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Haematology > Venous thrombosis > Flashcards

Venous thrombosis Flashcards

1
Q

What are some examples of thrombotic events?

A
  • Arterial - coronary, cerebral, peripheral
  • Venous - DVT, PE
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2
Q

What is the underlying mechanism of action in arterial thrombosis and how is it treated?

A
  • High pressure system
  • Atherosclerosis
  • Platelet rich thrombus
  • Treatment - aspirin and other anti-platelet drugs modify risk factors for atherosclerosis
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3
Q

What is the underlying mechanism of action in venous thrombosis?

A
  • Low pressure system
  • Platelets not activated
  • Activates coagulation cascade - rich in fibrin clot
  • Virchow’s triad - hypercoagulability, vessel wall injury, stasis
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4
Q

How is a venous thrombosis treated?

A

Heparin/warfarin/new oral anticoagulants

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5
Q

What are the clinical features of DVT?

A
  • Limb feels hot, swollen, tender
  • Pitting oedema
  • Top differential for DVT is cellulitis
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6
Q

What occurs in a pulmonary embolism?

A
  • Pulmonary infarction
  • Pleuritic chest pain
  • Cardiovascular collapse/death
  • Hypoxia
  • Right heart strain
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7
Q

What is the prevalence of venous thrombo-embolism?

A
  • Risk 1/1000 per annum
  • Young adults 1/10,000 per annum - this risk is increased by up to 7 times in women taking the COC pill
  • Elderly 1/100 per annum
  • Lifetime risk of 2.5%
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8
Q

What are some risk factors for VTE?

A

Age, marked obesity, pregnancy, puerperium, oestrogen therapy, *previous DVT/PE*, trauma, surgery, malignancy, paralysis, infection, thrombophilia

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9
Q

What are the risk factors associated with hypercoagulability and with release of tissue factor, raised VWF and factor VIII?

A

Age, pregnancy, puerperium, oestrogen therapy, trauma/surgery, malignancy, infection

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10
Q

What is thrombophilia?

A

Familial or acquired disorder of the haemostatic mechanism which is likely to predispose to thrombosis

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11
Q

What are the potential mechanisms of thrombophilia?

A
  • Increased coagulation activity - platelet plug formation, fibrin clot formation
  • Decreased fibrinolytic activity
  • Decreased anti-coagulant activity
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12
Q

Name the naturally occurring anti-coagulants

A
  • Serine protease inhibitors - anti-thrombin
  • Protein C and protein S
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13
Q

What are hereditary thrombophilias?

A

A group of genetic defects in which affected individuals have an increased tendancy to develop premature, unusual and recurrent thromboses

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14
Q

What are some causes of hereditary thrombophilias?

A
  • Factor V Leiden
  • Prothrombin 20210 mutation
  • Anti-thrombin deficiency
  • Protein C deficiency
  • Protein S deficiency
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15
Q

When is hereditary thrombophilia screening considered?

A
  • Venous thrombosis <45 years
  • Recurrent venous thrombosis
  • Unusual venous thrombosis
  • Family history of venous thrombosis
  • Family history of thrombophilia
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16
Q

How are hereditary thrombophilias managed?

A
  • Advice on avoiding risk
  • Short term prophylaxis to prevent thrombotic events during periods of known risk
  • Short term anti-coagulation to treat thrombotic events
  • Long term anti-coagulation if recurrent thrombotic events
17
Q

What causes acquired thrombophilia?

A
  • Anti-phospholipid syndrome
  • Stronger risk factor for thrombosis than the hereditary thrombophilias!
18
Q

What are the clinical features of anti-phospholipid syndrome (APS)?

A
  • Recurrent thromboses - arterial, including TIAs and venous
  • Recurrent miscarriages
  • Mild thrombocytopenia
19
Q

What is the pathogenesis of APS?

A

Antibodies lead to a conformational change in beta-2- glycoprotein-1 which leads to activation of both primary and secondary haemostasis and vessel wall abnormalities

20
Q

What are anti-phospholipid antibodies?

A

Autoantibodies which have specificity for anionic phospholipids and which prolong phospholipid dependent coagulation tests in vitro

Also known as lupus anticoagulants

21
Q

What conditions are associated with anti-phospholipid syndrome?

A
  • Autoimmune disorders
  • Lymphoproliferative disorders
  • Viral infections
  • Drugs
22
Q

How is APS treated?

A
  • Activation of both primary and secondary haemostasis - aspirin
  • Arterial and venous thrombosis - warfarin

Haematology (22 decks)

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