Drug Topics - January 14, 2008 - (Page 33) 33 the incidence of cardiovascular disease. GOAL To provide pharmacists and technicians with knowledge and skills to appropriately manage drug therapy for hypertensive patients Pathophysiology The pathogenesis of hypertension remains uncertain. There are various physiological mechanisms that may lead to essential hypertension. BP may be modulated by the kidneys, the central nervous system (CNS), peripheral nervous system (PNS), and the vascular endothelium. Normal BP is dependent on a balance between cardiac output and peripheral resistance. In essential hypertension, there is a higher level of vascular resistance and usually a normal cardiac output. This may lead to excessive vasoconstriction of the smooth muscle, inducing structural changes to the arteriolar vessel. Renin, a hormone secreted by the kidneys, is produced when there is a lack of perfusion in the glomerulus, reduced salt intake, or in response to stimulation of the sympathetic nervous system (SNS). Renin plays an important role in the renin-angiotensin-aldosterone system (RAAS). RAAS plays a significant role in regulating BP and blood volume. In the presence of renin, angiotensinogen converts to angiotensin I. Angiotensin I converts to angiotensin II via angiotensin converting enzyme. The action of angiotensin II is mediated by the activation of the AT1 receptor. Angiotensin II is a potent vasoconstrictor elevating BP. Aldosterone is also secreted from the adrenal gland in the presence of angiotensin II. Aldosterone causes sodium (Na+) and water retention, leading to elevated BP. Excess stimulation of the SNS may result in peripheral vasoconstriction, elevated heart rate (HR), and release of norepinephrine resulting in elevated BP. Sympathetic stimulation can also lead to vasoconstriction in the renal efferent artery, decreasing renal blood flow and increasing vascular resistance. Hypertension may also be caused by environmental factors such as excess sodium intake, obesity, stress, and genetic factors, such as family history and race. People with two or more first-degree relatives diagnosed with hypertension before age 55 are approximately at four times greater risk for developing hypertension before age 50. The incidence of hypertension is more common and severe in blacks than whites. The reason for the increased incidence among blacks is unknown, but studies have shown lower renin levels. Also, at normal levels of arterial blood pressure, the renal excretion of sodium is not increased to the same degree in response to excess sodium intake. Proteinuria is most commonly seen in conjunction with kidney disease. A patient with normal renal function excretes minimal amounts of protein because albumin is filtered in small amounts due to its large size and anionic character. The glomerular filtration barrier possesses negatively charged proteins, which repel the albumin. Three types of proteinuria can occur in nondiabetic patients with kidney disease: glomerular, tubular, and overflow. Glomerular proteinuria occurs when excess amounts of albumin are transported across the glomerular filtration barrier be- CREDIT This lesson provides two hours of CE credit and requires a passing grade of 70%.* OBJECTIVES Upon completion of this article, the pharmacist and technician should be able to: Describe the pathophysiology of hypertension and proteinuria Discuss the diagnosis and clinical presentations of hypertension and proteinuria and proteinuria’s impact on other disease states Discuss current pharmacologic treatment options for hypertension in conjunction with proteinuria Identify clinical efficacy and safety among the different classifications of antihypertensive agents Explain the role of the pharmacist in hypertension management *To receive credit you must score 70% or higher on the quiz and complete the evaluation. Upon successful completion, the University of Florida College of Pharmacy will mail Statements of Credit for written quizzes within 10 working days. Participants completing the program on-line may print a Statement of Credit after successfully completing the program. cause the glomerular filtration barrier lost its charge and size selectivity allowing excess protein to leak. In tubular proteinuria, smaller molecular weight proteins are unable to be reabsorbed by the proximal tubular cells. Overflow proteinuria is usually caused by the use of immunoglobulin for multiple myelomas. This will induce large amounts of low molecular weight proteins to be excreted secondary to increased production of proteins. Proteinuria occurs when the amount of protein filtered exceeds the reabsorptive capacity of the proximal tubule. In diabetic patients, the physical properties of albumin change. The albumin is in a glycated state secondary to elevation of blood glucose and transforms to an antigenic-like molecule forming free radicals. This causes direct injury to the glomerular filtration barrier leading to loss of size selectivity and impaired ability to filter proteins by the glomerulus. This mechanism allows excess amounts of albumin to be excreted. Diagnosis and clinical presentation of hypertension and proteinuria, and impact on other disease states Hypertension has been called the silent killer because it is usu-
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