Lec 28 Pathology of Coronary and Peripheral Artery disease

Question 1

What is pathology of atherosclerosis?

Answer 1

intiama cellular and matrix changes with remodelling of media and adventitia
due to chronic inflammatory and fibro lipid proliferative process

Question 2

What makes up the atherosclerotic plaque?

Answer 2

fibrous cap overlying necrotic lipid core

evolves from foam selves and develops into an atheroma

Question 3

What are key pathogenic features of plaque progression?

Answer 3

• inflammation
• neovascularization
• intra-plaque hemorrhage

Question 4

What type of atherosclerotic plaque is highest risk for plaque rupture and thrombosis?

Answer 4

thin capped fibro atheroma [TCFA]

Question 5

What causes true arterial aneurysm development?

Answer 5

intrinsic weakening of vessel wall; most commonly due to atherosclerosis with thickened intima, ischemia of media, and loss of elastic fibers

Question 6

How do you determine risk of rupture of an aortic aneurysm?

Answer 6

bigger diameter = bigger risk of rupture

Question 7

What is most common site of atherosclerotic aortic aneurysm development?

Answer 7

abdominal aorta below the renal arteries

Question 8

What is a genetic cause of aortic aneurysm?

Answer 8

marfan syndrome –> cystic degeneration of aortic media leading to aortic aneurysm of ascending aorta

Question 9

What arteries typically involved in PAD?

Answer 9

• distal abdominal aorta
• iliiac arteries
• distal arteries of lower extremities

Question 10

What happens in plaque neovascularization?

Answer 10

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 =

1. vasa vasorum interna arise from lumen
2. vasa vasorum externa arise from adventitia
3. venous vasa vasorum drain into veins

Question 11

What is effect of intra-plaque hemorrhage?

Answer 11

increased oxidative stress in plaque due to release of free hemoglobin
- increase size of plaque due to lipid core expansion

Question 12

What is type I atherosclerosis?

Answer 12

initial lesion
have isolated macrophages and foam cells
clinically silent, start in teens

Question 13

What is type II atherosclerosis?

Answer 13

fatty streak lesion
mainly intracellular lipid accumulation
clinically silent, start in teens

= intracellular lipid

Question 14

What is type III atherosclerosis?

Answer 14

intermediate pre-atheroma lesion = type II changes and small extracellular lipid pools
clinically silent, starts in 30s

= extracellular lipid

Question 15

What is type IV atherosclerosis?

Answer 15

atheroma lesion = type II changes and core of extracellular lipid

= fibrous cap formation

Question 16

What is type V atherosclerosis?

Answer 16

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

Question 17

What is type VI atherosclerosis?

Answer 17

complicated lesion = surface dfect, hematoma-hemorrhage, thrombus

disrupted plaque

Question 18

What is an erosion-thrombus?

Answer 18

no communication between thrombus and necrotic core

seen in post-menopausal smokers

Question 19

What happens in re-stenosis?

Answer 19

vessel wall injury –> proliferation of myofibroblasts from media into intma to generate neointimal/neoatherosclerosis

Question 20

How does histology of secondary venous graft atherosclerosis differ from primary atherosclerosis?

Answer 20

in primary = see lipid core and cap

in secondary = mostly fibrous tissue and some inflammatory tissue, usually concentric/diffuse

Question 21

HTN is a risk factor which which type of aortic aneurysm?

Answer 21

ascending aortic aneurysm

Question 22

What is loey’s dietz syndrome?

Answer 22

autosomal dominant genetic mutation in TGF-beta receptor

have abnormal elastin, collagen

at risk for ascending aortic aneruysm

Question 23

What is marfans syndrome?

Answer 23

defective fibrillin –> weakened elastic tissue and cystic medial necrosis

at risk for ascending aortic aneurysm

Question 24

what is ehler’s danlose syndrome?

Answer 24

defective type III collagen synthesis

at risk for ascending aortic aneurysm

Question 25

What nutritional deficiency assocaited wtih aortic aneurysm?

Answer 25

vitamine C deficiency

Question 26

What is majore complication of aortic aneurysm?

Answer 26

rupture

Question 27

What do you see histologically in aortic aneurysm?

Answer 27

thick fibrotic intima; elastic fiber degradation; much narrower media

Question 28

What happens in marfans syndrome aorta?

Answer 28

cystic medial degeneration

• have fragmentation of elastic fibers in media + degeneration

Question 29

Who is at risk for aortic dissection?

Answer 29

men 40-60 w/ HTN

younger pt with connective tissue disorders [ie marfans]

Question 30

What is most common site of aortic dissection?

Answer 30

ascending aorta