Week 7: Chp 31: Arteriosclerosis/ Atherosclerosis

Question 1

What is the primary culprits of many vascular disorders?

Answer 1

• arteriosclerosis

- atherosclerosis

Question 2

Arteriosclerosis

Answer 2

thickening or hardening of the arterial wall that is often associated with aging
-also causes stiffness and a loss of elasticity

Question 3

Arteriosclerosis includes 3 possible pathological processes..

Answer 3

1. Medial calcific sclerosis; occurs when calcium is deposited in the arterial wall
2. Arteriolar sclerosis; involves the thickening of smaller arterioles
3. Atherosclerosis; occurs when low-density lipoprotein (LDL) particles build up in the arterial wall

Question 4

Does a patient with Atherosclerosis have arteriosclerosis?

Answer 4

Yes

Question 5

Risk Factors that potentially stimulate atherosclerotic changes, causing damage to the arterial wall, include:

Answer 5

-elevated cholesterol levels
-elevated triglycerides
-elevated low-density lipoprotein cholesterol (LDL-C)
-low high-density lipoprotein cholesterol (HDLC)
>others include; hypertension, diabetes, smoking, family history, obesity, sedentary lifestyle, hyperlipidemia

Question 6

What greatly worsens atherosclerosis and accelerates growth in the coronary arteries, aorta, and arteries in the legs?

Answer 6

Tobacco smoke
-although cigarette smoke does not directly cause atherosclerosis, cigarette smoke and the by-products of tobacco cause vasoconstriction, hypertension, endothelial cell, and platelet dysfunction and increase circulating cholesterol

Question 7

What is Atherosclerosis?

Answer 7

a disease in which LDL-C particles build up in the arterial wall
-slow, complex disease that typically starts in childhood and progresses while people grow older

Question 8

The lesions of atherosclerosis accumulate where?

Answer 8

large and medium sized arteries

Question 9

How does atherosclerosis begin?

Answer 9

begins from vessel damage

-the vessel damage then causes an inflammatory response

Question 10

Process of Atherosclerosis

Answer 10

• damage to the vessel
• damaged vessel starts an inflammatory response
• LDL goes to the area of damage (damage to endothelium, gives LDL a place to collect/ plaque)
• monocytes respond becoming macrophages that overgorge on the LDL and die becoming foam cells
• while dying the macrophages signal for more help
• LDL continues to call more LDL to “hang out”
• process continues and plaque builds; lumen becomes constricted
• the smooth muscle starts to migrate to “contain” the plaque creating a wall around the plaque
• fatty streaks appear from this inflammatory process
• the plaque continues to grow

Question 11

Process of atherosclerosis from the textbook

Answer 11

• thought to begin from vessel damage that causes an inflammatory response
• after the vessel becomes inflamed, a fatty streak appears on the intimal surface, or inner lining of the artery
• researchers believe that high circulating cholesterol levels promote the deposit of lipids into the arterial wall
• in the presence of inflammatory mediators, they are oxidized by macrophages and perpetuate the inflammatory condition (best described as an inflammatory process comprising a series of highly specific cellular and molecular reactions that lead to the accumulation of atherosclerotic plaque)
• the presence of plaque thickens the inner layer of the artery
• the inner diameter of the artery shrinks, causing a decrease in blood flow, ultimately reducing oxygen supply to the affected tissues

Question 12

What can plaques do?

Answer 12

• can grow large enough to significantly reduce blood flow through an artery
• can rupture that may cause blood clots to form that can block blood flow entirely
• ruptured plaques also have the potential to travel to other parts of the body

Question 13

Clinical Manifestations of Atherosclerosis

Answer 13

may be no symptoms until there is critical narrowing of the artery that results in emergency

• depending on the artery involved, the coronary or carotid arteries, plaque formation and/or rupture can lead to myocardial infarction, unstable angina, sudden cardiac death, or stroke
• atherosclerotic disease in coronaries can result in chest pain or angina, SOB, fatigue, and arrhythmias; also cardiac death
• atherosclerotic disease in the carotids may result in a stroke

Question 14

Atherosclerosis in the coronary arteries can lead to?

Answer 14

• myocardial infarction
• chest pain or angina, unstable angina
• SOB
• fatigue
• arrhythmias
• cardiac death

Question 15

Atherosclerosis in the carotid arteries can lead to?

Answer 15

a stroke
(stroke symptoms; sudden weakness (often one side), dizziness and loss of coordination, difficulty talking, facial droop, sudden vision problems, and sudden and severe headache)

Question 16

Manifestations of a stroke

Answer 16

sudden weakness (sometimes noted more on one side than the other), dizziness and loss of coordination, difficulty talking, facial droop, sudden vision problems, and sudden and severe headache

Question 17

What happens if the blood supply to the arms or legs is reduced?

Answer 17

cause significant pain and difficulty walking (intermittent claudification)

Question 18

What happens if the blood supply is completely occluded peripherally to the affected body part?

Answer 18

can lead to gangrene

death of tissues of the body; can affect any part of the body; toes, fingers, hands, and feet

Question 19

Surgical Intervention

Answer 19

reserved for irreversible manifestations of atherosclerosis such as chest pain or gangrene

• intractable chest pain caused by coronary artery disease requires coronary revascularization which can be done percutaneously or by surgical coronary artery bypass surgery
• gangrene may require amputation

Question 20

Nursing Diagnosis

Answer 20

• risk for ineffective tissue perfusion

- pain r/t decreased blood flow

Question 21

Nursing Interventions: Assessments

Answer 21

-Complete patient history and cardiovascular assessment (genetic and environmental link to cardiovascular disease)
-Assess BP in both arms (hypertension is a risk factor for atherosclerosis)
Palpate pulses at all major sites on the body and note any differences (weak pulses may suggest poor flow through the artery)
-Auscultate for bruits (a turbulent, swishing sounds that can be soft or loud in pitch. It is heard as a result of blood trying to pass through a narrowed artery)
-Fast lipid profile (High LDL-C levels indicate an increased risk for atherosclerosis, target level is < 100; low HDL levels indicate an increased risk for atherosclerosis, target >40)
-Triglyceride levels (may elevate with atherosclerosis; level of 150 or above indicates hypertriglyceridemia)
-Homocysteine (sulfur-containing amino acid derived from a dietary protein. high serum levels may block production of nitric oxide on the vascular endothelium, making the cell walls less elastic and permitting plague to build up
-Glycosylated hemoglobin A1c (HgbA1) (hyperglycemia is a risk for development of atherosclerosis; a hgbA1c of greater than 7% may indicate poor glycemic control)

Question 22

Nursing Interventions: Actions

Answer 22

-administer medications as ordered (antihypertensive, lipid-lowering therapy including statin therapy)

Question 23

Nursing Interventions: Teaching

Answer 23

• BP management
• Healthy diet (low-fat, low-cholesterol; homocysteine levels may be lowered by a diet enriched with B-complex vitamins, particularly folic acid)
• smoking cessation
• Exercise (may lower LDL and increase HDL

Question 24

Nursing Interventions: Auscultate for bruits

Answer 24

bruits is a turbulent, swishing sound that can be soft or loud in pitch
-it is heard as a result of blood trying to pass through a narrowed artery

Question 25

Nursing Interventions: Assess homocysteine level

Answer 25

homocysteine is a sulfur-containing amino acid derived from a dietary protein
-high serum levels may block the production of nitric oxide on the vascular endothelium, making the cell walls less elastic and permitting plaque to build up