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Plaque Formation and Risk Factors

Plaque formation is initiated by risk factors that cause elevated LDL levels and reactive oxygen species in the bloodstream. This damages the endothelium and allows LDL to lodge in the artery wall where it becomes oxidized. Macrophages are attracted to the area and ingest the oxidized LDL, becoming foam cells and releasing growth factors. This causes smooth muscle cells to accumulate and form fibrous plaque over the foam cell core. Over time plaque can narrow the arteries and rupture, risking thrombosis. Chronic low-grade infection and endothelial dysfunction contribute to this pathogenic process.

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38 views3 pages

Plaque Formation and Risk Factors

Plaque formation is initiated by risk factors that cause elevated LDL levels and reactive oxygen species in the bloodstream. This damages the endothelium and allows LDL to lodge in the artery wall where it becomes oxidized. Macrophages are attracted to the area and ingest the oxidized LDL, becoming foam cells and releasing growth factors. This causes smooth muscle cells to accumulate and form fibrous plaque over the foam cell core. Over time plaque can narrow the arteries and rupture, risking thrombosis. Chronic low-grade infection and endothelial dysfunction contribute to this pathogenic process.

Uploaded by

Lynerthean
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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Plaque Formation

Key:
^ is up, _ is down
Pr (something) is probability of something happening
ROS = reactive oxygen species (oxygen-containing compounds that easily
react with other molecules)
Ox = oxidise or oxidised
M = macrophage (immune cell, eats bacteria + produced immune signalling

0 Risk Factors (see above)


cause
^ LDL in systemic circulation/peripheral tissues
o d/t: obesity
o smaller + denser than normal
o stay in systemic circulation longer
o ^ Pr (lodge in the artery wall) + ^ Pr (get oxidised)
^ reactive oxygen species
o d/t: hypertension etc
o will Ox the LDL and mess up the endothelium

1 Conditions Ripe for Plaque Formation


have Ox-LDL infection, smoking etc
^ prodn Ox-LDL
o by endothelium, SM & M
o ^ amt Ox-LDL overall (duh)
O
x o adhesions molecules on endothelium - ^P-selectin
- o chemotactic factors (by endothelium) attract M
L o get diapedesis (tether, activate & attach) monocytes + T-cells to
D endothelia
Monocytes/M
L move to subendothelial space stay here
o And eat more LDL and Ox-LDL
c o And release ROS Ox more LDL hyper-Ox-LDL
a o Positive feedbacks
Highly
u Ox-LDL sucked up by M via scavenger receptor
s o Get fatty streak (precursor to plaque)
e o Foam cells secrete growth factors lure in SM jam into intima
expression
o Getsofbigger
SM cells make fibrous tissue
o Fibrous plaque w/ fibrous cap
o Core of plaque is fatty = full of foam cells
Accumulation of lipid and fibrous connective tissue (plaque)
in intima of medium and large arteries (not veins)
requires high arterial pressures to form
Endothelial dysfunction and low-grade chronic inf. important in pathogenesis
Eventually stenosis (narrowed lumen), impaired vasodilation, plaques at risk of
rupture + pro-thrombotic environment.

Is more-or-less standard inf. (but sub-clinical/low grade + develops over years)

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