Atherosclerosis I Flashcards
Arteriosclerosis
“hardening of the arteries”
- affects mainly arterioles
- associated with chronic hypertension (response to HTN)
- narrowing of lumen
Tissue response to endothelial damage/injury:
Inflammation and Healing Response
-intimal thickening as site of accumulation of lipid
deposition and macrophage activation
-hyperplasia of media due chronic inflammation
-smooth muscle cells synthesis of extracellular matrix
molecules that directly influence the hardening (act as
fibroblasts)
-proliferation and migration into intima
two forms of atherosclerosis
-two forms: hyaline arteriolosclerosis, hyperplastic
arteriolosclerosis
Atherosclerosis
-basic lesion is atheroma (fibrofatty plaque)
-disease of large elastic arteries and large and medium
sized muscular arteries
-prime targets: aorta, coronary arteries, cerebral
arteries
characteristics of atherosclerosis
-progressive (inflammatory) disease of the walls of
large and medium sized muscular arteries of
-older adults
-lipid-containing plaques result in narrowing of the
vessel lumen
-chronic inflammatory reaction to deposited
oxidized lipid
-thrombotic/embolic obstruction of blood vessels of
the heart, brain, kidney, and lower extremities
pathogenesis of atherosclerosis
-Inflammatory/healing reaction of the endothelium of large
and medium sized arteries
-focal lesions within the intima (NOT involving media or
adventitia except secondarily)
what are the two main features separate this reaction from normal inflammatory events seen in small blood vessels
- accumulation of cholesterol as a result of insudation and
uptake of oxidized LDL by monocytes/macrophages and
smooth muscle cells - substitution of smooth muscle cells for fibroblasts in the
healing phase which give rise to a fibrous cap and
deposition of ECM components.
cell types involved
- endothelial cells
- monocytes/macrophages
- smooth muscle cells which migrate from the media
- platelets
- lymphocytes
6th major component
consists of serum lipids in the form of LDL or VLDL. These lipoproteins carry cholesterol, triglycerides, and phospholipids to peripheral tissues
evolution of atherosclerosis lesions
-local endothelial injury/accumulation of lipid
-endothelial cell activation
-adhesion of platelets and monocytes
-secretion of inflammatory cytokines
-migration/proliferation of cells activated by
cytokines which then secrete extracellular matrix
components (in this case smooth muscle cells).
lesions progression of age
Earliest lesions are tiny accumulations of lipid
within monocytes which give rise to fatty streaks
-flat, multifocal
With aging, the lesions become raised and
coalesce into plaques
-plaques are raised and show evidence of
extracellular lipid accumulation and
migration/proliferation of smooth muscle cells in the
intima (from the media).
characteristic distribution
- abdominal aorta
- carotid arteries
- coronary arteries
- proximal arteries of the lower extremities
where can atherosclerotic be found
Found at branching points and ostia of vessels
-increased blood flow and turbulence of flow
appear to play a role
consequences of lesions in middle sized vessels
progressive luminal narrowing
-results in progressive compromise of blood flow and
chronic ischemia
-thrombotic events associated with fissuring or rupture of
the atherosclerotic plaque are associated with acute
infarction
consequences of lesions in large vessels
(aorta) weakening of the arterial wall also results in aneurysms
- distortion of the wall architecture
- release of embolic material from disrupted plaques
