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1B Cardiorespiratory > thrombosis > Flashcards

thrombosis Flashcards

1
Q

how does a disorder of thrombosis usually present?

A
  1. pulmonary embolism
  2. deep vein thrombosis
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2
Q

what are the symptoms of pulmonary embolism?

A
  • Tachycardia
  • Hypoxia
  • Shortness of breath
  • Chest pain
  • Haemoptysis
  • Sudden death
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3
Q

what is the presentation of deep vein thrombosis

A
  • Painful leg
  • Swelling
  • Red
  • Warm
  • May embolise to lungs causing pulmonary embolism
  • Post-thrombotic syndrome
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4
Q

what factors contribute to thrombosis?

A
  1. blood (dominant in venous thrombosis)
  2. vessel wall (dominant in arterial thrombosis)
  3. blood flow (dominant in arterial and venous thrombosis)
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5
Q

how does vessel wall affect thrombosis?

A
  1. Many proteins active in coagulation are expressed on surface of endothelial cells and their expression altered in inflammation
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6
Q

how does blood flow affect thrombosis?

A
  1. Reduced flow (stasis) increases risk of thrombosis
    1. Surgery, pregnancy, long haul travel
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7
Q

what do the 3 contributory factors to thrombosis make up?

A

virchow’s triad

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8
Q

what is venous thrombosis called?

A

thrombophilia

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9
Q

how does thrombophilia present?

A
  • Thrombosis at young age
  • ‘spontaneous thrombosis’- no clear risk factor
  • Multiple thromboses
  • Thrombosis whilst anticoagulated
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10
Q

what can tip the balance towards venous thrombosis?

A

the decrease in fibrinolytic factors (decrease breakdown clots)

increase coagulant factors & platelets

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11
Q

what are the main proteins involved in anticoagulation?

A

antithrombin

protein c

protein s

  • antithrombin inactivates thrombin (F2a) and F10a
  • Protein C and Protein S inactivate F5a and F8a
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12
Q

what is the treatment of venous thrombosis?

A
  1. Prevention (Thromboprophylaxis)
    • Assess and prevent risks
    • Prophylactic anticoagulant therapy
  2. Reduce risk recurrence/ extension
    • Lower procoagulant factors
      • Warfarin, DOACs
    • Increase anticoagulant activity
      • Heparin
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13
Q

when does anticoagulant therapy have therapeutic effect?

A
  1. Venous thrombosis
    1. Initial treatment to minimise clot extension/ embolism (<3months)
    2. Long term treatment to reduce risk of recurrence
  2. Atrial fibrillation
    1. To reduce risk of embolic stroke
  3. Mechanical prosthetic heart valve
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14
Q

when can anticoagulant therapy have preventative effects?

A

(thromboprophylaxis)

Following surgery, during hospital admission, during pregnancy

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15
Q

what are the different types of heparin?

A
  • Long chains- unfractionated (UFH)- intravenous administration, short half life
  • Low molecular weight (LMWH)- subcutaneous administration
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16
Q

what are the actions of unfractionated heparin?

A
  • Enhancement of antithrombin
    • Inactivation of throbin (Hep binds AT + thrombin)
    • Inactivation of FXa (hep binds AT only)
    • (Inactivation of FIXa, FXIa, FXIIa)
  • Increases APTT
17
Q

what are the actions of low molecular weight heparin?

A
  • Contain pentasaccharide sequence for binding AT
  • Predictable dose response in most cases so does not require monitoring -measure anti-Xa as doesn’t change APTT
  • Action predominantly against factor Xa with some antithrombin effect
18
Q

what is an examples of a vitamin K antagonist?

A

warfarin

19
Q

how does warfarin work?

A

competes with Vit K reduction from epoxide to hydroquinone

reduces the production of functional coagulation factors

induces an anticoagulated state slowly

reversible

20
Q

what is the difficulty of VKA?

A

narrow therapeutic index and requires monitoring

21
Q

how can VKA be reversed?

A
  • Reversed slowly by vit K administration- takes several hours
  • Reversed rapidly by infusion of coagulation factors
    • POCC (prothrombin complex concentrate- contains factors II, VII, IX and XI)
    • FFP (fresh frozen plasma)
22
Q

what are the side effects of VKAs?

A
  • Bleeding
  • Skin necrosis
    • Severe protein C deficiency- 2-3 days after starting warfarin
    • Thrombosis predominantly in adipose tissue
  • Purple syndrome
    • Disrupted atheromatous plaques bleed
    • Cholesterol emboli lodge in extremities
  • Embryopathy
    • Chondrodysplasia punctata
      • Early fusion of epiphyses
      • Warfarin teratogenic in 1st trimester
23
Q

what can cause resistance to warfarin?

A
  • Lack of patient compliance
    • Measure warfarin levels
    • Proteins induce by vit k absence (PIVKA)
  • Diet, increased vit K intake
  • Increased metabolism Cyt P450 (CYP2C9)
  • Reduced binding (VKORC1)
24
Q

what are some examples of direct oral anticoagulants (DOACS)?

A

rivaroxaban

apixaban

dabigatran

25
Q

where do DOACs act on the coagulation pathway?

A
26
Q

what is the difference between warfarin and DOACs?

A
27
Q

what therapeutic treatment is used in venous thrombosis?

A
  • Initial treatment to minimise clot extension/ emoblisation (<3month)
    • DOAC or LMWH for first few days followed by DOAC or warfarin (not started immediately as takes time to work and avoid skin necrosis)
  • Long term treatment to reduce risk of recurrence
    • DOAC or warfarin
28
Q

what therapeutic treatment is used in atrial fibrillation?

A
  • To reduce risk of embolic stroke
    • DOAC or warfarin
29
Q

what therapeutic treatment can be used for mechanical prosthetic heart valve?

A
  • Warfarin (DOACS not effective and should be avoided)
30
Q

when can an anticoagulant preventative be used and what type of drug is more appropriate?

A
  • Lower doses used
  • Following surgery
    • LMWH or DOAC
  • During hospital admission
    • DOAC not effective for use as medical thromboprophylaxis
    • LMWH used
  • During pregnancy
    • LMWH
    • DOACs not safe in pregnancy – cross placenta

1B Cardiorespiratory (15 decks)

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