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Lecture 14

BIOC 3300 Lecture Notes - Lecture 14: Fibrous Cap, Foam Cell, Atheroma


Department
Biochem & Molecular Biology
Course Code
BIOC 3300
Professor
Mc Leod Roger
Lecture
14

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1. What defines a
type I lesion?
Isolated macrophage foam cells
Modest lipid accumulation
Present in first decade
Clinically silent
Possibly reversible
2. What defines a
type II
lesiationon?
Fatty streak
Mainly intracellular lipid accumulation
present in first decade
clinically silent
3. What defines a
type III lesion?
Intermediate
Type II lesion changes to contain small
extracellular lipid pools
Growth of lesion in mainly through further
lipid accumulation
Present from third decade
Clinically silent
4. What defines a
type IV lesion?
Atheroma
Type III lesion progresses to contain a core
of extracellular lipid
Growth is mainly through further lipid
accumulation
Present from third decade
Clinically silent or overt
5. What defines a
type V lesion?
Fibroatheroma
Contains lipid core and fibrous cap
Proliferation of smooth muscle and
extensive collagen
Present from fourth decade
Clinically silent or overt
6. What defines a
type VI lesion?
Defect develops in fibrous cap
presence of thrombus and hematoma
From fourth decade
Usually overt, potentially fatal
7. What are the
four theories of
atherogenesis?
Lipid infiltration
Thrombogenic
Monoclonal
Response to injury
8. What are the
components of
a fibrous cap?
Smooth muscle cells, macrophages, foam
cells, lymphocytes, collagen, elastin,
proteoglycans
9. What are the
components of
a necrotic
center?
cell debris cholesterol crystals, foam cells,
calcium
10. What is the
thrombogenic
theory?
Atherosclerotic lesions develop as a result
of repeated clot formation and
organization, eventually occluding the
vessels
Lipids accumulated by trapping in clot
Not an initiating event
11. What is the monoclonal
theory?
Atherosclerotic lesions
develop from a single cell
which changes to a
proliferative state at the
lesion site
viral or chemical mutagen
12. What is the lipid infiltration
theory?
Atherosclerotic lesions
develop as a result of an
imbalance on the entry
and exit of lipoproteins
from the intima
Supporting evidence:
Atherosclerosis associated
with increased LDL and
decreased HDL
Focal lesions - sites of stress
or injury are sites of lipid
accumulation
13. What are high-risk
lipoprotein level indicators
of atherosclerotic lesions
according to the lipid
infiltration theory?
High LDL = High risk
Low HDL = High risk
14. What are the major lipids
present in plaques?
cholesterol and esters
15. Where do oxygen free
radicals that modify LDL
come from, and where does
OxLDL go?
macrophages
taken up by macrophages
16. What happens when there is
unregulated OxLDL uptake
into macrophages?
causes foam cell formation
stimulates recruitment and
retention of macrophages
stimulates release of growth
factors and cytokines
17. What are the steps involved
in the response to injury
hypothesis?
1. Chronic endothelial
'injury'
2. endothelial dysfunction
and platelet adherance
3. SMC migration,
macrophage activation
4. Cellular lipid accumulation
5. SMC proliferation, matrix
deposition, cell necrosis
18. What are activators of
endothelial cell activity in
the response to injury
hypothesis?
Cytokines
Bacterial products
Hemodynamic forces
Lipid products
advanced glycosylation end
products
viruses
complement products
hypoxia
Lecture 14 - Atherosclerosis
Study online at quizlet.com/_17yoom
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