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Kat's Pathology > Thrombosis: Aetiology and Management > Flashcards

Thrombosis: Aetiology and Management Flashcards

1
Q

Why are venous thrombosis important

A

Common
Significant sequelae
PE is the cause of 5-10% of hospital deaths
25000 deaths pa from hospital related VTE
Difficult to reverse and leads to morbidity
Preventable

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2
Q

Consequences of thromboembolism

A

Death - mortality 5%
Recurrence - 20% in first 2 years and 4% pa thereafter
Thrombophlebitic syndrome (recurrent pain, swelling and ulcers)
Pulmonary hypertension - 4% at 2 years

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3
Q

Virchow’s triad

A

Blood
Vessel wall
Blood flow

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4
Q

What underpins thrombosis formation

A

Virchow’s triad

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5
Q

Blood factors in virchow’s triad

A

Viscosity: Haematocrit
Protein/paraprotein, Platelet count

Coagulation system: Triggered by tissue factor, Generates thrombin, Thrombin converts fibrinogen to fibrin (the clot)

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6
Q

Procoagulant factors

A 
V
VIII
XI
IX
X
II
Fibrinogen 
Platelets
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7
Q

What regulates coagulation

A

TFPI
Protein C and S
Antithrombin

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8
Q

Anticoagulation factors

A 
TFPI
Protein C
Protein S
Thrombomodulin 
EPCR
Antithrombin 
Fibrinolysis
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9
Q

What causes thrombophilia

A

A disturbance in the balance between increased coagulation factors and platelets and decreased fibrinolytic factors and anticoagulant proteins

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10
Q

Why is the vessel wall normally antithrombotic

A

Expresses anticoagulant molecules: Thrombomodulin, Endothelial protein C receptor, Tissue factor pathway inhibitor, Heparans

Does not express tissue factor

Secretes antiplatelet factors: Prostacyclin, NO

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11
Q

What causes the vessel wall to become prothrombotic

A

Infection, malignancy, vasculitis, trauma

Effects: 
Anticoagulant molecules (eg TM) are down regulated
Adhesion molecules upregulated
TF may be expressed
Prostacyclin production decreased
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12
Q

What blood flow factors promote thrombosis

A

Blood stasis promotes thrombosis

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

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13
Q

Causes of blood stasis

A

Immobility: surgery, paraparesis, travel
Compression: tumour, pregnancy
Viscosity: polycythaemia, paraprotein
Congenital: vascular abnormalities

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14
Q

Pregnancy risk factors for thrombosis

A

Increased FVIII< fibrinogen
Decreased Protein S
Increased blood flow

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15
Q

Malignancy risk factors for thrombosis

A

Tissue factor on tumour
Inflammation
Increased blood floq

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16
Q

Surgery risk factors for thrombosis

A

Trauma
Inflammation
Blood flow

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17
Q

Surgery risk factors for thrombosis

A

Trauma
Inflammation
Blood flow

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18
Q

Principles of preventing VTE

A

Identifying high risk patients and high risk situations

19
Q

Principles of treating VTE

A

Prompt diagnosis and inhibition of coagulation

20
Q

Principles of long term prevention of VTE

A

Assess risk and rebalance coagulation

21
Q

High dose anticoagulation therapy

A

Therapeutic

22
Q

Low dose anticoagulation therapy

A

Prophylactic

23
Q

Anticoagulation drugs

A

Immediate: herparin (unfractionated, LMWH), direct acting anti-Xa and anti-IIa

Delayed: vitamin K antagonists (Warfarin)

24
Q

Mode of admission of herparins

A

Unfractionated heparin: iv infusion
Low molecular weight heparin: sub cut
Pentasaccharide: sub cut

25
Q

MOA of herparin

A

All act by potentiating antithrombin

Provide immediate effect (eg for treatment of thrombosis)
Long term disadvantage - injections, risk of osteoporosis
Variable renal dependence

26
Q

Monitoring herparin therapy

A

Low molecular weight heparin (LMWH):
Reliable pharmacokinetics so not usually required
Can use anti-Xa assay eg: Renal failure (CrCl<50)
Extremes of weight or risk

Unfractionated heparin
Variable kinetics
Variable dose-response
Always monitor therapeutic levels with APTT or anti-Xa

27
Q

Anti-Xa anticoagulants

A

DIrect acting anticoagulants
Rivaroxaban
Apixaban
Edoxaban

28
Q

Anti-IIa anticoagulants

A

Direct acting anticoagulants

Dabigatran

29
Q

Properties of direct acting anticoagulants

A 
Includes anti-Xa and anti-IIa
Oral administration
Immediate acting –peak in approx. 3-4 hours (cf LMWH)
Also useful in long term
Short half-life
No monitoring
30
Q

Long-term anticoagulation therapy

A

Warfarin

31
Q

Features of warfarin therapy

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

32
Q

Monitoring on warfarin therapy

A

Always essential
Measure of effect is the INR
International normalised ratio (INR)
Derived from prothrombin time

Difficult because numerous interactions:
Dietary Vitamin K
Variable absorption
Interactions with other drugs: Protein binding, competition/induction of cytochromes
Teratogenic
33
Q

Anticoagulants increase the risk of….

A

Bleeding

34
Q

Who is at 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

35
Q

Thromboprophylaxis therapy

A

Low molecular weight heparin (LMWH): Eg: Tinzaparin 4500u/ Clexane 40mg
Not monitored
Rivaroxaban
TED Stockings (for surgery or if heparin C/I)
Intermittent compression (increases flow)

36
Q

What needs to be dome with all patients admitted to hospital

A

All admissions to hospital should be assessed for thrombotic risk and unless contraindication exists, receive heparin prophylaxis.

37
Q

What patient factors put the patient at increased risk for VTE

A 
Age > 60yrs
Previous VTE
Active cancer
Acute or chronic lung disease
Chronic heart failure
Lower limb paralysis (excluding acute CVA)
Acute infection
BMI>30
38
Q

What procedure factors may put the patient at increased risk for VTE

A 
Hip or knee replacement
Hip fracture
Other major orthopaedic surgery
Surgery >  30mins
Plaster cast immobilisation of lower limb
39
Q

What patient factors may put the patient at increased risk of bleeding

A 
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
40
Q

What procedure factors may put the patient at increased risk of bleeding

A

Neuro, spinal or eye surgery
Other with high bleeding risk
Lumbar puncture/spinal/epidural in previous 4 hours

41
Q

Treatment of DVT/PE

A

Immediate anticoagulation is essential: start LMWH (e.g. tinzaparin 175u/kg + warfarin) and stop LMWH when INR<2 for 2 days and continue for 3-6 months.
In patients with cancer: continue LMWH and not warfarin

Alternatively, can just start DOAC and continue for 3-6 months

42
Q

When should thrombolysis be used for VTE

A

Only for life threatening PE or limb threatening DVT
Risk of haemorrhage (ICH) ~4%
Reduces subsequent post-phlebitic syndrome
Indications broadening slowly

43
Q

What determines long-term anticoagulation therapy

A

Risk of recurrence: morbidity and mortality of recurrence

Risk of therapy (bleeding): morbidity and mortality of bleeding, variation of risks with different therapies

44
Q

Anticoagulation and recurrence after first VTE

A

Very low after surgical precipitant: No need for long term anticoagulation

High recurrence after idiopathic VTE (20% in 2yrs): Consider long term anticoagulation

Minor precipitants (COCP, flights, trauma): Usually 3 months adequate, Longer duration may be dictated by presence of other thrombotic and haemorrhagic risk factors

Kat's Pathology (105 decks)

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