NURS 210 Exam 2: Cardiac Review Questions
and Answers 100% Solved
Atherosclerosis: -Atherosclerotic plaque formation
-Injury to the endothelium (coronary arteries and peripheral arterial walls)
-Cigarette smoking injury endothelium
-Chronic hemodynamic wall stress (hypertension)
-Increased risk for permeability
-LDL molecules into vessel wall
-Oxidized damage to endothelium
-Macrophages arrive and engulf lipids - foam cells
-Causes inflammatory mediators to release
Lipid core Excess lipid and debris accumulate in vessel wall
Plaques with a large lipid core are prone to rupture
C-reactive protein (CRP) Marker of inflammation
,Elevated levels indicate an increased risk for disease state
Formation of atherosclerosis 1. Ruptured plaque
2. Platelet aggregation
3. Thrombus formation
Elevated LDL and cholesterol increase the risk for atherosclerosis True
Arteriosclerosis Any thickening or hardening of the arterial wall
Atherosclerosis and coronary heart disease: Almost all caused by atherosclerosis
Insufficient delivery of oxygen to the heart (ischemic heart disease)
Treatment: Lower cholesterol levels in the blood
Decrease LDL
Increase HDL
-Prescribed medicine
, -Healthy diet (DASH diet)
-Losing weight
-Exercise (increases HDL)
Hydroxymethylglutaryl Coenzyme A reductase inhibitors Statins
-Prevent nonfatal and fatal ASCVD (atherosclerotic cardiovascular disease) events
-Reduce the risk of disability from nonfatal stroke (women greater risk than men)
4 statin benefit groups: -Individuals with clinical ASCVD
-With primary elevations of LDL >190 mg/dl
-40-75 years with DM with LDL 70-189 mg/dl
-Without clinical ASCVD or DM 40-75 y.o. LDL 70-189 mg/dl with estimated 10-year ASCVD risk
7.5% or higher
Clinical ASCVD -Acute coronary syndrome
-History of MI
-Stable or unstable angina
and Answers 100% Solved
Atherosclerosis: -Atherosclerotic plaque formation
-Injury to the endothelium (coronary arteries and peripheral arterial walls)
-Cigarette smoking injury endothelium
-Chronic hemodynamic wall stress (hypertension)
-Increased risk for permeability
-LDL molecules into vessel wall
-Oxidized damage to endothelium
-Macrophages arrive and engulf lipids - foam cells
-Causes inflammatory mediators to release
Lipid core Excess lipid and debris accumulate in vessel wall
Plaques with a large lipid core are prone to rupture
C-reactive protein (CRP) Marker of inflammation
,Elevated levels indicate an increased risk for disease state
Formation of atherosclerosis 1. Ruptured plaque
2. Platelet aggregation
3. Thrombus formation
Elevated LDL and cholesterol increase the risk for atherosclerosis True
Arteriosclerosis Any thickening or hardening of the arterial wall
Atherosclerosis and coronary heart disease: Almost all caused by atherosclerosis
Insufficient delivery of oxygen to the heart (ischemic heart disease)
Treatment: Lower cholesterol levels in the blood
Decrease LDL
Increase HDL
-Prescribed medicine
, -Healthy diet (DASH diet)
-Losing weight
-Exercise (increases HDL)
Hydroxymethylglutaryl Coenzyme A reductase inhibitors Statins
-Prevent nonfatal and fatal ASCVD (atherosclerotic cardiovascular disease) events
-Reduce the risk of disability from nonfatal stroke (women greater risk than men)
4 statin benefit groups: -Individuals with clinical ASCVD
-With primary elevations of LDL >190 mg/dl
-40-75 years with DM with LDL 70-189 mg/dl
-Without clinical ASCVD or DM 40-75 y.o. LDL 70-189 mg/dl with estimated 10-year ASCVD risk
7.5% or higher
Clinical ASCVD -Acute coronary syndrome
-History of MI
-Stable or unstable angina
