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)2 How does acidosis, such as caused by ketones or CO2 retention, alter the delivery of oxygen to the tissues? (Pulmonary System MO2,5,9,11,12,16)3 What is a V/Q ratio and how does it affect oxygenation of blood in health and disease? In late stages of COPD, such as seen above, how is V/Q altered (Hint, see fig. 27-17) (Pulmonary System MO5,6,9,10)4 Why does she have ankle edema? What role does the lung play in hydrostatic pressure changes seen here? What is the effect pulmonary artery pressure and resultant changes to the right side of the heart? (Pulmonary System MO9,13,14,18,25,30)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 should 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)6 What actions (list 4) of renin lead to increased blood pressure? (Endocrine MO1-4; Cardiovascular MO13; Renal MO6)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)