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Clinical Year 4 > Anticoagulation > Flashcards

Anticoagulation Flashcards

1
Q

Give examples of when anticoagulation is used for primary prevention

A

Arterial:
- Stroke prevention in patients with AF

Venous:
- Prevention of DVT or PE (i.e VTE) in high risk patients

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2
Q

Give examples of when anticoagulation is used for secondary prevention

A

Arterial:
- Acute MI, thrombotic/embolic stroke and prevention of recurrence

Venous:
- Treatment of VTE and prevention of recurrence

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3
Q

What are the main hereditary risk factors for venous thromboembolism (VTE)?

A

Deficiency of anticoagulant

  • Antithrombin
  • Protein C
  • Protein S

Abnormal protein

  • Factor V Ledien
  • Fibrinogen

Increased procoagulant

  • Prothrombin
  • Factor VIII

Abnormal metabolism
- Hyperhomocysteinaemia

Putative mechanisms

  • Thrombomodulin defects
  • Fibrinolytic defects
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4
Q

What should be used in patients with renal failure for venous thromboprophylaxis? (eGFR

A

Unfractionated Heparin (UFH)

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5
Q

Well’s score for diagnosis of DVT

A

1 point each for

  • Active Cancer
  • Paralysis, paresis or recent plaster
  • Recently bedridden and/or major surgery
  • Localised tenderness along the distribution of the deep vein system
  • Entire leg swollen
  • Calf swelling 3cm compared to other leg
  • Pitting Oedema in the symptomatic leg
  • Collateral superficial veins (non-varicose)

-2 points for Alternative diagnosis

More than 2 points = High risk
1-2 points = Moderate risk
Less than 1 point = Low risk

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6
Q

Well’s score for diagnosis of PE

A

3 points for

  • Clinical signs/symptoms of DVT
  • Alternative diagnosis deemed less likely than PE
  1. 5 points each for
    - Heart rate higher than 100 bpm
    - Immobilisation or surgery in previous 4 weeks
    - Previous DVT or PE

1 point each for

  • Haemoptysis
  • Cancer (or treated in last 6 months)

More than 6 points = High risk
2-6 points = Moderate risk
Less than 2 points = Low risk

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7
Q

Clotting cascade

A

Look at diagram in lecture

LEARN!!

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8
Q

In relation to Factor Xa and Thrombin inhibition, UFH and LMWH inhibit which better?

A

LMWH inhibits Factor Xa better than Thrombin

UFH inhibits Thrombin better than Factor Xa

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9
Q

How do Heparins work?

A

They bind to Lys and Arg on antithrombin and increase it’s activity

Antithrombin inhibits the activity of Thrombin (Factor IIa), Factor Xa, Factor IXa and Factor XIa

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10
Q

What monitoring is needed for UFH?

A

aPTT and anti-factor Xa assay

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11
Q

What is the aPTT?

A

Activated Partial Thromboplastin Time (aPTT)

It measures the activity of the intrinsic and common pathways of coagulation.

aPTT normal is around 27-35 seconds
aPTT ratio = APTT/Control
Do no confuse with INR!

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12
Q

What investigations should be carried out before prescribing LMWH?

A

FBC, INR & APTT
U&Es
LFTs

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13
Q

Heparin-induced thrombocytopenia

A

Need to monitor platelet count when using UFH or LMWH

Greater than 30% reduction in platelets indicates thrombocytopenia

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14
Q

Mechanism of action of Vitamin K antagonists/Coumarins

A

Vit K epoxide reductase inhibitors

Inhibits synthesis of clotting factors II, VII, IX, X (2, 7, 9 and 10)

Prevents the gamma-carboxylation of serine proteases which leads to the production of non-carboxylated proteins (known as PIVKAs). This leads to limited thrombin generation.

Also inhibits protein C and protein S which are inhibitors of (Factor Va and Factor IIIa) - they are anticoagulants and therefore warfarin is initially a prothrombotic!

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15
Q

What is Prothrombin Time (PT)

A

Used to measure time to clot formation

Extrinsic pathway

Used to calculate INR
INR = (patient PT/mean normal PT)^ISI

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16
Q

What monitoring is needed for Warfarin/

A

PT/INR

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17
Q

Starting warfarin

A

Check baseline INR, FBC and LFTs

Given alongside a LMWH for at least 5 days and 2 consecutive INR readings in the therapeutic range are needed before stopping the LMWH

Reduce dose in elderly patients and those with impaired liver function

Adjust dose according to interacting medication

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18
Q

Why is the heparin-warfarin overlap necessary?

A

Warfarin inhibits the effective synthesis of biologically active forms of the vitamin K-dependent clotting factors: II, VII, IX and X, as well as the regulatory factors protein C, and protein S

Protein C is an innate anticoagulant that, like the procoagulant factors that warfarin inhibits, requires vitamin K-dependent carboxylation for its activity

Protein S is a vitamin K-dependent anticoagulant protein

Since warfarin initially decreases protein C and protein S levels faster than the coagulation factors, it can paradoxically increase the blood’s tendency to coagulate when treatment is first begun

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19
Q

What is the major risk of INR being too high?

A

Intracranial bleed and other major bleeding

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20
Q

What are the main reasons for the search for alternatives to VKAs?

A

Poor TTR (Time in the Therapeutic Range)

Drug interactions common

INR monitoring is not practical

Side effects (hair loss, skin rash)

VKA resistance

Renal Impairment

21
Q

What is the main problem with a poor TTR for warfarin?

A

the ability to prevent strokes falls significantly

If the patient has a TTR below 40% then the risk of stroke is actually higher than patients not on warfarin!

22
Q

Bleed risks of NOACs

A

Rivaroxaban has a similar bleed risk to warfarin.

Dabigatran and Apixaban both have a lower bleed risk than warfarin.

23
Q

Practical considerations with Dabigatran

A 
Large capsule (difficult to swallow)
Cannot go in a dosette box
Cannot go down an NGT or PEG
Does have a reversibility agent
24
Q

Practical considerations with Rivaroxaban

A

Small tablet
Can go in a dosette box
Can go down an NGT or PEG
Lack of reversibility

25
Q

Practical considerations with Apixaban

A

Small tablet
Can go in a dosette box
Can go down an NGT or PEG
Lack of reversibility

26
Q

Advantages of NOACs

A 
Oral
Reproducible pharmacokinetics
Rapid onset
No INR monitoring required
Licensed and NICE approved
27
Q

Unresolved issues with NOACs

A

No published comparisons with each other

Limited duration of follow up data

Short half life means missed doses are more significant

Lack of reversibility (except dabigatran)

28
Q

Which NOAC if high risk of bleeding?

A

Dabigatran (lower dose aka 110) or Apixaban

  • Lowest incidence of bleeding
29
Q

Which NOAC if previous GI bleeding or high risk of GI bleeding?

A

Apixaban

  • Lowest incidence of GI bleeds
30
Q

Which NOAC if high risk of ischemic stroke, low bleeding risk?

A

Dabigatran (150)

  • Considered to give best reduction of ischemic stroke
31
Q

Which NOAC if previous stroke?

A

Apixaban or Dabigatran (150)

  • Greatest reduction of stroke
32
Q

Which NOAC if CAD, previous MI or high-risk for ACS/MI?

A

Rivaroxaban

  • As it has positive effects in ACS
33
Q

Which NOAC if renal impairment?

A

Rivaroxaban or Apixaban

  • As they are less dependent on renal function
34
Q

Which NOAC if GI upset/disorders?

A

Rivaroxaban or Apixaban

  • As no reported GI effects
35
Q

Which NOAC if want a once daily formulation?

A

Rivaroxaban

36
Q

Which choice of anticoagulant would you use if looking at CrCl?

A

less than 15 = Warfarin

15-30 = Rivaroxaban or apixaban

37
Q

Which anticoagulant would you choose if the patient’s weight was very low or high?

A

Warfarin

38
Q

Which anticoagulant would you choose in children?

A

Warfarin

39
Q

Which anticoagulant would you choose if the patient had a prosthetic heart valve?

A

Warfarin

40
Q

Which anticoagulant would you choose if the patient had a high GI bleed risk?

A

Warfarin or Apixaban

41
Q

Which anticoagulant would you choose if the patient had a previous MI?

A

Warfarin or Xa inhibitor

42
Q

What is D-Dimer?

A

A fibrin breakdown product that is present in the blood after a blood clot is broken down by fibrinolysis

Can be used to help diagnose thrombosis

43
Q

What are the main contraindications for fibrinolysis in acute MI?

A 
Recent haemorrhage
Trauma
Surgery
Coagulation defects
Peptic ulceration
Severe hypertension
Acute pulmonary disease esp cavitation
Acute pancreatitis
Severe liver disease
Previous allergic reaction
44
Q

What are the prothrombotic risk factors for an increased risk of venous thrombosis?

A 
Age
Obesity
Varicose veins
Family history of VTE
Thrombophilias
Thrombotic states
45
Q

NOAC monitoring

A

Renal function
Liver function
BP
Prothrombin time

46
Q

LMWH monitoring

A

Platelet counts

Potassium (hyperkalaemia)

47
Q

UFH monitoring

A

INR
APTT
Platelet count
Potassium (hyperkalaemia)

48
Q

Warfarin monitoring

A

Baseline INR
FBCs
LFTs

49
Q

How do you initiate long-term warfarin or a NOAC after LMWH treatment in hospital for a DVT?

A

Take LMWH and warfarin overlapping for a minimum of 5 days, then wait until INR in therapeutic range for two days, then stop LMWH

Stop LMWH before initiating NOAC. 5 days of LMWH then 150mg BD of dabigatran.

Clinical Year 4 (12 decks)

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