VTE/anticoagulation Flashcards

1
Q

How does tPA work?

A

Converts plasminogen to plasmin –> (1) cleaves fibrin and fibrinogen, (2) destroys coagulation factors, (3) blocks platelet aggregation

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2
Q

What’s Virchow triad?

A

Hypercoagulable state
Endothelial damage
Disruption to blood flow

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3
Q

How does the endothelial wall prevent thrombosis?

A

(1) Secrete tPA
(2) Secrete NO, and prostacyclin
(3) Block exposure to subendothelial collagen
(4) Secrete heparin-like molecules - augmentin antithrombin III
(5) Secrete thrombomodulin

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4
Q

List 5 examples of hypercoagulable states that make you prone to VTE

A

(1) Factor V leiden - mutated factor V that can’t be deactivated by protein C or S
(2) Protein C or S deficiency - Protein C or S normally inactivate factor V and VIII
(3) Prothrombin 20210A - increased prothrombin
(4) ATIII deficiency - heparin like molecules released from the endothelium normally activate ATIII which inactivates thrombin and coagulation factors
(5) OCP - estrogen increases production of coagulation factors

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5
Q

What is warfarin skin necrosis and how does it happen?

A

When you first take warfarin, you get temporary deficiency in protein C and S due to shorter half life
If you are already protein C or S deficient, and you take warfarin, it increases your risk of thrombosis, especially in the skin, leading to warfarin skin necrosis

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6
Q

How much of distal DVTs will extend proximally without treatment?

A

1/3

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7
Q

How much of proximal DVTs will become PEs without treatment?

A

15-25%

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8
Q

List 3 strong risk factors for VTE

A

Major surgery especially TKR, THR
Lip or hip fracture
Multiple trauma e.g. spinal cord injury

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9
Q

Wells score is not validated in …

A

Pregnancy

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10
Q

When do you thrombolyse PE?

A

Massive PE with haemodynamic instability

Has not shown improved survival in submassive PE (trop rise and RV dysfunction)

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11
Q

When are IVC filters indicated?

A

Can’t anticoagulate

Recurrent PE despite anticoagulation

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12
Q

How long can IVC filters stay in for?

A

2-4/52
If not, risk overgrowth around filter and then you won’t be able to remove it. Will need lifelong anticoagulation in that case.

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13
Q

Which NOACs can you use for DVT/PE?

A

Rivaroxaban and apixaban only

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14
Q

Duration of anticoagulation for
PE/proximal DVT
Distal DVT

A

PE/proximal DVT: minimum 3/12
Distal DVT: 6/52 - 3/12

Whether its provoked or unprovoked, will determine duration

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15
Q

Thrombophilia screen

A
Lupus anticoagulant (only one to do in the acute setting)
Protein C, protein S
Factor V leiden 
Anticardiolipin ab 
Prothrombin G20210A
Antithrombin
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16
Q

When to do a thrombophilia screen?

A
Recurrent VTE
VTE before age 45
Arterial and venous thrombosis (antiphospholipid) 
VTE at unusual places
VTE while on OCP, HRT or pregnant 
Unprovoked VTE 
FHx of VTE
17
Q

What’s post-thrombotic syndrome?

A

Clot damages valve –> fluid goes backwards –> venous hypertension –> reduced blood supply to muscle

Symptoms can mimic recurrent DVT - pain, oedema, heaviness, fatigue
Gets better with elevation and rest. Worst later in the day.

18
Q

Rx post-thrombotic syndrome

A

If proximal DVT (ileofemoral), consider direct thrombolysis

Graduated compression stockings can improve symptoms of swelling but no benefit in RCT

19
Q

What factors make it high risk for recurrent VTE?

A

Unprovoked proximal DVT/symptomatic PE (especially if more than one episode)
Active cancer
Antiphospholipid syndrome
Anti-thrombin deficiency

= indefinite anticoagulation

Consider indefinite anticoagulation in minimally provoked DVT/PE e.g. travel related, immobility (non-surgery), minor surgery

20
Q

Indications for NOACs

A

DVT, PEs (except dabigatran)
Non-valvular AF
Post TKR

21
Q

In what population groups do we have less experience with NOACs?

A

Obesity or BMI >40
Cancer - NOACs are accepted now
Antiphospholipid syndrome (particularly triple positive) - don’t use

22
Q

In what population groups can we not use NOACs?

A
CrCl <30
Poor compliance (quick onset and offset)
Extremes of weight
Cancer
Antiphospholipid syndrome
Metal heart valves
Valvular AF
Lactation, pregnancy
Child Pugh B, C
23
Q

How does NOAC compared to warfarin?

A

Similar efficacy

Less serious bleeding especially ICH

24
Q

Reversal agent for dabigatran

A

Praxbind/Idaricizumab (monoclonal ab)

Immediate reversal

25
When to stop NOAC before procedure?
24-48 hours
26
How to manage bleeding in someone on NOAC?
Stop NOAC Praxbind for dabigatran If significant bleeding, consider prothrombinex, tranexamic acid (anecdotal evidence)
27
Which NOAC would you choose in renal impairment?
Apixaban (less renally cleared) | But still CI in CrCl <30
28
How to monitor (A) Apixaban (B) Rivaroxaban (C) Dabigatran
(A) Apixaban - anti Xa (B) Rivaroxaban - anti Xa, PT (C) Dabigatran - TT (very sensitive), APTT
29
How does antipsohpholipid syndrome present?
``` Arterial, venous or small vessel thrombus - most common is DVT and stroke Pregnancy loss Mild thrombocytopenia Autoimmune haemolytic anaemia PE/chronic thromboembolic pulmonary hypertension ARDS Diffuse alveolar haemorrhage Valvular thickening Libman-sacks endocarditis Livedo reticularis + livedo racemosa ```
30
Antiphospholipid syndrome is associated with which disorder?
SLE
31
What is a clinically significant antiphospholipid profile?
1 out of 3 antiphospholipid ab (anti-cardiolipin ab, anti-B2 glycoprotein ab, lupus anticoagulant)
32
How to manage antiphospholipid syndrome?
VTE --> anticoagulate with heparin then warfarin Secondary prevention of VTE --> warfarin Pregnant --> LMWH Primary prevention of VTE is not recommended
33
What's catastrophic antiphospholipid syndrome?
Widespread thrombotic disease with multiorgan failure 3+ new organ thromboses in one week Biopsy confirms microthrombus
34
Rx: catastrophic antiphospholipid syndrome
Rx: anticoagulation, steroids, and in severe cases, plasma exchange and/or IVIG
35
Causes of prolonged INR/PT
INR/PT looks at extrinsic pathway (factor VII) and common pathway (II, V, X) - Factor VII deficiency - Vitamin K deficiency or warfarin - Liver disease - Anti-Xa inhibitors e.g. rivaroxaban
36
Causes of prolonged APTT
APTT looks at intrinsic pathway (XII, XI, IX, VIII) and common pathway (II, V, X) - Factor VIII, IX, XI, XII deficiency - Liver disease - Anti-Xa inhibitor e.g. rivaroxaban - Unfractionated heparin/LMWH - vWD disease (vWF stabilises factor VIII) - Lupus anticoagulant
37
Causes of prolonged APTT and PT
DIC Liver disease Common pathway deficiency Direct thrombin inhibitor or anti Xa inhibitor
38
``` Warfarin INR goals AF VTE treatment/prophylaxis Mechanical mitral valve replacement Other valve replacement ```
AF 2-3 VTE treatment/prophylaxis 2-3 Mechanical mitral valve replacement 2.5-3.5 Other valve replacement 2-3