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. Explain the pathophysiology of chronic bronchitis and how it relates to COPD Chronic bronchitis is caused by inhalation of irritants that promote bronchial inflammation. This inflammation causes bronchial Edema, increase in the size and number of mucus glands and goblet cells, smooth muscle hyper trophy with fibrosis and narrowing of the airway. Explain the pathophysiology of chronic bronchitis and how it relates to COPD Increased secretions of thick mucus that patient cannot cough up due to impairment of ciliary function. Explain the pathophysiology of chronic bronchitis and how it relates to COPD As disease progresses, the smaller airways are involved as well as the large airways. These airways, due to hyper trophy, cause narrowing of smooth muscle and obstruct airflow, especially during expiration. The obstruction can lead to VQ mismatches. Patient was hypoxic as evidence by the low PaO2. Explain the pathological processes that caused this patient's hypoxemia Arterial hypoxemia early in acute pneumococcal pneumonia is principally caused by persistence of pulmonary artery blood flow to the consolidated lung resulting in an intrapulmonary shunt, and by ventilation perfusion mismatch later. Patient was hypoxic as evidence by the low PaO2. Explain the pathological processes that caused this patient's hypoxemia Release of mediators cause widespread inflammation of the bronchial structures, especially the alveolar capillary membrane. The alveoli collapse due to an inactivation of surfactant and the alveoli fill with exudate, decreasing surface area for gas exchange. Explain why patients with COPD are at risk for malnutrition Many of the patients with severe COPD are lean, and frequently in a malnourished and under nourished state, which is characterized by loss of fat free body mass causing muscle wasting. Explain why patients with COPD are at risk for malnutrition The muscle wasting in COPD not only leads to decrease skeletal muscle function associated with reduce exercise capacity but it also is a major determinant of mortality in COPD. Explain why patients with COPD are at risk for malnutrition Patients with COPD require a low carbohydrate diet as increased CHO can lead to hypercapnia as the end products of CHO metabolism are CO2 and H2O. What factors may have contributed to the development of PUD Stress secondary to divorce and financial situations, cigarette smoking, alcohol consumption, use of NSAIDs, excess coffee consumption, positive h pylori test How do these factors contribute to the formation of peptic ulcer's Chronic use of NSAIDs causes suppression of mucosal prostaglandin and a direct irritative topical effect. High gastrin level and excessive gastric acid production is often seen in Zollinger-Ellison syndrome which can be caused by gastrinoma. How do these factors contribute to the formation of peptic ulcer's Smoking impairs healing by vasoconstriction. H pylori causes gastritis and interferes with mucosa What causes GERD? GERD manifestations result directly from gastric acid reflux into the esophagus. Pyrosis, the classic symptom, is a substernal burning sensation typically described as heartburn. It may be accompanied by regurgitation, particularly in someone who has recently eaten. What causes GERD? The lower esophageal sphincter (LESS) relaxes due to certain medications (calcium channel blockers), hiatal hernia, and obesity allows stomach contents into the lower esophagus causing inflammation and possibly erosion of the esophagus What factors can contribute to an upper G.I. bleed Upper G.I. bleeds can be caused by peptic ulcer disease (PUD) which remains the most common cause of you UGIB. Esophageal bleeding from a Mallory-wise tear What can cause diverticulitis in the lower G.I. tract Diverticulitis is defined as an inflammation of one or more diverticula. Fecal material or undigested food particles may collect in a diverticula causing obstruction. The obstruction can cause vascular compromise. What can cause diverticulitis in the lower G.I. tract Increased intraluminal pressure or food particles cause erosion of the diverticular wall, resulting in inflammation, localized necrosis, and perforation. How does cirrhosis cause portal hypertension Portal hypertension results from an increase in resistance or blood flow in the portal venous system. How does cirrhosis cause portal hypertension In cirrhosis the most common cause of portal hypertension is the formation of scar tissue and regenerative nodules that lead to an increase in intrahepatic vascular resistance and consequently portal pressure. How does cirrhosis cause portal hypertension Hepatitis and the resultant inflammation and subsequent scarring also contributes to portal hypertension. Chronic right sided heart failure can also cause portal hypertension due to the increase in preload that the right ventricle cannot pump effectively Discuss how ascites develops as a result of portal hypertension There are several theories that contribute to ascites. In the underfilling theory the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed to the portal hypertension and a subsequent decrease in effective circulating blood volume. Discuss how ascites develops as a result of portal hypertension This underfilling theory activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention. Discuss how ascites develops as a result of portal hypertension The overflow theory postulates that increased portal pressure along with decreased serum albumin cause capillary hydrostatic pressure to exceed capillary oncotic pressure pushing transudative fluid into the peritoneal cavity Overflow theory of ascites postulates that increased portal pressure along with decreased serum albumin cause capillary hydrostatic pressure to exceed capillary oncotic pressure pushing transudative fluid into the peritoneal cavity Underfilling theory of ascites