Nursing 581-Week 5 Questions - Copy

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QUESTIONS: WEEK 5 NURSING 581: ADVANCED PATHOPHYSIOLOGY FIONNUALA BROWN, DNP, MSN, FNP-C, APRN GROUP 4 HALEY DONOVAN BETH FEUSTEL CAROL GIJIMA LEANNE NIXON ANNE GIAMPIETRO

1. How does sarcomere cross-bridge formation lead to muscle cell contraction? • Contraction of cardiac muscle is accomplished by shortening of individual sarcomeres. This is due to increased overlap of actin and myosin filaments. • Myosin heads bind to specific sites on actin and pull the thin filaments toward the center of the sarcomere, resulting in contraction. • Cross-bridging energy is provided by ATP hydrolysis. When myosin has a high affinity for actin, it binds to sites on actin and pulls thin filaments in, resulting in cardiac muscle contraction. When myosin has a low affinity for actin, the cross- bridge is broken and the muscle relaxes. Figure 1. https://courses.lumenlearning.com/suny-ap1/chapter/muscle-fiber-contraction-and-relaxation /

2. How are action potentials generated and conducted in myocardial and pacemaker cells? • The ratio of intracellular to extracellular K+ determines the membrane potential which is approximately –80 mV. When the membrane potential reaches threshold (+20mV), voltage-gated sodium channels open and there is a rapid influx of Na+. This results in depolarization. • The sodium channels then close and potassium enters the cell through K+ channels. This results in the inside of the cell being more positively charged and K+ leaves the cell. As K+ ions leave, calcium ions enter through slow voltage gated calcium channels. • Calcium ions entering the cell causes muscle contraction. Calcium channels then close and there is also a rapid efflux of K+ from the cell through potassium channels, causing a return to resting membrane potential. • Pacemaker discharge is the result of spontaneous generation of action potentials which occur due to Na+ and calcium leaking into the cell through channels that open during repolarization. • The pacemaker rate is determined by the rate of cation leak into the cell. K+ efflux slows the rate and is controlled by the PNS. Na+ and calcium influx increases the rate and is controlled by the SNS. Figure 2. https://www.ezmedlearning.com/blog/actionpotential

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3.What is the role of injury, inflammation, and lipid oxidation in coronary plaque initiation and progression? • Step 1: In normal conditions, the vascular endothelium is smooth and creates almost no friction with blood, along with creating a barrier for numerous molecules and cells found in the blood. But once this homeostasis is disrupted by some factor, such as wall stress such as in hypertension, or certain toxins, such as those from cigarettes, this endothelium becomes damaged and leaky. • Step 2: In such conditions, LDL particles enter the intima of the blood vessel from the blood, where they are recognized by the endothelial macrophages. These macrophages oxidize those LDL particles which begin the sequence of reactions. Additionally, the injury to the vascular endothelium also initiates an inflammatory reaction with the recruitment of the leukocytes. • Step 3: As the macrophages are in contact with oxidized LDL particles, they start to produce additional cytokines which will further attract leukocytes to that site and prolong the inflammation equally important, some of these cytokines will stimulate the proliferation of the smooth muscle tissue in the intima of the blood vessels where it normally shouldn't be found. • Step 4: As the inflammation is continuously stimulating incoming leukocytes, the endothelium continues to be leaky and if LDLs are abundant in blood, they continue to enter the intima, where they become oxidized. As more and more debris and macrophages with engulfed LDLs (foam cells) accumulate, the bigger and bigger the atherosclerotic plaque becomes. • Step 5: As the plaque becomes bigger, the structure of the endothelium changes more and more and becomes more unstable. Apart from decreasing the lumen of the blood vessel, these atheroma are also likely to rupture over time, leading to thrombosis of the vessel where they are located, with brain and coronary arteries being the most dangerous locations. Figure 3. https://www.mdpi.com/2076-3921/11/10/1958

4. How do the clinical features of the coronary heart disease syndromes differ? Coronary syndromes are a group of disorders that include: 1. Angina pectoris- stable angina, Prinzmetal variant angina 2. Acute coronary syndrome- unstable angina and MI Clinical features of angina pectoris are: • Stable angina: Stable angina pectoris is predictable and involves narrow, atherosclerotic coronary vessels that decrease coronary blood flow, leading to intermittent myocardial tissue ischemia. Narrowed coronary arteries cannot respond to increased cardiac workload with effective dilation. This is usually recurrent and can be brought on by anything that increases myocardial oxygen demand: exercise, stress, activation of the SNS, increased preload or afterload, changes in heart rate, or increased muscle mass. Pain symptoms resolve with nitroglycerin and rest. • Prinzmetal variant angina - Vasoplastic angina involves spasming of the coronary arteries, unrelated to any kind of exertion or increased myocardial oxygen demand. Vasospastic angina is unpredictable chest pain, sometimes at rest. It is unrelated to physical or emotional exertion. Clinical features of the acute coronary syndrome are: • Acute coronary syndrome is a result of acute occlusion and include unstable angina and MI. Clinical presentation for unstable angina and MI are similar with sudden onset of chest pain, which is severe and lasts longer that typical angina, nausea, diaphoresis, and shortness of breath. • In unstable angina , the occlusion is partial, or the clot is dissolved before the death of myocardial tissue. • In MI , the occlusion is complete, with the thrombus persisting long enough for irreversible damage to the myocardial cell to occur. This can result in necrosis. Treatment in the acute phase includes acute reperfusion with fibrinolytic therapy.

5. How does heart failure with primarily systolic dysfunction differ from heart failure with primarily diastolic dysfunction? • Systolic dysfunction is heart failure with a low ejection fraction. In this type of heart failure, contractility of the heart muscle is reduced, either because of the damaged and lost muscle cells, beta1 receptor down-regulation, impaired production of ATP, or impaired calcium ion regulation. Heart failure with reduced ejection fraction = systolic dysfunction. Systolic dysfunction is impaired contraction. • Diastolic dysfunction is heart failure with preserved ejection fraction. The muscle of the heart is non-compliant and relaxation is impaired. A person with diastolic dysfunction has all the symptoms of heart failure just like the ones with systolic dysfunction, but his/her ejection fraction is normal. Heart failure with preserved ejection fraction = diastolic dysfunction. Diastolic dysfunction is impaired relaxation.

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6. What are the clinical manifestations of heart failure? Signs and symptoms of heart failure are: • Forward effects are the same for either right-sided, left-sided, or biventricular failure and include confusion, anxiety, impaired memory, mental fatigue, and restlessness. Urine output will decrease resulting in fluid retention (due to poor kidney perfusion). There may also be activity intolerance, fatigue, and lethargy. • Backward effects depend on the ventricle affected. In left-sided heart failure, the backward effects are due to pulmonary dysfunction which results in pulmonary edema. Clinical findings/signs include SOB, nonproductive cough, orthopnea, dyspnea upon exertion, paroxysmal nocturnal dyspnea, respiratory crackles, presence of S3 gallop, hypoxemia, and high left atrial pressure. Figure 4. https://ksumsc.com/download_center/Archive/3rd/437/Teamwork/1-Medicine/1st%20Semester/4-Heart%20 Failure.pdf Figure 5. https://ksumsc.com/download_center/Archive/3rd/437/Teamwork/1-Medicine/1st%20Semester /4-Heart%20Failure.pdf • In right-sided heart failure, backward effects are due to systemic venous congestion which results in impaired function of the kidneys, liver, brain, portal system, peripheral subcutaneous tissue, and the spleen. Clinical findings/signs include ascites, hepatomegaly, splenomegaly, JVD, subcutaneous edema, abdominal discomfort and anorexia.

References Figure 1. https://courses.lumenlearning.com/suny-ap1/chapter/muscle-fiber-contraction-and-relaxation/ Figure 2. https://www.ezmedlearning.com/blog/actionpotential Figure 3. https://www.mdpi.com/2076-3921/11/10/1958 Figure 4. https://ksumsc.com/download_center/Archive/3rd/437/Teamwork/1-Medicine/1st%20Semester/4-Heart%20F ailure.pdf Figure 5. https://ksumsc.com/download_center/Archive/3rd/437/Teamwork/1-Medicine/1st%20Semester/4-Heart%20F ailure.pdf

Nursing 581-Week 5 Questions - Copy

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