TThrombosis, Emboli and Atheroma Flashcards

1
Q

What are the 4 zones of a platelet?

A

Peripheral
Sol gel
Organelle
Membrane

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2
Q

What constitutes the peripheral zone of platelets?

A

Rich in glycoproteins needed for platelet adhesion and aggregation

Contains platelet Factor 3 - which promotes clotting during aggregration

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3
Q

What constitutes the Sol-gel zone of platelets?

A

Contains microtubule and microfilaments

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4
Q

What constitutes the Organelle zone of platelets?

A
  • Contains alpha granules which contain:
    factor VIII, V,
    fibrinogen
    fibronectin
    platelet derived growth factor
    chemotactic factors
  • Contains dense bodies that contain ADP, 5HT and calcium
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5
Q

What constitutes the membrane zone of platelets?

A

Contains the dense tubular system responsible for platelet contractile function and PG synthesis

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6
Q

Name examples of thrombotic factors

A
  • vWB factor (produced by endothelial cells allowing PLT adherence)
  • Binding factors IXa and X
  • Factor V
  • Thromboplastin (endothelium)
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7
Q

Name examples of anti-thrombotic factors

A
  • tPA (converts plasminogen to plasmin which digests the thrombus)
  • Anti-thrombin III (inactivates thrombin and factor XIIa, XIa, Xa and IXa)
  • Thrombomodulin (alters thrombin to activate protein C)
  • Protein C destroys factors V and VIII
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8
Q

What is the inheritance of Protein C deficiency?

A

AD - clinically affected individuals are heterozygous, with a protein C concentration of 50%

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9
Q

What is Protein C?

A

A Vitamin K dependent serine protein that potently inhibits factors Va and VIIIa

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10
Q

What is the prevalence of protein C deficiency in patients with venous thrombosis?

A

6-8%

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11
Q

What is factor V leiden mutation?

A

It results in the resistance of factor V to breakdown by protein C

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12
Q

What % of the white populations are carriers of factor V Leiden?

A

5 % - most common inherited thrombophilia

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13
Q

What is protein S?

A

A Cofactor in the inactivation of factor Va and VIIIa by activated protein C

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14
Q

What is the prevalence of protein S deficiency in young patients?

A

5-8%

It is AD

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15
Q

What is the prevalence of anti-thrombin III deficiency in patients with venous thrombosis?

A

0-5%

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16
Q

What is Virchovs triad?

A
  1. Change in blood flow e.g. venous stasis, arrhythmia, valvular disease
  2. Change in vessel wall e.g. atherosclerosis, trauma, inflammation, neoplasia
  3. Change in blood constituents e.g. increased PLTs or altered PLT function
17
Q

Where can AIR emboli originate from?

A

Can occur during thyroid surgery

18
Q

Where can SEPTIC emboli originate from?

A

Subacute bacterial endocarditis leading to Roth spots

19
Q

Where can AMNIOTIC emboli originate from?

A

Complication of delivery particularly if the foetus is manipulated

20
Q

How are atheroma formed?

A
  • Vascular endothelial cell damage
  • Platelets adhere to the endothelium and promote SM cells within the vessel wall intima to proliferate
  • The stimulation factor is platelet derived growth factor
  • Intracellular and extracellular lipid accumulate at the site due to breakdown in the endothelial cell barrier - this forms a FIBROPIPID/ATHEROSCLEROTIC PLAQUE
21
Q

What is a true aneurysm?

A

True aneurysms contain all three layers of the vessel wall.

22
Q

What is a pseudoaneurysm?

A

A false aneurysm or pseudoaneurysm is a haematoma that forms outside the vessel wall, and is contained by surrounding tissues, as a result of a leaking artery.

23
Q

What is a Berry aneurysm?

A

Berry aneurysm is found in the Circle of Willis and is caused by vessel wall deficiency.

24
Q

What is a Saccular aneurysm?

A

Saccular aneurysm involves only part of the circumference of the vessel wall

25
Q

What is a fusiform aneurysm?

A

fusiform aneurysm involves the entire circumference of a vessel wall

26
Q

Why does a dissecting aneurysm occur?

A

Dissecting aneurysm occurs in arterial media deficiency as in Marfan’s syndrome.