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Primary essential hypertension

Hypertension is one of the two principal risk factors of many cardiovascular diseases, such as coronary heart disease (CHD), stroke, and CHF. Individuals are considered hypertensive if their systoHc arterial blood pressure is over 140 mm Hg (18.7 Pa) or their diastoHc arterial blood pressure is over 90 mm Hg (12 Pa). Over 60 million people, or one-third of the adult population in the United States are estimated to be hypertensive (163). About 90% of these patients are classified as primary or essential hypertensive because the etiology of their hypertension is unknown. It is generally agreed that there is a very strong genetic or hereditary component to this disease. [Pg.132]

The aim of therapy is straightforward reduction of blood pressure to within the normal range. When hypertension is secondary to a known organic disease, such as renovascular disease or pheochromocytoma, therapy is directed toward correction of the underlying malady. Unfortunately, about 90% of cases of hypertension are of unknown etiology. The therapy of primary, or essential hypertension, as these cases are generally called, is often empirical. [Pg.226]

Prazosin [MinipressJ. Prazosin is a competitive alpha-1 antagonist that has emerged as one of the primary alpha-1 selective agents. It tends to produce vasodilation in both arteries and veins, and is used primarily in the long-term management of essential hypertension.38 Prazosin has also been used to reduce alpha-1 receptor mediated activity in congestive heart failure, Raynaud phenomenon, pheochromocytoma, and BPH. Prazosin is administered orally. [Pg.281]

In most cases, elevated blood pressure is associated with an overall increase in resistance to flow of blood through arterioles, while cardiac output is usually normal. Meticulous investigation of autonomic nervous system function, baroreceptor reflexes, the renin-angiotensin-aldosterone system, and the kidney has failed to identify a primary abnormality as the cause of increased peripheral vascular resistance in essential hypertension. [Pg.226]

North of England Hypertension Guideline Development Group (2006) Essential hypertension managing adult patients in primary care. Centre for Health Services Research, University of Newcastle upon Tyne. Available at http //www.nice.org.uk/ nicemedia/pdf/CG18background. pdf [Accessed 3 July 2008],... [Pg.23]

The adverse effect of smoking on renal function in patients without primary renal disease has also been well documented. Smoking was the most powerful predictor of progression in patients with severe essential hypertension in the study of Regalado [40] and, as reflected by an increase of serum creatinine > 3 mg/dl, also in the study of Bleyer [41]. [Pg.897]

Interpretation Responses must be defined for the assay technique used. Patients with renin-dependent forms of hypertension (e.g., renovascular hypertension) show values that are approximately five times normal. Stimulated responses are also seen in patients with high-renin essential hypertension, pheochromocytoma, and Barttei s syndrome. Patients with hypertension firom mineralocorticoid excess (e.g., primary aldosteronism) usually have PRA below the concentration of assay sensitivity. Patients with hyporeninemic hypoaldosteronism usually have low concentrations of plasma renin and low aldosterone concentrations. Figure 51-17 shows typical responses. [Pg.2020]

The determination of plasma renin responsiveness, however, is not sufficient to diagnose primary aldosteronism because suppressed PRA also occurs in about 25% of patients with essential hypertension. Primary aldosteronism can be differentiated from other hypermineralocorticoid states on the basis of inappropriate secretion of aldosterone. The demonstration of an elevated concentration of aldosterone in blood or urine in a patient with an unequivocally suppressed PRA concentration (a plasma aldosterone/ plasma PRA ratio >50) is presumptive evidence of primary aldosteronism. Because hypokalemia has a suppressive effect on aldosterone secretion, the potassium deficit should be replaced before aldosterone measurements are done. To establish aldosterone autonomy, the clinician may attempt to suppress aldosterone production with rapid volume expansion (see Box 51-10), with a potent mineralocorticoid (see Box 51-11), or as mentioned with captopril. Failure... [Pg.2032]

Schwartz GL, Turner ST. Screening for Primary Aldosteronism in Essential Hypertension Diagnostic Accuracy of the Ratio of Plasma Aldosterone Level to Plasma Renin Activity. Clin Chem 2005 51 386-94. [Pg.2052]

Fardella CE, Mosso L, Gomez-Sanchez C, et al. Primary hyperaldosteronism in essential hypertensives Prevalence, biochemical profile, and molecular biology. J Clin Endocrinol Metab 2000 85 1863-1867. [Pg.1405]

Hypertension is classified as either essential (primary) or secondary. Essential hypertension comprises approximately 90% of all cases. Its causes are still unknown. The disease is incurable but treatable (i.e., it is controllable, with drugs). The remaining 10% constitute a number of hypertensive diseases with causes that are known. Some can be cured. The following outline is a classification of hypertension. [Pg.418]

Essential hypertension Hypertension of unknown cause also called primary hypertension... [Pg.98]

TYPES. High blood pressure is classified as (1) secondary hypertension, or (2) primary or essential hypertension. Most individuals suffer from primary or essential hypertension. [Pg.557]

Printary or Essential Hypertension. Unfortunately, relatively few individuals demonstrate a clear-cut cause of hypertension. Rather, about 90% of the people suffering from high blood pressure show no single, easily identifiable cause. This type of high blood pressure is called primary, or essential, or sometimes idiopathic hypertension. [Pg.557]

PREVENTION. Most Americans who suffer from high blood pressure suffer from primary or essential hypertension—a condition without specific causes. Hence, preventive measures are difficult to designate. However, some suggestions can be made based on the current knowledge. [Pg.558]

It sooms to us therefore... that the theory of primary renal origin is unproved. So tar as the genesis of essential hypertension is concerned, the kidney appears to be the victim rather than the culprit. ... [Pg.549]

Treatment of essential or primary hypertension emphasizes not only the lowering of the elevated blood pressure, but also individualized therapy for each patient, providing each patient with minimized unnecessary side effects. The patient s cardiovascular morbidity and mortaUty should be decreased and end organ damage reversed or reduced (184,185). [Pg.132]


See other pages where Primary essential hypertension is mentioned: [Pg.14]    [Pg.416]    [Pg.14]    [Pg.416]    [Pg.142]    [Pg.275]    [Pg.607]    [Pg.124]    [Pg.295]    [Pg.692]    [Pg.214]    [Pg.144]    [Pg.28]    [Pg.49]    [Pg.288]    [Pg.289]    [Pg.299]    [Pg.307]    [Pg.247]    [Pg.275]    [Pg.607]    [Pg.111]    [Pg.130]    [Pg.205]    [Pg.2032]    [Pg.186]    [Pg.191]    [Pg.193]    [Pg.410]    [Pg.1116]    [Pg.38]    [Pg.107]    [Pg.109]    [Pg.557]    [Pg.341]   
See also in sourсe #XX -- [ Pg.416 ]




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