ADVANCED PATHOPHYSIOLOGY EXAM 3 NEWEST
QUESTIONS AND CORRECT ANSWERS (VERIFIED
ANSWERS) | A+ GRADE
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
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 arterial wall causing platelet
aggregation and smooth muscle proliferation
android obesity - ✔✔ANSWER✔✔-excess body fat that is placed
predominantly within the abdomen 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 - ✔✔ANSWER✔✔-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
at risk for premature CAD as well as stroke
elevated high sensitivity c reactive protein and CAD (hs-CRP) -
✔✔ANSWER✔✔-acute phase reactant 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
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
QUESTIONS AND CORRECT ANSWERS (VERIFIED
ANSWERS) | A+ GRADE
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
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 arterial wall causing platelet
aggregation and smooth muscle proliferation
android obesity - ✔✔ANSWER✔✔-excess body fat that is placed
predominantly within the abdomen 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 - ✔✔ANSWER✔✔-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
at risk for premature CAD as well as stroke
elevated high sensitivity c reactive protein and CAD (hs-CRP) -
✔✔ANSWER✔✔-acute phase reactant 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
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
