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Venous thromboembolism Flashcards

1
Q

Define thrombosis

A

Pathological clot formation within blood vessel

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2
Q

Describe the difference between venous thrombi and arterial thrombi

A

Venous- red cells in fibrin mesh (red clot)

Arterial- platelets and fibrin (white clot)

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3
Q

Define embolism

A

Clot breaks off and travels through circulation until obstructed by vessels of smaller diameter

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4
Q

What is difference between distal and proximal DVT

A 
Distal= confined to calf vein
Proximal= involved popliteal vein and above
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5
Q

Where do majority of pulmonary embolisms arise from

A

DVT

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6
Q

Where do majority of DVTs arise from

A

Calf venous sinuses

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7
Q

What % of DVTs extend proximally to popliteal vein or above

A

25

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8
Q

Of the DVTs that extend proximally to popliteal vein, what % embolise

A

40

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9
Q

Of the DVTs that embolise, how many are fatal

A

20

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10
Q

What is the third most common cause of cardiovascular death

A

Pulmonary embolism

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11
Q

What is the mortality of untreated and treated pulmonary embolism

A

30% untreated

<5% when treated

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12
Q

What are the causes of venous thromboembolism (Virchows triad)

A

Static blood
Vessel wall disorder
Hypercoagulability

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13
Q

Name the strong risk factors for VTE (5)

A
  • Hip/ pelvis fracture
  • Hip/ knee replacement
  • Major general surgery
  • Major trauma
  • Spinal cord injury
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14
Q

Name the moderate risk factors for VTE (7)

A
  • Previous VTE
  • Cancer outpatient
  • Resp failure
  • Pregnancy
  • Combined OC pill/ HRT
  • Central venous line
  • Thrombophilia
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15
Q

Name the weak risk factors for VTE (5)

A
  • Bed rest > 8 days
  • Travel
  • Obesity
  • Day case srugery
  • Varicose veins
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16
Q

Signs and symptoms of DVT (8)

A 
Tenderness
Erythema
Pain
Palpable cord
Superficial venous dilation
Ipsilateral oedema
Warmth
Swelling
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17
Q

Why is it important to get objective diagnosis of DVT

A
  • 75% of suspected patients negative on investigation

- Drugs used to treat VTE cause serious side effects

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18
Q

3 steps of diagnosing DVT?

A

1) Clinical pre-test probability (Wells score)
2) D-dimer test
3) Radiological assessment

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19
Q

What is D-dimer

A

Blood test for non specific marker of fibrin formation

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20
Q

What radio-logical assessment is usually used to diagnose DVT and why?

A

Compression ultrasound as non invasive

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21
Q

Gold standard for radiological assessment

A

Venography

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22
Q

Name some components of a Wells score test

A 
Active cancer
Paralysis
Recently bedridden
Localised tenderness
Entire leg swollen
Calf swelling
Pitting oedema
Collateral superficial veins
Previous documentated DVT`
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23
Q

What is post-thrombotic syndrome

A

Recurrent pain and swelling in leg that may progress to local skin pigmentation and ulceration

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24
Q

Is post-thrombotic syndrome more or less common in distal or proximal DVT

A

Proximal (30-50% of proximal cases)

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25
Q

What causes post-thrombotic syndrome

A

Occurs due to venous hypertension (obstruction and valve damage) as well as abnormal microcirculation with reversal of blood flow from deep to superficial veins

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26
Q

Signs of pulmonary embolism

A

Tachypnoea and tachycardia
Crepitations
Pleural rub

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27
Q

What % of PE patients have isolated breathlessness

A

25

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28
Q

What % of PE patients have collapse/ hypotension/ shock

A

10

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29
Q

What does an ECG of somebody with PE show

A

Sinus tachycardia
Right heart strain
T wave inversion
S1Q3T3

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30
Q

What would chest x-ray show

A

Focal oligaemia
Peripheral wedge shaped density above diaphragm
Arterial blood gases show hypoxia, low CO2

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31
Q

What are the components of wells score for PE

A
  • Clinical signs and symptoms DVT
  • Alternative diagnosis less likely
  • Pulse >100
  • Immobilisation or surgery
  • Previous DVT/ PE
  • Cancer
32
Q

What is the % mortality of pulmonary embolism within 1 hour of symptoms onset

33
Q

What is the % mortality of pulmonary embolism within 2 weeks if untreated

34
Q

What is the % mortality of treated pulmonary embolism

35
Q

What is 1 year mortality of pulmonary embolism

36
Q

What blood tests are used to manage vte

A

FBC
Clottting screen
D dimer
U&E

37
Q

Describe treatment outline for VTE

A
  • Blood tests
  • Start low molecular weight heparin unless contraindication
  • Confirm diagnosis
  • Continue heparin and start warfarin
  • Stop heparin, continue warfarin
  • Review after 3 months
38
Q

When can heparin be stopped?

A

After minimum of 5 days and when INR is in therapeutic range (2-3) for 2 consecutive days

39
Q

What do anti-coagulants do (brief)

A

Prevent extension and recurrence (not clot busters)

40
Q

Why is low molecular weight heparin used?

A
  • As effective as and safer than unfractioned heparin
  • More predictable response
  • No monitoring required
  • Easier to use
41
Q

How is low molecular weight heparin adminster

A

Subcutaneously

42
Q

What is half life of low molecular weight heparin

43
Q

Brief mechanism of low molecular weight heparin

44
Q

What is the half life of unfractionated heparin

A

60-90 mins

45
Q

When is unfractionated heparin usually used

A

When rapid reversibility is important

46
Q

How is unfractionated heparin monitored

47
Q

What is fondaparinux

A

Synthetic pentasacchairde

48
Q

Half life of fondaparinux

49
Q

When is fondaparinus unsuitable

A

Renal impairment (GFR<30mL/min)

50
Q

Site of action of vitamin K antagonists

A

Factor IX
Factor VII
Factor X
Factor II

51
Q

Site of action of heparin

A

Factor Xa

Thrombin

52
Q

Site of action of apixaban, edoxaban, rivaroxaban

53
Q

Site of action of dabigatran

54
Q

Name 3 side effects of heparin

A
  • Major bleeding
  • Heparin induced thrombocytopenia
  • Osteroporosis
55
Q

What % of patients have major bleeding due to heparin within first week of treatment

56
Q

How can heparin related bleeding be treated

A

Specific heparin antagonist (protamine sulphate)

57
Q

What are the features of heparin induced thrombocytopenia

A

Onset of moderate thrombocytopenia and high risk of thrombosis
Develops 5-14 days after treatment

58
Q

Does osteoporosis occur after exposure to low molecular weight heparin, unfractionated heparin or both

59
Q

Briefly state mechanism of action of warfarin

A

Vitamin K antagonist

60
Q

Half life of warfarin?

61
Q

What measurement does warfarin primarily affect

A

Prothrombin time (INR)

62
Q

By how much does warfarin decrease recurrence of VTE

63
Q

How should you manage bleeding that occurs when on warfarin

A
  • Stop warfarin
  • Consider vitamin K 0.5-5mg orally or IV
  • Prothrombin complex concentrate if patient needs rapid reversal
64
Q

How long does the vitamin K used to treat warfarin related bleeding take to work

A

4 hours via IV

Maximum of 12-24 hours

65
Q

When in the treating of VTE can the following drugs be used:

a) Rivaroxaban
b) Apixaban
c) Dabigatran
d) Edoxaban

A

a) Start day 1- no need for heparin lead in
b) Start day 1- no need for heparin lead in
c) Heparin lead in required: 5-10 days
d) Heparin lead in required 5-10 days

66
Q

3 options for treating VTE

A
  • LMWH bridged to warfarin
  • LMWH followed after 5 days by dabigatran or edoxaban
  • Rivaroxaban or apixaban without LMWH
67
Q

What is DOAC stand for

A

direct oral anticoagulant

68
Q

How should VTEs be treated in pregnant women

A
  • Warfarin and DOACS closs placenta- warfarin causes bleeding and DOACs may
  • Use LMWH
69
Q

Which drugs are safe and which drugs are unsafe for women while they breastfeed

A

LMWH and warfarin safe

Not DOACs

70
Q

What drug is most effective in patients with cancer-associated thrombosis

A

LMWH is more effective than warfarin

71
Q

When is thrombolysis (clot busting) treatment used?

What is main risk factor

A

Massive PE or limb threatening DVT

1-3% intracranial bleeding risk

72
Q

When is inferior vena cava filter used

A

If major contraindication to anticoagulation

If PE recurrss despite adequate anticoagulation

73
Q

What is thrombophilia

A

Laboratory detected predisposition to thrombosis

74
Q

Name some heritable causes of thrombophilia

A 
Factor V Leiden
Prothrombin gene mutation
Protein C deficiency
Protein S deficiency
Antithrombin deficiency
75
Q

Clinical manifestation of antiphospholipid syndrome

A 
Migraines, strokes
PE
CAD
Renal vein thrombosis, renal infarction,
Recurrent miscarriage, pre-eclampsia
DVT
76
Q

Describe how antiphospholipid syndrome affects pregnancies/ fertility

A
  • Unexplained fetal deaths after 10 weeks
  • Premature deliveries
  • Miscarriages
77
Q

How many preventable PE deaths are there a year in England

CR 2 (33 decks)

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