NSG 533 Advanced Pathophysiology Exam 3
1. List the novel risk factors 1) markers of inflammation, ischemia, and thrombosis (elevated high
for CAD sensitivity C-reactive protein, troponin, fibrinogen) 2) adipokines
(leptin, adiponectin) 3) CKD 4) air pollution and ionizing radiation
5) medications (NSAIDs) 6) coronary artery calcification and carotid
wall thickness and 7) microbiome 8) small dense LDL particles and
lipoprotein(a) 9) Hyperhomocysteinemia
2. List nonmodifiable risk Advanced age, male gender or woman after menopause, and family
factors for CAD history (genetics, shared environmental exposure).
3. List modifiable risk factors Dyslipidemia, hypertension, cigarette smoking, diabetes and insulin
for CAD resistance, obesity and sedentary lifestyle, and an atherogenic diet.
4. How does dyslipidemia High levels of LDL in the bloodstream leads to LDL oxidation, migra-
contribute to CAD? tion into the vessel wall, and phagocytosis by macrophages, all key
steps in the pathogenesis of atherosclerosis.
5. Atherosclerosis A chronic inflammatory condition that results in damage to the ar-
teries. Thickening and hardening of the vessels are caused by the
accumulation of lipid-laden macrophages (foam cells) within the
arterial walls, leading to the formation of a plaque.
6. Optimal lipid panal results Total cholesterol (< 200), LDL (< 100), triglycerides (< 150)
7. What is the re- The earliest event in atherogenesis is injury to the endothelium, which
sponse-to-injury hypothe- could be triggered by hypertension, circulation of ROS (smoking,
sis in the development of pollutants), dyslipidemia, and elevated A1C.
atherosclerotic lesions?
8. When foam cells accu- a lesion called a fatty streak; inflammatory cytokines, damaging en-
mulate in a significant zymes, and growth factors.
amount within the arteri-
, NSG 533 Advanced Pathophysiology Exam 3
al wall, they form ______ .
What is then released?
9. Growth factors released smooth muscle cell proliferation; produce collagen and migrate over
released in atherogenesis the fatty streak to form a fibrous plaque.
stimulate _______ , which
________ .
10. Plaques that have rup- complicated plaques
tured are called ______ .
11. Plaque rupture occurs be- inflammatory activation of proteinases, apoptosis of cells within the
cause of the ______ . plaque, and bleeding within the lesion (plaque hemorrhage).
12. What happens once a The underlying tissue is exposed and causes platelet adhesion, initi-
plaque ruptures? ation of the clotting cascade, and rapid thrombus formation that can
suddenly occlude the vessel, resulting in ischemia and infarction.
13. Stable atheromatous le- A fibrous plaque that has calcified, protruded into the vessel lumen,
sions and obstructs blood flow, causing chest pain during exercise (stable
angina)
14. Unstable atheromatous Plaques that are prone to rupture even before they affect blood flow
lesions (clinically silent until rupture). The fibrous cap is typically thinner in
an unstable plaque.
15. List the acute coronary Unstable angina, NSTEMI, and STEMI
syndromes
16. What are the clinical fea- Chest pain at rest, new-onset, or increasing in severity or frequency.
tures and physical exam ST segment depression and T wave inversion that often resolves with
findings in unstable angi- relief of pain, transient abnormal heart sounds. Possible tachycardia
na? and pulmonary congestion. Patient might be dyspneic, diaphoretic,
or anxious. Troponin and CK are normal.
1. List the novel risk factors 1) markers of inflammation, ischemia, and thrombosis (elevated high
for CAD sensitivity C-reactive protein, troponin, fibrinogen) 2) adipokines
(leptin, adiponectin) 3) CKD 4) air pollution and ionizing radiation
5) medications (NSAIDs) 6) coronary artery calcification and carotid
wall thickness and 7) microbiome 8) small dense LDL particles and
lipoprotein(a) 9) Hyperhomocysteinemia
2. List nonmodifiable risk Advanced age, male gender or woman after menopause, and family
factors for CAD history (genetics, shared environmental exposure).
3. List modifiable risk factors Dyslipidemia, hypertension, cigarette smoking, diabetes and insulin
for CAD resistance, obesity and sedentary lifestyle, and an atherogenic diet.
4. How does dyslipidemia High levels of LDL in the bloodstream leads to LDL oxidation, migra-
contribute to CAD? tion into the vessel wall, and phagocytosis by macrophages, all key
steps in the pathogenesis of atherosclerosis.
5. Atherosclerosis A chronic inflammatory condition that results in damage to the ar-
teries. Thickening and hardening of the vessels are caused by the
accumulation of lipid-laden macrophages (foam cells) within the
arterial walls, leading to the formation of a plaque.
6. Optimal lipid panal results Total cholesterol (< 200), LDL (< 100), triglycerides (< 150)
7. What is the re- The earliest event in atherogenesis is injury to the endothelium, which
sponse-to-injury hypothe- could be triggered by hypertension, circulation of ROS (smoking,
sis in the development of pollutants), dyslipidemia, and elevated A1C.
atherosclerotic lesions?
8. When foam cells accu- a lesion called a fatty streak; inflammatory cytokines, damaging en-
mulate in a significant zymes, and growth factors.
amount within the arteri-
, NSG 533 Advanced Pathophysiology Exam 3
al wall, they form ______ .
What is then released?
9. Growth factors released smooth muscle cell proliferation; produce collagen and migrate over
released in atherogenesis the fatty streak to form a fibrous plaque.
stimulate _______ , which
________ .
10. Plaques that have rup- complicated plaques
tured are called ______ .
11. Plaque rupture occurs be- inflammatory activation of proteinases, apoptosis of cells within the
cause of the ______ . plaque, and bleeding within the lesion (plaque hemorrhage).
12. What happens once a The underlying tissue is exposed and causes platelet adhesion, initi-
plaque ruptures? ation of the clotting cascade, and rapid thrombus formation that can
suddenly occlude the vessel, resulting in ischemia and infarction.
13. Stable atheromatous le- A fibrous plaque that has calcified, protruded into the vessel lumen,
sions and obstructs blood flow, causing chest pain during exercise (stable
angina)
14. Unstable atheromatous Plaques that are prone to rupture even before they affect blood flow
lesions (clinically silent until rupture). The fibrous cap is typically thinner in
an unstable plaque.
15. List the acute coronary Unstable angina, NSTEMI, and STEMI
syndromes
16. What are the clinical fea- Chest pain at rest, new-onset, or increasing in severity or frequency.
tures and physical exam ST segment depression and T wave inversion that often resolves with
findings in unstable angi- relief of pain, transient abnormal heart sounds. Possible tachycardia
na? and pulmonary congestion. Patient might be dyspneic, diaphoretic,
or anxious. Troponin and CK are normal.
