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Haematology > VTE/anticoagulation > Flashcards

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
Q

When to stop NOAC before procedure?

A

24-48 hours

26
Q

How to manage bleeding in someone on NOAC?

A

Stop NOAC
Praxbind for dabigatran
If significant bleeding, consider prothrombinex, tranexamic acid (anecdotal evidence)

27
Q

Which NOAC would you choose in renal impairment?

A

Apixaban (less renally cleared)

But still CI in CrCl <30

28
Q

How to monitor
(A) Apixaban
(B) Rivaroxaban
(C) Dabigatran

A

(A) Apixaban - anti Xa
(B) Rivaroxaban - anti Xa, PT
(C) Dabigatran - TT (very sensitive), APTT

29
Q

How does antipsohpholipid syndrome present?

A 
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
Q

Antiphospholipid syndrome is associated with which disorder?

A

SLE

31
Q

What is a clinically significant antiphospholipid profile?

A

1 out of 3 antiphospholipid ab (anti-cardiolipin ab, anti-B2 glycoprotein ab, lupus anticoagulant)

32
Q

How to manage antiphospholipid syndrome?

A

VTE –> anticoagulate with heparin then warfarin
Secondary prevention of VTE –> warfarin
Pregnant –> LMWH

Primary prevention of VTE is not recommended

33
Q

What’s catastrophic antiphospholipid syndrome?

A

Widespread thrombotic disease with multiorgan failure
3+ new organ thromboses in one week
Biopsy confirms microthrombus

34
Q

Rx: catastrophic antiphospholipid syndrome

A

Rx: anticoagulation, steroids, and in severe cases, plasma exchange and/or IVIG

35
Q

Causes of prolonged INR/PT

A

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
Q

Causes of prolonged APTT

A

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
Q

Causes of prolonged APTT and PT

A

DIC
Liver disease
Common pathway deficiency
Direct thrombin inhibitor or anti Xa inhibitor

38
Q 
Warfarin INR goals
AF
VTE treatment/prophylaxis
Mechanical mitral valve replacement 
Other valve replacement
A

AF 2-3
VTE treatment/prophylaxis 2-3
Mechanical mitral valve replacement 2.5-3.5
Other valve replacement 2-3

Haematology (7 decks)

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