Nov22 M2-Pathology - Atherosclerosis

Question 1

ats composition

Answer 1

soft granulous necrotic core + thick fibrous cap

Question 2

ats step 1

Answer 2

endoth injury: lets lymphocytes, macrophages, monocytes through

Question 3

ats step 2 (after macrophages in)

Answer 3

are activated, secrete ECM and induce other cells to do so. LDL gets in intima, oxidized and taken up by activated macrophages

Question 4

ats step 3

Answer 4

macrophages activated form foam cells

Question 5

ats step 4

Answer 5

SM cells, normally contractile, become synthetic: mitosis + make ECM + move from media to intima

Question 6

ats step 5

Answer 6

SM cells activate macrophages, take lipids and form foam cells

Question 7

foam cells origin

Answer 7

from macrophages and SM that take cholesterol (LDL)

Question 8

why calcification in ats sometimes

Answer 8

SM (now synthetic) can become chondrocytes, deposit Ca, calcification

Question 9

effect of ats on platelets

Answer 9

aggregate and adhere bc endoth dysfunctional now

Question 10

how are fatty streaks caused

Answer 10

when both SM and macrophages engulf cholesterol

Question 11

what causes stenosis

Answer 11

thickening of intima

Question 12

fibrotic cap name + origin

Answer 12

atheroma. origin is ECM from SM

Question 13

what’s found in center of atheroma

Answer 13

CH esters, lipid debris

Question 14

fibrous cap components

Answer 14

SM cells, inflam cells, collagen, elastin, proteoglycans, new vessels

Question 15

necrotic center composition

Answer 15

cell debris, cholesterol crystals, foam cells, calcium

Question 16

vulnerable plaque def

Answer 16

big lipid core, thin fibrous cap. likely to rupture

Question 17

stable plaque def

Answer 17

thick fibrous cap, less lipid core: less likely to rupture

Question 18

inflam in vuln vs stable plaque

Answer 18

stable less inflammed

Question 19

why vuln plaque can rupture

Answer 19

lot of inflam, macrophages’ metalloproteinases, thin fibrous cap

Question 20

consequence of cap rupture

Answer 20

thrombus formation (core is very thrombogenic)

Question 21

complicated plaques

Answer 21

fissures, erosion, ulceration, calcification, thrombus, rupture

Question 22

pathophgy of aneurysm and rupture

Answer 22

thick cap and core, SM atrophy

Question 23

thrombotic stroke def

Answer 23

ulceration, rupture and thrombus or hemorrhage in plaque cause narrowing of lumen

Question 24

ats risk factor not usually covered

Answer 24

homocysteine mild elevation (can cause endoth damage and promote thrombosis)

Question 25

risk factor for ats of less importance

Answer 25

infection. conc. of antibodies assoc with severity

Question 26

why estrogen protective in ats

Answer 26

reduces LDL, increases HDL. antiplatelet action