ATHEROSCLEROSIS By Joshua Bower Easter Revision 2014 [email protected].
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Transcript of ATHEROSCLEROSIS By Joshua Bower Easter Revision 2014 [email protected].
![Page 1: ATHEROSCLEROSIS By Joshua Bower Easter Revision 2014 J.Bower@warwick.ac.uk.](https://reader036.fdocuments.in/reader036/viewer/2022062516/56649d835503460f94a6a0ec/html5/thumbnails/1.jpg)
ATHEROSCLEROSIS By Joshua BowerEaster Revision [email protected]
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Distinguish arteriosclerosis, atherosclerosis and arteriolosclerosis
• ARTERIOSCLEROSIS – generic term meaning ‘hardening of the arteries’ which encompasses the other 2
• ATHEROSCLEROSIS – intimal lesions of arteries caused by atheromas
• ARTERIOLOSCLEROSIS – arteriolar hardening seen in HTN and DM
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Intima:• Endothelium• BM• Subendothelial connective tissue• Internal elastic lamina
Media:• SMCs• Connective Tissue
Externa/Adventitia• Connective tissue• External elastic lamina• Vasa vasorum
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What are vasa vasorum?
• Network of small blood vessels supplying walls of large blood vessels• Provide blood supply and nourishment to tunica adventitia and outer
part of tunica media
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What is an atheroma?
• Chronic intimal lesion occurring in arteries• Causes lumen narrowing and weakening of vessel wall
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Atheromas are characterised by accumulation of what FOUR things? [4]
• Vascular SMCs (vascular smooth muscle cells)• ECM• Inflammatory cells• Lipids
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List FOUR modifiable and non-modifiable risk factors for atherosclerosis
• Hyperlipidaemia• HTN• Smoking• DM
• Older• Male• FHx• Genetics (e.g. ?)
Modifiable Non-modifiable
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Give an example of a genetic abnormality which may contribute to atheroma development
• Apolipoproteins• APLs package fats e.g. LDL• Some APLs act as ligand for receptors for uptake into cells
• Abnormal APL or receptors means:• Reduced uptake• Reduced excretion
• Thus increased serum LDL
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What are the THREE key features of chronic inflammation? [3]
• Ongoing inflammation• Ongoing tissue destruction• Ongoing tissue repair
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List the steps leading to atheroma development [6]
1. Chronic endothelial injury (e.g. HTN, smoking)2. Endothelial dysfunction (becomes more permeable, cholesterol-rich
LDLs enter and becomes oxidised3. Monocytes enter, becomes macrophages and attempt to digest the
cholesterol – become foam cells (visible as a fatty streak) 4. Foam cells release growth factors, stimulating SMC infiltration from
the media, which then proliferate5. Collagen and ECM becomes deposited, forming fibrofatty plaque6. SMCs calcify as they degenerate in aged plaques, making them
more vulnerable to rupture
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Suggest THREE outcomes of atheroma [3]
Atheroma
Chronic Narrowing of lumen
Chronic reduction in blood flow
Chronic ischaemia
Weakening of vessel wall
AneurysmPlaque rupture
Bleeding into atheroma
Thrombus
Occlusion
Embolus
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List THREE features of vessels which may make them more vulnerable to atheroma development [3]
• High pressure• Bifurcation (e.g. abdominal aorta)• Narrow lumen with high flow (e.g. cerebral vasculature)
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An obese 67yo diabetic male presents to his GP with pain in his lower leg which becomes worse after he has been walking for a while. Diagnosis?
• Peripheral vascular disease• Intermittent claudication• Pain at rest• Ischaemic limb
• These are atherosclerotic blockages outside of the coronary tree – usually lower limb
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The effects of the atheroma on distal tissue is dependent on what THREE things? [3-5]• Size of lumen• Stability of plaque• Degree of degeneration of underlying wall• Natural Hx of plaque• Type of blood supply
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How can atheroma be treated? [3]
• Reduce risk• Stenting by PCTA• Bypass grafting via CABG
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QUESTIONS? By Joshua BowerEaster Revision [email protected]