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Haematology - Path > Venous thrombosis - aetiology and management > Flashcards

Venous thrombosis - aetiology and management Flashcards

1
Q

Why is knowing about venous thrombosis important?

A

Common, and has significant complications. They can be difficult to reverse yet easily preventable Can turn into a PE, and a PE causes 5-10% of hospital deaths.

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2
Q

What is the prevalence of venous thromboembolism?

A

1 in 1000-10000 per annum Incidence doubles with each decade

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3
Q

What are the consequences of thromboembolism?

A

Death - mortality 5% Recurrence - 20% in the first 2 years and 4% per annum thereafter Thrombophlebitic syndrome (recurrent pain, swelling and ulcers) - preventable risk by wearing stockings. 23% affected within 2 years, only 11% in those who wore stockings Pulmonary hypertension - 4% at 2 years

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4
Q

What are three contributory factors to thrombosis?

A

Virchow’s triad Blood Vessel wall blood flow

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5
Q
  1. What affects the viscosity of blood? 2. What else in the blood contributes to thrombosis?
A
  1. Haematocrit and protein/paraprotein 2. Platelet count and coagulation system
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6
Q

What are the procoagulant factors in order of the cascade?

A

5, 8, 9, 11, 10, 2, Fibrinogen and platelets –> all leads to fibrin formation

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7
Q

What are the anticoagulant factors?

A

Fibrinolysis, antithrombin, EPCR, Thrombomodulin, protein S, protein C and TFPI

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8
Q

What is thrombophilia?

A

Thrombophilia is a a disturbed balance where there is an increase in coagulation factors and platelets but a decrease in fibrinolytic factors and anticoagulant proteins

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9
Q

Is the vessel wall antithrombotic or thrombotic and how?

A

Antithrombotic

Expresses anticoagulant molecules:

  • Thrombomodulin
  • Endothelial protein C receptor
  • Tissue factor pathway inhibitor
  • Heparans

Does not express tissue factors

Secretes antiplatelet factors:

  • Prostacyclin
  • Nitrous oxide
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10
Q
  1. What makes the endothelium prothrombotic?
  2. What are the effects of this?
A
  1. Inflammation and injury makes a the vessel wall thrombotic: Stimuli:
  • Infection
  • Malignancy
  • Vasculitis
  • Trauma
  1. Effects include
  • Anticoagulant molecules e.g. TM are downregulated
  • Adhesion molecules upregulated
  • TF may be expressed
  • Prostacyclin production decreased
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11
Q

What is the mechanism of blood stasis than can promote thrombosis?

A

Blood stasis promotes thrombosis: mechanism:

  • Accumulation of activated factors
  • Promotes platelet adhesion
  • Promotes leukocyte adhesion and transmigration
  • Hypoxia produces inflammatory effect on endothelium
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12
Q

What are the possible causes of blood stasis?

A
  • Immobility
    • Surgery
    • Paraparesis
    • Travel
  • Compression
    • Tumour
    • Pregnancy
  • Viscosity
    • Polythycaemia
    • Paraprotein
  • Congenital
    • Vascular abnormalities
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13
Q

Describe combined thromotic risks

A
  • Thrombotic risk factors often combine to produce thrombosis
  • Thrombotic factors may have powerful interactions - these can be unpredicatable

e.g OC and factor V leiden on their own have a relative risk of 5-10% of thrombosis. However, when both are present there is a 35% relative risk of thrombosis

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14
Q

What the differences between high dose and low dose anticoagulant therapy?

A
  • High dose = theraputic
  • Low dose = prophylactic
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15
Q
  1. What anticoagulant drugs work immediately?
  2. What anticoagulant drugs have a delayed effect?
A
  1. Immediate
  • Heparin
    • Unfractionated heparin
    • Low molecular weight heparin
  • Direct acting anti-Xa and anti-IIa
  1. Delayed:
  • Vitamin K antagonists
    • Warfarin
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16
Q
  1. What are the main heparins and how are each of them given?
  2. How do they act and the disadvantages?
A

1.

  • Unfractionated heparin - I.V infusion
  • Low molecular weight heparin - sub cut
  • Pentassaccharide - sub cut

2.

  • All act by potentiating antithrombin
  • Provides immediate effect for treatment of thrombosis
    • Long term disadvantage - injections, risk of osteoporosis
    • Variable renal dependence
17
Q

Describe monitoring heparin therapy for the following:

  1. Low molecular weight heparin
  2. Unfractionated heparin
A
  1. Low molecular weight therapy:
  • Reliable pharmacokinetics so not usually required
  • Can use anti-Xa assay e.g. renal failure, or extremes of weight or risks
  1. Unfractionated heparin
  • Variable kinetics
  • Variable dose-response
  • Always monitor theraputic levels with APTT or anti-Xa
18
Q
  1. What are the different groups of direct acting anticoagulants?
  2. What are their prroperties?
A

1.

  • Anti-Xa: Rivaroxaban, apixaban and edoxaban
  • Anti-IIa: Dabigatran
  1. Properties
  • Oral administration
  • Immediate acting - peak in approx. 3-4 hours
  • Also useful in long term
  • Short half life
  • No monitoring
19
Q
  1. What is the most commonly used delayed anticoagulant?
  2. Mechanism
  3. Which factor is affected first, and falls the most with this drug?
A
  1. Warfarin

2.

  • Given orally
  • Indirect effect by preventing recycling of vitamin K, therefore onset of action is delayed
  • Levels of procoagulant factors 2, 7, 9 and 10 fall
  • Levels of anticoagulant protein C and protein S also fall
  1. Factor 7, followed by 9, then 10 and then 2
20
Q
  1. How is warfarin measured?
  2. What are the difficulties with warfarin therapy?
A

1.

  • Always essential to measure of the the effect of warfarin by the INR
  • INR is the international normalised ratio (INR) and is derived from prothrombin time
  1. Difficulties because of numerous interactions
  • Dietary vitamin K
  • Variable absorption
  • Interactions with other drugs - protein binding, competition/induction of cytochromes
  • Teratogenic
21
Q

Draw a table and briefly describe the following about heparin, warfarin and DOACs:

  1. Administration
  2. Action
  3. Onset
  4. Monitoring
  5. Half life effect
  6. Reversal
  7. Use and pregnancy?
A
22
Q
  1. What is the main risk benefit and risks of anticoagulants?
  2. Describe what the INR means
A

Anticoagulants are effective in preventing thrombosis, but they also increase the risk of bleeding

Balancing the INR:

Want to keep it between 2.5-5 as this is the period when there is a balance between thrombosis risk being reduced, and the risk of bleeding being reduced. The higher the INR the higher then risk of bleeding, but the lower the INR then the higher the risk of thrombosis

23
Q

Which patients are at an increased risk of thrombosis?

A
  • Medical in patients
    • Infection/inflammation, immobility inc stroke, age
  • Patients with cancer
    • Procoagulation molecules, inflammation, flow obstruction
  • Surgical patients
    • Immobility, trauma and inflammation
  • Previous VTE
  • Family history and genetic traits
  • Obese
  • Elderly
24
Q

Describe what can be used in thromoboprophylaxis

A
  • Low molecular weight heparin
    • e.g. Tinzaparin 4500u/Clexane 40mg OD
    • Not monitored
  • TED stockings (for surgery)
  • Flotron - intermittent compression (increases blood flow)
  • Sometimes DOAC +/- aspirin (orthapaedics)
25
Q
  1. Which patients are at higher risk of developing a VTE?
  2. Which procedures have a higher risk of VTE after surgery?
A
  1. Patient
  • Age >60 years
  • Previous VTE
  • Active cancer
  • Acute or chronic lung disease
  • Chronic heart failure
  • Lower limb paralysis
  • Acute infection
  • BMI>30
  1. Procedure:
  • Hip or knee replacement
  • Hip fracture
  • Other major orthopaedic surgery
  • Surgery >30 minutes
  • Plaster cast
  • Immobilisation of lower limb
26
Q
  1. Which patients are at a higher risk of bleeding?
  2. What procedures causes a higher risk of bleeding?
A
  1. Patient
  • Bleeding diathesis e.g. haemophilia, Von willebrand disease
  • Platelets <100
  • Acute CVA in previous month
  • BP > 200 sytsolic or 120 diastolic
  • Severe liver disease
  • Severe renal disease
  • Active bleeding
  • Anticoagulation or anti-platelet therapy
  1. Procedure
  • Neuro, spinal or eye surgery
  • Other with high bleeding risk
  • Lumbar puncture/spinal/epidural in previous 4 hours
27
Q

What are the possible treatments for DVT/PE?

A

Immediate coagulation is essential (high risk of death from PE)

  1. Start LMWH (175u/kg) add warfarin
  2. Stop LWMH when INR>2 for 2 days
  3. Continue for 3-6 months

OR

  1. Start DOAC
  2. Continue DOAC for 3-6 months
28
Q

Describe the thrombolysis and use in VTE

A
  • Only for life threatening PE or limb threatening DVT
  • Risk of haemorrhage approx 4%
  • Reduces subsequent post-phlebitic syndrome
  • Indications broadening slowly
29
Q

Long term anticoagulation

Does the risk of thrombosis if untreated outweight the risk of bleeding if treated?

A
  • Need to assess
    • Risk of recurrence - mortality and morbidity of recurrence
  • Risk of therapy
    • Bleeding - mortality and morbidity
    • Variation of risks with different techniques
30
Q

Describe the need for anticoagulation in recurrence of VTE in the following situations:

  1. Surgical precipitant
  2. Following an idiopathic VTE
  3. After minor precipitants e.g. COCP, flights and trauma
A
  1. Very low risk of recurrence after sugical preciptant
    * No need for long term anticoagulation
  2. High risk of recurrence (10-20% in 2 years)
    * Consider long term anticoagulation
  3. After minor precipitants e.g. COCP, flights or trauma
  • Usually 3 months adequate
  • Longer duration may be dictated by presence of other thombotic and haemorrhagic risk factors

Haematology - Path (11 decks)

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