NSG 533/ NSG533 Exam 3 V1 – Advanced
Pharmacology Guide| Wilkes (Latest 2026/ 2027
Update) 100% Verified Questions & Answers |
Grade A
List the novel risk factors for CAD
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
Advanced age, male gender or woman after menopause, and family history (genetics, shared
environmental exposure).
List modifiable risk factors for CAD
Dyslipidemia, hypertension, cigarette smoking, diabetes and insulin resistance, obesity and
sedentary lifestyle, and an atherogenic diet.
How does dyslipidemia contribute to CAD?
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
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
Total cholesterol (< 200), LDL (< 100), triglycerides (< 150)
What is the response-to-injury hypothesis in the development of atherosclerotic lesions?
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?
a lesion called a fatty streak; inflammatory cytokines, damaging enzymes, and growth factors.
Growth factors released released in atherogenesis stimulate , which .
smooth muscle cell proliferation; produce collagen and migrate over the fatty streak to form a
fibrous plaque.
Plaques that have ruptured are called .
complicated plaques
, Plaque rupture occurs because of the .
inflammatory activation of proteinases, apoptosis of cells within the plaque, and bleeding within
the lesion (plaque hemorrhage).
What happens once a plaque ruptures?
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
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
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
Unstable angina, NSTEMI, and STEMI
What are the clinical features and physical exam findings in unstable angina?
Pharmacology Guide| Wilkes (Latest 2026/ 2027
Update) 100% Verified Questions & Answers |
Grade A
List the novel risk factors for CAD
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
Advanced age, male gender or woman after menopause, and family history (genetics, shared
environmental exposure).
List modifiable risk factors for CAD
Dyslipidemia, hypertension, cigarette smoking, diabetes and insulin resistance, obesity and
sedentary lifestyle, and an atherogenic diet.
How does dyslipidemia contribute to CAD?
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
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
Total cholesterol (< 200), LDL (< 100), triglycerides (< 150)
What is the response-to-injury hypothesis in the development of atherosclerotic lesions?
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?
a lesion called a fatty streak; inflammatory cytokines, damaging enzymes, and growth factors.
Growth factors released released in atherogenesis stimulate , which .
smooth muscle cell proliferation; produce collagen and migrate over the fatty streak to form a
fibrous plaque.
Plaques that have ruptured are called .
complicated plaques
, Plaque rupture occurs because of the .
inflammatory activation of proteinases, apoptosis of cells within the plaque, and bleeding within
the lesion (plaque hemorrhage).
What happens once a plaque ruptures?
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
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
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
Unstable angina, NSTEMI, and STEMI
What are the clinical features and physical exam findings in unstable angina?
