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Haematology > Haemostasis and Thrombosis > Flashcards

Haemostasis and Thrombosis Flashcards

1
Q

What percentage of PEs cause hospital deaths?

A

5-10%

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2
Q

What are the consequences of thromboembolism?

A

o Death – mortality 5%
o Recurrence – 20% in first 2 years and 4% pa after
o Thrombophlebitis syndrome (recurrent pain, swelling, ulcers) – severe TPS in 25% at 2y (11% with stockings)
o Pulmonary hypertension (if a PE isn’t cleared properly) – 4% at 2y

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3
Q

State Virchow’s Triad?

A
  • Blood
  • Vessel Wall
  • Blood flow
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4
Q

What in the blood affects the risk of thrombosis?

A
  • Viscosity (haematocrit, protein/paraprotein)
  • Platelet count
  • Coagulation System (net excess pf procoagulant activity)
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5
Q

Describe the coagulation cascade.

A
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6
Q

What factors in the blood increase the risk of thrombosis?

A 
	Reduced prothrombin 
	Thrombocytopenia 
	Reduced protein C 
	Elevated anti-thrombin 
	Increased fibrinolysis
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7
Q

How is the vessel wall antithrombotic?

A

o Expresses anticoagulant molecules

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

o Does not express tissue factor

o Secretes antiplatelet factors

  • Prostacyclin (PGI2) from vessel wall
  • NO
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8
Q

What can make the vessel wall prothrombotic?

A

infection
malignancy (3% thrombosis incidence)
vasculitis
trauma

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9
Q

What are the effects of the vessel wall becoming pro-coagulant?

A
  • anticoagulants (i.e. TM) downregulated
  • adhesion molecules upregulated
  • TF expressed
  • prostacyclin decreased
  • von Willebrand factor is released –> platelet and neutrophil capture + neutrophil extracellular traps (NETs) form
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10
Q

How does blood stasis promote thrombosis?

A
  • Accumulation of activated factors
  • Promotes platelet adhesion
  • Promotes leukocyte adhesion and transmigration
  • Hypoxia –> inflammatory effect on endothelium - adhesion, release of vWF
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11
Q

What are the causes of blood stasis?

A
  • Immobility –>surgery, paraparesis, travel
  • Compression –> tumour, pregnancy
  • Viscosity–>polycythaemia, paraprotein
  • Congenital–>vascular abnormalities
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12
Q

Which factor confers the highest risk of thrombosis?

A

Antithrombin deficiency

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13
Q

How do we use anticoagulants in thrombosis?

A

o Low dose –> prophylactic

o High dose –> therapeutic

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14
Q

What are the immediate anticoagulant drugs?

A

Heparin –> potentiates anti-thrombin activity
• Unfractionated
• LMWH

Direct acting anti-Xa and anti-IIa (thrombin)

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15
Q

What are the delayed anticoagulant drugs?

A

Vitamin K antagonists - warfarin

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16
Q

What are the long-term disadvantages of heparin?

A

Injections
Risk of osteoporosis
Variable Renal dependance

17
Q

Name Anti-Xa drugs

A

rivaroxaban, apixaban, edoxaban

18
Q

Name Anti-IIa drugs

A

dabigatran

19
Q

Name properties of direct acting anticoagulants

A
  • Oral admin
  • Immediate acting – peak in 3-4 hours
  • Useful long-term
  • Short half life
  • No monitoring – advantages over Warfarin
20
Q

Name properties of warfarin

A
  • Oral
  • Indirect effect on preventing recycling of Vitamin K
  • Onset of action delayed (slow onset; ~14 days to onset fully)
  • Procoagulants 2,7,9,10 fall (indirectly by inhibiting vitamin K) –> 2 and 1 take several days to become stable
  • Levels of anticoagulant protein C and S also fall
21
Q

In what order does warfarin delay the reduction in coagulation factors?

A

7, 9, 10 and 2

22
Q

How is warfarin monitored?

A

International Normalised Ratio (INR) –> derived from PT

23
Q

Why is warfarin therapy difficult?

A
  • Dietary vitamin K
  • Variable absorption
  • Interactions with other drugs – protein binding, competition/induction of cytochromes
  • Teratogenic (don’t give in pregnancy)
24
Q

What patients are at increased risk of thrombosis?

A
  • Medical in-patients –> Infection , immobility (including stroke), age
  • Patients with cancer –> procoagulant molecules, inflammation, flow obstruction
  • Surgical patients –> immobility, trauma, inflammation
  • Previous VTE, family history, genetic traits
  • Obese
  • Elderly
25
Q

Describe thromboprophylaxis.

A

-LMWH e.g. Tinzaparin 4500u/Enoxaparin 40mg od
Not monitored

  • TED stockings
  • Intermittent pneumatic compression (increases flow)

-Sometimes DOAC +/- aspirin (orthopaedics)

26
Q

What are the 3 main goals of anticoagulant therapy?

A

1) Prevent thrombosis
2) Treat thrombosis
3) Prevent recurring thrombosis

27
Q

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

A
  • Risk of recurrence – morbidity and mortality

- Risk of therapy – bleeding – morbidity and mortality, variation of risks with different therapies

28
Q

How should you give anticoagulation after first VTE?

A
  • If very low risk after surgical precipitant –> no need for long term anticoagulation
  • High risk after idiopathic VTW (10-20% in 2 yrs)–> consider long-term anticoagulation - esp with DOAC
  • After minor precipitants (COCP, flight, trauma) –> usually 3 months adequate + longer duration may be dictated by presence of other thrombotic and haemorrhage risk factors

Haematology (16 decks)

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