Cardio-path- atheroscelosis Flashcards
What is the fundamental basis for the vast majority of vascular disorders.?
Injury to the vessel wall—and in particular to endothelial cells
Blooc vessel Endotherlial Cell injury/dysfunction may contribute to pathologic processes including thrombosis, hypertensive lesions and atherosclerosis.
vascular
Vascular injury leading to Endothelial Cell loss or dysfunction stimulates growth of what?
smooth muscle cells, extra-cellular matrix synthesis, and thickening of the vascular wall.
As a result of vascular injury, smooth muscles cells migrate to the ?
intima -SMCs then proliferate, synthesize ECM, forming a neo-intima covered by an intact EC layer.
Though Smooth muscle cell proliferation and matrix synthesis can help to repair a damaged vessel wall, it can also cause what negative effect?
lead to luminal occlusion.
What ) is characterized by intimal lesions called atheromas (atheromatous/atherosclerotic plaques) that impinge on the vascular lumen, and can rupture to cause sudden occlusion?
atherosclerosis
What pathology underlies the pathogenesis of coronary, cerebral, and peripheral vascular disease, and causes more morbidity and mortality in the Western world than any other disorder!*?
atherosclerosis
Raised lesions composed of soft friable (crumbly) lipid cores covered by fibrous caps:
Atheromatous plaques
Thickness of the intimal lesions also may be sufficient to decrease perfusion of the , leading to ischemia and changes in the ECM caused by subsequent .
media, inflammation.
Subsequent tunica media hypoxia and inflammation from thick intimal atherosclerotoc plaques can weaken the media, and lead to the formation of?
aneurysms
What are constitutional risk factors?
non-modifiable
What is the most important independent risk factor for atherosclerosis?
Family history
Most familial risk is not related to , but related to multifactorial traits, including hypertension, and, diabetes
familial hypercholesterolemia
Familial hypercholesterolemia is a “receptor disease” caused by of-function mutations in the gene encoding the receptor, which is involved in the transport and metabolism of .
loss; LDL; cholesterol.
Describe the LDL receptor disesase familial hypercholesterolemia?
loss-of-function mutations in the gene encoding the LDL receptor
impair the intracellular transport and catabolism of LDL, resulting in accumulation of LDL cholesterol in the plasma.
elevated levels of cholesterol induce premature atherosclerosis and greatly increase the risk of MI.
Atherosclerosis is considered silent until about what age?
middle age or later
Which group of women are protected against atherosclerosis?
premenopausal women
Hyperlipidemial is a major risk factor, why?
The main cholesterol component associated with increased risk is low-density lipoprotein (LDL) cholesterol (“bad cholesterol”); LDL distributes cholesterol to peripheral tissues.
How does the liver get rid of excess cholesterol?
through the bile
HTN can increase the risk of ischemic heart disease by %
60
Foamy cells (macs with lipids) in intima
What are the 2 key features of atherosclerotic plaques?
intimal thickening and lipid accumulation
They are white to yellow raised lesions; they range from 0.3 to 1.5 cm in diameter but can coalesce to form larger masses.
Thrombus superimposed on ulcerated plaques gives a red-brown color.
Describe the morphology of an atherosclerotic plaque?
patchy, usually involving only a portion of any given arterial wall.
note: the image is a trichrome stain
blue is fibrosis
C is cholesterol
What are the 3 main components of the atherosclerotic plaques?
(1) Cells, including SMCs, macrophages, and T cells;
(2) ECM, including collagen, elastic fibers, and proteoglycans; and
(3) Intracellular and extracellular lipid.
note: the red circles surround cholesterol (lipids)
Atheromas generally over time.
• They also often undergo .
enlarge; calcification
note: calcified plaque
Which vessel has the ulcerated plaque and which is occluded by a clot?
left image- rupture of plaque
right image- clot or thrombus
