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
how do Physiological anticoagulants work?
Direct blocking effect on thrombin If antithrombin is deficient then thrombin generation continues and you have fibrin clot formation
26
what is Microvascular thrombus?
* 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
what is DIC? who does it occur in and what does it cause?
* 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
Summary: * \_ main types of thrombosis * Different ____ factors for each * Varying ____________ \_\_\_\_\_\_\_\_ depending on type of clot
3 risk management strategies