atheroma Flashcards
what is Atherosclerosis?
Inflammatory process characterised by hardened plaques in the intima of systemic arteries
in which vessels does Atherosclerosis tend to take place?
- in the intima of large and medium-sized systemic arteries (a higher pressure system)
- not pulmonary arteries
what is the main risk of Atherosclerosis?
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
what are common sites affected by Atherosclerosis?
coronary arteries, carotid arteries, renal arteries, aorta, or in peripheral arteries
when do complications of atherosclerotic plaques tend to occur in life?
40s-80s
list 5 non-modifiable risk factors to Atherosclerosis
Age
Gender
Race
Family History
poorly controlled Diabetes (Type 1)
list 5 modifiable risk factors to
Smoker
Lack of exercise
Weight
(Borderline) Diabetes (type 2)
Hypertension
High cholesterol (Hypercholesterolemia)
low SES?
what are the main constituents of an atherosclerotic plaque
predominantly Lipids
Necrotic core
Connective tissue
Fibrous “cap”
lymphocytes
in short, what is the Main reason atherosclerotic plaques can form?
the endothelial cell damage theory
what are the 3 main headings to plaque formation:
- damage to endothelial cells
- LDLs start fatty streak formation
- foam cells products and contents cause plaque growth
in what layer of the artery does the atherosclerotic plaque form?
the tunica intima
list some common outcomes of atherosclerosis
- aortic aneurysm
- myocardial infarct
explain step 1 in plaque formation
1.damage to endothelial cells
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
explain step 2 in plaque formation
- LDLs start fatty streak formation
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
explain step 3 in plaque formation
- foam cells products and contents cause plaque growth
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