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Haematology > Venous Thrombosis > Flashcards

Venous Thrombosis Flashcards

1
Q

Give examples of arterial thrombotic events.

A
  • Coronary
  • Cerebral
  • Peripheral
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2
Q

Give examples of venous thrombotic events.

A
  • DVT

* PE

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3
Q

____ muscles squeeze blood up through the veins

A

Calf

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4
Q

What kind of system are arterial thrombus found?

A

High pressure system

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5
Q

What process has a role in the formation of an arterial thrombus?

A

Atherosclerosis

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6
Q

What is the thrombus formed in an arterial thrombus like?

A

Rich in platelets !!

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7
Q

How is an arterial thrombus treated?

A
  • Aspirin and other anti-platelet drugs

* Modify risk factors for atherosclerosis

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8
Q

What kind of system is a venous thrombus found in?

A

LOW pressure system

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9
Q

What is the main risk factor for a venous thrombus?

A

Blood stasis !!

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10
Q

What does NOT happen in the formation of a venous thrombosis?

A

Platelet activation

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11
Q

What is the clot like in a venous thrombosis?

A

Rich in fibrin – due to activation of the coagulation cascade

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12
Q

What triad helps us to understand how a venous thrombosis occurs?

A

Virchow’s triad: stasis, vessel wall, hypercoagulability

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13
Q

What is the ‘vessel wall’ mentioned in virchows triad referring to?

A

Valves

(esp. if had a previous VT as valve will already be damaged, and blood will be able to fall backwards).

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14
Q

Why does the risk of venous thrombosis increase with age?

A

Valves degenerate with age

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15
Q

How is a venous thrombosis treated?

A

Anti-coagulation

(not anti-platelets as platelets aren’t the problem here)

e.g. heparin / warfarin / new oral anti-coagulants

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16
Q

How does a DVT present?

A
  • Limb feels hot, swollen and tender

* Pitting oedema

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17
Q

What Ix do you want to do to find out where a clot is in the leg?

A

Doppler US

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18
Q

List various causes of a PE.

A
  • Pulmonary infarction.
  • Pleuritic chest pain – knife-like pain on inspiration.
  • Cardiovascular collapse/death.
  • Hypoxia.
  • Right heart strain.
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19
Q

What ECG pattern is suggestive of a PE?

A

SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T wave in III.

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20
Q

What is the population risk of a VTE?

A

1/1000 per year

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21
Q

What is the yearly risk of a VTE in: i) young adults? Ii) elderly people?

A

i) 1/10,000

ii) 1/100

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22
Q

What is the lifetime risk of a VTE?

A

2.5%

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23
Q

What are the risk factors for a VTE?

A
  • Age
  • Obesity
  • Pregnancy
  • Puerperium
  • Oestrogen therapy - OCP, HRT
  • Previous DVT/PE
  • Trauma/surgery
  • Malignancy
  • Paralysis
  • Infection
  • Thrombophilia
24
Q

What is the biggest risk factor for a VTE?

A

A previous VTE

25
Q

What are the risk factors for a VTE in terms of STASIS?

A
  • Age
  • Obesity
  • Pregnancy
  • Previous DVT/PE
  • Trauma/surgery
  • Malignancy
  • Paralysis
26
Q

What are the risk factors for a VTE in terms of VESSEL WAL?

A
  • Age

* Previous DVT/PE

27
Q

What are the risk factors for VTE in terms of HYPERCOAGULABILTY?

A
  • Age
  • Pregnancy
  • Puerperium
  • Oestrogen therapy - OCP, HRT
  • Trauma/surgery
  • Malignancy
  • Infection
  • Thrombophilia
28
Q

Clotting factors are acute phase proteins, so being unwell pushes clotting factors up

A

T

29
Q

Oestrogen-containing pill – increases factor VIII, fools body into thinking you’re pregnant, risk of VTE rises 10-fold

A

T

30
Q

How do all the risk factors for hypercoagulability increased the risk of a VTE?

A

They are associated with the release of tissue factor, raised VWF and factor VIII

31
Q

What is thrombophilia?

A

Familial or acquired disorders of the haemostatic mechanism which are likely to predispose to thrombosis.

32
Q

Outline the potential mechanism for a thrombophilia.

A
  • Increased coagulation activity
  • platelet plug formation
  • fibrin clot formation
  • Decreased fibrinolytic activity
  • Decreased anticoagulant activity
33
Q

Name 2 naturally occurring anticoagulants.

A
  • Anti-thrombin

* Protein C and Protein S

34
Q

How does anti-thrombin work?

A

Switches off thrombin and other blood clotting factors.

35
Q

How does PC and PS work?

A

Switch off VIII/IXa and V/Xa

36
Q

What – in relation to proteins C and S – can lead to thrombophilia?

A

Factor V leiden

37
Q

What does factor V leiden do?

A

Results in a single base pair change in factor V, meaning that protein C and protein S can’t switch factor V off as well as they should be able to

38
Q

What are hereditary thrombophilias?

A

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

39
Q

Give examples of inherited thrombophilias.

A
  • Factor V Leiden.
  • Prothrombin 20210 mutation.
  • Antithrombin deficiency.
  • Protein C deficiency.
  • Protein S deficiency.
40
Q

When should screening for inherited thrombophilias be considered?

A
  • Venous thrombosis <45y/o.
  • Recurrent venous thrombosis.
  • Unusual venous thrombosis (e.g. upper limb, cerebral veins).
  • Family history of venous thrombosis.
  • Family history of thrombophilia.
41
Q

What should be considered in the management of inherited thrombophilias?

A
  • Advice on avoiding risk e.g. avoid COCP.
  • Short term prophylaxis – to prevent thrombotic events during periods of known risk.
  • Short term anticoagulation – to treat thrombotic events.
  • Long term anticoagulation – if recurrent thrombotic events.
42
Q

Why do some people with hereditary thrombophilia NEVER suffer a thrombosis?

A

Hereditary thrombophilias greatly increase risk of thrombosis, but from a very low baseline rate, meaning risk is still very low

43
Q

What does long term anticoagulation need to achieve a balance between?

A

Risk of recurrent thrombosis vs Risk of serious haemorrhage

44
Q

What is much more important than the results of thrombophilia screening?

A

History + history of previous thrombosis

45
Q

What is an acquired thrombophilia?

A

An autoimmune condition which leads to an increased tendency to thrombosis

46
Q

Give an example of an acquired thrombophilia.

A

Antiphospholipid antibody syndrome

47
Q

What imposes a higher risk for thrombosis - acquired or hereditary thrombophilia?

A

ACQUIRED

48
Q

What are the clinical features of APLS?

A
  • Recurrent thromboses
  • arterial, including TIA’s
  • venous
  • Recurrent foetal loss
  • 3 consecutive miscarriages, or an unexplained late miscarriage
  • Mild thrombocytopenia
49
Q

What does APLS involve the activation of?

A

Both primary and secondary haemostasis

50
Q

Explain the pathogenesis of APLS.

A

Antibodies lead to a conformational change in β2 glycoprotein 1 (a protein with unknown function in health) which leads to activation of both primary and secondary haemostasis and vessel wall abnormalities.

51
Q

What are antiphospholipid antibodies?

A

Autoantibodies which have specificity for anionic phospholipids, and which prolong phospholipid dependent coagulation tests in vitro (e.g. false prolonged APTT).

52
Q

What is another name for antiphospholipid antibodies?

A

Lupus anticoagulants

53
Q

Give examples of things/conditions associated with antiphospholipid antibodies.

A
  • Autoimmune disorders, especially SLE.
  • Lymphoproliferative disorders.
  • Viral infections.
  • Drugs.
  • Primary.
54
Q

What does the treatment of APLS need to tackle?

A
  • Activation of both primary and secondary haemostasis

* Arterial and venous thrombosis

55
Q

What drugs are prescribed to patients with APLS?

A

Both aspirin and warfarin

Haematology (26 decks)

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