Week 2- Atherosclerosis

Front 1

Generic tem for thickening and inelasticity of arterial wall

Back 1

arteriosclerosis

Front 2

Form of arteriosclerosis, fibrofatty deposits produce arterial wall thickening; affects large and medium-sized arteries

Back 2

atherosclerosis

Front 3

Basic lesion of atherosclerosis, a raised intimal and subintimal local lesion containing a core of cholesterol and cholesterol esters covered by fibrous plaque

Back 3

Atheroma

Front 4

What layer of arteries does atherosclerosis begin?

Back 4

Tunica intima (endothelial cells)

Front 5

What is the principle locations you might find atheromas?

Back 5

aorta, coronary arteries, and cerebral arteries

Front 6

What is the first lesion of atherosclerosis?

Back 6

The fatty streak

Front 7

What are the three lesions of atherosclerosis?

Back 7

1. fatty streak
2. raised lesion/atheromatous plaque
3. complicated plaquw

Front 8

What is a fatty streak? When is it seen? What kind of cells? What kind of lipid?

Back 8

seen in children/teenagers

subendothelial collection of FOAM CELLS (fat-laden macrophages)

lipid is cholesterol and cholesterol ester derived from LDL

Front 9

What's an atheroma?

structure
type of lipids

Back 9

fibrous cap that overlies a lipid-rich necrotic core

inta-and extra-cellular lipids, cholesterol and cholesterol esters

smooth muscle and extracellular matrix at edge of lipid core

capillaries at edge of fibrous cap

Front 10

What type of lesion consists of a fibrous cap that overlies a necrotic core?

Back 10

atheroma

Front 11

Which type(s) of lesion(s) have smooth muscle at edge of lipid core? Why?

Back 11

atheromas, complicated/advanced legions

smoo

Front 12

What type of lesion has a necrotic core + hemorrhage?

Back 12

advanced/complicated

Front 13

What are the hallmarks of advanced/complicated legions?

Back 13

necrotic core + hemorrhage
calcium
plaque rupture and thrombosis

Front 14

What are the components of atherosclerotic lesions?

Back 14

Smooth muscle cells
macrophages
lymphocytes
connective tissue matrix (colalgen, elastin, proteoglycan)
lipid (cholesterol esters, free cholesterol)

Front 15

When is the earliest onset of atheromas?

Back 15

30s

Front 16

Which lesion is marked by a fibrous cap overlying a localized deposit of lipids including cholesterol, and
cholesterol esters?

Back 16

atheromatous lesions

Front 17

What are the preferential sites of atherosclerosis?

Back 17

Intimal irregularities and sites of turbulent flow

Front 18

What are compensatory measures for atherosclerotic obstruction of muscular arteries?

Back 18

Increased arterial diameter

the formation of collateral vessel

Front 19

What causes localized vasoconstriction?

Back 19

decreased nitric oxide and upped endothelin

Front 20

Describe the difference between stable and unstable lesions

Back 20

circumferential lesions are circumferential and lipid-poor

unstable lesions are eccentric and lipid-rich, ulcerated

Front 21

Where are the places where atherosclerotic lesions are most severe?

Back 21

branch points!

carotid artery, subclavian artery, celiac artery, iliac artery, etc

Front 22

atherosclerosis risk factors

Back 22

blood pressure
serum cholestrol
smoking
weight
glucose intolerance
age, sex

Front 23

How do we view the pathogenesis of atherosclerosis?

Back 23

Atherosclerosis is a chronic immunoinflammatory,
fibroproliferative disease of large
and medium-sized arteries.

Front 24

Describe the importance of CD40-CD40L interactions in atherosclerosis

Back 24

activated platelets express CD40L (T cell surface) which triggers a cascade of inflammation (B cellzz)

activation of CD40-CD40L upregulates adhesion molecules, destabilizes lesions

patients with unstable angina have mad CD40L

Front 25

What is the Marek virus?

Back 25

plaques in chickens, causes paralysis and T cell lymphoma

Front 26

describe role of c reactive protein in atherosclerois

Back 26

acute phase reactant

inflammatory marker as good as cholesterol in predicting coronary events

increased with hypertension, smoking inactivity and diabetes

Front 27

Describe early atherosclerosis

Back 27

platelet aggregation
platelets release factors 3 and 4 (factor 3, procoagulant that activates prothrombin factor 4, procoagulant, chemotactic for monocytes)

Front 28

What mediates the expression of adhesion of monocytes to endothelium?

Back 28

adhesion molecules on endothelial cells

upregulation of adhesion molecules are important in early atherogenesis!

Front 29

Upregulation of what molecules plays an important role in early atherogenesis?

Back 29

Adhesion molecules!

Front 30

What happens after adhesion molecules bind to endothelium in atherogenesis?

Back 30

monocytes migrate into intima and become macrophage foam cells

Front 31

Summarize the early events of atherogenesis

Back 31

uptake of LDL by arterial wall
binding and migration of circulating monocytes into intima
endothelial cell injury

Front 32

Late effects of endothelial injury!

Back 32

smooth muscle cells proliferate!
fibroblasts make collagen

damaged arterial wall permeable to lipids

incomplete endothelial regeneration further sequesters liquid

Front 33

Summarize the events of atherosclerosis

Back 33

LDL causes endothelial injury
Platelet adherence and aggregation
release of PDGF
smooth muscle cell proliferation, secretion of connective tissue matrix elements while cholesterol accumulates
atheroma!

Front 34

Consequences of atherosclerosis

Back 34

no effect
gradual occlusion leading to cerebral ischemia, myocardial ischemia, and renal ischemia
sudden occlusion leading to thrombosis- myocardial infarction, cerebral infarction, embolism
hemorrhage resulting from leakage or rupture of aortic aneurysm