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Year 5 Haematology > 2: Venous Thrombosis > Flashcards

2: Venous Thrombosis Flashcards

1
Q

Coagulation Cascade and regulation

A
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2
Q

Thrombophlebitis syndrome (superficial or DVT) triad

A

recurrent pain, swelling, ulcers

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3
Q

Virchow’s triad

A

blood, vessel wall, blood flow

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4
Q

Blood in Virchow’s triad, what increased thrombosis risk?

A

Viscosity (hct, protein/paraprotein), plt count, coagulation system

Imbalance → thrombophilia or thrombosis

Risk of thrombosis increased by:

  • reduced prothrombin
  • thrombocytopenia
  • reduced protein C
  • elevated anti-thrombin
  • increased fibrinolysis
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5
Q

Vessel wall in Virchow’s triad

A

Normally antithrombotic

  • thrombomodulin
  • endothelial protein C receptor
  • TFPI
  • Heparans

Does NOT express tissue factor

Secretes anti platelet factors

  • PGI2 from vessel wall
  • NO
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5
Q

Vessel wall in Virchow’s triad

A

Normally antithrombotic

  • thrombomodulin
  • endothelial protein C receptor
  • TFPI
  • Heparans

Does NOT express tissue factor

Secretes anti platelet factors

  • PGI2 from vessel wall
  • NO
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6
Q

What happens when vessel wall experiences inflammation or injury

A

Inflammation or injury makes the vessel wall PROTHROMBOTIC e.g. infection, malignancy, vasculitis, trauma

Stimulus: infection, malignancy (3% thrombosis incidence), vasculitis, trauma

Effects: anticoagulants (i.e. TM) downregulated; adhesion molecules upregulated; TF expressed; prostacyclin decreased

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7
Q

Blood flow in Virchow’s triad

A

Stasis promotes thrombosis

Causes of stasis thrombosis → compression, congenital, viscosity, immobility

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8
Q

Which factor confers the highest risk of thrombosis?

A

Antithrombin deficiency > APC (+S) > FVL

  • Other risk factors = Factor V Leiden, FHx of thrombosis, Reduced F8 level, plane flight
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9
Q

Plane flight risk of thrombosis and compound risk factors

A

Plane flight risk increases gradually:

  • 3-6hrs = 0.11 / million
  • 9-12hrs = 2.66 / million
  • >12hrs = 4.77 / million

Risk factors can COMPOUND to produce a higher effect

  • Risk with OC is 4x
  • Risk with Factor V Leiden is 7x
  • Both together is 35x
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10
Q

VTE and anticoagulants

A
  • Preventing VTE → IDENTIFY high risk patients, high risk situations
  • Treating VTE → prompt Dx and inhibition of coagulation
  • Long term prevention → assess risk and rebalance coagulation
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11
Q

What is the difference between low dose and high dose anticoagulant dosages

A
  • Low dose → prophylactic
  • High dose → therapeutic
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12
Q

Give an example of an immediate anticoagulant to increase anticoagulant activity and it’s mechanism of action, GIVE TWO MORE EXAMPLES and their mechanism of action

A

Heparin -→ potentiates anti-thrombin activity

  • unfractionted = IV
  • LMWH = SC
  • Pentasaccharide = SC

other examples = anti-10a (Rivaroxaban, apixaban)

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13
Q

Long term disadvantages of immediate anticoagulant therapy

A

injections, risk of osteoporosis, variable renal dependence

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14
Q

How do we monitor heparin therapy?

A

LMWH

  • reliable pharmacokinetics
  • MONITOR: anti-Xa assay → renal failure (creatinine clearance <50), extremes of weight or risk

Unfractionated heparin

  • variable kinetics
  • variable dose-response
  • MONITOR: APTT or anti-Xa assay
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15
Q

How do we monitor direct acting anticoagulants?

A

Anti-Xa → rivaroxaban, apixaban, edoxaban

Anti-2a → dabigatran

Properties:

  • oral administration
  • useful long-term
  • no monitoring = advantage over warfarin

Immediate acting = peak in 3-4 hours

Short half-life

16
Q

Factors half-life

17
Q

Give an example of delayed anticoagulants and their mechanism of action

A

Warfarin

  • vitamin K antagonist stops synthesis of 2,7,9 and 10
  • factor 7 and protein C drop first
  • Vit K epoxide reductase (VKER) inhibitor

Reversible

  • give vit K if high INR (12 hours)
  • quickly (1 minute) = 2,7,9 and 10 infusion
18
Q

How do we monitor warfarin

A

Measure of effect is INR – international normalised ratio derived from PT

Difficult because numerous interactions

  • Dietary vitamin K
  • Variable absorption
  • Interactions with other drugs – protein binding, competition/induction of cytochromes
19
Q

why do western LMWH with warfarin

A

N.B. LMWH started with warfarin due to immediate procoagulant effect (inhibit APC) of warfarin that wears off after a few days…

20
Q

Heparin vs warfarin vs DOACs

21
Q

INR graph

22
Q

Risk assessment for VTE

23
Q

Bleeding risk assessment

24
Treating DVT/PE
25
3 goals of anticoagulant therapy
1. Prevent thrombosis 2. Treat thrombosis 3. Prevent recurring thrombosis
26
Preventing thrombosis → identify patients at increased risk of thrombosis thromboprophylaxis examples
* Medical → infection/inflammation, immobility, age * Cancer patients → procoagulation, inflammation, flow obstruction * Surgical patients → immobility, trauma, inflammation * Previous VTE, FHX, Genetic traits * Obese & the elderly **Thromboprophylaxis** * **LMWH** – Tinzaparin or Clexane, not monitored * **TED stockings** for surgery or if heparin CI * **Flowtron** – intermittent compression – increases flow * Sometimes **DOAC** +/- aspirin **Prevention short-term – _assess thrombotic risk_**
27
Treating thrombosis
* Only for life-threatening PE or limb threatening DVT * Risk of haemorrhage (ICH) ~4% * Reduces subsequent postphlebitic syndrome * Indicates broadening slowly * Anticoagulants don’t bust the clot; they just stop it moving
28
Preventing recurrence → high-risk patients may need long-term anticoagulation
* Does the risk of thrombosis if untreated outweigh the risk of bleeding if treated? * There is a need to assess… * Risk of recurrence – morbidity and mortality * _Circumstance_ under which patient had thrombosis – **see graph overleaf** * After a _surgical precipitant_, no long-term anticoagulation needed * After _minor precipitants_, 3 months anticoagulation usually adequate * If _idiopathic cause_  long-term anticoagulation (10-20% recurrence in 2 years) * _Men_ have a higher recurrence rate than women [M\>F] * People that have a _proximal thrombosis_ have a higher recurrence rate * PE  likely to have a PE again; DVT  likely to have a DVT * Risk of therapy – bleeding – morbidity and mortality, variation of risks with different therapies
29
**Which patient is most likely to benefit from long term anticoagulation after their DVT?** * 57y M, after flying from Moscow * 27y W, during pregnancy * 33y W, on OCP * 77y M, after hip replacement – *relatively low long-term risk; cause is surgery* * *30y M, after long walk - can't blame the long walk, so idiopathic - least external factors (big intrinsic risk)*

Year 5 Haematology (7 decks)

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