Thrombotic Disorders Flashcards

1
Q

What are the elements of haemostasis?

A

Primary haemostasis - primary plug formation
Blood coagulation
Fibrinolysis

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2
Q

What are the elements of primary haemostasis?

A

Vasoconstriction mediated by substances e.g. catecholamines, nitric oxide, calcium
Platelet adhesion to damaged endothelium
Platelet aggregation

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3
Q

What is involved in coagulation?

A

Insoluble fibrin formation - fibrin cross linking

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4
Q

What is the end goal of haemostasis?

A

Fibrin production which leads to fibrinolytic pathways

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5
Q

What promotes the breakdown of plasminogen to plasma?

A

tPA and factor XII

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6
Q

What is a thrombus and what is a thromboembolism?

A

Thrombus is a clot arising in the wrong place, thromboembolism is the movement of a clot along a vessel

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7
Q

What are the elements of Virchow’s triad?

A

Stasis
Hypercoagulability
Vessel damage

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8
Q

What are the types of thrombosis?

A

Arterial
Venous
Microvascular

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9
Q

What are the features of venous thrombus?

A

Red thrombus - predominantly fibrin, also red cells
Results in back pressure
Principally due to stasis and hypercoagulability

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10
Q

What are the types of venous thromboembolism?

A
Deep vein thrombosis
Pulmonary embolism 
Visceral venous thrombosis
Intracranial venous thrombosis 
Superficial thrombophlebitis
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11
Q

What systemic diseases are associated with venous thrombosis?

A

Cancer - some patients present with VTE as first sign of malignancy
Myeloproliferative neoplasm e.g. polycythaemia
Autoimmune disease
- IBD
- connective tissue disease e.g. SLE
- anti-phospholipid syndrome

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12
Q

What should be considered in an unprovoked DVT/PE with no obvious trigger?

A

Occult malignancy

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13
Q

How is venous thrombosis diagnoses?

A

Pretest probability scoring - Wells score/Geneva score

Laboratory testing - D-dimer

Imaging

  • doppler ultrasound
  • ventilation/perfusion scan
  • CTPA
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14
Q

When is it recommended to go straight to imaging investigation of venous thrombosis?

A

If pretest probability is high

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15
Q

What does it mean if the d-dimer is negative?

A

Essentially excludes VTE if negative
If positive it does not confirm VTE as it can go up in a number of other conditions, needs to be considered in appropriate clinical circumstances

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16
Q

What feature on doppler ultrasound should raise suspicion of a clot?

A

If vein is non-compressible

17
Q

What are the aims of management of VTE?

A

Prevent clot extension
Prevent clot embolisation
Prevent clot recurrence in long-term treatment

18
Q

What drug type breaks down clots?

A

Thombolytics promote fibrinolysis so break down clots, anticoagulants do not break down clots

19
Q

What do anticoagulants do?

A

Do not break down the clot - work to prevent clot formation or prevent pre-existing clot from getting larger

20
Q

What drugs are used in management of VTE?

A

Anticoagulants

  • LMWS
  • coumarins e.g. warfarin
  • direct oral anticoagulants

Thrombolysis only in selected cases e.g. massive PE

21
Q

What is heritable thrombophilia?

A

An inherited predisposition to venous thrombosis

22
Q

What are the causes of heritable thrombophilia?

A

Common - mutation in factor V Leiden or prothrombin G20210A

Rare - anti-thrombin deficiency, protein C deficiency, protein S deficiency

23
Q

What are the features of factor V Leiden mutation?

A

Results in factor Va
Va should be broken down by activated aPC but with the mutation it becomes resistant to this
Activated protein C and protein S should break down factor V and VIII to keep haemostatis balance but there is a block of breakdown of factor V in this mutation

24
Q

What are the physiological anticoagulants?

A

Protein C and S

If these are mutated, natural anticoagulation will not occur so predisposition to VTE occurs

25
Q

What is the clinical utility of heritable thrombophilia?

A

The majority are not predictive of a recurrent event
Screening of asymptomatic family members is not recommended
Limited thrombophilia screening - restricted to high risk heritable thrombophilia e.g. anti-thrombin deficiency

26
Q

What are the features of microvascular thrombus?

A

Combination of platelets and/or fibrin
Results in diffuse ischaemia
Marked ischaemia in peripheries
Principally in disseminated intravascular coagulation

27
Q

What are the features of disseminated intravascular coagulation?

A

Diffuse systemic coagulation activation
Occurs in septicaemia, malignancy and eclampsia
Causes tissue ischaemia - gangrene, organ failure
Trigger activates coagulation cascade, excessive drive towards fibrin formation which leads to microthrombi being deposited, often in extremities
Clotting factors and platelets then begin to reduce in number as they are being used up in microvascular thrombin so there is now an increased risk of bleeding

28
Q

In what patients does disseminated intravascular coagulation predominantly occur in?

A

Thrombotic phenotype patients

29
Q

What is the management of disseminated intravascular coagulation?

A

Support clotting factor levels in those with bleeding
Management is around balancing thrombosis risk with bleeding risk
Low dose cautious anticoagulation treatment

30
Q

What are the features of arterial thrombus?

A

White clot - predominantly platelets, also fibrin
Results in ischaemia and infarction
Principally secondary to atherosclerosis

31
Q

What are some common presentations of arterial thrombus?

A

Coronary thrombosis - Mi, unstable angina
Cerebrovascular thromboembolism - stroke, TIA
Peripheral embolism - limb ischaemia

32
Q

What is the management of arterial thrombus?

A

Primary prevention - focus on lifestyle modification and addressing/treating vascular risk factors
Acute presentation - thrombolysis, anti-platelet/anti-coagualtion drugs
Secondary prevention - address vascular risk factors e.g. anti-thrombotic medication such as an anti-platelet or anti-coagulation

33
Q

What are the risk factors for arterial thrombosis?

A
Age
Smoking 
Sedentary lifestyle
Hypertension
Diabetes mellitus
Obesity 
Hypercholesteroaemia
34
Q

What are the risk factors for venous thrombosis?

A
Stasis/hypercoagulability 
Increasing age
Pregnancy 
Hormonal therapy - OCP, HRT 
Tissue trauma 
Immobility 
Surgery 
Obesity 
Systemic disease
Family history - specific to first degree relatives only