Exam 3) NSG 533 Exam 3: Questions & Answers
(5) Non-modifiable risk factors for CAD - ANSWER:(1) Age
(2) Gender
(3) Ethnicity
(4) Family history
(5) Genetic predisposition
(6) Traditional modifiable risk factors for CAD - ANSWER:(1) Dyslipidemia (abnormal serum lipoproteins)
(2) HTN (endothelial injury and myocardial hypertrophy)
(3) Cigarette Smoking (endothelial injury and oxygen radicals)
(4) Diabetes (endothelial injury and vessel wall damage)
(5) Obesity/Sedentary Lifestyle (strongest link to CAD)
(6) Atherogenic Diet (high in salt, fat, trans fat, carbs)
(10) Novel risk factors for CAD - ANSWER:(1) Markers of Inflammation, ischemia and thrombosis (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 - ANSWER: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
Lipoproteins - ANSWER:Refers to lipids, phospholipids, cholesterol, and triglycerides bound to carrier
proteins.
,- LDL (low-density lipoprotein): contain mostly cholesterol and protein.
- HDL (high-density lipoprotein): mainly phospholipids and protein
- VLDL (very-low-density lipoprotein): mainly triglyceride and protein
Atherosclerosis - ANSWER:- Progressive, multifactorial disease process that generally 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 in high 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 between HDL (high-density lipoprotein), LDL (low-density lipoprotein), VLDL
(very-low-density lipoprotein), and CAD - ANSWER:Low levels of HDL pose risk for CAD. HDL is
responsible for returning excessive cholesterol to the liver for elimination or conversion to cholesterol-
containing steroids. HDL can also remove excessive cholesterol through the arterial wall. It can protect
LDL from oxidation, preserve endothelial 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 for CAD (dyslipidemia criteria) - ANSWER:<200 = desirable
200-239 = borderline
≥240 = high
LDL risk levels for CAD (dyslipidemia criteria) - ANSWER:<100 = optimal
100-129 = near optimal
130-159 = borderline
160-189 = high
≥190 = very high
HDL risk levels for CAD (dyslipidemia criteria) - ANSWER:<40 = low
≥60 = high
Triglyceride risk levels for CAD (dyslipidemia criteria) - ANSWER:<150 = desirable
150-199 = borderline
200-499 = high
≥500 = very high
, Atherosclerotic plaque/lesion - ANSWER:- Likely to develop following endothelial injury; areas of
increased shear wall stress are
especially vulnerable
Fatty streak → Fibrous-fatty plaque → Advanced complicated lesion
Fatty streak (early damage to vessel wall) - ANSWER:- Focal thickening of the intima
- Increase in smooth muscle cells and extracellular matrix
- Smooth muscle cells migrate and proliferate into the intima
- Lipid deposits accumulate
- Macrophages and T-lymphocytes (early damage to vessel wall)
Fibrous-fatty plaque (evolves from fatty streak) - ANSWER:- Accumulation of connective tissue
- Increased number of smooth muscle cells laden with lipids
- Deeper extracellular lipid pool
- 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
Advanced complicated lesion - ANSWER:- Smooth muscle cells, numerous macrophages, T-cells , often
associated with lipid core and necrotic material
- Covered by a fibrous cap (smooth muscle cells surrounded by CT matrix)
- Thick cap - provides stability to the lesion
- Thin, non-uniform cap, macrophage-rich - lesion is unstable
(5) Non-modifiable risk factors for CAD - ANSWER:(1) Age
(2) Gender
(3) Ethnicity
(4) Family history
(5) Genetic predisposition
(6) Traditional modifiable risk factors for CAD - ANSWER:(1) Dyslipidemia (abnormal serum lipoproteins)
(2) HTN (endothelial injury and myocardial hypertrophy)
(3) Cigarette Smoking (endothelial injury and oxygen radicals)
(4) Diabetes (endothelial injury and vessel wall damage)
(5) Obesity/Sedentary Lifestyle (strongest link to CAD)
(6) Atherogenic Diet (high in salt, fat, trans fat, carbs)
(10) Novel risk factors for CAD - ANSWER:(1) Markers of Inflammation, ischemia and thrombosis (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 - ANSWER: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
Lipoproteins - ANSWER:Refers to lipids, phospholipids, cholesterol, and triglycerides bound to carrier
proteins.
,- LDL (low-density lipoprotein): contain mostly cholesterol and protein.
- HDL (high-density lipoprotein): mainly phospholipids and protein
- VLDL (very-low-density lipoprotein): mainly triglyceride and protein
Atherosclerosis - ANSWER:- Progressive, multifactorial disease process that generally 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 in high 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 between HDL (high-density lipoprotein), LDL (low-density lipoprotein), VLDL
(very-low-density lipoprotein), and CAD - ANSWER:Low levels of HDL pose risk for CAD. HDL is
responsible for returning excessive cholesterol to the liver for elimination or conversion to cholesterol-
containing steroids. HDL can also remove excessive cholesterol through the arterial wall. It can protect
LDL from oxidation, preserve endothelial 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 for CAD (dyslipidemia criteria) - ANSWER:<200 = desirable
200-239 = borderline
≥240 = high
LDL risk levels for CAD (dyslipidemia criteria) - ANSWER:<100 = optimal
100-129 = near optimal
130-159 = borderline
160-189 = high
≥190 = very high
HDL risk levels for CAD (dyslipidemia criteria) - ANSWER:<40 = low
≥60 = high
Triglyceride risk levels for CAD (dyslipidemia criteria) - ANSWER:<150 = desirable
150-199 = borderline
200-499 = high
≥500 = very high
, Atherosclerotic plaque/lesion - ANSWER:- Likely to develop following endothelial injury; areas of
increased shear wall stress are
especially vulnerable
Fatty streak → Fibrous-fatty plaque → Advanced complicated lesion
Fatty streak (early damage to vessel wall) - ANSWER:- Focal thickening of the intima
- Increase in smooth muscle cells and extracellular matrix
- Smooth muscle cells migrate and proliferate into the intima
- Lipid deposits accumulate
- Macrophages and T-lymphocytes (early damage to vessel wall)
Fibrous-fatty plaque (evolves from fatty streak) - ANSWER:- Accumulation of connective tissue
- Increased number of smooth muscle cells laden with lipids
- Deeper extracellular lipid pool
- 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
Advanced complicated lesion - ANSWER:- Smooth muscle cells, numerous macrophages, T-cells , often
associated with lipid core and necrotic material
- Covered by a fibrous cap (smooth muscle cells surrounded by CT matrix)
- Thick cap - provides stability to the lesion
- Thin, non-uniform cap, macrophage-rich - lesion is unstable
