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CPT > Anticoagulants > Flashcards

Anticoagulants Flashcards

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1
Q

Anticoagulant drugs prevent thrombus formation and growth.

List 3 natural inhibitors of the clotting cascade

A
  • Antithrombin III (especially with regards to Heparin’s action)
  • Protein C
  • Protein S
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2
Q

Which ion is a cofactor for the clotting cascade?

What can be given with a blood transfusion to prevent clotting?

A
  • Calcium

- EDTA (Chelates Ca, preventing it from being used to clot)

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3
Q

Most heparins are sourced from animals

Compare the Heparins: UFH and LMWH in terms of size

How do Heparins work?

A

Unfractionated Heparins;
- Large

Low Molecular Weight Heparins;
- Smaller

  • Heparins work by enhancing Antithrombin III activity (in vivo AND in vitro)
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4
Q

In what form are Heparin preparations?

A

Prepared in Units (IU) per ml

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5
Q

List the targets of the following Heparins;

  • UFH
  • LMWH
  • Fondaparinux (A synthetic LMWH)
A

UFH;
- Acts on Thombin IIa and Xa mainly (also on 12a, 11a, 9a)

LMWH;
- Acts on Xa

Fondaparinux;
- Acts on Xa

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6
Q

Describe the Pharmacodynamics of UFH

A
  • Fast onset of action
  • 30 mins half life at Low doses
  • 2 hours half life at high doses
  • This difference in half life results in mixed elimination so is unpredictable elimination kinetics
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7
Q

Describe the Administration of UFH

A
  • Typically, IV Bolus followed by Infusion

- Can be given Subcutaneously for prophylaxis, but low bioavailability

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8
Q

Describe the mechanism of action of UFH

A
  • Binds to ATIII causing conformational change and increased activity
  • To catalyse Thrombin IIa inhibition, UFH must bind to ATIII AND IIa
  • To catalyse Xa inhibition, UFH only need to bind to ATIII
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9
Q

What kind of drug are Dalteparin and Enoxaparin?

State their administration, half life and bioavailability

A
  • LMWHs
  • Almost always given SC (can be IV) as high bioavailability
  • Half life of 2hrs plus

(Slower onset of action)

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10
Q

Why are LMWHs more predictable than UFHs?

A

LMWHs are smaller and don’t bind to Endothelial cells (partial elimination of UFH here)

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11
Q

How do LMWHs work?

A

Enhance ATIII activity to inhibit Xa

Not long enough to inactivate Thrombin IIa

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12
Q

Compare Fondaparinux with the natural LMWHs

A

Fondaparinux;

  • Same mechanism of action and administration route
  • Longer half life of 18 hours
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13
Q

List 4 indications for use of Heparins

A
  • Venous thromboembolism prevention (before/ after operations as patients have been immobile)
  • During pregnancy (do not cross placenta)
  • Treating + secondary prevention of DVT and PE (prior to DOACs)
  • Acute Coronary Syndrome/ ACS (NSTEMI), in the short term
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14
Q

List 4 ADRs of Heparins

A
  • Bruising + bleeding (Intracranial, Site of injection, GI, Nose)
  • Heparin Induced Thrombocytopenia, HIT (Autoimmune response, more common with UFH)
  • Hyperkalaemia (Inhibition of Aldosterone secretion)
  • Osteoporosis (Rare, long term use, higher risk with UFH, more common in pregnancy)
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15
Q

Describe Heparin Induce Thrombocytopenia (HIT)

A
  • Antibodies to Heparin-Platelet factor IV complex
  • Platelets depleted
  • IN SOME, can lead to Thrombosis as more platelets activated by endothelial damage
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16
Q

List 2 contraindications of Heparins

A
  • Clotting disorders

- Renal impairment (LMWH + Fondaparinux)

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17
Q

List DDIs of Heparins

A
  • Other antithrombotics

- ACEi/ ARBs + Spirionalctone (Increased risk of Hyperkalaemia)

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18
Q

Which form of Heparin requires more monitoring?

Against what value is the dose titrated?

A
  • UFH

- APTT (Intrinsic pathway: XII, XI, IX, VIII + Common)

19
Q

Suggest a drug used for Heparin Reversal Therapy

How does it work?

A
  • Protamine Sulphate (given IV)

- Irreversibly forms inactive complex with Heparin, dissociating it from ATIII

20
Q

Compare the effects of Protamine Sulphate on;

  • UFH
  • LMWH
  • Fondaparinux
A

Protamine Sulphate;

  • Greater effect on UFH
  • Weaker effect on LMWH
  • No effect on Fondaparinux
21
Q

Name a Vitamin-K Antagonist

How do these drugs work as anticoagulants?

A
  • Warfarin
  • Inhibit conversion of Vit-K to active form via Competitive Inhibition of VKOR
  • Thus, inhibited activation of Vit-K dependent clotting factors (7,9,10,2)
22
Q

How is Vitamin K involved in production of Factors II, VII, IX and X

A

Hepatic synthesis of the clotting factors requires Vit-K as a cofactor for activation

23
Q

Why does Warfarin have a delayed onset of action?

How can we speed this up?

A
  • Already circulating active clotting factors are present for days
  • Active factors can be cleared and replaced with non-carboxylated forms
24
Q

State the half life of Warfarin

A

36 to 48 hours (some variation)

25
Q

Warfarin is generally used in the longer-term compared to Heparin, and due to its delayed onset of action so a Heparin cover is often needed for immediate anticoagulation.

List some indications for Warfarin use

A
  • Venous thromboembolism
  • DVT + PE (secondary prevention)
  • Superficial Vein Thrombosis
  • AFib with high risk of stroke
  • Heart valve replacement
26
Q

Describe the Pharmacokinetics of Warfarin

A
  • Good GI absorption (95% Bioavailability)
  • CYP 2C9 polymorphism= Significant variability
  • [Plasma] doesn’t correlate with clinical effect
  • Mixture of R and S enantiomers which have different Potency and Metabolisms
27
Q

List 2 contraindications of Warfarin

A
  • Hepatic Disease

Crosses Placenta so;

  • Avoided in Trimester 1 (Teratogenic)
  • Avoided in Trimester 3 (Haemorrhagic)
28
Q

Suggest 3 things that affect the response to Warfarin

A
  • CYP 2C9
  • Vitamin K intake
  • Alcohol
29
Q

State the primary ADR of Warfarin

A
  • Bleeding (Epistaxis, Spontaneous Retroperitoneal bleeding in some old people)
30
Q

Describe Warfarin Reversal Therapy

A
  • Vitamin K1 is most effective
  • Addition of IV Prothrombin complex concentrate

(Warfarin replaced with Heparin for a short time before and after surgery)

31
Q

List 5 groups of DDIs of Warfarin

A
  • PPIs can increase effect of Warfarin
  • Amiodarone, Clopidogrel and large doses of alcohol (inhibit hepatic metabolism)
  • Cephalosporin ABs (Reduce Vit K by eliminating gut bacteria involved in production)
  • NSAIDs + drugs that decrease Vit K GI absorption (increase INR)
  • Barbiturates, Phenytoin, Rifampicin, St Johns Wort accelerate Warfarin metabolism (decrease INR)
32
Q

Compare High and Low INR

A

High INR;
- More anti-coagulated (more risk of bleeding)

Low INR;
- Less anti-coagulated

33
Q

Factor VII is the most sensitive to Vitamin K deficiency.

What is the clinical significance of this?

A
  • Factor VIII is used in measuring Prothrombin Time

- This is referred to as the INR, used to measure clotting time

34
Q

What kind of drugs are Apixaban, Edoxaban, Rivaroxaban and Dabigatran

A

Apixaban, Edoxaban, Rivaroxaban are Direct Xa DOACs

Dabigatran is a Direct IIa DOAC

35
Q

Compare the Direct Xa and Direct IIa DOACs

A

Direct Xa;

  • Inhibit Free Xa AND Xa Bound to ATIII
  • Don’t directly affect Thrombin IIa

Direct IIa;
- Competitive Thrombin IIa inhibitor (both circulating and thrombus bound IIa)

36
Q

List Anticoagulants that inhibit Xa

A
  • LMWH
  • Fondaparinux
  • Apixaban, Edoxaban, Rivaroxaban

(Also UFH)

37
Q

List Anticoagulants that inhibit IIa

A
  • UFH

- Dabigatran

38
Q

Describe the administration and monitoring of the DOACs

DOACs are often used in situations where Warfarin could be used

A
  • Oral administration

- Little to no monitoring required

39
Q

Suggest an ADR of DOACs

A
  • Bleeding (Lower intracranial bleed risk than Warfarin)

- (Dose adjustments particular in those at risk of GI bleed)

40
Q

List 3 contraindications of DOACs

A
  • Dabigatran contraindicated in Creatine clearance <30ml/min
  • Other DOACs are contraindicated in Creatine clearance <15ml/min
  • Avoid use in Pregnancy and Breastfeeding (little information)
41
Q

List DDIs of DOACs

A

Affected by CYP inducers/inhibitors (less frequent than Warfarin)

  • [Plasma] reduced by Carbamazepine, Phenytoin, Barbiturates
  • [Plasma] increased by Macrolides
42
Q

Andexanet and Idarucizumab are what kind of drugs?

These are expensive

A

DOAC Reversal drugs

43
Q

Of the DOACs, which are not used in lactose intolerant patients and why?

A

AApixaban and Rivaroxaban, as they contain lactose (otherwise they are 1st line DOACs as they don’t require bridging therapy)

CPT (19 decks)

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