Pathophysiology NSG 533 Exam 3 UPDATED ACTUAL Exam Questions and CORRECT Answers

Pathophysiology NSG 533 Exam 3
UPDATED ACTUAL Exam Questions and CORRECT Answers

Question 1.
(6) Traditional modifiable risk factors for CAD

Correct Answer: (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)


Question 2.
(10) Novel risk factors for CAD

Correct Answer: (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)


Question 3.
Lipids

Correct Answer: Refers to cholesterol in particular. Required by most cells for
manufacture/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


Question 4.
Lipoproteins

Correct Answer: 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


Question 5.
Atherosclerosis

Correct Answer: - Progressive, multifactorial disease process that generally
begins 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


Question 6.
Describe the relationship between HDL (high-density lipoprotein), LDL (low- density
lipoprotein), VLDL (very-low-density lipoprotein), and CAD

Correct Answer: Low levels of HDL pose risk for CAD. HDL is responsible for
returning excessive cholesterol 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


Question 7.
Total Cholesterol risk levels for CAD (dyslipidemia criteria)

Correct Answer: <200 = desirable 200-239 = borderline ≥240 = high


Question 8.
LDL risk levels for CAD (dyslipidemia criteria)

Correct Answer: <100 = optimal 100-129 = near optimal 130-159 = borderline
160-189 = high ≥190 = very high


Question 9.
HDL risk levels for CAD (dyslipidemia criteria)

Correct Answer: <40 = low ≥60 = high


Question 10.
Triglyceride risk levels for CAD (dyslipidemia criteria)

Correct Answer: <150 = desirable 150-199 = borderline 200-499 = high ≥500
= very high
• Atherosclerotic plaque/lesion -✓✓- Likely to develop following endothelial
injury; areas of increased shear wall stress are especially vulnerable
Fatty streak → Fibrous-fatty plaque → Advanced complicated lesion

, Question 11.
Fatty streak (early damage to vessel wall)

Correct Answer: - Focal thickening of the intima
- Increase in smooth muscle cells and extracellular matrix
- Smooth muscle cells migrate and proliferate into the intima
- Lipid deposits accumulate
- Macrophages and T-lymphocytes (early damage to vessel wall)


Question 12.
Fibrous-fatty plaque (evolves from fatty streak)

Correct Answer: - Accumulation of connective tissue
- Increased number of smooth muscle cells laden with lipids
- Deeper extracellular lipid pool
- Results in further endothelial cell dysfunction, necrosis of underlying vessel
tissue, and narrowing of the lumen as the lesion protrudes out from the vessel
wall


Question 13.
Advanced complicated lesion

Correct Answer: - Smooth muscle cells, numerous macrophages, T-cells , often
associated with lipid core and necrotic material
- Covered by a fibrous cap (smooth muscle cells surrounded by CT matrix)
- Thick cap - provides stability to the lesion
- Thin, non-uniform cap, macrophage-rich - lesion is unstable
- Thrombosis, hemorrhage, and/or calcification


Question 14.
Response to Injury Hypothesis

Correct Answer: (1) Endothelial cell dysfunction (2) Macrophage involvement
(3) Smooth Muscle cell involvement (4) Hyperlipidemia


Question 15.
Describe the response-to-injury hypothesis for the development of atherosclerotic
lesions

Correct Answer: - Various sources or risk factors may induce some form of
endothelial dysfunction/changes including alterations in permeability,
adhesive characteristics, and growth-stimulatory characteristics - These
changes/alterations lead to monocyte-endothelial attachment, adherence, and
transmigration - Monocytes then enter the sub-endothelium, become
activated as macrophages, and be joined by T-cells - Macrophages and T
lymphocytes compose the first lesion of atherosclerosis - the fatty streak -