054 Heart Disease Flashcards

1
Q

Globally, there are about 57m deaths per year. How many are dying from cardiovascular disease?

A

1/3 people (17m)

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2
Q

Is cardiovascular disease higher in LIC or HIC?

A

LIC - smoking, poor nutrition, poor health

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3
Q

What are the two top killers of 2030?

A

Heart disease and stroke

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4
Q

Which stages of atherosclerosis are reversible?

A

Stages 1-4

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5
Q

What is the cause of change during stages 1-4 compared to stages 5-6?

A

Stages 1-4 develop due to increasing accumulation of lipid. Stages 5 and 6 develop due to fibrous thickening and thrombus deposit formation.

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6
Q

In the UK, what are the differences in cardiovascular disease epidemiology?

A

Higher rates in the north, lower rates in south west and south east of London.

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7
Q

What are the three layers of a normal large artery?

A

Intima (endothelial cells on luminal side and elastic fibres on peripheral side)
Media (smooth muscle cells)
Adventitia (connective tissues with interdispersed fibroblasts)

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8
Q

What are the three most important cell types involved in atherosclerotic lesion development?

A

Monocytes
Smooth muscle cells
endothelial cells

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9
Q

What is the significance of endothelial cells in the development of atherosclerosis lesions?

A

Activated endothelial cells will express adhesion molecules and recruit inflammatory cells (monocytes). Lipid formation may also occur in the intima space of vessel wall.

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10
Q

What is adaptive thickening

A

Some people may have defined locations in the blood vessels where smooth muscles have thickened as a self limited response of the intima to thermodynamic forces present due to blood flow etc. These areas are not necessarily places where lesions will occur, although they do occur in areas that are progression prone.

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11
Q

Which types of lesions are most frequent >40 year olds

A

Type V and VI

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12
Q

Which types of lesions can be seen in young children?

A

Type I and II

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13
Q

Which types of lesions are symptom producing, and which symptoms are they?

A

Type V can cause angina due to thickened vessels. Type VI can be a cause of thrombus deposition

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14
Q

How do foam cells occur?

A

Lipid that is deposited gets oxidised by free radicals. Monocytes that have differentiated into macrophages have receptors that uncontrollably ingest the oxidised lipids, causing foam cells.

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15
Q

What is the role of macrophages/monocytes in the development of atherosclerosis lesions?

A

These immune cells will migrate and produce cytokines and growth factors. They will also induce smooth muscle cell migration.

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16
Q

What is the role of smooth muscles in the development of atherosclerosis lesions?

A

Smooth muscle cells change from contractile to repair phenotype. They will form a fibrous cap and generate extracellular matrix. This causes calcification.

17
Q

What do statins do?

A

Block formation of cholesterol and reducing it by 30%, also increases HDL.

18
Q

What is the relationship between cholesterol and NO production?

A

LDL inhibits NO production and constricts blood vessels. HDL stimulates and enhances vascular tone.