Thrombotic Disorders Flashcards

1
Q

Haemostasis is a fine balance and if there is a dysregulation of one or more components then complications that can arise is _________ or _________ at the other end of the spectrum

A

bleeding

thrombosis

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2
Q

what are the elements of haemostasis?

A
  • Primary haemostasis
  • Blood coagulation
  • Fibrinolysis
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3
Q

primary haemostasis is triggered by tissue damage which leads to what things?

A
  • Vasoconstriction
  • Platelet adhesion
  • Platelet aggregation
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4
Q

Coagulation - Coagulation cascade activated leading to what?

A
  • Insoluble fibrin formation
  • Fibrin cross-linking (to form a stable clot)
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5
Q

what is involved in the process of fibrinolysis?

A

Plasmin is activated by the activation of plasminogen

Plasmin breaks down the fibrin network

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6
Q

what is a thrombus?

A

‘Clot arising in the wrong place’

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7
Q

what is a thromboembolism?

A

‘Movement of clot along a vessel’

Picture showing DVT that has moved to lungs cause pulmonary embolism

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8
Q

how can Virchow’s Triad lead to a thrombus?

A

If one of more is upset this can lead to thrombus generation

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9
Q

what are some examples of when one of the components of Virchows triad can be upset

A
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10
Q

what are the 3 main types of thrombosis?

A
  • Arterial
  • Venous
  • Microvascular
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11
Q

what makes up a Arterial thrombus and what does it result in?

A
  • ‘White clot’~ consisted mainly of platelets and fibrin
  • Results in ischaemia and infarction
  • Principally secondary to atherosclerosis
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12
Q

what are some Examples of arterial thromboembolism?

A

•Coronary thrombosis – can lead to:

  • Myocardial Infarction
  • Unstable angina

•Cerebrovascular thromboembolism:

  • Stroke
  • Transient ischaemia

•Peripheral embolism:

  • Acute limb ischaemia
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13
Q

what are the risk factors for arterial thrombosis?

A
  • Age
  • Smoking
  • Sedentary lifestyle
  • Hypertension
  • Diabetes mellitus
  • Obesity
  • Hypercholesterolaemia

Family history is also an important risk factor

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14
Q

what is the Management (of arterial thrombosis)?

A

•Primary prevention:

  • Lifestyle modification
  • Treatment of vascular risk factors

•Acute presentation:

  • Thrombolysis
  • Antiplatelet/anticoagulant drugs

•Secondary prevention (focused on the treatment of identified risk factors)

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15
Q

what is venous thrombus made of, what is it due to and what does it result in?

A
  • ‘Red thrombus’~ mainly composed of fibrin and red cells
  • Results in back pressure
  • Principally due to stasis and hypercoagulability
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16
Q

what are some examples of venous thromboembolism?

A

•Limb deep vein thrombosis

•Pulmonary embolism

  • visceral venous thrombosis
  • intracranial venous thrombosis
  • superficial thrombophlebitis
17
Q

what are the Risk factors for venous thrombosis
Stasis/hypercoagulability?

A

increasing age

pregnancy

hormonal therapy: COCOP/HRT

Tissue trauma

immobility

surgery

obesity

systemic disease

family history

18
Q

Systemic disease and venous thrombosis:

what systemic diseases may be a risk factor for VTE?

A
  • Cancer
  • Myeloproliferative Neoplasm (MPNs)
  • Autoimmune disease:
  • Inflammatory bowel disease
  • Connective tissue disease e.g SLE
  • Antiphospholipid syndrome: arterial and venous thrombosis
19
Q

how is a diagnosis of venous thrombosis made?

A

•Pretest probability scoring:

  • Wells score
  • Geneva score

•Laboratory testing if pretest probability low:

  • D-dimer

•Imaging

Lab testing is appropriate if the patients pretest probability score is low and if that’s negative then you can exclude DVT

If person has low pretest probability but a positive d-dimer then they require imaging

Patients with high pretest probability got straight to imaging

20
Q

what is a common modality for imaging in VTE?

A

doppler US (Common modality for imaging are doppler US for upper and lower limb veins)

Ventilation/Perfusion scan (V/Q) - This image shows in perfusion image that the right lower lung is well perfused so the person has bilateral pulmonary embolism

CT Pulmonary Angiogram (Regarded as a gold standard for pulmonary embolism)

21
Q

What are the Aims of management (in venousthrombosis)?

A
  • Prevent clot extension
  • Prevent clot embolisation
  • Prevent clot recurrence in long term treatment
22
Q

what Drugs are used to manage patients with venothromboembolism?

A

•Anticoagulants:

  • LMWH
  • Coumarins (warfarin)
  • DOACs

•Thrombolysis only in selected cases:

  • Massive PE
23
Q

what are examples of Heritable thrombophilia?

(Thrombophilia is a condition in which there’s an imbalance in naturally occurring blood-clotting proteins, or clotting factors. This can put you at risk of developing blood clots)

A

Heritable conditions that can increase the individuals risk of venous thromboembolic events

24
Q

how does Factor V Leiden work?

A

Drive towards thrombin generation and a fibrin clot generation

25
Q

how do Physiological anticoagulants work?

A

Direct blocking effect on thrombin

If antithrombin is deficient then thrombin generation continues and you have fibrin clot formation

26
Q

what is Microvascular thrombus?

A
  • Involved Platelets and/or fibrin
  • Results in diffuse ischaemia
  • Principally in Disseminated Intravascular Coagulation [DIC]

Most commonly seen in very unwell patients in intensive care

27
Q

what is DIC? who does it occur in and what does it cause?

A
  • Diffuse systemic coagulation activation
  • Occurs in:
  • Septicaemia
  • Malignancy
  • eclampsia

•Causes tissue ischaemia

  • Gangrene
  • organ failure
  • Consumption of platelets and clotting factors leading to bleeding
  • Activation of coagulation leading to microvascular thrombosis deposition
28
Q

Summary:

  • _ main types of thrombosis
  • Different ____ factors for each
  • Varying ____________ ________ depending on type of clot
A

3

risk

management strategies