NSG 533 ADVANCED PATHOPHYSIOLOGY EXAM
3 QUESTIONS & ANSWERS LATEST
( A+ GRADED 100% VERIFIED)
List the novel risk factors for CAD - Answer - 1) markers of inflammation, ischemia, and
thrombosis (elevated high 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
List nonmodifiable risk factors for CAD - Answer - Advanced age, male gender or
woman after menopause, and family history (genetics, shared environmental exposure).
List modifiable risk factors for CAD - Answer - Dyslipidemia, hypertension, cigarette
smoking, diabetes and insulin resistance, obesity and sedentary lifestyle, and an
atherogenic diet.
How does dyslipidemia contribute to CAD? - Answer - High levels of LDL in the
bloodstream leads to LDL oxidation, migration into the vessel wall, and phagocytosis by
macrophages, all key steps in the pathogenesis of atherosclerosis.
Atherosclerosis - Answer - A chronic inflammatory condition that results in damage to
the arteries. 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.
Optimal lipid panal results - Answer - Total cholesterol (< 200), LDL (< 100),
triglycerides (< 150)
What is the response-to-injury hypothesis in the development of atherosclerotic lesions?
- Answer - The earliest event in atherogenesis is injury to the endothelium, which could
be triggered by hypertension, circulation of ROS (smoking, pollutants), dyslipidemia,
and elevated A1C.
When foam cells accumulate in a significant amount within the arterial wall, they form
______ . What is then released? - Answer - a lesion called a fatty streak; inflammatory
cytokines, damaging enzymes, and growth factors.
, Growth factors released released in atherogenesis stimulate _______ , which ________
. - Answer - smooth muscle cell proliferation; produce collagen and migrate over the
fatty streak to form a fibrous plaque.
Plaques that have ruptured are called ______ . - Answer - complicated plaques
Plaque rupture occurs because of the ______ . - Answer - inflammatory activation of
proteinases, apoptosis of cells within the plaque, and bleeding within the lesion (plaque
hemorrhage).
What happens once a plaque ruptures? - Answer - The underlying tissue is exposed
and causes platelet adhesion, initiation of the clotting cascade, and rapid thrombus
formation that can suddenly occlude the vessel, resulting in ischemia and infarction.
Stable atheromatous lesions - Answer - A fibrous plaque that has calcified, protruded
into the vessel lumen, and obstructs blood flow, causing chest pain during exercise
(stable angina)
Unstable atheromatous lesions - Answer - Plaques that are prone to rupture even
before they affect blood flow (clinically silent until rupture). The fibrous cap is typically
thinner in an unstable plaque.
List the acute coronary syndromes - Answer - Unstable angina, NSTEMI, and STEMI
What are the clinical features and physical exam findings in unstable angina? - Answer -
Chest pain at rest, new-onset, or increasing in severity or frequency. ST segment
depression and T wave inversion that often resolves with relief of pain, transient
abnormal 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 in a NSTEMI? - Answer - ST
depression and T wave inversion, early peak in CK level, and small elevation in
troponin.
What are the clinical features and physical exam findings in a STEMI? - Answer - ST
elevation, T wave inversion, and pathological Q waves. Elevation of CK, CK-MB,
myoglobin (peaks 1-4 hrs), troponin (begins to rise at 3 hrs), and LDH. Patient has
anxiety, cold perspiration and pallor, variable HR and BP response.
3 QUESTIONS & ANSWERS LATEST
( A+ GRADED 100% VERIFIED)
List the novel risk factors for CAD - Answer - 1) markers of inflammation, ischemia, and
thrombosis (elevated high 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
List nonmodifiable risk factors for CAD - Answer - Advanced age, male gender or
woman after menopause, and family history (genetics, shared environmental exposure).
List modifiable risk factors for CAD - Answer - Dyslipidemia, hypertension, cigarette
smoking, diabetes and insulin resistance, obesity and sedentary lifestyle, and an
atherogenic diet.
How does dyslipidemia contribute to CAD? - Answer - High levels of LDL in the
bloodstream leads to LDL oxidation, migration into the vessel wall, and phagocytosis by
macrophages, all key steps in the pathogenesis of atherosclerosis.
Atherosclerosis - Answer - A chronic inflammatory condition that results in damage to
the arteries. 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.
Optimal lipid panal results - Answer - Total cholesterol (< 200), LDL (< 100),
triglycerides (< 150)
What is the response-to-injury hypothesis in the development of atherosclerotic lesions?
- Answer - The earliest event in atherogenesis is injury to the endothelium, which could
be triggered by hypertension, circulation of ROS (smoking, pollutants), dyslipidemia,
and elevated A1C.
When foam cells accumulate in a significant amount within the arterial wall, they form
______ . What is then released? - Answer - a lesion called a fatty streak; inflammatory
cytokines, damaging enzymes, and growth factors.
, Growth factors released released in atherogenesis stimulate _______ , which ________
. - Answer - smooth muscle cell proliferation; produce collagen and migrate over the
fatty streak to form a fibrous plaque.
Plaques that have ruptured are called ______ . - Answer - complicated plaques
Plaque rupture occurs because of the ______ . - Answer - inflammatory activation of
proteinases, apoptosis of cells within the plaque, and bleeding within the lesion (plaque
hemorrhage).
What happens once a plaque ruptures? - Answer - The underlying tissue is exposed
and causes platelet adhesion, initiation of the clotting cascade, and rapid thrombus
formation that can suddenly occlude the vessel, resulting in ischemia and infarction.
Stable atheromatous lesions - Answer - A fibrous plaque that has calcified, protruded
into the vessel lumen, and obstructs blood flow, causing chest pain during exercise
(stable angina)
Unstable atheromatous lesions - Answer - Plaques that are prone to rupture even
before they affect blood flow (clinically silent until rupture). The fibrous cap is typically
thinner in an unstable plaque.
List the acute coronary syndromes - Answer - Unstable angina, NSTEMI, and STEMI
What are the clinical features and physical exam findings in unstable angina? - Answer -
Chest pain at rest, new-onset, or increasing in severity or frequency. ST segment
depression and T wave inversion that often resolves with relief of pain, transient
abnormal 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 in a NSTEMI? - Answer - ST
depression and T wave inversion, early peak in CK level, and small elevation in
troponin.
What are the clinical features and physical exam findings in a STEMI? - Answer - ST
elevation, T wave inversion, and pathological Q waves. Elevation of CK, CK-MB,
myoglobin (peaks 1-4 hrs), troponin (begins to rise at 3 hrs), and LDH. Patient has
anxiety, cold perspiration and pallor, variable HR and BP response.
