NSG 533 Advanced Pathophysiology Exam 3
Study online at https://quizlet.com/_cy8wko
1) markers of inflammation, ischemia, and thrombosis
(elevated high sensitivity C-reactive protein, troponin, fib-
rinogen) 2) adipokines (leptin, adiponectin) 3) CKD 4) air
List the novel risk factors for CAD 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
Advanced age, male gender or woman after menopause,
List nonmodifiable risk factors for CAD and family history (genetics, shared environmental expo-
sure).
Dyslipidemia, hypertension, cigarette smoking, diabetes
List modifiable risk factors for CAD and insulin resistance, obesity and sedentary lifestyle, and
an atherogenic diet.
High levels of LDL in the bloodstream leads to LDL oxida-
tion, migration into the vessel wall, and phagocytosis by
How does dyslipidemia contribute to CAD?
macrophages, all key steps in the pathogenesis of ather-
osclerosis.
A chronic inflammatory condition that results in damage to
the arteries. Thickening and hardening of the vessels are
Atherosclerosis caused by the accumulation of lipid-laden macrophages
(foam cells) within the arterial walls, leading to the forma-
tion of a plaque.
Optimal lipid panal results Total cholesterol (< 200), LDL (< 100), triglycerides (< 150)
The earliest event in atherogenesis is injury to the en-
What is the response-to-injury hypothesis in the develop- dothelium, which could be triggered by hypertension, cir-
ment of atherosclerotic lesions? culation of ROS (smoking, pollutants), dyslipidemia, and
elevated A1C.
a lesion called a fatty streak; inflammatory cytokines, dam-
aging enzymes, and growth factors.
, NSG 533 Advanced Pathophysiology Exam 3
Study online at https://quizlet.com/_cy8wko
When foam cells accumulate in a significant amount with-
in the arterial wall, they form ______ . What is then re-
leased?
Growth factors released released in atherogenesis stimu- smooth muscle cell proliferation; produce collagen and
late _______ , which ________ . migrate over the fatty streak to form a fibrous plaque.
Plaques that have ruptured are called ______ . complicated plaques
inflammatory activation of proteinases, apoptosis of cells
Plaque rupture occurs because of the ______ . within the plaque, and bleeding within the lesion (plaque
hemorrhage).
The underlying tissue is exposed and causes platelet ad-
hesion, initiation of the clotting cascade, and rapid throm-
What happens once a plaque ruptures?
bus formation that can suddenly occlude the vessel, re-
sulting in ischemia and infarction.
A fibrous plaque that has calcified, protruded into the
Stable atheromatous lesions vessel lumen, and obstructs blood flow, causing chest pain
during exercise (stable angina)
Plaques that are prone to rupture even before they affect
Unstable atheromatous lesions blood flow (clinically silent until rupture). The fibrous cap
is typically thinner in an unstable plaque.
List the acute coronary syndromes Unstable angina, NSTEMI, and STEMI
Chest pain at rest, new-onset, or increasing in severity or
frequency. ST segment depression and T wave inversion
What are the clinical features and physical exam findings that often resolves with relief of pain, transient abnor-
in unstable angina? mal heart sounds. Possible tachycardia and pulmonary
congestion. Patient might be dyspneic, diaphoretic, or
anxious. Troponin and CK are normal.
What are the clinical features and physical exam findings ST depression and T wave inversion, early peak in CK level,
in a NSTEMI? and small elevation in troponin.
What are the clinical features and physical exam findings
in a STEMI?
Study online at https://quizlet.com/_cy8wko
1) markers of inflammation, ischemia, and thrombosis
(elevated high sensitivity C-reactive protein, troponin, fib-
rinogen) 2) adipokines (leptin, adiponectin) 3) CKD 4) air
List the novel risk factors for CAD 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
Advanced age, male gender or woman after menopause,
List nonmodifiable risk factors for CAD and family history (genetics, shared environmental expo-
sure).
Dyslipidemia, hypertension, cigarette smoking, diabetes
List modifiable risk factors for CAD and insulin resistance, obesity and sedentary lifestyle, and
an atherogenic diet.
High levels of LDL in the bloodstream leads to LDL oxida-
tion, migration into the vessel wall, and phagocytosis by
How does dyslipidemia contribute to CAD?
macrophages, all key steps in the pathogenesis of ather-
osclerosis.
A chronic inflammatory condition that results in damage to
the arteries. Thickening and hardening of the vessels are
Atherosclerosis caused by the accumulation of lipid-laden macrophages
(foam cells) within the arterial walls, leading to the forma-
tion of a plaque.
Optimal lipid panal results Total cholesterol (< 200), LDL (< 100), triglycerides (< 150)
The earliest event in atherogenesis is injury to the en-
What is the response-to-injury hypothesis in the develop- dothelium, which could be triggered by hypertension, cir-
ment of atherosclerotic lesions? culation of ROS (smoking, pollutants), dyslipidemia, and
elevated A1C.
a lesion called a fatty streak; inflammatory cytokines, dam-
aging enzymes, and growth factors.
, NSG 533 Advanced Pathophysiology Exam 3
Study online at https://quizlet.com/_cy8wko
When foam cells accumulate in a significant amount with-
in the arterial wall, they form ______ . What is then re-
leased?
Growth factors released released in atherogenesis stimu- smooth muscle cell proliferation; produce collagen and
late _______ , which ________ . migrate over the fatty streak to form a fibrous plaque.
Plaques that have ruptured are called ______ . complicated plaques
inflammatory activation of proteinases, apoptosis of cells
Plaque rupture occurs because of the ______ . within the plaque, and bleeding within the lesion (plaque
hemorrhage).
The underlying tissue is exposed and causes platelet ad-
hesion, initiation of the clotting cascade, and rapid throm-
What happens once a plaque ruptures?
bus formation that can suddenly occlude the vessel, re-
sulting in ischemia and infarction.
A fibrous plaque that has calcified, protruded into the
Stable atheromatous lesions vessel lumen, and obstructs blood flow, causing chest pain
during exercise (stable angina)
Plaques that are prone to rupture even before they affect
Unstable atheromatous lesions blood flow (clinically silent until rupture). The fibrous cap
is typically thinner in an unstable plaque.
List the acute coronary syndromes Unstable angina, NSTEMI, and STEMI
Chest pain at rest, new-onset, or increasing in severity or
frequency. ST segment depression and T wave inversion
What are the clinical features and physical exam findings that often resolves with relief of pain, transient abnor-
in unstable angina? mal heart sounds. Possible tachycardia and pulmonary
congestion. Patient might be dyspneic, diaphoretic, or
anxious. Troponin and CK are normal.
What are the clinical features and physical exam findings ST depression and T wave inversion, early peak in CK level,
in a NSTEMI? and small elevation in troponin.
What are the clinical features and physical exam findings
in a STEMI?
