Atheroma, thrombosis, embolism and infarction Flashcards

1
Q

What is ischaemia?

A

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.

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2
Q

What is infarction?

A

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

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3
Q

What is haemostasis?

A

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.

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4
Q

What is thrombosis?

A

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

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5
Q

What is Virchows triad?

A

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

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6
Q

What is the role of platelets?

A

Close small breaches in vessel walls

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7
Q

What is the main function of an endothelial cell?

A

To maintain a permeability barrier

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8
Q

Give 7 causes of enfothelial injury

A
Hyperlipdaemia
Hypertension
Smoking
Toxins
Vasculitis 
Viruses 
Immune reactions
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9
Q

How would you describe normal blood flow in vessels?

A

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

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10
Q

What can disrupt laminar blood flow?

A

Stasis and turbulence

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11
Q

What are the effects of disrupted laminar flow?

A

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

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12
Q

What is hypercoagulability?

A

Any alteration in the coagulation pathway which predisposes to thrombosis

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13
Q

What two groups can hypercoagulable states be split into?

A

Acquired or genetic

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14
Q

What are high risk factors of developing acquired hypercoagulable states?

A

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

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15
Q

`Define cardiomyopathy

A

A chronic disease of the heart muscle

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16
Q

What are the lines of Zahn?

A

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

17
Q

What are the different fates of thrombi?

A

Propagation proximally, embolisation, fibrinolysis and organisation

18
Q

What is an embolism?

A

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

19
Q

Give 7 types of embolism

A

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

20
Q

When would you get fat embolism?

A

Following a major soft tissue trauma or major bone fractures

21
Q

When would you get gas/air embolism?

A

Barotrauma in divers, delivery or abortion and iatrogenic

22
Q

When would you get amniotic fluid embolism?

A

Post-partum

Amniotic fluid and debris enters torn veins and embolises to lungs

23
Q

Where do the majority of systemic embolism originate?

A

From thrombi within heart chambers or on valves

24
Q

What does systemic embolism in the limbs cause?

A

Gangrene

25
Q

What does systemic embolism in the brain cause?

A

Infarct/stoke

26
Q

Give 4 outcomes of athersclerosis

A
MI
Peripheral vascular disease (gangrene)
Mesenteric artery occlusion 
Ischaemic encephalopathy
Aortic aneurysm
27
Q

What are the risk factors for atherosclerosis?

A

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

28
Q

What size of arteries does atherosclerosis affect?

A

Small to medium arteries

29
Q

What happens as plaque size increases?

A

Luminal diameter decreases
Blood flow reduces
Ischaemia results once significant reduction

30
Q

What is the first stage of atherosclerosis?

A

Chronic endothelial injury

31
Q

What is the second stage of atherosclerosis?

A
Endothelial dysfunction:
Increased permeability
Monocyte adhesion
Monocyte migration
Platelet adhesion
32
Q

What does macrophage oxidation cause?

A

Lipoprotein oxidation
Production of cytokines
Production of growth factors

33
Q

How are foam cells produced?

A

Macrophages and smooth muscle cells engulf lipid to become foam cells

34
Q

How are foam cells seen?

A

As a fatty streak on the wall of the artery

35
Q

What happens when hypercholesterolaemia persists?

A

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

36
Q

Where is atherosclerosis commonly distributed?

A

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

37
Q

Which coronary artery is most affected by atherosclerosis?

A

Left anterior descending

38
Q

What are possible complications of atherosclerosis?

A

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