48 - Vascular Pathology II Flashcards

1
Q

Example of a factor on platelets, and its ligand on vascular endothelium

A

GP1b on platelets sticks to exposed Von Willebrand factor

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2
Q

What do platelets do when activated?

A

Change shape, release granules (factors, fibrinogen)

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3
Q

Thrombomodulin

A

Changes thrombin from activator of clotting to an inhibitor

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4
Q

Effector of fibrinolysis

A

Tissue plasminogen activator (tPA)

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5
Q

Mechanism of tissue plasminogen activator action

A

Tissue plasminogen activator binds to fibrin, activates plasmin. Plasmin degrades fibrin.

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6
Q

Thrombus

A

A blood clot within an intact, living cardiovascular system.

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7
Q

Contents of a thrombus

A

RBC, WBC, platelets

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8
Q

Appearance of a thrombus

A

Red and white stripes (layers of RBC and platelets+fibrin) - called ‘lines of Zahn’.

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9
Q

Difference in appearance between arterial and venous thrombi

A

Arterial are white.

Venous are red.

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10
Q

Why do arterial thrombi appear white?

A

Greater proportion of platelets and fibrin.

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11
Q

Why do venous thrombi appear red?

A

Higher proportion of RBC

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12
Q

What are arterial thrombi mostly associated with?

A

Endothelial dysfunction or damage

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13
Q

What are venous thrombi mostly associated with?

A

Blood stasis, hypercoagulability

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14
Q

Useful drug for preventing arterial thrombi

A

Aspirin (interferes with platelet thromboxane production)

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15
Q

Useful drug for preventing venous thrombi

A

Warfarin (interferes with coagulation cascade)

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16
Q

Outcome of laminar flow in blood vessels

A

Blood cells don’t touch vascular wall

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17
Q

Why do thrombi form?

A

Virchow’s triad of factors influencing clotting:

1) Endothelium (EG: injury)
2) Blood flow (EG: non-laminar flow)
3) Blood composition (EG: hypercoagulability)

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18
Q

How might endothelial abnormality occur (Virchow 1)

A

Endothelial activation or dysfunction from:

Inflammation (EG: from smoking, infection, toxins, hypertension, etc)

19
Q

How can abnormal blood flow (Virchow 2) lead to thrombus formation?
1)
2)
3)

A

Turbulence, stasis, or loss of laminar flow:

1) Endothelium is activated
2) Platelets come into contact with vascular wall
3) Allows any activated clotting factors to accumulate, initiate cascade

20
Q

How can abnormal blood coagulability (Virchow 3) come about?

A

1) Genetic (primary) - EG: Factor V Leiden

2) Non-genetic (secondary) - Oestrogen (contraceptive pill, pregnancy), cancer, smoking, obesity, age

21
Q

Factor V Leiden

A

Mutant of factor V protein in coagulation cascade. Confers hypercoagulability.
If heterozygous, 5x risk of thrombosis.
If homozygous, 50x risk of thrombosis.

22
Q
Examples of secondary risk factors for thrombosis
1)
2)
3)
4)
5)
6)
A

1) Prolonged immobilisation
2) Myocardial infarct
3) Atrial fibrillation
4) Tissue injury (EG: surgery, burn, fracture)
5) Cancer
6) Smoking

23
Q
Things that can happen to a thrombus
1)
2)
3)
4)
A

1) Dissolution - Fibrinolysis (with tissue plasminogen activator, protein C and S). Becomes less likely with age.
2) Organisation and recanalisation (granulation tissue formation
3) Propagation (grows)
4) Embolisation

24
Q

Embolus

A

Intravascular mass carried in the bloodstream (solid, liquid or gaseous- EG the bends)

25
Q

Examples of emboli causing disease
1)
2)

A

1) Pulmonary embolus

2) Arterial thromboembolism

26
Q

Where do emboli that result in pulmonary emboli often forM?

A

Usually in legs as a DVT

27
Q

Where do emboli that result in arterial thromboembolism often form?

A

Usually from atheroma (EG: atherosclerosis) or heart

28
Q

Outcomes of pulmonary embolism

A

Can be asymptomatic, cause transient hypoxia, sudden death

29
Q

Where do emboli causing pulmonary embolism often lodge?

A

Travels through right heart, lodges in pulmonary arteries.

30
Q

What does the formation of an arterial thromboembolism often involve?

A

Turbulence and/or platelets adhering to a dysfunctional blood vessel surface (EG: atherosclerosis, myocardial infarct, atrial fib)

31
Q

Where is it rare for emboli from the heart to lodge?

A

In the coronary arteries

32
Q

Difference between ischaemia and infarction

A

Ischaemia means ‘not enough blood supply.’

Infarction is tissue death as a result of too little blood supply

33
Q

Difference between ischaemia and hypoxia

A

Ischaemia is too little blood supply.
hypoxia is too little oxygen.
EG: If severely anaemic, can have hypoxia without ischaemia.

34
Q

Examples of acute ischaemia
1)
2)

A

1) Coronary thrombosis leading to myocardial infarct.

2) Shock, reducing blood supply to everything

35
Q

Examples of chronic ischaemia
1)
2)

A

1) Atherosclerotic disease leading to atrophy of lower limbs
2) Renal artery stenosis leading to renal atrophy

36
Q

Most common cause of infarction

A

Arterial occlusion

37
Q

Time taken for neurons to die from hypoxia

A

3-4 minutes

38
Q

Two appearances of infarctions

A

1) Red infarction

2) White infarction

39
Q

Red infarction

A

When there is haemorrhage in infarcted tissue

40
Q
Situations that could lead to red infarction
1)
2)
3)
4)
A

1) Dual blood supply to an organ (EG: Lungs)
2) Collateral blood supply (EG: intestine)
3) Venous infarction (EG: testicular torsion)
4) Reperfusion (common in emboli to the brain)

41
Q

How can reperfusion lead to a red infarct?

A

Infarction of tissue causes necrosis, breakdown of structure.
Blockage of artery is removed, blood enters now-damaged organ and leaks out into surrounding tissues.

42
Q

Pale infarction

A

When there is no bleeding in infarcted tissues

43
Q

When are pale infarcitons more common?

A

Due to a blocked end artery

44
Q

Why can an infarct lead to a thrombosis?

A

Abnormal, inflamed endothelium overlies infarct.