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The Cardiovascular System > Venous Thromboembolism > Flashcards

Venous Thromboembolism Flashcards

1
Q

What are the three components of Virchow’s Triad

A
  • Abnormal blood flow - stasis
  • Hypercoagulability
  • Vascular Injury
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2
Q

Which factors of the coagulation cascade are important in the generation of thrombin

A

Factors 5 and 8

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3
Q

What does tissue damage lead to the release of

A

Tissue factor

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4
Q

What two factors combine to form factor 10a

A

Factors 7a and tissue factor

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5
Q

What is kind of membrane is required for the clotting cascade to occur

A

A phospholipid membrane in the form of platelets or monocytes.

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6
Q

What does the tissue factor pathway inhibitor do

A

Prevents the generation of factor 10a.

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7
Q

What is post thrombotic syndrome

A

A permanent pain and swelling.

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8
Q

What are the risk factors for venous thromboembolism

A
  • Age
  • Obesity
  • Varicose veins
  • Previous VTE
  • Thombophilia
  • Cancer
  • Other thrombotic states
  • Hormone therapy
  • Pregnancy
  • Immobility
  • Hospitalisation
  • Anaesthesia
  • Central venous catheters.
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9
Q

What is the issue with diagnosis of VTE

A

80% of DVT are clinically silent.

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10
Q

What are the clinical symptoms of DVT

A
  • Pain
  • Swelling
  • Increased temperature of the limb
  • Dilatation of superficial veins
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11
Q

Is DVT usually unilateral or bilateral

A

Unilateral

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12
Q

When may a DVT be bilateral

A

If thrombosis is sited in the inferior vena cava

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13
Q

What are the differential diagnosis of DVT

A

Calf haematoma, ruptured Baker’s cyst, cellulitis

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14
Q

What is Well’s score used for

A

To predict which patients might have DVT. Patients are put into low, moderate and high risk categories depending on the score.

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15
Q

What investigations are used to diagnose DVT

A
  • Contrast venography
  • Venous ultrasoundography
  • D-dimer test
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16
Q

What are the diagnostic results of DVT in venous ultrasoundography

A

Non-compressibility of the common femoral vein or popliteal vein.

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17
Q

What are the clinical features of pulmonary embolism

A
  • Collapse, faintness, crushing central chest pain
  • Pleuritic chest pain
  • Difficulty breathing
  • Haemoptysis
  • Extertional dyspnoea
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18
Q

What is pleuritic chest pain

A

Pain in the chest which worsens when breathing in

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19
Q

What is haemoptysis

A

Coughing up blood

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20
Q

What investigations are used in the diagnosis of PE

A
  • Chest x-ray
  • Electrocardiogram
  • Arterial blood gases
  • D-dimer
  • Ventilation perfusion scan
  • CT angiogram
  • Echocardiogram
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21
Q

Why is a chest x-ray used in the diagnosis of PE

A

To rule out other possible diagnosis

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22
Q

What will be shown on an echocardiogram in someone with a pulmonary embolism

A

On an echocardiogram, a high right sided ventricular pressure will be shown due to resistance from the pulmonary circulation as a result of the PE.

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23
Q

What are the principles of anticoagulant therapy

A

Rapid initial anticoagulation followed by extended therapy.

24
Q

What can be given for rapid initial anticoagulation

A

Parenteral anticoagulant or direct oral anticoagulant

25
Q

What are examples of parenteral anticoagulants

A
  • Heparin
  • Low molecular weight heparin
  • Fondaparinux
26
Q

When are direct oral anticoagulants used

A

In emergency situations.

27
Q

Why are direct oral anticoagulants only used in emergency situations

A

Because it takes 4 hours for absorption so if a person has collapsed due to PE, they will be given parenteral heparin as this ensures absorption and brings about a response more quickly.

28
Q

What can be given for extended therapy after a PE

A

An orally active anticoagulant or a direct anticoagulant.

29
Q

What is an example of an orally active anticoagulant

A

A vitamin K antagonist such as warfarin.

30
Q

What is the aim of extended anticoagulant therapy

A

To prevent recurrent thrombosis and chronic complications such as post phlebitic syndrome

31
Q

What are DOACs

A

Direct oral anticoagulants

32
Q

What are four examples of DOACs

A

Dabigatran, Rivaroxaban, Edoxaban and apixaban

33
Q

What does dabigatran do

A

Dabigatran inhibits the action of thrombin in the formation of a thrombus

34
Q

What do rivaroxaban, edoxaban and apixaban

A

Rivaroxaban, edoxaban and apixaban inhibit factor 10a to prevent the progression of the clotting cascade

35
Q

Which two points are important in the clotting cascade and therefore are drug targets

A

The formation of factor 10a and thrombin action to convert fibrinogen into fibrin.

36
Q

What is sometimes given alongside DOACs

A

Heparin

37
Q

What is the action of DOACs

A

They enable rapid initial anticoagulation orally and then are given at a lower dose for secondary prevention of venothromboembolism.

38
Q

Which DOACs do not need to be given alongside heparin

A

Apixaban and rivaroxaban

39
Q

What investigations are used to investigate a procoagulant tendency

A
  • Full blood count
  • Antithrombin
  • Protien C
  • Protein S
  • Thrombin time
40
Q

In what situation is the DOAC argatroban used

A

Where the person is allergic to heparin.

41
Q

What factors are thrombin and prothrombin

A

Thrombin is factor IIa and prothrombin is factor II.

42
Q

What are two types of heparin

A

Unfractionated and low-molecular weight heparin.

43
Q

Which type of heparin is more bioavailable

A

Low molecular weight heparin

44
Q

How does heparin work

A

It binds to pentasaccharide on antithrombin and brings about its inhibitory action towards factor Xa and thrombin.

45
Q

What’s negative about prescribing unfractionated heparin

A

It has an unpredictable anticoagulant response due to binding to plasma proteins so requires monitoring using APTT.

46
Q

What conditions could develop due to unfractionated heparin

A

Osteoporosis and heparin-induced thrombocytopenia

47
Q

What is there a high risk of with unfractionated heparin

A

Bleeding.

48
Q

What are the two positives about the use of low molecular weight heparin

A

It has almost 100% bioavailability and no monitoring is required.

49
Q

What is the negative about the use of low molecular weight heparin

A

It is not reversible

50
Q

What are coumarins

A

They inhibit vitamin K dependent carboxylation of factors 2, 7, 9 and 10

51
Q

What is the most common coumarin

A

Vitamin K

52
Q

By what method are coumarins such as warfarin taken

A

Orally

53
Q

How are coumarins such as warfarin monitored

A

By the international normalised ratio (INR) derived from the prothrombin time (PT)

54
Q

How can the effect of warfarin be reversed

A

Dietary intake of vitamin K, fresh frozen plasma and concentrates of the factors inhibited by warfarin.

55
Q

What are the negative aspects of prescribing warfarin

A

There are many drug interactions with warfarin and requires monitoring at least monthly.

56
Q

What is the negative aspect about using DOACs instead of warfarin

A

Their effect cannot really be revered.

57
Q

Which is currently the only DOAC that can be reversed

A

Dabigatran. The factor 10a inhibitors cannot yet be reversed.

The Cardiovascular System (15 decks)

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