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LEADERSHIP N250 UNIT 2 EXAM QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS GRADED A++

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LEADERSHIP N250 UNIT 2 EXAM QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS GRADED A++ How is CAD characterized? and ACS (acute coronary syndrome)? -CAD—asymptomatic or chronic stable angina (chest pain) -Acute coronary syndrome (ACS) —unstable angina (UA) or myocardial infarction (MI) CAD negatively affects cardiac function; impaired ___________ ____________ and decreased perfusion cardiac output Facts about atherosclerosis •major cause of CAD •Characterized by lipid deposits within intima of artery •Endothelial injury and inflammation play a major role in development How does CAD progress? First stage? pathophysiology? •Fatty streak: earliest lesion; lipid filled smooth muscle cells; appears yellow •Start ~age 20 and increase as age •Tx to lower low-density lipoproteins (LDL) may slow process Second stage of CAD? pathophysiology? •Fibrous plaque •Beginning of progressive change in endothelium; ~age 30 •LDLs & growth factors stimulate smooth muscle proliferation & arterial wall thickens •Cholesterol & other lipids move into intima •Collagen covers & form grayish-whitish fibrous plaque w/ smooth or jagged edges •Narrowed vessel lumen reduces distal blood flow Third stage of CAD? pathophysiology? •Complicated lesion •Fibrous plaque grows; continued inflammation leads to plaque instability, ulceration, & rupture •Platelets accumulate resulting in thrombus that further narrows or occludes artery •Activation of platelets causes expression of glycoprotein IIb/IIIa receptors to bind fibrinogen resulting in increased size of thrombus Fourth stage of CAD? pathophysiology? •Collateral circulation •Arterial anastomoses (or connections) within coronary circulation •Contributing factors: •Inherited predisposition for angiogenesis •Presence of chronic ischemia •Slowly developing blockages increase collateral circulation & allow adequate blood & O2 to heart; except w/ increased workload (e.g. ,exercise) •Rapid-onset CAD or coronary spasm results in severe ischemia or infarction What are the normal levels for cholesterol, HDL, LDL and fasting triglycerides? •Cholesterol 200 mg/dL •High-density lipoproteins (HDL) 40 mg/dL •High HDLs prevent lipid accumulation in arteries •Low-density lipoproteins (LDL) 130 mg/dL •High LDLs increase atherosclerosis and CAD •Fasting triglycerides 150 mg/dL •High levels increase risk for CAD HTN is a major modifiable risk factor for CAD, what are the stages? •Normal BP 120/80 mm Hg •Elevated BP 120 to 129/80 mm Hg •Stage 1 HTN 130 to 139/80 to 89 mm Hg •Stage 2 HTN 140/90 mm Hg •Lifestyle changes for elevated BP & HTN; treat stage 1 or 2 HTN w/ drugs •Elevated BP—endothelial injury leads to LV hypertrophy & reduced SV How does tobacco use increase risk of CAD? second hand smoke? •Nicotine: Increased catecholamine results in increased HR & BP, peripheral vasoconstriction •Increased LDL, decreased HDL, increased oxygen radicals—vessel inflammation and thrombosis •Increased carbon monoxide—reduces O2 carrying capacity of Hgb •Second-hand smoke - Increased CAD 25% to 30% How does DM & metabolic syndrome increase risk for CAD? by how much? -DM—2-4 × CAD •Increased endothelial dysfunction •Altered lipid metabolism, increased cholesterol & triglycerides -Metabolic syndrome •Multiple risk factors related to insulin resistance in

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LEADERSHIP N250 UNIT 2 EXAM QUESTIONS AND

ANSWERS WITH COMPLETE SOLUTIONS GRADED A++


How is CAD characterized? and ACS (acute coronary syndrome)?

-CAD—asymptomatic or chronic stable angina (chest pain)

-Acute coronary syndrome (ACS) —unstable angina (UA) or myocardial infarction (MI)

CAD negatively affects cardiac function; impaired ___________ ____________

and decreased perfusion

cardiac output

Facts about atherosclerosis

•major cause of CAD

•Characterized by lipid deposits within intima of artery

•Endothelial injury and inflammation play a major role in development

How does CAD progress? First stage? pathophysiology?

•Fatty streak: earliest lesion; lipid filled smooth muscle cells; appears yellow

•Start ~age 20 and increase as age

•Tx to lower low-density lipoproteins (LDL) may slow process

Second stage of CAD? pathophysiology?

•Fibrous plaque

•Beginning of progressive change in endothelium; ~age 30

•LDLs & growth factors stimulate smooth muscle proliferation & arterial wall thickens

•Cholesterol & other lipids move into intima

,•Collagen covers & form grayish-whitish fibrous plaque w/ smooth or jagged edges

•Narrowed vessel lumen reduces distal blood flow

Third stage of CAD? pathophysiology?

•Complicated lesion

•Fibrous plaque grows; continued inflammation leads to plaque instability, ulceration, &

rupture

•Platelets accumulate resulting in thrombus that further narrows or occludes artery

•Activation of platelets causes expression of glycoprotein IIb/IIIa receptors to bind

fibrinogen resulting in increased size of thrombus

Fourth stage of CAD? pathophysiology?

•Collateral circulation

•Arterial anastomoses (or connections) within coronary circulation

•Contributing factors:

•Inherited predisposition for angiogenesis

•Presence of chronic ischemia

•Slowly developing blockages increase collateral circulation & allow adequate blood &

O2 to heart; except w/ increased workload (e.g. ,exercise)

•Rapid-onset CAD or coronary spasm results in severe ischemia or infarction

What are the normal levels for cholesterol, HDL, LDL and fasting triglycerides?

•Cholesterol >200 mg/dL

•High-density lipoproteins (HDL) < 40 mg/dL

•High HDLs prevent lipid accumulation in arteries

•Low-density lipoproteins (LDL) > 130 mg/dL

,•High LDLs increase atherosclerosis and CAD

•Fasting triglycerides >150 mg/dL

•High levels increase risk for CAD

HTN is a major modifiable risk factor for CAD, what are the stages?

•Normal BP <120/<80 mm Hg

•Elevated BP 120 to 129/<80 mm Hg

•Stage 1 HTN 130 to 139/80 to 89 mm Hg

•Stage 2 HTN >140/>90 mm Hg

•Lifestyle changes for elevated BP & HTN; treat stage 1 or 2 HTN w/ drugs

•Elevated BP—endothelial injury leads to LV hypertrophy & reduced SV

How does tobacco use increase risk of CAD? second hand smoke?

•Nicotine: Increased catecholamine results in increased HR & BP, peripheral

vasoconstriction

•Increased LDL, decreased HDL, increased oxygen radicals—vessel inflammation and

thrombosis

•Increased carbon monoxide—reduces O2 carrying capacity of Hgb

•Second-hand smoke - Increased CAD 25% to 30%

How does DM & metabolic syndrome increase risk for CAD? by how much?

-DM—2-4 × CAD

•Increased endothelial dysfunction

•Altered lipid metabolism, increased cholesterol & triglycerides

-Metabolic syndrome

, •Multiple risk factors related to insulin resistance including central obesity, HTN,

abnormal serum lipids, & high fasting blood glucose

How can type A personality contribute to CAD?

•Acute & chronic stress, depression, anxiety, hostility & anger, lack of social support

results in increased SNS stimulation results in increased catecholamines results in

endothelial injury, increased HR, increased force of myocardial contraction results in

increased O2 demand

What are some more modifiable risk factors for CAD?

• Increased homocysteine level

•Breakdown of essential amino acid methionine (protein)

•Damage endothelium, promote plaque buildup, enhance clotting

•Substance use like cocaine & meth results in coronary artery spasm resulting in CP &

MI

What does the FITT acronym stand for?

•FITT formula:

•Frequency, Intensity, Type and Time

•30 minutes most days plus weight training 2 days/wk

Which patients should be on statins?

•Patients with known CVD

•LDL cholesterol > 190 mg/dL

•Age 40 to 75 with diabetes and LDL 70 to 189 mg/dL

•Age 40 to 75 with LDL 70 to 189 mg/dL and 10-year risk for CVD at least 7.5%

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