Porth's Essentials of Pathophysiology, 4e

427

Disorders of Blood Flow and Blood Pressure

C h a p t e r 1 8

angiotensinogen and the ability of adipose tissue to increase aldosterone levels through the production of factors that induce aldosterone production. 40 Regular alcohol consumption plays a role in the development of hypertension. 41 The effect is seen with different types of alcoholic drinks, in men and women, and in a variety of ethnic groups. One of the first reports of a link between alcohol consumption and hyperten- sion came from the Oakland-San Francisco Kaiser Permanente Medical Care Program study that corre- lated known drinking patterns and blood pressure levels of 84,000 persons. 42 This study revealed that the regular consumption of three or more drinks per day increases the risk for hypertension. Systolic pressures were more markedly affected than diastolic pressures. Blood pres- sure may improve or return to normal when alcohol consumption is decreased or eliminated. Secondary Hypertension Secondary hypertension, which describes an elevation in blood pressure due to another disease condition, accounts for 5% to 10% of hypertension cases. 43 Unlike essential hypertension, many of the conditions causing secondary hypertension can be corrected or cured by surgery or specific medical treatment. Secondary hyper- tension tends to be seen in persons younger than 30 and older than 50 years of age. Among the most common causes of secondary hypertension are kidney disease (i.e., renovascular hypertension), adrenal cortical disor- ders, pheochromocytoma, and coarctation of the aorta. Oral contraceptive agents are also implicated as a cause of secondary hypertension. Cocaine, amphetamines, and other illicit drugs can also cause a significant eleva- tions in blood pressure, as can sympathomimetic agents (decongestants, anorectics), erythropoietin, and licorice (including some chewing tobaccos with licorice as an ingredient). Obstructive sleep apnea is an independent risk factor for secondary hypertension. Renal Hypertension. With the dominant role that the kidney assumes in blood pressure regulation, it is not surprising that the largest single cause of secondary hypertension is renal disease. Most acute kidney disor- ders result in decreased urine formation, retention of salt and water, and hypertension. This includes acute glo- merulonephritis, acute renal failure, and acute urinary tract obstruction. Hypertension also is common among persons with chronic pyelonephritis, polycystic kidney disease, diabetic nephropathy, and end-stage kidney dis- ease, regardless of cause. In older persons, the sudden onset of secondary hypertension often is associated with atherosclerotic disease of the renal blood vessels. Renovascular hypertension refers to hypertension caused by reduced renal blood flow and activation of the renin-angiotensin-aldosterone mechanism. It is the most common cause of secondary hypertension, accounting for 1% to 2% of all cases of hypertension. 44 The reduced renal blood flow that occurs with renovas- cular disease causes the affected kidney to release exces- sive amounts of renin, increasing circulating levels of

angiotensin II. Angiotensin II, in turn, acts as a vasocon- strictor to increase peripheral vascular resistance and as a stimulus for increased aldosterone levels and sodium retention by the kidney. One or both of the kidneys may be affected. When the renal artery of only one kidney is involved, the unaffected kidney is subjected to the detri- mental effects of the elevated blood pressure. There are two major types of renovascular disease: (1) atherosclerosis of the proximal renal artery, and (2) fibromuscular dysplasia, a noninflammatory vas- cular disease that affects the renal arteries and branch vessels. 44,45 Atherosclerotic stenosis of the renal artery accounts for 70% to 90% of cases and is seen most often in older persons, particularly those with diabetes, aortoiliac occlusive disease, coronary artery disease, or hypertension. 44 Fibromuscular dysplasia is more com- mon in women and tends to occur in younger age groups, often persons in their third decade. 45 Genetic factors may be involved, and the incidence tends to increase with risk factors such as smoking and hyperlipidemia. Diagnostic tests for renovascular hypertension may include studies to assess overall renal function, physi- ologic studies to assess the renin-angiotensin system, perfusion studies to evaluate renal blood flow, and imaging studies to identify renal artery stenosis. 44 Renal arteriography remains the definitive test for identifying renal artery disease. Duplex ultrasonographic scanning, contrast-enhanced CT scans, and magnetic resonance angiography (MRA) are other tests that can be used to screen for renovascular hypertension. 44 The goal of treatment for renal hypertension is to control the blood pressure and stabilize renal func- tion. Angioplasty or revascularization has been shown to be an effective long-term treatment for the disor- der. Angiotensin-converting enzyme (ACE) inhibitors may be used in medical management of renal steno- sis. However, these agents must be used with caution because of their ability to produce marked hypotension and renal dysfunction. Disorders of Adrenocortical Hormones. Increased levels of adrenocortical hormones also can give rise to hypertension. Primary hyperaldosteronism (excess pro- duction of aldosterone due to adrenocortical hyperplasia or adenoma) and excess levels of glucocorticoid (Cushing disease or syndrome) tend to raise the blood pressure 30,46 (see Chapter 32). These hormones facilitate sodium and water retention by the kidney; the hypertension that accompanies excessive levels of either hormone prob- ably is related to this factor. For patients with primary hyperaldosteronism, a sodium-restricted diet often pro- duces a reduction in blood pressure. Because aldosterone acts on the distal renal tubule to increase sodium absorp- tion in exchange for potassium elimination in the urine, persons with hyperaldosteronism usually have decreased potassium levels. Screening tests for primary hyperaldo- steronism involve the determination of plasma aldoste- rone concentration and plasma renin activity. Computed tomography and magnetic resonance imaging scans are used to localize the lesion. Persons with solitary adeno- mas are usually treated surgically. Potassium-sparing