Thrombosis, Embolism and Infarction Flashcards

(40 cards)

1
Q

What is a thrombus?

A

A solidification of blood contents that forms within the vascular system during life.

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2
Q

What three factors contribute towards thrombosis?

A
  1. Endothelial injury
  2. Abnormal blood flow
  3. Hypercoagulability
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3
Q

After injury to a vessel, what three important reactions do platelets undergo?

A
  1. Adhesion
  2. Secretion
  3. Aggregation
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4
Q

Explain the pathogenesis of thrombosis in terms of endothelial injury.

A
  1. endothelium is damaged. Matrix of injured vessel causes vasoconstriction to make the gap smaller.
  2. Platelets adhere to exposed collagen and in doing so, change their shape to a brick-like structure allowing them to accumulate and release granules.
  3. Granules released into the lumen causing further platelet recruitment.
  4. Fibrin acts as a glue between platelets and RBCs and WBCs get trapped in the fibrin mesh.
  5. If this is continued, it could be detrimental and so plasminogen is released to dissolve the clot.
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5
Q

What are the two types of blood flow?

A
  1. Turbulence (blood flows in all directions causing the alteration of blood flow. This can happen in arteries and also in the lumen of he heart. It contributes towards the development of arterial and cardiac thrombi.)
  2. Stasis (instead of laminar blood flow through the vessel, blood is very slow and this is a particular cause of DVT.)
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6
Q

What is hypercoagulability?

A

An alteration of the blood coagulation mechanism that, in some way, predisposes thrombosis.

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7
Q

What are primary (genetic) risk factors for hypercoagulability?

A
  • mutation in factor V gene (Lieden mutation)
  • antithrombin II deficiency
  • protein C and S deficiency
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8
Q

What are secondary (acquired) high risk factors for hypercoagulability?

A
  • bed rest
  • MI
  • tissue damage
  • prosthetic valve
  • DIC
    etc.
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9
Q

What are the secondary (acquired) low risk factors for hypercogulability?

A
  • oral contraceptive
  • smoking
  • sickle cell anaemia
  • cardiomyopathy
    etc.
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10
Q

What is the function of Von Willebrand’s factor?

A

Adheres platelets to exposed collagen in damaged endothelial wall

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11
Q

What is the function of GPIIB and GPIIIA?

A

Attach platelets to each other

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12
Q

What is the function of GPIB?

A

Attaches platelets to VW factor

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13
Q

What is the name of being deficient in GPIIIA/GPIIB?

A

Glanzmann’s thrombasthenia

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14
Q

What is the name of being deficient in GPIB?

A

Bernard Soulier syndrome

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15
Q

What is the result of Von Willebrand’s disease, Glanzmann’s thrombasthenia and bernard soulier syndrome?

A

Lack of blood clotting

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16
Q

What are the clinical features of arterial thrombosis?

A

loss of pulses distal to thrombus, area becomes perishing (cold, pale, painful) and eventually tissue dies and gangrene results. Gangrene can lead to autoimmune amputation.

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17
Q

What are the clinical features of saphenous venous thrombosis?

A

congestion, swelling, pain, tenderness (rarely embolise).

18
Q

What are the clinical features of deep venous thrombosis?

A

foot and ankle oedema, Homan’s sign, could be asymptomatic and only realise once embolised.

19
Q

What is the treatment for venous thrombosis?

A

Stocking are used as prevention as they push venous flow towards the heart.
Anticoagulant drugs aim to prevent growth of clot or embolism.
Heparin and Warfarin are commonly used anticoagulant drugs. Heparin is always used first as it is IV whereas warfarin is oral and therefore the effects of heparin are immediate.

20
Q

What are the three types of thrombi in the CV system?

A
  1. Mural
  2. Arterial
  3. Venous
21
Q

Describe the morphology of mural thrombi.

A

in chambers of the heart and aorta and are applied to one wall of underlying structure, occur in capacious lumina of chambers and aorta.

22
Q

Describe the morphology of arterial thrombi.

A

in arteries usually occlusive and may be mural. Frequently in coronary, cerebral and femoral arteries. They are grey-white and friable.

23
Q

Describe the morphology of venous thrombi.

A

in veins, invariably occlusive and dark red, affects veins and lower extremities (90%). Thrombophlebitis = inflamed and thrombosed.

24
Q

What is the histological appearance of thrombi?

A

dark bands = RBCs
pale bands = fibrin and platelets
There are laminations called the lines of Zahn (red and white lines)

25
What is an embolism?
a detached intravascular solid, liquid or gas mass that is carried by the blood to a site distant from its origin.
26
What is a pulmonary embolism?
occlusion of a large or medium sized pulmonary artery and is embolic in origin until proven otherwise. A large PE is the cause of instantaneous death. PEA (pulseless electrical activity)
27
Which 2 pathophysiological consequences do pulmonary emboli result in?
1. Respiratory compromise | 2. Haemodynamic compromise
28
What is a systemic emboli?
emboli that travel through arterial circulation. 80-85% arise from cardiac thrombi. Arterial emboli almost always cause infarction.
29
Where are the major sites of lodgement of systemic emboli?
lower extremities, brain, viscera.
30
What are air embolisms?
presence of bubbles in circulation which can obstruct blood flow and damage tissue just as thrombotic masses.
31
What is the pathophysiology of air embolisms?
delivery/abortion, performance of pneumothorax, Caisson disease (deep sea divers - treatment is recompression chamber), decompression sickness.
32
What is a fat embolism?
Minute fat globules can often be demonstrated in circulation following fractures of shaft of long bones.
33
What is the pathogenesis of fat embolisms?
very complex and involves both: - mechanical obstruction (microagregates of neutral fat cause occlusion) - chemical injury (free fatty acids released from fat globules result in toxic injury to vascular endothelium.
34
How are fat embolisms clinically characterised?
- pulmonary insufficiency - neurological symptoms - anaemia - symptoms appear after a 24-72hr latent period then sudden onset of tachycardia and tachyponia. Neurological symptoms can lead to delirium and coma.
35
What is an amniotic fluid embolism?
rare complication of labour and causes 86% of maternal mortalities. Caused by infusion of amniotic fluid into maternal circulation.
36
What is the clinical presentation of an amniotic fluid embolism?
- profound respiratory difficulty with deep cyanosis and CV shock - followed by convulsion and profound coma
37
What is an infarct?
An area of ischaemic necrosis
38
How is an infarct caused?
Caused by occlusion of arterial supply or venous drainage of a particular tissue. 99% are caused by embolisms and the other 1% are caused by vasospasm, expansion of atheroma and compression of the vessel.
39
What factors influence infarct development?
- rate of vessel occlusion - vulnerability to hypoxia - O2 of blood - nature of vascular supply
40
What types of infarcts are there?
Red (haemorrhagic), White (anaemic), Bland/septic infarctions