BIO 669 Assignment 3 Pulmonary and Renal System Latest updated 2022,100% CORRECT

BIO 669 Assignment 3 Pulmonary and Renal System Latest updated 2022 Pulmonary and Renal System Ms. MC is a 59 yo woman with long history of smoking 1-1.5 packs/day (20+ years) but is no longer smoking. She notices that she fatigues quickly, is often short of breath, coughs frequently and has ankle swelling. She has trouble sleeping but noted some improvement with extra pillows. You note an increase in anteroposterior chest diameter, prolonged expiratory phase with wheezing. She also has cyanosis of nailbeds with moderate pitting edema bilaterally. Lab tests reveal Hgb is high normal, PaO2 is low at 48 mmHg, O2 saturation is at 80%, PCO2 is significantly elevated (70 mmHg) and HCO3- is also elevated above normal (35 mEq/L). Your diagnosis is a combination of chronic bronchitis and emphysema (COPD). Pulmonary function tests revealed a decrease in Vital Capacity and Expiratory Flow Rate combined with an increase in both Residual Capacity and Functional Residual Capacity. These types of tests could also reveal other conditions, such as asthma, as well as guide treatment to prevent significant attacks. 1). What changes occurred in her airways that led to obstruction and increased airway resistance? (Hint: View it in two parts: 1) the airway changes and 2) the alveolar tissue changes relating to elasticity and compliance). (Pulmonary System MO2,3,5,7,8,23,26) Chronic bronchitis and emphysema are the two most common conditions that make up chronic obstructive pulmonary disease (COPD). The most important cause of COPD is smoking cigarettes(John Hopkins Medicine, 2021b). Ms. MC has 20+ year history of cigarette smoking that has directly impacted her health. According to John Hopkins Medicine (2021), chronic bronchitis causes inflammation of the bronchi, common in people who smoke cigarettes. It is defined as, “hypersecretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years (Huether & McCane, 2017, p. 701). Symptoms of bronchitis include: wheezing, productive cough (mucus), “smoker’s” cough, chest discomfort, frequent or severe infections of the lungs, trouble breathing, and narrowing or obstruction of the airway (bronchi). Symptoms may also include, but not always: bluish fingernails, lips, and skin because of hypoxia, sounds of wheezes and crackles when breathing, swelling of the feet and ankles, and heart failure (John Hopkins Medicine, 2021a). Emphysema is damage to lung tissue called alveoli (ALA, 2021). Alveoli are tiny air sacs in the lungs where the gas exchange of oxygen and carbon dioxide (CO2) occur. This is where oxygen is breathed in, that air passes through the alveoli and into the blood, while carbon dioxide is removed (Huether & McCane, 2017). The blood then carries the oxygen throughout the body. When damage occurs, air sacs can narrow, rupture, overinflate, or become stretched. This damage cannot be fixed, leaving permanent holes in the lung tissue. This causes air to get trapped inside the damaged tissue, preventing oxygen from passing through to the bloodstream. Additionally, this blockage causes the lungs to slowly overfill, causing a decrease in respiratory function and shortness of breath (ALA, 2021). Other symptoms can include, but not limited to: cough, rapid breathing, wheezing, sputum production, anxiety, fatigue, and depression (John Hopkins Medicine, 2021c). Ms. MC’s airway changes were caused by chronic bronchitis. In chronic bronchitis inhaled irritants, such as cigarettes can lead to vascular congestion, bronchospasm, mucus secretion, thickening of airway walls, impaired mucociliary function, and increased contractile response of bronchial smooth muscle (Huether & McCane, 2017). This response to irritants causes narrowing, and obstruction of the airway. Ms. MC’s alveolar tissue changes were caused by emphysema as a result of smoking. In emphysema the alveoli are destroyed due to the breakdown of elastin (Huether and McCane, 2017). This alveolar destruction produces large airspaces within the lungs leading to ineffective gas exchange. Expiration is also compromised due to loss of elastic recoil, and leads to air trapping. Ultimately, tobacco smoke is the irritant that caused Ms. MC’s COPD. After inhaling this irritant for many years, inflammation of the airway occurred. According to Huether and McCane (2017), when inflammation occurs, this activates an inflammatory response releasing cytokines that cause a continual irritation and inflammation of the airway, and breakdown of elastin in the connective tissue of the lungs. This has led Ms. MC to chronic bronchitis and emphysema, the two most common causes of COPD. Both bronchitis and emphysema cause airway obstruction, air trapping, ineffective gas exchange, and frequent exacerbations which leads to shortness of breath, cough, hypercapnia, hypoxemia, and cor pulmonale. 2). How does an increased PaCO2, respiratory acidosis, alter the delivery of oxygen to the tissues? (Pulmonary System MO2,5,9,11,12,16) Hypercapnia is increased levels of CO2 in arterial blood. It is caused by hypoventilation of alveoli, which occurs when there is ineffective gas exchange at the alveoli, leading to accumulation of CO2 (Huether & McCane, 2017). Ms. MC’s emphysema has destroyed the alveoli in her lungs, causing a loss of surface air for gas exchange, which has led to hypercapnia. There are many causes of hypercapnia, but two of those causes of large airway obstruction, and increase work of breathing or emphysema. Ms. MC’s condition has directly impacted her ability to get rid of CO2, instead she is retaining it causing hypercapnia, a buildup of CO2 in arterial blood. We know that with Ms. MC having COPD, her respiratory function has decreased, the alveoli are damaged, and gas exchange along with delivery of oxygen (O2) to the tissues, and the removal of CO2, are not taking place as it should. COPD makes in hard for an individual to breathe in oxygen that they need, and to breathe out CO2 the body needs to get rid of. CO2 is also present in bicarbonate ions, and bound to hemoglobin. In contrast, most of the oxygen carried in the blood is bound to hemoglobin, and very few are dissolved (Marhong & Fan, 2014). According to Huether and McCane (2017), the increased levels of CO2 and hydrogen ions decreases the attraction between O2 and hemoglobin. Thus, leading to a decrease in the amount of O2 carried from the lungs, and an increase in the amount of O2 released into the cells. 3) What is a V/Q ratio and how has it changed in Ms. MC’s case? (Pulmonary System MO5,6,9,10) The V/Q ratio is the relationship between ventilation and perfusion. In a healthy individual, a V/Q ratio of 0.8 is normal, where perfusion exceeds ventilation (Huether & McCane, 2017). In Ms. MC’s case, the V/Q ratio is decreased due to worsening ventilation, and decreased vital capacity in her late stages of COPD. In late stages of COPD the V/Q ratio is low due to the obstructed airways, causing hypoxemia. In a rather healthy individual, when hypoxia occurs, they have the ability to balance the V/Q ratio. In an individual with COPD, the person has been hypoxic, and has had an altered V/Q ration for a long period of time, resulting in a hypercapnic drive. The alveolar destruction that is caused by Ms. MC’s emphysema does not allow effective gas exchange, and results is V/Q mismatching and hypoxemia (Huether & McCane, 2017). 4) Why does she have ankle edema? (Hint: there is increased hydrostatic pressure on the venous side of the capillaries leading to an increase in fluid moving into the tissues. What role does the lung play in development of that increased hydrostatic pressure in terms of alveolocapillary membrane/lung changes. What is the effect on oxygen diffusion from the alveolus, on pulmonary artery pressure and resultant changes to the right side of the heart)? (Pulmonary System MO9,13,14,18,25,30) While COPD alone cannot directly cause peripheral edema, there are several other factors associated with COPD that can attribute to peripheral edema, such as: lungs, heart, oxygen level, kidneys, and fluid balance. According to Huether & McCane (2017), pulmonary hypertension is a result of lung disease. Ms. MC’s COPD has led to chronic hypoxemia and chronic acidosis. This chronic hypoxemia results in pulmonary artery vasoconstriction, causing the pulmonary artery pressure to rise. Eventually this increased pressure leads to fibrosis and hypertrophy of the smooth muscle layer of the pulmonary arteries. Over time this chronic pulmonary hypertension causes hypertrophy, and dilation of the right ventricle leading to right sided heart failure (Huether & McCane, 2017). These changes cause pulmonary artery blood flow resistance, increasing pressure in the pulmonary artery and right ventricle. The gas exchange is reduced because of the lung volume restriction (Huether & McCane, 2017, p. 708). When cor pulmonale occurs due to pulmonary hypertension, the right side of the heart loses its ability to pump blood effectively. When the heart cannot pump blood into the lungs, the blood backs up into the systemic circulation leading to an increase in hydrostatic pressure on the venous side of the capillaries. The increase in pressure leads to leaking of fluid from the capillaries into the tissues causing peripheral edema. Five years after being treated for hypercortisolism by you, Ms. J.S. returns with complaint of weight gain (she had lost weight after last visit led to removal of an anterior pituitary tumor that was promoting excessive ACTH release). Her blood pressure had improved as after the 5 year ago visit, but has been rising over the past three years. Stress at work has been worse and her diet suffered as a result. Current blood pressure is 175/110 and you note an abdominal bruit upon examination. This leads you to check plasma renin levels, which came back 10ng/mL per hr (normal is 0.9-3.3ng/mL per hr). A differential renal vein renin test was ordered and showed a difference of 1.6 (normal is 1). *NB The renal vein renin test is no longer used as less expensive and less invasive tests, such as duplex ultrasonography and computed tomographic angiography are now available. I am using this test in this context as a thought-provoking, though now outdated, exercise. The test results were consistent with renal artery stenosis, which an arteriogram confirmed was 85% blocked. An angioplasty is scheduled and her blood pressure is expected to return to normal after the procedure. 5) The turbulent blood flow through the renal artery, narrowed due to atherosclerosis, led to the sound detected upon examination. Why did the differential renal vein renin test show an increase in the blocked renal artery side secretion of renin, yet a drop in renin levels on the other (normal) side? (Renal MO3,4,26) A sampling of blood from the renal veins is taken to assess the blood renin levels. This is done to rule out whether renal artery stenosis is a contributor to an individuals' hypertension. According to Huether and McCane (2017), renin can increase systemic arterial pressure, and alter renal blood flow. This can occur with renal artery occlusion, from stenosis, resulting in a higher renal vein renin ration. The differential showed a drop on the normal side because an increase in pressure was not detected. In the case of Ms. J.S., her body began secreting increased amounts of renin due to the plaque buildup in the stenotic artery, and in turn decreased the blood flow in an effort to increase blood flow to the kidneys. 6) What actions (list 4) of renin lead to increased blood pressure? (Endocrine MO1-4; Cardiovascular MO13; Renal MO6) Renin, by itself, does not increase blood pressure. Renin converts inactive forms of angiotension that are produced by the liver, into active angiotensin I, which then has the capability of altering blood pressure. Once angiotensin is converted into angiotensin I, angiotensin-converting enzyme (ACE), and enzyme found in the lungs, converts angiotensin I into angiotensin II. Angiotensin II causes vasoconstriction, thus increasing blood pressure. Additionally, angiotensin II stimulates the release of aldosterone from the adrenal glands which causes the renal tubules to retain sodium and water, leading to an increase in blood volume (Huether & McCane, 2017). When the renin-angiotensin-aldosterone (RAAS) system becomes overactive, as demonstrated in Ms. J.S.’s case, blood pressure remains high (UKRO, 2020). 7) What medications are available to treat someone who had a genetic predisposition to higher than average renin production (or incomplete/unsuccessful repair of the renal artery stenosis), and thus prevent the adverse effects of high blood pressure? Describe why you feel this is an appropriate treatment (i.e. focusing treatment on the derangement as closely as possible). (Endocrine MO1-4; Cardiovascular MO13; Renal MO6) ACE, angiotensin-converting enzyme, inhibitors prevent the conversion of angiotensin I into angiotensin II, thus prevent vasoconstriction. This helps the body’s blood vessels to relax, decreasing blood pressure. This is an appropriate treatment for someone who has higher than average renin production, to prevent hypertension because it targets hypertension at the source. According to the Mayo Clinic (2019), ACE inhibitors are also commonly used as they lead to little or no side effects, and also treat other conditions, such as heart failure. This would be an appropriate treatment for Ms. J.S. given her heart failure secondary to COPD, and before her angioplasty, and after if the procedure is not successful.