Lec 28 Pathology of Coronary and Peripheral Artery disease Flashcards
What is pathology of atherosclerosis?
intiama cellular and matrix changes with remodelling of media and adventitia
due to chronic inflammatory and fibro lipid proliferative process
What makes up the atherosclerotic plaque?
fibrous cap overlying necrotic lipid core
evolves from foam selves and develops into an atheroma
What are key pathogenic features of plaque progression?
- inflammation
- neovascularization
- intra-plaque hemorrhage
What type of atherosclerotic plaque is highest risk for plaque rupture and thrombosis?
thin capped fibro atheroma [TCFA]
What causes true arterial aneurysm development?
intrinsic weakening of vessel wall; most commonly due to atherosclerosis with thickened intima, ischemia of media, and loss of elastic fibers
How do you determine risk of rupture of an aortic aneurysm?
bigger diameter = bigger risk of rupture
What is most common site of atherosclerotic aortic aneurysm development?
abdominal aorta below the renal arteries
What is a genetic cause of aortic aneurysm?
marfan syndrome –> cystic degeneration of aortic media leading to aortic aneurysm of ascending aorta
What arteries typically involved in PAD?
- distal abdominal aorta
- iliiac arteries
- distal arteries of lower extremities
What happens in plaque neovascularization?
new vessels proliferate from microvasculature [vasa vasorum] due to increased diffusion barrier from thickened blood vessel wall to try to get more oxygen to ischemic cells
these neovessels are thin walled and fragile thus prone to rupture and hemorrhage
3 types =
- vasa vasorum interna arise from lumen
- vasa vasorum externa arise from adventitia
- venous vasa vasorum drain into veins
What is effect of intra-plaque hemorrhage?
increased oxidative stress in plaque due to release of free hemoglobin
- increase size of plaque due to lipid core expansion
What is type I atherosclerosis?
initial lesion
have isolated macrophages and foam cells
clinically silent, start in teens
What is type II atherosclerosis?
fatty streak lesion
mainly intracellular lipid accumulation
clinically silent, start in teens
= intracellular lipid
What is type III atherosclerosis?
intermediate pre-atheroma lesion = type II changes and small extracellular lipid pools
clinically silent, starts in 30s
= extracellular lipid
What is type IV atherosclerosis?
atheroma lesion = type II changes and core of extracellular lipid
= fibrous cap formation
What is type V atherosclerosis?
fibroatheroma lesion = lipid core and fibrotic layer OR mulitple lipid cores and fibrotic layres OR mainly calcific OR mainly fibrotic
3 types
Va = fibro-atheroma, expansion of lipid core, collagen Vb = calcific plaque Vc = fibrotic plaque, fibrous tissue + collagen, no lipid core
What is type VI atherosclerosis?
complicated lesion = surface dfect, hematoma-hemorrhage, thrombus
disrupted plaque
What is an erosion-thrombus?
no communication between thrombus and necrotic core
seen in post-menopausal smokers
What happens in re-stenosis?
vessel wall injury –> proliferation of myofibroblasts from media into intma to generate neointimal/neoatherosclerosis
How does histology of secondary venous graft atherosclerosis differ from primary atherosclerosis?
in primary = see lipid core and cap
in secondary = mostly fibrous tissue and some inflammatory tissue, usually concentric/diffuse
HTN is a risk factor which which type of aortic aneurysm?
ascending aortic aneurysm
What is loey’s dietz syndrome?
autosomal dominant genetic mutation in TGF-beta receptor
have abnormal elastin, collagen
at risk for ascending aortic aneruysm
What is marfans syndrome?
defective fibrillin –> weakened elastic tissue and cystic medial necrosis
at risk for ascending aortic aneurysm
what is ehler’s danlose syndrome?
defective type III collagen synthesis
at risk for ascending aortic aneurysm
What nutritional deficiency assocaited wtih aortic aneurysm?
vitamine C deficiency
What is majore complication of aortic aneurysm?
rupture
What do you see histologically in aortic aneurysm?
thick fibrotic intima; elastic fiber degradation; much narrower media
What happens in marfans syndrome aorta?
cystic medial degeneration
- have fragmentation of elastic fibers in media + degeneration
Who is at risk for aortic dissection?
men 40-60 w/ HTN
younger pt with connective tissue disorders [ie marfans]
What is most common site of aortic dissection?
ascending aorta
