is primarily excreted through the kidneys.

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14
Q

How is Rivaroxaban primarily excreted?

A

Rivaroxaban is primarily excreted through the liver.

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15
Q

How is Apixaban and Edoxaban primarily excreted?

A

Apixaban and Edoxaban are primarily excreted through feces.

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16
Q

What is the reversal agent for Dabigatran?

A

The reversal agent for Dabigatran is Idarucizumab.

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17
Q

What are the reversal agents for Rivaroxaban and Apixaban?

A

The reversal agents for Rivaroxaban and Apixaban are Andexanet alfa.

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18
Q

What are the two main types of heparin?

A

Unfractionated ‘standard’ heparin and low molecular weight heparin (LMWH).

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19
Q

How do heparins generally act?

A

By activating antithrombin III.

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20
Q

What does unfractionated heparin inhibit?

A

Thrombin, factors Xa, IXa, XIa, and XIIa.

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21
Q

What does LMWH primarily inhibit?

A

Factor Xa.

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22
Q

What are the adverse effects of heparins?

A

Bleeding, thrombocytopenia, osteoporosis, and hyperkalaemia.

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23
Q

What is a notable side effect of heparin related to potassium levels?

A

Hyperkalaemia, thought to be caused by inhibition of aldosterone secretion.

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24
Q

What is the administration route for standard heparin?

A

Intravenous.

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25
What is the administration route for low molecular weight heparin (LMWH)?
Subcutaneous.
26
What is the duration of action for standard heparin?
Short.
27
What is the duration of action for LMWH?
Long.
28
What monitoring is required for standard heparin?
Activated partial thromboplastin time (APTT).
29
What monitoring is required for LMWH?
Anti-Factor Xa (routine monitoring is not required).
30
What is a key feature of heparin-induced thrombocytopenia (HIT)?
It is an immune-mediated condition.
31
What antibodies are involved in HIT?
Antibodies against complexes of platelet factor 4 (PF4) and heparin.
32
When does HIT usually develop?
After 5-10 days of treatment.
33
What is the treatment for heparin overdose?
Protamine sulphate.
34
What is a notable characteristic of HIT despite low platelets?
It is a prothrombotic condition.
35
What are the features of HIT?
Greater than 50% reduction in platelets, thrombosis, and skin allergy.
36
What can be used for ongoing anticoagulation in HIT?
Direct thrombin inhibitor e.g. argatroban or danaparoid.
37
What are parenteral anticoagulants used for?
Parenteral anticoagulants are used for the prevention of venous thromboembolism and in the management of acute coronary syndrome.
38
What is fondaparinux?
Fondaparinux activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa. It is given subcutaneously.
39
What are direct thrombin inhibitors?
Direct thrombin inhibitors are anticoagulants that inhibit thrombin directly. ## Footnote Examples include bivalirudin.
40
How are direct thrombin inhibitors generally administered?
Direct thrombin inhibitors are generally given intravenously.
41
What is dabigatran?
Dabigatran is a type of direct thrombin inhibitor that is taken orally.
42
How is dabigatran categorized?
Dabigatran is often grouped alongside the direct oral anticoagulants (DOACs).
43
What is Warfarin?
Warfarin is an oral anticoagulant that was used first-line for many years in both the management of venous thromboembolism and reducing stroke risk in patients with atrial fibrillation. It has now been largely superseded by the use of direct oral anticoagulants (DOACs).
44
What is the mechanism of action of Warfarin?
Warfarin inhibits epoxide reductase, preventing the reduction of vitamin K to its active hydroquinone form, which acts as a cofactor in the carboxylation of clotting factors II, VII, IX, and X.
45
What are the indications for Warfarin?
Indications include mechanical heart valves and as a second-line treatment after DOACs for venous thromboembolism and atrial fibrillation.
46
What is the target INR for mechanical heart valves?
The target INR depends on the valve type and location; mitral valves generally require a higher INR than aortic valves.
47
What is the target INR for venous thromboembolism?
Target INR = 2.5; if recurrent, target INR = 3.5.
48
What is the target INR for atrial fibrillation?
Target INR = 2.5.
49
How are patients monitored while on Warfarin?
Patients are monitored using the INR (international normalized ratio), which is the ratio of the prothrombin time for the patient over the normal prothrombin time.
50
What factors may potentiate Warfarin?
Factors include liver disease, P450 enzyme inhibitors (e.g., amiodarone, ciprofloxacin), cranberry juice, drugs displacing warfarin from plasma albumin (e.g., NSAIDs), and drugs that inhibit platelet function (e.g., NSAIDs).
51
What are the side effects of Warfarin?
Side effects include haemorrhage, teratogenic effects (though can be used in breastfeeding mothers), skin necrosis, and purple toes.
52
What happens when Warfarin is first started?
When Warfarin is first started, biosynthesis of protein C is reduced, resulting in a temporary procoagulant state, normally avoided by concurrent heparin administration.
53
What are general factors that may potentiate warfarin?
Liver disease, P450 enzyme inhibitors, cranberry juice, drugs that displace warfarin from plasma albumin (e.g., NSAIDs), and drugs that inhibit platelet function (e.g., NSAIDs).
54
What are the effects of P450 inducers on warfarin metabolism?
Inducers of the P450 system will decrease the INR. ## Footnote Examples include antiepileptics (phenytoin, carbamazepine), barbiturates (phenobarbitone), rifampicin, St John's Wort, chronic alcohol intake, griseofulvin, and smoking.
55
What are the effects of P450 inhibitors on warfarin metabolism?
Inhibitors of the P450 system will increase the INR. ## Footnote Examples include antibiotics (ciprofloxacin, clarithromycin/erythromycin), isoniazid, cimetidine, omeprazole, amiodarone, allopurinol, imidazoles (ketoconazole, fluconazole), SSRIs (fluoxetine, sertraline), ritonavir, sodium valproate, acute alcohol intake, and quinupristin.
56
What is the management for major bleeding with INR > 8.0?
Stop warfarin. Give intravenous vitamin K 5mg. Prothrombin complex concentrate - if not available then FFP.*
57
What is the management for minor bleeding with INR > 8.0?
Stop warfarin. Give intravenous vitamin K 1-3mg. Repeat dose of vitamin K if INR still too high after 24 hours. Restart warfarin when INR < 5.0.
58
What is the management for no bleeding with INR > 8.0?
Stop warfarin. Give vitamin K 1-5mg by mouth, using the intravenous preparation orally. Repeat dose of vitamin K if INR still too high after 24 hours. Restart when INR < 5.0.
59
What is the management for minor bleeding with INR 5.0-8.0?
Stop warfarin. Give intravenous vitamin K 1-3mg. Restart when INR < 5.0.
60
What is the management for no bleeding with INR 5.0-8.0?
Withhold 1 or 2 doses of warfarin. Reduce subsequent maintenance dose.