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Wilkes NSG 533 Exam 3 Advanced Pharmacology Study Guide 2025, 100% Verified. $11.49
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Wilkes NSG 533 Exam 3 Advanced Pharmacology Study Guide 2025, 100% Verified.
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Wilkes NSG 533 Exam 3 Advanced Pharmacology Study Guide 2025, 100% Verified. Ace your Wilkes University NSG 533 Exam 3 with the 2025 Advanced Pharmacology Study Guide, expertly designed for advanced nursing students preparing for this critical assessment. This comprehensive guide focuses on co...

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  • May 15, 2025
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NSG533 / NSG 533

EXAM 3 STUDY GUIDE

Advanced Pharmacology - Wilkes




THIS GUIDE CONTAINS:

NSG 533 Exam 3 Study Guide

key Terms and Definitions

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,1. (5) Non-modifiable risk factors for CAD:
(1) Age
(2) Gender
(3) Ethnicity
(4) Family history
(5) Genetic predisposition


2. (6) Traditional modifiable risk factors for CAD:
(1) Dyslipidemia (abnormal serum lipoproteins)
(2) HTN (endothelial injury and myocardial hypertrophy)
(3) Cigarette Smoking (endothelial injury and oxygen radicals)
(4) Diabetes (endothelial injury and vessel wall damage)
(5) Obesity/Sedentary Lifestyle (strongest link to CAD)
(6) Atherogenic Diet (high in salt, fat, trans fat, carbs)


3. (10) Novel risk factors for CAD:
(1) Markers of Inflammation, ischemia and thrombosis (c-reactive protein,
troponin, fibrinogen)
(2) Adipokines (adiponectin, leptin)
(3) CKD (as GFR declines, risk for CAD increases)
(4) Air Pollution and Ionizing Radiation
(5) Medications (NSAIDS increase risk for CAD)
(6) Coronary Artery Calcification and Carotid Artery Wall Thickness
(7) Microbiome (diet/lifestyle)
(8) Elevated Fibrinogen (inflammatory marker)
(9) Elevated LDL particle number (cholesterol concentration within particles)


,(10) Small, dense LDLs (vs. large fluffy lipoprotein)
4. Lipids:
Refers to cholesterol in particular. Required by most cells for manufac-
ture/repair of plasma membranes.


High dietary intake of cholesterol and fats results in high levels of LDL in the
bloodstream, which can lead to Atherosclerosis and contribute to CAD


5. Lipoproteins:
Refers to lipids, phospholipids, cholesterol, and triglycerides bound to
carrier proteins.


- LDL (low-density lipoprotein):
contain mostly cholesterol and protein.
- HDL (high-density lipoprotein):
mainly phospholipids and protein
- VLDL (very-low-density lipoprotein):
mainly triglyceride and protein


6. Atherosclerosis:
- Progressive, multifactorial disease process that generally be- gins in childhood;
clinical manifestations occur in middle to late adulthood, that results in the
variable composition of lesions


- High dietary intake of cholesterol and fats results in high levels of LDL in the





, bloodstream. LDL oxidation, migration into the vessel wall, and phagocytosis by
macrophages result in fatty deposits called plaques to form on the inner walls of
the arteries


7. Describe the relationship between HDL (high-density lipoprotein), LDL
(low-density lipoprotein), VLDL (very-low-density lipoprotein), and CAD:
Low levels of HDL pose risk for CAD. HDL is responsible for returning excessive
choles- terol to the liver for elimination or conversion to cholesterol-containing
steroids. HDL can also remove excessive cholesterol through the arterial wall. It
can protect LDL from oxidation, preserve endothelial function, and promote anti-
inflammatory and antithrombotic effects. VLDL pose risk for CAD, especially in
combination with other risk factors such as diabetes


8. Total Cholesterol risk levels for CAD (dyslipidemia criteria):
<200 = desirable 200-239 = borderline
e240 =high


9. LDL risk levels for CAD (dyslipidemia criteria):
<100 = optimal 100-129 = near optimal
130-159 = borderline
160-189 = high
e190 =very high


10. HDL risk levels for CAD (dyslipidemia criteria):
<40 = low e60 =high

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