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FIP > 20. Thrombosis/Embolism > Flashcards

20. Thrombosis/Embolism Flashcards

1
Q

Definition of thrombus

A

aggregate of coagulated blood containing platelets, fibrin, and RBC that occurs in FLOWING blood

  • diff from a clot
  • adhere to endothelium but can separate
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2
Q

Clinical consequence of separation of a thrombus from vessel

A

Becomes an embolus

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3
Q

Thrombus aetiology

A

Virchow’s triad

  • endothelial damage
  • abnormal blood flow
  • hypercoagulability
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4
Q

What happens during endothelial damage

A

Normal endothelial cells profuces substances that

  • reduce thrombi formation
  • prevent platelet aggregation
  • inhibit coagulation
  • encourage fibrinolysis
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5
Q

Substances that normal endothelial cells produce in a prothrombotic state

A
  1. prostacyclin - platelet inhibitor
  2. thrombomodulin - antithrombin
  3. plasminogen activator - degrades fibrin clots
  4. nitric oxide
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6
Q

Substances that damaged endothelial cells produce in a prothrombotic state

A
  1. platelet aggregating factor
  2. plasminogen activator inhibitors
  3. platelets produce thromboxane which causes further platelet aggregation
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7
Q

Causes of endothelial damage in arteries

A
  • ulcerated plaques in atherosclerotic arteries
  • vasculitis
  • endothelial dysfunction due to haemodynamic stresses of hypertension or turbulent flow over scarred valves
  • cigarette smoke
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8
Q

Effects of abnormal blood flow

A
  1. disrupts laminar flow and brings platelets into contact with the endothelium
  2. prevents dilution of activated clotting factors by fresh flowing blood
  3. slows inflow of clotting factor inhibitor and permits the build up of thrombi
  4. promotes endothelial cell activation
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9
Q

What cayses turbulence in arteries and heart

A
  1. endothelial injury or dysfunction
  2. countercurrents and local pockets of stasis
    - ulcerated atherosclerotic plaques
    - aneurysms
    - sites of arterial bifurcation
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10
Q

What causes stasis venous thrombi

A 
General
-prolonged immobilization in bed
-heart failure
-shock
Local
-external pressure
-aneurysm
-eddy currents
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11
Q

Primary disorders that increase coagulability

A

primary = genetic

  1. mutation in factor V gene (factor V Leiden)
  2. mutation in prothrombin gene
  3. antithrombin III deficiency
  4. Protein C and S deficiency
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12
Q

Secondary disorders (more common) that increase coagulability

A

secondary = acquired

  1. tissue damage (surgery, fracture, burns)
  2. cancer
  3. DIC
  4. APS
  5. OCP
  6. hyperestrogenic state (pregancy)
  7. nephrotic syndrome
  8. polycythaemia
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13
Q

What are the clinical consequences of

a) arterial thrombi
b) venous thrombi

A

a) ischaemia/infarction and emboli into other arteries/arterioles
b) emboli into venous side of circulation
- e.g. pulmonary arteries -> lungs -> infarction

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14
Q

Causes of thrombosis in

a) arteries
b) veins

A

a) atherosclerotic plaques, turbulence, stasis, hypertension, counter currents
b) stasis, hypercoagulability

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15
Q

What happens to a thrombus

A
  1. propagation
    - thrombus enlarges, leading to vessel obstruction
  2. embolisation
    - thrombus dislodges, travelling to a different site
  3. dissolution
    - thrombus degraded by fibrinolytic system
  4. organisation and recanalisation of blood vessels
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16
Q

Clinical effects of arterial thrombosis

A
  1. infarction
    - cell necrosis due to reduced blood supply with thrombus at site
    - e.g. MI, cerebral infarction, acute limb ischaemia
  2. embolise peripherally through arteries
    - infarcts brain, kidneys, spleem
17
Q

Difference between thrombus and embolus

A

Thrombosis occurs when a thrombus, or blood clot, develops in a blood vessel and reduces the flow of blood through the vessel.
Embolism occurs when a piece of a blood clot, foreign object, or other bodily substance becomes stuck in a blood vessel and largely obstructs the flow of blood.

18
Q

Effects of venous thrombosis

A
  1. Localised
    - may be asymptomatic
    - oedema, pain
    - may cause necrosis and gangrene
  2. Distant
    - PE
    - venous sinuses of the skull secondary to infection of the middle ear, mastoid or paranasal sinuses (less common)
19
Q

Causes of thrombosis in capillaries

A
  • frost bites
  • burns
  • haemolytic anaemia such as sickle cell disease or autoimmune disease with cold agglutinins
20
Q

Effects of thrombosis in capillaries

A

necrosis and ulceration

21
Q

Thrombosis in the heart

A
  1. mural thrombus post MI
  2. thrombotic vegetations on cardiac valves in infective endocarditis
  3. thrombosis in left atrium, esp auricular appendix in atrial fibrillation
22
Q

What is embolism

A

an embolus is a detached intravascular physical mass that arises from one part of the circulation and travels to another part of the circulation

  • can be systemic or pulmonary
  • can be solid, liquid or gas
23
Q

Characteristics of pulmonary embolism

A
  • arises mainly in the deep veins of the lower limbs, but occasionally can arise in the right side of the heart
  • carried in circulation along the IVC through the right side of the heart and gets caught in the lung circulation
24
Q

Types of pulmonary emboli

A
  1. massive
    - wedges in the pulmonary artery
    - resulting in sudden death
    - Saddle embolus - straddles the bifurcation of the pulmonary trunk extending to the left and right pulmonary arteries
  2. intermediate
    - may or may not cause infarction
    - lungs have dual blood supply (bronchial + pulmonary)
    - necrosis only occurs in patients whose circulation is already compromised (heart failure/shock)
  3. microemboli
    - large numbers of tiny emboli gets into the circulation
    - blocks small pulmonary arterioles -> right heart failure
25
Q

What are the cause of air/gas embolism

A
  • damage to the veins of head and neck
  • during inspiration, the negative pressure from the thorax is transmitted to the head and neck vein
  • damaged/cut veins causes air to be sucked in during inspiration
  • blood vessel blockage caused by one or more bubbles of air or other gas in the circulatory system

FIP (24 decks)

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