NURS 6501 Mod 1-4 Questions & Answers Solved 100% Correct!!

NURS 6501 Mod 1-4 Questions & Answers Solved 100% Correct!! Why is HDL considered good cholesterol? It's able to remove cholesterol from artery plaques and recycle it back to the liver. Why is HDL consider good cholesterol HDL is considered good cholesterol because it collects excess cholesterol in the body cells and transports it to the liver where it is excreted. HDL carries 20 to 25% of total plasma cholesterol. Explain the role inflammation has in the development of atherosclerosis Inflammation in the heart muscle caused by chronic inflammatory processes leads to mitochondrial damage that results in an increased free radical production that further activates the chronic inflammatory vicious cycle Explain the role inflammation has in the development of atherosclerosis Activated mast cells recruit inflammatory cells that provoke plaque formation and lead to atherosclerosis. Chronic inflammatory infiltrates occupy layers of arteries were stable plaques are formed and associated with atherosclerosis. Explain the role inflammation has in the development of atherosclerosis Additionally active inflammation involves a thinning at the fibrous Of atherosclerotic plaque which predisposes vulnerable plaque to rupture. Why does the APRN recognize as the result of the pleural friction rub? The inflammation of the pericardium due to either the underlying autoimmune disease or a post viral syndrome causes roughening of the pericardium. This causes the classic rug which can be best heard at the Apex of the heart and left sternal border. Explain how a positive strep test has caused the patient's symptoms Rheumatic heart disease RHD only develops after a pharyngeal infection with group a beta hemolytic streptococcus. It is an abnormal response to humoral and cell mediated response to M proteins. Inflammation causes proliferative and exudative lesions in connective tissue. Explain how a positive strep test has caused the patient's symptoms Inflammation causes scarring of the valve tissue. Inflammation usually affects the endocardium which contains the valves. Endocardial inflammation causes swelling of leaflets in the valves. Describe the factors that could have contributed to the development of a DVT in this patient and explain how each of the factors could cause DVT Virchow's Triad caused damage to the walls of the vessels. Injury to the intimal layer of the vessel, antiplatelet substances such as nitric oxide and prostacyclin, along with the expression of collagen on the vessel wall, causes adherence to the platelets to the vessel wall. Describe the factors that could have contributed to the development of a DVT in this patient and explain how each of the factors could cause DVT Platelets become activated, then aggregate, forming clots. Venous stasis is a result of obesity, patients advanced age, and inability to perform physical therapy therapy. Explain why large pulmonary embolus interferes with oxygenation The embolus lodges somewhere in the pulmonary circulation and causes a ventilation/perfusion mismatch V/Q. Ventilation perfusion mismatch or V/Q defects are defects in total long ventilation perfusion ratio. Explain why large pulmonary embolus interferes with oxygenation It is a condition in which one or more areas of the lung receive oxygen but no blood flow, or they receive blood flow but no oxygen due to obstruction somewhere in the pulmonary circulation. This causes a decreased area for oxygen exchange. Explain why a large pulmonary embolism causes right ventricular strain The V/Q mismatch causes release of neurohumeral substances and inflammatory mediators that cause vasoconstriction of the pulmonary vasculature further impeding oxygenation. Explain why a large pulmonary embolism causes right ventricular strain Hemodynamically this vasoconstriction results in pulmonary hypertension, making it difficult for the right ventricle to pump blood. Explain why a large pulmonary embolism causes right ventricular strain The V/Q mismatch also creates decreased production of surfactant causing atelectasis that further decreases surface area available for oxygen exchange. Explain early asthmatic responses in the cells responsible for the responses When there is an initial airway exposure to an antigen, an innate and adaptive immune response is initiated. Explain early asthmatic responses in the cells responsible for the responses Cells that can initiate the inflammation of the bronchial mucosa and hyperresonance of the airways include Dedrick cells, T-helper 2 cells, lymphocytes, B lymphocytes, mast cells, neutrophils, eosinophils, and basophils. Explain early asthmatic responses in the cells responsible for the responses Early asthmatic response is a phase of bronchospasm that peaks at about 30 minutes and usually resolves after about 3 hours. Explain late asthmatic responses in the cells responsible for the responses Late asthmatic responses are mediated by earlier exposure in early phase that causes a latent release of inflammatory mediators. These mediators, leukotrienes and prostaglandin D, cause bronchospasm, edema, and mucus secretions that obstruct airflow. Explain late asthmatic responses in the cells responsible for the responses Airway obstruction creates resistance to airflow and causes air trapping. Continued air trapping increases intrapleural and alveolar gas pressure, decreases ventilation and perfusion leading to uneven and variable ventilation/perfusion in the lung. Explain the pathophysiology of emphysema and how it relates to COPD Emphysema is a disease of the airways that causes permanent enlargement of the gas exchange airways. It is accompanied by destruction of the alveolar walls and does not appear to be fibrotic. Explain the pathophysiology of emphysema and how it relates to COPD Chronic exposure to irritants recruit neutrophils, macrophages, and lymphocytes to the lung resulting in progressive damage from inflammatory oxidative stress. Explain the pathophysiology of emphysema and how it relates to COPD Emphysema is characterized by destruction of alveoli leading to decrease surface area for gas exchange that causes significant ventilation/perfusion mismatch.