Venous Thrombosis Flashcards

1
Q

Where do arterial events occur and where do venous events normally occur?

A

Arterial

  • Coronary (MI)
  • cerebral (stroke)
  • peripheral (gangrene and loss of limb)

Venous

  • Deep venous thromboses
  • Pulmonary Embolism
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2
Q

How do the walls of arteries and veins differ?

A

arteries = high pressure => very muscular wall

veins = low pressure => valves to prevent backflow

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3
Q

How does clotting differ between an artery or a vein?

A

Arteries
- high pressure system ruptures atherosclerotic plaques in vessels

Veins

  • stasis of blood activates the coagulation cascade
  • no platelets are attracted as there is no “injury site”
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4
Q

What are the components of Virchow’s triad and how do these relate to the clotting of blood?

A
  • Stasis (low pressure venous system)
  • vessel walls (deterioration of valves due to age/ previous blood clots)
  • hypercoagulability (elevated clotting factor levels)
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5
Q

HOw is venous thrombosis usually treated?

A

Anticoagulants e.g. heparin/warfarin/DOAC’s

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6
Q

What are the clinical signs of a DVT?

A

Limb is:

  • hot
  • swollen
  • tender
  • potentially erythematous
  • pitting oedema present
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7
Q

What may be a differential diagnosis of a DVT based on the clinical signs?

A

Cellulitis

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8
Q

Where in the lungs tends to be affected by a PE?

A
  • infarcts usually occur in lung periphery
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9
Q

What symptoms do patients usually experience in a PE?

A
  • pleuritic chest pain (knife stuck into chest during every breath)
  • cardiovascular collapse
  • hypoxia
  • Right sided heart strain (due to pumping blood against increased lung pressure => this can be seen on ECG/ECHO)
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10
Q

What is the normal bacground risk of a patient experiencing a VTE?

A

Roughly 1/1000 patients per year
(young adults 1/10 000 and elderly 1/100)

Lifetime risk 2.5%

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11
Q

What are the potential risk factors for developing a VTE?

A
  • Age
  • Obesity
  • Pregnancy and Puerperium
  • Oestrogen therapy (COCP/HRT)
  • Previous DVT/PE
  • Trauma/Surgery
  • Malignancy
  • Paralysis (limited mobility)
  • Infection
  • Thrombophilia
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12
Q

Why are pregnant women and those in the puerperiium more at risk of a VTE?

A

Factor VIII levels rise up to 5x during pregnancy to prevent haemorrhage during childbirth

=> increased risk of clotting

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13
Q

What happens in a thrombophilia which puts patients more at risk of clotting?

A
  • familial disorder where coagulation activity is increased
  • fibrinolytic activity decreased => clots can expand easier
  • anticoagulation activity e.g. antithrombin/ Protein C/S may also be decreased (may be due to a deficiency)
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14
Q

What happens in Factor V Leiden and how does this condition put patients at an increased risk of clotting?

A

Small change in Factor V protein
=> means the Proteins C/S struggle to switch it off efficiently
=> body is 5x more likely to clot

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15
Q

Which of the risk factors for VTE are involved in blood STASIS?

A
Age
Obesity
Pregnancy
Previous DVT/PE
Trauma/Surgery
Malignancy
Paralysis
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16
Q

Which of the risk factors for VTE are involved in VESSEL WALL damage/changes?

A

Age

Previous DVT/PE

17
Q

Which of the risk factors for VTE are related to HYPERCOAGULABILITY?

A
Age
Pregnancy
Puerperium
Oestrogen therapy (COCP/HRT)
Trauma/Surgery
Malignancy
Infection
Thrombophilia
18
Q

In what patients would you consider doing a hereditary thrombophilia screen?

A
  • Venous thrombosis in patient <45 years
  • Recurrent venous thrombosis
  • Unusual venous thrombosis (e.g. in upper limb)
  • FHx of venous thrombosis or thrombophilia
19
Q

HOw is a hereditary thrombophilia usually managed?

A
  • Advice on avoiding risk (e.g. COCP not suitable)
  • Short term prophylaxis (if periods of known risk e.g pregnancy)
  • Short term anticoagulation (to treat thrombotic events)
  • Long term anticoagulation (if recurrent VTE)
20
Q

Why do many patients with a hereditary thrombophilia not experience a thrombosis solely due to their condition?

A

Much more commonly occurs if combined with other risk factor

- e.g. COCP, surgery/procedure causing immobility etc

21
Q

What is the risk/ benefit analysis of long term anticoagulation?

A

Weighing up risk of thrombosis with the risk of serious haemorrhage

22
Q

GIve an example of an acquired thrombophilia?

A

Antiphospholipid antibody syndrome

- change in β2 glycoprotein 1

23
Q

Acquired thrombophilias have a stronger risk factor for thrombosis than the hereditary thrombophilias. TRUE/FALSE?

A

TRUE

24
Q

What are the main features of Antiphospholipid antibody syndrome?

A

Recurrent thromboses

  • Arterial, including TIAs
  • Venous
  • Recurrent fetal loss (due to thrombosis in placenta)
    {babies carried to term may be SGA due to placental insufficiency}
  • Mild thrombocytopenia
25
Q

Why is the APTT prolonged in Antiphospholipid Ab Syndrome if there is no clotting factor deficiency?

A

Lupus anticoagulant interferes with the test

=> prolongs the APTT

26
Q

Why is warfarin commonly used to treat Antiphospholipid Ab syndrome?

A

It has protection against arterial events as well as venous

=> useful as this condition experiences both

27
Q

What other conditions are associated with Antiphospholipid Ab syndrome?

A
  • autoimmune
  • lympho-proliferative (lymphoma, SLE)
  • viral infection