atheroma Flashcards

1
Q

what is Atherosclerosis?

A

Inflammatory process characterised by hardened plaques in the intima of systemic arteries

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2
Q

in which vessels does Atherosclerosis tend to take place?

A
  • in the intima of large and medium-sized systemic arteries (a higher pressure system)
  • not pulmonary arteries
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3
Q

what is the main risk of Atherosclerosis?

A

The increased pressure and inflammation can cause the plaque to rupture.
A thrombus forms on the disrupted plaque (platelets adhere and clotting process begins)
blood flow can be impeded

OR the plaque occludes the artery and can cause angina

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4
Q

what are common sites affected by Atherosclerosis?

A

coronary arteries, carotid arteries, renal arteries, aorta, or in peripheral arteries

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5
Q

when do complications of atherosclerotic plaques tend to occur in life?

A

40s-80s

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6
Q

list 5 non-modifiable risk factors to Atherosclerosis

A

Age
Gender
Race
Family History
poorly controlled Diabetes (Type 1)

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7
Q

list 5 modifiable risk factors to

A

Smoker
Lack of exercise
Weight
(Borderline) Diabetes (type 2)
Hypertension
High cholesterol (Hypercholesterolemia)

low SES?

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8
Q

what are the main constituents of an atherosclerotic plaque

A

predominantly Lipids
Necrotic core
Connective tissue
Fibrous “cap”
lymphocytes

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9
Q

in short, what is the Main reason atherosclerotic plaques can form?

A

the endothelial cell damage theory

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10
Q

what are the 3 main headings to plaque formation:

A
  1. damage to endothelial cells
  2. LDLs start fatty streak formation
  3. foam cells products and contents cause plaque growth
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11
Q

in what layer of the artery does the atherosclerotic plaque form?

A

the tunica intima

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12
Q

list some common outcomes of atherosclerosis

A
  • aortic aneurysm
  • myocardial infarct
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13
Q

explain step 1 in plaque formation

1.damage to endothelial cells

A

Due to high levels of LDLs in blood stream (hyperlipidemia)
Smoking or air pollution (free radicals)
High cholesterol
Hypertension - causes physical injury
Turbulent blood flow, for example, where arteries branch
Chronically elevated blood glucose levels

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14
Q

explain step 2 in plaque formation

  1. LDLs start fatty streak formation
A

Dysfunctional endothelial cells allow Low density lipoproteins (LDLs) to move from lumen into tunica intima layer

The Dysfunctional cells release reactive oxygen species (eg. metalloproteases) which oxidise the LDLs

Oxidised LDLs cannot leave the intima, they are trapped

Dysfunctional endothelial cells + oxidised LDLs trigger endothelial cells to express adhesion molecules for WBCs (monocytes + T helper cells)

These monocytes attach and move into intima where they are now called macrophages

Macrophages have scavenger receptors that will engulf the oxidised LDLs to become a foam cell

A fatty streak has formed

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15
Q

explain step 3 in plaque formation

  1. foam cells products and contents cause plaque growth
A

Foam cells release products, then die and release contents. this forms the fibrous cap, the bulk of the plaque and increases inflammation.

Products released:

-chemokines, to attract more macrophages
IGF-1 ( a growth factor), that causes smooth muscle cells to proliferate and migrate from the media to the intima layer. These cells make collagen, which forms a hard, fibrous cap to the plaque

-proinflammatory cytokines and reactive oxygen species increase inflammation

-When the foam cells die they release lipid content, containing DNA materials which attract neutrophils to the site of Inflammation

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16
Q

what 2 factors cause plaque growth and increased inflammation

A
  1. increased vascular supply to plaque
  2. T cells
  • T cells bind onto the endothelial cells,
    -enter plaque area,
    -activated by macrophages to release IFN-Y
  • this promotes inflammation and activates endothelial cells to attract more WBCs
    -therefore plaque keeps growing and there is inflammation
17
Q

What can be done to prevent atherosclerosis?

A

Reduce risk factors and taking low dose aspirin regularly.

18
Q

Why can cigarette smoking lead to atherosclerosis?

A

Cigarette smoking releases free radicals, nicotine and CO into the body. These all damage endothelial cells.

19
Q

Why can hypertension lead to atherosclerosis?

A

A higher blood pressure means there is a greater force exerted onto the endothelial cells and this can lead to damage.