Atheroma, thrombosis, embolism and infarction

Question 1

What is ischaemia?

Answer 1

The result of impaired vascular perfusion depriving the affected tissue of nutrients. It can be reversible depending on the speed of onset, local demand and duration.

Question 2

What is infarction?

Answer 2

This is ischaemic necrosis of a tissue or organ secondary to the occlusion./reduction of arterial supply or venous drainage

Question 3

What is haemostasis?

Answer 3

Human body’s response to blood vessel injury and bleeding. It is a coordinated effort between platelets and blood clotting factors to form a clot.

Question 4

What is thrombosis?

Answer 4

The formation of a solid or semi-solid mass from the constituents of blood within the vascular system, during life.

Question 5

What is Virchows triad?

Answer 5

The 3 main factors that predispose to thrombosis:
Changes in vessel walls (endothelial injury)
Changes in blood constituents (hypercoagulability)
Changes in blood flow

Question 6

What is the role of platelets?

Answer 6

Close small breaches in vessel walls

Question 7

What is the main function of an endothelial cell?

Answer 7

To maintain a permeability barrier

Question 8

Give 7 causes of enfothelial injury

Answer 8

Hyperlipdaemia
Hypertension
Smoking
Toxins
Vasculitis 
Viruses 
Immune reactions

Question 9

How would you describe normal blood flow in vessels?

Answer 9

Laminar flow - a slower moving column of plasma separates the cells from the endothelium

Question 10

What can disrupt laminar blood flow?

Answer 10

Stasis and turbulence

Question 11

What are the effects of disrupted laminar flow?

Answer 11

Platelets come into contact with the endothelium
Activated clotting factors are not diluted by the normal rapid flow of blood
Inflow of anticoagulant factors is slowed
Activation of endothelial cells is promoted

Question 12

What is hypercoagulability?

Answer 12

Any alteration in the coagulation pathway which predisposes to thrombosis

Question 13

What two groups can hypercoagulable states be split into?

Answer 13

Acquired or genetic

Question 14

What are high risk factors of developing acquired hypercoagulable states?

Answer 14

MI, immobilisation, tissue damage, cancer, prosthetic heart valves, disseminated intravascular coagulation (DIC), heparin induced thrombocytopenia and antiphospholipid syndrome.

Question 15

`Define cardiomyopathy

Answer 15

A chronic disease of the heart muscle

Question 16

What are the lines of Zahn?

Answer 16

Thrombosis form under pressure and this results in alternating plate (platelet and fibrin) and dark (RBC/WBC) bands

Question 17

What are the different fates of thrombi?

Answer 17

Propagation proximally, embolisation, fibrinolysis and organisation

Question 18

What is an embolism?

Answer 18

Detached intravascular solid, liquid or gaseous mass which is carried by the bloodstream to a site distant from the point of origin.

Question 19

Give 7 types of embolism

Answer 19

Thromboembolism, fat embolism, marrow embolism, air embolism, septic embolism, amniotic fluid embolism and tumour embolism

Question 20

When would you get fat embolism?

Answer 20

Following a major soft tissue trauma or major bone fractures

Question 21

When would you get gas/air embolism?

Answer 21

Barotrauma in divers, delivery or abortion and iatrogenic

Question 22

When would you get amniotic fluid embolism?

Answer 22

Post-partum

Amniotic fluid and debris enters torn veins and embolises to lungs

Question 23

Where do the majority of systemic embolism originate?

Answer 23

From thrombi within heart chambers or on valves

Question 24

What does systemic embolism in the limbs cause?

Answer 24

Gangrene

Question 25

What does systemic embolism in the brain cause?

Answer 25

Infarct/stoke

Question 26

Give 4 outcomes of athersclerosis

Answer 26

``` MI Peripheral vascular disease (gangrene) Mesenteric artery occlusion Ischaemic encephalopathy Aortic aneurysm ```

Question 27

What are the risk factors for atherosclerosis?

Answer 27

Age, sex, genetics, hypertension, smoking, diabetes, hyperlipidaemia , lack of exercise, obesity, high carbohydrate or saturated fat diet, oestrogenic status and stress.

Question 28

What size of arteries does atherosclerosis affect?

Answer 28

Small to medium arteries

Question 29

What happens as plaque size increases?

Answer 29

Luminal diameter decreases Blood flow reduces Ischaemia results once significant reduction

Question 30

What is the first stage of atherosclerosis?

Answer 30

Chronic endothelial injury

Question 31

What is the second stage of atherosclerosis?

Answer 31

``` Endothelial dysfunction: Increased permeability Monocyte adhesion Monocyte migration Platelet adhesion ```

Question 32

What does macrophage oxidation cause?

Answer 32

Lipoprotein oxidation Production of cytokines Production of growth factors

Question 33

How are foam cells produced?

Answer 33

Macrophages and smooth muscle cells engulf lipid to become foam cells

Question 34

How are foam cells seen?

Answer 34

As a fatty streak on the wall of the artery

Question 35

What happens when hypercholesterolaemia persists?

Answer 35

Smooth muscle proliferation and collagen deposition which convert the fatty steak into a mature firbofatty atheroma

Question 36

Where is atherosclerosis commonly distributed?

Answer 36

The aorta, coronary arteries, superior and inferior mesenteric arteries, renal arteries, coeliac trunk, circle of Willis and the illiac arteries

Question 37

Which coronary artery is most affected by atherosclerosis?

Answer 37

Left anterior descending

Question 38

What are possible complications of atherosclerosis?

Answer 38

Ulceration of athermatous plaque thrombosis Haemorrhage into plaque with plaque rupture and embolism Critical stenosis Aneurysm formation