Vascular Physiology 3

Question 1

atherosclerosis: starts with? which allows?

Answer 1

endothelial activation/damage = entry of bad LDL cholesterol, macrophages. macrophages eat cholesterol = foam cells –> enough foam cells accumulated = fatty streak

Question 2

atherosclerotic plaque: how is it formed?

Answer 2

macrophages die = free cholesterol pool. other inflammatory cells move in. fibrotic cap of matrix and cells seal off core of necrotic/dead cholesterol pool = plaque

Question 3

atherosclerosis: as more chol. accumulates what happens?

Answer 3

vessel remodels and bulges outward so the inner diameter is maintained until late = no major stenosis

Question 4

progression of stable athersclerosis

Answer 4

more chol. accumulates. inner diameter (lumen) squeezed = stenosis. get symptoms from vessels slowly blocking. eventual calcification = hardening of arteries

Question 5

unstable atherosclerosis: what happens?

Answer 5

fibrous cap attacked by inflammation/stress. lose glycocalyx. blood contacts prothrombotic core = thrombus formation –> risk of emboli

Question 6

how does monocyte enter the vessel?

Answer 6

response to damage and inflammatory mediators; stick to wall. monocyte chemoattractant protein, made in fat, attracts it into the vessel

Question 7

obesity and inflammation?

Answer 7

more fat cells = release IL6 and TNFa = CRP

Question 8

normal person: what happens when they ingest carbs?

Answer 8

insulin goes up, inhibits HSL so less fat breakdown and more glycogen storage

Question 9

obese/insulin resistance person: what happens when they ingest carbs?

Answer 9

insulin resistance = less glycogen formation = more fat formation but also more breakdown into fatty acids

Question 10

PET scanning of vasculature?

Answer 10

see inflammation