092614 path of atherosclerosis

Question 1

examples of large or elastic blood vessels

Answer 1

aorta and major branches (innominate, subclavian, common carotid, iliac) and pulmonary artery

Question 2

ex of medium sized or muscular arteries

Answer 2

coronary arteries

renal arteries

Question 3

small arteries and arterioles are found where?

Answer 3

coursing within connective tissue of organs

Question 4

diff btwn elastic and muscular arteries w respect to the media

Answer 4

in elastic artery, elastic fibers alternate btwn sm muscle cells in media

in muscular artery, the media has primarily sm musc cells; elastic fibers are limited to internal and external elastic lamina

Question 5

arterioles’ elastic composition?

Answer 5

arterioles have thin internal elastic membrane

terminal arterioles have no elastica

Question 6

what does medial sm musc contraction in arterioles cause?

Answer 6

adjustment of blood pres and blood flow

arterioles have thin internal elastic membranes and are points of physiologic resistance

Question 7

size of capillaries in diameter

Answer 7

7-8 microns

Question 8

what other cells can capillaries by surrounded by other than endothelium

Answer 8

pericytes (smooth musc like cells)

Question 9

what are the vessels at which leukocytes emigrate in inflam?

Answer 9

venules

Question 10

characteristics of veins

Answer 10

large lumen, thin wall

Question 11

endothelial cells can do what

Answer 11

maintain barrier
anticoagulant, antithrombotic, fibrinolytic regulators
prothrombotic molecules
make ECM 
modulate blood flow
regulate inflam
regulate cell growth
oxidize LDL

Question 12

how do endothelial cells respond to injury?

Answer 12

two types of response (in terms of timing):

stimulation–is immediate response. rapid and reversible. independent of new protein synthesis. an example would be contraction of endothelial cells in response to histamine

activation–elaboration of gene products with biologic activity requires hours or days to develop

Question 13

how can endothelial cells be turned into activated state from its basal state?

Answer 13

by factors like turbulent flow, HTN, lipid products, advance glycation end-products, cigarette smoke, etc

Question 14

what do endothelial cells in the activated state do?

Answer 14

increase expression of procoagulants, adhesion molecules, proinflammatory factors

alter expression of chemokines, cytokines, growth factors

Question 15

role of vascular sm musc cells

Answer 15

vasoconstriction or dilation
making collagen, elastin, proteoglycans
elaboration of growth factors and cytokines

migration to intima and proliferation in normal vascular repair and pathologic processes such as atherosclerosis

Question 16

what are pro-growth factors on the vascular sm muscle cells

Answer 16

PDGF, endothelin, thrombin, FGF, IFN-gamma, IL-1

Question 17

what do sm musc cells do in response to vascular injury

Answer 17

migrate from media into intima
in intima, will undergo mitosis
then will make ECM
intima, as aresult, thickens

Question 18

intimal sm musc cells are different from normal sm musc cells how?

Answer 18

they cannot contract

Question 19

arteriosclerosis

Answer 19

hardening of the arteries

Question 20

types of arteriosclerosis

Answer 20

atherosclerosis-elastic arteries and large/medium muscular arteries

arteriolosclerosis–small arteries and arterioles

Monckeberg medial calcific sclerosis

Question 21

Monckeberg arteriosclerosis

Answer 21

calcific depositis in media and internal elastic lamina of MEDIUM sized muscular arteries (usually radial and ulnar arteries)

greater than 50 years of age

no obstruction to blood flow

ring shaped (vs eccentric for an atheroma)

usually not clinically significant

Question 22

two basic types of damage in atherosclerosis

Answer 22

aneurysm formation

stenosis

Question 23

morphology of fatty streak

Answer 23

multiple yellow, flat dots to streaks. usually in aorta and later in coronaries

may be a precursor of atheroma but not all fatty streaks develop into more advanced lesions

Question 24

atheroma

Answer 24

fibrofatty plaque

Question 25

how are lipids incorporated into macrophages?

Answer 25

LDL cholesterol is transported into vessel wall

then endothelial cells and monocytes or macrophages generate free radicals that oxidize the LDL, resulting in lipid peroxidation

oxidized LDL is taken up by macrophages through scavenger receptors

uptake of oxidized LDL activates macrophages and releases proinflammatory cytokines

Question 26

morphology of fibro fatty plaque

Answer 26

RAISED yellow-white plaque in intima with soft yellow core and white fibrous cap

Question 27

calcifications in Monckeberg vs fibro fatty plaque

Answer 27

fibro fatty plaques can have calcifications but they would be in the intima. Monckeberg has calcifications in the media

Question 28

advanced or vulnerable plaques are at risk for

Answer 28

rupture ulceration, erosion, and hemorrhage leading to thrombosis/embolism, progressive luminal narrowing

atheroembolism

aneurysm formation

Question 29

vulnerable plaque vs stable plaque

Answer 29

vulnerable plaque has a thin fibrous cap, lots of lymphocytes, and thick lipid core

stable cap has a thick fibrous cap, minimal finlam, and small lipid cores

Question 30

if atherosclerotic plaque ruptures, what forms?

Answer 30

thrombus

Question 31

what factors contribute to thrombosis

Answer 31

shear stress, high levels of LDL, smoking

Question 32

aneurysm formation in atherosclerosis is due to

Answer 32

atrophy (due to pressure and or ischemia) of media and destruction of elastic fibers

leading to thinned, wakened wall

Question 33

pathogenesis of atherosclerosis

Answer 33

chronic inflam response of arterial wall to ENDOTHELIAL INJURY

components: endothelial injury, hemodynamic distrubances, lipid accumulation, inflam, infection (possibly?), sm musc proliferation

Question 34

strongly suspected causes of chronic endothelial cell injury

Answer 34

hemodynamic disturbances (areas of disturbed flow patterns)

hypercholesterolemia

HTN, smoking toxins, homocysteine, infectious agents