CAD Risk Factors: Non-modifiable - ANSWER age
genetic disposition
family history
ethnic background
gender
CAD risk factors - ANSWER Age >55
male
fam hx
personal hx peripheral vasc/Cerebrovascular disease
smoking
lipid abnorm
DM
HTN
obesity
sedentary
cocaine
estrogen use
dyslipidemia - high LDL, low HDL, high triglycerides
what happens when LDL becomes oxidized - ANSWER becomes oxidized when exposed
to endothelial cells and smooth muscle cell
then exposed to macrophages
becomes foam cell
1
,makes up atherosclerotic plaque
what does HDL do - ANSWER reverse cholesterol transport
returns excess cholesterol from the tissue to the liver where it binds to hepatic receptors
and is processed or eliminated as bile or converted to cholesterol-containing steroids
protects LDL from oxidation
explain the relationship of lipoprotiens and diabetes as a risk factor for CAD - ANSWER
lipoproteins can be altered by glycation as a result of high glucose levels which causes a
greater integration into macrophages (engulf oxidized LDL) this then accumulates in the arte-
rial wall causing platelet aggregation and smooth muscle proliferation
android obesity - ANSWER excess body fat that is placed predominantly within the abdo-
men and upper body, as opposed to the hips and thighs
strongest link with CAD risk r/t insulin resistance, decreased HDL levels, increased blood
pressure, and inflammation
9 P21 - ANSWER genetic variant associated with a strong risk for CAD
what is the risk of having an MI in relation to the age that it occurred in a parent - AN-
SWER inverse relationship
if you have a parent who had an MI at 40 you have a higher risk than someone who's parent
had one at 70
Women typically present with CAD symptoms 10 years earlier than men
t/f - ANSWER false
lipoprotein (a) and CAD - ANSWER nontraditional risk factor
associated with atherosclerosis and thrombosis
genetically derived particle
2
,at risk for premature CAD as well as stroke
elevated high sensitivity c reactive protein and CAD (hs-CRP) - ANSWER acute phase reac-
tant or protein
made in liver
indirect measure of atherosclerotic plaque-related inflammation/progression
inflammatory marker
the more inflammation the more likely to have plaque ruptures
t/f lipoproteins increase risk for a cardiac event, thrombus, and stroke - ANSWER true
t/f high numbers of large and puffy LDL particles are associated with increased risk for CAD -
ANSWER false
high numbers of small dense LDL
total cholesterol levels - ANSWER desirable - <200
Borderline - 200-239
high - >240
LDL levels - ANSWER Optimal: <100
Near optimal: 100-129
Borderline high: 130-159
High: 160-189
Very high: >190
Triglycerides levels - ANSWER desirable - <150
borderline - 150 - 199
high - 200-499
3
, very high - >500
HDL levels - ANSWER low - <40
high - >60
response to injury hypothesis - ANSWER Atherosclerosis hypothesis where plaque build
up begins with the endothelial damage
changes in permeability
monocytes attach
move in
release oxygen free radicals
LDL becomes oxidized
monocyte becomes macrophage
cell dies
dead cells and oxidized LDLs form the plaque
cover by smooth muscle cell
fatty streak - ANSWER first lesion of atherosclerosis
-thickening of intima
-inc. in smooth muscle cells
-smooth muscle cells migrate and proliferate into intima
-lipid deposits accumulate
-macrophages cause damage
fibrous plaque - ANSWER second lesion of atherosclerosis
-evolves from fatty streak
-accumulation of connective tissue
-inc. in number of smooth muscle cells
4
genetic disposition
family history
ethnic background
gender
CAD risk factors - ANSWER Age >55
male
fam hx
personal hx peripheral vasc/Cerebrovascular disease
smoking
lipid abnorm
DM
HTN
obesity
sedentary
cocaine
estrogen use
dyslipidemia - high LDL, low HDL, high triglycerides
what happens when LDL becomes oxidized - ANSWER becomes oxidized when exposed
to endothelial cells and smooth muscle cell
then exposed to macrophages
becomes foam cell
1
,makes up atherosclerotic plaque
what does HDL do - ANSWER reverse cholesterol transport
returns excess cholesterol from the tissue to the liver where it binds to hepatic receptors
and is processed or eliminated as bile or converted to cholesterol-containing steroids
protects LDL from oxidation
explain the relationship of lipoprotiens and diabetes as a risk factor for CAD - ANSWER
lipoproteins can be altered by glycation as a result of high glucose levels which causes a
greater integration into macrophages (engulf oxidized LDL) this then accumulates in the arte-
rial wall causing platelet aggregation and smooth muscle proliferation
android obesity - ANSWER excess body fat that is placed predominantly within the abdo-
men and upper body, as opposed to the hips and thighs
strongest link with CAD risk r/t insulin resistance, decreased HDL levels, increased blood
pressure, and inflammation
9 P21 - ANSWER genetic variant associated with a strong risk for CAD
what is the risk of having an MI in relation to the age that it occurred in a parent - AN-
SWER inverse relationship
if you have a parent who had an MI at 40 you have a higher risk than someone who's parent
had one at 70
Women typically present with CAD symptoms 10 years earlier than men
t/f - ANSWER false
lipoprotein (a) and CAD - ANSWER nontraditional risk factor
associated with atherosclerosis and thrombosis
genetically derived particle
2
,at risk for premature CAD as well as stroke
elevated high sensitivity c reactive protein and CAD (hs-CRP) - ANSWER acute phase reac-
tant or protein
made in liver
indirect measure of atherosclerotic plaque-related inflammation/progression
inflammatory marker
the more inflammation the more likely to have plaque ruptures
t/f lipoproteins increase risk for a cardiac event, thrombus, and stroke - ANSWER true
t/f high numbers of large and puffy LDL particles are associated with increased risk for CAD -
ANSWER false
high numbers of small dense LDL
total cholesterol levels - ANSWER desirable - <200
Borderline - 200-239
high - >240
LDL levels - ANSWER Optimal: <100
Near optimal: 100-129
Borderline high: 130-159
High: 160-189
Very high: >190
Triglycerides levels - ANSWER desirable - <150
borderline - 150 - 199
high - 200-499
3
, very high - >500
HDL levels - ANSWER low - <40
high - >60
response to injury hypothesis - ANSWER Atherosclerosis hypothesis where plaque build
up begins with the endothelial damage
changes in permeability
monocytes attach
move in
release oxygen free radicals
LDL becomes oxidized
monocyte becomes macrophage
cell dies
dead cells and oxidized LDLs form the plaque
cover by smooth muscle cell
fatty streak - ANSWER first lesion of atherosclerosis
-thickening of intima
-inc. in smooth muscle cells
-smooth muscle cells migrate and proliferate into intima
-lipid deposits accumulate
-macrophages cause damage
fibrous plaque - ANSWER second lesion of atherosclerosis
-evolves from fatty streak
-accumulation of connective tissue
-inc. in number of smooth muscle cells
4
