Hypertension
An intermittent or a sustained elevation in diastolic or systolic blood pressure, hypertension occurs as two major types: essential (idiopathic) hypertension, the most common, and secondary hypertension, which results from kidney disease or another identifiable cause. Malignant hypertension is a severe, fulminant form of hypertension common to both types.
Hypertension is a major cause of stroke, heart disease, and renal failure. The prognosis is good if this disorder is detected early and if treatment begins before complications develop. Severely elevated blood pressure (hypertensive crisis) may be fatal.
Causes
Hypertension affects 15% to 20% of adults in the United States. If untreated, it carries a high mortality. Before age 55, a higher percentage of men than women have high blood pressure. This changes after age 55. (See Incidence of hypertension.)
Gender Influence: Incidence of hypertensionGender and age play a role in who suffers from hypertension.
Prior to age 55, men are more likely than women to have high blood pressure.
Between ages 55 and 74, women are slightly more likely than men to have high blood pressure, but after age 74, the incidence of high blood pressure in women becomes significantly higher than in men.
Women taking hormonal contraception (especially women who are overweight or obese) are two to three times more likely than women not taking them to have high blood pressure.
Risk factors
Family history, race (most common in blacks), stress, obesity, a high intake of saturated fats or sodium, use of tobacco, sedentary lifestyle, and aging are risk factors for essential hypertension. Insulin resistance has also been implicated in some patients.
Clinical TipSystolic hypertension poses a risk that’s equal to or greater than diastolic elevations. It’s commonly seen in elderly people and presents a risk for stroke or myocardial infarction (MI).
Secondary hypertension may result from renovascular disease; pheochromocytoma; primary hyperaldosteronism; Cushing’s syndrome; thyroid, pituitary, or parathyroid dysfunction; coarctation of the aorta; pregnancy; neurologic disorders; and use of hormonal contraceptives or other drugs,
such as cocaine, epoetin alfa, and cyclosporine.
such as cocaine, epoetin alfa, and cyclosporine.
Blood pressure regulators
Cardiac output and peripheral vascular resistance determine blood pressure. Increased blood volume, cardiac rate, and stroke volume as well as arteriolar vasoconstriction can raise blood pressure. The link to sustained hypertension is unclear. Hypertension may also result from the failure of the following intrinsic regulatory mechanisms:
Renal hypoperfusion causes the release of renin, which is converted by angiotensinogen, a liver enzyme, to angiotensin I. Angiotensin I is converted to angiotensin II, a powerful vasoconstrictor. The resulting vasoconstriction increases afterload.
Angiotensin II stimulates adrenal secretion of aldosterone, which increases sodium reabsorption. Hypertonic-stimulated release of antidiuretic hormone from the pituitary gland follows, increasing water reabsorption, plasma volume, cardiac output, and blood pressure.
Autoregulation changes the diameter of an artery to maintain perfusion despite fluctuations in systemic blood pressure. The intrinsic mechanisms responsible include stress relaxation (vessels gradually dilate when blood pressure rises to reduce peripheral resistance) and capillary fluid shift (plasma moves between vessels and extravascular spaces to maintain intravascular volume).
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