PATHO NSG 533 EXAM 3 / NEWEST
COMPREHENSIVE STUDY GUIDE – EXPERT
STRATEGIES, REVIEW OF KEY QUIZZES, AND
PRACTICE QUESTIONS FOR GUARANTEED SUCCESS
Terms in this set (117)
(5) Non-modifiable risk (1) Age
factors for CAD (2) Gender
(3) Ethnicity
(4) Family history
(5) Genetic predisposition
(1) Dyslipidemia (abnormal serum lipoproteins) (2)
HTN (endothelial injury and myocardial hypertrophy)
(3) Cigarette Smoking (endothelial injury and
(6) Traditional modifiable oxygenradicals)
risk factors for CAD (4) Diabetes (endothelial injury and vessel walldamage)
(5) Obesity/Sedentary Lifestyle (strongest link to
CAD)
(6) Atherogenic Diet (high in salt, fat, trans fat, carbs)
,(10) Novel risk factors for (1) Markers of Inflammation, ischemia and thrombosis
CAD (c-reactive protein, troponin, fibrinogen)
(2) Adipokines (adiponectin, leptin)
(3) CKD (as GFR declines, risk for CAD increases)
(4) Air Pollution and Ionizing Radiation
(5) Medications (NSAIDS increase risk for CAD)
(6) Coronary Artery Calcification and Carotid Artery
Wall Thickness
(7) Microbiome (diet/lifestyle)
(8) Elevated Fibrinogen (inflammatory marker) (9) Elevated
LDL particle number (cholesterol concentration within particles)
(10) Small, dense LDLs (vs. large fluffy lipoprotein)
Lipids Refers to cholesterol in particular. Required by most cells for
manufacture/repair of plasma membranes.
High dietary intake of cholesterol and fats results in high
levels of LDL in the bloodstream, which can lead to
Atherosclerosis and contribute to CAD
Refers to lipids, phospholipids, cholesterol, and triglycerides
bound to carrier proteins.
- LDL (low-density lipoprotein): contain mostlycholesterol and
Lipoproteins protein.
- HDL (high-density lipoprotein): mainly phospholipidsand
protein
- VLDL (very-low-density lipoprotein): mainlytriglyceride and
protein
,Atherosclerosis - Progressive, multifactorial disease process thatgenerally
begins in childhood; clinical manifestations occur in middle to
late adulthood, that results in the variable composition of
lesions
- High dietary intake of cholesterol and fats results inhigh
levels of LDL in the bloodstream. LDL oxidation, migration into
the vessel wall, and phagocytosis by macrophages result in fatty
deposits called plaques to form on the inner walls of the
arteries
Describe the relationship Low levels of HDL pose risk for CAD. HDL is responsible for
between HDL (highdensity returning excessive cholesterol to the liver for elimination or
lipoprotein), LDL (low- conversion to cholesterolcontaining steroids. HDL can also
density lipoprotein), VLDL remove excessive cholesterol through the arterial wall. It
(very-low-density can protect LDL from oxidation, preserve endothelial
lipoprotein), and CAD function, and promote anti-inflammatory and
antithrombotic effects. VLDL pose risk for CAD, especially in
combination with other risk factors such as diabetes
Total Cholesterol risk levels <200 = desirable
for CAD 200-239 = borderline
(dyslipidemia criteria) ≥240 = high
LDL risk levels for CAD <100 = optimal
(dyslipidemia criteria) 100-129 = near optimal
130-159 = borderline
160-189 = high
≥190 = very high
HDL risk levels for CAD <40 = low
(dyslipidemia criteria) ≥60 = high
<150 = desirable
Triglyceride risk levels for
150-199 = borderline
CAD (dyslipidemia
200-499 = high
criteria)
≥500 = very high
, Atherosclerotic - Likely to develop following endothelial injury; areas of
plaque/lesion increased shear wall stress are especially vulnerable
Fatty streak → Fibrous-fatty plaque → Advanced complicated lesion
Fatty streak (early damage to - Focal thickening of the intima
vessel wall)
- Increase in smooth muscle cells and extracellularmatrix
- Smooth muscle cells migrate and proliferate into theintima
- Lipid deposits accumulate
- Macrophages and T-lymphocytes (early damage tovessel wall)
- Accumulation of connective tissue
- Increased number of smooth muscle cells ladenwith lipids
Fibrous-fatty plaque
- Deeper extracellular lipid pool
(evolves from fatty streak)
- Results in further endothelial cell dysfunction,necrosis of
underlying vessel tissue, and narrowing of the lumen as the
lesion protrudes out from the vessel wall
COMPREHENSIVE STUDY GUIDE – EXPERT
STRATEGIES, REVIEW OF KEY QUIZZES, AND
PRACTICE QUESTIONS FOR GUARANTEED SUCCESS
Terms in this set (117)
(5) Non-modifiable risk (1) Age
factors for CAD (2) Gender
(3) Ethnicity
(4) Family history
(5) Genetic predisposition
(1) Dyslipidemia (abnormal serum lipoproteins) (2)
HTN (endothelial injury and myocardial hypertrophy)
(3) Cigarette Smoking (endothelial injury and
(6) Traditional modifiable oxygenradicals)
risk factors for CAD (4) Diabetes (endothelial injury and vessel walldamage)
(5) Obesity/Sedentary Lifestyle (strongest link to
CAD)
(6) Atherogenic Diet (high in salt, fat, trans fat, carbs)
,(10) Novel risk factors for (1) Markers of Inflammation, ischemia and thrombosis
CAD (c-reactive protein, troponin, fibrinogen)
(2) Adipokines (adiponectin, leptin)
(3) CKD (as GFR declines, risk for CAD increases)
(4) Air Pollution and Ionizing Radiation
(5) Medications (NSAIDS increase risk for CAD)
(6) Coronary Artery Calcification and Carotid Artery
Wall Thickness
(7) Microbiome (diet/lifestyle)
(8) Elevated Fibrinogen (inflammatory marker) (9) Elevated
LDL particle number (cholesterol concentration within particles)
(10) Small, dense LDLs (vs. large fluffy lipoprotein)
Lipids Refers to cholesterol in particular. Required by most cells for
manufacture/repair of plasma membranes.
High dietary intake of cholesterol and fats results in high
levels of LDL in the bloodstream, which can lead to
Atherosclerosis and contribute to CAD
Refers to lipids, phospholipids, cholesterol, and triglycerides
bound to carrier proteins.
- LDL (low-density lipoprotein): contain mostlycholesterol and
Lipoproteins protein.
- HDL (high-density lipoprotein): mainly phospholipidsand
protein
- VLDL (very-low-density lipoprotein): mainlytriglyceride and
protein
,Atherosclerosis - Progressive, multifactorial disease process thatgenerally
begins in childhood; clinical manifestations occur in middle to
late adulthood, that results in the variable composition of
lesions
- High dietary intake of cholesterol and fats results inhigh
levels of LDL in the bloodstream. LDL oxidation, migration into
the vessel wall, and phagocytosis by macrophages result in fatty
deposits called plaques to form on the inner walls of the
arteries
Describe the relationship Low levels of HDL pose risk for CAD. HDL is responsible for
between HDL (highdensity returning excessive cholesterol to the liver for elimination or
lipoprotein), LDL (low- conversion to cholesterolcontaining steroids. HDL can also
density lipoprotein), VLDL remove excessive cholesterol through the arterial wall. It
(very-low-density can protect LDL from oxidation, preserve endothelial
lipoprotein), and CAD function, and promote anti-inflammatory and
antithrombotic effects. VLDL pose risk for CAD, especially in
combination with other risk factors such as diabetes
Total Cholesterol risk levels <200 = desirable
for CAD 200-239 = borderline
(dyslipidemia criteria) ≥240 = high
LDL risk levels for CAD <100 = optimal
(dyslipidemia criteria) 100-129 = near optimal
130-159 = borderline
160-189 = high
≥190 = very high
HDL risk levels for CAD <40 = low
(dyslipidemia criteria) ≥60 = high
<150 = desirable
Triglyceride risk levels for
150-199 = borderline
CAD (dyslipidemia
200-499 = high
criteria)
≥500 = very high
, Atherosclerotic - Likely to develop following endothelial injury; areas of
plaque/lesion increased shear wall stress are especially vulnerable
Fatty streak → Fibrous-fatty plaque → Advanced complicated lesion
Fatty streak (early damage to - Focal thickening of the intima
vessel wall)
- Increase in smooth muscle cells and extracellularmatrix
- Smooth muscle cells migrate and proliferate into theintima
- Lipid deposits accumulate
- Macrophages and T-lymphocytes (early damage tovessel wall)
- Accumulation of connective tissue
- Increased number of smooth muscle cells ladenwith lipids
Fibrous-fatty plaque
- Deeper extracellular lipid pool
(evolves from fatty streak)
- Results in further endothelial cell dysfunction,necrosis of
underlying vessel tissue, and narrowing of the lumen as the
lesion protrudes out from the vessel wall
