Haemostasis and Thrombosis Flashcards

1
Q

What is the case mortality of VTE?

A

5%

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2
Q

What is thrombophlebitic syndrome?

A

Post-thrombotic syndrome resulting in recurrent pain, swelling, ulcers etc.

23% recurrence at 2-years (11% with TED stockings)

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3
Q

What can be a complication of PE?

A

Pulmonary hypertension (heart failure with high mortality)

4% recurrence at 2 years

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4
Q

Why is thrombosis important?

A

Significant sequelae (death is rapid) but is preventable thorugh thromboprophylaxis

Can also be indicator of underlying disease (cancer)

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5
Q

What is Virchow’s Triad?

A

Three contributory factors to thrombosis

  • Viscocity
  • Blood flow
  • Vessel wall damage
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6
Q

What can cause high viscocity of blood?

A

Increased haematocrits and protein paraprotein or high platelet count

More active blood coagulation pathway

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7
Q

How do heparans work?

A

They are a protein C coreceptor

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8
Q

How do endothelial protein C receptors (EPCR) contribute?

A

Decreases protein C

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9
Q

What are some stimuli for increased haemostasis?

A

Infection, malignancy, vasculitis, trauma

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10
Q

How do the stimuli result in increased haemostasis?

A

Thrombomodulin (TM) regulated

TF expressed

Prostacyclin production decreased

Adhesion molecules upregulated

vWB fragment expressed

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11
Q

What is netosis?

A

Neutrophils releasing DNA, vWF and histones

Activates XII to XIIIa

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12
Q

Why is netosis important?

A

Key to immunothrombosis

Inflamation is important drive of thrombosis

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13
Q

How does a change in blood flow affect thrombosis?

A

Can result in accumulation of activated factors

Promotion of platelet adhesion and leukocyte adhesion and transmigration

Hypoxia produces inflammatory effect on endothelium

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14
Q

What are some causes of stasis?

A

Immobility - long haul flights

Compression - tumours or pregnancy

Viscosity - polycythaemia, paraprotein

Congenital - vascular abnormalities

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15
Q

What is the difference in high dose and low dose anticoagulation?

A

High dose anticoagulation - therapeutic

Low dose anticoagulation - prophylactic

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16
Q

What are some immediate anticoagulation treatments?

A
  • Heparin, unfractionated and LMWH
  • Direct acting anti-Xa and anti-IIa
17
Q

What are some delayed anticoagulation treatments?

A

VitK antagonist (warfarin)

18
Q

How are heparins given?

A

They are immediate acting

Unfractionated - IV infusion
LMWH - subcut
pentasaccharide - subcut

19
Q

What is the long term disadvantage to heparins?

A

Osteoporosis

20
Q

How do DOACs work?

A

Bind directly to enzyme

Anti-Xa - rivaroxaban, apixaban

Anti-IIa - Dabigatran

21
Q

What are the pharmacodynamics and pharmacokinetics of DOACs?

A

Oral administration
Peak in approx 3-4 hours
Useful in long term
Short half life, no monitoring required

22
Q

What are the pharmacodynamics and pharmacokinetics of warfarin?

A

Orally, indirect effect
Onset of action is delayed
Levels of II, VII, IX, X fall
Protein C and protein S also fall

23
Q

Can you give warfarin in an emergency?

A

No

Also no point in giving larger dose since it’s delayed no matter what

24
Q

What is always important to consider when giving warfarin?

A

Need to measure INR (derived from prothombin time)

25
Q

What are some of the complications of warfarin?

A
  • Dietry VitK
  • Variable absorption
  • Interaction with other drugs - protein binding, competition induction of cytochromes
  • Teratogenic, so can’t be used through pregnancy, must stop within 6 weeks or risk of fetal malformation
26
Q

What are some things which can be given for prophylaxis?

A

Tinz or Enox

TED stockings

DOAC +/- aspirin (orthopaedics)

27
Q

Why are DOACs preferred over other methods of anticoagulation?

A

They reduce the risk of bleeding by half compared to other drugs