NSG 533 Advanced Pathophysiology Exam 3
Study online at https://quizlet.com/_cy8wko
1. List the novel risk factors 1) markers of inflammation, ischemia, and
for CAD thrombosis (elevated high sensitivity C-reactive
protein, troponin, fibrinogen) 2) adipokines (lep-
tin, adiponectin) 3) CKD 4) air pollution and ion-
izing radiation 5) medications (NSAIDs) 6) coro-
nary artery calcification and carotid wall thick-
ness and 7) microbiome 8) small dense LDL
particles and lipoprotein(a) 9) Hyperhomocys-
teinemia
2. List nonmodifiable risk Advanced age, male gender or woman after
factors for CAD menopause, and family history (genetics, shared
environmental exposure).
3. List modifiable risk fac- Dyslipidemia, hypertension, cigarette smoking,
tors for CAD diabetes and insulin resistance, obesity and
sedentary lifestyle, and an atherogenic diet.
4. How does dyslipidemia High levels of LDL in the bloodstream leads to
contribute to CAD? LDL oxidation, migration 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 arteries. Thickening and harden-
ing of the vessels are caused by the accumu-
lation 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), triglyc-
erides (< 150)
7. What is the re- The earliest event in atherogenesis is injury to
sponse-to-injury hypothe- the endothelium, which could be triggered by
sis in the development of hypertension, circulation of ROS (smoking, pol-
atherosclerotic lesions? lutants), dyslipidemia, and elevated A1C.
8. When foam cells accu- a lesion called a fatty streak; inflammatory cy-
mulate in a significant tokines, damaging enzymes, and growth factors.
, NSG 533 Advanced Pathophysiology Exam 3
Study online at https://quizlet.com/_cy8wko
amount within the arteri-
al wall, they form ______ .
What is then released?
9. Growth factors released smooth muscle cell proliferation; produce colla-
released in atherogenesis gen and migrate over the fatty streak to form a
stimulate _______ , which fibrous plaque.
________ .
10. Plaques that have rup- complicated plaques
tured are called ______ .
11. Plaque rupture occurs be- inflammatory activation of proteinases, apopto-
cause of the ______ . sis of cells within the plaque, and bleeding within
the lesion (plaque hemorrhage).
12. What happens once a The underlying tissue is exposed and causes
plaque ruptures? platelet adhesion, initiation of the clotting cas-
cade, and rapid thrombus formation that can
suddenly occlude the vessel, resulting in is-
chemia and infarction.
13. Stable atheromatous le- A fibrous plaque that has calcified, protruded into
sions the vessel lumen, and obstructs blood flow, caus-
ing chest pain during exercise (stable angina)
14. Unstable atheromatous Plaques that are prone to rupture even before
lesions they affect blood flow (clinically silent until rup-
ture). 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
tures and physical exam severity or frequency. ST segment depression
findings in unstable angi- and T wave inversion that often resolves with
na? relief of pain, transient abnormal heart sounds.
Possible tachycardia and pulmonary congestion.
Study online at https://quizlet.com/_cy8wko
1. List the novel risk factors 1) markers of inflammation, ischemia, and
for CAD thrombosis (elevated high sensitivity C-reactive
protein, troponin, fibrinogen) 2) adipokines (lep-
tin, adiponectin) 3) CKD 4) air pollution and ion-
izing radiation 5) medications (NSAIDs) 6) coro-
nary artery calcification and carotid wall thick-
ness and 7) microbiome 8) small dense LDL
particles and lipoprotein(a) 9) Hyperhomocys-
teinemia
2. List nonmodifiable risk Advanced age, male gender or woman after
factors for CAD menopause, and family history (genetics, shared
environmental exposure).
3. List modifiable risk fac- Dyslipidemia, hypertension, cigarette smoking,
tors for CAD diabetes and insulin resistance, obesity and
sedentary lifestyle, and an atherogenic diet.
4. How does dyslipidemia High levels of LDL in the bloodstream leads to
contribute to CAD? LDL oxidation, migration 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 arteries. Thickening and harden-
ing of the vessels are caused by the accumu-
lation 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), triglyc-
erides (< 150)
7. What is the re- The earliest event in atherogenesis is injury to
sponse-to-injury hypothe- the endothelium, which could be triggered by
sis in the development of hypertension, circulation of ROS (smoking, pol-
atherosclerotic lesions? lutants), dyslipidemia, and elevated A1C.
8. When foam cells accu- a lesion called a fatty streak; inflammatory cy-
mulate in a significant tokines, damaging enzymes, and growth factors.
, NSG 533 Advanced Pathophysiology Exam 3
Study online at https://quizlet.com/_cy8wko
amount within the arteri-
al wall, they form ______ .
What is then released?
9. Growth factors released smooth muscle cell proliferation; produce colla-
released in atherogenesis gen and migrate over the fatty streak to form a
stimulate _______ , which fibrous plaque.
________ .
10. Plaques that have rup- complicated plaques
tured are called ______ .
11. Plaque rupture occurs be- inflammatory activation of proteinases, apopto-
cause of the ______ . sis of cells within the plaque, and bleeding within
the lesion (plaque hemorrhage).
12. What happens once a The underlying tissue is exposed and causes
plaque ruptures? platelet adhesion, initiation of the clotting cas-
cade, and rapid thrombus formation that can
suddenly occlude the vessel, resulting in is-
chemia and infarction.
13. Stable atheromatous le- A fibrous plaque that has calcified, protruded into
sions the vessel lumen, and obstructs blood flow, caus-
ing chest pain during exercise (stable angina)
14. Unstable atheromatous Plaques that are prone to rupture even before
lesions they affect blood flow (clinically silent until rup-
ture). 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
tures and physical exam severity or frequency. ST segment depression
findings in unstable angi- and T wave inversion that often resolves with
na? relief of pain, transient abnormal heart sounds.
Possible tachycardia and pulmonary congestion.
