Thrombosis Flashcards

1
Q

What is a clot?

A

General term for mass of coagulated blood (can occur outside the body or after death)

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2
Q

What is a Thrombus?

A

Blood clot formed in situ in a blood vessel or heart chamber during life

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3
Q

What is an Embolus?

A

Detached intravascular material that is carried from origin to distant site (not just thrombotic material)

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4
Q

What are the 5 types of embolus?

A

Thrombus (DVT)
Fat embolus
Air embolus
Amniotic fluid embolus
Foreign material

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5
Q

What is Virchow’s triad?

A

A model that describes and categorises the risks of thrombosis (has 3 main components that contribute to the risk)

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6
Q

What are the 3 main components of Virchow’s triad?

A

Stasis
Vessel wall injury
Hypercoagulability

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7
Q

What is stasis?

A

Anything that stops your blood from flowing

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8
Q

What are risk factors for Vessel wall injury?

A

Endothelial dysfunction
- Smoking
- Hypertension
Endothelial damage
- Surgery
- Catheter (PICC lines)
- Trauma

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9
Q

What are hereditary risk factors for hypercoagulability?

A
  • Factor V Leiden
  • Prothrombin G20210A
  • Protein C and S deficiency
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10
Q

What are acquired risk factors for hypercoagulability?

A
  • Cancer
  • Chemotherapy
  • OCR/HRT
  • Pregnancy
  • Obesity
  • HIT
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11
Q

What are clinical risk factors for stasis?

A

Immobility
Polycythemia

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12
Q

What is factor V Leiden?

A

-FVL= inherited thrombophilia
-Autosomal dominant (incomplete penetrance)
-3-5% white european pop. are heterozygous
- Often need acquired risk to produce symptoms

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13
Q

What is heterozygous risk for FVL?

A

5-10x risk

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14
Q

What is homozygous risk for FVL?

A

16-18x

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15
Q

What is the mutant form of Factor V?

A

Lack Arg506 cleavage site

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16
Q

What does a mutant form of Factor V cause?

A

Resistant to degradation by activated protein C, this results in hypercoagulable state
Can lead to unprovoked VTE & recurrent pregnancy loss

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17
Q

What is anti- phospholipid syndrome?

A
  • Acquired thrombophilia
  • Autoimmune condition
  • 3-5% of general population
  • Common in SLE (LUPUS) but most don’t have SLE
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18
Q

What autoantibodies are involved in Anti-phospholipid syndrome?

A

B2glycoprotein 1
Anti- cardiolipin
Lupus anticoagulant

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19
Q

What type of thrombosis risk is increased in anti- phospholipid syndrome?

A

Increased risk of arterial or venous thrombosis

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20
Q

How is anti- phospholipid antibody syndrome diagnosed?

A
  • Positive test on 2 occasions
  • 6-12 weeks apart
  • Venous or arterial thrombosis, thrombocytopaenia or recurrent fetal loss
  • Most need to take aspirin daily
  • Catastrophic form= large volume of antibodies produced, can lead to organ failure
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21
Q

What causes an arterial thromboses?

A
  • Usually due to endothelial injury/ atherosclerosis
  • High pressure & shear stress
22
Q

What is an arterial thrombus?

A
  • “White” platelet- rich thrombus
  • Adherent to vessel wall
23
Q

Where to Arterial thromboses usually occur?

A

Coronaries
Carotids
Cerebral vessels
Lower limb arteries

24
Q

What causes Venous thromboses?

A
  • Usually in non-injured veins and due to stasis
  • Low pressure and low flow
  • Red blood cell rich thrombus
  • Loosly attached and friable
25
Q

Where do Venous thromboses usually occur?

A
  • Lower limb veins (DVT)
  • Pulmonary veins (PE)
  • Cerebral venous sinus
26
Q

What is DVT?

A

Deep vein thrombosis
Formation of a blood clot (thrombus) in a deep vein

27
Q

Where does DVT most commonly affect?

A

Leg veins (femoral or popliteal vein)
OR
the deep veins of the pelvis

28
Q

How many people get DVT in their lifetime?

A

1/20

29
Q

What is VTE?

A

Venous thromboembolism is a common disease that is often asymptomatic

30
Q

How many people do clinical symptoms present in of VTE?

A

1-2 per 1000 people every year
Approx 2/3 of all cases are DVT & 1/3 PE

31
Q

What is the incidence of DVT during pregnancy?

A

Approx 1 in 1000 live births

32
Q

What is the incidence of DVT in critically ill people?

A

37.2%

33
Q

What is the DVT wells score?

A

scoring system based on risk factor

34
Q

What is the D- dimer test?

A

Test has 93-95% sensitivity
Negative test= virtually rules out VTE

35
Q

What are false negatives of the D- dimer test?

A

False negatives- rare, sample delayed or too early, patient on anticoagulation

36
Q

What are false positives of the D- dimer test?

A

Liver disease, inflammation malignancy, trauma, pregnancy, recent surgery, advanced cancer

37
Q

What is a pulmonary embolus?

A

Blockage of an artery in the lungs by a substance that has moved from elsewhere in the body or bloodstream

38
Q

What are the 8 presenting symptoms of PE?

A
  • Dyspnoea
  • Tachynoea
  • Pleuritic chest pain
  • Cough
  • Haemoptysis
  • Haemodynamic instability
  • Collapse/ syncope
  • Sudden death
39
Q

What is the PE wells score?

A

More than 4 points (PE likely)
Less than 4 points (PE unlikely)

40
Q

What is CVA?

A

Cerebrovascular accident

41
Q

What is a stroke?

A

A rapidly developing loss of brain function due to a disturbance in the blood supply to the brain

42
Q

What are the two types of stroke?

A

Ischaemic (80%)
Haemorrhagic (20)

43
Q

What are the 3 types of Ischaemic stroke?

A

Thrombotic- occlusion of small or large vessels in situ
Embolic- occlusion due to embolus; often from heart or blood vessels
Hypoperfusion

44
Q

What are the two types of Haemorrhagic stroke?

A

Intra- cerebral haemorrhage (ICH)
Subarachnoid haemorrhage (SAH)

45
Q

What does treatment of thrombosis depend on?

A

The type of thrombosis & what risk factors are present (length of risk factors)

46
Q

What do antiplatelets treat?

A

Arterial thrombosis
(Aspirin, clopidogrel, dipyridamole)

47
Q

What do thrombolysis treat?

A

drugs which rapidly destroy clots, given straight after stroke

48
Q

What does thromboectomy treat?

A

break up clot (caution as can make the clot migrate somewhere else)

49
Q

What do anticoagulants treat?

A

work against different steps in the clotting cascade, manage underlying risk factors

50
Q

What is the natural history of a thrombus if it is not treated?

A

Organisation
1. Acute inflammatory reaction (neutrophils)
2. Chronic inflammatory reaction (lymphocytes)
3. Capillary revascularisation
4. Fibroblasts from granulation tissue and scar
5. Phagocytosis (macrophages)
6. Recanalisation

51
Q

What is the organisation of a clot?

A

Break it apart/ prevent clot thrombolysing

52
Q

What does organisation and recanalisation do?

A

Make small channels so blood can still flow