Vascular Pathology 1 - Atherosclerosis, Aneurism, Dissection Flashcards

1
Q

What is ischaemia?

A

Deficiency of blood in a tissue causing a shortage of oxygen and impaired aerobic respiration

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2
Q

What is ischaemia due to?

A

increased demand for oxygen that is not met, local vascular narrowing or occlusion, systemic reduction in tissue perfusion

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3
Q

What is hypoxia?

A

A deficiency of oxygen in tissues

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4
Q

What is hypoxia due to?

A

Ischaemia, impaired respiratory function, decrease in oxygen carrying capacity of the blood

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5
Q

What is an infarct?

A

An area of necrosis caused by acute ischaemia

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6
Q

What is a thrombus?

A

A clotted mass of blood that forms within the cardiovascular system during life

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7
Q

What is an embolus?

A

An intravascular solid, liquid or gaseous mass carried in the blood stream to a site remote from its origin

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8
Q

What is atherosclerosis?

A

An accumulation of lipid and fibrous connective tissue in the intima of medium and large arteries

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9
Q

What is the first step in the pathogenesis of atherosclerosis?

A

Chronic endothelial injury due to hyperlipidaemia, hypertension, smoking, hemodynamic factors, toxins, viruses, immune reactions

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10
Q

What is the response to the chronic endothelial injury?

A

Endothelial dysfunction

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11
Q

What happens in endothelial dysfunction?

A

Increased vascular permeability, platelet adhesion (by exposure of the subendothelial ECM), monocyte adhesion (by expression of selectins, VCAM-1 and ICAM-1), release of PDGF, decreased releasing factors to inhibit clotting, production of ROS, altered release of vasoactive substances

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12
Q

What is the result of endothelial dysfunction?

A

LDLs can gain entry to the intima

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13
Q

What happens to LDLs once they enter the intima?

A

They are oxidised by ROS

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14
Q

What causes the recruitment of monocytes to the intima?

A

the leukocyte adhesion molecules on the endothelium (selectins, VCAM-1, ICAM-1) and the chemoattractant signals (IL-8, MCP-1)

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15
Q

How are foam cells formed?

A

By the phagocytosis of LDL by macrophages

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16
Q

Why do smooth muscle cells migrate from the media into the intima?

A

In response to the PDGF released from the endothelium and macrophages as well as FGF and TGF

17
Q

What do smooth muscle cells in the intima do?

A

Secrete ECM (mostly collagen) to wall off the lipid core of the plaque

18
Q

How is the lipid rich necrotic core of the plaque formed?

A

The break down of foam cells by apoptosis and the breakdown of collagen by matrix metalloproteinases

19
Q

What are the results of atherosclerosis?

A

vessel stenosis, impaired vasodilation, plaques vulnerable to rupture, local prothrombotic environment

20
Q

What are the risk factors for atherosclerosis?

A
  • age
    • gender
    • family history
    • hypertension
    • diabetes mellitus
    • smoking
    • hypercholesterolaemia
    • obesity
    • physical inactivity
    • proteinuria
    • type A personality
    • infections
21
Q

Why is diabetes a risk factor for atherosclerosis?

A

Because hyperglycaemia causes oxidative stress and damages endothelium and patients have smaller denser LDL which is more atherogenic

22
Q

At what stage of atherosclerosis do you see fatty streaks?

A

When there are foamy macrophages present but before migration of smooth muscle cells

23
Q

What other features are seen histologically in atherosclerosis?

A

cholesterol clefts, calcification, lymphocytes

24
Q

What are the complications of atherosclerosis?

A

ischaemia (narrowing), infarction (athero-embolism or thrombo-embolism), aneurysm

25
Q

What is an aneurysm?

A

A localised abnormal dilation of a blood vessel or the heart

26
Q

What is a true aneurysm?

A

Where the dilation occurs but the wall is intact

27
Q

What is a false aneurysm?

A

Where there is a defect in the vascular wall so that blood can go in the intravascular space

28
Q

What is a dissection?

A

Blood between two layers of the vascular wall

29
Q

What is a fusiform dilation?

A

The dilation of the entire circumference

30
Q

What is a saccular dilation?

A

A focal dilation

31
Q

What are the causes of aneurysm?

A

atherosclerosis, congenital weakness in the wall, systemic hypertension, infection in an artery wall

32
Q

What are the complications of an aneurysm?

A

Rupture, narrowing

33
Q

What is Marfan syndrome?

A

A genetic abnormality in fibrin meaning that the elastin isn’t made right - can lead to an aneurysm

34
Q

What is arteriosclerosis?

A

Hardening of the arteries - includes atherosclerosis and age related changes

35
Q

What happens to elastic arteries with age?

A

Degeneration of elastic tissue and intimal fibrosis

36
Q

What is arteriolosclerosis?

A

Deposition of plasma proteins and collagen in the endothelium of small arteries and arterioles - arteriole wall becomes thickened with eosinophilic glassy material and the lumen is narrowed

37
Q

What are the consequences of arteriolosclerosis?

A

stroke due to rupture of weakened vessels, ischaemia/infartction in the retina or chronic ischaemia in the kidney