Pathophysiology NSG 533 Exam 3 Latest
Questions and Answer Key with Detailed
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(2026)
• (6) Traditional modifiable risk factors for CAD -✓✓(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 -✓✓(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 -✓✓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 -✓✓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 -✓✓- 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 -✓✓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) -✓✓<200 =
desirable
200-239 = borderline
≥240 = high
• LDL risk levels for CAD (dyslipidemia criteria) -✓✓<100 = optimal
100-129 = near optimal
130-159 = borderline
160-189 = high
≥190 = very high
• HDL risk levels for CAD (dyslipidemia criteria) -✓✓<40 = low
≥60 = high
• Triglyceride risk levels for CAD (dyslipidemia criteria) -✓✓<150 = desirable
150-199 = borderline
200-499 = high
≥500 = very high
, • Atherosclerotic plaque/lesion -✓✓- 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) -✓✓- 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) -✓✓- 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 -✓✓- 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
- Thrombosis, hemorrhage, and/or calcification
• Response to Injury Hypothesis -✓✓(1) Endothelial cell dysfunction
Questions and Answer Key with Detailed
Explanations (Verified Answers) |
Already Graded A+ | Premium Study Set
(2026)
• (6) Traditional modifiable risk factors for CAD -✓✓(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 -✓✓(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 -✓✓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 -✓✓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 -✓✓- 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 -✓✓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) -✓✓<200 =
desirable
200-239 = borderline
≥240 = high
• LDL risk levels for CAD (dyslipidemia criteria) -✓✓<100 = optimal
100-129 = near optimal
130-159 = borderline
160-189 = high
≥190 = very high
• HDL risk levels for CAD (dyslipidemia criteria) -✓✓<40 = low
≥60 = high
• Triglyceride risk levels for CAD (dyslipidemia criteria) -✓✓<150 = desirable
150-199 = borderline
200-499 = high
≥500 = very high
, • Atherosclerotic plaque/lesion -✓✓- 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) -✓✓- 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) -✓✓- 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 -✓✓- 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
- Thrombosis, hemorrhage, and/or calcification
• Response to Injury Hypothesis -✓✓(1) Endothelial cell dysfunction
