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Haematology - Path > Venous thrombosis > Flashcards

Venous thrombosis Flashcards

1
Q

Who is at a higher risk of venous thromboemoblism?

A

People above the age of 50

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2
Q

What are the consequences of thromboemolism?

A
  • Death
  • Recurrence - 20% in 2 years
  • Thrombophleblitic syndrome - recurrent pain, swelling and ulcers
  • Pulomonary hypertension - 4% at 2 years
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3
Q

Describe vichow’s triad

A

Blood

Vessel wall

Blood flow

Three contributory factors ot thrombosis

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4
Q

What can be affected in the blood?

A
  • Viscocity
    • Haematocrit - polycythemia
    • Protein/paraprotein
  • Platelet count
  • Coagulation system
    • Net excess of procoagulant activity
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5
Q

Describe the end point of the blood coagulation system

A

Series of enzymatic events that leads to the formtion of thrombin (IIa) and then the conversion of fibrinogen to fibrin which forms the blood clot

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6
Q

What are the procoagulant factors?

A
  • V
  • VIII
  • XI
  • IX
  • X
  • II
  • Fibrinogen
  • Platelets

Leading to fibrin formation

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7
Q

What are the anticoagulant factors?

A
  • TFPI
  • Protein C
  • Protein S
  • Thrombomodulin
  • EPCR
  • Antithrombin
  • Fibrinolysis
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8
Q

Define the basics of thrombophilia

A
  • Thrombophilia is a disturbed balance
  • An increase in the level of coagulation factors and platelets
  • A decrease in fibrinolytic factors and anticoagulant proteins
  • Disturbing the delicate equilibrium and causing increased clots
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9
Q
  1. Is the vessel wall normally thrombotic or antithrombotic?
  2. How does the vessel wall achieve this?
A
  1. Antithrombotic
  2. The vessel wall expresses anticoagulant molecules:
  • Thrombomodulin
  • Endothelial protein C receptor
  • Tissue factor pathway inhibitor
  • Heparans

The vessel wall does not express tissue factor

Secretes antiplatelet factors such as

  • Prostacyclin
  • Nitric oxide
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10
Q
A
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11
Q
  1. What makes the vessel wall prothrombotic?
  2. How does the vessel wall become thrombotic?
A
  1. Inflammatory/injury such as:
  • Infection
  • Malignancy
  • Vasculitis
  • Trauma
  1. The vessel wall becomes thrombotic:
  • Anticoagulant molecules e.g. thrombomodulin are down regulated
  • Adhesion molecules upregulated
  • Tissue factor may be expressed
  • Prostacyclin production decreased
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12
Q

Blood flow makes up part of Virchow’s triad. Stasis promotes thrombosis. What is the mechanism?

A
  • Accumulation of activated factors
  • Promotes platelet adhesion
  • Promotes leukocyte adhesion and transmigration
  • Hypoxia produces inflammatory effect on endothelium
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13
Q

What are the possible causes of stasis?

A
  • Immobility - e.g. surgery, paraparesis and travel
  • Compression - e.g. tumour or pregnancy
  • Viscocity e.g. Polycythemia, paraprotein
  • Congenital e.g. Vascular abnormalities
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14
Q

Describe combined thrombotic risks

A
  • Thrombotic risk factors often combine to produce thrombosis
  • Thrombotic factors may have powerful interactions - these are unpredictable

Example: Oral contraceptive pill and factor V Leiden

  • Combination of both of these increases the relative risk from RR 10 individually to a RR of 35 when they appear together of developing a VTE
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15
Q

Describe the basic uses of high dose and low dose anticoagulant therapy

A
  • High dose - theraputic
  • Low dose - prophylactic
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16
Q

Describe the:

  1. Immediate acting anticoagulants
  2. The anticoagulants that have a delayed action
A
  1. Immediate
  • Heparin
    • Unfractionated heparin
    • Low molecular weight heparin
  • Direct acting anti-Xa and anti-IIa (rivoroxaban)
  1. Delayed action
  • Vitamin K antagonists
    • Warfarin
    • Affects factor 2, 7, 9 and 10
17
Q
  1. Describe the different heparins
  2. Describe how heparins act
  3. Uses and disadvantages of heparins
A
  1. Different types of heparins
  • Unfractionated heparins - I.V infusion
  • Low molecular weight heparin - sub cut
  • Pentasaccharide - sub cut

2.Action

  • All act by potentiating antithrombin
  • Provide immediate effect - e.g. can be used as immediate treatment for thrombosis
  1. Uses and disadvantages:
  • LMWH provides a more controlled/uniformed action
  • Long term disadvantage - many injections, also increased risk of osteoporosis
  • Variable renal dependence
18
Q

Describe the monitoring of:

  1. LMWH
  2. Unfractionated heparin
A
  1. Low molecular weight heparin:
  • Reliable pharmacokinetics so not usually required
  • Can use anti-Xa assay e.g.
    • Renal failure (CrCl <50)
    • Extremes of weight or risk
  1. Unfractionated heparin:
  • Variable kinetics
  • Variable dose-response
  • Always monitor theraputic levels with APTT or anti-Xa assay
19
Q
  1. Describe the direct-acting anticoagulants
  2. Describe their properties
A
  1. Directing acting anti-coagulants
  • Anti-Xa
    • Rivoroxaban, apixaban and edoxaban (all have X in!!)
  • Anti-IIa
    • Dabigatran

Properties

  • Oral administration
  • Immediate acting - peak in approx 3-4 hours
  • Useful in long-term
  • Short half life
  • No monitoring needed
20
Q

Describe the properties of Warfarin

A
  • Given orally
  • Indirect effect by preventing recycling of Vit K
  • Therefore onset of action is delayed
  • Levels of procoagulant factors II, VII, IX & X fall
  • Levels of anticoagulant protein C and protein S also fall
  • Doesn’t inhibit 2,7,9 and 10 just blocks synthesis
21
Q
  1. Describe how warfarin is measured
  2. Why does Warfarin need monitoring?
A
  1. Monitoring of warfarin
  • Always essential
  • Measure of effect is the INR - international normalised ratio - derived from prothrombin time
  1. Difficult drug as Warfarin ahas numerous interactions
  • Dietary vitamin K
  • Variable absorption
  • Interactions with other drugs
    • Protein binding
    • Competition/induction of cytochromes
  • Teratogenic - Warfarin crosses the placenta
22
Q

Why is it important to keep people in the theraputic range when on anticoagulants?

A

The benefit of being on anticoagulants is that they reduce the risk of thrombosis, however this means they are also at a higher risk of bleeding

Keep in the theraputic range to keep a balance between reducing thrombotic risk and the risk of bleeding

23
Q

Which patients are at a higher risk of thrombosis?

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

Describe what thromboprophylaxis should be given to someone with a higher risk of developing thrombosis

A
  • Low molecular weight heparin (LMWH)
    • Eg: Tinzaparin 4500u/ Clexane 40mg od
    • Not monitored
  • TED Stockings (for surgery or if heparin C/I)
    • Flotron - Intermittent compression (increases flow)
  • Sometimes DOAC +/- aspirin (orthopaedics)
25
Q
  1. What patient factors increase the risk of developing a VTE?
  2. Which procedures increase the risk of developing a VTE?
A
  1. Patient factors
  • Age > 60yrs
  • Previous VTE
  • Active cancer
  • Acute or chronic lung disease
  • Chronic heart failure
  • Lower limb paralysis (excluding acute CVA)
  • Acute infection
  • BMI>30

Procedures:

  • Hip or knee replacement
  • Hip fracture
  • Other major orthopaedic surgery
  • Surgery > 30mins
  • Plaster cast immobilisation of lower limb
26
Q
  1. Which patient factors increase the risk of bleeding?
  2. Which procedures have the highest risk of bleeding?
A
  1. Patient factors:
  • Bleeding diathesis (eg haemophilia, VWD)
  • Platelets < 100
  • Acute CVA in previous month (H’gge or thromb)
  • BP > 200 syst or 120 dias
  • Severe liver disease
  • Severe renal disease
  • Active bleeding
  • Anticoag or anti-platelet therapy
  1. Procedures
  • Neuro, spinal or eye surgery
  • Other with high bleeding risk
  • Lumbar puncture/spinal/epidural in previous 4 hours
27
Q

Describe the treatment for DVT/PE

A

Immediate coagulation is essential - otherwise there is a high risk of death from PE

  • Start LMWH e.g. Tinzaparin 175u/kg + warfarin
  • Stop LMWH when INR >2 for 2 days
  • Continue warfarin for 3-6 months

OR

Immediately start a DOAC and continue for 3-6 months

28
Q
  1. When should thrombolysis be used?
  2. What are the risks?
A
  1. Only for life threatening PE or limb threatening DVT

2.

  • Risk of haemorrhage (Intra cranial) ~4%
  • Reduces subsequent post-phlebitic syndrome
  • Indications broadening slowly
29
Q

How do we assess the risk of thrombosis when left untreated to the risk of bleeding if treated?

A

Need to assess

  • Risk of recurrence
    • Morbidity and mortality of recurrence
  • Risk of therapy (bleeding)
    • Morbidity and mortality of bleeding
    • Variation of risks with different therapies
30
Q

Which are at a higher risk of VTE recurrence men or women?

A

men

31
Q

Describe site and types of recurrence

A

If you have a DVT first, if it recurs its likely to be another DVT not a PE. if a PE develops first, a recurrent thrombotic episode is likely to be another PE

32
Q

What is the recurrence risk like for the following and how should they be managed?

  1. Surgical precipitant
  2. Idiopathic VTE
  3. COCP/flights/trauma
A
  1. Very low recurrence risk after after surgical precipitant
    * No need for long term anticoagulation
  2. High risk of recurrence after idiopathic VTE (10-20% in 2yrs)
    * Consider long term anticoagulation
  3. After minor precipitants (COCP, flights, trauma)
  • Usually 3 months adequate - anticoagulant therapy
  • Longer duration may be dictated by presence of other thrombotic and haemorrhagic risk factors

Haematology - Path (11 decks)

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