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
Examples of emboli causing disease 1) 2)
1) Pulmonary embolus | 2) Arterial thromboembolism
26
Where do emboli that result in pulmonary emboli often forM?
Usually in legs as a DVT
27
Where do emboli that result in arterial thromboembolism often form?
Usually from atheroma (EG: atherosclerosis) or heart
28
Outcomes of pulmonary embolism
Can be asymptomatic, cause transient hypoxia, sudden death
29
Where do emboli causing pulmonary embolism often lodge?
Travels through right heart, lodges in pulmonary arteries.
30
What does the formation of an arterial thromboembolism often involve?
Turbulence and/or platelets adhering to a dysfunctional blood vessel surface (EG: atherosclerosis, myocardial infarct, atrial fib)
31
Where is it rare for emboli from the heart to lodge?
In the coronary arteries
32
Difference between ischaemia and infarction
Ischaemia means 'not enough blood supply.' | Infarction is tissue death as a result of too little blood supply
33
Difference between ischaemia and hypoxia
Ischaemia is too little blood supply. hypoxia is too little oxygen. EG: If severely anaemic, can have hypoxia without ischaemia.
34
Examples of acute ischaemia 1) 2)
1) Coronary thrombosis leading to myocardial infarct. | 2) Shock, reducing blood supply to everything
35
Examples of chronic ischaemia 1) 2)
1) Atherosclerotic disease leading to atrophy of lower limbs 2) Renal artery stenosis leading to renal atrophy
36
Most common cause of infarction
Arterial occlusion
37
Time taken for neurons to die from hypoxia
3-4 minutes
38
Two appearances of infarctions
1) Red infarction | 2) White infarction
39
Red infarction
When there is haemorrhage in infarcted tissue
40
``` Situations that could lead to red infarction 1) 2) 3) 4) ```
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
How can reperfusion lead to a red infarct?
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
Pale infarction
When there is no bleeding in infarcted tissues
43
When are pale infarcitons more common?
Due to a blocked end artery
44
Why can an infarct lead to a thrombosis?
Abnormal, inflamed endothelium overlies infarct.