Thrombotic Disorders Flashcards

1
Q

What causes venous vs arterial thrombi?

What are the general outcome of venous and arterial [3] thrombi and give examples of each

A

Arterial - Secondary to Atherosclerosis
- Result in ischemia and infarction - coronary thrombosis, stroke, peripheral embolism

Venous - Secondary to Stasis & Hypercoagulability
- Result in back pressure - DVT, PE, visceral venous thrombosis, intracranial venous thrombosis, superficial venous thrombophlebitis

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2
Q

Risk factors for an arterial thrombosis? [4]

A
  • Age
  • Smoking
  • HTN, Hypercholesterolaemia
  • DM, obesity, sedentary lifestyle
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3
Q

How do we manage an arterial thrombus? [3]

A

Primary prevention with lifestyle modification and treating the risk factors

Acutely: thrombolysis & Anti-platelets or Anti-coags

Secondary prevention

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4
Q

Risk factors for a DVT or PE? [5]

A
Age
Surgery, Tissue Trauma
Immobility, obesity
Pregnancy, hormonal Therapy
FH and systemic disease
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5
Q

What systemic diseases put you at risk of a DVT? [4]

A

Cancers
Myeloproliferative Neoplasm
Autoimmune diseases eg IBD, APS
CT disease eg SLE

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6
Q

How can we test for a DVT/PE (venous thrombus)? [4]

A

Clinical probability simplified score
* DVT likely: 2 points or more
* DVT unlikely: 1 point or less

If a DVT is ‘likely’ (2 points or more)
* leg vein ultrasound should be carried out within 4 hours
* if US result is negative > D-dimer
* if US cannot be done within 4 hours, start DOAC
* if US scan negative but the D-dimer is positive, repeat proximal leg vein ultrasound scan 6 to 8 days later

If a DVT is ‘unlikely’ (1 point or less)
* perform a D-dimer test within 4 hours.
* If not, interim therapeutic anticoagulation should be given until the result is available
* if D-dimer is positive then a proximal leg vein ultrasound scan should be carried out within 4 hours
*

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7
Q

How can we treat a DVT/PE? [2]

A

Anticoagulants e.g. LMWH, Warfarin & DOACs

Thrombolysis only if massive PE

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8
Q

What are the 2 commonest Inheritable thrombophilias?
What’s the major cause of microvascular Thrombus?
Components of microvascular thrombi [2]

A

Factor V Leiden and Prothrombin G20210A

Disseminated Intravascular Coagulation (DIC)

Microvascular thrombus made up of platelets and/or fibrin

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9
Q

What triggers DIC? [4]

A

Septicaemia
Malignancy
Eclampsia, placental abruption, amniotic fluid embolism
Microangiopathic haemolytic anaemia

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10
Q

What are the consequences of DIC? [2]

A

Diffuse Tissue ischaemia –> Gangrene & Organ Failure

Consumes platelets/clotting factors –> Bleeding

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11
Q

What investigation if pre-test probability score is high?

A

Skip lab test

Imaging modality - VQ or CTPA

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12
Q

Appearance of VTE on doppler ultrasound scan? [2]

A

In DVT, thrombosed vein enlarged, non-compressble

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13
Q

Factor V Leiden
Describe the mutation associated with this bleeding disorder
Describe inheritance pattern and penetrance of this genetic condition

A

Mutation of human Factor V leading to hyper coagulable state
- So inhibitor of Factor V can no longer inhibit it leading to unregulated coagulation
AD - incomplete penetrance

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14
Q

DIC symptoms and signs [4]

Investigations: FBC [3], Clotting [3], D-dimer

A
  • Bleeding from at least unrelated sites
  • confusion, fever
  • ARDS
  • petechiae, skin necrosis, acral cyanosis
  • FBC and film: low platelets, schistocytes (microangiopathic haemolytic anaemia)
  • Clotting profile: prolonged PT, prolonged APTT, prolonged bleeding time
  • D-dimer: raised
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15
Q

DIC management
Treat underlying cause!!
When is platelet transfusion indicated?
What do you do for active bleeding and prolonged PT and APTT? [2]
What do you do if critically ill but not bleeding [1]

A
  • High risk of bleeding and platelets <50x109/L: platelet transfusion
  • Active bleeding and prolonged PT and APTT: FFP (if persists can give fibrinogen concentrate or cryoprecipitate)
  • Critically ill BUT NOT BLEEDING: LMWH
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16
Q

Antiphospholipid syndrome - lab test [2]

A

Lupus anticoagulant and anticardiolipin ab

17
Q

What is the inheritance of factor V leiden and anti-thrombin III deficiency?

A

Autosomal dominant

18
Q

What is the pathophysiology of factor V leiden?

A

Gain of function in factor V leiden protein - activated factor V is inactivated 10x more slowly by activated protein C

19
Q

What is the prevalence and risk of VTE in factor V Leiden?

A

Prevalence 5%

Risk of VTE 4% (homozygotes 10% but prevalence 0.05%)

20
Q

What is the inheritance of protein C deficiency?

A

Autosomal co-dominant

21
Q

What are the features of protein C deficiency?

A

VTE

Skin necrosis following commencement of warfarin (temporary pro-coagulant state –> thrombosis in venules)

22
Q

How is protein C deficiency diagnosed?

A

Copperhead snake venom assay

23
Q

What is the function of anti-thrombin?

A

Inhibits thrombin, factor C, factor IX, and mediates the effects of heparin

24
Q

What is monitored in anti-thrombin deficiency?

A

Anti-Xa to ensure adequate anticoagulation

As there is a degree of resistance to heparin

25
Q

What does Protein S do?

A

Activates protein C in the degradation of factor Va and VIIIa

26
Q

What are the features of anti-phospholipid syndrome

A

Arterial and venous thromboses
Recurrent foetal loss
Thrombocytopenia
Prolonged APTT