L26. Vascular Pathology

Question 1

How is the endothelium normally an anti-clotting surface?

Answer 1

Produces thrombomodulin which inhibits thrombin (and thrombosis)
Produces Protein C and Protein S which change thrombin from a pro into anti thrombotic factor

Question 2

What is a thrombus?

Answer 2

An abnormal clotted mass of blood in an unruptured cardiovascular system (Ie. blood clot formed without needing to be formed or persisting long after it needs to)

Question 3

What are the components of clotted blood?

Answer 3

RBCs, WBCs, Platelets and Fibrin

Question 4

What causes the formation of layers of red and white in these clots? What are these called?

Answer 4

Thombosis occurs in FLOWING BLOOD leading to the formation of clumped cells and platelets followed by fibrin formation and then more clots and then fibrin causing this streaked appearance = LINES OF ZAHN

Question 5

What causes thrombosis?

Answer 5

An imbalance between thrombogenesis and thrombolysis

Question 6

What is the difference between arterial and venous thrombi?

Their formation, appearance and treatments

Answer 6

ARTERIAL:
Higher platelets in the clot
White Thrombus due to endothelial dysfunction or damage (high stress environment)
Aspirin is more useful for the prevention of arterial thrombosis

VENOUS:
Higher red cells
Red thrombus due to blood stasis or hypercoaguability causing accumulation of clotting factors
Warfarin is more useful for preventing venous thrombus

Question 7

Why is aspirin better in prevention of arterial thrombosis and warfarin better for venous?

Answer 7

Because aspirin (a blood thinner) prevents thromboxane formation in platelets (arterial clots are platelet heavy). And warfarin is an anti-coagulant which prevents the formation of clotting factors and coagulatives in the blood (venous thrombosis is a result of hypercoaguability)

Question 8

What underlying abnormalities lead to thrombosis?

Answer 8

Virchov’s Triad:

1. Abnormal endothelium: loss of endothelium and vWF and TF exposure, dysfunction due to inflammation, reduced anticoagulant activity
2. Abnormal Flow: turbulence, stasis, loss of laminar flow,, accumulation of active platlets
3. Abnormal contents: genetic problems, oestrogen (pill or pregnancy), cancer, smoking, obesity, age and others

Question 9

What are the possible outcomes of thrombosis? [4]

Answer 9

1. Dissolution (fibronlysis)
2. Organisation and recanalisation (granulation tissue)
3. Propagation (grow longer and more crumblier due to continual platelet activation)
4. Embolism (mass carrier through the blood stream)

Question 10

What is an embolus?

Answer 10

An intravascular mass carried in the blood that can be solid, liquid or gaseous carried to a remote site from its origin or point of entrance causing blockage of the vessel.

Question 11

Describe an arterial embolism

Answer 11

Usually occurs as a result of turbulence in the blood.
The thromboembolis gets stuck in a downstream (smaller) artery causing ischaemia to an organ that the artery supplies (eg. the brain, intestines, kidneys, legs, spleen).

Question 12

Describe a venous embolism

Answer 12

Significant thromboemboli usually arise in the deep veins of the legs or pelvis and travels back into the veins and drains into the right side and often lodge in the pulmonary arteries (Pulmonary Embolism)

Question 13

What is ischaemia? What is infarction?

Answer 13

Ischaemia is when there is not enough blood supply and infarction is tissue death as a result of inadequate blood supply.

Question 14

What are some causes of Ishaemia? [3]

Answer 14

Local vascular narrowing or occlusion (stops oxygen delivery)
Increased demands for oxygen that are not met (eg. angina)
Systemic reduction in tissue perfusion (like cardiac or respiratory failure)

Question 15

What are some examples of acute ischaemia?

Answer 15

Coronary thrombosis leading to MI
Thromboembolism to the brain causing ischaemic stroke or transient ischaemic heart attack (TIA)
Atheroscelrotic narrowing causing claudication and angina
Torsion or twisting of some areas blocking a vein
Shock - reduced blood volume

Question 16

What are some examples of chronic ischaemia?

Answer 16

Atherosclerotic disease leading to atrophy
Renal artery stenosis causing renal atrophy
Hyaline atherosclerosis leading to benign nephrosclerosis

Question 17

What kind of vessel is the main problem (occluded) causing infarction?

Answer 17

Mainly arteries being blocked: because they deliver the oxygen

Question 18

What are the outcomes of infarction? What does it depend upon?

Answer 18

Depends upon the type of tissue

• Some are more sensitive (eg. Neurons die within minutes)
• Some have multiple blood supplies that can compensate somewhat
• Some have collateral supplies that are activated upon chronic ischamiea

Question 19

What kind of necrosis occurs in the heart as a result of infarction?

Answer 19

Coagulative Necrosis:
Death of cardiac cells that leads to ghost outlines of cells followed by acute inflammation and from the cell content leakage. Then to healing by granulation tissue and eventual scar formation

Question 20

What is the difference between a red and a pale infarction?

Answer 20

RED:

• Haemorrhage into the infarction: due to dual (liver, lungs) or collateral (intestine) blood supply.
• Venous infarction (testicular torsion)
• Reperfusion injury

PALE:

• No Haemorrhage
• Due to blocked ‘end arteries’
• Occurs in most organs: heart, kidney, spleen leading to a wedge shaped infarct